CLINICAL PROFILE, RADIOLOGICAL AND OPERATIVE FINDINGS...

CLINICAL PROFILE, RADIOLOGICAL AND OPERATIVE

FINDINGS OF SURGICALLY MANAGED INTERNAL CAROTID

ARTERY COMMUNICATING SEGMENT ANEURYSM:

A RETROSPECTIVE STUDY

Submitted for M.Ch Neurosurgery

By

Dr. Shashank Aroor

October 2017

Department of Neurosurgery

Sree ChitraTirunal Institute for Medical Sciences

& Technology

Thiruvananthapuram – 695011

CLINICAL PROFILE, RADIOLOGICAL AND OPERATIVE

FINDINGS OF SURGICALLY MANAGED INTERNAL CAROTID

ARTERY COMMUNICATING SEGMENT ANEURYSM:

A RETROSPECTIVE STUDY

Submitted by : Dr. Shashank Aroor

Programme : M.Ch Neurosurgery

Month & year of submission : October, 2017

DECLARATION

This thesis titled ―Clinical profile, radiological and

operative findings of surgically managed Internal Carotid Artery

communicating segment aneurysm: A retrospective study‖, is a

consolidated report based on a bonafide study of the period from

January 2013 to May 2017, done by me under the Department of

Neurosurgery, Sree Chitra Tirunal Institute for Medical Sciences

& Technology, Thiruvananthapuram.

This thesis is submitted to SCTIMST in partial fulfillment

of rules and regulations of MCh Neurosurgery examination.

Dr. Shashank Aroor,

Department of Neurosurgery,

SCTIMST,

Thiruvananthapuram.

CERTIFICATE

This is to certify that the thesis entitled ―Clinical profile,

radiological and operative findings of surgically managed Internal

Carotid Artery communicating segment aneurysm: A retrospective

study‖ is a bonafide work of Dr.Shashank Aroor and was conducted in

the Department of Neurosurgery, Sree Chitra Tirunal Institute for

Medical Sciences & Technology, Thiruvananthapuram (SCTIMST),

under my guidance and supervision.

Prof. Mathew Abraham,

Professor and Head of the Department,

Department of Neurosurgery,

SCTIMST,

Thiruvananthapuram

ACKNOWLEDGEMENT

The guidance of Prof. Mathew Abraham, Professor and Head of the

Department of Neurosurgery, has been invaluable and I am extremely

grateful and indebted for his contributions and suggestions, which were

of invaluable help during the entire work. He will always be a constant

source of inspiration to me.

I owe a deep sense of gratitude to Dr. Suresh Nair for his

invaluable advice, encouragement and guidance, without which this work

would not have been possible. His critical remarks, suggestions, helped

me in achieving a high standard of work.

I am deeply indebted to Dr. Easwer H. V, Dr. Krishnakumar K.,

Dr. George Vilanilam, Dr Jayanand Sudhir, Dr. Prakash Nair, Dr Tobin

George and colleagues and I thank them for their constant encouragement

and support.

I am also deeply indebted to Dr Santhosh Kumar (Department of

imaging sciences and interventional radiology, SCTIMST) for guiding

and helping me in the radiological interpretation.

I owe a deep sense of gratitude to all my patients without whom

this work would not have been possible.

I am very grateful to my family for their constant encouragement

and moral support.

INDEX

INTRODUCTION 1

AIM AND OBJECTIVE 3

MATERIALS AND METHODS 4

REVIEW OF LITERATURE 9

RESULTS 42

DISCUSSION 63

CONCLUSION 79

LIMITATION OF THE STUDY 80

BIBLIOGRAPHY 81

ANNEXURES 98

i. Proforma

ii. IEC approval

iii. Originality index

iv. Master chart abbreviations

v. Master Chart

Introduction

1

INTRODUCTION

The communicating segment of the internal carotid artery is the

segment between the origin of posterior communicating artery (PcoA)

and the bifurcation of internal carotid artery (ICA).(1,2) The

communicating artery aneurysm are the second most common location

for anterior circulation aneurysm. The incidence of PcoA aneurysm as

quoted in the literature is 15%–25% of all intracranial aneurysms. (12,30)

Communicating segment aneurysm can present with subarachnoid

hemorrhage or third nerve palsy. Successful surgical management of

aneurysms of the PCoA depends on precise understanding of their unique

microsurgical anatomy, avoidance of pitfalls, and the surgeon’s

experience. PCoA gives rise to many important branches supplying the

optic chiasm, oculomotor nerve, mammillary body, tuber cinerum,

cerebral crura, ventral thalamus, and rostral portion of the caudate

nucleus. (3) Interruption of flow through these vessels may result in

ischemic damage to the diencephalon with significant morbidity, even

after an apparently uneventful surgical procedure.

The outcome depends on pre operative, intra operative and post

operative factors. Various factors like Glasgow coma scale at the time of

admission, Fischer grade on computerised tomography scan, presence of

Introduction

2

third nerve palsy, intra operative rupture, need for temporary clipping,

direction of aneurysm, presence of hydrocephalus, post operative

vasospasm will affect the final outcome. The literature available till date

is descriptive of risk factors, clinical presentation and surgical outcome of

communicating segment aneurysms. (5,7)There are comparisons in

literature on endovascularly and surgically treated aneurysms. (24)

Studies to determine the outcome based on multiple preoperative,

intra operative and post operative factors are lacking. In this study we

have tried identifying multiple pre operative , intra operative and post

operative risk factors which could affect outcome.

Aim and objective

3

AIM AND OBJECTIVE

AIM : To understand the varied clinical picture, radiological and

operative findings of good grade patients with symptomatic,

angiographically proven, surgically managed ICA communicating

segment aneurysm.

OBJECTIVE:

1.To study the outcome of operated posterior communicating artery

aneurysm.

2.Factors influencing outcome

The outcome would be measured as quality of life, presence or

absence of neurological deficit and independence to work using modified

rankin score.

Material and Methods

4

MATERIAL AND METHODS

Total of 100 consecutive patients who underwent surgical clipping

for symptomatic angiographically proven Internal carotid artery (ICA)

communicating segment aneurysm between January 2013 and May 2017

were analysed. Retrospective data of patients was recorded from the

SCTIMST database. Follow up at 3 months was done based on SCTIMST

records database.

Inclusion criteria:

Patients who presented with symptomatic angiographically proven

ICA communicating segment aneurysm and then underwent

surgical management.

WFNS grade 1 and 2

Exclusion criteria:

Giant aneurysm; size > 2.5 cm

Patient lost to follow up


5

The following factors were studied:

Pre operative factors :

1. Age

2. Sex

3. Symtom to surgery

4. Presenting complaints like headache, vomiting, diplopia, seizure.

5. Neurological deficits like third nerve palsy, hemiparesis or

hemiplegia.

6. Radiological features like Fischer grading, presence of

hydrocephalus, infarct, intraventricular blood, hematoma.

7. Aneurysmal factors like shape, number of lobes, direction of

fundus, size of aneurysm and neck, relation to PCoA and

perforators, presence of teet or bleb, fetal PCoA.

Intra operative factors:

1. Intra operative rupture

2. Temporary clipping

3. Duration of temporary clipping


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4. Type of clip used

5. Number of clip

6. Fundus opened or not

7. Relation to third nerve

8. Presence of atherosclerosis and calcification

9. Opening of lamina terminalis

Post operative factors:

1. Early and late infarct

2. Hematoma

3. Vasospasm

4. Need for CSF diversion like VP shunt

5. Decompressive craniectomy

6. Tracheostomy

7. Duration on ventilator

8. Post operative hospital stay

9. GCS at day 5 and discharge


7

10. Rankin score at disharge

11. Deficit at discharge

12. Death

Follow up at 3 months:

1. Rankin score

2. Deficit

3. GCS

Outcome parameters: Rankin score at discharge and follow up at 3

months was primary outcome parameter. Factors predicting the outcome

were studied. Rankin score 0 and 1 was considered as excellent functional

outcome, 2 as mild disability, 3 and more as poor outcome. (43,61)

Statistical analysis: All pre operative, intra operative and post

operative variables were compared between the groups based on outcome

variables. Two -tailed Student t-tests , Mann- Whitney U test and Kruskal

Wallis test for continuous variables and Fisher exact test or Chi square

test for categorical variables was used. For factors which had association

with outcome variables simple logistic regression analysis was performed

to look at the odds ratio and confidence interval. For those which were


8

significant after simple regression analysis multivariable regression

analysis was performed to adjust the effect in order to see the independent

factors predicting outcome. A p value of 0.05 or less was considered

statistically significant. All statistical calculations were made with widely

available SPSS software (SPSS 22.0).

Review of Literature

9

REVIEW OF LITERATURE

Posterior communicating artery aneurysm are the aneurysm that

arise from the communicating segment of internal carotid artery.

ANATOMY:

The posterior communicating artery (PCoA) bisects the supra-

clinoid internal carotid artery (ICA) into an ophthalmic segment from the

distal dural ring to the PCoA, and a communicating segment from the

PCoA to ICA bifurcation. (Fig 1)The PCoA originates from the

posterolateral surface of the proximal internal carotid artery, curves after

its origin and then sweeps posteromedially. It travels along the superior

surface of the oculomotor nerve, and intersects the posterior cerebral

artery (PCA) to mark the end of the P1 segment and the beginning of the

P2 segment. Approximately eight anterior thalamoperforating arteries

originate from the superior surface of the PCoA along its course and

ascend to the hypothalamus, anterior thalamus, internal capsule, tuber

cinereum, floor of third ventricle, posterior perforated substance, optic

chiasm and tract, and pituitary stalk.(1-3). PCoA aneurysms almost

always arise from the superior aspect of the PCoA along the lateral

surface of the ICA.(Fig 2)The anterior choroidal artery (AChA) is the

most important branch associated with PCoA aneurysms, lying adjacent


10

to the distal neck. The AChA arises from the posterior wall of the

communicating segment, but can also arise from the PCoA,ICA

bifurcation and the proximal M1 segment. Damage to AchA can cause

hemiplegia, hemianesthesia, and hemianopsia. Hence while treating

PCoA Aneurysm PCoA, thalamoperforators and AchA should be taken

care of. (3)

Figure 1:Superior view showing origin of Posterior communicating

artery dividing ICA into communicating and ophthalmic segment.

Figure 2: Showing the origin of PCoA aneurysm.

BA: Basilar artery, Tent: Tentorium, MCA: Middle cerebral artery, ICA: Internal carotid artery, OphA:

Ophthalmic artery, PCA: Posterior cerebral artery, SCA, Superior cerebellar artery, III: Third nerve, II:

Optic nerve

Figure 1 Figure 2


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Fetal posterior cerebral artery (PCA) is an important variant.

During embryogenesis, the PCoA initially supplies the occipital lobe, but

the P1 segment enlarges to supply this territory and the PCoA shrinks to

produce the classic circle of Willis anatomy. The transformation fails to

occur in as many as 20% of patients, and the P1 segment remains

hypoplastic or atretic. The fetal PCA must be recognised and preserved

when clipping PCoA aneurysms because its compromise can result in

occipital lobe infarction.(4)

The direction of the dome of the PCoA aneurysm has significant

surgical implications. A classification system was described by

Yasargil.(4) When the fundus points anterolaterally, the origin of the

PCoA artery may be hidden by the aneurysm. In addition, the aneurysm

may be adherent to the clinoid process requiring careful dissection so that

the fundus may be mobilised and the origin of the PCoA is visualised

during application of a clip. A superolateral fundus is occasionally

encountered in which the dome points into the sphenoid ridge.

Haemorrhage of these aneurysms may cause a subdural hematoma. In

contrast, a posterolateral superior fundus points into the temporal lobe

and is often associated with an intraparenchymal hemorrhage and/or

hemorrhage into the temporal horn of the ventricle. A posterolateral

inferior fundus often penetrates the Liliquist membrane pointing into the


12

interpeduncular fossa. These aneurysms are also associated with

oculomotor nerve palsy. A posteromedial inferior dome is rarely

encountered. These aneurysms are often sidewall aneurysms of the

ICA.(5)

Pathology of formation of aneurysm:

The underlying mechanism in formation of aneurysm are

multifactorial (6).Cebral JR et al in their study on aneurysm have

analysed that the rupture of saccular aneurysm is the consequence of the

inability of the wall to contain the hemodynamic loads and rupture occurs

when wall stress exceeds wall strength (7). Aneurysm occur by

degenerative changes secondary to hemodynamic stress (8). Degeneration

and repair have a balance until aneurysm rupture. Hemodynamic stress

leads to degenerative endothelial damage which exposes collagen leading

to formation of a fibrin matrix that triggers a repair process that remodels

the wall of the aneurysm, modifying the geometry and creating aberrant

flow conditions in the lumen. As the repair and degeneration process

continues the repair mechanisms are interrupted and the aneurysm wall

matrix degenerates and becomes too fragile to resist hemodynamic

pressure and eventually the aneurysm ruptures (9)

The location of the aneurysm is an important factor that influences

the hemodynamics, wall structure and determines whether the peri-


13

aneurysmal environment is constraining or protective for aneurysmal

rupture. (7). Saccular aneurysms usually arise at the distal carina of

arterial bifurcations, where the vessels are exposed to maximum impact

of wall shear stress.(10). PCoA aneurysm tend to be more common

because of the turbulence created by the arterial origin at an angulation

with ICA. Several studies have shown that smooth contact of the

aneurysm with surrounding structures provide protective support to the

aneurysm dome by decreasing the wall stresses near the fundus, while

increased wall stresses can be created by sharp contacts(11). PCoA

aneurysm touch the surrounding intra cisternal and juxta cisternal

structures including cranial nerves, adjacent brain parenchyma, cranial

base bone, dural folds, dura mater, bridging and surface veins, small

arteries, and arachnoid trabeculae. A PCoA aneurysm projecting laterally

will be unable to extend beneath the oculomotor nerve and will compress

the superomedial aspect of the oculomotor nerve. In addition, when the

PCoA aneurysm extends laterally, the aneurysm dome comes into contact

with surrounding hard structures such as the tentorial free edge and

deformation may be observed on the dome(12). Hence PCoA aneurysm

attached to tentorium are more susceptible for rupture whereas those

attached to third nerve can present with symptomatic third nerve palsy.


14

Risk factors for aneurysmal rupture:

Age and gender: The incidence of aneurysm increase with

increasing age. The maximum incidence is between 50 - 70 years

thereafter decreases(12, 13). Female gender is considered to be risk factor

for both aneurysm formation and growth, with aneurysms 1.6 times more

likely to occur in women than in men.(12) The cause of increased female

predilection is not clear as most of the risk factors like smoking,

hypertension, atherosclerosis are more common in men. (14) As the

incidence of subarachnoid haemorrhage (SAH) is found to occur more in

the post-menopausal period, a mechanism involving compromised arterial

integrity as a result of a drop in estrogen levels has been proposed. (14,

15)

Hypertension: Hypertension is considered as an independent risk

factor for SAH. Rivero Rodriguez et al in their study on patients with

subarachnoid haemorrhage found unfavourable outcome with

hypertension.(16). The underlying mechanism is proposed to be the

endothelial damage and remodelling created by hypertension leads to

increase incidence of aneurysmal formation and rupture.Intracranial

arteries are composed of the outer layer of the adventitia, a muscular

media that maintains most of the vessel wall integrity and the inner layer

of intima. They are different from other vessels in the body as they do not


15

possess external elastic lamina. Therefore, there is less elasticity of the

media in addition to the thinner adventitia compared to the extracranial

artery wall. These vessels are also situated in the subarachnoid space,

which has no surrounding connective tissue to support the vessels. These

factors make intracranial arteries susceptible to the formation of saccular

aneurysms, making their occurrence fairly common in hypertensive

patients. (17,18,19)

Hyperglycemia: Hyperglycemia has been associated with

morbidity and poor outcome in patients with SAH(16, 20). Several

studies have shown that systemic glucose levels affect glucose

availability to the brain and can impact cellular metabolism and energy

production. Aneurysmal SAH patients have impaired glucose transport

and systemic glucose levels fluctuation can significantly affect the

cerebral metabolic demand(16, 21)

Other like ethnic race, family history, cigarette smoking are

considered as risk factors for aneurysm formation and rupture. Prevalence

of aneurysm is higher in Caucasian than in African American patients.

(7). Autosomal Dominant Polycystic Kidney Disease (ADPKD) or Ehlers

- Danlos Syndrome (EDS) Type IV, have been associated with

intracranial aneurysms.(7)


16

Clinical presentation:

Symptomatic third nerve palsy and sub arachnoid haemorrhage

(SAH) are the most common presentations of PCoA aneurysm. 1.3-7.9%

of aneurysms may present with a subdural hematoma (SDH) and PCoA

aneurysm is responsible for the haemorrhage is 43% of cases.(5, 22)

Presentation as third nerve palsy:

The course of the oculomotor nerve parallels the PCoA. The nerve

originates from the interpeduncular fossa of the midbrain, courses

between the P1 PCA and superior cerebellar artery (SCA). It attaches to

the membrane of Liliequist and climbs to the oculomotor triangle, a dural

space bordered by the tentorial edge laterally, the petrous apex

posteriorly, and the interclinoidal line medially (the line between the

anterior and posterior clinoid processes). The nerve enters its dural sleeve

at the triangle’s anterior apex to exit the subarachnoid space and travel in

the roof of the cavernous sinus, just below the anterior clinoid process.

PcoA aneurysm projecting posteriorly laterally and slightly inferiorly will

impact the nerve in the cisternal segment of nerve. Resulting palsy will

cause diplopia, the eye deviation laterally and inferiorly, or the ―down

and out‖ eye. Involvement of pupillary fibres will cause mydriasis. Palsy

of levator palpebrae superioris will cause ptosis. (23). These palsies may

be complete or incomplete.(24)


17

Approximately 38% of patients with PCoA aneurysms develop

oculomotor palsy as their presenting symptom(3, 25). Roughly 70% of

patients present with a complete oculomotor nerve palsy, while 30%

present with a partial oculomotor nerve palsy (5). Acute third nerve palsy

can occur with an expanding PCoA aneurysm. Therefore, such a clinical

presentation requires urgent evaluation and treatment. Compression,

either by enlargement of the aneurysm or pulsation of the aneurysm, is

considered as the main cause for third nerve palsy.(26). Absence of

oculomotor palsy indicates that the aneurysm may either be small in size,

or be projecting posterolaterally above the tentorium or medially

involving the inferior wall of the ICA.(3) Treatment of intracranial

aneurysms should not be delayed even if patients do not have

subarachnoid haemorrhage(26). Long-term nerve compression results in

neuronal injury and neural degeneration affecting postoperative recovery.

Several studies found that oculomotor palsy is irreversible even after

decompression if the symptoms lasted more than 4 weeks.(26)

The size of the aneurysm is considered to be one of the most

important reasons for direct compression of the nerve. Teasdale et al.

reported in their series of 27 patients with unruptured PCoA aneurysms

found that third nerve palsy is caused by anuerusym that are 7 mm or

greater (81). The curve of ICA also determines the risk of third nerve


18

palsy. Yanaka et al. has mentioned that unruptured aneurysms measuring

less than 10 mm can cause third nerve palsy when the anterior cavernous

genu of the ICA forms an acute angle and the supraclinoid portion runs

posterolaterally.(29) Kurokawa et al. also pointed out that when the

intracranial part of the ICA ran horizontally, rather than vertically, along

the cranial base, even small ICA–AChA aneurysms could cause third

nerve palsy(27, 28)

The ICA to anterior -posterior clinoid process distance is the novel

concept used to explain the presence of absence of third nerve palsy. All

ICAs run under the anterior–posterior clinoid (ACP) process, and it is

easy to measure the ICA–APC distance using the recently developed

radiological modalities. In study by Anan et al, the ICA– APC distance

was significantly shorter in patients with positive third neve palsy than in

the negative third nerve palsy group. (27, 29). This means that the PCoA

aneurysm should be closer to the third nerve when the ICA runs closer to

the skull base. The pulsatility of the ICA may more easily affect the nerve

when the ICA–APC distance is short.(27)


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Presentation as SAH:

Size, location, shape and projection determining risk of rupture :

PCoA aneurysm even if they are unruptured carries a high risk of

rupture. International Study of Unruptured Intracranial Aneurysms

(ISUIA) study gives the impression that small aneurysms < 7mm in

anterior circulation have a minimal risk of rupture(12). But the rupture

risk for PCoA aneurysm matches that of rupture risk of posterior

circulation aneurysm. (5)The prevalence of small ruptured PCoA

aneurysms are particularly high, with 87.5% of aneurysms measuring less

than 10 mm in diameter and 40% measuring less than 5 mm in diameter.

(7, 12). According to Laplace’s law (which states that the tension

required to withstand a given pressure increases with the diameter of a

vessel), the critical diameter for rupture is proportional to the average

wall thickness. This suggests that aneurysms at smaller arteries may

rupture at smaller sizes since they had initially thinner walls. These

observations seem to indicate that rupture risk depends on the location,

and that aneurysms at the PCoA are more prone to rupture than

aneurysms at other locations even in smaller size(7)

Japanese study on the natural course of unruptured cerebral

aneurysms (Unruptured Cerebral Aneurysm Study [UCAS]) also showed

that a PCoA aneurysm is more likely to rupture(12) .


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The bleb formation is frequently associated with rupture. In a

recent study focusing on bleb formation in an effort to gain insight into

the mechanisms underlying aneurysm rupture, the highest shear stress

values were at or adjacent to the bleb formation(12). Non-spherical

shapes (oval, oblong and multilobulated) are found to be associated with

rupture. (7) Similarly true PCoA aneurysm have also higher chance of

rupture at smaller size. (5)

Similarly laterally projecting aneurysm are more likely to rupture

due to peri aneurysmal environment characteristics like attachment to

tentorium.

Morphological and hemodynamic factors affecting rupture:

Morphological factors like Aspect ratio, size ratio, inflow angle

and hemodynamic factors like wall shear stress, oscillatory shear index,

normalised wall shear stress are considered as risk factors for aneurysmal

rupture. The aspect ratio (AR) between ruptured and unruptured

aneurysms was found to be significantly different, with almost 80% of

ruptured aneurysms having AR>1.6 while almost 90% of unruptured

aneurysm having AR<1.6 (7). In a study by Lv N et al the inflow angle

was considered as significant factor for aneurysm rupture.Aneurysm with

more inflow angle had higher risk of rupture.(30). But once the aneurysm


21

ruptures it is difficult to measure these morphological and hemodynamic

factors.

True PcoA aneurysm and risk of rupture:

―True‖ PCoA aneurysms are the on in which the aneurysm actually

arises from the PCoA artery as opposed to the junction with the ICA.

They are rare, accounting for 4.6–13% of PCoA aneurysms (0.1–2.8% of

all intracranial aneurysms)(31) True PCoA aneurysms typically arise

within 2–3 mm of the ICA (31, 32). They tend to be smaller than

junctional PCoA aneurysms, but have higher risk of rupture(7)They have

have a classic appearance on imaging where dome projects posteriorly.

True PCoA aneurysms are often associated with a dominant PCoA, in

which the PCoA is the major blood supply to the posterior cerebral artery.

(31).The thalamoperforating arteries can arise from the PCoA both

proximal and distal to the aneurysm(31). Hence preservation of both

PcoA and thalamoperforating arteries are important in clipping of these

aneurysms. (31)


22

Imaging of PCoA aneurysm:

CT plain:Plain CT is used as an initial investigating tool for

detecting subarachnoid blood. In acute setting the higher attenuation of

blood as compared to normal parenchyma allows 100 % sensitivity for

diagnosis SAH within first 6 hours.(33). Although CT is an excellent

modality for evaluating acute subarachnoid hemorrhage, in the subacute

setting, from six hours to one week after hemorrhage, the ability to detect

subarachnoid hemorrhage with CT drops dramatically because of the

brain’s normal degradation of hemorrhagic blood products. The

sensitivity drops as the days passes after SAH and comes down to 85 %

after five days, 50 % after one week, and 30 % after two weeks (33, 34)

In one study the sensitivity of CT to detect SAH dropped to 36.5% after

five days. (33)A ruptured PCoA aneurysm is suggested when clots are

located in the ipsilateral carotid cistern, which may extend into the

interpeduncular and the Sylvian cisterns. Massive rupture of an aneurysm

may cause a temporal lobe hematoma or an intraventricular hemorrhage.

Persistent localised clot on delayed CT confirms the location of the

ruptured aneurysm in cases of multiple aneurysms.(3). Attention should

be paid to the calcified ICA because temporary clips cannot be applied to

the stiff ICA. Exposure of the carotid artery from the neck is mandatory

in such patients.


23

Several grading systems have come through ages to predict the

severity of SAH and risk of developing vasospasm. Davis et al used a

four-point scale and correlated with development of vasospasm (35, 36).

The primary limitation of this classification was that it did not allow

distinctions to be made between large and small collections of blood in a

specific subarachnoid compartment.

Friedman et al in a retrospective study found a high correlation

between severe vasospasm and the presence of subarachnoid clots greater

than 5 X 3 mm in diameter in cisterns and fissures in horizontal plane and

clot greater than 1 mm thickness in vertical plane. They graded the blood

in cisterns and fissures to assess the risk of vasospasm. (36, 37). Fischer

grade is used to assess the degree of SAH based on the cisternal blood.

Hijdra and colleagues demonstrated the importance of intra

ventricular blood(IVH). (36, 38). Classen et al used the IVH in addition

to cisternal blood and demonstrated that a modified Fischer scale is better

predictor of outcome in terms of vasospasm. (36, 39)


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Table 1: Showing modified Fischer grading for SAH(36,38):

Grade Description

0 No subarachnoid blood

1 Minimal / thin SAH, no IVH in both lateral ventricle

2 Minimal / thin SAH, with IVH in both lateral ventricle

3 Thick SAH and no IVH in both lateral ventricle

4 Thick SAH with IVH in both lateral ventricle

CT angiogram: This is helpful in determining the location and

aetiology of the haemorrhage.(33)Studies have shown 97 % sensitivity

rate for detection of all aneurysm sizes(33, 40) The relationship between

anterior clinoid process and aneurysm can be found on CT angiogram.

Prominent posterior clinoid process can hinder the process of clip

placement and can be assessed pre operatively on CT angiogram. (3)

MRI for detection of SAH and aneurysm: MRI has advantages

over CTA in that it does not use ionising radiation and offers the ability to

obtain images without the need for administration of intravenous contrast

agents. Fluid attenuated inversion recovery (FLAIR) sequences produce

strong T2 weighting while suppressing the cerebrospinal fluid (CSF)

signal and can be particularly useful for detecting subarachnoid


25

haemorrhage especially in subacute period. (33) Rocha et al had

demonstrated 100 % sensitivity for subacute SAH for MRA as compared

to 66 % for CTA (41). The use of time-of-flight (TOF) sequences on

MRA eliminates the need for administration of contrast agents(33). MRA

is generally not the diagnostic test of choice for the evaluation of cerebral

aneurysms in the acute setting and is reserved as a screening test or for

follow-up.

Angiogram: Angiography is the most reliable study to define the

precise location, size, neck, shape, and direction of the aneurysm, and to

confirm the presence of multiple aneurysms. It can separately evaluate

the arterial, capillary, and venous phases. (33) The direction of PCoA

aneurysm gives the idea of attachment to surrounding structures. Postro

laterally projecting aneurysm can be attached to oculomotor nerve or

tentorium while laterally projecting aneurysm may be attached to

temporal lobe. The latter condition might require removal of uncus. A

short and dilated ICA or closed carotid siphon hinders use of a temporary

clip on the ICA proximal to the PCoA. It may be necessary to drill off the

anterior crinoid process or expose the carotid artery in the neck for

proximal control in such cases. PCoA is found medial to the ICA on the

anterior-posterior view of the angiogram. This means that the PCoA can

be exposed easily in the opticocarotid triangle. Fetal type PCoA appears


26

overlapped with the ICA on the anterior-posterior projection of the

angiogram.The relationship between the AChoA and the aneurysm

should be defined to ensure that this vital artery remains patent after clip

placement. The assessment of collateral circulation on cross- compression

study may predict the tolerance of temporary occlusion of the ICA. It is

also important to assess the venous drainage pattern of the sylvian and the

deep venous systems, all of which should be preserved to prevent

postoperative venous infarction. (3)

Predicting whether the anterior clinoidectomy is needed or not can

be done by pre operative angiogram. It was first mentioned by Ochiai et

al. in 1989 (42). In the study by Ochiai et al, anterior clinoidectomy was

necessary in 3 patients with internal carotid–PCoA aneurysms. The

authors noted that the distance between the posterior wall of the carotid

―knee‖ of the clinoidal ICA and the proximal neck of the aneurysm on

lateral angiography in 3 cases of anterior crinoid process resection was

shorter than 9.6 mm. (42) However, the number of cases was too small to

reveal any statistical significance. Along with measurement of the

distance from the aneurysm to the ACP, evaluation of the tortuosity of the

ICA, provide valuable parameters to predict the necessity of ACP

removal in PCoA aneurysm surgery. (15)


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Treatment options:

The treatment options for ruptured PCoA aneurysm is either

clipping or coiling. Several studies have shown that the mortality and

morbidity is equal for both clipping and coiling with respect to ruptured

PCoA aneurysm. International Subarachnoid Hemorrhage Aneurysm

Trial (ISAT) showed that coiling is better in terms of functional outcome

based on mRS score with respect to PCoA aneurysm.(43). But the rate of

rebreeding and recurrence was higher in coiling group. Several

drawbacks are associated with ISAT trial as only 20% of patients were

randomised, study was done mainly in European centres, predominantly

small aneurysm and low grade haemorrhages were taken to consideration,

used CT angiogram to randomise instead of angiogram.

This lead to Barrow ruptured aneurysm trial and Chinese trial. (44,

45) BRAT 6 year follow up showed clipping is as good as coiling for

anterior circulation aneurysm and coiling to be better for posterior

circulation aneurysm. In BRAT trial PCoA was grouped under anterior

circulation. Chinese study had also not shown difference between coiling

and clipping for PCoA aneurysm. Lanzino et al conducted a meta-

analsysis on the 3 prospective controlled studies. Pooled data showed

poor outcome at 1 year to be lower in the immobilisation group and no

difference in mortality between group. Rebleeding rates within the first


28

month were higher in coiled patients. Long term follow up showed

similar results between the groups(46). Surgical clipping has lower re

operative rates, lower rebelled rates and can also relieve the

hydrocephalus. The treatment for ruptured PCoA aneurysm is mainly

clipping. Over the years due to microsurgical techniques the outcome of

clipped PCoA aneurysm have significantly improved.(47,48)

Intra operative characters and technique of clipping:

Craniotomy:

The standard pterional craniotomy position, head elevation with

neck extension and rotation of 30 degree to opposite side is used for

clipping of these aneurysm. (3). In patients with short supraclinoid

ophthalmic segment of the ICA, dilated and calcified arteriosclerotic ICA

or closed carotid siphon, the draping of neck for cervical carotid exposure

is required for proximal control. (3)A standard pterional craniotomy is

fashioned for an exposure allowing a wide range of inclination for the

clip-applying forceps.The sphenoid ridge is drilled off down to the

superior orbital fissure, and the orbital roof and the subtemporal bone are

flattened to get an unobstructed view along the cranial base. The dura is

incised based on sphenoid ridge and margin of dura is everted and pulled

over a sponge with traction stitches to minimise epidural bleeding and to

prevent blood from dripping into the field (3)


29

Brain relaxation:

Brain relaxation is the key to the rapid and atraumatic exposure of

PCoA aneurysms in the carotid cistern. Adequate brain relaxation can be

obtained by opening the cisterns. It may sometimes be necessary to open

the Liliequist membrane or lamina terminalis to relieve the intracranial

pressure. Opening of lamina terminalis is an effective way of relieving

intra cranial pressure. (3,4)

Opening of sylvian fissure:

The frontal operculum can be detached from the temporal lobe by

opening the Sylvian fissure. Incision of the arachnoid membrane

connecting the fissure is easy and atraumatic when the brain is fully

relaxed and the fissure is filled with CSF or blood. (Fig 4 )After

assessment of the cerebral venogram including the venous drainage

pattern through the Sylvian and deep venous system, the distal Sylvian

fissure is entered on the frontal side of the Sylvian vein (86).One or more

veins bridging the Sylvian fissure may be encountered, and these may be

sacrificed as necessary. Deep cerebral veins such as the deep middle

cerebral vein, the basal vein of Rosenthal, and the deep vein of the orbital

lobe in the fissure should be preserved to prevent venous infarction even

if the deep veins limit the opening of the fissure. A sharp dissection

prevents injury of the pial membrane of the frontal operculum.


30

As the fissure is split, the frontal lobe can be mobilised and

retracted progressively. Dissection is then directed to the chiasmatic

cistern overlying the optic nerve. As the thick arachnoid bands connect

the frontal side of the proximal Sylvian fissure with the temporal side, it

is necessary to cut the bands to release the frontal and temporal lobes.

Wide opening of the Sylvian fissure exposes the M1 and M2 segments of

the middle cerebral artery and the carotid bifurcation. After this

procedure, the whole length of the supraclinoid ICA as well as the

aneurysm can be exposed with minimal brain retraction.(3,4,86)

Figure 4: Steps of dissection for approaching posterior communicating

artery aneurysm (86)

Approach to neck of aneurysm:

The carotid cistern is opened along the medial border of the ICA.

The proximal ICA is prepared for temporary occlusion. If the exposed

ophthalmic segment of the ICA is too short for temporary clip placement,


31

it is necessary to drill off the anterior clinoid process. Sometimes the

aneurysm is hidden under the uncus or embedded in a large amount of

clot. Therefore, it can be very dangerous to expose the aneurysm by

removing the clot from the dome of the aneurysm before applying the

temporary clips. The distal PCoA is usually identified in the opticocarotid

triangle, which is the space formed by the ICA, the optic nerve, and the

A1 segment of the anterior cerebral artery. It may be difficult to expose

the fetal type PCoA before clip placement because the artery is usually

hidden beneath the ICA or the aneurysm. As the dissection is continued

toward the carotid bifurcation, the AChoA can be identified, and the

distal neck of the aneurysm is usually found immediately proximal to the

artery. It may be much safer to remove the uncus around the aneurysm by

a small subpial resection than by attempting hazardous dissection and

retraction to expose the neck of the aneurysm and the proximal PCoA.

This subpial dissection is an appropriate technique for safe exposure of

the aneurysm, because it leaves the pia and arachnoid attached to the

dome, and reduces the risk of mechanical violation. (3)Temporary clips

may be used when further dissection of the neck of the aneurysm appears

risky.


32

Identification of aneurysm neck:

Majority of PCoA artery aneurysm originate distal to the PCoA

origin. Tracing the posterolateral wall of the proximal ICA can help in

identification PCoA origin, which is often visualised as a knuckle (Fig

4)(47).

In contrast to traditional PCoA aneurysms, for which the aneurysm

dome may be readily visible, true PCoA aneurysms most commonly arise

in what is typically an intra-operative blind spot 2–3 mm posterior to the

origin of the PCoA at the ICA. The PCoA should thus be followed

posteriorly to visualise the neck of the aneurysm. (31)

Clip placement:

Once the neck of the aneurysm is defined, the clip is advanced

between the PCoA and the AChoA. For wide-necked aneurysms, the clip

is placed parallel to the ICA to avoid ―dog ear‖ remnants or stenosis of

the ICA. Care should be taken to exclude branches of the ICA from the

clip blades.

When it is impossible to clip an inferior wall aneurysm of the ICA

because of the branches, wrapping-with-clipping can be done. Wrapping

includes placing a muscle or cellulose fabric circumferentially which

leads to fibrosis around the aneurysm. A bent clip is applied over the


33

fabric that is encircling the ICA and the aneurysm, while both ends of the

fabric are held together with forceps (3). When branches or perforators

prevent circumferential application of the fabric, it may be necessary to

split the fabric partially into two or three strips to accommodate the

branches or perforators without squeezing. If the neck of the aneurysm is

torn during dissection or clip placement, a piece of cellulose fabric sheet

or muscle is placed on the torn site and a clip is used to seal the tear.

Papaverine solution is instilled around the ICA and its major

branches to relieve possible vasospasm caused by manipulation after

removing the temporary clips. Direct application of concentrated

papaverine on the oculomotor nerve is avoided as it may cause mydriasis.

The clip and the aneurysm neck are inspected to confirm the

complete occlusion of the aneurysm and the sparing of the branches,

including the PCoA and the AChoA and perforators.

It is also important to check for the possibility of clip movement or

rotation after release of the brain retractors, because the repositioning of

the frontal operculum or the temporal pole may push the handle of the

clip. (3)


34

Complications:

Intra operative complications relating to the nature of aneurysm:

PCoA aneurysms with a posterior projection is correlated with a

higher incidence of intraoperative complications than those with a lateral

projection. Posterior projecting aneurysm will have adhesions to

perforators, the posterior part of aneurysm is obscured behind the ICA,

and the dome is surrounded by only arachnoid trabeculae. All these

factors contribute to difficulty in clipping of these aneurysm and high

incidence of intra operative rupture. (49). On the other hand, the dome of

an aneurysm with a lateral projection often attaches to the brain

parenchyma of the temporal lobe, which enables subpial dissection of the

aneurysm, decreasing the risk of rupture. Posterior projecting aneurysms

often have a wide neck involving the origin of a fetal PCoA. At

intraoperative rupture, clamping of not only the ICA but also the fetal

PCoA is required for flow control, and a longer clip blade must be

applied to the wide neck in the limited surgical corridor created by

multiple temporary clips. (49)

PCoA aneurysms with lateral projection are more likely to cause

intracerebral hematoma as a result of attachment to the temporal lobe.

Patients with these aneurysms presents with poorer initial neurological

status by rapidly increasing intracranial pressure(49, 50). Thus the poor


35

outcome of laterally projecting aneurysm is related to poor initial grade

than the aneurysm factor per se.

Superolateral projecting aneurysm are also reported to have worse

prognosis. One theory might be that the hemodynamics of its location

produce more shear stress on the wall of the aneurysm making it more

prone to rupture and produce a greater amount of SAH and/or that they

have more space to grow quickly debilitating the aneurysm wall at a

higher rate. (51)

Large/giant size is reported as another risk factor of procedure

related complications of the aneurysm surgery.(49)The size of an

aneurysm is not a good predictor of rupture. Aneurysms develop and

grow at different rates and the hemodynamics of their location differ

depending on their orientation in the parent vessel. (51)

Post operative complications:

Vasospasm: Blood released under high pressure into the basal

subarachnoid cisterns as a result of a ruptured aneurysm can trigger a

cascade of molecular events that leads to a narrowing of the major

intracranial arteries, which is called cerebral vasospasm. Extreme

vasospasm can lead to infarction. Vasospasm follows a typical time

course in that its onset usually occurs within 1 week after the


36

hemorrhage, it reaches its maximum severity between Days 7 and 10

post-SAH, and it usually dissipates after 14 to 21 days. 5 to 11% of

patients continue to suffer permanent disability as a result of

vasospasm.(36)

A mainstay in the prophylaxis and treatment of cerebral vasospasm

in the past was hyperdynamic therapy, also known as ―triple-H therapy,‖

which utilised the three approaches of hypervolemia, induced

hypertension, and slight hemodilution with the aim of improving cerebral

blood ow (CBF). Lennihan et al. demonstrated that hypervolemic therapy

resulted in increased cardiac filling pressures and fluid intake but did not

increase CBF or blood volume compared with normovolemic therapy,

concluding that prophylactic hypervolemic therapy is unlikely to confer

benefit. (52, 53)Prophylactic hyperdynamic therapy was found to have

greater costs and more frequent complications such as excess bleeding,

congestive heart failure, and infections (53) Hence at present the

recommendation for hyper dynamic therapy is for treatment and not for

prophylaxis.(53)

Hydrocephalus: Acute hydrocephalus within the first 24 h of

hemorrhage may develop due to blood within the basal cisterns or in the

ventricular system causing CSF obstruction. Acute hydrocephalus within

the first 24 h of hemorrhage may develop due to blood within the basal


37

cisterns or in the ventricular system causing CSF obstruction. In a study

by Varelas et al on 108 patients, hydrocephalus was present in 30% of the

patients with aneurysmal SAH and found that shunt dependent

hydrocephalus was more in patients who underwent coiling. The

rationale behind this being subarachnoid blood may be cleared by intra

operative lavage which is not possible for coiling group. (54)However, in

a an another retrospective study comparing 100 matched patients who had

suffered SAH, either clipping or coil embolization, did not significantly

affect the development of chronic hydrocephalus.(55) In an another study

by Woernle et al shunt dependency was found in 23.6 % of patients and

GCS 3-7 at admission and coiling were predictors of shunt

dependency.(56)

Infarct: The incidence of infarct in aneurysm surgery is reported to

be between 24 to 35 %(57). Early onset infarct are those infarcts which

develops within 0–5 days. Etiology of such infarct is mostly related to

site of ruptured aneurysm. They are thought to be due to either perforator

injury or due to permanent or temporary occlusion of artery or retraction

injuries. They are usually deep or cortical in distribution and are mostly

ipsilateral to the parent vessel bearing aneurysm. Secondly, late onset

infarcts were those infarcts that develops mostly after first week of

surgery. They are mostly diffuse, patchy, multiple and bilateral,


38

etiologically perhaps due to a diffuse process like vasospasm.The

mortality among late onset infarct is also higher. (57). In PcoA aneurysm

the deep infarcts are secondary to occlusion of perforators supplying

basal ganglia and internal capsule. Literature quotes poor grade at

presentaion, higher Fisher’s grade on CT, intraoperative rupture and

prolonged temporary clipping as predictors of developing infarct in

operated cases of aneurysm.(57)

Outcome:

Approximately 10% to 15% of patients with ruptured aneurysm die

before reaching hospital. Of those who survive, 42% will be dependent,

46% will have some form of disability, and 12% will be left severely

impaired.(58)

Population based study informed mortality rates range from 8% to

67% with a significant morbidity among survivors (16). Some factors has

been related with mortality are female sex, severity of clinical

presentation, rebleeding, older age, preexisting severe medical illness,

global cerebral edema on computed tomography (CT) scan,

intraventricular and intracerebral haemorrhage, symptomatic vasospasm,

delayed cerebral infarction (especially if is multiple), hyperglycemia,

fever, anaemia, and other systemic complications such as pneumonia and

sepsis (16)


39

In the ISAT trial involving 2143 patients, the long term mortality

among the clipped aneurysms was 14%. (43)

In a study by Ghani et al at three months after discharge, 33.3%

had the mRS score of 0 with no symptoms at all, and 33.3% had the mRS

score of 6 or had died. (19)

In a study by Lee K chang et al in their study on 424 operated cases

of PCoA aneurysm found that 7.3% had poor outcome.(3)

Hop et al.analyzed disabilities 1-48 months after the onset and

found that on average, 10-20% of survivors of aneurysmal SAH become

so disabled that they lose their independence and have to rely on others to

carry on in their daily lives(59)

In the meta-analysis by Nieuwkamp et al,55% of patients remained

independent and 19% were dependent on help for activities of daily living

1-12 months after the onset. (60)

In a study by Pegoli et al excellent outcome was noted in 236

patients (63.3%), including an mRS score of 0 in 122 (32.7%) and an

mRS score of 1 in 114 (30.6%). (61)


40

Third nerve recovery

Some studies that compared coiling and clipping showed no

difference in results between these two treatments. Chen et al described a

series of 13 patients of whom 6 were treated with coil embolisation and 7

were treated with surgical clipping. Only two patients in the endovascular

cohort made a complete recovery, while six patients in the surgical cohort

made a complete recovery . Also they reported that 86% vs 33% of

patients had complete resolution of third nerve palsy after clipping and

coiling, respectively.(5, 62) Chang SI et al study showed a 70% complete

recovery rate which is similar to recovery rates in previous studies(26) .

In the case of a ruptured PCoA aneurysm, the aim of the treatment

is not only to safely exclude the aneurysm but also to increase the chance

of third nerve recovery. In meta-analysis by Gabarel et al, they have

shown that clipping achieved better oculomotor outcomes than coiling.

(24)

Although the studies done on oculomotor nerve recovery are small

and non randomised the general conclusion in literature is that patients

with can have slightly higher chance of recovery with clipping as

compared to coiling. (5)


41

Study by Golshani et al have also shown that factors associated with a

higher likelihood of recovery include time to treatment, partial third nerve

deficit, and presence of sub arachnoid hemorrhage.(5)

Results

42

RESULTS

Total of 100 consecutive cases of communicating segment aneurysm

clipped between January 2013 to May 2017 were analysed. All cases had

underwent surgery at SCTIMST, Trivandrum.

The total number 554 aneurysm cases were clipped during this period.

Incidence: As per the aneurysm cases operated the incidence of PcoA

aneurysm was 18.05 %.

Age: The average age of presentation was 55.2 years.(Median 56 years).

Age didn't affect the outcome and there was no difference in outcome

whether patient is young or old. (Table 2)

Table 2: Relationship of age with mRS at 3 month follow up

Age median Total

Less than 56

years

More than

56 years

Modified

Rankin score

(mRS) at 3

month follow

up

Excellent (mRS 0

and 1)

42 38 80

Mild (mRS 2) 2 3 5

Moderate to

severe including

death(mRS 3 - 6)

6 9 15

Total 50 50 100

Results

43

Sex: Out of 100 patients 75 were male and 25 were female. The incidence

of SAH was more in female as compared to male. Other than the

incidence ,the functional outcome based on mRS, recovery from third

nerve palsy, duration of hospital and ventilatory stay and death was not

statistically significant between male and female.

Comorbidities:

Hypertension: The incidence of hypertension in the study was 42%.

There was no statistical significance for poor or good outcome with

hypertension.

Other comorbidities and risk factors: Diabetes was found in 11%, asthma

3%, hypothyroid 4 %, dylipidemia 12%, seizure and history of cerebral

25%

75%

Male Female

Results

44

vascular accident in 1% each. 14 % had multiple comorbidites and 52 %

had no comorbidity at all. None of these factors were predictors of

outcome.

Smoking and alcohol consumption was found in 32 % and 27 %

respectively and was not significantly associated with outcome.

Symptom, deficits and severity at presentation:

Headache was the most common presenting symptom seen in 90 % of

patients. Vomiting was seen in 40 %, third nerve palsy 27 %, loss of

consciousness 28 %, seizure 4 % and focal weakness in 7 %.

16 patients presented as unbled aneurysm out of which 8 patients had

third nerve palsy and the rest were incidentally detected or had multiple

aneurysm.

42

11

21

58

89

52

0.0

50.0

100.0

Hypertension Diabetes Other

Per

cen

tag

e

Present Absent

Results

45

27 patients had third nerve palsy at presentation and 20 patients had

associated SAH.(Table 3)

Table 3: Frequency of occurrence of third nerve palsy

Third nerve palsy Percent

Yes 27.0

No 73.0

Total 100.0

The GCS was 15 for 95 % of patients, 14 and 13 for 2% each and 12 for

1%.

90

40

27 28

4 7

0.0

50.0

100.0

Headache Vomiting 3rd nervepalsy

LOC Seizure Focalweakness

Per

cen

tage

Symptom at presentation (Percentage)

Results

46

The WFNS grade at presentation was 68% for Grade 1 and 16 % for

grade 2. 16 % were unbled aneurysm.

1 2 2

95

0.0

50.0

100.0

12 13 14 15

Per

cen

tag

e

GCS at presentation

68

16 16

0.0

50.0

100.0

1 2 Unbled aneurysm

Per

cen

tag

e

WFNS grade at presentation

Results

47

Radiological factors:

CT plain was done in all patients. CT angiogram (CTA) was done

in 90 % of patients, MRI angiogram (MRA) in 25 % and angiogram

(DSA) was done in 38 % of patients.

Modified Fischer grading was used to assess the severity of SAH.

16 % of patients were unbled, 11 % were in grade 1, 27 % in grade II, 25

% in grade III and 21 % in grade IV.

0

25

50

75

100

CTAMRA

DSA

Pre op radiology

Results

48

The severity of SAH based on modified Fischer grading didn't

affect the outcome. 8 patients had post operative vasospasm and its

relation with pre operative Fischer grading couldn't achieve statistical

significance as the number was small. (Table 4)

Table 4: Modified Fischer grade relation with Vasospasm

Vasospasm Total

0 1

Modified Fischer

grade

0 16 0 16

1 10 1 11

2 24 3 27

3 24 1 25

4 18 3 21

Total 92 8 100

16 11

27 25 21

0.0

50.0

100.0

0 1 2 3 4

Perc

enta

ge

CT Fischer grade

Results

49

Pre operative imaging features hydrocephalus, IVH, infarct, hematoma

didn't affect the outcome in terms of mRS or recovery from third nerve

deficit or death.

Although the number of patients with vasospasm was small, none of these

factors predicted the occurrence of vasospasm.

Similarly only one patient required VP shunt out of 13 patients who had

hydrocephalus.

20 16

7 13

2

80 84

93 87

98

0.0

50.0

100.0

IVH NoSAH(Unbled)

Pre op infarct Hydrocephalus Hematoma

Per

cen

tage

Pre op CT findings

Present Absent

Results

50

Aneurysmal factors:

All patients had PCoA aneurysm. 31% had multiple aneurysm. 5

patients had mirror aneurysm. Acom was the most common location

found in cases of multiple aneurysm.

Direction and relation of PCoA to aneurysm: Most of the aneurysm

were directed poster infer lateral direction (68 %). 64 % of the cases

PCoA was arising proximal to aneurysm 19 % from neck of aneurysm

and 17 % opposite to the origin of the aneurysm .

Morphology and size: 92 % were saccular aneurysm and 13 had

complex morphology in terms of bi or multilobes. Average neck size was

2.52 mm and average dome height was 5.2 mm and dome width 3.6 mm.

39 % of the aneurysm had a narrow neck(< 2.5 mm) and 49 % had wide

neck (2.5 - 5mm) with 5.4 % having very wide neck(> 5 mm). 90% of the

aneurysm were smaller than 10 mm.

47%

43%

10%

Aneurysm size

< 5mm 5-10 mm >10 mm

Results

51

Fetal PCoA and attachment to third nerve: 10 % of the patients had

fetal PCoA. The aneurysm was attached to third nerve in 22 % of

patients.

Intra operative factors:

Intra operative rupture occurred in 24 %. Clip and wrap technique was

used in 20 patients. Fundus was opened in 21 patients. 17 % had

atherosclerosis and 3 % had into aneurysmal thrombus.

Lamina terminals was opened in 24 % of patients and uncus was removed

in 4 % and clinoidectomy was done in 6 %.

Bilateral PCoA was operated at interval in 6 patients.

Temporary clipping was used in 38 patients and the average duration of

temporary clipping was 2.4 minutes.

Calcification was present in 2 % and atherosclerosis was present in 17%.

22 % had attachment to third nerve.

Straight clip was used in 47 % , curved in 25 %, right angled in 10 % and

fenestrated in 9 %.

Results

52

Post operative factors:

Post operative hospital stay was less then 12 days in 71 % of

patients and > 12 days in 29 % of patients. 94 % of the patient had

hospital stay of < 20 days. 17 patients had hemiparesis, with only 6

patients having immediate post op hemiplegia. Presence of hemiparesis ,

any post operative complication and duration of temporary clipping > 12

minutes affected the post operative hospital stay (> 12 days) after simple

logistic regression. (p < 0.05).

Duration on ventilator: 74 % of the patients had stay < 1 day on

ventilator. The presence of any complication prolonged ventilator stay.

Presence of third nerve palsy, intra operative rupture, temporary clipping,

presence of hemiparesis were significant after univariate analysis. No

factor was statistically significant for predicting the duration on ventilator

after multivariate analysis.

Infarct: The incidence of pre op infarct was 7 %. 22 patients developed

post operative infarct. Out of which 11 had early radiological infarct and

11 had late infarct which manifested clinically. 14 out of 22 (63.63%)

patients had underwent temporary clipping. 24 out of 78 (30.7%) patients

had underwent temporary clipping in the other group who didn't had

infarct (Table 5). Temporary clip, intra op rupture and use of complex

clip were predictors of infarct after simple logistic regression. No factor

Results

53

was statistically significant for predicting the infarct after multivariate

analysis.

The average duration of temporary clipping was 5.72 minutes as

compared to 1.48 minutes for those patients who didn't had infarct. The

incidence of infarcts in WFNS grade I and II patients was 20 % and 31.5

%.

Table 5: Relation of infarct with temporary clipping

Temp clip Total

No Yes

Early plus late

infract

(Radiological and

clinical)

No 54 24 78

Yes 8 14 22

Total 62 38 100

Results

54

The post operative complications are listed in the table 6.

Table 6: Post operative complications

POST Operative complication

Complication Number

Early infarct 11

Late infarct 11

Hematoma 3

Decomp craniectomy 6

Vasospasm 8

Tracheostomy 7

Hemiparesis 17

3rd nerve deficit 16

Aphasia 1

Vegetative state 1

Hyponatremia 5

Pulmonary embolism 6

DVT 1

VP shunt 1

COPD 1

Pneumothorax 1

MI 1

EDH 1

Chemical angioplasty 3

SDH/ EDH 2

Results

55

OUTCOME:

FUNCTIONAL OUTCOME:

Modified rankin score was used to assess the outcome at discharge

and at follow up of 3 months. mRS 0 and 1 were considered excellent

functional outcome, 2 as mild disability including the presence of third

nerve palsy, 3 or more than three as poor outcome including death

48 % had excellent outcome, 23% had mild disability, 29 % had

moderately to severe disability which includes 9% mortality. Follow up at

3 months patients had significant recovery with 80 % showing excellent

functional outcome with 5 % having mild disability and 6 % severe

disability.

Intra operative rupture, temporary clip and post operative infarct

were significant predictors of poor outcome after simple logistic

regression (Table 7,8). Presence of post operative infarct (OR : 0.125 95

% CI 0.030 - 0.531) affected the outcome in terms of mRS at discharge

after multivariable logistic regression analysis. This included radiological

and clinical infarct. Out of 27 patients who had poor outcome 12 patients

had intra operative rupture and 18 had temporary clipping.

Results

56

None of the factors affected improvement in terms of rankin score at

follow up of 3 months.

None of the factors predicted poor outcome as per the GCS at discharge

or follow up

Table 7 : Relationship of intra operative rupture(IOR) Vs mRS at

discharge

IOR Total

Absent Present

mRS at discharge Excellent 40 8 48

Mild 19 4 23

Poor 17 12 29

Total 76 24 100

Table 8: Relationship of temporary clip vs mRS at discharge

Temp clip

Total Present Absent

mRS at discharge Excell

ent 37 11 48

Mild 14 9 23

Poor 11 18 29

Total 62 38 100

Results

57

THIRD NERVE DEFICIT:

Factor affecting the recovery of third nerve deficit:

In 16 patients who had third nerve deficit after surgery the dome

was attached to the nerve in 10 patients, 10/16 (62.5 %) as against 10/66 (

37.5 %) in those who didn't have deficit(Table 9). This was statistically

significant (p < 0.05). The average size of aneurysm for third nerve

deficit and without deficit are 6.2mm and 4.3mm respectively. This was

not statistically significant.

Temporary clipping was also significant predictor of long term

third nerve deficit at 3 months. (p < 0.05) 68.5% of patients who had third

nerve palsy with associated SAH recovered after surgery. But only 37.5

% of patients who had third nerve palsy as the presenting symptom

recovered(Table 10).

Results

58

Table 9: Relation of third nerve deficit in post operative (op) period

with attachment of dome of the aneurysm to nerve during surgery

Relation to 3rd

nerve to

dome of aneurysm

Total

Not

attached Attached

3 rd nerve

deficit post

op

No 56 10 66

Yes 6 10 16

Total 62 20 82

Table 10: Recovery of third nerve palsy and relationship to SAH

THIRD NERVE DEFICIT and RECOVERY

Before surgery After surgery 3 months

Third nerve

palsy present

27 16 11

Third nerve

palsy absent

73 84 89

100 100 100

Relation of third nerve palsy and associated SAH

Third nerve +

Unbled

Third nerve +

SAH

Total

Pre op third

nerve deficit

8 19 27

Post op third

nerve at 3

months

5 6 11

Recovery

percentage

3/8(37.5%) 13/19(68.5 % )

Results

59

Table 11: mRS at discharge and factors affecting outcome.

Excellent

functional

outcome

Mild

disability

mod to

severe

disability

Percentag

e(%)

p value

Age

< 56 years 27 12 11 50 0.289

> 56 years 21 11 18 50

Sex 0.881

Male 13 5 7 25

Female 35 18 22 75

Co morbidities

Hyppertension 21 9 12 42 0.931

Diabetes 4 3 3 11 -

Other co

morbidities

Presenting symptoms

Vomiting 19 15 6 40 0.15

Third nerve

deficit

11 10 6 27 0.53

Focal deficit 3 0 4 7 -

GCS

15 47 23 25 95

14 1 0 1 2

13 0 0 2 2

12 0 0 1 1

WFNS

2 6 5 5 16

1 35 16 19 70

Unbled 7 4 5 16

Results

60

Pre op CT characteristics

IVH 8 4 8 20 0.478

Pre op infarct 4 1 2 7

Cisternal blood 31 15 19 65 0.996

Hydrocephalus 5 2 6 13

Pre op investigations

MRA 9 9 7 25 0.177

CTA 41 22 27 90

DSA 21 6 11 38 0.357

Multiple

aneurysm

13 8 10 31 0.718

Aneurysm characters

Direction 0.484

Posteriorly

inferiorly

laterally

31 18 19 68

Other direction 17 5 10 32

Relation to

PCoA

0.864

Arising distal to

PCoA

32 14 18 64

Arising from

neck/opposite to

PCoA

16 9 11 36

Aneurysm size

< 5 mm 37 14 22 73

5 - 10 mm 11 8 4 23

> 10 mm 0 1 3 4

Operative characters

IOR 8 4 12 24 0.02

Temporary

clipping

11 9 18 38 0.003

Results

61

Wrap + clip 6 5 9 20 0.140

Attached of

aneurysm to 3 rd

nerve

8 5 9 22 0.337

Open lamina

terminalis

7 5 12 24 0.27

Fetal PCoA 1 3 6 10 -

Atherosclerosis 6 4 7 17 -

Duration of temporary clip

< 3min 39 18 13 70

3- 6 min 5 3 8 16

6- 12 min 3 2 5 10

> 12 min 1 0 3 4

Post operative factors

Tracheostomy 0 3 5 8

Infarct 0 2 20 22 0.04

Decompressive

craniotomy

0 1 5 6

Vasospasm 0 2 6 8

Hemiparesis 0 2 11 13

GCS at

discharge

-

15 48 23 15 86

13-15 0 0 1 1

<13 0 0 4 4

MRS at

discharge

48 23 29

Results

62

Mortality:

Nine patients expired out of operated 100 patients. Only 3 patients

died due to complication related to subarachnoid haemorrhage like

vasospasm. 6 patients died due to medical complication (2 patients

COPD, 1 patients due to MI and 3 patients due to pulmonary embolism).

The number was too small to derive any statistical significance or

to find any factor that predicted mortality.

Discussion

63

DISCUSSION

Incidence of PCoA: 100 cases out of 554 clipped aneurysms between

January 2013 and May 2017 were PCoA aneurysm. The incidence of

PCoA in our study was 18.05 %. The incidence of PCoA aneurysm as

quoted in the literature is 15%–25% of all intracranial aneurysms. (12,

30)

PRE OPERATIVE CHARACTERS:

Age : The average age of presentation of PCoA aneurysm in this study

was 55.2 years. The median was 56 years. In a study by Matsukawa et al

the average was less than 60 years. Several studies have shown that

incidence of SAH increased with increasing age, reaching the maximum

level at the age of 50–70 years but declined after that. (12). In an another

study the average age at presentation was 55.8 +/- 13.3 years. (61)

Sex: In our study 75 % were female and 25 % were male. The incidence

of aneurysm being higher in female is reported in literature. Park et al in

their study on 53 patients have found that the incidence is more common

in female as compared to men(15). In a study by Ghods et al on

unruptured aneurysms, the incidence among women was 54–37% and

29– 15% among men(14). Similarly in a study by Pegoli et al 64% of

their 381 patients were female. The most important mechanism quoted in

Discussion

64

literature for increased incidence in female is due to altered hemodynamic

stress and vascular remodelling secondary to decreased oestrogen level.

In our study difference in sex didn't affect the outcome parameters (61).

Risk factors and comorbidities:

Hypertension and smoking: Hypertension has been considered as

an independent risk factor for aneurysmal formation. Our results co relate

with previous studies with 42% of patients having hypertension. In a

study by Taylor et al the prevalence of hypertension in patients with

unruptured aneurysms was 43.2% compared with 34.4% in the random

sample.(63) In a meta analysis by Backes et al hypertension was

significant factor in 11 studies and had 1.24 (0.98–1.58) risk ratio of

aneurysmal formation and rupture as compared to the control group. (64)

32 % of patients in our study had history of smoking. In a study

smoking had risk ratio of 2.03 (1.52–2.71) over the control group.(64)

The mechanism cited for both hypertension and smoking as a risk

factor for aneurysm formation and rupture ,is the endothelial damage

leading to repair and regeneration process ultimately leading to aneurysm

formation and rupture.(16, 63, 64)

Discussion

65

Other comorbidities and risk factors like diabetes, asthma,

dyslipidemia, hypothyroidism, alcohol consumption, did not significantly

affect the outcome in our study.

Symptom at presentation: Ninty percent of patients had headache at

presentation. Vomiting and third nerve palsy were also common

presenting symptoms. 16 % of the patients were unbled aneurysm.

Presentation as 3rd

nerve palsy:

In our study 27 % had third nerve palsy at presentation and

19/27(71.8 %) of those patients had associated SAH. The incidence of

oculomotor nerve palsy in patients with posterior communicating

aneurysm has been reported to vary from 9% to 50% (26, 62, 65). In

study by Chang et al among a total of 99 patients with 103 aneurysms, 13

(13.1%) patients had oculomotor palsy.(26)

The mechanisms by which PCoA aneurysm causes oculomotor

nerve palsy are through direct compression by the enlarging aneurysm or

through pulsation of the aneurysm(26). In unbled aneurysm the palsy is

usually secondary to some conformational change in dome of the

aneurysm and often indicates an impending rupture.(5, 65)

Discussion

66

RADIOLOGICAL FINDINGS AND PARAMETERS AFFECTING

OUTCOME:

CT angiogram was done in 90 % of patients, MRA in 25 % and

angiogram was done in 38 % of patients. Modified Fischer grading was

used to assess the severity of SAH. Even though 46% were among grade

III and grade IV group, this didn't affect the outcome or the occurrence of

vasospasm.

Pre operative imaging features like hydrocephalus, IVH, infarct,

hematoma didn't affect the outcome in terms of mRS or recovery from

third nerve deficit.

Aneurysm characters :

Projection: Most of the aneurysm were directed posteriorly,

inferiorly and laterally(51 %). Sola T et al studied the projection of

aneurysm with outcome. In their study inferolateral was the most

common projection. (51)

The incidence of intra operative rupture (IOR) is co related with

direction of aneurysm. In our study the incidence of intra operative

rupture was higher for aneurysm that were not directed posteriorly,

inferiorly and laterally. (62.5 % vs 20.2 %) In a study by Fukuda et al

pure posteriorly directed aneurysm had higher chance of rupture , need of

Discussion

67

complex clipping like use of fenestrated clip, risk of injury to perforators

as compared to laterally directed aneurysm. (49). Also superolateral

projecting aneurysm are reported to have worse prognosis. (51)

Table 12: Direction of aneurysm with intra operative rupture.

Direction Number IOR Percentage

Posterior inferior lateral 84 17 20.2

Other direction 16 7 62.5

Size: Most of the aneurysm were less than 10 mm . (90%) Average neck

size was 2.52 mm and average dome height was 5.2 mm and dome width

3.6 mm.In a study on PCoA aneurysm 90 % were < 10mm, 40 % < 5mm

in diameter. (66). Forget et al showed that the prevalence of small

ruptured PCoA aneurysms is high, with 87.5% of aneurysms measuring

less than 10 mm in diameter and 40% measuring less than 5 mm in

diameter having ruptured. (7, 12, 66).Similarly in our study aneurysm <

5mm were 47 % and had ruptured. This contradicts the ISUIA trial

stating that aneurysm < 7mm of anterior circulation have less chance of

rupture. PCoA Aneurysm have rupture risk equal to that of posterior

circulation aneurysm.(5)

Bleb and large aneurysm: The percentage of aneurysm with bleb in

our study was 3%. Tsukahara et al.reported a global rupture rate of 3.42%

Discussion

68

per year and a rupture rate of 28.3% per year in aneurysms that contained

bleb formation. (67) The poor outcome on large sized aneurysm is

reported. In a study by Thiarawat et al large aneurysm (15 - 25 mm)

required longer time of surgery, higher incidence of intra operative

rupture and longer temporary clipping. (47)10 % of our study had

aneurysm had size > 10 mm.

INTRA OPERATIVE CHARACTERS :

Adequate drainage of CSF, minimal brain retraction, and

identification of all perforators are the important steps in clipping of

PCoA aneurysm. (47) Selecting the proper clip, use of temporary clipping

when needed with achieving proximal and distal control is of utmost

importance. (47)

Intra Operative Rupture: Intraoperative rupture occurred in 24% of the

patients and 50 % of them had moderate to severe disability at discharge.

There are multiple factors which can affect intra operative rupture. As

said earlier postero medially directed aneurysm have high chance of

rupture. Similarly aneurysm attached to temporal lobe or uncus have high

chance of rupture. The retraction of temporal lobe should be avoided

because dome of the aneurysm might be attached to the medial wall of

temp lobe. This can lead to premature rupture of aneurysm. (47) Patients

Discussion

69

who had intra operative rupture had higher chance of poor functional

outcome at discharge but this was nullified at follow up of 3 months.

Leipzig et al, reviewed a large series of aneurysm clipping looking

for risk factors of intra-operative rupture. PCoA aneurysms had the

second highest rate of intra-operative rupture amongst anterior circulation

aneurysms (9.3%). (68) Risk factors for intra-operative rupture included

an immediate history of subarachnoid hemorrhage as well as temporary

clipping.(5, 68)

Wrapping: Wrapping and clipping is a technique applied to

ruptured aneurysms where the lesion is wrapped with autogenous tissue

or absorbable material to reconstruct the integrity of the vessel and then

clip is placed over it.(58) This is helpful when there is avulsion at neck of

aneurysm.

Barrow and Spetzler reported a cotton-clipping technique using

cotton as bolster and clip together with an aneurysm. (69) The use of

muscle as a replacement for cotton has been reported in very few studies.

We used muscle as a replacement for cotton. The pieces of muscle are

used to cover the perforate site of the neck, and they are held in place

with a suction tip. Then, muscle is clipped onto the torn neck together

with the aneurysm neck(47)

Discussion

70

The rationale for using muscle is that the foreign body reaction is

less but it still can form a good coagulum. Skeletal muscle is very

vascularised. The arterioles and capillaries that are present in muscle are

known for releasing several procoagulative factors after a piece of muscle

is harvested (70, 71) This is much more aggravated when it is smashed or

crushed. Pro coagulant factors along with platelets, amplify, and

propagate the natural hemostasis process at the point of injury.This,

combined with a mechanical tamponade resulting from the muscle piece

results in a strong hemostatic plug. Sometimes just placing the piece of

muscle against the bleeding point for 2 minutes may be sufficient to stop

the bleeding(71, 72) This can be used when the neck of aneurysm gets

avulsed.

Relation to 3rd

nerve: The infratentorial with laterally projecting

aneurysms have a higher tendency to present with preoperative

oculomotor palsy. In 20 patients aneurysm was attached to third nerve.

The recovery of third nerve deficit in patients who present with SAH with

oculomotor nerve palsy was better than patients who presented with third

nerve deficit without SAH. The identification of the oculomotor nerve

before clip application should be avoided because of the increased risk of

premature aneurysm rupture.(22, 47)

Discussion

71

Lamina terminalis opening: Lamina terminals was opened in 24 %

of cases. This is achieved after identification of optic nerve and chiasm.

With release of CSF the dissection of sylvan fissure becomes more easier

with less need for retraction. (47)In almost all patients with pre operative

hydrocephalus and intraventricluar blood lamina terminals was opened.

This has lead to decreased incidence of shunt in post operative period.

Temporary Clipping: Temporary clipping is done on proximal

ICA. The average time for temporary clipping in our study was 2.4

minutes. Studies have shown that temporary clipping upto 12 minutes is

safe and temporary clipping with intermittent release can safely be done

as long as 27 minutes (47) In our study the use of temporary clipping has

affected functional outcome at discharge but there was no difference in

outcome at follow up of 3 months.

Discussion

72

POST OPERATIVE COMPLICATIONS:

Hydrocephalus:

In our study thirteen patients had pre op hydrocephalus and only

one patient required VP shunt.

Clipping patients have less incidence of long term hydrocephalus

as compared to coiling patients. Literature also supports this fact. Varelas

et al in their study on 108 patients found that hydrocephalus was present

in 30% of the patients with aneurysmal SAH and shunt dependent

hydrocephalus was more in patients who underwent coiling.(54). In a

study by Woernele et al the shunt dependency for aneurysmal SAH was

26.5 %. GCS 3- 7 at admission and coiling were predictors for shunt

dependency. (56)

The very low incidence of requirement of VP shunt in our study

can be explained by the aggressive opening of lamina terminals in cases

of hydrocephalus. In our study lamina terminals was opened for all

patients who had pre operative hydrocephalus or IVH on pre op scan.

This lead to effective drainage of CSF and there by reducing the

incidence of requirement of shunt.

Discussion

73

Infarct:

The incidence of pre op infarct was 7 %. The incidence of post op

infarct in our study was 22%. This included the radiological presence of

infarct. The average incidence of infarct in various studies is around 39%.

In a study done by Umbredkar et al the quoted incidence of infarct

was24.5% for Fischer grade 1 patients and 33% for Fischer grade II

patients. The incidence of infarct co relate with grade of SAH at

presentation. (57). In our study all good grade SAH were included hence

poor grade patients affecting infarct was not studied. The average

duration of temporary clipping was 5.72 minutes for patients who

developed infarct as compared to 1.48 minutes for those patients who

didn't had infarct.This was statistically significant. Patients with infarct

had prolonged hospital stay and poor recovery. Also the incidence of

mortality is high among the group who develop late infarct.(73, 74).

Decompressive craniectomy : In our study 6 patients required

decompressive craniectomy secondary to vasospasm induced infarct. In a

study by Schirmer et al decompressive craniotomy was performed in 16

patients with poor grade SAH. They found that 64 % had good outcome

in terms of mRS score and early craniectomy ( < 48 hrs) is associated

with good outcome. In our study the number was too small for any

statistical conclusion. (75)

Discussion

74

Vasospasm: The incidence of vasospasm reported in literature is 15 to 35

%. (76, 77). In our series only 8 % developed vasospasm.Symptomatic

vasospasm patients were treated with chemical angioplasty. The number

was small to derive any statistical significance.

Seventeen patients had developed hemiparesis which improved

gradually. Hyponatremia (5%), pulmonary embolism(6%), DVT (1%)

were other complications.

OUTCOME:

In our study the functional outcome was measured in terms of

excellent outcome (mRS score 0 and 1), mild disability (mRS score of 2)

and poor functional outcome (mRS > 3)

At discharge 48 % had excellent outcome, 23% had mild disability,

29 % had moderately to severe disability which includes 9% mortality.

Follow up at 3 months patients had significant recovery with 80 %

showing excellent functional outcome with 5 % having mild disability

and 6 % severe disability. The presence of third nerve palsy was included

in mild disability.

In the multicenter International Study of Aneurysm Treatment

(ISAT), 49% of patients has an mRS score of 0–1 at 1 year (21% with

mRS score of 0 and 28% with mRS score of 1)(43)

Discussion

75

Pegoli et al in their study on 373 patients of clipped aneurysm

considered mRS 0 and 1 as excellent functional outcome. Excellent

outcome was noted in 236 patients (63.3%), including an mRS score of 0

in 122 (32.7%) and an mRS score of 1 in 114 (30.6%). The factors that

predicted good functional outcome in their study was good grade at

presentation, no intraparenchymal hematoma, no infarct, not recieving

blood transfusion. (61)

In a study by Lee K chang et al on 424 operated cases of PCoA

aneurysm , the incidence of poor outcome at follow up was 7.3%. (3)

In the meta-analysis by Nieuwkamp et al55% of patients remained

independent and 19% were dependent on help for activities of daily living

1-12 months after the onset. (60)

Hop et al analysed disabilities 1-48 months after the onset and

found that on average, 10-20% of survivors of aneurysmal SAH become

so disabled that they lose their independence and have to rely on others to

carry on in their daily lives (59)

Our series shows the functional outcome of operated cases of

PCoA aneurysm is better than what quoted in literature. The factors that

predicted moderate to severe disability at discharge were intra operative

rupture, temporary clipping and post operative infarct. The presence of

post operative infarct predicted poor outcome at discharge after multi

Discussion

76

variable logistic regression analysis. None of the factors determined poor

outcome at follow up of 3 months.

Sanai et al in their study on technical difficulties in clipping of

PCoA aneurysm have found that temporary clipping and use of

fenestrated clip is associated with poor outcome indicating the

complexity of aneurysm. (78)

Recovery of 3rd

nerve deficit

In our study 27 patients had third nerve palsy at presentation and

20 patients had associated SAH. After surgery 11 patients recovered.

(40.7%) 16 patients had either partial or complete third nerve deficit.

Full recovery of third nerve palsy has been reported to range

between 32% and 85% after treatment.(24, 79)Several studies have been

conducted to predict the recovery of occulomotor nerve palsy. In a study

by Guresier et al after multivariate analysis they found that patients with

incomplete third nerve palsy at admission were more likely to attain full

recovery from the palsy than were those with complete third nerve palsy

at admission(79)

In our study the usage of temporary clipping more than 7 minutes

affected the outcome in terms of post operative third nerve palsy at

discharge and at 3 months. The recovery of third nerve palsy was

significantly better for those patients who had presented with SAH. This

Discussion

77

can be attributed to the fact that along with clipping the decompression of

hematoma or blood surrounding the nerve might have benefited in

recovery. In other studies other factors like symptom to surgery,

aneurysm size has found to affect the third nerve palsy recovery but these

were not significant in our study.(27, 80)

Teasdale et al. in their series of 27 patients with unruptured PCoA

aneurysms found that aneurysm measuring 7mm or greater had higher

incidence of third nerve deficit. (81)In our study the average size of

aneurysm for third nerve deficit and without deficit are 6.2mm and

4.3mm respectively showing that the size of aneurysm was larger in

patients who presented with third nerve palsy. But this was not

statistically significant.

Time duration from presentation to clipping determines the

outcome. The average duration from symptom to surgery for those who

had permanent deficit was 60.5 days as against 23.5 days for those who

improved. The number was small to derive statistical significance.

Botterell et al, and Grayson et al, found that presence of oculomotor

nerve palsy greater than 10 days prior to operative intervention was

associated with a reduced likelihood of a full recovery.(82, 83). In an

another study by Chang et al the time to surgery and the severity at

presentation were the predictors of recovery.(26) The mechanism

Discussion

78

underlying non improvement for patients presenting late are long-term

nerve compression leading to neuronal injury and neural degeneration..

Kyriakides et al reported that most of the patients operated on in the first

week had a complete recovery and they also found a statistical correlation

between incomplete palsies and good postoperative recovery. (84)

Mortality:

Nine patients expired out of operated 100 patients. Only 3 patients

died due to complication related to sub arachnoid haemorrhage like

vasospasm. 6 patients died due to medical complication( 2 patients

COPD, 1 patients due to MI and 3 patients due to pulmonary

embolism).The reported rates of mortality in literature is 7 - 45 %. Case

fatality rates have decreased by 17% during the last three decades.(61).

Various factors predicting the mortality have been studied in literature.

like female sex, severity of clinical presentation, re bleeding, older age,

preexisting severe medical illness, cerebral edema on computed

tomography (CT) scan, intraventricular and intracerebral hemorrhage,

symptomatic vasospasm, delayed cerebral infarction (especially if is

multiple), hyperglycemia, fever, anemia, and other systemic

complications such as pneumonia and sepsis (16, 85) In our study the

number was too small to derive any statistical significance or to find any

factor that predicting mortality.

Conclusion

79

CONCLUSION

The following conclusions can be made from our study on PCoA

aneurysm

• The presence of post operative infarct predicted poor outcome in terms

of modified rankin score at discharge. (mRS ≥ 3). But no factors

predicted poor outcome at 3 month follow up.

• The incidence of intra operative rupture was more in aneurysms that

were not directed posteriorly, laterally and inferiorly.

• The wrap clip technique using autologous muscle was an effective way

of securing the neck of aneurysm.

• Opening of lamina terminals significantly reduced the need for post

operative CSF diversion in patients who had hydrocephalus at

presentation.

• The recovery of third nerve palsy was better if the patient had an

associated SAH as compared to the patients who had only third nerve

palsy as presentation. The use of temporary clipping > 7 minutes was

associated with long term third nerve deficit.

Successful surgical management of PCoA aneurysm depends on

precise understanding of their unique microsurgical anatomy, avoidance

of pitfalls and the surgeon’s experience.

Limitation of the study

80

LIMITATION OF THE STUDY

A deficiency of our analysis is that it was a retrospective study. All

data was collected retrospectively from database including the imaging

data, operative records and follow up details. Even though the database

was well maintained there were some missing details in records. mRS

was used as a functional outcome measurement but still some patients

might have cognition impairment which required neuropshychometric

testing. However mRS score of o and 1 indicate excellent functional

outcome with almost near to normal life activities. Also most of the

patients who were doing well despite third nerve palsy were grouped

under mild disability according to modified rankin scale (mRS). This

affected the mRS scores at discharge and follow up.The factors predicting

mortality was not done due to low number of patients who expired after

surgery. Further prospective studies can overcome these drawbacks faced

in this study.

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81

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Annexures

98

ANNEXURE I

PROFORMA

A. GENERAL INFORMATION

Anonymized Patient ID:

Age, sex, comorbidites:

B.CLINICAL DETAILS

Symptom:

Symtom to surgery

Neurological deficits:

GCS on admission:

WFNS grade at admission:

Radiological features: Fischer grading, presence of hydrocephalus,

infarct, intraventricular blood, hematoma

Aneurysmal factors : Shape, number of lobes, direction of fundus, size of

aneurysm and neck, relation to PCoA , fetal PCoA.

C. INTRAOPERATIVE EVENTS

Clipping or wrapping:

Intra operative rupture:

Temporary clipping

Duration of temporary clipping

Type of clip used

Number of clip

Fundus opened or not

Relation to third nerve

Annexures

99

Presence of atherosclerosis and calcification

Opening of lamina terminalis

Relation to perforator:

D. POST-OPERATIVE EVENTS

Vasospasm:

Infract Early:

Late:

Re-exploration / Decompression

Duration of the ventilator support:

Tracheostomy:

Duration of ICU stay:

Duration of post-op hospital stay:

GCS on POD 5

Need for other procedures like VP shunt

E. STATUS ON DISCHARGE

GCS

Motor and speech status

Any other deficit

Modified rankin score

F. Follow up (3 months)

GCS

Motor and speech status

Any other deficit

Modified rankin scale

Annexures

100

Glasgow coma scale: (GCS):

WFNS Grade:

Grade 1 – Glasgow Coma Score (GCS) of 15, motor deficit absent

Grade 2 – GCS of 13-14, motor deficit absent

Grade 3 – GCS of 13-14, motor deficit present

Grade 4 – GCS of 7-12, motor deficit absent or present

Grade 5 – GCS of 3-6, motor deficit absent or present

Modified Fischer grade:

Grade Description

0 No subarachnoid blood

1 Minimal / thin SAH, no IVH in both lateral ventricle

2 Minimal / thin SAH, with IVH in both lateral ventricle

3 Thick SAH and no IVH in both lateral ventricle

4 Thick SAH with IVH in both lateral ventricle

Annexures

101

MODIFIED RANKIN SCALE (mRs)

Score Description

0 No symptoms at all

1 No significant disability despite symptoms; able to carry out all usual duties

and activities

2 Slight disability; unable to carry out all previous activities, but able to look

after own affairs without assistance

3 Moderate disability; requiring some help, but able to walk without assistance

4 Moderately severe disability; unable to walk without assistance and unable to

attend to own bodily needs without assistance

5 Severe disability; bedridden, incontinent and requiring constant nursing care

and attention 6 Dead

TOTAL (0–6): _______

Reference:

1 Risselada R, Lingsma HF, Molyneux AJ, Kerr RS, Yarnold J, Sneade M,

Steyerberg EW, Sturkenboom MC. Prediction of two month modified Rankin

Scale with an ordinal prediction model in patients with aneurysmal

subarachnoid haemorrhage. BMC medical research methodology. 2010;10:86.

2.Bonita R, Beaglehole R. ―Modification of Rankin Scale: Recovery of motor

function after stroke.‖ Stroke 1988;19:1497-1500

Annexures

102

ANNEXURE II

Annexures

103

Annexures

104

ANNEXURE III

INTERNET SOURCES: ------------------------------------------------------------------------------------------- 0% - https://en.wikipedia.org/wiki/Internal_c 0% - Empty 1% - http://www.sciencedirect.com/science/art 0% - http://www.tandfonline.com/doi/full/10.3 0% - http://www.sciencedirect.com/science/art 0% - http://www.sciencedirect.com/science/art 0% - http://dspace.sctimst.ac.in/jspui/bitstr 0% - https://www.researchgate.net/publication 0% - https://www.researchgate.net/publication 0% - https://www.hindawi.com/journals/nri/201 0% - http://www.pjo.com.pk/23/3/Abid%20Naseem 0% - https://jbppni.biomedcentral.com/article 0% - https://link.springer.com/content/pdf/10 0% - https://link.springer.com/article/10.100 0% - http://thejns.org/doi/10.3171/jns.1995.8 0% - https://www.researchgate.net/publication 1% - http://www.turkishneurosurgery.org.tr/pd 1% - http://www.turkishneurosurgery.org.tr/pd 1% - http://surgicalneurologyint.com/surgical 0% - https://www.researchgate.net/publication 1% - http://surgicalneurologyint.com/surgical 0% - http://europepmc.org/articles/PMC3779399 0% - http://europepmc.org/articles/PMC2859623 0% - http://thejns.org/doi/full/10.3171/2013. 0% - https://2475432.r.bat.bing.com/?ld=d36Pt 1% - http://europepmc.org/articles/PMC3011114 1% - http://surgicalneurologyint.com/surgical 1% - http://surgicalneurologyint.com/surgical 1% - http://surgicalneurologyint.com/surgical 0% - https://www.researchgate.net/profile/Jun

Annexures

105

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Annexures

106

ANNEXURE IV

CODING

1. Sex; Male - 1, Female 2

2. Hypertension- Yes - 1, No - 0

3. Diabetes - Yes - 1, No - 0

4. Other comorbidity - Seizure 1, Cerebovascular accident 2, Asthma- 3,

Dyslipidemia 4, Hypothyroid 5, Alcohol 7, Smoking 8

5. Headcahe- Yes - 1, No - 0

6. Vomiting - Yes - 1, No - 0

7. 3 rd nerve palsy- Yes - 1, No - 0

8. Other symptoms - Giddiness 1, Previous hematoma/bleed/sentinel headache 2,

LOC 3, Seizure 4, Focal weakness 5

9. 3 rd nerve - Yes - 1, No - 0

10. Focal deficit - Yes - 1, No - 0

11. IVH: Yes - 1, No - 0

12. Unbled - Yes - 1, No - 0

13. Infarct- Yes - 1, No - 0

14. Cisternal blood- Yes - 1, No - 0

15. Hydrocephalus- Yes - 1, No - 0

16. Other - Hematoma , Yes - 1 , No- 0

17. Pcom aneurysm Yes - 1, No - 0

18. Other location - Prom 1 Acom 2, ICA bifn 3, Choroidal 4,Ant choroidal 5, MCA

bifurcation 6, PCA 7, ACA 8, Vertebral 9, Basilar 10, Superior hypophyseal 11,

Cavernous 12, SCA 13, Ophthalmic segment 14.

19. Multiple- Yes - 1, No - 0

20. Direction: Posterior + inf + Lat 1, Posterior + Inferior 2, Posterior + Lateral 3,

Post + superior + Lateral 4,Post + inf + medial 5, Post medial 6, Post+ superior +

Medial 7, Anterior + Inf + Lat 8.

21. Relation to Pcom: Proximal1, Neck 2, opposite 3

22. Teet, Bleed, Perforator loss, Fetal PCOM , Intra op rupture ,temp clip, wrap,

perforator loss,calcification, atherosclerosis, thrombus, open lamina terminalis—-

Yes - 1, No -0

23. Type of clip - Curved 1,Straight 2,Right angle 3,Fenestrated 4,Angled 5

24. Relation to 3 rd nerve - Attached -1, Not attached - 0

25. Other features - Clinoidectomy 1, Uncus removed 2, B/l pcom 3

26. Early and late infarct, decompressive craniectomy, vasospasm, hematoma,

hydertensive (HHH) therapy, tracheostomy - Yes - 1, No - 0

27. Neurodeficit - Hemiparesis 1 ,3rd nerve deficit 2, Aphasia 3, Vegetative state 4.

28. Severity of hemiparesis- No weakness 0, flicker 1, Movement with gravity 2,

Against gravity 3, against minimal resistance 4, against full resistance 5

29. Other complication- Hyponatremia 1 ,SDH 2 ,Pulmonary embolism 3, DVT 4, VP

shunt 5, COPD 6, Pneumothorax 7, MI 8, EDH 9, Chemical angioplasty 10, SDH

11.

30. Deficit at follow up of 3 months- Hemiparesis 1 ,3rd nerve deficit 2, Aphasia 3,

Vegetative state 4, Patients who have expired: No entry

31. Death - Yes -1 No 0

32. Cause of death- COPD 1, MI 2, Vasospasm 3, Pilmonary embolism 4

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29 212280 52 2 0 0 0 0 1 0 0 0 3 0 0 14 2 4 1 0 0 1 1 0 1 0 0 1 8 1 1 1 0 1 0 0 0 0 1 0

30 376238 64 2 0 0 0 7 0 0 0 3 1 0 0 15 1 3 0 0 0 1 0 0 1 0 0 1 0 0 1 1 2 2 5 8 9 1 0 0

31 374509 31 1 0 0 0 0 1 0 0 1 90 0 0 15 0 0 0 1 0 0 0 0 0 0 1 1 0 0 2 1 0 1 3.6 3.9 0 0 0 0

32 377343 57 2 1 0 0 0 1 0 1 0 6 1 0 15 1 2 0 0 0 1 0 0 1 0 0 1 0 0 7 1 0 1 4.6 13.5 8.6 0 0 0

33 379741 47 2 0 0 0 8 1 0 0 0 3 0 0 15 1 4 1 0 0 1 1 0 1 0 0 1 0 0 3 1 0 1 2.3 6.3 5.1 0 0 0

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1 0 0 1 1 1 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 1 2 0 5 8 22 13 15 5 4 15 1 3 0 0

1 1 1 1 1 0 5 0 0 0 0 0 0 0 1 0 0 1 0 0 1 1 1 0 21 34 49 4 10 5 4 13 1 1 0 0

0 0 1 3 1 0 3 0 0 0 0 0 0 0 0 0 0 0 0 0 0 3 0 0 0 1 7 15 15 1 1 15 3 0 0 0

0 0 0 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 5 15 15 1 0 15 0 0 0 0

0 0 0 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 0 0 1 1 1 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 0 0 3 1 1 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 6 15 15 1 0 15 0 0 0 0

0 0 0 5 1 0 0 0 0 0 0 0 0 2 0 0 0 0 0 0 0 0 0 0 2 3 15 15 15 2 1 15 0 0 0 0

0 0 1 1 1 1 2 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 2 11 15 15 2 1 15 0 0 0 0

0 0 0 4 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 12 15 15 2 1 15 2 0 0 0

0 0 1 0 1 1 6 0 0 0 0 0 1 0 0 0 0 0 1 1 0 0 0 0 1 2 13 15 15 2 0 15 0 0 0 0

0 0 0 5 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 1 0 1 16 15 15 3 0 15 0 0 0 0

0 0 0 5 1 0 0 0 0 0 0 1 1 0 0 0 0 0 0 0 0 0 0 5 1 3 13 15 15 3 1 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 1 0 0 1 1 0 1 1 6 5 5 0 3 6 0 1 1

0 1 1 4 1 0 12 0 0 0 0 0 0 0 0 1 0 0 0 0 0 1 2 7 5 6 20 12 13 5 3 15 1 3 0 0

0 0 0 0 1 1 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 1 3 3 4 7 21 13 15 4 2 15 1 4 0 0

0 1 1 4 1 0 9 0 0 0 0 0 0 2 0 0 0 0 0 0 0 0 0 0 2 3 17 15 15 3 1 15 0 0 0 0

0 0 0 3 1 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 2 0 0 0 1 6 15 15 1 0 15 2 0 0 0

0 0 1 2 1 0 2 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 12 15 15 2 0 15 0 0 0 0

0 1 1 2 1 0 5 0 0 0 0 1 0 2 0 0 0 0 0 0 0 2 0 0 0 1 11 15 15 1 1 15 2 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 1 4 0 1 2 13 15 15 1 0 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 2 0 0 0 1 8 15 15 2 1 15 2 0 0 0

0 1 1 5 1 1 5 0 1 1 1 0 1 0 1 0 1 0 0 0 0 1 1 0 2 2 0 0 6 1 1 1

0 0 0 1 1 0 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 1 2 11 15 15 2 0 15 0 0 0 0

0 0 0 2 1 1 0 0 0 0 0 0 0 3 0 0 0 0 0 0 0 0 0 0 1 2 9 15 15 1 0 15 0 0 0 0

0 1 0 2 1 0 0 0 0 1 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 1 1 2 1 0 2 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 1 1 1 1 1 5 0 0 0 0 0 1 3 0 0 0 1 1 1 0 4 0 8 7 7 0 0 6 0 1 3

0 0 1 2 1 0 9 0 0 0 0 1 0 0 0 0 0 0 0 0 0 1 4 0 1 2 7 15 15 1 0 15 0 0 0 2

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 0 0 3 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 10 15 15 1 0 15 0 0 0 0

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34 379978 34 2 0 0 3 0 1 1 0 0 50 0 0 15 1 1 0 0 1 1 0 0 1 0 1 1 3 1 2 2 0 1 2.1 2.1 1.7 0 1 0

35 349951 57 2 1 0 0 0 1 1 0 0 312 0 0 15 0 0 0 1 0 0 0 0 1 0 1 1 1 1 1 3 1 1 4.5 1.7 1.3 0 0 0

36 379816 25 2 0 0 0 7 1 0 1 0 10 1 0 15 2 1 0 0 0 0 0 0 1 1 0 1 0 0 3 3 0 1 2.7 7.9 6.2 0 1 0

37 381087 60 2 1 0 0 8 1 1 1 0 7 1 0 15 1 4 1 0 0 0 0 0 1 0 0 1 0 0 2 1 0 1 5 6.9 4.8 0 0 0

38 327026 70 2 1 0 0 0 0 0 0 0 381 0 0 15 0 0 0 1 0 0 0 0 1 0 1 1 0 0 1 1 0 1 5.1 5.1 2.4 0 0 0

39 381895 56 1 1 0 0 7 1 1 0 0 3 0 0 15 1 3 0 0 0 1 0 0 0 0 1 1 0 0 1 1 0 1 3.2 6.1 2.9 1 1 0

40 382453 53 2 1 0 0 8 1 0 0 0 8 0 0 15 1 2 0 0 0 1 0 0 1 0 0 1 0 0 1 2 2 1 0 0 0 0 1 0

41 380465 38 1 0 0 0 8 1 0 0 0 1460 0 0 15 1 0 0 0 0 0 0 0 1 0 1 1 0 0 6 2 0 1 3.6 13.2 8.7 0 0 0

42 382831 49 2 0 0 0 8 1 0 1 0 5 1 0 15 1 4 1 0 0 1 0 0 1 1 0 1 0 0 1 1 0 1 2.8 13.6 10 1 1 0

43 383010 51 2 1 0 0 7 1 1 0 3 15 0 0 15 1 2 0 0 1 0 0 0 1 1 1 1 2 1 1 1 0 2 0 0 0 0 0 0

44 382898 56 2 1 0 0 0 0 0 0 5 42 0 1 15 0 0 0 1 1 0 0 0 1 1 1 1 10 0 4 3 0 1 4.9 12.1 16.9 0 0 0

45 383745 51 1 0 0 0 0 0 0 1 0 150 1 0 15 0 0 0 1 0 0 0 0 1 0 0 1 0 0 2 2 0 1 2.6 10 6 0 0 0

46 385280 54 1 0 0 0 7 1 0 0 1 13 0 0 13 2 4 1 0 0 1 0 0 1 0 0 1 0 0 1 1 0 1 0 0 0 0 0 0

47 385806 77 2 1 1 0 0 1 0 0 0 7 0 0 15 1 3 0 0 0 1 0 0 1 0 0 1 3 1 2 3 0 1 2.2 3.6 2.8 0 1 0

48 387281 53 1 0 0 0 7 1 0 1 0 15 1 0 15 1 1 0 0 0 1 0 0 1 1 0 1 0 0 2 1 0 1 1.2 2.5 1.6 0 0 0

49 386650 53 1 0 1 0 8 1 1 0 3 28 0 0 15 1 4 1 0 0 1 1 0 1 0 0 1 1 1 3 2 0 1 0.7 2.3 2 0 1 0

50 387696 70 2 1 0 0 0 1 0 1 0 8 1 0 15 1 2 0 0 0 1 0 0 1 1 0 1 12 1 1 2 0 1 3 7.4 4.6 0 0 0

51 389334 50 2 0 0 0 0 1 1 1 0 16 1 0 15 1 4 1 0 1 1 0 0 1 1 0 1 1 1 1 1 0 1 0 0 0 0 1 0

52 389295 67 2 0 0 0 8 1 0 1 0 22 1 0 15 1 2 0 0 0 1 0 0 1 1 0 1 0 1 1 1 0 1 4 6.3 4.3 0 0 0

53 390365 60 2 1 1 0 7 1 1 0 0 8 0 0 15 1 1 0 0 0 0 0 0 1 0 0 1 0 0 1 1 2 1 0 0 0 0 0 0

54 390480 72 2 1 0 3 0 1 1 0 3 67 0 0 15 1 3 0 1 0 1 0 0 1 0 0 1 0 0 1 1 0 1 3 5.6 3 0 1 0

55 391656 60 2 1 1 0 0 1 1 1 0 15 1 0 15 1 2 0 0 0 1 0 0 1 1 0 1 0 0 2 2 0 1 2.5 8 4 0 0 0

56 391729 50 2 0 0 0 8 1 0 0 0 12 0 1 15 1 0 0 0 0 0 0 0 1 0 1 5 0 1 1 1 0 1 1.7 5.2 2.7 0 0 0

57 392592 59 2 1 0 0 0 1 0 0 0 18 0 0 14 2 2 0 0 0 0 0 0 1 0 1 1 13 1 1 2 1 1 0 0 0 0 0 0

58 393383 60 1 0 0 0 0 0 0 0 3 7 0 1 13 2 3 0 0 0 1 0 0 1 0 0 1 0 0 1 3 0 1 0 0 0 0 0 0

59 394625 51 1 1 1 0 7 1 0 0 0 20 0 0 15 1 2 0 0 0 1 0 0 1 0 0 1 0 0 1 1 0 1 0 0 0 0 0 0

60 395114 43 2 0 0 0 8 1 0 0 4 12 0 0 15 1 2 0 0 0 0 0 0 1 0 1 1 0 0 3 1 0 1 0 0 0 0 0 0

61 395523 61 2 1 0 0 7 1 1 0 0 4 0 0 15 1 1 0 0 0 0 0 0 1 0 0 1 0 0 2 1 0 1 3.2 8.3 7.7 0 0 0

62 397738 47 1 0 0 0 0 1 0 0 3 8 0 0 15 1 2 0 0 0 0 0 0 1 0 0 1 0 0 3 3 0 1 0 0 0 0 0 0

63 398015 37 2 0 0 4 0 1 0 0 3 25 0 0 15 1 2 0 0 0 1 0 0 1 0 0 1 0 0 1 1 0 1 0 0 0 0 0 0

64 398155 62 2 1 0 5 8 0 0 1 0 21 1 0 15 0 0 0 0 0 0 0 0 1 1 1 1 0 0 5 2 0 1 4 1.6 1.2 0 0 0

65 398775 65 2 0 0 0 0 1 1 0 0 9 0 0 15 1 1 0 0 0 0 0 0 1 0 0 1 0 0 1 2 0 1 3.2 4 3.3 0 0 0

66 398739 85 2 1 0 0 7 1 0 0 3 10 0 0 15 1 2 0 0 0 1 0 0 1 1 0 1 2 1 4 1 0 1 3.2 8 6 1 0 0

3

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1 0 0 1 1 0 0 0 0 0 0 0 0 3 0 0 0 0 0 0 0 0 0 0 0 1 6 15 15 1 0 15 0 0 0 0

0 1 1 2 2 1 3 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 2 1 15 2 0 0 0

0 0 0 1 1 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 2 0 0 0 1 11 15 15 1 1 15 2 0 0 0

0 0 0 1 1 0 0 0 0 0 0 0 0 3 0 1 0 0 0 0 0 1 4 0 0 1 13 15 15 4 3 15 1 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 6 15 15 1 0 15 0 0 0 0

0 1 1 2 2 1 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 6 15 15 1 0 15 0 0 0 0

0 0 1 2 1 0 16 1 0 0 0 1 0 0 1 0 0 0 0 0 0 1 1 0 2 5 16 15 15 4 2 15 1 4 0 0

0 0 0 0 0 1 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 11 15 15 1 0 15 0 0 0 0

0 0 1 1 2 1 10 0 1 1 0 1 1 4 0 0 0 0 0 0 0 2 4 0 2 3 13 15 15 4 1 15 1 4 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 2 0 0 0 1 7 15 15 2 1 15 2 0 0 0

0 0 1 2 1 0 3 0 0 0 0 0 0 4 0 1 0 0 0 0 1 1 3 0 6 8 18 10 14 4 1 15 1 4 0 0

0 0 1 5 2 0 7 0 0 0 0 0 1 0 1 0 0 0 0 0 1 2 1 0 8 8 8 10 6 0 1 2

0 0 0 1 1 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 2 0 0 0 1 6 15 15 1 0 15 0 0 0 0

0 0 0 2 2 1 0 0 0 0 0 1 0 3 0 0 0 0 0 0 0 0 0 1 1 3 13 15 15 2 0 15 0 0 0 0

0 1 1 2 1 0 1 0 0 1 0 1 0 0 0 0 0 0 0 0 0 2 0 0 0 1 7 15 15 2 1 15 2 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 2 0 0 1 2 9 15 15 2 0 15 0 0 0 0

0 0 0 1 1 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 2 0 0 0 1 7 15 15 2 0 15 0 0 0 0

1 0 0 2 1 0 0 0 0 0 0 0 0 2 0 1 0 0 0 0 0 1 4 0 2 4 19 15 15 2 1 15 1 4 0 0

0 0 0 2 1 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 1 0 3 1 2 11 15 15 2 1 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 14 15 15 1 1 15 0 0 0 0

0 1 0 2 1 0 0 0 0 0 0 1 0 4 0 0 0 0 0 0 0 0 0 0 0 1 10 15 15 1 0 15 0 0 0 0

0 0 0 4 1 0 0 0 0 0 0 0 1 0 0 1 0 1 0 0 1 1 3 9 6 6 6 4 6 0 1 2

0 0 0 2 1 0 0 0 0 0 0 1 0 0 0 1 0 0 0 0 0 0 0 3 8 8 8 6 6 0 1 4

0 1 1 2 1 0 8 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 0 1 2 1 0 4.5 0 0 1 0 0 0 0 0 0 0 0 1 0 0 1 3 10 1 2 21 12 15 2 0 15 0 0 0 0

0 0 0 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 8 15 15 1 0 15 0 0 0 0

0 1 1 1 1 1 6 0 0 0 1 1 0 0 1 0 0 0 0 0 0 2 3 0 1 2 14 15 15 3 2 15 0 0 0 0

0 0 1 2 1 0 3 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

1 0 0 1 1 1 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 2 0 1 1 2 19 15 15 2 0 15 0 0 0 0

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67 399446 65 2 1 1 0 8 1 1 0 0 13 0 0 15 1 4 1 0 0 1 1 0 1 0 1 1 6 0 4 3 0 1 0 0 0 0 1 0

68 399576 57 2 0 0 5 0 1 0 1 0 186 1 0 15 0 0 0 1 0 0 0 0 1 0 1 1 11 1 4 2 0 1 2.3 9.1 4.8 0 0 0

69 399842 59 2 0 0 0 0 1 0 0 0 8 0 0 15 1 1 0 0 0 0 0 0 1 0 1 1 4 1 4 2 0 1 0 5.9 4.1 0 0 0

70 400315 62 1 0 0 0 7 1 0 0 0 8 0 0 15 1 2 0 0 0 1 0 0 1 1 1 1 14 0 2 1 0 1 7.5 13 11.2 0 0 0

71 401123 45 2 1 0 0 0 1 1 0 3 12 0 0 15 1 4 1 0 0 1 1 0 1 0 0 1 0 0 1 1 0 1 2.2 7.4 4.3 0 0 0

72 401066 55 1 0 0 0 8 1 1 0 3 9 0 0 15 1 4 1 0 1 1 0 0 1 1 0 1 2 1 1 1 0 1 2.7 4.7 4.3 0 0 0

73 401354 38 2 0 0 0 0 1 1 0 0 5 0 0 15 1 3 0 0 0 1 0 0 1 0 0 1 0 0 4 1 0 1 2.5 8 5 0 0 0

74 403299 60 2 1 0 4 7 1 0 0 3 2 0 0 15 1 2 0 0 0 1 0 0 1 0 0 1 0 0 2 1 0 1 2 5.5 3.5 0 0 0

75 403570 66 2 0 0 0 0 1 0 1 3 16 1 0 15 1 0 0 1 0 0 0 0 1 1 1 1 0 0 1 1 1 1 3.5 10.5 10.3 0 0 0

76 404655 59 1 0 0 0 8 1 1 0 0 25 0 0 15 1 2 0 0 0 1 0 0 1 1 1 1 0 0 2 1 0 1 3 8 5 0 0 0

77 408056 58 1 1 0 0 8 1 0 0 5 5 0 0 15 1 3 0 0 1 1 0 0 1 0 0 1 0 0 4 1 0 1 3.2 6 2.7 1 1 0

78 255645 46 2 0 0 0 7 1 1 0 3 13 0 0 15 1 3 0 0 0 1 0 0 1 0 1 1 0 0 3 1 0 1 0 0 0 0 0 0

79 408681 48 2 0 0 0 8 1 0 0 3 15 0 0 15 1 4 1 0 0 1 0 0 1 0 0 1 0 0 1 3 0 1 2 5.6 3.8 0 0 0

80 410050 57 2 0 0 0 7 1 1 0 0 6 0 0 15 1 3 0 0 0 1 0 0 1 0 0 1 0 0 1 1 0 1 4.8 4.5 4.3 0 0 0

81 409762 55 2 0 0 0 8 1 0 0 0 22 0 0 15 1 2 0 0 0 0 0 0 1 0 0 1 0 0 1 3 0 1 3.1 9.7 4.9 0 0 0

82 410234 48 2 1 0 0 0 1 1 0 3 3 0 0 15 1 3 0 0 0 1 0 0 1 0 0 1 0 0 8 1 0 1 3.7 8.2 9.4 0 0 0

83 411866 67 2 1 1 0 0 1 1 0 0 4 0 0 15 1 4 1 0 0 1 1 0 1 0 1 1 0 0 2 1 0 1 2.2 5 3 0 0 0

84 413050 68 2 0 0 0 0 0 0 0 3 7 0 0 15 1 4 1 0 0 1 0 0 1 0 1 1 0 0 1 3 0 1 4.2 13.2 11.7 0 0 0

85 413150 60 2 1 1 5 8 1 0 0 0 7 0 0 15 1 1 0 0 0 1 0 0 1 0 1 1 11 1 1 1 0 1 2.2 5 3.8 1 1 0

86 399526 57 2 0 0 5 0 1 0 1 0 420 1 0 15 0 0 0 1 0 0 0 0 1 0 1 1 11 1 1 1 0 1 5.4 9.1 4.8 0 0 0

87 416458 65 2 1 0 0 8 1 0 0 0 10 0 0 15 1 3 0 0 0 1 0 0 1 0 1 1 5 1 1 1 0 1 3.9 4.5 3.8 1 1 0

88 289935 43 2 0 0 0 0 1 1 1 0 6 1 0 15 1 0 0 1 0 0 0 0 1 0 1 1 0 0 3 2 0 1 4.2 9.6 5.5 0 0 0

89 419437 53 2 1 0 0 0 1 1 0 0 7 0 0 15 1 4 1 0 0 1 1 0 1 1 0 1 0 0 1 1 0 1 0 6.7 5.3 0 0 0

90 419732 65 2 1 0 0 7 1 0 0 3 7 0 0 15 1 3 0 0 0 1 1 0 1 0 1 1 0 0 1 3 1 1 6.3 12.6 7.5 0 0 0

91 421018 62 2 0 0 0 8 1 0 1 0 7 1 0 15 0 0 0 1 0 0 0 0 1 1 0 1 0 0 3 2 0 1 3.2 8.8 6.2 0 0 0

92 422045 73 1 1 0 0 7 1 1 0 0 3 0 1 15 1 3 0 0 0 1 0 0 1 0 0 1 0 0 2 2 0 1 3.7 6.9 5.1 0 0 0

93 422161 48 2 1 0 0 0 1 0 0 0 7 0 0 15 1 3 0 0 0 1 0 0 1 0 0 1 0 0 1 3 1 1 4.8 8.6 6 1 1 0

94 422182 70 2 1 0 0 0 1 0 0 3 5 0 0 15 1 4 1 0 0 1 1 0 1 0 1 1 2 1 3 2 0 1 4 6 4 0 0 0

95 423300 44 1 0 0 0 8 1 0 1 0 6 1 0 15 1 2 0 0 0 1 0 0 1 0 0 1 0 0 1 1 0 1 3.2 7 5.3 0 0 0

96 395816 54 2 1 0 0 7 1 0 0 5 23 0 1 15 2 3 0 0 0 1 0 0 1 0 1 1 12 1 4 1 0 1 3 3 2.7 0 0 0

97 426826 57 2 0 0 0 8 1 1 0 0 13 0 0 15 1 4 1 0 0 1 0 0 1 0 1 1 10 1 5 1 0 1 3.6 3.9 2.7 0 0 0

98 428811 55 2 1 0 0 0 1 1 1 3 7 1 0 15 2 3 0 0 0 1 0 0 1 0 0 1 0 0 2 1 0 1 3 4.8 2 0 0 0

99 429360 48 2 0 0 0 8 1 1 0 4 21 0 0 15 1 1 0 0 0 0 0 0 0 0 1 1 1 1 1 1 2 1 2.5 5 3.4 0 0 0

5

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67

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0 0 0 2 1 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

1 0 1 1 1 0 3 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 1 13 15 15 1 0 15 0 0 0 0

0 2 1 3 1 0 14 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 10 15 15 1 0 15 0 0 0 0

0 2 1 2 1 1 2 0 0 0 0 0 0 0 0 1 0 1 1 1 1 0 0 0 9 9 9 5 6 0 1 3

0 0 1 4 2 0 5 0 0 0 0 1 0 0 1 0 0 0 0 0 0 1 3 0 1 3 15 15 15 4 3 15 2 4 0 0

0 0 0 2 1 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 1 1 3 1 0 4 0 0 0 0 0 1 0 1 0 0 0 0 0 0 1 4 0 2 4 14 15 15 3 1 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 4 0 1 8 15 15 2 0 15 0 0 0 0

0 0 0 3 1 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 9 15 15 1 0 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 10 15 15 1 0 15 0 0 0 0

1 0 0 1 1 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 6 15 15 1 0 15 0 0 0 0

0 1 1 2 2 0 4 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

0 1 1 3 1 1 29 0 0 0 0 0 1 1 1 0 0 1 1 1 1 1 1 0 4 4 0 3 6 0 1 3

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 1 9 15 15 1 1 15 0 0 0 0

0 0 0 4 1 0 0 0 0 0 0 1 1 0 0 0 0 0 0 0 0 2 0 0 1 2 8 15 15 4 2 15 2 0 0 0

0 0 0 2 2 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 2 11 15 15 1 0 15 0 0 0 0

0 1 1 2 2 0 1 0 0 0 0 0 0 0 0 0 1 0 0 0 0 2 0 0 1 2 13 15 15 2 0 15 1 0 0 0

0 1 1 1 2 1 5 1 0 0 0 1 1 0 1 0 0 1 0 0 0 1 2 0 3 5 20 9 12 4 4 15 1 2 0 0

0 0 0 2 1 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 1 12 15 15 2 0 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 0 2 0 0 0 1 9 15 15 1 0 15 0 0 0 0

0 0 0 2 1 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 1 4 11 3 5 18 12 15 3 1 15 0 0 0 0

1 0 0 5 1 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 2 12 15 15 1 0 15 0 0 0 0

0 1 0 4 2 0 0 0 0 1 0 0 0 0 0 1 0 0 0 0 1 0 0 11 7 10 27 9 15 4 1 15 0 0 0 0

0 0 0 2 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 2 0 0 0

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0 0 0 5 1 0 0 0 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 7 15 15 1 0 15 0 0 0 0

6

CLINICAL PROFILE, RADIOLOGICAL AND OPERATIVE FINDINGS...

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