Peak age for aneurysmal subarachnoid hemorrhage aSAH is 55-60 years, about 20% of cases occur between ages 15-45 yrs.
30% of aSAHs occurs during sleep
50% of patients with aneurysms have warning symptoms, usually 6-20 days before SAH
headache ls lateralized in 30%, most to the side of the aneurysm.
soft evidence suggests that rupture incidence is higher in spring and autumn
patients > 70 yrs age have a higher proportion with a severe neurologic grade.
Estimated annual rate of aneurysmal subarachnoid hemorrhage in most western populations: 6-8 per 100,000 population.
Aneurysmal subarachnoid hemorrhage (aSAH) accounts for only 3-5% of all strokes.
Aneurysmal subarachnoid hemorrhage (aSAH) is more common in women than in men.
Women outnumbered men among aSAH patients, especially along increasing age strata, and had increased global disease severity on admission. No other significant differences between genders were found 4).
The age and gender information of 4,895 case of aneurysmal SAH (3,016 females, 1,879 males) were collected retrospectively from eight institutions in mainland China. The prevalence of aneurysmal SAH of men and women at different ages was analyzed.
The data showed women had a higher incidence of aneurysmal SAH than men starting at late thirties, and men might have a higher incidence of aneurysmal SAH than women only before 37-year-old.
Menopause may not be the only dominant factor causing higher incidence of aneurysmal SAH in women than in men 5).
Following cocaine abuse
Alcohol consumption: controversial
Diurnal variations in blood pressure
Pregnancy and parturition
Slight increased risk during lumbar puncture and/or cerebral angiography in patient with cerebral aneurysm
Slight increased risk with advancing age
Conditions with an increased incidence of cerebral aneurysms
The inherent variability in the incidence and presentation of ruptured cerebral aneurysms has been investigated in association with seasonality, circadian rhythm, lunar cycle, and climate factors.
Rosenbaum et al., aimed to identify an association between solar activity (solar flux and sunspots) and the incidence of aneurysmal SAH, all of which appear to behave in periodic fashions over long time periods. The Nationwide Inpatient Sample (NIS) provided longitudinal, retrospective data on patients hospitalized with SAH in the United States, from 1988 to 2010, who underwent aneurysmal clipping or coiling. Solar activity and SAH incidence data were modeled with the cosinor methodology and a 10-year periodic cycle length. The NIS database contained 32,281 matching hospitalizations from 1988 to 2010. The acrophase (time point in the cycle of highest amplitude) for solar flux and for sunspots were coincident. The acrophase for aneurysmal SAH incidence was out of phase with solar activity determined by non-overlapping 95% confidence intervals (CIs). Aneurysmal SAH incidence peaks appear to be delayed behind solar activity peaks by 64 months (95% CI; 56-73 months) when using a modeled 10-year periodic cycle. Solar activity (solar flux and sunspots) appears to be associated with the incidence of aneurysmal SAH. As solar activity reaches a relative maximum, the incidence of aneurysmal SAH reaches a relative minimum. These observations may help identify future trends in aneurysmal SAH on a population basis. 6).
By using high-quality meteorological data analyzed with a sophisticated and robust statistical method no clearly identifiable meteorological influence for the SAH events considered can be found. Further studies on the influence of the investigated parameters on SAH incidence seem redundant 7).
Pathophysiological processes following subarachnoid hemorrhage (SAH) present survivors of the initial bleeding with a high risk of morbidity and mortality during the course of the disease. As angiographic vasospasm is strongly associated with delayed cerebral ischemia (DCI) and clinical outcome, clinical trials in the last few decades focused on prevention of these angiographic spasms. Despite all efforts, no new pharmacological agents have shown to improve patient outcome. As such, it has become clear that our understanding of the pathophysiology of SAH is incomplete and we need to reevaluate our concepts on the complex pathophysiological process following SAH. Angiographic vasospasm is probably important. However, a unifying theory for the pathophysiological changes following SAH has yet not been described. Some of these changes may be causally connected or present themselves as an epiphenomenon of an associated process. A causal connection between DCI and early brain injury (EBI) would mean that future therapies should address EBI more specifically. If the mechanisms following SAH display no causal pathophysiological connection but are rather evoked by the subarachnoid blood and its degradation production, multiple treatment strategies addressing the different pathophysiological mechanisms are required. The discrepancy between experimental and clinical SAH could be one reason for unsuccessful translational results 8).
Many pathological mechanisms ensue after cerebral aneurysm rupture, including hydrocephalus, apoptosis of endothelial cells and neurons, cerebral edema, loss of blood-brain barrier, abnormal cerebral autoregulation, microthrombosis, cortical spreading depolarization and macrovascular vasospasm.
There is significant theoretical evidence for the potential role of estrogen and progesterone use in altering the pathogenesis of SAH. Nevertheless, this has received mixed reviews in both case controlled studies and cohort analysis within the literature 9)
Patients with good aSAH grades are generally hemodynamically stable and less prone for perioperative adverse events.
The diagnosis of aSAH itself may not be a challenge as the classical presentation is sudden severe headache described as “worst headache ever experienced in life.” Other manifestations such as brief loss of consciousness, sentinel headache, nausea and vomiting, photophobia, neck stiffness, seizures and focal deficits may however cause diagnostic confusion 10).
Focal cranial nerve deﬁcits may occur (e.g. third nerve palsy from aneurysmal compression, causing diplopia and/or ptosis).
Low back pain may develop due to irritation of lumbar nerve roots by dependent blood.
The most common symptom is headache, present in up to 97% of cases. Usually severe (classic description: “the worst headache of my life”) and sudden in onset. They may clear and the patient may not seek medical attention (referred to as a sentinel hemorrhage or headache, or warning headache; they occur in 30-60% of patients presenting with SAH). If severe or accompanied by reduced level of consciousness, most patients‘ present for medical evaluation. Patients with H/A due to minor hemorrhages will have blood on CT or LP. However, warning. headaches may also occur without SAH and maybe due to aneurysmal enlargement or to hemorrhage conﬁned within the aneurysmal wall.
Warning H/A are usually sudden in onset, severe, and clear within 1 day.
Evidence based information on the epidemiology, risk factors and prognosis, as well as recommendations on diagnostic work up, monitoring and management are provided, with regard to treatment possibilities in Croatia in the article of Solter et al. 11) 12).
There is high variability in the election of treatment modality among centres in Spain. Endovascular treatment allows more patients to have their aneurysm treated. Guideline adherence is moderate 13).
Mijiti et al, retrospectively reviewed the medical records of 542 consecutive aSAH patients admitted to neurosurgery department of the First Affiliated Hospital of Xinjiang Medical University in Urumqi city of China between January 1, 2011 and December 31, 2015. AV, SV and cerebral infarction were defined based on clinical data and neuroimaging findings. Univariate and multivariate analyses were performed to identify predictors of AV, SV or cerebral infarction.
343 (63.3%) patients fulfilled the inclusion and exclusion criteria. Of them, 182(53.1%) developed AV, 99 (28.9%) developed SV, and 87 (25.4%) developed cerebral infarction. A history of hypertension, poor modified Fisher grade (3-4) and poor Hunt-Hess grade (4-5) on admission were common risk factors for AV, SV and cerebral infarction. Patients from Uyghur ethnic group or other minorities were less likely to develop AV, SV or cerebral infarction, compared to those from Han ethic group after adjustment of other potential confounders. Additionally, age ≥53 years, leukocyte count ≥11× 109/L on admission and being current or former smokers were independent risk factors of cerebral infarction. Leukocyte count ≥11× 109/L on admission and aneurysm size ≥ 10 mm were independent risk factors of SV. Serum glucose level ≥7.0 mmol/L on admission was an independent risk factor of AV.
Risk factors of different definitions of CVS were diverse in Chinese patients with aSAH; however, risk factors of SV and cerebral infarction seem to be similar. We recommend early and aggressive therapy in these patients at-risk of CVS 14).
In a retrospective study, from all 142 adult patients admitted to a surgical intensive care unit (ICU) with SAH between March 2004 and November 2010.
The mean patient age was 54 ± 14 years, 62.7 % were female, and the median Hunt and Hess score was 3. The proportions of patients with poor outcome (Glasgow Outcome Score ≤3) were 58.4, 54.2, and 52.1 % at 3, 6, and 12 months, respectively, after the SAH. The ICU and hospital mortality rates were both 12.7 %, and the median lengths of stay in the ICU and the hospital were 16 (IQ 7-25) and 26 (IQ 18-34) days, respectively. In multivariable analysis, older age and greater cumulative fluid balance within the first 7 days in the ICU were independently associated with a greater risk of poor outcome.
In this cohort of patients, older age and greater cumulative fluid balance were independently associated with a greater risk of poor outcome up to 1 year after the initial insult. The data suggest that mild hypovolemia may be beneficial in the management of these patients 15).
Seventy-one patients were treated in two periods: 2010-2011 (32 patients; 19 clipped, 6 coiled, 7 untreated), and 2012-2013 (39 patients, 3 clipped, 34 coiled, 2 untreated). No significant differences were found in age, sex, clinical grade at admission, type and location of aneurysm, Fisher score, or in hospital mortality (28.1% vs 25.6%, P=.35), GOS (except for GOS 5: 43.37% vs 53.8%, P=.045), rate of hydrocephalus and rate of vasospasm. The second cohort obtained better results for aggregated GOS 1+2+3 (36.3% vs 43.75%, P=.034) and for GOS 4+5 (61.5% vs 56.25%, P=.078). The percentage of patients left untreated was significantly lower in the second period (5.1% vs 21.8%, P<.01), as well as the rate of re-bleeding (0% vs 9.4%, P<.01). Patients were treated earlier (2.51 vs 3.95 days), and hospital and total stay were lower (15.2 and 24.6 vs 10.3 and 18 days) in the second period, these differences not reaching statistical significance.
Endovascular therapy allowed treating more patients with aSAH, and with a lower re-bleeding rate. This led to a modest reduction in morbidity and mortality 16).
Five hundred ninety patients (40.4%) reported LOC at onset of SAH. Loss of consciousness was associated with poor clinical grade, more subarachnoid and intraventricular hemorrhage seen on admission computed tomographic scan, and a higher frequency of global cerebral edema (P < .001). Loss of consciousness was also associated with more prehospital tonic-clonic activity (22.7% vs 4.2%; P < .001) and cardiopulmonary arrest (9.7% vs 0.5%, P < .001) vs patients who did not experience LOC. In multivariable analysis, death or severe disability at 12 months was independently associated with LOC after adjusting for established risk factors for poor outcome, including poor admission clinical grade (adjusted odds ratio, 1.94; 95% CI, 1.38-2.72; P < .001). There was no association between LOC at onset and delayed cerebral ischemia or aneurysm rebleeding.
The distribution of cisternal blood in relation to the development of acute hydrocephalus was studied in 246 consecutive patients with aneurysmal subarachnoid hemorrhage who were admitted within 72 hours. Patients with evidence on the initial computed tomograph (CT) of subarachnoid hemorrhage caused by other than a ruptured aneurysm and patients with a negative angiography were excluded. Acute hydrocephalus (defined as a bicaudate index, measured on the initial CT or on a repeat CT within 1 week after subarachnoid hemorrhage, exceeding the 95th percentile for age) was found on the initial CT in 50 (20%) of the 246 patients and on a repeat CT in 9 other patients. Ventricular blood was found significantly more often in patients with acute hydrocephalus than in those in whom acute hydrocephalus did not develop (28 of 59 [47%] versus 58 of 187 [31%]; chi 2 = 4.634, p = 0.031). When the analysis was restricted to the 86 patients with ventricular blood, no significant differences were found in the total amount of cisternal blood and in the distribution of cisternal blood between patients with and without hydrocephalus. In contrast, among the 160 patients without ventricular blood, hydrocephalus was associated with a slightly higher total amount of cisternal blood (Wilcoxon's rank sum test, p = 0.023), and significantly more patients with acute hydrocephalus had a higher score in both ambient cisterns than patients without acute hydrocephalus (20 of 31 [65%] versus 41 of 129 [32%]; chi 2 = 10.007, p = 0.002) 18).