Endovascular interventions have become the standard option for the management of cerebral aneurysms compared to surgical clipping. Since 1990, detachable coils designed by Guglielmi were considered an innovation in the era of modern endovascular neurosurgery [7]. Significant advances in the coil industry and coil assisting devices have grown up significantly [8]. Assisting devices include balloons and stents to maintain the patency of the parent vessel and to promote proper coil packaging [9]. Balloon assisted coiling helps in proximal control in case of procedural aneurysmal rupture and prevents coil migration during embolization [10].
The main complications of endovascular interventions for cerebral aneurysms include aneurysmal perforations and thromboembolic events. The incidence, and management of these complications is well established. On the other hand, perianeurysmal vasogenic edema after endovascular embolization is not extensively studied, however, there is still uncertainty about the exact mechanism. Postoperative imaging may show perianeurysmal edema, aneurysmal wall enhancement, recanalization and occasionally, delayed hydrocephalus [11]. De novo edema after coil embolization has been frequently reported in some patients, while others with preoperative edema had their edema resolved after aneurysm occlusion [12].
The clinical significance and impact of perianeurysmal edema after embolization is not well-defined. Arterial pulsatile flow that stresses the aneurysmal wall and could be transmitted to the surrounding brain parenchyma could be a contributing factor [13]. Aneurysmal expansion, and thrombus formation could exert a mass effect on the surrounding brain causing edema [14]. Aneurysm thrombosis exerts a mass effect and can induce an inflammatory reaction. In a case report, a giant vertebral artery aneurysm continued to grow after endovascular treatment, and MRI showed perianeurysmal enhancement. Histological examination of the surrounding tissue showed inflammation and neovascularization surrounding the coils [15]. Moreover, inflammatory mediators produced in the aneurysmal wall could contribute to post-coiling thrombus formation exacerbating perianeurysmal edema Fig. 1 [16]. Postmortem examination of the wall of aneurysms treated with embolization suggested an inflammatory reaction that is associated with aneurysmal wall enhancement [17]. Some patients develop post-embolization hydrocephalus. The mechanism by which those patients develop hydrocephalus is not fully understood. Patients with unruptured aneurysms treated with bioactive coils developed hydrocephalus [18]. It is hypothesized that embolization coils could induce inflammatory meningitis that might cause a low grade obstructive hydrocephalus [19].
The incidence of perianeurysmal edema is 7.6–8.6% on regular postembolization MRI examination [20]. Typical radiological features include punctuate, nodular or annular areas of enhancement and T2-hyperintensities involving the leptomeninges, cortex and subcortical areas close to the treated aneurysm. The clinical presentations are variable and include headache, seizure, motor deficit, altered mental status, visual, and speech disturbances [12, 13, 21]. Female sex was associated with a higher incidence of PE after EVT. Generally, women have a higher risk of aneurysmal rupture than men [24, 28]. Several studies have reported that females have a higher risk for cerebral aneurysm formation than men and they are more likely to have multiple cerebral aneurysms than males which may explain the increased incidence of perianeurysmal post embolization edema among females [29, 30]. The exact prevalence of PE in patients with cerebral aneurysms treated with EVT is unknown.
PE occurred with all aneurysmal sizes and there was no predilection for large sized ones. Through our pooled analysis, we noticed that most patients were asymptomatic, while the most frequent presentation was headache [22, 23, 24] followed by seizures due to cortical irritation. However, several patients with parenchymal embedding of the aneurysms were completely asymptomatic. The most common aneurysms associated with post ETV edema were main ICA and bifurcation aneurysms followed by basilar tip aneurysms. We noticed that a large number of the aneurysms were embedded in the brain parenchyma which may explain the impact of dynamic water hammer flow on the wall and the surrounding brain. Based on pulsatility theory, careful attention should be given to large aneurysms in contact with parenchyma, and close to the brainstem.
Interestingly, we noticed that the most common coil used was the platinum type, and edema was less observed with the use of flow diversion and stents. The time of edema onset is highly variable from a single day to several years following EVT, indicating the need for long-term follow-up protocols for the late detection of PE. Factors that predispose to the differential onset of edema are not well-defined. In a certain case report, it took two days after EVT to develop edema, while in others it took more than a year [22, 23] Aneurysm recanalization and expansion was reported in about 12 patients, suggesting aneurysmal incomplete occlusion as a possible etiology for PE. A second endovascular intervention in those cases with aneurysm expansion is required to completely occlude the aneurysm which may potentially improve the edema. Steroid therapy is considered the first line treatment for post-embolization perianeurysmal edema [25, 26]. In most of the patients, symptoms resolved without treatment, and patients who presented with seizures were treated with anti-seizure medications. The follow up of seizures incidence over a long term follow up is not available in the available case reports. There is no general consensus about the management of post-endovascular perianeurysmal edema. If the edema was related to aneurysm expansion or recanalization, a second treatment or embolization would be the best treatment option [6, 27].
Limitations:
Due to the infrequent occurrence of post ETV PE, the sample size of available case reports is small. Our heterogeneous data and the small sample size challenged the statistical robustness, which further limited the pooled analysis. A larger sample would allow for more detailed analysis. The unavailability of several studies data and reported results of the included literature further limited our review findings. The short follow up periods do not allow us to establish a proper evidence based outcome assessment. The difference of the degree of edema or inflammatory reactions stratified by the method of embolization is not well known in human studies. In experimental animal aneurysms, inflammatory and wound healing molecules were higher in coiled aneurysms than following flow diversion, however, this comparison is not substantiated in humans [43]. Researchers should recruit animal models for properly identifying the exact mechanism of edema that could affect the brain after endovascular interventions for cerebral aneurysms.