12 Chapter 1 higher prevalence of intracranial aneurysms,6 which leads to the conclusion that there must be a higher risk for rupture of the aneurysms in these countries. Several factors have been found to predict the risk of rupture: smoking, hypertension and heavy alcohol use all appear to be independent risk factors.18-21 Incidence of rupture increases with age and is 1.24 times higher in women than in men; the exception being the Central & South American population in which the incidence of rupture was found to be slightly higher in men.15 Size, location and morphological characteristics of the aneurysm itself are also predictors of risk of rupture.12,22-25 Other investigations have focused on flow dynamics and wall shear stress factors26-29 in order to predict risk of rupture, and some report seasonal variations due to meteorological factors,30,31 whereas others find no such correlation.32 Apart from aneurysm rupture, any of the following may cause non-traumatic SAH: rupture of an intracranial arteriovenous (AV) malformation or fistula, dissection of an intracranial artery, a bleeding disorder or drug abuse. In two thirds of the patients in whom no aneurysm can be found after SAH, computed tomographic (CT) imaging reveals a perimesencephalic pattern of hemorrhage, with the bleed confined to the CSF spaces around the midbrain.33,34 These patients invariably have a good prognosis regarding the risk of rebleeding.35,36 Patients suffering a SAH due to aneurysm rupture have high rates of morbidity and mortality. Although case fatality rates have improved markedly over the past years,15,37,38 there is still a 30-day mortality rate of more than 20%.16,17,37 The risk of a rebleed from an aneurysm, especially in the period shortly after the first rupture, is much higher than the average risk of initial rupture: the case fatality rate of patients suffering from a rebleed is up to 70%.16 Timely discovery and treatment of the causative aneurysm therefore, is vital. Confirmation of Subarachnoid Hemorrhage When a patient presents to the hospital with acute-onset headache, the first step is to exclude or confirm a SAH. This can be achieved through CT or magnetic resonance imaging (MRI), or through the examination of CSF obtained by lumbar puncture (LP). The usual diagnostic strategy is to perform non- contrast enhanced CT (NECT), followed by a LP if the CT is negative.16,34,39-41 NECT is highly sensitive for the detection of SAH in the first 12 hours after the onset of symptoms, with sensitivities ranging from 93 – 100%,42-47 but this decreases steadily in the ensuing hours and days, until sensitivity is no more than 50% after one week.48 On the other hand, CSF examination is not reliable in the first 12 hours after SAH due to the fact that bilirubin is not formed until 9 – 15 hours after a bleed.39 The role of LP is under debate45,47,49,50 due to its potential complication rate51 and due to the higher sensitivity of newer generation CT scanners.52 An alternative diagnostic strategy may be the combination of NECT and CT angiography (CTA), in which CTA functions as a diagnostic back-up to detect an intracranial aneurysm as possible cause of SAH in case of a negative NECT.47,52,53 After all, the absolute diagnostic priority in a patient with a possible SAH lies in establishing the presence of an aneurysm. If diagnostic emphasis lies on aneurysm detection by CTA, a (false) negative NECT finding in the absence of an aneurysm becomes less relevant.52,54 The risk of missing an aneurysmal SAH with the combination NECT and CTA is small, ranging from 0.2%-0.8%, depending on the assumed dependency of the two tests.47 The role of MRI in detecting SAH has always been under discussion.55-58 In the early years of MRI it was thought that this modality was insensitive for detecting acute SAH.58 Explanations for this lack of
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