Etiology
Rupture of an intracranial saccular aneurysm is the leading cause of nontraumatic SAH, accounting for approximately 80% of cases. The remaining 20% are attributed to nonaneurysmal perimesencephalic SAH, arteriovenous malformations, arterial dissections, use of anticoagulants, and other rare conditions.[15] This distinction is crucial, as aneurysmal SAH has a different spectrum of complications and outcome, requiring more specific treatment and management. This topic focuses on the diagnosis and management of subarachnoid hemorrhage caused by aneurysm (i.e., aneurysmal SAH)
Cerebral saccular aneurysm formation is an acquired process. Very little is known about this process, but evidence suggests structural abnormalities are acquired in the intimal and medial layers of cerebral vessels, and could result from an inflammatory process occurring within these layers.[16][17][18] Structural abnormalities may be influenced by smoking, hypertension, and alcohol abuse.[15] Patients with previous SAH are at substantial risk for new aneurysm formation and enlargement of previously diagnosed and untreated aneurysms. This suggests that aneurysm formation is a dynamic, continuous process.[19][20][21] Hereditary and genetic factors may also contribute. Patients with Ehlers-Danlos syndrome, Marfan syndrome, pseudoxanthoma elasticum, adult polycystic kidney disease, and neurofibromatosis type I are at increased risk of aneurysm formation and SAH.
Pathophysiology
Cerebral aneurysms arise at the bifurcation of major arteries that form the circle of Willis. The majority are located at the anterior communicating/anterior cerebral artery junction (Acom/ACA), distal internal carotid artery/posterior communicating artery junction (ICA/Pcom), and middle cerebral artery bifurcation (MCA). Less than 10% arise from the vertebral or basilar arteries. Up to 19% of patients are found to have multiple aneurysms.[11][12] Greater pressures at the apexes of arterial bifurcation, pulsatile flow patterns, and turbulence have been suggested as explanations for the predilection of aneurysm growth at these sites.[17][22]
The risk of aneurysm rupture depends on its size, location, the presence of symptoms, the presence of multiple aneurysms, and whether previous aneurysms have ruptured.[17][23][24][25][26][27] Patient-related predictors of rupture are age and smoking. Small, asymptomatic aneurysms (<7 mm) are less prone to rupture than bigger ones that exert mass effect on surrounding structures. Aneurysms located at the basilar tip, in the vertebrobasilar, posterior cerebral distribution, or posterior part of the circle of Willis are more likely to rupture compared with aneurysms in other locations.[24][28] The 5-year cumulative rupture rate of an aneurysm <7 mm in diameter is 0% when located on ICA, Acom, or MCA and 2.5% when located on Pcom or posterior cerebral, vertebral, or basilar arteries.[28] An unruptured aneurysm discovered during workup for SAH (caused by a different aneurysm) has a higher annual incidence of rupture than a single unruptured aneurysm.[17][25][26] In this case, the 5-year cumulative rupture rate ranges between 1.5% and 3.4% for aneurysms <7 mm and between 2.6% and 18.4% for aneurysms between 7 mm and 24 mm.
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