Although ruptured aneurysms are increasingly amenable to modern endovascular techniques, antiplatelet and heparin administration are frequently required, thus raising concerns regarding ventriculostomy related ICH.
In this series, VS-ICH occurred in 13.1% of all cases, which is in line with other studies reporting rates from 10 to 20% [3, 10]. While the observed predominance of ICH in the endovascular group confirms previously reported data from Scheller et al, this difference was no longer present among patients receiving no antiplatelet therapy [21]. Accordingly, the major finding of this study is that the administration of any antiplatelet therapy was the most prominent risk factor for VS-ICH.
Previous studies reporting on the impact of dual antiplatelet therapy on VS-ICH showed controversial results: while some authors reported an increased risk for ventriculostomy-related ICH after peri- and postprocedural administration of acetylsalicylic acid and clopidogrel (ranging from 7 to 63%), others could not demonstrate any correlation between dual antiplatelet therapy and VS-ICH, [1, 3, 10, 11, 15] and data elucidating the impact of specific substances are sparse. Only one study compared the administration of acetylsalicylic acid and clopidogrel, defining both as a risk factor for VS-ICH [7]. While some reports identified tirofiban as a risk factor for VS-ICH, [2, 19] this could not be confirmed by other studies [13, 24, 25] Of note, the number of ventriculostomies in these studies was either low or even neglected. The heterogeneous cohort and consequently small subgroups in the present study did not allow a sound statistical evaluation of the individual antiplatelet agents. To answer this question, larger, multicenter studies are warranted.
Periprocedural heparin administration had no effect on the rate of VS-ICH, consistent with the largely homogeneous results of previous studies [2, 9, 15, 16, 23]. Conflicting results may be explained by different time intervals between ventriculostomy and heparinization [8].
In general, conflicting results with regards to antithrombotic medication may be explained by statistical limitations and differences in study design; also dosage regimes are not standardized and rely on local standards, resulting in variable loading and maintenance dosages. Furthermore, non-responder rates of up to 40% may limit the explanatory power of these analyses [3, 4, 7].
The issue of ventriculostomy timing in relation to anticoagulation treatment has been controversially discussed in literature, in particular addressing the question of whether the initiation of antiplatelet therapy shortly after or prior to ventriculostomy is safer. Performing the ventriculostomy before starting antiplatelet therapy has been recommended based on reports of a higher incidence of ICH in case of subsequent ventriculostomy [5, 18, 20, 22]. Indeed, in this study ventriculostomy prior to aneurysm occlusion was significantly more frequent in the endovascular group, despite comparable clinical status, which may be explained by a more deliberate indication for prophylactic external ventricular drain placement in order to avoid ventriculostomy under antiplatelet therapy. However, our data did not show an impact of ventriculostomy timing on bleeding rates, neither in the overall population nor the subgroup on antiplatelet drugs, which is in line with the results of two recent studies [17, 19].
While most studies report VS-ICH rates following a single ventriculostomy, this does not necessarily reflect the clinical reality since many patients require subsequent ventriculo-peritoneal shunting or their device exchanged due to obstruction or infection. Consequently, the number of ventriculostomies by far exceeded the number of patients in this study. Since each surgical procedure implies a separate surgical risk, the aspect of repeated surgery must not be neglected in this patient group. In this present study the number of ventriculostomies was a significant risk factor for VS-ICH in both uni- and multivariate analysis. Considering that previous studies frequently ignore this issue, the actual risks for ICH may be underestimated.
Besides an increased risk of VS-ICH, our findings show that antiplatelet therapy was associated with an increased hematoma volume, which is in line with previous data [6, 9]. In this regard, the primary objective of our study was to assess the risk of VS-ICH between endovascular and surgical treatment, as this is frequently debated in our clinical practice. While previous reports found no effect of VS-ICH on clinical outcome [3, 8, 16, 21], we chose not to analyze clinical outcome in our study because we do not believe that, in the context of a retrospective study, a meaningful correlation can be drawn between these largely minor hemorrhages and the overall clinical outcome in patients often severely affected by the subarachnoid hemorrhage.
Furthermore, this study carries all the limitations of a single-center retrospective analysis. Additionally, response to antiplatelet drugs was not monitored and antiplatelet dosing was not standardized. However, with respect to the number of ventriculostomies, this is the largest study so far investigating VS-ICH in endovascular and surgical patients suffering from subarachnoid hemorrhage.
In conclusion, endovascular treatment of ruptured aneurysms requiring antiplatelet drugs carries an increased risk of VS-ICH. This aspect needs to be considered when weighing endovascular and surgical treatment options.