2. A cerebral aneurysm (also called an intracranial aneurysm or
brain aneurysm) is a bulging, weakened area in the wall of an
artery in the brain, resulting in an abnormal widening,
ballooning, or bleb.
3. Currently, the cause of cerebral aneurysms is not clearly understood. Brain aneurysms are
associated with several factors, including smoking, hypertension, and family history
(genetic:Polycystic kidney disease ). The ultimate cause of a brain aneurysm is an abnormal
degenerative (breaking down) change (weakening) in the wall of an artery, and the effects of
pressure from the pulsations of blood being pumped forward through the arteries in the brain.
Certain locations of an aneurysm may create greater pressure on the aneurysm, such as at a
bifurcation (where the artery divides into smaller branches).
7. Subarachnoid haemorrhage (SAH) is one of the types of extra-axial intracranial haemorrhage and denotes
the presence of blood within the subarachnoid space.
SAH may occur as a result of a head injury or spontaneously, usually from a ruptured cerebral aneurysm.
8. Spontaneous subarachnoid haemorrhage accounts for 3% of stroke and 5% of stroke
deaths.
Up to 80% of patients with a spontaneous subarachnoid haemorrhage have ruptured
an aneurysm and 90% of these aneurysms are located in the anterior circulation
(carotid system), with 10% are found in the posterior circulation (vertebrobasilar
system).
9. Symptoms of Subarachnoid Hemorrhage:
headache - described as "thunderclap"
neck stiffness (non-specific)
acute confusion, neurological signs or reduced conscious level
seizures
nausea
vomiting
photophobia
Diagnosis of subarachnoid hemorrhage:
CT scan and CT angiogram.
Lumbar Puncture.
MRI and MR angiogram.
Cerebral angiography- DSA.
10.
11. The Hunt and Hess grading system:
Grade 0 - Unruptured aneurysm
Grade I - Asymptomatic or mild headache and slight nuchal rigidity
Grade Ia - Fixed neurological deficit without acute meningeal/brain reaction
Grade II - Cranial nerve palsy, moderate to severe headache, nuchal rigidity
Grade III - Mild focal deficit, lethargy, or confusion
Grade IV - Stupor, moderate to severe hemiparesis, early decerebrate rigidity
Grade V - Deep coma, decerebrate rigidity, moribund appearance
12.
13. Prodromal signs and symptoms usually are the result of one or more of the
following:
Sentinel or "warning" leaks with minor loss of blood from the aneurysm are
reported to occur in 30-50% of aneurysmal SAHs.
Mass effect of aneurysm expansion.
Emboli originating from intra-aneurysmal thrombus formation can cause
transient ischemic attacks.
14. Ruptured Aneurysm-Aneurysmal
Subarachnoid haemorrhage
(SAH)
The overall incidence of SAH is 9.1
per 100,000 person-years in most
regions, and is higher in Finland and
Japan; in the European community
that means around 36,000 SAH
cases per year.
43% of all SAH patients die without recovering
from the initial bleeding.
Of those, 74% die within the first 24 h,
7% within 2–3 days,
12% within 4–7 days,
5% within week 2,
1% within week 3,
and 1% later than 3 weeks after the initial SAH.
15. Mortality and Morbidity of Subarachnoid Hemorrhage
Approximately 10%–15% (and in some references up to 30%) of patients with aSAH
die before obtaining medical attention.
For those who survive until hospital arrival, another 30%–60% will die because of the
initial hemorrhage or secondary sequelae.
Secondary Injury After aSAH
1. Aneursymal rebleeding.
2. Acute hydrocephalus.
3. Cerebral vasospasm and delayed cerebral ischemia.
4. Seizures.
5. Cardiac abnormalities.
6. Cerebral hyponatremia.
7. Fever.
16. Rebleeding.
Up to 15% of patients rebleed during the first few hours after the initial haemorrhage, that is, during
transportation or before the treatment team is able to occlude the aneurysm.
Patients surviving the first day after the initial SAH have a cumulative risk of 35–40% to suffer rebleeding of the
aneurysm with a mortality rate of about 40%. After 4 weeks the risk of rebleeding decreases to about 3%/year.
• Aneurysm should be treated as early as logistically and technically possible to reduce the risk of rebleeding;
if possible it should be aimed to intervene at least within 72 h after onset of first symptoms.
17. Intracerebral
hematoma.
Although rupture of cerebral aneurysms usually results in SAH, some degree of intraparenchymal bleeding is
often seen. A cooperative study reported by Locksley showed that 90% of patients with SAH who died within 72
hours also had intracerebral clots. Only 4 to 17% patients with aneurysmal SAH, however, have clinically
significant hematomas.
It is well known that the presence of an ICH after aneurysm rupture negatively influences the patient’s
clinical course and outcome. The overall mortality rate ranges from 36 to 58%.
18. Intraventricular haemorrhage.
Intraventricular haemorrhage (IVH)
can serve as an independent predictor of
worse outcome and increasing morbidity
and mortality after subarachnoid
hemorrhage (SAH), and can lead to
severe complications, such as
hydrocephalus.
Hydrocephalus itself may contribute to
increased mortality following IVH, and
can be used as an independent predictor
of higher mortality and worse prognosis.
19. Hydrocephalus may be communicating or non-communicating.
Communicating hydrocephalus occurs when the flow of cerebrospinal fluid (CSF)
is blocked after it exits the ventricles.
Non-communicating (obstructive) hydrocephalus occurs when the flow of CSF is
blocked along one or more of the narrow passages connecting the ventricles.
Its onset can be acute, within 48 hours after SAH, or rarely chronic, occurring in a
delayed fashion weeks and even months after the hemorrhage.
Hydrocephalus.
20. ACUTE
• Occurs within the first 24 hours after hemorrhage.
• Occurs in up to 20% to 67% of affected patients within 3 days following SAH.
• Associated with intraventricular hemorrhage or excessive blood in the basal cisterns of posterior fossa.
• Characterized by the abrupt onset of stupor or persistence of coma.
• Management: immediate ventriculostomy to drain the CSF periodically, especially when ICP is elevated above a
predetermined level such as 20 mm Hg.
Hydrocephalus.
Hydrocephalus, defined as a bicaudate index on the CT scan exceeding the 95th percentile for age, occurs in
approximately 20% of patients during the acute phase and in about 10% during the chronic phase after SAH.
21. SUBACUTE
• Occurs within the first few days to 7 days after hemorrhage.
• Associated with blood in the CSF secondary to SAH.
• Characterized by drowsiness, the onset of which is gradual, although an abrupt onset is possible.
• Management: ventriculostomy, or serial lumbar puncture or lumbar drainage of CSF.
DELAYED
Occurs 10 or more days after hemorrhage.
Associated with blood in the CSF secondary to SAH.
Characterized by a gradual onset of symptoms when the patient is recovering from surgery; symptoms include gait
difficulty, behavioral changes (dull, quiet, and blunted animation).
Management: surgical placement of a ventriculoperitoneal shunt.
Because signs and symptoms of hydrocephalus are nonspecific, changes in responsiveness may be attributed to
other problems, thus delaying appropriate treatment.
Hydrocephalus.
22. Cerebral Vasospasm.
Of the 18,000 persons annually who survive initial aneurysmal rupture, 3,000 either die or are disabled from
cerebral vasospasm.
Vasospasm occurs in approximately 30% of patients.
By definition, cerebral vasospasm is narrowing of a cerebral blood vessel and causes reduced blood flow distally,
which may lead to delayed ischemic deficit and cerebral infarction if left untreated.
Besides the damage done by the initial SAH, brain damage produced by vasospasm is an important cause of
morbidity and mortality after hemorrhage, with 14% to 36% of patients suffering disability and death.
Vasospasm develops 3 to 14 days after SAH (peaking at 7 to 10 days), although the onset may be delayed up to
21 day.
23. Cerebral Vasospasm.
Vasospasm may be differentiated as either angiographic or symptomatic.
Angiographic vasospasm refers to narrowing of a cerebral arterial territory, as noted on angiography, without
clinical symptoms.
Symptomatic vasospasm is the clinical syndrome of delayed cerebral ischemia associated with
angiographically documented narrowing of a major cerebral arterial territory and TCD (transcranial Doppler)
elevation of a specific arterial territory.
The present rescue therapies, includes “triple H therapy” HHH, (hypertension/hypervolemia/ hemodilution),
interventional procedures such as balloon angioplasty, intra-arterial nicardipine and other vasodilators.
Since improved treatment of aneurysmal subarachnoid hemorrhage has occurred with early and improved
microsurgery, new endovascular techniques and better post operative care and monitoring, vasospasm has
significantly decreased as the cause of death over the last ten years (from 35% in the seventies to less than 10%
at this time.
27. Unruptured Intracranial Aneurysms
Unruptured intracranial aneurysms (UIA) are relatively common in
the general population, found in ≈3.2% of the adult population
(mean age 50 years) worldwide.
Unruptured intracranial aneurysms (UIA) may be incidental
findings as a result of complaints unrelated to the aneurysm or
detected as they grow and cause compression on adjacent
brain structures.
Such compressions include middle cerebral artery aneurysms causing
hemiparesis, visual field defect, or seizure, posterior communicating
artery or basilar artery aneurysms causing third cranial nerve palsy,
cavernous sinus aneurysms causing a cavernous sinus syndrome,
basilar distribution aneurysms causing compression of the brainstem,
and, on rare occasions, an embolus from the aneurysmal sac causing
transient ischemic attack or cerebral infarction due to distal
embolisation. Other cranial nerves can be involved, including trochlear
and abducens nerves and the first division of the trigeminal nerve .
28. Unruptured Intracranial Aneurysms
Optimum management of an unruptured intracranial aneurysm should involve the
comparison of the risk of aneurysmal rupture without any intervention with the risks of
surgical clipping or endovascular treatment. The factors that should be considered
include:
(1) aneurysmal factors, such as location, size, morphology, whether a thrombus exists
within the aneurysm, and the presence of a daughter sac or multiple lobes, and
(2) patient factors such as age, medical history, history of subarachnoid hemorrhage,
and family history of subarachnoid hemorrhage.
29. Unruptured Intracranial Aneurysms.
The large majority of UIAs will never rupture. For example, of the 1 million adults in the
general population with a mean age of 50 years, ≈32 000 harbor a UIA, but only 0.25% of
these, or 1 in 200 to 400, will rupture.
Among patients with no history of SAH, the rupture risk was 0.05% per year for aneurysms
<10 mm in diameter and ≈1% per year for larger aneurysms; aneurysm size (relative risk,
[RR] 11.6 for 10–24 mm and 59 for >25 mm compared with <10 mm) and location in the
posterior circulation (RR 13.8 for basilar tip and RR 13.6 for vertebrobasilar or posterior
cerebral versus anterior circulation) or posterior communicating artery (RR, 8.0) were
predictors of rupture risk in this group.
Among those with a history of SAH from a different aneurysm, the rupture risk was 0.5% per
year for those <10 mm and ≈0.7% per year for larger aneurysms; basilar tip aneurysms (RR,
5.1) and older age were predictors of rupture risk in this group.
33. Unruptured Intracranial Aneurysms
1. All symptomatic UΙAs, with rare exceptions, should be treated. Severe
concomitant diseases, advanced age, and complex anatomical characteristics of the
aneurysm may be contraindications for surgery if risks of death and disability after
treatment reach a total of 25%.
2. Small asymptomatic aneurysms of less than 3 mm in diameter should remain under
observation practically in all cases.
3. Patients under 60 years of age with aneurysms of more than 5 mm should be
treated if there are no serious contraindications. In patients older than 60 years,
treatment tactics is less clear. In these cases, the aneurysm location plays an
important role. Also, it is necessary to remember that aneurysms of the anterior
communicating artery, posterior communicating artery, and main artery bifurcation are at a
higher risk of rupture than aneurysms with other locations. In these cases, treatment is
reasonable if there are no serious concomitant diseases.
Guidelines for the Management of Patients With Unruptured Intracranial Aneurysms: A Guideline
for Healthcare Professionals From the American Heart Association/American Stroke Association.
European Stroke Organization guidelines for the management of intracranial aneurysms and
subarachnoid haemorrhage.
34. Unruptured Intracranial Aneurysms
4. Asymptomatic aneurysms of more than 10 mm should be treated in all patients
under the age of 70 years. The indications for older patients are less convincing.
5. Microsurgical clipping is the method of choice in young patients with small
aneurysms of the anterior circle of Willis. In cases of large and giant aneurysms and
aneurysms with a high neck to body size ratio, outcomes of microsurgical treatment are
usually better than those of endovascular treatment (however, with the introduction of flow-
diverting stents, this statement has become controversial). In cases of complex
aneurysms, combined procedures (e.g., performing an arterial bypass, followed by
proximal endovascular occlusion of the parent vessel) are important.
6.The experience of surgeons, availability of various techniques for exclusion of
aneurysms, and hospital facilities are of great importance.
Guidelines for the Management of Patients With Unruptured
Intracranial Aneurysms: A Guideline for Healthcare Professionals From
the American Heart Association/American Stroke Association.
European Stroke Organization guidelines for the management of
intracranial aneurysms and subarachnoid haemorrhage.
