General considerations

Ruptured cerebral aneurysms account for 77% of SAH cases.105 Chason and Hindman demonstrated 137 cerebral aneurysms, a 5% incidence, in an autopsy study of 2786 patients who died of causes unrelated to SAH. Forty-two per cent of these aneurysms had evidence of prior rupture. This would be consistent with other reports that have demonstrated a history of prior haemorrhage in 60% of aneurysms discovered in people under 60 years of age.106,107

Autopsy studies demonstrate a higher incidence of ruptured aneurysms than clinical or radiological studies because aneurysm rupture is a frequent cause of sudden death. Although many series reflect widely variable epidemiological statistics, an approximate occurrence rate for aneurysm rupture is 10 per 100 000 population per year. There is an average prevalence rate of unruptured aneurysms of 5% in the adult population.

Three basic theories attempt to explain the pathogenesis of cerebral aneurysms. One theory proposes that a congenital weakness in the muscular layer of cerebral arteries allows the intimal layer to herniate and eventually distend and destroy the elastic membrane, leading to outpouching of an aneurysmal sac. Other theories have attributed aneurysm formation to postnatal degeneration within the vessel wall that leads to deterioration of the internal elastic lamina and resultant aneurysm formation. Others have postulated that it is a combination of congenital and degenerative effects that lead to aneurysm formation.108 The law of LaPlace relates wall stress to radius and transmural pressure and can be used to show that as the radius of the aneurysm enlarges, significantly less force is required to cause further enlargement or rupture of the sac.109

Aneurysms tend to occur at vascular bifurcations, although they may occur unassociated with vessel branches.110 Forbus used a rigid glass model to demonstrate that the point of greatest stress on the artery wall occurs at the apex of a vascular bifurcation in line with the direction of flow.111

The average size of ruptured aneurysms is 7 5 mm. Two per cent of aneurysms under 5 mm rupture, in contrast to 40% of those between 6 mm and 10 mm in external diameter.112114 Unruptured but symptomatic giant aneurysms (2 5 cm) carry a grave prognosis related to both mass effect and future rupture. The commonly held perception that giant aneurysms do not bleed and can be managed conservatively is dangerously misleading. Between 30% and 70% of giant aneurysms that become symptomatic are associated with SAH.115,116

Approximately 20% of SAH patients demonstrate multiple aneurysms.6 This makes it imperative to visualise all cerebral vessels on diagnostic angiography when SAH is investigated. The presence of multiple aneurysms will significantly affect surgical planning. When multiple aneurysms are present, the most proximal, irregularly shaped, and largest will be the most likely source of SAH.117 Aneurysms with small secondary outpouchings are thought to be particularly prone to rupture and these outpouchings may actually be false sacs from previous haemorrhages.118 DuBoulay has hypothesised that secondary aneurysm bulges are regions where the aneurysm wall is most unstable. Asymptomatic aneurysms rarely had secondary protuberances. He also found the mortality rate of such aneurysms to be twice that of smooth walled lesions.119 To help determine which of multiple aneurysms is the most likely source of SAH, one must correlate the history of the ictal event, clinical examination, CT scan, angiogram, and MRI study. The patient may lateralise the initial headache when bilateral aneurysms are present and the clinical exam may demonstrate unilateral weakness or cranial nerve palsy. When multiple aneurysms are diagnosed, CT localisation of subarachnoid blood, ventricular shift, and the site of an intraparenchymal haematoma are helpful findings. Local vasospasm may be present near the ruptured lesion on angiography. The aneurysm most likely to have bled will often be the largest, have the most irregular contour, or have a nipple-like secondary bulge. Nehls found statistical evidence that aneurysms associated with the anterior communicating complex, the basilar apex, and the posterior inferior cerebellar artery-vertebral junction were the most likely aneurysms to bleed when multiple aneurysms were diagnosed.120 MRI can be valuable in detecting subarachnoid clot beyond the time clot is visible on the CT scan and in localising the causative source of haemorrhage in cases with multiple aneurysms. Focal increased signal intensity is often found around a ruptured aneurysm on T2 weighted MR scans.64

After the diagnosis of ruptured cerebral aneurysm has been confirmed as the cause of SAH, treatment plans need to be considered. The treatment for SAH secondary to a ruptured aneurysm is a complex decision depending upon multiple factors. Treatment in the past has been primarily surgical, however, the development of Guglielmi Detachable Coils (GDC) (Target Therapeutics, Fremont, CA) has made interventional neuroradiologic management a viable option in selected cases.121-131 In general, aneurysms with a small neck to fundus ratio are more favourable for endovascular therapy than wide-necked lesions.132,133 Endovascular technology continues to improve, however, and techniques are evolving that further the spectrum of endovascular therapy options.132,134-137 The long-term durability of GDC embolisation of aneurysms is still largely unknown.138,139 The decision between surgical or endovascular therapy for any given aneurysm must be tailored to the specific patient, and this is best performed by a cerebrovascular team composed of cerebrovascular neurosurgeons, endovascular neurosurgeons, and interventional neuroradiologists.140,141

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