Non-traumatic subarachnoid hemorrhage (SAH) is a major life-threatening emergency. In 80% of cases, it is caused by the rupture of a saccular intracranial aneurysm (sIA). Other common causes are dissecting aneurysms, cerebral arteriovenous malformations and vasculitis [1, 2, 3].
The hallmark symptom is a sudden and severe headache. Associated signs include nausea, vomiting, photophobia, neck stiffness, focal neurologic deficits, seizure or depressed consciousness [1, 2, 4]. The initial clinical severity is determined by simple validated grading system like the World federation of Neurosurgical Societies (WFNS) that is the most used indicators and considered as a major determinant of the prognosis [4, 5].
SAH may cause acute hydrocephalus and brain edema. Later complications include vasospasm and delayed cerebral ischemia that are associated with serious damages even after the aneurysm treatment [1, 2, 5].
Aneurysmal SAH are most often treated within 24 – 72 hours [3, 4, 5]. Neurosurgical clipping and endovascular treatment (EVT) by endosaccular coiling are both effective for the treatment of saccular intracranial aneurysms. These treatments have been compared and EVT is now considered as the first therapeutic option in most cases. Treatment choice is made by a multidisciplinary team including interventional neuroradiologists (INR), neurosurgeons, intensivists, and neurologists [3, 4, 5, 6, 7, 8, 9].
The aim of our study is to evaluate, over a 14-year period in a single high-volume center, the results of EVT of ruptured intracranial aneurysm.
This study was approved by our institutional ethical committee (n°P2019/152). Our prospectively maintained database was retrospectively analyzed to identify, between April 2004 and June 2018, all patients treated only by endovascular approach for a ruptured IA.
Available data were collected from the admission date in different institutions to collect the first bleeding time. The outcomes of our patients were followed until they were discharged from our hospital, or another medical institution and no clinical results were collected beyond three months of follow-up after EVT.
All EVT were performed by an INR from our institution. As it is reflected in Figure 1, the majority of patients were treated within the first days following the SAH (median = day 1 and interquartile range = 2 days).
Placement of an external ventricular drainage (EVD) was decided by our neurovascular team. Patients were then monitored in our intensive care unit until the overall stabilization of their condition.
The sample was analyzed by descriptive statistics. Quantitative data were expressed in mean values ± standard deviation (SD) or medians and 95% confidence intervals (CI) or interquartile range, accordingly, after verification of normality of distributions by the Kolmogorov-Smirnov test. Qualitative data were expressed by the way of percentages.
Four hundred sixty-eight patients were identified. In eleven patients, there was a failure of EVT (2.4%). These patients were excluded from the present analysis and are detailed in Appendix.
Our final cohort includes 457 patients successfully treated by endovascular approach. Patient characteristics are detailed in Table 1.
|AGE (YEARS)||52 ± 14.2 (SD)|
|WFNS(before the first procedure)|
|Grade 1||231 (50.6%)|
|Grade 2||75 (16.4%)|
|Grade 3||8 (1.8%)|
|Grade 4||81 (17.7%)|
|Grade 5||62 (13.6%)|
Imaging characteristics of 457 patients successfully treated by endovascular approach are detailed in Table 2.
|ORIGIN OF SAH (N = 457)|
|Saccular aneurysm||414 (90.6%)|
|Fusiform aneurysm||10 (2.2%)|
|Dissecting aneurysm||33 (7.2%)|
|Anterior communicating complex (ACom)||189 (41.4%)|
|Middle cerebral artery (MCA)||65 (14.3%)|
|Posterior communicating artery (PCom)||79 (17.3%)|
|Internal carotid artery (ICA)||38 (8.4%)|
|Pericallosal artery||4 (1.8%)|
|Basilar artery tip||28 (6.1%)|
|Posterior inferior cerebellar artery (PICA)||17 (3.8%)|
|Vertebral artery||14 (3.1%)|
|Size range of aneurysm ab (n = 424)|
|Small (<10 mm)||352 (83%)|
|Large (10 to 25 mm)||70 (16.5%)|
|Giant (>25 mm)||8 (1.9%)|
|Associated lesion c (n = 457)|
|Cerebral arteriovenous malformation||10 (2.2%)|
|Other aneurysm||113 (24.7%)|
|Carotid stenosis||3 (0.7%)|
|Carotid thrombosis||1 (0.2%)|
|Major decreased cerebral perfusion||2 (0.4%)|
|Number of associated aneurysms||Median = 1 ; 95% CI [1, 2, 3]|
Figure 2 shows the endovascular technique used for EVT. In 6.3% of the cases (n = 29/457), a second EVT was necessary to completely exclude the aneurysm or the arterial dissection. Figure 3 shows the second endovascular method.
Regarding aneurysm or arterial dissection occlusion, EVT achieved a complete occlusion in 65.7% of the cases. There was a neck remnant in 28.2% and an incomplete occlusion in 6.1% of the cases.
Procedure-related complications occurred in 27 cases (5.9%) in 26 patients.
Complications included 9 thromboembolic events (2%), 6 aneurysm perforations (1.3%), 5 vasospasms (1.1%), 2 coil migrations (0.4%), 4 arterial dissections (0.9%), one WEB device migration (0.2%). These complications were associated with clinical consequences in 6 patients with 5 worsening of neurological exam and 1 death. Immediate EVT-related morbidity and mortality were thus 1.1% and 0.2% respectively.
Immediate clinical outcomes were collected within 24 hours after EVT and are detailed in Figure 4.
Clinical complications occurred in 246/457 (53.8%) patients. These events are detailed in Table 3.
|Vasospasm and delayed cerebral ischemia (DCI)||166 (67.5%)|
|Intracranial hypertension||54 (22%)|
|Epileptic seizure||38 (15.5%)|
|Septic shock||11 (4.5%)|
|Terson syndrome||9 (3.7%)|
|Status epilepticus||9 (3.7%)|
|Cardiogenic shock||5 (2%)|
|EVD related hemorrhage||5 (2%)|
|Pulmonary embolism||4 (1.6%)|
|Digestive ischemia||3 (1.2%)|
|Acute respiratory distress syndrome (ARDS)||2 (0.8%)|
|Aneurysm rebleeding||2 (0.8%)|
|Transient ischemic attack||1 (0.4%)|
|Myocardial infarction||1 (0.4%)|
|Cardiorespiratory arrest||1 (0.4%)|
|Intra-stent stenosis||1 (0.4%)|
Aneurysm rebleeding occurred in 2/457 patients (0.4%):
Overall EVT-related morbidity and mortality were thus 1.3% and 0.4% respectively.
There were 37 ventriculitis and 2 meningitis among 192 EVDs placed. Overall EVD-related infections were thus 20.3%.
Modified Rankin Scale (mRS) at discharge is shown in Figure 5.
The report of the clinical results (mRS) at discharge according to the initial WFNS grade is detailed in Table 4.
|grade 1||0 = No symptoms at all||154||66.7|
|1 = No significant disability despite symptoms||35||15.2|
|2 = Slight disability||19||8.2|
|3 = Moderate disability||6||2.6|
|4 = Moderate severe disability||2||0.9|
|5 = Severe disability||1||0.4|
|6 = Dead||14||6.1|
|grade 2||0 = No symptoms at all||27||36.0|
|1 = No significant disability despite symptoms||20||26.7|
|2 = Slight disability||7||9.3|
|3 = Moderate disability||5||6.7|
|4 = Moderate severe disability||2||2.7|
|5 = Severe disability||2||2.7|
|6 = Dead||12||16.0|
|grade 3||0 = No symptoms at all||0||0|
|1 = No significant disability despite symptoms||3||37.5|
|2 = Slight disability||2||25|
|3 = Moderate disability||2||25|
|4 = Moderate severe disability||1||12.5|
|5 = Severe disability||0||0|
|6 = Dead||0||0|
|grade 4||0 = No symptoms at all||10||12|
|1 = No significant disability despite symptoms||20||25|
|2 = Slight disability||14||17|
|3 = Moderate disability||7||9|
|4 = Moderate severe disability||3||4|
|5 = Severe disability||1||1|
|6 = Dead||26||32|
|grade 5||0 = No symptoms at all||2||3|
|1 = No significant disability despite symptoms||7||11|
|2 = Slight disability||5||8|
|3 = Moderate disability||6||10|
|4 = Moderate severe disability||10||16|
|5 = Severe disability||3||5|
|6 = Dead||29||47|
In this study, the proportion of saccular intracranial aneurysms (90.6%) and arterial dissection (7.2%) is probably higher because we have excluded etiologies that did not require an EVT. The most common sites of ruptured aneurysms are the ACom, the Pcom and the MCA with often unique aneurysm which are in line with our results. The median size of ruptured aneurysms is around 6 mm and most of intracaranial aneurysms are smaller than 1 cm (around 80–90% of cases) like in our study which highlights the rupture risk even with small aneurysms [2, 6, 7, 9, 10, 11, 14, 15, 16, 17].
Our results show high use of intracranial stents and vascular occlusion. It can be explained by several factors: (1) a high percentage (9.4%) of dissections and fusiform aneurysms; (2) stents are more often used for larger aneurysms (18.4% in our study) and/or wide neck aneurysms (although neck size was not measured in our data).
Regarding thromboembolic events (2% in our study), the range in the literature is between 2.5% and 28.0% [19, 21, 22, 23]. Good results can possibly be explained by the use of a strict heparinization protocol, the same as for unruptured aneurysms. The aim is to double the activated clotting time (ACT) during EVT, and to control it every 30 minutes. Heparinization is then prolonged for 12-24h in most patients. Some studies showed comparable good results using continuous heparin for 24h without a significant increase of hemorrhagic complications [22, 24].
The rate of intraoperative rupture in our study was 1.3% which is lower to the reported rates found in literature (4.4–7.6%) [19, 21, 23]. Practitioner experience and centers with high number of patients have lower complication rate and improve outcomes from SAH which could also explain our good results. Indeed, in our center, around 250 IA are yearly treated, most of them being unruptured and referred by other centers [4, 13, 19, 21, 22].
In our series, delayed cerebral ischemia (DCI) occurred in 166 patients (36.3%) and was the most frequent complication. Our results are thus in accordance with the literature.
The incidence of acute re-rupture after coiling embolization of ruptured saccular intracranial aneurysms is between 1.0% to 3.6% [21, 25]. Dissecting aneurysms have different etiological and anatomical characteristics. The recurrence of SAH is not uncommon with a rate of 40% specifically for patient treated conservatively [16, 21, 25]. In the present series, two patients suffered from an early rebleeding. One was a saccular intracranial aneurysm with an acute re-rupture probably due to an incomplete occlusion during the first EVT. The second is a dissection treated by stenting. Our results compare favorably with the literature (0.4%).
The ISAT study showed 74.6% of modified Rankin Scales (mRS) between 0 – 2 and 25.4% of mRS between 3 – 6 which are like our results even if we have more patients without any symptom (42%) and more fatalities (17.8%) compared to ISAT (20% and 7.5% respectively) [7, 8].
As illustrated in Figure 6, a significant proportion of patients at discharge are in a worse clinical condition than immediately after EVT. Post-procedural events like DCI, intracranial hypertension or epileptic seizure may explain this worsening.
Our monocentric retrospective study has several limitations despite the fact that our database was prospectively maintained. Some data could have been collected to provide interesting information such as the aneurysm neck size, patient risk factors, the severity of the bleeding on CT scan, the detailed presentation of SAH. On the other hand, mid- and long-term results were not evaluated in the present study. Aneurysm recanalization and late rebleeding are significant issues and could be part of a complementary study to evaluate long-term results of EVT of ruptured IA [5, 12, 17, 25]. Finally, data concerning patients treated by surgical clipping were not evaluated.
This study shows that EVT is safe and effective for patients with ruptured intracranial aneurysms, especially when high practitioner experience and high-volume centers are available. However, even if SAH management has improved over the years, associated complications still lead to significant neurological impairment in some patients. Further research on these topics is mandatory to improve the clinical course of these patients.
|PATIENT GENDER/AGE||WFNS BEFORE EVT||EVD||ANEURYSM CHARACTERISTICS||REASON OF THE EVT FAILURE|
|M/57||2||Yes||ACom, large||Risk of vascular occlusion|
|M/78||4||Yes||ACom, small||Carotid stenosis|
|F/56||1||Yes||ACom, small||Coil instability|
|F/54||2||Yes||PICA, small||Risk of vascular occlusion|
|F/43||5||Yes||ACom, small||Risk of vascular occlusion|
|F/84||1||Yes||PCom, large||Coil instability|
|F/74||2||Yes||ACom, small||Carotid stenosis|
|F/50||1||Yes||ACom, large||Coil instability|
|M/56||1||Yes||MCA, small||Coil instability|
|M/53||1||No||PCom, small||Too small aneurysm size|
The authors have no competing interests to declare.
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