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doi: 10.1227/01.neu.0000430290.93304.33
Research-Human-Clinical Studies: Editor's Choice

The Epidemiology of Admissions of Nontraumatic Subarachnoid Hemorrhage in the United States

Rincon, Fred MD, MSc, MBE, FACP, FCCP, FCCM*,‡; Rossenwasser, Robert H. MD, FACS, FAHA; Dumont, Aaron MD, FACS, FAHA

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*Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania;

Department of Neurosurgery, Thomas Jefferson University, Philadelphia, Pennsylvania

Correspondence: Fred Rincon, MD, MSc, MBE, Department of Neurological Surgery, Thomas Jefferson University and Jefferson College of Medicine, Division of Critical Care and Neurotrauma, 909 Walnut St, 3rd Floor, Philadelphia, PA 19107. E-mail:

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (

Received January 13, 2013

Accepted March 20, 2013

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BACKGROUND: Subarachnoid hemorrhage (SAH) is the cause of 5% to 10% of strokes annually in the United States.

OBJECTIVE: To study the incidence and mortality trends of admissions of SAH from 1979 to 2008 using a nationally representative sample of all nonfederal acute-care hospitals in the United States: The National Hospital Discharge Survey.

METHODS: The sample was obtained from the hospital discharge records according to the International Classification of Disease, 9th Revision, Clinical Modification code 430.

RESULTS: We reviewed data on approximately 1 billion hospitalizations in the United States over a 30-year study period and identified 612 500 cases of SAH, which was more common in women (relative risk 1.71, 95% confidence interval 1.7-1.72) and nonwhite persons than white persons (relative risk 1.46, 95% confidence interval 1.4-1.5). The estimated incidence rate of admission after SAH was 7.2 to 9.0 per 100 000/year and did not significantly change over the study period. Overall, in-hospital mortality after SAH fell from 30% during the period from 1979 to 1983 to 20% during the subperiod from 2004 to 2008 (P = .03) and was lower in larger treating hospitals. The average days of care for SAH hospitalizations decreased, but the rate of discharge to long-term care facilities increased.

CONCLUSION: The incidence rate of admission after SAH has remained stable over the past 30 years. Total deaths and in-hospital mortality after SAH have decreased significantly. In-hospital mortality after SAH is lower in larger treating hospitals.

ABBREVIATIONS: CI, confidence interval

ICD-9-CM, International Classification of Disease, 9th Revision, Clinical Modification

NHDS, National Hospital Discharge Survey

RSE, relative standard error

RR, risk ratio

SAH, subarachnoid hemorrhage

SE, standard error

Subarachnoid hemorrhage (SAH) causes 5% to 10% of strokes annually in the United States.1 Population-based studies indicate that the incidence varies according to the geographic region.2,3 The outcome depends on several factors including age, severity, timing of treatment, intensive care unit management, and the incidence of medical complications.1 Updated long-term nationwide studies regarding the epidemiology and trends in overall in-hospital mortality after SAH in the United States are currently lacking. In this study, we investigated the temporal trends in admissions of SAH using a representative sample of all nonfederal hospitals with specific attention to its admission rate, disposition, and in-hospital mortality. We hypothesized that the incidence rate of admissions and in-hospital mortality after SAH have not significantly changed over the past 30 years.

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Data Source

The National Center for Health Statistics has conducted the National Hospital Discharge Survey (NHDS) continuously since 1965. Since 1979, the NHDS has conformed to the guidelines of the Uniform Hospital Discharge Data Set for consistency of reporting in records. The NHDS represents a sample of discharges from noninstitutional hospitals, exclusive of federal, military, and Veterans Administration hospitals, located in the 50 states and the District of Columbia including approximately 500 hospitals. The database is constructed by surveying inpatient discharge records from each participating institution, representing approximately 1% of all hospitalizations, or 350 000 discharges annually. Demographic information (age, sex, racial background, geographic location, and marital status), dates of hospital admission and discharge, sources of payment, and disposition at discharge are abstracted by National Center for Health Statistics personnel using International Classification of Disease, 9th Revision, Clinical Modification (ICD-9-CM) criteria. A maximum of 7 diagnostic codes is assigned for each sampled abstract; in addition, if the medical information included surgical or nonsurgical procedures, a maximum of 4 codes for these procedures is assigned (for information:

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Sample, Definitions, and Hospitalization Data

Admissions of patients with a primary diagnosis of SAH were identified by querying of the database between 1979 and 2008 by using the ICD-9-CM code 430.4,5 Tirschwell et al6 demonstrated that the code used to identify SAH admissions in the primary diagnosis field has a sensitivity of 90%, specificity of 97%, and positive predictive value of 94%. Individual's age, sex, and race were obtained from the NHDS records. The NHDS coded race as white, African-American, American/Indian Eskimo, Asian-Pacific Islander, other, or not stated. Querying all secondary fields identified organ dysfunctions during hospitalization characteristically seen in SAH cohorts7 as suggested by other studies using similar data sets8-10 and included cardiovascular dysfunction, respiratory dysfunction, renal dysfunction, hepatic dysfunction, neurological dysfunction, metabolic dysfunction (acidosis), and hematologic dysfunction (see the Table, Supplemental Digital Content,, which illustrates the ICD-9-CM-based classification of SAH and acute organ dysfunctions used in this study). We divided the hospitals according to the Halpern criteria11 into small to medium size (≤300 beds), large (301-499 beds), and extra large (>500 beds). No data on the severity of disease, imaging findings, physiology during hospitalization, or hospital type (urban-academic, urban-private, or rural) are available in the NHDS database.

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Statistical Analyses

Admission rates per 100 000 were adjusted for the 2000 census population distribution. National estimates were calculated according to accepted guidelines for the accuracy of the NHDS data. Our methodology for calculating national estimates from the NHDS has been published previously.12 In brief, only absolute, unweighted samples of more than 60 patients with relative standard error (RSE) measures of less than 30% were included in data analyses. The standard error (SE) was calculated by multiplying the RSE by the estimated admission rate and mortality, and 95% confidence intervals (CI) were calculated from these standard errors. Differences between calculated incidence rates and weighted national prevalence estimates were quantified with the Z-score test by using conventional online calculators ( Data for continuous variables were compared by the 1-way analysis of variance and the difference in means compared with the Tukey-Kramer post hoc test; data for categorical variables were compared by using the χ2 test. Annual data are divided into 6 subperiods (1979-1983, 1984-1988, 1989-1993, 1994-1998, 1999-2003, and 2004-2008) based on the total amount of years included in the study period allowing for more accurate calculation of RSE and SE and better trend interpretation. Age (less than 45 years, 45-64 years, and older than 65 years) and race (white and nonwhite) were divided into subgroups according to NHDS recommendations to allow for specific calculation of RSE and age- and race-adjusted estimates. Blacks and other nonwhites were grouped into 1 single group (the nonwhite group) because lower unweighted samples in the other nonwhite groups would have not allowed for adequate estimation of RSE and the SE. Since the data on were was missing in up to 17% of the sample, these persons were excluded only from the calculations of race-adjusted specific estimates but were included in all other calculations. We used commercially available statistical software (JMP 9.0, SAS Institute, Cary, North Carolina). P-values are 2-sided, and statistical significance was judged when P < .05.

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Over the 30-year period, there were more than 1 billion hospitalizations and 612 500 cases of SAH, representing 0.07% of total hospitalizations in the United States. The demographic characteristics in the population of admissions with SAH are shown in Table. The average age of SAH patients increased over time, from 52.9 years in the first subperiod to 56.6 in the last subperiod (difference 3.8 years, 95%CI 1.1-6.5, P < .001). The mean age among women was 56.7 compared with 53.4 years in men (difference 3.3 years, 95%CI 2.3-4.4, P < .001). The overall age-adjusted risk of SAH was higher in women in comparison with men (risk ratio [RR] 1.71, 95%CI 1.7-1.72). According to age group, the risk of SAH was higher in women older than 65 years (RR 3.37, 95%CI 3.3-3.4; vs RR 1.9, 95%CI 1.86-1.9 for 45-64 age group; vs RR 1.4, 95%CI 1.34-1.4 for <45 age group).

TABLE Characteristic...
TABLE Characteristic...
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Admission Incidence Rate

The number of reported SAH admissions per year increased from an average 15 000 cases during the first subperiod to an average 24 400 cases during the last subperiod (P < .001) (Table), or an increase in 1.3% per year. The admission rate of SAH remained stable over the 30-year period (7.2 cases per 100 000 person-years during the first subperiod and 7.8 cases per 100 000 person-years during the last subperiod, Table). The rate of admission after SAH was higher in women throughout the study period (Figure 1). Nonwhites had a higher risk of SAH than whites (RR 1.46, 95%CI 1.4-1.5) (Table).

Figure 1
Figure 1
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Organ Dysfunctions and Mortality

Development of complications occurred with more SAH admissions developing organ dysfunctions throughout the study period (Table). In the first subperiod, 9.1% of SAH admissions had reported organ dysfunctions compared with 35.6% during the last subperiod (P < .001). The number of organ dysfunctions increased significantly in the last subperiod compared with the first subperiod (P < .001) (Table).

The overall in-hospital mortality declined over the 30-year period, from an average of 30% (95%CI 21%–39%) during the first subperiod to 20% (95%CI 16%–24%) during the last subperiod (P = .03) (Figure 2). This difference was also significant when comparing the second subperiod (33%, 95%CI 29%–35%) and last subperiod (P = .01) (Figure 2 and Table). The increase in the number of SAH admissions did not result in a higher number of in-hospital deaths, which declined from 6930 in 1979 to 4425 in 2008, a reduction of 1.2% per year (P < .001).

Figure 2
Figure 2
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Overall, in-hospital mortality after SAH was higher in women than in men (RR 1.13, 95%CI 1.1-1.14, P < .001), admissions older than 65 years (39% vs 22% in 45-64 age subgroup vs 17% in <45 age subgroup, P < .001), and in whites compared with nonwhites (RR 1.1, 95%CI 1.05-1.1, P < .001); however, older men >65 years were more likely to die (41% vs 38% in women >65 years, P < .001). Organ dysfunctions were significantly associated with in-hospital mortality. The mortality in admissions with no reported organ dysfunction was 17%, 1 organ dysfunction was 50%, 2 organ dysfunctions was 64%, and 3 or more organ dysfunctions was 72% (P < .001). According to bed size, mortality was higher in smaller hospitals (38.5%) than in large (36%) and extralarge hospitals (25.6%) (P < .001).

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Disposition of Patients and Days of Care

Overall, more patients were discharged to home and short-term care facilities combined (Table). However, the number of discharges to long-term facilities increased from 9% during the first subperiod to 16.3% in the last subperiod (P < .001). The average length of stay decreased significantly from an average of 16.5 days in the first subperiod to an average of 11.3 days in the last subperiod (difference 5.2 years, 95%CI 2.4-8.0 years, P < .001) (Table).

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The results of this study based on a representative sample of hospitals from all the geographic regions of the United States suggest that the estimated incidence rate of admissions of SAH has not significantly changed over the past 30 years. In contrast, however, our study suggests that the total number of hospital deaths after SAH and in-hospital mortality decreased significantly. In support of our results, the demographic and epidemiological characteristics of our cohort resemble reported estimates of the incidence of SAH from population-based studies and reflect known disparities in the risk of SAH based upon age, sex, and race.2,13-15 In our cohort, nonwhites had a higher incidence of SAH, a characteristic that has been established by previous observational studies in the United States.15 Therefore, despite our study being non-population-based, it provides similar epidemiological estimates about the incidence of SAH in the United States according to other studies.2,5,13,15

Epidemiological studies from administrative repositories are important for the delineation of trends, impact of treatments, and allocation of health care resources and research budgets.8,10,16 Specific data on the epidemiology of SAH are available from cohort studies17-22 and meta-analysis,2,13 but these have been limited by the lack of inclusion of cohorts from the United States. According to a recent meta-analysis of population-based studies, the overall incidence of SAH in the world is 9.0 per 100 000 person-years.2 The incidence rate per region of the world varies substantially with higher incidence rates in Japan (22.7, 95%CI 21.9-23.4), Finland (19.7, 95%CI 18.1-19.3), followed by other countries (9.1, 95%CI 8.8-9.5) and South/Central American countries (4.2, 95%CI 3.1-5.7).2 Studies in North America have suggested that the incidence rate of SAH may be 6 to 8 per 100 000 person-years.13 In the United States the reported incidence rate from population-based studies in the Olmsted County (Rochester, Minnesota) during the 1950s to 1980s was 10.5 per 100 000 person-years, but these studies may have not fully relied on computed tomography (CT) scanning to ascertain the diagnosis of SAH.20 In support of our results, Linn et al13 also demonstrated that the incidence of SAH did not change between 1960 and 1990, which is in contradiction of earlier reports that claimed a decline in the incidence of SAH in the United States.17-19 The results of these studies17-19 may have been explained by the infrequent use of CT scanning before 1980 after which CT scan imaging became a more commonly used assessment tool in the diagnosis of stroke.13

The stable estimated incidence of SAH contrasts with the impressive decline in total deaths and in-hospital mortality seen in our study, which mirrors overall stroke-related mortality in the United States.23 The mortality in the white SAH population increased substantially between 1950 and 1970, possibly related to the better diagnostic definition and differentiation of SAH and intracerebral hemorrhage.22,24 After 1970, mortality trends in SAH populations were demonstrated in smaller cohorts,22,25 and a recent population-based study in England and pooled analysis from all available population-based studies demonstrated a significant decrease in mortality after SAH.26 However, in this pooled analysis large updated population studies from the United States were lacking. To this end, our study supports those reported trends in mortality reduction after admission for SAH and provides further epidemiological information on trends after admission for SAH in the United States.

The sharp decline in total deaths and in-hospital mortality from the first subperiods to the last subperiod and the significant reduction in the average days of care can also be attributed to the potential effect of specific improvements in neurosurgical interventions and timing for obliterating cerebral aneurysms, nonspecific improvements in neurological critical care,27,28 advances in neuroprotective strategies,29 and more patients being discharged earlier to long-term and short-term facilities based on hospital overcrowding and health insurance practices. We cannot overstate the role of CT scanning in the diagnosis of SAH, which revolutionized our diagnostic ability in the neurosciences and may have also influenced the trend in mortality seen in our cohort.

The increase in the number of organ dysfunctions may be a reflection of more patients being treated after SAH based on the known relationship between more aggressive medical and surgical interventions and the onset of complications and organ dysfunctions,7 the interaction between age and outcome after critical illness, and the improvement in the physician's nihilistic views when assessing the role of treatments vs expected outcomes. This may be reflected by the significant change in the average age of the cohort from the first subperiod in comparison with the last subperiod, suggesting that more older patients were being treated and surviving after admission for SAH, or related to improved longevity of the US population30 or a healthy aging effect. However, evolving billing and coding practices that encourage greater attention to the onset of specific organ failures may also explain this trend.

The role of specialized high-volume centers in the management of SAH and its effect on outcomes is supported by the lower in-hospital mortality seen in these hospitals31-33 with availability of appropriate specialty neurointensive care units, neurointensivists, vascular neurosurgeons, and interventional neuroradiologists that provide the essential elements of care.28 Center-specific higher case load has been associated with better outcomes in SAH cohorts31; however, the effect of comprehensive neuroscience centers and its effect on mortality after SAH was also demonstrated in a recent study.33 If operator-specific higher case load in these neuroscience centers is the driving factor associated with lower mortality remains to be answered by future studies. Preliminary studies also suggest that neurointensivist-directed neurocritical care units may result in reduced mortality in patients with SAH at high-volume centers.34 To this end, our study supports the concept of management of SAH at high-volume centers and encourages the implementation of public health policies to pursue regionalization while ensuring adequate and timely geographic spread of access to neurocritical care.33,35

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Our study has limitations. First, our analysis was observational in nature, which limits the inferences that can be made about etiological or causal relationships. Second, ICD-9-CM codes have historically been of questionable accuracy, particularly because they may change over time. The accuracy of the ICD-9-CM code used in our study has been validated in a prior study6 carrying a 94% probability of identifying true cases of SAH.6 However, we may have underestimated the true incidence of SAH based on the historical use of CT scanning to accurately diagnose SAH, which may have been limited during the earlier subperiods of the study period, so our results should be interpreted with this in mind. We may have also potentially missed cases of SAH not evaluated at an acute care hospital. There may also be inaccuracies such as the attribution of the cause of death to SAH on the basis of crude mortality data, rather than direct data from death certificates or autopsies. It is important to explicitly point out that this analysis does not address longer-term or overall SAH-related mortality, which may be more important from a public health perspective. Further, data on the disposition of patients at discharge may have been influenced by the overall increase in the use and transfers to long-term health care facilities in the United States predicated on the recent changes in insurance reimbursement and hospital overcrowding. We were also unable to examine or link mortality data beyond the hospital admission. However, in support of our results, the demographic characteristics of this cohort of SAH admissions are similar to those that have been identified in previous cohort studies of SAH.5,13,36 Third, our data are limited by the quality of the NHDS repository, but the advantages of our robust sample size are potentially offset by our inability to audit the data elements. Fourth, the NHDS data do not include important outcomes after hospitalizations classically used in research of SAH cohorts. Despite these limitations, the NHDS database is robust because it allows investigators to estimate national trends of several variables important for understanding the behavior of certain diseases.8,16 Fifth, the NHDS does not allow us to evaluate the effects of other variables that may have confounded our observed associations such as the time of onset of SAH, additional comorbidities, severity and characteristics of SAH, rates of DNR orders, and timing of treatments.

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The rate of admission of aneurysmal SAH has remained stable over the past 30 years in the United States. Our reported incidence rate of admission is comparable to that of population-based incidence studies of SAH. Total deaths and the in-hospital mortality after SAH have decreased significantly, and, more importantly, in-hospital mortality was lower in larger treating hospitals. Our results may be used in support of population-based studies of aneurysmal SAH providing important information for the evaluation of health care delivery related to stroke, the allocation of health care resources, clinical practice, public health, and research budgets in general.

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Dr Rincon has received salary support from the American Heart Association (AHA 12CRP12050342). Dr Dumont is supported by 1K08NS067072 from the National Institute of Neurological Disorders and Stroke. The authors have no personal financial or institutional interest in any of the drugs, materials, or devices described in this article.

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1. Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. N Engl J Med. 2006;354(4):387–396.

2. de Rooij NK, Linn FH, van der Plas JA, Algra A, Rinkel GJ. Incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender and time trends. J Neurol Neurosurg Psychiatry. 2007;78(12):1365–1372.

3. Nieuwkamp DJ, Setz LE, Algra A, Linn FH, de Rooij NK, Rinkel GJ. Changes in case fatality of aneurysmal subarachnoid haemorrhage over time, according to age, sex, and region: a meta-analysis. Lancet Neurol. 2009;8(7):635–642.

4. Johnston SC. Effect of endovascular services and hospital volume on cerebral aneurysm treatment outcomes. Stroke. 2000;31(1):111–117.

5. Claassen J, Bateman BT, Willey JZ, et al.. Generalized convulsive status epilepticus after nontraumatic subarachnoid hemorrhage: the nationwide inpatient sample. Neurosurgery. 2007;61(1):60–64; discussion 64-65.

6. Tirschwell DL, Longstreth WT Jr. Validating administrative data in stroke research. Stroke. 2002;33(10):2465–2470.

7. Wartenberg KE, Schmidt JM, Claassen J, et al.. Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med. 2006;34(3):617–623; quiz 624.

8. Martin GS, Mannino DM, Eaton S, Moss M. The epidemiology of sepsis in the United States from 1979 through 2000. N Engl J Med. 2003;348(16):1546–1554.

9. Qureshi AI, Suri MF, Nasar A, et al.. Thrombolysis for ischemic stroke in the United States: data from National Hospital Discharge Survey 1999-2001. Neurosurgery. 2005;57(4):647–654; discussion 647-654.

10. Rincon F, Ghosh S, Dey S, et al.. Impact of acute lung injury and acute respiratory distress syndrome after traumatic brain injury in the United States. Neurosurgery. 2012;71(4):795–803.

11. Halpern NA, Pastores SM, Thaler HT, Greenstein RJ. Changes in critical care beds and occupancy in the United States 1985-2000: differences attributable to hospital size. Crit Care Med. 2006;34(8):2105–2112.

12. Rincon F, Mayer SA. The epidemiology of intracerebral hemorrhage in the United States from 1979 to 2008 [published online ahead of print]. Neurocrit Care. 2012.

13. Linn FH, Rinkel GJ, Algra A, van Gijn J. Incidence of subarachnoid hemorrhage: role of region, year, and rate of computed tomography: a meta-analysis. Stroke. 1996;27(4):625–629.

14. Teunissen LL, Rinkel GJ, Algra A, van Gijn J. Risk factors for subarachnoid hemorrhage: a systematic review. Stroke. 1996;27(3):544–549.

15. Broderick JP, Brott T, Tomsick T, Huster G, Miller R. The risk of subarachnoid and intracerebral hemorrhages in blacks as compared with whites. N Engl J Med. 1992;326(11):733–736.

16. Birkmeyer JD, Siewers AE, Finlayson EV, et al.. Hospital volume and surgical mortality in the United States. N Engl J Med. 2002;346(15):1128–1137.

17. Pakarinen S. Incidence, aetiology, and prognosis of primary subarachnoid haemorrhage. A study based on 589 cases diagnosed in a defined urban population during a defined period. Acta Neurol Scand. 1967;43(suppl 29):1–28.

18. Brewis M, Poskanzer DC, Rolland C, Miller H. Neurological disease in an English city. Acta Neurol Scand 1966;42(suppl 24):21–89.

19. Ingall TJ, Whisnant JP, Wiebers DO, O'Fallon WM. Has there been a decline in subarachnoid hemorrhage mortality? Stroke. 1989;20(6):718–724.

20. Phillips LH II, Whisnant JP, O'Fallon WM, Sundt TM Jr. The unchanging pattern of subarachnoid hemorrhage in a community. Neurology. 1980;30(10):1034–1040.

21. Bonita R, Thomson S. Subarachnoid hemorrhage: epidemiology, diagnosis, management, and outcome. Stroke. 1985;16(4):591–594.

22. Sacco RL, Wolf PA, Bharucha NE, et al.. Subarachnoid and intracerebral hemorrhage: natural history, prognosis, and precursive factors in the Framingham Study. Neurology. 1984;34(7):847–854.

23. Roger VL, Go AS, Lloyd-Jones DM, et al.. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. 2012;125(1):e2–e220.

24. Whisnant JP, Phillips LH II, Sundt TM Jr. Aneurysmal subarachnoid hemorrhage: timing of surgery and mortality. Mayo Clin Proc. 1982;57(8):471–475.

25. Bonita R, Beaglehole R, North JD. Subarachnoid hemorrhage in New Zealand: an epidemiological study. Stroke. 1983;14(3):342–347.

26. Lovelock CE, Rinkel GJ, Rothwell PM. Time trends in outcome of subarachnoid hemorrhage: population-based study and systematic review. Neurology. 2010;74(19):1494–1501.

27. Diringer MN, Edwards DF. Admission to a neurologic/neurosurgical intensive care unit is associated with reduced mortality rate after intracerebral hemorrhage. Crit Care Med. 2001;29(3):635–640.

28. Diringer MN, Bleck TP, Claude Hemphill J III, et al.. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society's Multidisciplinary Consensus Conference. Neurocrit Care. 2011;15(2):211–240.

29. Pickard JD, Murray GD, Illingworth R, et al.. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ. 1989;298(6674):636–642.

30. Kulkarni SC, Levin-Rector A, Ezzati M, Murray CJ. Falling behind: life expectancy in US counties from 2000 to 2007 in an international context. Popul Health Metr. 2011;9(1):16.

31. Leake CB, Brinjikji W, Kallmes DF, Cloft HJ. Increasing treatment of ruptured cerebral aneurysms at high-volume centers in the United States. J Neurosurg. 2011;115(6):1179–1183.

32. Cowan JA Jr, Dimick JB, Wainess RM, Upchurch GR Jr, Thompson BG. Outcomes after cerebral aneurysm clip occlusion in the United States: the need for evidence-based hospital referral. J Neurosurg. 2003;99(6):947–952.

33. McNeill L, English SW, Borg N, Matta BF, Menon DK. Effects of institutional caseload of subarachnoid hemorrhage on mortality: a secondary analysis of administrative data. Stroke. 2013;44(3):647–652.

34. Cross DT III, Tirschwell DL, Clark MA, et al.. Mortality rates after subarachnoid hemorrhage: variations according to hospital case volume in 18 states. J Neurosurg. 2003;99(5):810–817.

35. Ward MJ, Shutter LA, Branas CC, Adeoye O, Albright KC, Carr BG. Geographic access to US Neurocritical Care Units registered with the Neurocritical Care Society. Neurocrit Care. 2012;16(2):232–240.

36. Claassen J, Vu A, Kreiter KT, et al.. Effect of acute physiologic derangements on outcome after subarachnoid hemorrhage. Crit Care Med. 2004;32(3):832–838.

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This is an interesting report on the incidence and mortality trends of admissions of SAH from 1979 to 2008 using a nationally representative sample of all nonfederal acute-care hospitals in the US: The National Hospital Discharge Survey. Basically the authors were able to demonstrate that the NHDS data provide, besides the mentioned limitations, sufficient data to analyze some epidemiological factors in patients with aneurismal SAH in the United States. Additionally, this study underlines in contrast to ischemic stroke a quite stable incidence over the last decades and its correlation to ethnicity. At least, the study expresses clearly that there is the need of more detailed registers integrating a high amount of information from patients experiencing aneurismal SAH to achieve a better understanding of the disease.

Daniel Hänggi

Düsseldorf, Germany

This is a very definitive epidemiological study of SAH incidence and mortality over a period of 30 years in the United States. By the use of a large administrative database, 612 500 nontraumatic SAH cases were analyzed. The main finding confirms something that neurosurgeons and neurointensivists have known for many years, but that to date has only been confirmed in smaller studies and systematic reviews: SAH mortality is falling, and mortality is lower in high-volume centers that concentrate clinical experience and expertise. As a result of our ability to save more poor-grade patients, the need for intensive host-hospital rehabilitation and long-term care has increased. This article is destined to become widely cited, and raises an interesting point regarding health care policy. The data show that hospital care has become more efficient, resulting in decreased hospital length-of-stay, but clinicians on the frontlines also recognize that our current payer system hampers effective transitioning of critically ill stroke survivors from the intensive care unit to rehabilitation. As we increasingly move toward global fees for hospital care, data of this type can be used to plan and justify innovative programs that bundle surgery, critical care, and rehabilitation into a single global plan of care.

Stephan A. Mayer

New York, New York


Aneurysm; Epidemiology; NHDS; National Hospital Discharge Survey

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