Cerebral Aneurysm: The Right Clinical Information, Right Where It's Needed

Cerebral aneurysm
The right clinical information, right where it's needed
Last updated: Apr 19, 2018

Table of Contents
Summary 3
Basics 4
Definition 4
Epidemiology 4
Aetiology 4
Pathophysiology 4
Classification 5
Prevention 6
Screening 6
Diagnosis 7
Case history 7
Step-by-step diagnostic approach 7
Risk factors 8
History & examination factors 9
Diagnostic tests 10
Differential diagnosis 11
Diagnostic criteria 12
Treatment 13
Step-by-step treatment approach 13
Treatment details overview 14
Treatment options 15
Follow up 19
Recommendations 19
Complications 19
Prognosis 21
Guidelines 22
Diagnostic guidelines 22
Treatment guidelines 22
Evidence scores 23
References 24
Images 28
Disclaimer 31
Summary
◊ Typically asymptomatic until ruptured, resulting in a subarachnoid haemorrhage.
◊ Head CT usually confirms the diagnosis of subarachnoid haemorrhage, but lumbar puncture is
indicated if the CT is negative and suspicion persists.
◊ Cerebral angiogram is the definitive investigation. CT angiography or magnetic resonance

angiography may also be used.
◊ Definitive treatment aims to obliterate the aneurysm from the cerebral circulation. Options include
endovascular coiling or open surgical clipping.
◊ Screening with non-invasive neuroangiography is recommended for at-risk populations.

Cerebral aneurysm Basics
Definition
A cerebral aneurysm is a focal abnormal dilation of the wall of an artery in the brain. Intra-cranial aneurysms
are most commonly located at branching points of the major arteries at the base of the brain, which course
BASICS
through the subarachnoid space. Cerebral aneurysms can, by nature of their size, compress neighbouring
nerves or brain tissue or, more devastatingly, rupture and cause significant morbidity and mortality.
Epidemiology
Autopsy studies indicate that cerebral aneurysms are fairly common in adults, with a prevalence ranging
between 1% and 5%.[3] [4] Prevalence of intra-cranial aneurysms among adults is estimated between 1.0%
and 3.2%.[5] [6] Therefore, 3 to 12 million Americans harbour intra-cranial aneurysms. The incidence of
reported ruptured aneurysms is about 6 to 7 in every 100,000 people per year.[7]
Cerebral aneurysms can occur at any age but are more common in adults than children. Women are more
likely to harbour cerebral aneurysms than men. Epidemiological studies show that 7% to 20% of patients with
aneurysmal subarachnoid haemorrhage have a first- or second-degree relative with a confirmed intra-cranial
aneurysm.[8]
Aetiology
Although once thought to be congenital, saccular aneurysms are now regarded as an acquired,
haemodynamically induced injury to the vascular wall. Other less common causes include trauma, infection,
tumour, arteriovenous malformations/fistulas, and drug abuse.
The well-known association with heritable connective tissue diseases and the familial occurrence support
a genetic factor. It is considered specifically in patients with autosomal dominant polycystic kidney disease,
Ehlers-Danlos syndrome type IV, neurofibromatosis type 1, and Marfan's syndrome.[9]
All population studies have consistently shown that cigarette smoking increases the risk for aneurysmal
subarachnoid haemorrhage (SAH).[10] [11] [12] [13]
Moderate- to high-level alcohol consumption is an independent risk factor for aneurysmal subarachnoid
haemorrhage (SAH).[13]
Pathophysiology
Blood vessels are composed of three layers: tunica intima, tunica media (muscularis), and tunica externa
(adventitia). The intima and media are separated by the lamina elastica interna, and the media and adventitia
are separated by the membrana elastica externa. In cerebral vessels the media is thinner and the membrana
elastica externa is negligible.
Although the pathophysiology of traumatic and infectious cerebral aneurysms is obvious, that of spontaneous
saccular aneurysms is less clear. Hypertension and smoking are thought to contribute significantly to the
vascular changes associated with saccular cerebral aneurysms.[9] One hypothesis relates to the effect
cigarette smoking has on inhibitors of proteases, which results in degradation of various connective tissues,
including arterial walls.[14] In pathology specimens, the tunica media is decreased and the aneurysm sac
is therefore reduced to a single layer of endothelial cells and a thin fibrous layer. The lamina elastica interna
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 19, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
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subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Cerebral aneurysm Basics
ends at the entrance to the aneurysm sac.[15] Continuous arterial pressure directed on this abnormal section
of the artery leads to aneurysmal out-pouching, particularly at arterial branch points, where the pressure is
higher.[9]
BASICS
With increased availability and improved sensitivity of non-invasive cerebral imaging techniques, more
unruptured cerebral aneurysms are being detected. Although they are often discovered incidentally,
unruptured aneurysms can cause symptoms through the mass effect on neighbouring cranial nerves or brain
parenchyma.
Classification
Morphological types of cerebral aneurysm[1]
1. Saccular
• Often termed a berry aneurysm, as it resembles a berry hanging from a vine

• Rounded out-pouching attached by a neck or stem to a brain artery.
2. Fusiform
• Also called atherosclerotic aneurysm

• Forms as media damage leads to arterial stretching and elongation
• Intra-luminal clots may form.
3. Dissecting
• Often termed pseudo-aneurysm

• Forms as blood accumulates within a tear between the layers of the cerebral artery
• Depending on which plane is dissected, either luminal narrowing or a sac-like out-pouching can
occur.
Classification of cerebral aneurysm based on size[2]

• Small: 2 to 7 mm in diameter
• Medium: 7 to 12 mm in diameter
• Large: 13 to 24 mm in diameter
• Giant: >25 mm in diameter.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 19, 2018.
5
Cerebral aneurysm Prevention
Screening
Screening for asymptomatic cerebral aneurysms is warranted, as rupture is associated with a very poor
prognosis and treatment of unruptured aneurysms is associated with a low morbidity and mortality.[9]
Magnetic resonance angiography (MRA) is considered the appropriate first test in cerebral aneurysm
screening, as it is non-invasive and safe. The primary limitation is the inability to reliably detect aneurysms
<3 mm in diameter.[26] CT angiography (CTA) adds the small risk associated with giving a bolus of non-ionic
contrast, but it is particularly helpful in visualising cerebral vasculature with clips in place.
Screening for cerebral aneurysms is indicated for patients with two or more family members affected by
cerebral aneurysm or subarachnoid hemorrhage. In these cases, history of hypertension, smoking, and
female sex are risk factors associated with aneurysm occurrence.[27] Screening is also indicated with certain
genetic syndromes, such as Ehlers-Danlos syndrome type IV, Marfan syndrome, neurofibromatosis type 1,
and autosomal dominant polycystic kidney disease.[28] It is also judicious to offer CTA or MRA to patients
with coarctation of the aorta, and patients with microcephalic osteodysplastic primordial dwarfism.[27] Finally,
screening those with a first-degree family history of cerebral aneurysm is advised, as a positive family history
increases the risk of cerebral aneurysm up to sevenfold.[29]
Patients with a prior history of cerebral aneurysms also have a higher rate of future de novo aneurysm
PREVENTION
formation and should be screened at 5-year intervals.[30]
Cerebral aneurysm Diagnosis
Case history
Case history #1
A 45-year-old woman was having dinner when she felt the sudden onset of a severe headache, unlike
anything she had ever experienced. She vomited many times before her husband brought her to seek
medical attention. On presentation she requires stimulation to maintain alertness and has mild nuchal
rigidity. Her blood pressure is elevated but examination is otherwise normal. CT of the brain reveals
subarachnoid blood in the anterior interhemispheric fissure. Angiography reveals a 7-mm aneurysm in the
anterior communicating artery.
Case history #2
An anxious 30-year-old woman seeks medical attention because of recent worsening headaches and
visual disturbances. She is a smoker and has a sibling who was admitted to hospital for a ruptured
cerebral aneurysm. Examination discloses slight ptosis of the left eye. On neurological examination, her
left pupil is dilated, minimally reactive to light, and pointing inferiorly and laterally at rest. CT of the brain
shows no subarachnoid blood. Lumbar puncture is normal. Magnetic resonance angiography of the brain
reveals a 5-mm aneurysm in the left posterior communicating artery.
Other presentations
At the brief moment of aneurysmal rupture, intra-cranial pressure rises to approach mean arterial
pressure, thereby dropping the cerebral perfusion pressure. This may explain the transient or persisting
decreased consciousness that can occur. The severity of the haemorrhage and its effects on intra-cranial
pressure ultimately determine the severity of the presenting symptoms. Prodromal symptoms may point
to the location of an unruptured aneurysm and suggest progressive enlargement, such as in a posterior
communicating artery aneurysm compressing the third cranial nerve. A sudden unexplained headache in
any location should arouse suspicion of subarachnoid haemorrhage.
DIAGNOSIS
Step-by-step diagnostic approach
Patients with an unruptured cerebral aneurysm may be asymptomatic. As the aneurysm increases in size it
may cause symptoms of increased intra-cranial pressure (such as headaches and vomiting) or focal cranial
nerve lesions. Rupture of a cerebral aneurysm with resulting subarachnoid haemorrhage (SAH) is the most
feared clinical manifestation of cerebral aneurysms.
History
Unruptured aneurysms are often asymptomatic and are detected either incidentally or on screening.
Aneurysms can rupture at any time, but rupture may be associated with exertion or stress.[17] An
unusual, unexpected abrupt-onset headache is the most common symptom and is usually accompanied
by nausea and/or vomiting, and possibly an abrupt change in consciousness. Patients sometimes report
an unusual headache several weeks prior, which may represent a minor leak of blood into the wall of the
aneurysm or into the subarachnoid space (known as a sentinel headache).[18] In some cases the severity
7
of the headache can be quite mild and misleading. In every patient complaining of a new headache, SAH
should be considered as an important secondary cause and be investigated when appropriate.
Physical examination
In an unruptured aneurysm, the examination is usually unremarkable. However, a pressure effect from
the aneurysm may produce focal neurological signs.[19] The classic syndrome is that of a third nerve
palsy with pupillary dysfunction from a posterior communicating artery aneurysm exerting mass effect.
In a ruptured aneurysm, findings depend on the severity and location of the SAH; there may be nuchal
rigidity and intraocular haemorrhage. The neurological examination may be normal in an SAH, show focal
neurological signs due to a local mass effect from a haematoma, or the patient may be in a deep coma
with decerebrate rigidity.
Investigations
CT head scan without contrast is the preferred initial diagnostic test when SAH is suspected. Modern,
third-generation CT scanners are highly sensitive (92.9%) and specific (100%) for identifying patients
with SAH, particularly if performed within 6 hours when sensitivity improves to 97% to 100%.[20] If the CT
scan does not show subarachnoid blood and there is high clinical suspicion, a lumbar puncture should be
performed. Grossly bloody cerebrospinal fluid (CSF) that does not clear suggests SAH. A more definitive
finding is the presence of xanthochromia, a yellowish discoloration of CSF coming from breakdown
products of haemoglobin. This usually takes about 12 hours to develop.[21]
Conventional cerebral angiography is still the preferred imaging modality for a cerebral aneurysm,
ruptured or unruptured. With a resolution of 50 micrometres, conventional cerebral angiography,
including 3-dimensional reconstructions, not only has the highest sensitivity but also allows for better
characterisation of the morphology, orientation, neck size, adjacent vessels, and any additional
aneurysms. However, CT angiography is an alternative investigation with high accuracy and increased
sensitivity in diagnosing cerebral aneurysms.[22] CT angiography is also useful in that it can be quickly
obtained and can help guide the decision making and urgency of subsequent studies. Magnetic-
resonance angiography takes longer to perform than CT angiography and is therefore more problematic
DIAGNOSIS
in critically ill patients. However, it is the investigation of choice for screening because it is non-invasive
and safe.
[Fig-1]
[Fig-2]
[Fig-3]
Risk factors
Strong
smoking
• Consistently identified in all populations studied.
moderate- to high-level alcohol consumption

• Moderate- to high-level alcohol consumption is an independent risk factor for aneurysmal
subarachnoid haemorrhage (SAH).[13]
FHx subarachnoid haemorrhage
• Highest in siblings. No single Mendelian model but several possible patterns of inheritance identified.
Most likely autosomal dominant.[9]
previous subarachnoid haemorrhage

• Multiple aneurysms are consistently seen in follow-up studies of patients with subarachnoid
aneurysmal haemorrhage.
heritable connective tissue disease

• Considered specifically in patients with autosomal dominant polycystic kidney disease, Ehlers-Danlos
syndrome type IV, neurofibromatosis type 1, and Marfan's syndrome.[9]
Weak
hypertension
• Hypertension is a weak risk factor for aneurysm formation and rupture, although population studies
examining its importance have produced conflicting results.
head trauma
• May cause damage to the vascular wall leading to aneurysm formation.
intracranial infection
• May cause damage to the vascular wall leading to aneurysm formation.
tumour
• The presence of an intracranial tumour can lead to aneurysm formation.
arteriovenous malformations or fistulas

• Arteriovenous malformations or fistulas in the intracranial circulation can develop into aneurysms.
DIAGNOSIS
drug abuse
• Drug abuse can lead to cerebral aneurysm formation (particularly amphetamines, cocaine, and
ecstasy).[16]
History & examination factors

Key diagnostic factors
presence of risk factors (common)
• Key risk factors include smoking, moderate- to high-level alcohol consumption, previous subarachnoid
haemorrhage (SAH), FHx SAH and heritable connective tissue diseases.
headache (common)
• New, never-before-experienced headache suggests ruptured cerebral aneurysm.
• The character of the headache can be quite variable.
9
Other diagnostic factors

seizures (uncommon)
• New, never-before-experienced focal or generalised seizures.
nuchal rigidity (uncommon)

• New neck stiffness that includes pain on stretching the neck meninges with manoeuvres. More
commonly found in subarachnoid haemorrhage.
decreased level of consciousness (uncommon)

• More commonly found in subarachnoid haemorrhage. Usually related to concurrent hydrocephalus.
focal neurological deficit (uncommon)

• Variable, depending on mass effect of aneurysm and/or haematoma. More commonly found in
subarachnoid haemorrhage.
• The classic syndrome is that of a third nerve palsy with pupillary dysfunction from a posterior
communicating artery aneurysm exerting mass effect.[19]
Diagnostic tests
1st test to order
Test Result
conventional catheter-based angiogram aneurysm in relation to
• Highest spatial resolution in determining aneurysm size, location, and arteries
morphology in relation to nearby arteries.
• Three-dimensional reconstruction allows for further resolution of
aneurysm configuration.
• Initial test after ruptured aneurysm has been diagnosed on CT or
DIAGNOSIS
lumbar puncture.
[Fig-1]
[Fig-2]
[Fig-3]
CT angiography aneurysm location/size
• Shows cerebral vessels in 3 dimensions. May be helpful in
establishing a baseline from which to monitor for cerebral
vasospasm.
• Sensitivity from 0.77 to 0.97. Sensitivity drops for aneurysms <3 mm.
Specificity from 0.87 to 1.00.[19]
magnetic resonance angiography aneurysm location/size
• Takes longer to perform than CT angiography, therefore more
problematic in critically ill patients.
• Can be used as an initial test for unruptured cerebral aneurysms and
is the investigation of choice for aneurysm screening.
• Sensitivity from 0.69 to 0.99. Like CT angiography, sensitivity drops
for aneurysms <3 mm in size. Specificity is 1.00.[19]
Emerging tests
Test Result
CT head scan subarachnoid blood
in ruptured or leaking
• Preferred initial diagnostic study in subarachnoid haemorrhage.
aneurysm; calcified or
• About 95% of patients have evidence of subarachnoid blood on a
thrombosed aneurysm
non-contrast head CT obtained within the first 48 hours after rupture.
may also be seen on CT
lumbar puncture elevated red blood cell

count with xanthochromia
• Contraindicated if there is a suspicion for a mass lesion (lateralising
neurological deficits or papilloedema).
• Reserved for about 5% of patients in whom head CT is normal with
suspected subarachnoid haemorrage.
• Bloody cerebrospinal fluid (CSF) that does not clear with continued
egress of fluid raises index of suspicion.
• The presence of xanthochromia, a yellowish discoloration of CSF
representing bilirubin, is more specific than elevated red cell count in
CSF.
Differential diagnosis
Condition Differentiating signs / Differentiating tests

symptoms
Arteriovenous • Subacute presentation. • Diagnostic cerebral
malformation • Presents more often with angiography and/or MRI
seizures. of the brain will show an
arteriovenous malformation.
Hypertensive intra- • Age >55 years. • Diagnostic cerebral

cerebral haemorrhage • Hx of hypertension. angiography will be normal.
• Headache with focal • CT or MRI of the brain will
DIAGNOSIS
neurological deficit. show a focal haematoma
more typical for a
hypertensive haemorrhage.
Cerebral venous sinus • Middle-aged woman. • Diagnostic cerebral

thrombosis • Subacute presentation. angiography will show slow
• May have known arteriovenous transit if there
hypercoagulable state. is venous hypertension,
• Papilloedema seen on and a flow defect in a major
examination. sinus.
• Pattern of haemorrhage on
CT or MRI will be adjacent to
cortical vein or sinus.
Traumatic subarachnoid • Older patient with a fall. • CT or MRI will show

haemorrhage • Headache usually less haemorrhage focused along
severe. the bony contour, sometimes
with an associated skull
fracture.
11
Condition Differentiating signs / Differentiating tests

symptoms
Haemorrhagic tumour • Hx of primary malignancy, • CT or MRI may show a
particularly lung or renal mass with surrounding
carcinoma. haemorrhage.
• A thrombosed aneurysm
may produce surrounding
oedema and haemorrhage
mimicking a mass.
Diagnostic criteria
Hunt and Hess grading scale for subarachnoid haemorrhage[23]
• Grade 1: asymptomatic or minimal headache and slight nuchal rigidity
• Grade 2: moderate to severe headache, nuchal rigidity, and no neurological deficit other than cranial
nerve palsy
• Grade 3: drowsiness, confusion, or mild focal deficit
• Grade 4: stupor, moderate to severe hemiparesis, and, possibly, early decerebrate rigidity and
vegetative disturbance
• Grade 5: deep coma, decerebrate rigidity, and moribund appearance.
World Federation of Neurological Surgeons scale for subarachnoid

haemorrhage[24]
• Grade 1: Glasgow coma score (GCS) of 15, motor deficit absent
• Grade 2: GCS 13-14, motor deficit absent
• Grade 3: GCS 13-14, motor deficit present
•
DIAGNOSIS
Grade 4: GCS 7-12, motor deficit absent or present

• Grade 5: GCS 3-6, motor deficit absent or present.
Fisher scale[25]
Radiological classification based on findings on CT of head:
• Group 1: no blood detected

• Group 2: diffuse deposition of subarachnoid blood, no clots, and no layers of blood >1 mm
• Group 3: localised clots and/or vertical layers of blood ≥1 mm in thickness
• Group 4: diffuse or no subarachnoid blood but intra-cerebral or intra-ventricular clots are present.
Cerebral aneurysm Treatment
Step-by-step treatment approach

The main goal of treatment is to exclude the aneurysm sac from the intracranial circulation while preserving
the parent artery. In unruptured aneurysms, the decision as to whether to treat or observe the aneurysm is
made on a case-by-case basis.[31] In ruptured aneurysms, early treatment is essential.
Unruptured aneurysms
For aneurysms that have not ruptured, the choice is observation or treatment.[27] Observation consists
of periodic imaging studies of increasingly greater duration along with regular visits to the physician.
Treatment consists of either open surgical clipping or endovascular obliteration. The choice of observation
or treatment needs to be made on a case-by-case basis by a specialist experienced in the management
of cerebral aneurysms. Factors to consider include:
• Patient age: increased risk of treatment and shorter life expectancy tend to favour observation in
older patients with asymptomatic aneurysms.
• Aneurysm location: the risk of rupture varies depending on the location of the aneurysm.
Cavernous carotid artery aneurysms carry the lowest risk, anterior circulation aneurysms carry an
intermediate risk, and posterior circulation aneurysms carry the highest risk of rupture.
• Aneurysm size: the risk of rupture increases with the size of the aneurysm. In asymptomatic
patients without a history of subarachnoid haemorrhage, small aneurysms (i.e., <7 mm) can
generally be observed.[3]
• Presence of symptoms: symptomatic aneurysms should be considered for treatment regardless of
size. Urgent consideration for treatment is needed for symptomatic intradural aneurysms.
• Comorbid medical illness: increases the risk of treatment.
• Risks of treatment: the 2 main risks are surgery-related death and poor neurological outcomes.
Ruptured aneurysms
Treatment is instituted early for those with a ruptured aneurysm, particularly those with clinically
favourable Hunt and Hess grades. Treatment of unruptured co-existing aneurysms should also be
considered. Surgery for cerebral aneurysm involves placing a clip across the neck of an intra-cranial
aneurysm and has a long track record of demonstrated efficacy. It was originally performed in 1936, and
recent advances with microsurgical techniques, the operating microscope, bipolar coagulation, and an
array of self-closing aneurysm clips mean that the attributable risk of the procedure is fairly low.[9] The
size, location, and configuration of the aneurysm, along with brain oedema, vasospasm, and surrounding
tenacious clot, all complicate microsurgical clipping and can increase procedural complications.
Endovascular therapy for cerebral aneurysms involves insertion of soft metallic coils within the lumen
of the aneurysm, which are detached once they are in place.[32] 1[C]Evidence The coils, some bare
platinum, some with various surface additives, all promote thrombosis within the aneurysm dome.[33]
A comparison of hydrogel-coated coils versus bare platinum coils did not show an improvement in long-
term clinical outcome with the coated device, although it did seem to reduce major recurrence.[34] Factors
that complicate endovascular treatment are the presence of a wide neck, a giant aneurysm with intra-
TREATMENT
aneurysm thrombus, and the presence of eloquent arterial branches emanating from the aneurysm
dome. Adjunctive devices, such as balloons and intra-cranial stents, can enable aneurysms that were
previously difficult to coil to be successfully treated.[35] Flow-diverter devices can also be used to treat
13
cerebral aneurysms. Evidence shows that treatment of cerebral aneurysms with flow-diverter devices is
an effective endovascular procedure with high complete occlusion rates.[36]
The International Subarachnoid Aneurysm Trial (ISAT) compared the safety and efficacy of endovascular
coil treatment and surgical clipping for the treatment of ruptured cerebral aneurysms.[37] The primary
results of ISAT were that, among patients equally suited for both treatment options, endovascular coil
treatment yielded substantially better outcomes than surgery in terms of survival free of disability at
1 year. A follow-up study of the ISAT participants demonstrated that endovascular coil treatment was
also associated with increased long-term survival (at 10 years) when compared with neurosurgical
repair.[38] Extracranial-intracranial bypass can be considered if a clip application or coiling procedure
cannot be performed.[39]
[Fig-4]
[Fig-5]
Supportive care for ruptured aneurysms

The patient should be monitored in a quiet room in the neurointensive care unit. If the patient is agitated,
mild sedation is recommended. The head end of the bed should be kept raised to around 30°.
The systolic blood pressure should be maintained at no more than 130 mmHg to 140 mmHg until the
aneurysm has been excluded from the circulation and there is no clinical evidence of vasospasm.
Calcium-channel blockade with nimodipine is given to all patients.
Stool softeners are given to prevent Valsalva manoeuvres that may cause peaks in systolic blood
pressure and intra-thoracic pressure.
Treatment details overview

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Acute ( summary )
unruptured aneurysm
1st observation and/or exclusion of

the aneurysm from the intra-cranial
circulation
ruptured aneurysm
1st cardiopulmonary support
plus exclusion of the aneurysm from the intra-

cranial circulation
TREATMENT
adjunct prevention of vasospasm
adjunct blood pressure (BP) control
adjunct stool softener
Treatment options
Acute
unruptured aneurysm
1st observation and/or exclusion of

the aneurysm from the intra-cranial
circulation
Primary options
» observation
OR
» surgical clipping
OR
» endovascular obliteration
» Observation consists of periodic imaging

studies of increasingly greater duration along
with regular visits to the physician. Treatment
consists either of open surgical clipping or
endovascular obliteration.
» The choice of observation or treatment needs

to be made on a case-by-case basis by a
specialist experienced in the management of
cerebral aneurysms.
» Small aneurysms (i.e., <7 mm) can generally

be observed.[3]
» Cavernous carotid artery aneurysms carry the

lowest risk, anterior circulation aneurysms carry
an intermediate risk, and posterior circulation
aneurysms carry the highest risk of rupture.
» Symptomatic aneurysms should be considered

for treatment regardless of size. Urgent
consideration for treatment is needed for
symptomatic intradural aneurysms.
» Increased risk of treatment and shorter life

expectancy tend to favour observation in older
patients.
» Comorbid medical illness also increases the

risk of treatment.
TREATMENT
ruptured aneurysm
1st cardiopulmonary support
» Patients should be admitted to the intensive

care unit.
15
Acute
» Consciousness level should be assessed
using the Glasgow Coma Scale, and need
for endotracheal intubation and mechanical
ventilation should be established. Blood
pressure, heart rate, and respiratory function
should be closely monitored.[40]
plus exclusion of the aneurysm from the intra-
cranial circulation
Primary options
» surgical clipping
OR
» endovascular obliteration
Secondary options
» extracranial-intracranial bypass
» Treatment is instituted early for those with

a ruptured aneurysm, particularly those with
clinically favourable Hunt and Hess grades.
» Surgery involves placing a clip across the neck

of an intra-cranial aneurysm. The attributable
risk of the procedure is fairly low.[9] The size,
location, and configuration of the aneurysm,
along with brain oedema, vasospasm, and
surrounding tenacious clot, all complicate
microsurgical clipping and can increase
procedural complications.
» Endovascular therapy for cerebral aneurysms

involves insertion of soft metallic coils within
the lumen of the aneurysm, which are detached
once they are in place.[32] 1[C]EvidenceThe
coils promote thrombosis within the aneurysm
dome.[33] Factors that complicate endovascular
treatment are the presence of a wide neck, a
giant aneurysm with intra-aneurysm thrombus,
and the presence of eloquent arterial branches
emanating from the aneurysm dome. Adjunctive
devices including balloons and intra-cranial
stents can be used in difficult cases. Flow-
diverter devices can also be used to treat
cerebral aneurysms. Evidence shows that
treatment of cerebral aneurysms with flow-
diverter devices is an effective endovascular
procedure with high complete occlusion
rates.[36]
TREATMENT
» The preferred treatment depends on

patient factors (age, clinical grade after the
haemorrhage, comorbidities, and expected
longevity) and aneurysm factors (location, size,
Acute
shape, dome-to-neck ratio, and presence of
calcification).
» Extracranial-intracranial bypass can be

considered if a clip application or coiling
procedure cannot be performed.[39]
» Treatment of unruptured co-existing

aneurysms should also be considered.
[Fig-4]
[Fig-5]
adjunct prevention of vasospasm
Primary options
» nimodipine: 60 mg orally every 4 hours for

21 days
» Nimodipine is standard treatment for

the prevention of ischaemia from cerebral
vasospasm following subarachnoid
haemorrhage. There is evidence that nimodipine
may improve the clinical outcome in patients
with aneurysmal subarachnoid haemorrhage
and decrease the incidence of symptomatic
cerebral vasospasm, delayed neurological
deficits, and cerebral infarction.[41] It is
speculated to act at the cellular level, perhaps as
a neuroprotectant.[42]
» Therapy should be started within 96 hours of

haemorrhage.
adjunct blood pressure (BP) control
Primary options
» labetalol: 20 mg intravenous bolus initially,

followed by 40-80 mg every 10 minutes
according to response, maximum 300 mg
total dose; 0.5 to 2 mg/min intravenous
infusion, maximum 300 mg total dose;
switching from intravenous therapy: 200 mg
orally initially when BP controlled, followed by
200-400 mg every 6-12 hours
OR
» enalaprilat: 0.625 to 1.25 mg intravenously

every 6 hours
TREATMENT
Secondary options
» nicardipine: 5 mg/hour intravenous infusion

initially, increase by 2.5 mg/hour increments
every 15 minutes according to response,
maximum 15 mg/hour
17
Acute
» Anti-hypertensive agents are used to control
BP. Mean arterial pressure can be used as a
parameter and should be kept <100 mmHg.
adjunct stool softener
» May be given to prevent Valsalva manoeuvres

that may cause peaks in systolic blood pressure
and intra-thoracic pressure.
TREATMENT
Cerebral aneurysm Follow up
Recommendations
Monitoring
FOLLOW UP
In patients who have suspected subarachnoid haemorrhage (SAH) but no angiographical evidence for
aneurysms or arteriovenous malformations on any studies, angiography is repeated within 1 week, and
then again in 1 to 6 weeks.[42] Patients with a confirmed SAH and aneurysms generally have a post-
operative angiogram if clipped, or a 6-month follow-up angiogram if coiled.
Any suspicion of an incomplete occlusion during aneurysm treatment should be followed with repeat
angiography at 6 months, then periodically with non-invasive imaging with increasing duration between
investigations.
Patients with a history of cerebral aneurysms, who are at higher risk for developing future de novo
cerebral aneurysms, should undergo periodic non-invasive cerebral vascular imaging, including magnetic
resonance or CT angiography of the brain.
Patient instructions
Complications
Complications Timeframe Likelihood

subarachnoid haemorrhage#(SAH)-related death short term medium
About 12% of patients with SAH die before they receive medical attention,[44] and 40% of patients
admitted to hospital die within 1 month after the rupture.[45]
SAH-related vasospasm short term medium
This seems to be a reaction of basal cerebral blood vessels to the breakdown products of the
subarachnoid blood. It is related to prolonged and intense smooth muscle contraction associated with
smooth muscle cell proliferation, fibrosis, and inflammatory changes.[46]
It is the main cause of delayed morbidity or death and occurs in up to 30% of patients with SAH.[47]
Vasospasm typically occurs 4 to 10 days after haemorrhage onset and correlates with the amount of
subarachnoid clot adjacent to the basal vessel. It clinically manifests as acute neurological deficit.
The Fisher grade uses a 4-point scale to describe the amount of blood on non-contrast CT of the head
and has been shown to correlate with the complication of vasospasm.[25]
Trans-cranial Doppler is effective for monitoring the degree of vasospasm.
Nimodipine is the standard treatment for preventing ischaemia related to vasospasm. Medical
management is with triple H therapy (hypertension, haemodilution, and hypervolaemia).
Intra-arterial vasodilator or balloon angioplasty may be required if medically refractory.
SAH-related hyponatraemia short term medium
19

Hyponatraemia may be due to syndrome of inappropriate anti-diuretic hormone secretion (SIADH) or
cerebral salt wasting (CSW).[47] SIADH represents a primary disruption in water regulation, with intact
FOLLOW UP
sodium and volume regulation. In CSW, hyponatraemia results from renal sodium loss, leading to intra-
vascular volume loss (an opposite mechanism to that found in SIADH).
Fluid restriction to an amount less than urinary output (while attempting to maintain normal sodium intake)
gradually corrects hyponatraemia in most cases due to SIADH.
CSW should be treated with enteral sodium and intravenous hypertonic saline.[47]
risks of treatment procedures short term low
The risks of endovascular obliteration include arterial dissection, parent artery occlusion, and
thromboembolic complications. Intra-procedural rupture of the aneurysm during advancement of the
catheter into the aneurysm is one of the most serious complications.
The risks of surgical aneurysm repair include vessel injury, stroke, infection, and injury to the brain
parenchyma.
aneurysm recurrence short term low
Even with immediate obliteration of the aneurysm with coiling, recurrence is an issue that may potentially
increase the risk of rebleeding.[19] Larger aneurysms that are coiled tend to recanalise. The risks
associated with aneurysm recanalisation after coil embolisation are yet to be defined. Aneurysms that are
clipped tend not to recur.
Aneurysm recurrence after coiling or clipping is usually treated with further endovascular embolisation.
aneurysmal rebleeding short term low
This is usually diagnosed after an acute neurological decline and more SAH on non-contrast head CT.
Aneurysmal rebleeding carries significant morbidity and mortality. Highest incidence occurs within the first
24 hours after haemorrhage.
Endovascular coiling or surgical clipping for aneurysm obliteration is the primary means of eliminating risk
of rebleeding.
Measure intra-cranial pressure invasively in a critical care setting with intra-parenchymal or intra-
ventricular probes. Maintain cerebral perfusion pressure (cerebral pressure = mean arterial pressure
minus intra-cranial pressure) at 50 mmHg to 70 mmHg with a beta-blocker, such as labetalol.
seizures short term low
Seizures are more often witnessed in the pre-hospital setting.
Start anticonvulsants after witnessed seizure. Some initiate anticonvulsants prophylactically, but then
discontinue them days after the aneurysm has been definitively treated.
delayed aneurysm recurrence long term medium

One retrospective study of 383 cerebral aneurysms treated with endovascular coiling showed that 33.6%
of treated aneurysms that were followed up showed aneurysm recurrence at a mean of 1 year. Major
FOLLOW UP
recurrences presented in 20.7% at a mean time of 16 months.[48]
SAH-related hydrocephalus variable low
Acute hydrocephalus usually occurs after intra-ventricular haemorrhage or from excess blood in the basal
cisterns. It clinically manifests as an abrupt onset of stupor or persistence of coma after initial rupture.
Non-contrast head CT is the primary means of diagnosis.
Subacute hydrocephalus develops days to weeks after SAH and presents as progressive drowsiness or
a quiet abulic state. Ventriculostomy with external ventricular drain can be given. Acutely, the ventricular
drainage system may be left open to drain at 10 cm above the external auditory meatus. Improvement may
be immediate and dramatic.
Prognosis
The prognosis for a patient with a ruptured cerebral aneurysm depends on the extent and location of the
aneurysm and the person's age, general health, and neurological condition. A formal comprehensive grading
system has been published that incorporates age, aneurysm size, density of subarachnoid haemorrhage
(if present), and clinical condition of the patient. This system predicts outcome ≥6 months after aneurysm
treatment.[43] In particular, there is a significant correlation between the Hunt and Hess scale, the Fisher
scale, and the patient's age on outcomes, regardless of treatment with clipping or coiling. Aneurysm size had
less influence on endovascular outcomes than on surgical outcomes. Posterior circulation aneurysms fared
worse than those in the anterior circulation.
21
Cerebral aneurysm Guidelines
Diagnostic guidelines
North America
Guidelines for the management of patients with unruptured intracranial

aneurysms
Published by: American Heart Association/American Stroke Association Last published: 2015
Treatment guidelines
Europe
Coil embolisation of ruptured intracranial aneurysms

GUIDELINES
Published by: National Institute for Health and Care Excellence Last published: 2005
Coil embolisation of unruptured intracranial aneurysms

Supraorbital minicraniotomy for intracranial aneurysm

North America
Guidelines for the management of patients with unruptured intracranial

aneurysms
Published by: American Heart Association/American Stroke Association Last published: 2015
Asia
Clinical practice guideline for the management of intracranial aneurysms

Published by: Korean Society of Interventional Neuroradiology Last published: 2014
Cerebral aneurysm Evidence scores
Evidence scores
1. Mortality and disability: there is poor-quality clinical evidence to suggest that, compared with
surgical clipping, endovascular coiling may be more effective at reducing the proportion of people
with spontaneous aneurysmal subarachnoid haemorrhage who have a poor outcome (death or
dependence) at 1 year.
Evidence level C: Poor quality observational (cohort) studies or methodologically flawed randomized
controlled trials (RCTs) of <200 participants.
EVIDENCE SCORES
23
Cerebral aneurysm References
Key articles
• Schievink WI. Intracranial aneurysms. N Engl J Med. 1997 Jan 2;336(1):28-40. Abstract
REFERENCES
• Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage
visualized by computerized tomographic scanning. Neurosurgery. 1980 Jan;6(1):1-9. Abstract
• Maeder PP, Meuli RA, de Tribolet N. Three-dimensional volume rendering for magnetic resonance
angiography in the screening and preoperative workup of intracranial aneurysms. J Neurosurg. 1996
Dec;85(6):1050-5. Abstract
• Etminan N, Brown RD Jr, Beseoglu K, et al. The unruptured intracranial aneurysm treatment score: a
multidisciplinary consensus. Neurology. 2015 Sep 8;85(10):881-9. Full text Abstract
• Guglielmi G, Vinuela F, Sepetka I, et al. Electrothrombosis of saccular aneurysms via endovascular

approach. Part 1: Electrochemical basis, technique, and experimental results. J Neurosurg. 1991
Jul;75(1):1-7. Abstract
• Molyneux A, Kerr R, Stratton I, et al. International Subarachnoid Aneurysm Trial (ISAT) of

neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial
aneurysms: a randomised trial. Lancet. 2002 Oct 26;360(9342):1267-74. Abstract
• Liu GJ, Wang ZJ, Wang YF, et al. Efficacy and safety of prophylactic use of nimodipine in patients
with aneurysmal subarachnoid hemorrhage: a meta-analysis. Chinese Journal of Cerebrovascular
Diseases. 2011;8:28-33.
• Ogilvy CS, Cheung AC, Mitha AP, et al. Outcomes for surgical and endovascular management of
intracranial aneurysms using a comprehensive grading system. Neurosurgery. 2006;59:1037-1042.
Abstract
References
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2. International Study of Unruptured Intracranial Aneurysms Investigators. Unruptured intracranial

aneurysms - risk of rupture and risks of surgical intervention. N Engl J Med. 1998;339:1725-1733. Full
text Abstract
3. Wiebers DO, Whisnant JP, Huston J 3rd, et al. Unruptured intracranial aneurysms: natural
history, clinical outcome, and risks of surgical and endovascular treatment. Lancet. 2003 Jul
12;362(9378):103-10. Abstract
4. Korja M, Kaprio J. Controversies in epidemiology of intracranial aneurysms and SAH. Nat Rev Neurol.
2016 Jan;12(1):50-5. Abstract
5. Atkinson JL, Sundt TM Jr, Houser OW, et al. Angiographic frequency of anterior circulation intracranial
aneurysms. J Neurosurg. 1989 Apr;70(4):551-5. Abstract
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6. Vlak MH, Algra A, Brandenburg R, et al. Prevalence of unruptured intracranial aneurysms, with
emphasis on sex, age, comorbidity, country, and time period: a systematic review and meta-analysis.
Lancet Neurol. 2011 Jul;10(7):626-36. Abstract
7. Asaithambi G, Adil MM, Chaudhry SA, et al. Incidences of unruptured intracranial aneurysms and
subarachnoid hemorrhage: results of a statewide study. J Vasc Interv Neurol. 2014 Sep;7(3):14-7. Full
text Abstract
8. Norrgard O, Angquist KA, Fodstad H, et al. Intracranial aneurysms and heredity. Neurosurgery. 1987
Feb;20(2):236-9. Abstract
9. Schievink WI. Intracranial aneurysms. N Engl J Med. 1997 Jan 2;336(1):28-40. Abstract
10. Petitti DB, Wingerd J. Use of oral contraceptives, cigarette smoking, and risk of subarachnoid
haemorrhage. Lancet. 1978 Jul 29;2(8083):234-5. Abstract
11. Bonita R. Cigarette smoking, hypertension and the risk of subarachnoid hemorrhage: a population-
based case-control study. Stroke. 1986 Sep-Oct;17(5):831-5. Full text Abstract
12. Knekt P, Reunanen A, Aho K, et al. Risk factors for subarachnoid hemorrhage in a longitudinal
population study. J Clin Epidemiol. 1991;44(9):933-9. Abstract
13. Juvela S, Hillbom M, Numminen H, et al. Cigarette smoking and alcohol consumption as risk factors
for aneurysmal subarachnoid hemorrhage. Stroke. 1993 May;24(5):639-46. Full text Abstract
14. Schievink WI, Katzmann JA, Piepgras DG, et al. Alpha-1-anti-trypsin phenotypes among patients with
intracranial aneurysms. J Neurosurg. 1996;84:781-784. Abstract
15. Krex D, Schackert HK, Schackert G. Genesis of cerebral aneurysms - an update. Acta Neurochir.
2001;143:429-448. Abstract
16. McEvoy AW, Kitchen ND, Thomas DG. Intracerebral haemorrhage and drug abuse in young adults. Br
J Neurosurg. 2000 Oct;14(5):449-54. Abstract
17. Schievink WI, Karemaker JM, Hageman LM, et al. Circumstances surrounding aneurysmal
subarachnoid hemorrhage. Surg Neurol. 1989 Oct;32(4):266-72. Abstract
18. Leblanc R. The minor leak preceding subarachnoid hemorrhage. J Neurosurg. 1987 Jan;66(1):35-9.
Abstract
19. Brisman JL, Song JK, Newell DW. Cerebral aneurysms. N Engl J Med. 2006 Aug 31;355(9):928-39.
Abstract
20. Perry JJ, Stiell IG, Sivilotti ML, et al. Sensitivity of computed tomography performed within six hours of
onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011
Jul 18;343:d4277. Full text Abstract
25
21. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med.
2000 Jan 6;342(1):29-36. Abstract
REFERENCES
22. Menke J, Larsen J, Kallenberg K. Diagnosing cerebral aneurysms by computed tomographic

angiography: meta-analysis. Ann Neurol. 2011 Apr;69(4):646-54. Abstract
23. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial
aneurysms. J Neurosurg. 1968;28:14-20. Abstract
24. Ogungbo B. The World Federation of Neurological Surgeons scale for subarachnoid haemorrhage.
Surg Neurol. 2003;59:236-237. Abstract
25. Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage
visualized by computerized tomographic scanning. Neurosurgery. 1980 Jan;6(1):1-9. Abstract
26. Maeder PP, Meuli RA, de Tribolet N. Three-dimensional volume rendering for magnetic resonance
angiography in the screening and preoperative workup of intracranial aneurysms. J Neurosurg. 1996
Dec;85(6):1050-5. Abstract
27. Thompson BG, Brown RD Jr, Amin-Hanjani S, et al. Guidelines for the management of patients with
unruptured intracranial aneurysms: a guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke. 2015 Aug;46(8):2368-400. Full text Abstract
28. Schievink WI. Genetics of intracranial aneurysms. Neurosurgery. 1997 Apr;40(4):651-62; discussion
662-3. Abstract
29. Nakagawa T, Hashi K. The incidence and treatment of asymptomatic, unruptured cerebral aneurysms.
J Neurosurg. 1994 Feb;80(2):217-23. Abstract
30. Rinne JK, Hernesniemi JA. De novo aneurysms: special multiple intracranial aneurysms.
Neurosurgery. 1993 Dec;33(6):981-5. Abstract
31. Etminan N, Brown RD Jr, Beseoglu K, et al. The unruptured intracranial aneurysm treatment score: a
multidisciplinary consensus. Neurology. 2015 Sep 8;85(10):881-9. Full text Abstract
32. Guglielmi G, Vinuela F, Sepetka I, et al. Electrothrombosis of saccular aneurysms via endovascular
approach. Part 1: Electrochemical basis, technique, and experimental results. J Neurosurg. 1991
Jul;75(1):1-7. Abstract
33. Kurre W, Berkefeld J. Materials and techniques for coiling of cerebral aneurysms: how much scientific
evidence do we have? Neuroradiology. 2008 Nov;50(11):909-27. Abstract
34. White PM, Lewis SC, Gholkar A, et al; HELPS trial collaborators. Hydrogel-coated coils versus bare
platinum coils for the endovascular treatment of intracranial aneurysms (HELPS): a randomised
controlled trial. Lancet. 2011 May 14;377(9778):1655-62. Abstract
35. Bodily KD, Cloft HJ, Lanzino G, et al. Stent-assisted coiling in acutely ruptured intracranial aneurysms:
a qualitative, systematic review of the literature. AJNR Am J Neuroradiol. 2011 Aug;32(7):1232-6. Full
text Abstract
36. Brinjikji W, Murad MH, Lanzino G, et al. Endovascular treatment of intracranial aneurysms with flow
diverters: a meta-analysis. Stroke. 2013 Feb;44(2):442-7. Abstract
REFERENCES
37. Molyneux A, Kerr R, Stratton I, et al. International Subarachnoid Aneurysm Trial (ISAT) of
neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial
aneurysms: a randomised trial. Lancet. 2002 Oct 26;360(9342):1267-74. Abstract
38. Molyneux AJ, Birks J, Clarke A, et al. The durability of endovascular coiling versus neurosurgical
clipping of ruptured cerebral aneurysms: 18 year follow-up of the UK cohort of the International
Subarachnoid Aneurysm Trial (ISAT). Lancet. 2015 Feb 21;385(9969):691-7. Full text Abstract
39. Schaller B. Extracranial-intracranial bypass to reduce the risk of ischemic stroke in intracranial
aneurysms of the anterior cerebral circulation: a systematic review. J Stroke Cerebrovasc Dis. 2008
Sep;17(5):287-98. Abstract
40. Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal
subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke. 2012 Jun;43(6):1711-37. Full text Abstract
41. Liu GJ, Wang ZJ, Wang YF, et al. Efficacy and safety of prophylactic use of nimodipine in patients
with aneurysmal subarachnoid hemorrhage: a meta-analysis. Chinese Journal of Cerebrovascular
Diseases. 2011;8:28-33.
42. van Gijn J, Rinkel GJ. Subarachnoid haemorrhage: diagnosis, causes and management. Brain. 2001
Feb;124(Pt 2):249-78. Full text Abstract
43. Ogilvy CS, Cheung AC, Mitha AP, et al. Outcomes for surgical and endovascular management of
intracranial aneurysms using a comprehensive grading system. Neurosurgery. 2006;59:1037-1042.
Abstract
44. Schievink WI, Wijdicks EF, Parisi JE, et al. Sudden death from aneurysmal subarachnoid hemorrhage.
Neurology. 1995 May;45(5):871-4. Abstract
45. Sacco RL, Wolf PA, Bharucha NE, et al. Subarachnoid and intracerebral hemorrhage: natural history,
prognosis, and precursive factors in the Framingham Study. Neurology. 1984 Jul;34(7):847-54.
Abstract
46. Findlay JM, Weir BK, Kanamaru K, et al. Arterial wall changes in cerebral vasospasm. Neurosurgery.
1989 Nov;25(5):736-45; discussion 745-6. Abstract
47. Biller J, Godersky JC, Adams HP Jr. Management of aneurysmal subarachnoid hemorrhage. Stroke.
1988 Oct;19(10):1300-5. Full text Abstract
48. Raymond J, Guilbert F, Weill A, et al. Long-term angiographic recurrences after selective endovascular
treatment of aneurysms with detachable coils. Stroke. 2003 Jun;34(6):1398-403. Full text Abstract
27
Cerebral aneurysm Images
Images
Figure 1: Cerebral angiogram showing aneurysm

From the personal collection of Dr M. Chen, Columbia College of Physicians and Surgeons
IMAGES
Figure 2: Comparison of 2-dimensional catheter angiography (left) with 3-dimensional catheter angiography
(right) showing a basilar tip aneurysm
From: Sellar M. Practical Neurology. 2005;5:28-37. Used with permission
IMAGES
Figure 3: Three-dimensional catheter angiogram showing a basilar tip aneurysm
29
Figure 4: Example of a coil used to treat cerebral aneurysms
IMAGES
Figure 5: Progressive angiography images of a small dissecting aneurysm of the distal basilar artery after a
subarachnoid and intraventricular haemorrhage on day 3 (A), day 23 (B), and day 30 (C), and 6 months after
stent-assisted coiling (D). Arrows indicate proximal and distal stent markers
From: Peluso JP, van Rooij WJ, Sluzewski M. BMJ Case Reports 2009; doi:10.1136/bcr.2007.121533. Used
with permission
Cerebral aneurysm Disclaimer
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Publishing Group Ltd ("BMJ Group") tries to ensure that the information provided is accurate and up-to-
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31
Contributors:
// Authors:
Giovanni Grasso, MD, PhD

Associate Professor
Department of Clinical Neurosciences, Neurosurgical Unit, University of Palermo, Palermo, Italy
DISCLOSURES: GG declares that he has no competing interests.
// Acknowledgements:
Dr Grasso would like to gratefully acknowledge Dr Michael Chen, the previous contributor to this
monograph. MC is an author of a reference cited in this monograph.
// Peer Reviewers:
Jae H. Choi, MD
Research Director
Stroke Center/The Neurological Institute, Columbia-Presbyterian Medical Center, New York, NY
DISCLOSURES: JHC declares that he has no competing interests.
Peter Martin, MA, BM BCh, MD, FRCP

Consultant Neurologist
Addenbrookes Hospital, Cambridge, UK
DISCLOSURES: PM declares that he has no competing interests.

Cerebral Aneurysm: The Right Clinical Information, Right Where It's Needed

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Cerebral aneurysm

The right clinical information, right where it's needed

Last updated: Apr 19, 2018

◊ Typically asymptomatic until ruptured, resulting in a subarachnoid haemorrhage.

◊ Cerebral angiogram is the definitive investigation. CT angiography or magnetic resonance

◊ Screening with non-invasive neuroangiography is recommended for at-risk populations.

• Often termed a berry aneurysm, as it resembles a berry hanging from a vine

• Also called atherosclerotic aneurysm

• Often termed pseudo-aneurysm

Classification of cerebral aneurysm based on size[2]

formation and should be screened at 5-year intervals.[30]

moderate- to high-level alcohol consumption

previous subarachnoid haemorrhage

heritable connective tissue disease

arteriovenous malformations or fistulas

History & examination factors

Other diagnostic factors

nuchal rigidity (uncommon)

decreased level of consciousness (uncommon)

focal neurological deficit (uncommon)

lumbar puncture elevated red blood cell

Condition Differentiating signs / Differentiating tests

Hypertensive intra- • Age >55 years. • Diagnostic cerebral

Cerebral venous sinus • Middle-aged woman. • Diagnostic cerebral

Traumatic subarachnoid • Older patient with a fall. • CT or MRI will show

Condition Differentiating signs / Differentiating tests

World Federation of Neurological Surgeons scale for subarachnoid

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

• Group 1: no blood detected

Step-by-step treatment approach

Supportive care for ruptured aneurysms

Calcium-channel blockade with nimodipine is given to all patients.

Treatment details overview

1st observation and/or exclusion of

1st cardiopulmonary support

plus exclusion of the aneurysm from the intra-

adjunct prevention of vasospasm

adjunct blood pressure (BP) control

adjunct stool softener

1st observation and/or exclusion of

» Observation consists of periodic imaging

» The choice of observation or treatment needs

» Small aneurysms (i.e., <7 mm) can generally

» Cavernous carotid artery aneurysms carry the

» Symptomatic aneurysms should be considered

» Increased risk of treatment and shorter life

» Comorbid medical illness also increases the

1st cardiopulmonary support

» Patients should be admitted to the intensive

» Treatment is instituted early for those with

» Surgery involves placing a clip across the neck

» Endovascular therapy for cerebral aneurysms

» The preferred treatment depends on

» Extracranial-intracranial bypass can be

» Treatment of unruptured co-existing

» nimodipine: 60 mg orally every 4 hours for

» Nimodipine is standard treatment for

» Therapy should be started within 96 hours of

» labetalol: 20 mg intravenous bolus initially,

» enalaprilat: 0.625 to 1.25 mg intravenously

» nicardipine: 5 mg/hour intravenous infusion

» May be given to prevent Valsalva manoeuvres

Complications Timeframe Likelihood