Epidemiology and pathophysiology of cerebral aneurysms
Dr Roger Traill
Department of Anaesthetics, RPAH, Sydney, Australia
A
Cerebral Aneurysm is a balloon like weakness of a cerebral blood vessel
usually occurring at a branch point. They are important due to their
propensity to rupture (sub-arachnoid haemorrhage - SAH) leading to high
morbidity and mortality. About a third of patients will die at the time
of the bleed and of the remaining patients who make it to hospital ,a
further third will die, a third will have some deficit and only a third
will have no deficit!
They are broadly classified into:
Saccular (like a "sac")
Fusiform - like an abdominal aortic aneurysm and are associated with atherosclerosis
If the aneurysm is greater than 2.5cm in diameter it is called a giant aneurysm.
Most aneurysms arise sporadically but occasionally they may be:
dissecting (resulting from a luminal endothelial tear), traumatic
(usually within 2-3 weeks after severe head injury) or mycotic (as a
result of embolism of infected material)
Saccular Aneurysms are mostly due to a pre-existing vascular weakness
however the relative roles of genetics and other factors are not
clearly elucidated. It is clear however that there is a familial
relationship to cerebral aneurysms as studies have shown that siblings
(RR 6:1) and first-degree relatives (RR 3-7:1) have a higher incidence
than the background population. There have also been relatively small
numbers of families described with a Mendelian dominant inheritance. No
single gene has been found so far to be responsible for cerebral
aneurysms.
A number of conditions are associated with cerebral aneurysm formation.
The most important of these is the presence of an AVM. Another
important association is the presence of the autosomal dominant type of
polycystic kidneys that has a 5-40% incidence. Screening for aneurysms
is recommended for these patients by CT or MRI angiography. Other
conditions with an increased incidence are; fibromuscular dysplasia,
Marfan's syndrome and Ehlers-Danlos syndrome (type IV).
Other causative factors are hypertension, smoking, cocaine use and "heavy" alcohol use.
90% of Aneurysms occur in the anterior circulation (30% Internal
Carotid Artery, 40% Anterior Cerebral or Anterior Communicating Artery,
20% Middle Cerebral Artery) and 10% in the Posterior Circulation
(Vertebro-Basilar systems).
The risk of rupture is greater (per year) the larger the aneurysm is but 90% of aneurysms that rupture are <12mm in size.
La Places Law (T=2PR) would explain a linear increase in the risk of
rupture as size increases however there is also thinning of the
aneurysm wall that occurs as they expand and the aneurysm wall is not
uniform in size. This leads to the risk being greater than La Place's
Law would predict, one study indicating that the risk of rupture is
related to the third power of the aneurysm radius.
The overall prevalence of aneurysms is unclear as it can only be
determined by autopsy studies or screening of the normal population
with cerebral angiography or one of the less invasive alternatives (CT
or MRI angiography).
Several autopsy and screening studies have found rates between 0.2 and
9.9%. It may be higher in Japan and Finland and the average prevalence
of all these studies is about 2%.
It is estimated that there is an average risk of rupture is 1-2% per
year but this varies greatly on the size and location of the aneurysm.
It is estimated that between 50-80% will never rupture.
The incidence of Sub-Arachnoid Haemorrhage is about 10 per 100,000 per
year in Western Europe and the US. The rate is higher in Japan and
Finland (about 15 per 100,000 per year)
The International Study of Unruptured Intracranial Aneurysms (ISUIA)
looked at a retrospective analysis of cerebral aneurysms as well as a
prospective analysis. The initial, retrospective analysis, indicated
minimal risk of rupture if the aneurysm is <10mm in size but
subsequent prospective analysis has revealed that only if the aneurysm
is <7mm in size, is located in the anterior circulation and their
have been no previous SAHs is the risk minimal, location in the
Anterior circulation, larger size and previous SAH increases the
likelihood of rupture.
The decision to treat however depends on an individual assessment of
the risks of bleeding versus the risks of treatment (surgery or
endovascular). The risks of treatment must be considered in the light
of the success and complication rate of the treating centre. In many
cases high risk of bleeding is associated with a high risk of treatment.
Bibliography:
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