Epidemiology of Aneurysmal Subarachnoid Hemorrhage
Section snippets
Incidence
Spontaneous (nontraumatic) SAH most commonly is the result of aneurysmal rupture. Ruptured intracranial aneurysms account for approximately 75% to 80% of spontaneous SAH.1 Overall, its incidence is between 6 and 8 per 100,000 persons per annum in most Western civilizations.2, 3 There is estimated to be between 16,000 and 30,000 new cases of aSAH in the United States annually.4, 5 Wide variations in aSAH incidence are observed between study populations, with rates reported to be as low as 2.2
Presentation
Sudden onset of worst headache of life often signals a catastrophic event and is associated with high suspicion for aSAH. However, only 25% of individuals with severe, acute, paroxysmal headache actually have aSAH.18 Other possibilities include benign thunderclap headaches and benign orgasmic cephalgia, both of which do not have subarachnoid blood on computed tomographic (CT) imaging or lumbar puncture. Benign thunderclap headaches may present similarly to SAH, with emesis in approximately 50%
Risk factors
Modifiable and nonmodifiable risk factors play an important role in aneurysmal subarachnoid hemorrhage epidemiology. The prevalence of risk factors for aSAH and the ability to address those risk factors may contribute to the wide variation in disease burden of aSAH between regions.17, 27
Diagnosis
The evaluation of the patient with symptoms suggestive of SAH begins with confirmation of the presence of subarachnoid blood. This confirmation is primarily accomplished with a noncontrast CT scan, which in the first 12 hours after SAH has a 98% to 100% sensitivity for SAH. This number drops to 93% at 24 hours after SAH, and60, 61, 62, 63, 64 after 6 days decreases further to 57% to 85%.65, 66 In the setting of suggestive symptomatology a negative CT scan should be followed up with a lumbar
Treatment
Treatment of SAH requires a multifaceted, collaborative team approach. In addition to acute neurologic concerns aSAH patients are medically ill and require intensive management. Following medical stabilization the primary concern is rebleeding of the ruptured aneurysm, a fact that has resulted in a shift toward early definitive management by either surgical or endovascular means. Of the aforementioned methods of treatment, clipping has long been the mainstay of neurosurgical treatment of
General Trends and Grading
Over the past 2 decades, mortality following SAH has decreased dramatically.90 Previous death rates consistently occurred in a range around 50%,2, 8 whereas more recently they have been found in the 10%91 to 24% range.89 These reductions likely stem from advances in multiple aspects of SAH management, including improved diagnostic capabilities, aggressive neurocritical care management, and use of modern microsurgical and endovascular instruments and techniques.26
The 3 SAH-specific scales most
Summary
aSAH is a form of hemorrhagic stroke that affects up to 30,000 individuals per year in the United States. The incidence of aSAH has been shown to be associated with numerous nonmodifiable (age, gender, ethnicity, family history, aneurysm location and size) and modifiable (hypertension, BMI, tobacco and illicit drug use) risk factors. Although early repair of ruptured aneurysms and aggressive postoperative management has improved overall outcomes, it remains a devastating disease, with mortality
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2022, Brain HemorrhagesCitation Excerpt :Subarachnoid hemorrhage (SAH) is a devastating stroke subtype that affects up to 30,000 people in the U.S. annually which generally affects a significantly younger population than other stroke subtypes.1 SAH has mortality rates as high as 67%2 and significant morbidity to survivors leading to a large economic burden.3–5 In order to better understand the pathological events, molecular mechanisms, and therapeutic targets, several animal models of SAH have been developed.
Delayed Cerebral Ischemia Following Subarachnoid Hemorrhage: Hope for a New Therapy?
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2021, Journal of Clinical NeuroscienceCitation Excerpt :In patients who survive the initial bleeding, delayed cerebral infarction (DCI) is one of the leading causes of poor outcome. The pathogenesis of DCI is hypothesized to be multifactorial and includes angiographic vasospasm, but also cortical spreading ischemia, microthrombosis and microcirculation constriction[3,4]. Seventy percent of aSAH patients develop angiographic vasospasm and 20–30% progress to develop DCI[5].