Clinical Aspects of Subarachnoid Hemorrhage

Introduction

Aneurysmal rupture leading to subarachnoid hemorrhage (SAH) represents a dire clinical entity with profound neurologic and systemic manifestations. Despite several advances in microsurgical and endovascular technology, mortality rates remain high, and survivors often suffer substantial neurologic morbidity; of all patients with aneurysm rupture, 25% die within the first 24 h and nearly half die within 30 days . As such, proper diagnostic evaluation and early clinical management of patients with ruptured aneurysms is essential, and delays in this process have been shown to significantly worsen outcome . Here we provide a brief review of the epidemiology and natural history of aneurysmal SAH as well as recommendations regarding the present state of diagnosis and management of this clinical entity.

Epidemiology

In the United States, incidence of aneurysmal SAH is 2 per 100,000 population—approximate number of cases annually . In Japan and the Netherlands, incident rates reach as high as 22 per 100,000, suggesting a genetic and/or environmental component to their incidence. The average age at presentation is 55 years with a female predilection, which is thought to be related to hormonal influences and estrogen deficiency in postmenopausal women .

Cerebral aneurysms occur mainly as saccular or fusiform lesions. Saccular aneurysms are the most common cause of aneurysmal SAH and are thought to occur because of persistent pressure on a branch point or turning point, or as a result of a diseased vessel in the setting of underlying vascular disease. As with systemic vascular disease, several modifiable risk factors such as hypertension, smoking, and cocaine use are associated with a higher incidence of these lesions . Fusiform lesions are thought to represent the end product of a prior dissection, atherosclerotic changes, or defects in collagen synthesis (e.g., Ehlers–Danlos type IV syndrome, Marfan syndrome, autosomal dominant polycystic kidney disease, pseudoxanthoma elasticum) . Histologically, this manifests as a vessel outpouching with vessel intima and adventitia without the presence of arterial media, accounting for the fragility of these lesions and their tendency to rupture.

As demonstrated in the Nordic twin cohort, most aneurysms in practice are only modestly influenced by genetic predisposition when compared to environmental risk factors . However, this should be weighed against the fact that a family history of aneurysmal SAH has been shown to be among the strongest independent predictors . Even when excluding the aforementioned rare inherited connective tissue disorders, first-degree relatives of patients with SAH are at significantly increased risk when compared to the general population .

Most unruptured aneurysms do not rupture . The greatest risk of rupture in incidentally discovered lesions is a history of SAH. Further risk stratification to determine the need for prophylactic surgical or endovascular obliteration is performed based on other known modifiers such as aneurysm size, interval growth of an aneurysm, aneurysm location, and irregular morphology .