Epidemiology and treatment of atraumatic subarachnoid hemorrhage over 10 years in a population-based registry

Abstract

Introduction:

Incidence of atraumatic subarachnoid hemorrhage (SAH) is decreasing over time and its treatment is changing. We reported epidemiologic data on aneurysmal (a-) and non-aneurysmal (na-) SAH over 10 years.

Patients and Methods:

Our prospective population-based registry included patients with first-ever SAH occurring from January 2011 to December 2020. Clinical and neuroimaging records were screened to evaluate the presence and location of intracranial aneurysms, to identify naSAH subtypes and to retrieve information on surgical treatments. Incidence rates were standardized to the 2011 Italian and European population. We also estimated 30-day and 1-year case-fatality rates after SAH. Multivariate hazard ratios for 30-days and 1-year fatality were estimated with Cox regression analysis.

Results:

194 patients (60.8% women; mean age 62.5 ± 16.0 years) were included (76.8% aSAH and 23.2% naSAH). The crude incidence rates per 100,000 person-years of SAH, aSAH, and naSAH were 6.5 (95% CI 5.6–7.5), 5.0 (95% CI 4.2–5.9), and 1.5 (95% CI 1.1–2.0), respectively, and remained stable over time. Compared to aSAH, naSAH patients had higher age (68.8 ± 19.7 yearsvs 60.6 ± 14.2 years; p = 0.012), lower cigarette smoking (17.9%vs 36.4%; p < 0.001) and higher atrial fibrillation (15.7% vs 2.8%; p = 0.005). SAH case-fatality rates within 30-days and 1-year were 28.4% (95% CI 21.4–36.9) and 37.1% (95% CI 29.0–46.7), respectively. The relative proportion of surgically treated patients did not change over time.

Conclusion:

We found a low and stable incidence of SAH over the 2011–2020 period. naSAH remained rare and deserves further investigation in larger prospective cohorts.

Graphical abstract.

Introduction

Subarachnoid hemorrhage (SAH) refers to bleeding into the subarachnoid space. Non-traumatic SAH is the least common type of stroke with a relative proportion of 5% of all cerebrovascular disease. ¹ Most cases of non-traumatic SAHs are attributed to the rupture of cerebral arterial aneurysms potentially amenable to surgical correction. A minority of cases is attributable to causes different from aneurysms including arteriovenous malformations, cerebral amyloid angiopathy, cerebral vasculitis, posterior reversible encephalopathy syndrome (PRES), other uncommon etiology, or unknown causes. ²

According to a meta-analysis, the overall incidence of SAH is 7.9 per 100,000 person-years and is higher in Asian compared with Western populations. ³ A trend toward a decreasing incidence of SAH was found in recent years, possibly related to public health interventions and lifestyle modifications with an increasing control of vascular risk factors, including arterial hypertension and smoking. Those two risk factors have a great impact on the risk of SAH.^4,5 Worldwide decrease in SAH incidence has also been attributed to growing prophylactic treatment of unruptured aneurysms. In fact, compared to past decades, more and more brain aneurysms are detected before their rupture, either as incidental findings or as screening in relatives of subjects with known aneurysms.^5–7 Moreover, literature suggests an increase in surgical clipping and endovascular coiling of ruptured and unruptured aneurysms over time as well as an improvement in surgical techniques ⁸ that might have had an impact on SAH treatment. For all those reasons, it is important to provide an updated account of the epidemiology of SAH. The aim of the present work is to provide a comprehensive report of SAH incidence, classification, treatments, and outcomes in a well-defined geographical area over a decade.

Methods

Study design and population

We followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) guidelines to report the results of the present study. The study is part of a prospective population-based registry including patients with first-ever stroke and transient ischemic attack in the resident population of 298,343 inhabitants ⁹ of the district of L’Aquila, central Italy. ¹⁰ The registry includes all cases of cerebrovascular events occurring in the district, which are regularly reported by local physicians, validated by the study staff, and followed-up; it complies with epidemiological criteria for stroke incidence studies ¹¹ and was approved by the Internal Review Board of the University of L’Aquila with protocol numbers 13/2018 and 57/2019. Patients were treated according to routine clinical practice and following national and international guidelines. Among all cases of stroke, we registered cases of SAH occurring in the district of L’Aquila over a 10-year period, from January 1, 2011 until December 31, 2020. We only considered patients who had first-ever SAH and were residing in the district of L’Aquila at the time of stroke; patients with SAH occurring after a previous stroke event, non-residents in the district, and patients whose SAH was found to originate from a trauma were excluded. For the present study, SAH classification was performed retrospectively via neuroimaging review after the prospective collection of cases. The district of L’Aquila is a mountainous area of 5034.46 km² provided by four public hospitals with 24/7 availability of brain CT, intensive care units and general medicine wards; two hospitals have neurology wards and one a neurosurgical ward. Medical care in the district is completely free of charge with easy access to medical services for the acute phase of a stroke.

Case-finding procedures

All events in this study were identified by active monitoring of all health services in the district and nearby areas. Patients admitted for a cerebrovascular event were examined by a vascular neurologist to validate the event. The records of patients with a possible diagnosis of TIA, dizziness, vertigo, confusion, seizures, headache, and transient global amnesia were also reviewed. The 118 Emergency Medical Service, emergency rooms, neuroradiology, neurophysiology and neurosonology services were systematically checked. Regular contacts were also maintained with rehabilitation and long-term care services. The study purpose was explained in advance to all general practitioners and on-call physicians, who were asked to refer all stroke cases or give information about patients evaluated at home. Death certificates were checked monthly and clinical data of all deceased patients who died with a diagnosis of stroke not otherwise included in the registry, were reviewed.

Data collection and follow-up

Demographic, clinical and laboratory data were collected through consultation of medical records and stored in a computerized database in a fully anonymized form. We used Research Electronic Data Capture (REDCap), a web application for building and managing online surveys and databases, for data input. ¹² We collected medical history, cardiovascular and neurological evaluations, and routine laboratory blood tests. We also recorded vascular risk factors including arterial hypertension, diabetes mellitus, atrial fibrillation, hypercholesterolemia, cigarette smoking, alcohol abuse, coronary heart disease, and peripheral artery disease. Where available, we also included the results of ancillary investigations such as 12-lead electrocardiography, transthoracic echocardiography, transesophageal echocardiography, Doppler ultrasonography of neck vessels, transcranial Doppler, brain CT and MRI, CT, and magnetic resonance angiography. Brain CT and MRI were carefully screened to confirm SAH and to evaluate the presence and location of intracranial aneurysms. Surgical treatments for ruptured aneurysms, including endovascular coiling and neurosurgical clipping, were also recorded. Furthermore, we recorded level of consciousness at stroke onset according to the Glasgow Coma Scale (GCS) score and neurological impairment on admission and at discharge based on the National Institutes of Health Stroke Scale (NIHSS) score. ¹³

Classification of SAH

We defined SAH as a collection of blood into the subarachnoid space. In the presence of an intraparenchymal component, cases were defined as intracerebral hemorrhage even if caused by aneurysms and were not included in the present study. Cases of SAH studied with brain imaging were classified as aneurysmal (aSAH) or non-aneurysmal (naSAH). We classified aSAH basing on intracerebral arterial aneurysms location according to brain CT and CT angiography. Among patients with aSAH, we retrospectively measured aneurysm size according to the maximum aneurysm diameter by reviewing imaging data; we also made a distinction between those who underwent conservative or interventional treatment (clipping or endovascular coiling). naSAH refers to condition when no bleeding source can be identified despite repetitive radiological imaging. ¹⁴ In those cases, we made a distinction, according to the blood distribution, into two subgroups, namely perimesencephalic and non-perimesencephalic SAH. ¹⁵ In perimesencephalic naSAH blood is confined to perimesencephalic and prepontine cisterns, anterior to the brainstem that could extend to the ambiens cistern and basal parts of the sylvian fissures, while in non-perimesencephalic naSAH blood has a more diffuse distribution exceeding the above-mentioned territories. ¹⁵

Statistical analysis

Incidence rates were standardized by age and sex with the direct method to the 2011 Italian and European population. ¹⁶ We provided a global incidence rate and an incidence trend over the 10-year observation period. Poisson regression analysis was performed to evaluate incidence trends. Descriptive statistics are reported as absolute numbers with percentages or mean ± standard deviation (SD), as appropriate. Comparisons between patients with aSAH and those with naSAH were performed using Student’s t-test for continuous variables and Pearson’s χ ² test for discrete variables. Missing values were not entered for continuous data when assessing baseline variables; we entered missing values using the median of the variables when performing regression analyses, where applicable. For risk factors, missing data were double-checked against patients’ treatments to obtain complete information. Where not confirmed by the investigators’ double-check against patients’ history or treatments, risk factors were considered absent.

Thirty-day and 1-year case-fatality rates (CFRs) were reported as numbers and percentages with the corresponding 95% confidence intervals (CIs). Univariate and multivariate estimates of the hazard ratios (HRs) of factors influencing 30-day and 1-year case-fatality were calculated according to the Cox regression analysis. Variables for multivariate analyses were selected as those with p-value <0.05 at univariate analyses. Two-sided statistical significance was set at a p level <0.05. All statistical analyses were performed with R software, version 4.1. ¹⁷

Results

From January 1, 2011, to December 31, 2020, we identified 194 patients with a first-ever SAH of whom 118 (61.0%) were women; the mean age at SAH onset was 62.5 ± 16.0 years. The most frequent vascular risk factors were arterial hypertension (97 patients, 51.0%) and cigarette smoking (58 patients, 33.3%) (Table 1). SAH was attributed to a ruptured intracranial aneurysm or arteriovenous malformation (aSAH) in 149 patients (76.8%) while 45 patients (23.2%) had naSAH. as no primary lesion was identified. All patients with arteriovenous malformations also had brain aneurysms and were therefore classified within the aSAH group. All patients with arteriovenous malformations also had brain aneurysms and were therefore classified within the aSAH group.

Table 1.

Characteristics of patients with first-ever subarachnoid hemorrhage.

Female, n (%)	118 (61.0)
Age (years), mean ± SD	62.5 ± 16.0
Systolic blood pressure at onset (mmHg), mean ± SD	155.5 ± 31.1
Diastolic blood pressure at onset (mmHg), mean ± SD	87.7 ± 17.0
International normalized ratio, mean ± SD	1.13 ± 0.60
Risk factors, n (%)
Arterial hypertension	97 (51.0)
Cigarette smoking	58 (33.3)
Hypercholesterolemia	19 (11.6)
Diabetes mellitus	19 (10.3)
Coronary heart disease	10 (5.6)
Atrial fibrillation	10 (5.6)
Alcohol abuse	6 (3.5)
Peripheral artery disease	2 (1.1)
Previous treatments, n (%)
Antiplatelets	35 (18.0)
Anticoagulants	5 (2.6)

All patients performed non-contrast brain CT and CT angiography, while 92 patients (47.4%) underwent conventional angiography. Brain MRI was performed in 26 (13.4%) patients. All imaging examinations were performed within 24 h from symptom onset, except from three CT angiograms and three conventional angiographies that were performed between 24 and 48 h. Patients with aSAH performed conventional angiography more often than those with naSAH (53.0% vs 28.9%, respectively; p = 0.008; Supplemental Table 1).

The most frequent aneurysmal location was in the anterior communicating artery (n = 41; 21.0%), followed by proximal (M1-horizontal segment), middle cerebral artery (n = 15; 7.7%) and at the bifurcation of the internal carotid artery (n = 14; 7.2%) (Supplemental Figure 1). Most patients (n = 135; 90.6%) had a single aneurysm, while the remaining 14 (9.4%) had multiple aneurysms beside the ruptured one. The mean diameter of ruptured aneurysms was 8.0 ± 5.8 mm; 51 patients (34.2%) had a small aneurysm (<5 mm diameter), 65 (43.6%) a medium aneurysm (5–9 mm in diameter), 30 (20.2%) a large aneurysm (10–25 mm in diameter), and 3 (2.0%) a giant aneurysm (>25 mm in diameter). There was no change in aneurysm size over the years (p = 0.117) (Supplemental Table 2).

Incidence of SAH

The crude annual incidence rate of first-ever SAH in the 2011–2020 period was 6.5 per 100,000 person-years (95% CI 5.6–7.5). The incidence rate was 6.3 per 100,000 (95% CI 5.4–7.2) when standardized to the Italian population and 5.8 per 100,000 (95% CI 5.0–6.7) when standardized to European population (Table 2). Incidence rates of SAH were stable over time (p for trend = 0.764; Figure 1). Considering age groups, incidence rates were highest in women aged 64–74 and in men over 85 years (Table 2). The crude incidence rates per 100,000 person-years of aSAH and naSAH were 5.0 (95% CI 4.2–5.9) and 1.5 (95% CI, 1.1–2.0), respectively. Incidence rates were 4.9 (95% CI 4.1–5.7) and 1.4 (95% CI 1.0–1.9), respectively, when standardized to the Italian population, and 4.6 (95% CI 3.9–5.4) and 1.3 (95% CI 0.9–1.7), respectively, when standardized to the European population. Incidence rates were stable over time for both aSAH (p for trend = 0.831) and naSAH (p for trend = 0.815; Figure 2).

Table 2.

Crude incidence rates of first-ever subarachnoid hemorrhage according to age and sex over the 2011–2020 period.

		2011–2020
Age group (years)	Population at risk (2011)	N	Incidence × 100,000	95% CI
Men
0–44	75,276	16	2.1	1.2–3.5
45–54	22,438	17	7.6	4.4–12.1
55–64	20,067	14	7.0	3.8–11.7
65–74	14,094	14	9.9	5.4–16.7
75–84	10,142	8	7.9	3.4–15.5
⩾85	3323	7	21.1	8.5–43.4
All	145,340	76	5.2	4.1–6.5
Standardized (Italy)	28,745,507		5.1	4.0–6.3
Standardized (Europe)	244,302,577		4.8	3.7–6.0
Women
0–44	72,385	10	1.4	0.7–2.5
45–54	22,868	27	11.8	7.8–17.2
55–64	20,295	22	10.8	6.8–16.4
65–74	15,435	23	24.0	16.9–33.0
75–84	14,774	25	16.9	11.0–25.0
⩾85	7246	11	15.2	7.6–27.2
All	153,003	118	7.7	6.4–9.2
Standardized (Italy)	30,688,237		7.4	6.1–8.9
Standardized (Europe)	256,398,176		6.9	5.7–8.3
Both
0–44	147,661	26	1.8	1.2–2.6
45–54	45,306	44	9.7	7.1–13.0
55–64	40,362	36	8.9	6.2–12.3
65–74	29,529	37	12.5	8.8–17.3
75–84	24,916	33	13.2	9.1–18.6
⩾85	10,569	18	17.0	10.1–26.9
All	298,343	194	6.5	5.6–7.5
Standardized (Italy)	59,433,744		6.3	5.4–7.2
Standardized (Europe)	500,700,753		5.8	5.0–6.7

Figure 1.

Incidence trend for subarachnoid hemorrhage over the 2011–2020 period.

Figure 2.

Incidence trend of aneurysmal and non-aneurysmal subarachnoid hemorrhage over the 2011–2020 period.

Characteristics of SAH subtypes and risk factors of aSAH versus naSAH

Comparing the 149 patients with aSAH with the 45 patients with naSAH, we found that mean age was lower in patients with aSAH than in those with naSAH (60.6 ± 14.2 years vs 68.8 ± 19.7 years; p = 0.012); cigarette smoking was more prevalent in patients with aSAH than in those with naSAH (36.4% vs 17.9%; p < 0.001), while atrial fibrillation was less prevalent in those with aSAH than in those with naSAH (2.8% vs 15.7%; p = 0.005; Table 3). Arterial hypertension and cigarette smoking were the most prevalent risk factors in both groups.

Table 3.

Patient characteristics, risk factors and 30 -days/1 year survival of aneurysmal and non-aneurysmal subarachnoid hemorrhage over the 2011–2020 period.

	aSAH (n = 149)	naSAH (n = 45)	p
Age, mean ± SD	60.6 ± 14.2	68.8 ± 19.7	0.012
Women, n (%)	94 (63.0)	24 (53.3)	0.240
Systolic blood pressure at onset (mmHg), mean ± SD	154.7 ± 31.9	157.8 ± 28.4	0.560
Diastolic blood pressure at onset (mmHg), mean ± SD	87.2 ± 16.6	89.3 ± 18.3	0.517
International normalized ratio, mean ± SD	1.14 ± 0.67	1.10 ± 0.21	0.544
Arterial hypertension, n (%)	72 (48.9)	25 (58.1)	0.395
Diabetes mellitus, n (%)	12 (8.3)	7 (16.6)	0.138
Atrial fibrillation, n (%)	4 (2.8)	6 (15.7)	0.005
Hypercholesterolemia, n (%)	15 (11.4)	4 (12.1)	0.816
Cigarette smoking, n (%)	51 (36.4)	7 (17.9)	0.016
Alcohol abuse, n (%)	6 (4.5)	0	0.171
Coronary heart disease, n (%)	6 (4.2)	4 (11.1)	0.196
Peripheral artery disease, n (%)	1 (0.7)	1 (2.7)	0.367
Case-fatality rate at 30 days, n (%)	39 (26.1)	16 (35.5)	0.221
Case-fatality rate at 1 year, n (%)	53 (35.5)	19 (42.2)	0.418
Previous treatments, n (%)
Antiplatelets	23 (15.4)	11 (24.4)	0.242
Anticoagulants	3 (2.0)	2 (4.4)	0.715

Treatment of aSAH

Over the study period, 103 (69.1%) of the 149 patients with aSAH were surgically treated, of whom 53 (35.6%) underwent neurosurgical clipping and 50 (33.6%) endovascular coiling. The relative proportion of patients treated with clipping or coiling did not change over the years (p for trend = 0.678; Figure 3).

Figure 3.

Proportions of patients undergoing interventional treatment of aneurysmal subarachnoid hemorrhage over the 2011–2020 period.

SAH case-fatality rates

Within 30 days from SAH, 55 patients died, while 72 patients died within 1 year. The corresponding CFRs were 28.4% (95% CI 21.4–36.9) and 37.1% (95% CI 29.0–46.7), respectively. Ten patients (5.2%) died within 24 h. Fifty-seven patients (29.4%) died in the hospital, of whom 51 (89.5%) died within 30 days. Complications found in patients with SAH are reported in Supplemental Table 3. All deaths occurring within 30 days were related to SAH, while among the 72 deaths occurring within 1 year, 62 (86.1%) were neurological, 4 (5.6%) cardiac deaths, and 6 (8.3%) were due to other causes.

Thirty-day and 1-year CFRs did not differ between aSAH and naSAH (Table 3). Comparing the two types of naSAH, the perimesencephalic subtype affected younger patients compared to non-perimesencephalic naSAH (57.8 ± 16.2 years vs 75.5 ± 18.7 years; p = 0.002) and 30-day and 1-year case-fatality rates were far higher for non-perimesencephalic naSAH (p = 0.022) (Supplemental Table 4). The multivariate Cox regression analysis showed that low Glasgow Coma Scale (GCS) score was the only independent predictor of 30-day (HR 0.92, 95% CI 0.86–0.98, p = 0.010) and 1-year (HR 0.92, 95% CI 0.86–0.97, p = 0.003) case-fatality (Supplemental Table 5). Among patients with aSAH, the multivariate Cox regression analysis showed that interventional treatment (including either clipping or coiling) was the only independent predictor of 30-day case-fatality (HR 0.45, 95% CI 0.22–0.94, p = 0.033). No predictors of death were found at 1-year (Supplemental Table 6).

Discussion

Our study provides a 10-year insight into the epidemiology of SAH and either aSAH and naSAH together with case-fatality and patients profile in terms of risk factors.

Although we found a roughly stable incidence over time for both SAH subtypes, recent population-based studies have reported a worldwide decline in SAH incidence, especially in Western countries.^3,18,19 Our value of 6.5 cases per 100,000 person-years in the 2011–2020 period was lower than the value of 7.9 reported by a 2019 meta-analysis. ³ However, the same meta-analysis showed that the incidence of SAH globally declined to a value of 6.1 cases per 100,000 person-years in 2010, which is more in line with our data. Additionally, we observed a modest reduction in SAH incidence compared to the previous population study conducted in the L’Aquila district between 1994 and 1998 in which the crude annual incidence rate was 7.9 per 100,000 inhabitants (95% CI 6.5–9.6). ²⁰ A possible explanation of this finding is that SAH incidence has decreased in recent years, as a result of enhanced management of vascular risk factors and improved identification and treatment of unruptured aneurysms. Another explanation may rely on the shift of SAH incidence toward older age. Indeed, in our population, we recorded the highest SAH incidence in patients aged >75 years. Our data are in line with worldwide trends pointing toward an increasing age at SAH onset probably due to improved control of vascular risk factors.^4,21 The most prevalent risk factors in patients with SAH were arterial hypertension and cigarette smoking, thus confirming their key role in promoting intracranial aneurysm growth and rupture.^4,22,23 Our 28.7% 30-day case-fatality rate of SAH was slightly higher than those found in other reports,^7,18,23,24 probably as a consequence of the relatively high mean age of our sample.

In line with literature, most patients with SAH (75%) had aSAH and aneurysms were mostly located at branching points along intracranial arteries where hemodynamic stress may weaken the wall between exiting branches. ²⁵ The proportion of patients with ruptured aneurysms treated with surgical procedures was stable over our study period; in particular, there was no predilection for neurosurgical or endovascular approach. Our data differ from those in literature that highlight the marked increase in coiling use for both ruptured and unruptured aneurysms.^26,27 Different factors could explain this discrepancy. First, our data are more recent than the available ones. The two US large case series refer to the 1997–2007²⁶ and 2004–2014²⁷ period, respectively, when updated recommendations for treatment of ruptured and unruptured aneurysms were issued. During our study period (2011–2020), the most recent recommendations for treatment of ruptured and unruptured aneurysms might have already been implemented. The proportion of ruptured aneurysms treated with coiling was relatively high since 2011 (Figure 2). It should also be noted that our cases only encompass ruptured aneurysms mostly treated with urgent procedures. Clipping might be still performed in many of those procedures, even if the proportion is decreasing in favor of coiling. ²⁶ Notably, in our population the decision of not treating aneurysms was determined equally by clinical indication or by early death, as 25 (54.3%) of the 46 non-treated patients with aSAH died within 30 days from symptom onset.

In our study about one quarter of SAH cases were non-aneurysmal, which is a higher proportion compared with a similar population-based study. ²⁸ Evidence suggest an increasing trend of naSAH incidence over time that could be attributed to the increasing use of antithrombotic medication. ²⁹ Compared with a previous study which found an incidence of naSAH of 2.8 cases per 100,000 person-years, our incidence rate of 1.54 cases per 100,000 person-years was lower. ²⁸ Nevertheless, the relative proportion of naSAH over the total number of SAH cases was only slightly lower than that found in the previous population-based study (23% vs 28%). ²⁸ Contrary to a previous study, ²⁹ we did not find any specific trend in the incidence of naSAH over time, probably because our 10-year timespan was not sufficient to identify any incidence trend, or because antithrombotic medication and other risk factors implied in naSAH were stable over time in our population.

When comparing with aSAH, we found that naSAH patients were older and had higher prevalence of cigarette smoking and atrial fibrillation (Table 3). This risk profile might empower an association between subtle ischemic changes and naSAH. Indeed, ipsilateral convexity SAH has been sparsely reported in the context of subcortical strokes, either atherosclerotic or cardioembolic, probably because of the development of compensatory leptomeningeal collaterals’ susceptibility to dilatation, rupture and bleed.^30,31 Additionally, there was a considerable difference in the utilization of conventional angiography between aSAH and naSAH patients, with a significantly higher proportion of aSAH patients undergoing the procedure (52.3% vs 28.9% for naSAH). This difference primarily stems from the need to assess eligibility for surgical treatment of the ruptured aneurysm. We also found difference in case-fatality rates, suggesting that identifying naSAH subtypes might be of prognostic relevance. Previous population-based studies were unable to compare fatality rates between different naSAH subtypes, which were assessed only in retrospective studies.^16,32 Notably, our study confirms that non-perimesencephalic naSAH is associated with worse prognosis compared with perimesencephalic naSAH. ³²

A strength of our study is the relatively high number of patients included in a population-based registry which allowed the gathering of a wide range of clinically relevant information. Additionally, all patients had a diagnosis confirmed by brain neuroimaging studies. However, the study has some limitations. Being an observational study, some data were inevitably missing. We cannot exclude that in our registry other cases of SAH were included among the ill-defined or unclassified cerebrovascular events due to early death, without any autopsy confirming the diagnosis of SAH We may also have missed some diagnoses of aSAH due to the lack of available conventional angiography.

Nevertheless, all patients included in our study performed at least a CT angiogram. Unfortunately, our registry did not collect thorough information about neurological outcome data or complications related either to SAH itself (delayed cerebral ischemia, hydrocephalus, rebleeding) or to aneurysm treatment. Additionally, we could not retrieve data on angiographic examinations. Our registry data do not include information on the shape of ruptured aneurysms, which could have influenced the choice of aneurysm repair methods, as well as on unruptured aneurysms that were repaired before causing SAH. We also did not collect information on surgical techniques, which could have influenced the decision of intervening with clipping or coiling, as they were detailed only in surgical registries. Furthermore, as expected, we recorded few cases of naSAH, thus limiting the significance of naSAH subtypes comparisons.

Conclusion

Our study investigated the epidemiology of SAH in a high-income, predominantly Caucasian population from 2011 to 2020. In line with existing literature, we found a low incidence of SAH with a potential shift of SAH burden toward the elderly population. Of note, our findings reveal that the majority of patients with aSAH underwent surgical endovascular treatment, which likely played a significant role in improving their survival. As advancements in controlling vascular risk factors and treating both ruptured and unruptured aneurysms continue to improve, the burden of aSAH may decrease even more. naSAH is a rare and heterogeneous entity and the distinction between its subtypes (perimesencephalic and non-perimesencephalic) is of prognostic relevance. Considering the lower frequency of naSAH, larger prospective cohort studies are warranted to confirm our observations.