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Essay: Aneurysmal subarachnoid hemorrhage (aSAH)

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  • Aneurysmal subarachnoid hemorrhage (aSAH)
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Aneurysmal subarachnoid hemorrhage (aSAH) is a significant cause of stroke and it is often associated with death or severe disability. Approximately 5’15% of stroke cases are secondary to ruptured cerebral aneurysms. Data from population-based studies suggest that the incidence rates vary from 6 to 16 per 100 000, with the highest rates reported from Japan and Finland [12], [66], [85] and [130]. The overall mortality rates from 32% to 67% with 10’20% of patients with long-term dependence due to brain damage [61]. Twelve percent of patients affected by aneurismal SAH die before medical treatment can be given [65] and 25% die within 24 h [13]. A further 40’60% mortality rate occurs within 30 days [13].
Outcome after aneurysmal subarachnoid hemorrhage depends on a myriad of interrelated factors, including the severity of the initial event, rebleeding, perioperative medical management and the timing and technical success of surgery. Surgical obliteration of the ruptured aneurysm is the primary concern in all patients after subarachnoid hemorrhage, but the contribution of perioperative medical management can be considerable. The first 14 days after aneurysmal rupture is the peak period for morbidity and mortality, principally because of the effects of hemorrhage, vasospasm, cerebral ischemia and rebleeding. In theory, optimization of the medical management of rebleeding and cerebrovascular dysfunction can result in substantial benefit to the patient.
Cerebral vasospasm and brain ischemia are critical clinical complications that occur after SAH.
Cerebral vasospasm occurs in 70% of patients with aneurysmal SAH and leads to symptomatic brain ischemia in 36% of patients [9]. It can be considered as a delayed and self-limited condition that usually occurs when cerebral vessels are exposed to blood in the subarachnoid space following aneurysmal rupture. It typically occurs 4’14 days after the SAH, with a peak incidence between 6 and 10 days. Given that the vast majority of intracranial aneurysms are located in the circle of Willis, the large proximal vessels are the ones most frequently affected by vasospasm. The volume, density and prolonged presence of subarachnoid blood are important predictors of vasospasm [1, 2].
Cerebral vasospasm was reported first by Ecker and Riemenschneider [38] by using angiographic visualization and is correlated with a 1.5- to 3-fold increase in mortality in the first 2 weeks after SAH [9]. Intracranial arterial spasm has been recognized as a detrimental clinical entity for more than 40 years, but the etiology and pathogenesis of such symptomatic cerebral vasospasm are still not well understood. Despite numerous attempts at prevention and treatment, it is still associated with significant mortality and an unfavorable outcome [9].
Along with the intravascular volume depletion and impaired cerebral autoregulation commonly seen after aneurysmal SAH (aSAH), vasospasm contributes to decreasing cerebral blood flow (CBF), resulting in delayed ischemic injury. Indeed, vasospasm constitutes one of the most common treatable causes of morbidity and mortality following aSAH. Approximately 70% of aSAH patients will demonstrate angiographic evidence of vasospasm; however, only 40% will have clinical symptoms, and approximately 30% will have delayed ischemic injury. Up to 20% of patients will die or have severe deficits as a result of vasospasm [1, 2, 4’28].
One of the most important and critical aspects of SAH-induced vasospasm and brain ischemia is its failure to consistently respond to treatment. Pharmacological interventions have been assessed in experimental studies and in clinical trials [83] with only partial success. Therefore, it is clear that further basic and clinical research is needed to better clarify the underlying mechanisms of SAH-induced cerebrovascular dysfunction.

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