HomeStrokeVol. 40, No. 3Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBGuidelines for the Management of Aneurysmal Subarachnoid HemorrhageA Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Heart Association Joshua B. Bederson, MD, E. Sander ConnollyJr, MD, FAHA, H. Hunt Batjer, MD, Ralph G. Dacey, MD, FAHA, Jacques E. Dion, MD, FRCPC, Michael N. Diringer, MD, FAHA, John E. DuldnerJr, MD, MS, Robert E. Harbaugh, MD, FAHA, Aman B. Patel, MD and Robert H. Rosenwasser, MD, FAHA Joshua B. BedersonJoshua B. Bederson Search for more papers by this author , E. Sander ConnollyJrE. Sander ConnollyJr Search for more papers by this author , H. Hunt BatjerH. Hunt Batjer Search for more papers by this author , Ralph G. DaceyRalph G. Dacey Search for more papers by this author , Jacques E. DionJacques E. Dion Search for more papers by this author , Michael N. DiringerMichael N. Diringer Search for more papers by this author , John E. DuldnerJrJohn E. DuldnerJr Search for more papers by this author , Robert E. HarbaughRobert E. Harbaugh Search for more papers by this author , Aman B. PatelAman B. Patel Search for more papers by this author and Robert H. RosenwasserRobert H. Rosenwasser Search for more papers by this author Originally published22 Jan 2009https://doi.org/10.1161/STROKEAHA.108.191395Stroke. 2009;40:994–1025is corrected byCorrectionOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 22, 2009: Previous Version 1 Subarachnoid hemorrhage (SAH) is a common and frequently devastating condition, accounting for ≈5% of all strokes and affecting as many as 30 000 Americans each year.1,2 The American Heart Association (AHA) previously published “Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage.”3 Since then, considerable advances have been made in endovascular techniques, diagnostic methods, and surgical and perioperative management paradigms. Nevertheless, outcome for patients with SAH remains poor, with population-based mortality rates as high as 45% and significant morbidity among survivors.4–9 Several multicenter, prospective, randomized trials and prospective cohort analyses have influenced treatment protocols for SAH. However, rapid evolution of newer treatment modalities, as well as other practical and ethical considerations, has meant that rigorous clinical scientific assessment of the treatment protocols has not been feasible in several important areas.To address these issues, the Stroke Council of the AHA formed a writing group to reevaluate the recommendations for management of aneurysmal SAH. A consensus committee reviewed existing data in this field and prepared the recommendations in 1994.3 In an effort to update those recommendations, a systematic literature review was conducted based on a search of MEDLINE to identify all relevant randomized clinical trials published between June 30, 1994, and November 1, 2006 (search terms: subarachnoid hemorrhage, cerebral aneurysm, trial; Table 1). Each identified article was reviewed by at least 2 members of the writing group. Selected articles had to meet one of the following criteria to be included: randomized trial or nonrandomized concurrent cohort study. Case series and nonrandomized historical cohort studies were reviewed if no studies with a higher level of evidence were available for a particular topic covered in the initial guidelines. These were chosen on the basis of sample size and the relevance of the particular studies to subjects that were covered in the initial guidelines.10 The committee’s recommendations were made by applying the standard AHA evidence rating scheme11,12 (Tables 2 and 3). These recommendations are intended to summarize the best available evidence for treatment of patients with aneurysmal SAH and to identify areas of future research. Treatments for specific patients need to be individualized. Table 1. Randomized Clinical Trials in Aneurysmal SAH: 1995 to 2006 (by Therapeutic Modality)AuthorsYearTherapynBenefitDIND indicates delayed ischemic neurological deficits; GDC, Guglielmi detachable coil; ET, endothelin; TD NTG, transdermal nitroglycerin; rtPA, recombinant tissue-type plasminogen activator; F-NA, female patient subgroup–North American cohort; F-E, female patient subgroup–European cohort; NA, North American cohort; and E, European cohort.Van den Bergh et al4152006Aspirin161No less DINDHop et al4162000Aspirin50No improvement in 4-mo outcomeSchmid-Elsaesser4992006Magnesium113No better outcome than nimodipineWong et al1762006Magnesium60No better outcomeVan den Bergh et al4092005Magnesium283Less DCI and poor outcomeVeyna5002002Magnesium40No less clinical vasospasmMolyneux et al1852005GDC2143Less mortality/epilepsy, more rebleedingMolyneux et al2582002GDC2143Less mortality, better outcomeKoivisto et al2592000GDC109No improvement in 12-mo outcomeVanninen5011999GDC109No improvement in 3-mo outcomeVajkoczy et al4252005ET antagonist32Less incidence/intensity angiographic vasospasmShaw et al4262000ET antagonist420Trend to less DIND, no better outcomeLynch et al4282005Statin (simvastatin)39Reduced incidence of clinical vasospasmTseng et al4292005Statin (pravastatin)80Less mortality/incidence of TCD vasospasmAnderson5022006Hypothermia1001No neuropsychological benefit at 3 moTodd et al3642005Hypothermia1001No improvement in 3-mo outcomeKaribe5032000Hypothermia24Immediate CBF improvementHindman5041999Hypothermia114Improved outcome at 3 and 6 moDiringer5052004Normothermia296Reduced fever burden with catheterReinert et al4272004TD NTG17Raised CBFKlopfenstein et al4692004Drain wean81No difference in shunted hydrocephalusWurm et al4172004Enoxaparin117No less TCD vasospasmSiironen et al4182003Enoxaparin170No improvement in 3-mo outcomeMoro5062003Hydrocortisone28Improved sodium balanceMori et al4961999Fludrocortisone30No improvement in 6-mo outcomeMayer et al39119985% Albumin43Improved sodium balanceHamada5072003IT urokinase110Reduced symptomatic vasospasmFindlay5081995IT rtPA91No decrease in angiographic vasospasmHillman et al1402002Tranexamic A505Reduced rebleeding, no effect on outcomeRoos5092000Tranexamic A462Reduced rebleeding, no effect on outcomeEgge et al3892001Hypervolemia32No effect on clinical/TCD vasospasmLennihan et al3852000Hypervolemia82No less symptomatic vasospasmLanzino et al4191999Tirilazad (F-NA)823No improvement in 3-mo outcomeLanzino et al4201999Tirilazad (F-E)819No improvement in 3-mo outcomeHaley et al4211997Tirilazad (NA)897No improvement in 3-mo outcomeKassell et al4221996Tirilazad (E)1015No improvement in 3-mo outcomeSaito et al4231998Ebselen286No less DIND but improved outcomeAsano et al4241996Ebselen162Decreased incidence of DINDTable 2. Definitions of Classes and Levels of Evidence Used in AHA Stroke Council RecommendationsClass IConditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effectiveClass IIConditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatmentClass IIa: the weight of evidence or opinion is in favor of the procedure or treatmentClass IIb: usefulness/efficacy is less well established by evidence or opinionClass IIIConditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmfulTherapeutic recommendations Level of Evidence AData derived from multiple randomized clinical trials Level of Evidence BData derived from a single randomized trial or nonrandomized studies Level of Evidence CConsensus opinion of expertsDiagnostic/prognostic recommendations Level of Evidence AData derived from multiple prospective cohort studies using a reference standard applied by a masked evaluator Level of Evidence BData derived from a single grade A study or ≥1 case-control studies or studies using a reference standard applied by an unmasked evaluator Level of Evidence CConsensus opinion of expertsDownload figureDownload PowerPointTable 3. Applying Classification of Recommendations and Level of Evidence*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.Incidence and Prevalence of Aneurysmal SAHA large multinational World Health Organization study found that the age-adjusted annual incidence of SAH varied 10-fold between different countries, from 2.0 cases per 100 000 population in China to 22.5 per 100 000 in Finland.13 Community-based studies reported an incidence that ranged from 8.1 per 100 000 in Australia and New Zealand to 23 per 100 000 in Japan.14–16 One Japanese study suggested that if early deaths attributed to SAH were included, the rate would be as high as 32 per 100 000.17 Using data collected from nonfederal hospitals in the United States, the National Hospital Discharge Survey of 199018 reported that 25 000 patients had an SAH during the previous year. Data from Rochester, Minn, for 1975 through 1984 suggest that an additional 12% of persons with SAH do not receive prompt medical attention19 and that many cases of SAH are misdiagnosed.20–26 The annual prevalence of aneurysmal SAH in the United States may therefore exceed 30 000 persons. Population-based studies have indicated that the incidence rate for SAH has not changed dramatically over the past 4 decades,27,28 whereas others have suggested a slight decline in incidence in New Zealand from the 1980s to the 1990s29 and a decreased mortality from SAH in Sweden as a result of declining incidence in men and decreased death rates after SAH in women.30 The incidence of SAH increases with age, occurring most commonly between 40 and 60 years of age (mean age ≥50 years), but SAH can occur from childhood to old age and is ≈1.6 times higher in women than in men,4,31 although this difference does not carry across all populations.13 Studies have suggested that the gender difference is related to hormonal status, with premenopausal women,32 those of older age at the birth of their first child, and those of older age at the onset of menarche at reduced risk for SAH.33 There appear to be racial differences in risk of SAH. Black Americans are at higher risk than white Americans.34 Maori and Pacific people are at higher risk than white New Zealanders.14 Population-based mortality rates for SAH appear to have declined from the 1970s and 1980s.28 More recent studies have suggested that the trend either is continuing or has leveled off.27 Racial differences in mortality have emerged, with white Americans having a lower mortality rate than black Americans, Hispanic Americans, American Indians/Alaskan Natives, and Asian/Pacific Islanders in the United States.35Risk Factors for Aneurysmal SAHRisk factors for SAH have been studied in a number of settings. Multivariate models have found hypertension, smoking, and heavy alcohol use to be independent risk factors for SAH in the United States,36,37 Japan,38 the Netherlands,39,40 Finland,41,42 and Portugal.43 Sympathomimetic drugs, including cocaine44,45 and phenylpropanolamine,46 have been implicated as a cause of SAH. Cocaine-related SAH occurs in younger patients and has an outcome similar to that in other SAH patients.44 Diabetes does not appear to be a risk factor for SAH.47 Interestingly, some of the same risk factors for SAH also have been shown to increase the risk of multiple aneurysms (ie, smoking, female gender, hypertension, family history of cerebrovascular disease, and postmenopausal state).48–50There has also long been interest in the influence of meteorological and temporal factors on the incidence of SAH. Studies have provided variable results, but there appears to be a somewhat higher incidence of SAH in the winter months14,51 and in the spring.52 This, however, was not found in a Japanese study.53 Finally, another study found a modest correlation between atmospheric pressure and change in pressure and number of SAHs per day.54Certain genetic syndromes have also been associated with an increased risk of SAH and support the concept of inherited susceptibility to aneurysm formation. These include autosomal dominant polycystic kidney disease and type IV Ehlers-Danlos syndrome.55–60 These syndromes support the theory of inherited susceptibility to aneurysm formation.61–76 In a small review of published sibships with SAH, angiography performed in asymptomatic siblings found an aneurysm in one third of cases.77 This finding is in contrast to the true familial intracranial aneurysm syndrome, which occurs when 2 first- through third-degree relatives have intracranial aneurysms.10,78–83 This is associated with SAH at a younger age, a high incidence of multiple aneurysms, and hemorrhages among siblings and mother-daughter pairings.78,83,84 In family members with the familial intracranial aneurysm syndrome, the risk of harboring an unruptured aneurysm was 8%73 with a relative risk of 4.2.85 A study of 23 families with familial SAH found that having ≥3 affected relatives tripled the risk of SAH. When magnetic resonance angiography (MRA) was used to screen 8680 asymptomatic individuals for intracranial aneurysms, the overall incidence of aneurysms was 7.0% but rose to 10.5% in those with a family history of SAH.86 However, another magnetic resonance imaging (MRI) study reported that 4% of relatives of sporadic SAH patients had aneurysms.87 In a large case-control study,88 family history was found to be an independent risk factor for SAH. The specific genes involved have not yet been identified, and when polymorphisms in matrix metalloproteinase genes were studied, they had no relationship to the development of aneurysms.89Finally, in patients who have been treated for a ruptured aneurysm, the annual rate of new aneurysm formation is 1% per year to 2% per year.81,84,90–95 Patients with multiple intracranial aneurysms may be particularly susceptible to new aneurysm formation.47,93,96 It is not clear whether this is due to genetic or acquired factors.Prevention of SAHBecause no randomized controlled trials have specifically examined whether treatment of medical risk factors reduces the occurrence of SAH, available evidence is derived from observational cohort studies. It has been suggested that control of these major risk factors may have a greater impact on SAH in younger than in older patients.97 Hypertension is a common risk factor for hemorrhagic stroke. In a review by Collins et al,98 an average reduction in diastolic blood pressure of 6 mm Hg by antihypertensive medication produced an aggregate 42% reduction in stroke incidence. However, there are few data on aneurysmal SAH in these studies because of limited sample size for SAH events. Although there has been a marked improvement in blood pressure control in the general population, there has been little change in the incidence of SAH during that time.99–101 Regardless of whether hypertension control reduces the incidence of SAH, it may reduce the severity; untreated hypertension appears to be an independent risk factor for poor outcome after SAH.102 Similarly, only indirect evidence exists to indicate that smoking cessation reduces risk for SAH. In a case-control study,103 former smokers had a lower relative risk than light or moderate smokers, and there was an inverse relationship between time since the last cigarette and risk of SAH. In a prospective study of 117 006 women, it was observed that former smokers also had a lower relative risk of SAH than current smokers and that duration since quitting was associated with a decreased risk.104Because of the poor prognosis from SAH and the relatively high frequency of asymptomatic intracranial aneurysms, the role of elective screening has been a subject of discussion in the literature. In evaluations of the clinical efficacy of screening for asymptomatic intracranial aneurysms, the costs of screening should be weighed against the risks and consequences of SAH. Several assumptions must be made to estimate these costs, for example, about how an aneurysm would be managed if detected, although this unrealistically simplifies the medical decision-making process. Several factors, including aneurysm incidence, risk of rupture (natural history), and risk of treatment, influence the analysis of cost-effectiveness for asymptomatic unruptured aneurysms.73,85,93,105 Of these factors, the risk of rupture is the most important. To date, there have been no population-based clinical studies of cost-effectiveness of screening for intracranial aneurysms. Therefore, screening for asymptomatic intracranial aneurysms in the general population is currently not supported by the available literature. Patients with environmental risk factors such as cigarette smoking and alcohol use have an increased incidence of SAH, but this has not been associated with an increased incidence of intracranial aneurysms,94,103,106–108 and general screening for aneurysms does not appear to be warranted in this population either.In populations with the familial intracranial aneurysm syndrome, although screening detects an increased incidence of intracranial aneurysms, the cost-effectiveness of screening has not been demonstrated.40,105 Until the efficacy of screening has been evaluated in a population-based clinical study, most studies suggest that screening should be considered on an individual basis. In contrast to asymptomatic individuals, the annual rate of new aneurysm formation in patients treated for aneurysmal SAH is 1% to 2%. In this group, late radiological evaluation of this population has been considered reasonable by some.91Nevertheless, the appropriate techniques for aneurysm detection screening remain a matter of debate. Many of the issues pertaining to screening for incidental aneurysm also pertain to detecting ruptured aneurysm and are discussed below in the section on diagnosis. Although early studies have suggested that MRA may miss aneurysms detected by conventional angiographic techniques,109 data suggest that MRA combined with computed tomography (CT) angiography (CTA) is comparable to conventional angiography in detecting aneurysms. Another small prospective study suggested that digital subtraction angiography and MRA were complementary.110 However, in a review of the available literature, Wardlaw and White111 concluded that “quality of data testing their [MRA and CTA] accuracy is limited.” Thus, until better data become available, the appropriate technique for initial screening should be individualized; however, when it is clinically imperative to know if an aneurysm exists, catheter angiography remains the gold standard.As discussed, the case fatality rate for aneurysmal SAH remains high,4–7 and it is recognized that the main determinant of outcome is the severity of the initial bleed.8,112 If SAH could be prevented before aneurysm rupture, poor outcomes related to SAH could theoretically be avoided. However, because only a minority of asymptomatic aneurysms go on to rupture and because all aneurysm treatments carry some risk, the management of patients harboring an unruptured aneurysm remains controversial. Recommendations were published for the management of unruptured intracranial aneurysms in 2000.113 Subsequent advances in treatment modalities and better understanding of the natural history of unruptured intracranial aneurysms have occurred, and a separate writing committee has been commissioned to update these recommendations.Prevention of SAH: Summary and RecommendationsThe relationship between hypertension and aneurysmal SAH is uncertain. However, treatment of high blood pressure with antihypertensive medication is recommended to prevent ischemic stroke, intracerebral hemorrhage, and cardiac, renal, and other end-organ injury (Class I, Level of Evidence A).Cessation of smoking is reasonable to reduce the risk of SAH, although evidence for this association is indirect (Class IIa, Level of Evidence B).Screening of certain high-risk populations for unruptured aneurysms is of uncertain value (Class IIb, Level of Evidence B); advances in noninvasive imaging may be used for screening, but catheter angiography remains the gold standard when it is clinically imperative to know if an aneurysm exists.Natural History and Outcome of Aneurysmal SAHAn estimated 6700 annual in-hospital deaths from aneurysmal SAH occur in the United States,114 with evidence that incidence rates remain relatively stable, but death rates from SAH may have declined during the past several decades in other geographic locations. The mortality rate for SAH in the 1966 Cooperative Study on Intracranial Aneurysms was 50% at 29 days115 and 33% in a recent analysis of in-hospital deaths among SAH patients admitted through an emergency department (ED).102 In a population-based study by Broderick et al,8 the 30-day mortality rate among all patients who suffered SAH was 45%, with the majority of deaths occurring in the first days after SAH. Other studies have suggested slightly declining mortality rates in this and other countries.27,28,30There are many influences on outcome after SAH, with wide variations in case fatality rates reported between different countries and regions.13 The factors that strongly influence outcome after SAH can be divided into patient factors, aneurysm factors, and institutional factors. Patient factors include the severity of initial hemorrhage, age, sex, time to treatment, and medical comorbidities such as untreated and treated hypertension, atrial fibrillation, congestive heart failure, coronary artery disease, and renal disease.102 Aneurysm factors include size, location in the posterior circulation, and possibly morphology.116 Institutional factors include the availability of endovascular services,117 the volume of SAH patients treated,102,117–119 and the type of facility in which the patient is first evaluated.120Of patient factors, by far the most important determinant of poor outcome is the deleterious effect of acute SAH on the brain (reviewed by Sehba and Bederson121). SAH causes profound reductions in cerebral blood flow (CBF), reduced cerebral autoregulation, and acute cerebral ischemia.122–126 These pathophysiological processes are linked to raised intracranial pressure and decreased cerebral perfusion pressure,122,127,128 decreased availability of nitric oxide,126,129 acute vasoconstriction123,130,131 and microvascular platelet aggregation,132 activation of microvascular collagenases, loss of microvascular collagen,133 and endothelial barrier antigen leading to decreased microvascular perfusion and increased permeability.132,133 Despite recent advances in the understanding of the mechanisms of SAH-induced brain injury, few effective treatments exist, and further research is needed.Recurrent hemorrhage remains a serious consequence of aneurysmal SAH, with a case fatality rate of ≈70% for persons who rebleed, and is currently the most treatable cause of poor outcomes. Previous studies delineated several patterns of rebleeding.134,135 In the prospective Cooperative Aneurysm Study,136 rebleeding was maximal (4%) on the first day after SAH and then constant at a rate of 1% per day to 2% per day over the subsequent 4 weeks. Several prospective follow-up cohorts137,138 have demonstrated that the risk of rebleeding with conservative therapy is between 20% and 30% for the first month after hemorrhage and then stabilizes at a rate of ≈3% per year.139 Several potential risk factors for acute rebleeding have been identified from prospective and retrospective studies. A longer interval from hemorrhage to admission and treatment, higher initial blood pressure, and worse neurological status on admission have been related to recurrent hemorrhage in the first 2 weeks after SAH. Recent evidence indicates that the risk of “ultraearly rebleeding” (within 24 hours of initial SAH) may be 15%, which is considerably higher than previously recognized,140,141 with high mortality rates. In 1 study, 70% of ultraearly rebleeds occurred within 2 hours of initial SAH.141 In another study, all preoperative rebleeding occurred within 12 hours of initial SAH.142 In recent studies, poor neurological status,142 high Hunt-Hess grade, and larger aneurysm diameter143 were independent predictors of acute hydrocephalus, intraventricular blood, and the use of ventricular drains.137–139,143–147 Recent data suggest that when preoperative ventriculostomy is followed by early treatment of the ruptured aneurysm, the risk of rebleeding is not increased by the ventriculostomy.148Numerous systems have been reported for grading the clinical outcome in patients with SAH from a ruptured intracranial aneurysm, but the current literature remains substantially deficient with respect to intraobserver and interobserver uniformity or consistency.9,149–151 Recent reports have tended to use the Glasgow Coma Scale or Glasgow Outcome Scale.149,150,152–178 It should be noted that the Glasgow Coma Scale was designed to predict outcome after head injury and has not been fully assessed in outcome after SAH. In addition, patients who have no grossly evident neurological deficits after SAH frequently have subtle cognitive or neurobehavioral difficulties that impair their social adjustment and ability to return to their previous occupations.179–183 At least 1 study has suggested that these neurobehavioral deficits are not correlated with tissue loss as seen on recent MRI184; therefore, it is likely that they are due to a diffuse effect of SAH. At the present time there is no standardized method of measuring these deficits in patients with SAH, and a wide variety of standard neuropsychological tests have been used by a variety of investigators.179–182,184 In the recent International Subarachnoid Aneurysm Trial (ISAT), written questionnaires were sent to patients to determine a modified Rankin Scale.185,186 Perhaps the most meaningful and simplest measure of the effect of these deficits is whether the patient is able to return to his or her previous occupation.182 It is reasonable to recommend that studies reporting on SAH contain as a minimum the admission Glasgow Coma Scale score and factors commonly believed to influence prognosis as discussed previously.150Natural History and Outcome of Aneurysmal SAH: Summary and RecommendationsThe severity of the initial bleed should be determined rapidly because it is the most useful indicator of outcome after aneurysmal SAH, and grading scales that rely heavily on this factor are helpful in planning future care with family and other physicians (Class I, Level of Evidence B).Case review and prospective cohorts have shown that for untreated, ruptured aneurysms, there is at least a 3% to 4% risk of rebleeding in the first 24 hours—and possibly significantly higher—with a high percentage occurring immediately (within 2 to 12 hours) after the initial ictus, a 1% per day to 2% per day risk in the first month, and a long-term risk of 3% per year after 3 months. Urgent evaluation and treatment of patients with suspected SAH are therefore recommended (Class I, Level of Evidence B).In the triage of patients for aneurysm repair, factors that may be considered in determining the risk of rebleeding include severity of the initial bleed, interval to admission, blood pressure, gender, aneurysm characteristics, hydrocephalus, early angiography, and the presence of a ventricular drain (Class IIb, Level of Evidence B).Clinical Manifestations and Diagnosis of Aneurysmal SAHThe clinical presentation of aneurysmal SAH is one of the most distinctive in medicine. The sine qua non of SAH in an awake patient is the complaint of “the worst headache of my life,” described by ≈80% of patients who can give a history, but a warning or sentinel headache is also described by ≈20% of patients.187,188 Most intracranial aneurysms remain asymptomatic until they rupture. Although aneurysmal SAH occurs frequently during physical exertion or stress, SAH can occur at any time.189,190 The onset of headache may be associated with ≥1 additional signs and symptoms, including nausea and/or vomiting, stiff neck, a brief loss of consciousness, or focal neurological deficits (including cranial nerve palsies). Fontanarosa191 retrospectively studied 109 patients with proven SAH and found headache in 74%, nausea or vomiting in 77%, loss of consciousness in 53%, and nuchal rigidity in 35%.4 As many as 12% die before receiving medical attention.189Despite the classic presentation of SAH, individual findings occur inconsistently, and because the type of headache from SAH is sufficiently variable, misdiagnosis or delayed diagnosis is common. Misdiagnosis of SAH occurred in as many as 64% of cases before 1985, with more recent data suggesting an SAH misdiagnosis rate of ≈12%.4,21,192–195 Misdiagnosis was associated with a nearly 4-fold higher likelihood of death or disability at 1 year in patients with minimal or no neurological deficit at the initial visit.21 The most common diagnostic error is failure to obtain a noncontrast cranial