(Stroke. 1998;29:2298-2303.)
© 1998 American Heart Association, Inc.
Original Contributions |
Changes in Subarachnoid Hemorrhage Mortality, Incidence, and Case Fatality in New Zealand Between 1981–1983 and 1991–1993
From the University Geriatric Unit, Faculty of Medicine and Health Science, University of Auckland (T.T., R.B., J.D.); the Department of Medicine, Faculty of Medicine and Health Science, University of Auckland, and Department of Neurology, Auckland Hospital (N.E.A.); and the Department of Neurosurgery, Auckland Hospital (E.M.), Auckland, New Zealand; and the 4Danish Epidemiology Science Center at the Institute of Preventive Medicine, Copenhagen University Hospital (T.T.), Copenhagen, Denmark.
Correspondence to Associate Professor Ruth Bonita, University Geriatric Unit, North Shore Hospital, Private Bag 93 503, Takapuna, Auckland 9, New Zealand. E-mail r.bonita{at}auckland.ac.nz
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Abstract |
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Background and Purpose—As with total stroke, mortality rates from subarachnoid hemorrhage (SAH) have declined in New Zealand since the mid-1970s. Data from the Auckland Region Stroke studies allow an understanding of reasons for the change, as SAH incidence and 28-day case fatality rates were measured as part of population-based stroke registers.
Methods—National death registrations were used to describe the trends in mortality rates from SAH (International Classification of Diseases [ICD] code 430) among men and women in New Zealand. Changes in incidence and case fatality rates were determined from 2 large-scale population-based stroke registries carried out in 1981–1983 and 10 years later in Auckland. Similar methodology and case ascertainment techniques were used in both studies.
Results—The mortality rates from SAH declined in both men and women after the mid-1970s. The mortality rate remained higher among women than men. The incidence of SAH was lower in 1991–1993 (11.3 per 100 000) compared with 1981–1983 (14.6 per 100 000). In the younger age groups, the decrease was mostly due to a lower incidence among men, whereas in the older age groups women older than 65 years had a lower incidence. There was no consistent change in case fatality rates between the 2 periods in either men or women.
Conclusions—Mortality rates from SAH have decreased in both men and women. This decrease may be explained by a decrease in the incidence of SAH, because case fatality rates showed no change.
Key Words: cerebrovascular disorders • epidemiology • incidence • mortality • New Zealand • subarachnoid hemorrhage
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Introduction |
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Subarachnoid hemorrhage (SAH) constitutes approximately 5% of all strokes in most affluent countries.1 In contrast to other stroke subtypes, it occurs in relatively younger people and has a higher case fatality.2 3 Most SAHs are caused by rupture of an intracranial aneurysm; in a recent meta-analysis it was estimated that the prevalence of aneurysms in adults is approximately 2%, with an annual risk of rupture of 0.7%.4 The incidence of SAH shows considerable variation between countries with reported rates from approximately 6 to >30 cases per 100 000 person-years.5 6
In New Zealand, mortality from cerebrovascular disease (International Classification of Diseases, 8th Revision [ICD-8] codes 430 to 438) has decreased since the mid-1970s in both men and women.7 Because most strokes result from cerebral infarction or intracerebral hemorrhage, we wanted to investigate the pattern for SAH separately and examine explanations for trends in SAH mortality. We analyzed data from a large, population-based stroke register in the city of Auckland, whose population accounts for approximately one quarter of New Zealand's total population. The incidence and 28-day case fatality rates of SAH in Auckland have been reported for the early 1980s8,9; the present study compared these results with the incidence rates and 28-day case fatality in the same population 10 years later.
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Subjects and Methods |
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National Mortality Data
Mortality rates for all strokes and for SAH for the period 1950 to 1994 have been calculated from information provided by the New Zealand Health Information Service.10 Direct standardization was done using the total 1950 population of New Zealand. Different classifications of the ICD have been used (rubric 330 in the seventh revision between 1950 and 1968, and rubric 430 in the rest of the years in the eighth and ninth revisions), but the changes have had no effect on classification rules.
The Auckland Region Stroke Study
Residents of the Auckland region who had a SAH were identified
as part of large, population-based studies of
stroke11 12 in 2 sequential 2-year periods, the
first in 1981–1983 and the second in 1991–1993. Whereas the time
frame for the larger study of stroke was 1 year, case finding for SAHs
extended over 2 years because of small numbers. The Auckland population
represented approximately one quarter of New Zealand's
total population in both periods; in the 1981 census the total Auckland
population was 829 454, and in the 1991 census it was 945 369.
The definition of SAH was an abrupt onset of a severe headache and/or impaired consciousness or focal neurological signs associated with at least 1 of the following findings: uniform blood staining of the cerebrospinal fluid; CT evidence of blood in the subarachnoid space; cerebral angiographic identification of an aneurysm or arteriovenous malformation, and identification of SAH at surgery or at autopsy. This definition excludes primary intracerebral hemorrhage with extension into the subarachnoid space and subarachnoid bleeding due to trauma, neoplasms, or infections.
The methods of the study and identification of patients with SAH have been described previously.8 Briefly, to ensure detection of all SAHs, admission lists of all public hospitals were examined daily, together with a systematic search of hospital discharges, postmortem and coroner's reports, death certificates, and visits to the neurosurgical and neurological ward at Auckland Hospital. As a part of the larger study, a representative sample of the general practitioners in the Auckland region referred suspected cases from their practices to ensure detection of nonfatal nonhospitalized cases. This did not yield any cases of SAH. The second 12-month period of registration of SAH events undertaken at both sequential periods did not include general practitioners as a source of case finding for nonfatal nonhospitalized events.
Trained nurse interviewers under the direction of a neurologist used standard questionnaires to obtain information about the current event, past medical history, and sociodemographic variables from the patient, or if this was not possible, from a close family member. The same interviewers were used in both study periods. The information concerning management and investigations (lumbar puncture, CT, cerebral angiography) was obtained from the medical records and from discussions with a neurosurgeon or a neurologist.
Case fatality was defined as death within 28 days from onset of symptoms related to the SAH. To compare incidence rates between the 2 periods, we standardized use of the direct method to the total 1991 population in Auckland. To compare case fatality, the proportions for each age and sex group from each of the 2 periods were standardized to the 1991–1993 case distribution.
For comparison of proportions, Fisher's 2-sided exact test was used, and the confidence intervals (CIs) for standardized rate ratios were calculated according to Flanders.13 Confidence intervals around age- and sex-specific rates were based on a normal distribution. The statistical software package STATA14 was used for the calculations.
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Results |
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Mortality Rates
Since the 1950s mortality rates from cerebrovascular disease (ICD-8 codes 430 to 438) in New Zealand have decreased in both men and women (Figure 1
). Until the 1960s, women
had a slightly higher mortality rate than men, followed by a period of
similar rates in both men and women. From the end of the 1970s, men
have had a higher mortality rate than women. There was a trend to
decreasing mortality from the mid-1970s for both men and women. Between
1975 and 1994, stroke mortality rates declined in men and women, from
80 per 100 000 to 40 per 100 000.
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The mortality rates for SAH (ICD-8 code 430) over the same period are
shown in Figure 2. The period from 1950
until the 1970s was characterized by an increase in mortality from SAH;
since the mid-1970s there has been a decreasing trend. For the period
relevant to this study, 1981–1983 to 1991–1993, there was a decline
in SAH mortality in New Zealand from approximately 12 to 8 per 100 000
population in women and 8 to 6 per 100 000 population in men. This
pattern of decline occurred uniformly in different age groups and in
both men and women (data not shown). In contrast to total stroke
mortality, the mortality rates for SAH were consistently higher
among women.
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The Auckland Region Stroke Study
In the first study period (1981–1983) there were 180 cases of
SAH, of which 65 (36.1%) occurred in men and 115 (63.9%) in women; 4
patients experienced a recurrent event within the study period. In
1991–1993 there were 168 cases, 59 (35.1%) in men and 109 (64.9%) in
women; 2 patients experienced a recurrent event within the study
period. One further case, identified through a more intensive
case-finding procedure in 1991–1993 than was possible in 1981–1983,
was excluded. Recurrent events in both periods were omitted from the
calculation of incidence and case fatality rates. The proportion with
aneurysmal SAH was similar in the 2 studies: 78.1% in
1981–1983 and 79.4% in 1991–1993. Arteriovenous malformation was the
cause of SAH in 5 patients in both periods. The mean age increased in
men between the 2 periods from 44 to 52 years and decreased in women
from 56 to 52 years.
The incidence rates decreased for all age groups (men and women
combined) except for people aged 55 to 64 years (Table 1). This decline in incidence was
significant in people aged 35 to 44 years (rate ratio [RR], 0.49;
95%CI, 0.29 to 0.83), with most of this decline explained by a lower
incidence in men (RR, 0.27; 95% CI, 0.09 to 0.73). In women of the
same age there was also a lower incidence in 1991–1993 compared with
1981–1983, but this was not statistically significant (RR, 0.64; 95%
CI, 0.33 to 1.24). Among people aged 
65 years, the overall incidence
rate decreased (RR, 0.62; 95% CI, 0.38 to 1.04), which was largely
explained by a decrease in women, (RR, 0.45; 95% CI, 0.25 to 0.82).
The increase in the incidence of SAH in men aged 65 years was not
statistically significant (RR, 1.82; 95% CI, 0.58 to 6.69).
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The age-standardized incidence rates of SAH decreased in men from 10.9 per 100 000 in 1981–1983 to 8.4 per 100 000 in 1991–1993, and decreased in women from 17.5 per 100 000 in 1981–1983 to 14.1 per 100 000 in 1991–1993. For men and women combined, the decrease was from 14.6 per 100 000 to 11.3 per 100 000 between the 2 periods. The corresponding standardized rate ratios were 0.77 (95% CI, 0.59 to 1.02) in men, 0.80 (95% CI, 0.65 to 0.99) in women, and 0.77 (95% CI, 0.66 to 0.91) for men and women combined.
The age- and sex-specific case fatality rates from SAH showed no
consistent change between the 2 periods (Table 2). Within different age groups there was
no statistically significant change in case fatality except for people
aged 25 to 34 years. After standardization of the 28-day case fatality
rate to the case distribution in 1991–1993, there was no statistically
significant change in the overall rate in men
(
21=0.09;
P=0.77), women
(21=2.32; P=0.13),
or both sexes (21=1.86;
P=0.17). In 1981–1983, 26 people (14%) died before medical
attention or hospitalization; in 1991–1993 a similar proportion of
patients (15%) died before admission. Of the 154 patients who were
hospitalized in 1981–1983, 136 (88%) were admitted within 48 hours of
onset of symptoms. In 1991–1993, 139 patients were admitted to the
hospital; of these, 123 (88%) were admitted within 48 hours of the
onset. The median time from onset to hospitalization decreased from 5.3
hours in 1981–1983 to 2.5 hours in 1991–1993.
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The use of investigations in the 2 study periods showed an increased
use of CT (Table 3). In the first study
period, the diagnosis of SAH was based on an abnormal CT alone in only
7% of the patients, whereas in the second study period the proportion
was 20%. Lumbar puncture was more often used as the first
diagnostic investigation in 1981–1983: of 55 patients who
had both CT and lumbar puncture, 35 (64%) had lumbar puncture first,
while in 1991–1993 lumbar puncture was the first investigation in only
3 (8%) of 36 patients who had both procedures performed (information
on the sequence was not available for 3 and 12 patients, respectively,
in the 2 periods). Of all patients who were admitted to hospital, CT
was used in 61% in 1981–1983 and in 95% in 1991–1993. The
corresponding proportions for lumbar puncture were 62% in 1981–1983
and 26% in 1991–1993.
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Autopsy rates among patients who died decreased between the 2 periods from 47% to 35% (P=0.09). Autopsy was performed on 78% and 43% of deaths which occurred within 48 hours of onset in 1981–1983 and 1991–1993, respectively, (P<0.01). The proportion of events in which the diagnosis of SAH was based on autopsy only decreased from 24% in 1981–1983 to 16% in 1991–1993.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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As with the continuing decline in mortality rates from all strokes, the mortality rates from SAH have shown a similar trend.15 The decline in the mortality of SAH is probably real and not due to a shift in coding practices or diagnostic classification. In contrast to overall deaths from cerebrovascular disease, women have higher mortality rates from SAH than men. The incidence of SAH decreased between the early 1980s and the early 1990s in almost all age groups, in line with the mortality trends for this period. This decrease in incidence was mostly due to a fall in the incidence among men in the younger age groups; the decrease in older people was, in contrast, due to a lower incidence rate in women. There was no change in 28-day case fatality in either men or women except for 1 age group, indicating that the most likely explanation for the observed trend in mortality for SAH was decreased incidence.
SAH incidence rates from the Auckland Region Stroke Study were significantly lower in 1991–1993 than in 1981–1983 only for men and women aged 35 to 44 years. The incidence rates for other age groups did not reach statistical significance, possibly because of the relatively small numbers of SAHs. However, the uniform trends toward lower incidence rates indicate that the decrease is probably real. The standardized incidence rate ratios for men and women also suggest a decrease in incidence, although the summarized rates must be interpreted with caution because they hide variation within different age groups. In contrast to the incidence, the 28-day case fatality rate showed no trend in either men or women. The statistically significant decrease in case fatality in men and women aged 25 to 34 years could be a random result.
Unlike many other studies of SAH, the Auckland Stroke study is large by world standards. Since SAH is a relatively rare condition, accurate assessment of incidence rates and case fatality relies both on a large population and thorough identification of all events. The identification of patients with SAH occurring in Auckland residents was undertaken by the same nurses in both study periods, and the same definition of SAH was used. Incomplete identification of nonhospitalized cases would lead to a lower incidence and case fatality, as most would be due to people who die before medical attention. However, in both study periods 26 patients with SAH were identified who died before hospital admission could be arranged. Similar proportions of fatal out-of-hospital patients have been found in other studies.15 16 17 Incomplete identification of hospitalized cases would lead to lower incidence rates and higher case fatality rates, which was not found; furthermore, the proportion of patients admitted to the hospital within 48 hours in the 2 study periods was identical. The lower autopsy rates in 1991–1993 were in accordance with the general tendency for fewer autopsies in recent years. Furthermore, because the time delay before admission to hospital was reduced between the 2 study periods by almost 3 hours, more patients would have had investigations before death, making autopsy unnecessary. We feel confident that all eligible cases were identified.
The frequency of CT scanning increased while the use of lumbar puncture decreased between the 2 periods. Red blood cells and xanthochromia can be detected in the cerebrospinal fluid in virtually all patients with SAH between 12 hours and 2 weeks after the bleeding.18 Lumbar puncture alone is less specific than CT for SAH, and it may falsely suggest a diagnosis of SAH if there has been a traumatic tap or in patients with an intracerebral hematoma.18 19 However, review of the clinical presentation by a neurologist and exclusion of all cases in whom the diagnosis of SAH was in doubt probably excluded most cases in which the subarachnoid bleeding was secondary to extension of an intracerebral hematoma into the subarachnoid space. Thus, the impact of the changes in diagnostic investigations between 1981–1983 and 1991–1993 on incidence and case fatality was probably minimal.
Our results are not in accord with the conclusions from recent meta-analyses that investigated differences in SAH incidence5 and case fatality20 for a number of studies which have spanned the last 3 decades. An apparent decline in incidence over the time period investigated was explained by increased use of CT. The authors concluded that misclassification of other types of intracranial hemorrhages as SAH may have led to artificially high incidence rates in the early period. Other authors21 have suggested that the introduction of CT may lead to an increase in incidence, because less-severe cases would be diagnosed. However, there is an apparent trend of increasing incidence of SAH when only those studies with more than 70% of CT scans are included in the analysis, suggesting that a linear relation between the frequency of CT and the incidence of SAH is unlikely to be an adequate explanation. The investigation of case fatality in the meta-analyses suggested that there had been a decrease in case fatality; none of the results were statistically significant. Meta-analysis carries a risk of publication and language bias22–24; furthermore, conflicting results emerge when the studies differ in size, scope, and time period.
Case fatality at 28 days after SAH has not improved in Auckland during the 1980s. Earlier clipping of an aneurysm and use of the calcium antagonist nimodipine have been shown to improve outcome after SAH.25 26 27 The median time from hospitalization to surgery fell from 8 days in 1981–1983 to 4 days in 1991–1993, with a corresponding improvement in survival 2 weeks after surgery (from 83.4% in the earlier period to 91.5% in the later period). Overall, only 5.8% of hospitalized patients received nimodipine; because of the high early case fatality of SAH, selective use in a small proportion of patients is unlikely to have an impact on overall case fatality.
A decrease in the incidence of SAH may be a result of a declining exposure to risk factors. Most SAHs result from a ruptured intracranial aneurysm, and to a lesser extent are due to vascular malformations. Also, a few arise as a result of arteriosclerotic aneurysms, mycotic aneurysms, and neoplastic aneurysms, causes that have been excluded because of the definition of SAH in the present study. Although there are equivocal results concerning the impact of risk factors for SAH, and whether the effect is on creation of an aneurysm and/or rupture of an aneurysm, exposure to smoking and hypertension have been clearly identified as hazardous factors.1 28 29 30 31 Oral contraception, alcohol consumption, hypercholesterolemia, and physical activity also have been suggested as risk factors for SAH,32 33 34 35 although interpretation of the data is often hampered by small numbers of patients. In the Auckland population it has previously been estimated that the population-attributable risks of SAH associated with smoking and hypertension were 43% and 28%, respectively.28 Between 1983 and 1994 the prevalence of smoking and hypertension declined in the general Auckland population aged 35 to 64 years.36 Such a decrease may have contributed to a decrease in the incidence of SAH.
We conclude that mortality from SAH has decreased in New Zealand and that the most likely explanation for the observed mortality trend is a fall in incidence rates, rather than improvement in case fatality rates.
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Acknowledgments |
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The authors wish to acknowledge Joanna Broad and Ulf Leth Dahl for statistical advice and Susan Hawkins for her involvement in the collection of data. The Auckland Stroke Study was funded by the Health Research Council of New Zealand with assistance from the Stroke Foundation of New Zealand and the Neurological Foundation of New Zealand.
Received June 16, 1998; revision received August 28, 1998; accepted August 28, 1998.
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