Complications of endovascular treatment for intracranial aneurysms: Management and prevention

Abstract

Endovascular coiling for intracranial aneurysms has become an accepted treatment with good clinical results and provides adequate protection against rebleeding and rupture of aneurysms. However, despite the experience, preparation, or skill of the physician, complications during endovascular treatment still occur. The main complications of endovascular coiling are: procedural aneurysmal perforations by the microcatheter, micro-guidewire, or coil, and thromboembolic events. Such situations are unexpected, complex, and can have devastating consequences. In this article, we present a comprehensive review of the two most common complications, aneurysmal perforation and thromboembolism during endovascular coiling, and how we can prevent or overcome these complications to achieve a satisfactory outcome. In addition, as the flow diverter has been become an important tool for management of large, wide necked, and other anatomically challenging aneurysms, we also describe complications stemming from the use of the tool, which remains a novel treatment option for complex aneurysms.

Introduction

Intracranial aneurysm is one of the most common neurovascular afflictions. For the last few decades, the method used to decrease the morbidity and mortality rates of unruptured intracranial aneurysms has been treatment before rupture; treatment for ruptured aneurysms focuses on the prevention of rebleeding. Endovascular coiling has become a mainstay in intracranial aneurysm treatment since the International Subarachnoid Aneurysm Trial (ISAT).¹ However, coiling has inherent complications compared to clipping surgery.

Coiling complications can be divided into the following categories: complications in the intracranial artery, complications in the extracranial artery, complications related to the placing of the guiding catheter, and complications related to the puncture site. Most often, two types of complications occur during coiling in the intracranial artery: intraprocedural aneurysm ruptures (IARs) and thromboembolic events. We describe these most common complications during coiling and how we can prevent or overcome these unexpected events. We will also briefly address complication that may arise from the use of the flow diverter, a novel endovascular treatment option for complex aneurysms such as fusiform or giant aneurysms. Although this tool has demonstrated positive outcomes, there have been reports of complications to which research efforts have not yet been dedicated. In this article, we address some of these complications from the perspective of hemorrhagic and thromboembolic events.

IAR during coiling

Incidence

The reported percentage of IARs during coiling varies among studies. A wide spectrum of IAR rates have been reported, and it is currently estimated to be between 1% and 5%.^2,3 Although procedural iatrogenic ruptures are more often seen with surgical clipping of aneurysms, IAR occurrence with coiling is associated with a higher risk of mortality, ranging up to a rate of 40%. The clinical seriousness of IAR may be variable, ranging from a slight leakage of contrast material into subarachnoid space to a massive hemorrhage with severe intracranial hypertension.

The Cerebral Aneurysm Rupture After Treatment (CARAT) trial examined 1010 unselected patients with ruptured cerebral aneurysms treated by either coil embolization or surgical clipping at nine high-volume clinics over a period of five years. They found IARs occurred in 148 (14.6%) patients and these ruptures during coiling (5%) or clipping (19%) increased the risk of periprocedural death/disability fourfold and twofold, respectively (p = 0.12).⁴ A meta-analysis showed the risk of aneurysm perforation during coil embolization is much higher in patients with previously ruptured aneurysms than in those with unruptured aneurysms.⁵ Yet, the unquestionably poor clinical outcome that is an IAR of a previously ruptured aneurysm can be obscured by the tragic outcome of a ruptured aneurysm.

IARs are more frequent in acutely ruptured aneurysms, small aneurysms, and aneurysms in the anterior communicating artery (A-ComA).⁶

Mechanism

Multiple factors are associated with the risk of an IAR. It may be induced by coil, microcatheter, or the micro-guidewire. Cloft et al. reported that the morbidity and mortality rates of perforations caused by coil (39%) and microcatheter (33%) were similar. The morbidity and mortality rates of IARs caused by micro-guidewire were considerably lower (0%, n = 4) than the rates caused by coils or microcatheters.⁵ Kawabata et al. also reported that clinical outcomes depended on the cause of the IAR, and rupture by microcatheter showed the worst outcomes. And they also reported the rates of good clinical outcomes of IARs induced by coils, micro-guidewires, and microcatheters were 90%, 100%, and 57%, respectively.⁷

Over-packing of the aneurysm, oversized coils, and the use of stiff 3D coils have been reported to be associated with IARs.⁸

The higher risk of rupture in small aneurysms is believed to be due to the increased restriction of microcatheter movement within the aneurysm, resulting in greater stress within the aneurysm sac. In terms of aneurysmal location, Oishi et al. reported a trend toward a higher incidence of iatrogenic rupture located in the A-ComA.⁹ This may be because an A-ComA aneurysm usually has an unfavorable dome-neck ratio, and an acute angle between the internal carotid artery and the anterior cerebral artery.¹⁰

Some studies have shown that the balloon-assisted technique is not associated with an increased incidence of IARs,^11–13 while other studies have demonstrated an increase of IARs compared with conventional coil embolization.¹⁴ Nevertheless, using a balloon can be beneficial to control hemorrhaging after the occurrence of an IAR.⁸ Vascular tortuosity might increase the risk of perforation by decreasing the level of control of the operator.⁵

Coil embolization can be performed under local anesthesia or general anesthesia. In a retrospective study of 186 patients with subarachnoid hemorrhage (SAH), the rate of IARs was significantly higher under local anesthesia than general anesthesia. It is thought that patient's unexpected movements under local anesthesia are to blame for the higher rate of IARs, given that such motions can displace the micro-instruments being used in the procedure.¹⁵

Recognition and management

Decreasing the risk of death and permanent neurologic disability as a result of an IAR is dependent on immediate and proper action after a perforation occurs.⁵ Therefore, quick recognition of the IAR is very important. The first radiographic sign of a perforation is a breach of any device out of the aneurysmal boundary on a road-map image. This breach is followed by a rise in blood pressure and an increase in the pulse rate. On occasion, false breaching can appear due to a patient's feeble movement, a partially thrombosed aneurysm, or a superimposed parent artery. Blood pressure also abruptly increases without an IAR when an endovascular device stimulates the endothelium of a cerebral artery or in the event of diminished anesthesis.¹⁶ In such a situation, a careful angiogram through the guiding catheter with a minimum amount of contrast material can confirm the presence or absence of an IAR. Contrast stagnation that does not wash out in the venous phase indicates blood in the extravascular space. The Dyna CT (Siemens' cone-beam CT which can be obtained during interventions) can serve as a useful tool to confirm the existence of an extravascular hemorrhage in the equivocal circumstances.

After identifying an IAR, the neurointerventionist should advise the anesthesiologist to proceed with blood pressure control while the neurointerventionist takes additional steps to control the hemorrhage.

If an aneurysmal perforation is detected during the procedure, quickly managing the situation is critical. After identifying contrast leakage from the aneurysm, treatment of the aneurysmal perforation starts with the immediate reversal of anticoagulants. Heparin reversal in the setting of an intraprocedural rupture involves 1 mg of protamine sulfate, intravenously, per 100 units of heparin administered. In the short term, 5–10 mg of protamine sulfate is usually sufficient for the doses administered during coil embolization. Cardiopulmonary side effects can occur after protamine administration. These may include hypotension, anaphylaxis, and pulmonary hypertension. Since cardiopulmonary side effects can occur and rapid mechanical hemostasis by coil or balloon should not be delayed, we recommend skipping the protamine administration if rapid mechanical hemostasis can be achieved. The skipping of protamine administration has been reported in a study of endovascular aortic aneurysm repair.¹⁷ Antiplatelets such as aspirin and clopidogrel can be also reversed,¹⁶ but it is important that these anticoagulation or antiplatelet reversals should not delay mechanical hemostasis.

If the perforation is caused by micro-guidewire, it may be minimal, and management involves the continuation of embolization. If the perforating device is a coil or microcatheter it should not be removed because the device may be partially occluding the perforation, and removal of the device may result in further injury to the aneurysmal wall. Tears caused by a coil can be mitigated by leaving the perforating coil in place. To do so, deploy part of the coil outside of the aneurysm and withdraw the microcatheter tip from proximity of the aneurysm wall, and upon positioning the microcatheter tip, deliver the rest of the coil into the aneurysm as normal. With the use of a second microcatheter, pack the aneurysm with coils temporarily leaving the first microcatheter in place.¹⁸ This multiple microcatheter technique is more advantageous than a single microcatheter technique for an immediate and proper response to an IAR. In addition, applying a balloon across the aneurysmal neck at the time of rupture allows for immediate and effective control of the hemorrhage. However, neurointerventionists need to be more careful when using balloons because their use may increase risk factors for secondary procedural complications in this situation.

If the rupture point is either unclear or near the aneurysmal neck, additional coils cannot be deployed. In such a circumstances, multiple stents or liquid adhesives such as n-butyl cyanoacrylate can be considered for the closure of the aneurysmal rupture.¹⁹

In addition, the authors of this paper emphasize the role of immediate external ventricular drainage (EVD) or a craniectomy for the urgent management of severe SAH and intracranial hypertension after coiling procedure.

Even though thromboembolic events are more frequent and associated with higher morbidity rates, IARs are more distressing. This is because in the event of an IAR, the operator may often feel rushed to take pressing action, amplifying the amount of stress associated with the procedure. This calls for a crisis-management algorithm that doctors might employ to achieve good outcomes following IAR events. We have drafted just such a thing, and by adopting the example workflow algorithm described in Figure 1, physicians might be better able to manage IAR events and successfully minimize the stress of these high-pressure scenarios.

Figure 1.

Example of workflow algorithm in the situation of intraprocedural aneurysm ruptures (IARs) during coiling. BP: blood pressure; CT: computed tomography.

Prevention

To try to reduce the rate of IARs, it is important to determine which factors affect the rate of occurrence. McDougall et al. reported the uncontrolled advancement of the microcatheter can be a factor leading to an IAR. The incidence of microcatheter perforation can be decreased by ensuring that no forward pressure is exerted on the microcatheter before the micro-guidewire is removed and by removing the micro-guidewire very slowly while under fluoroscopic visualization.²⁰

As mentioned above, the presence of a balloon allows for immediate and effective control of IARs. Santillan et al. propose using a balloon in assisting the embolization of aneurysms with high risk of IARs.⁸ The balloon-assisted technique in the treatment of aneurysms is analogous to the use of temporary clips in the neurosurgical treatment of aneurysms.

Proper positioning of the microcatheter is very important for prevention of IARs. If the microcatheter tip is positioned too close to the aneurysm wall, IAR by coil is more likely to occur. And neurointerventionists should know that microcatheters have a radiolucent distal segment approximately 0.5–1 mm in length between the distal marker visible on fluoroscopy and the actual microcatheter tip.²¹

Thromboembolic events related to coiling

Incidence

A thromboembolic event is defined as any event with complete or partial occlusion of arteries at the site of the aneurysm, distal to the vascular territory where the endovascular procedure was performed, or in any other vascular territory. Although thromboembolic complications occur more frequently and are associated with higher morbidity rates compared to IARs, ascertaining a thromboembolism is more difficult than confirming the existence of aneurysmal perforations. This is because the latter is radiologically and/or clinically obvious in most cases, but evidence suggests that a significant number of minor embolic events may go unfound unless detected by a rigorous angiographic analysis or by a follow-up diffusion magnetic resonance imaging (MRI).

The incidence of thromboembolic complication within 24 h after coil embolization is generally reported in a wide range of procedures (2–15%).^9,22,23 Altay et al. reported nine (4.9%) clinically evident strokes out of 184 patients with treated aneurysm who underwent MRI within 72 h of the procedure.²⁴ Ries et al. observed 48 cases (9.3%) of thromboembolism in his series of 515 patients, and eight incidents were observed during embolization of unruptured aneurysms (8/174; 4.6%) despite the oral administration of clopidogrel for three days preoperatively.²⁵

Mechanism

Thromboembolic complications may be caused by clot formation in the guiding catheter, on the coil mashes, or in parent vessels caused by the induced vasospasm or malposition of coils. Prolapsed coil loops serve as a site for platelet aggregation, leading to local thrombosis or distal thromboembolism.²⁶ Several reports have also suggested that explainable embolic sources are air embolisms, atheroma dislodged during catheterization, thrombus formation from the device used over the course of the procedure, and hydrophilic coating from catheters and wires.^27,28

Regardless of the technique used, thromboembolic complications are more common in patients with a ruptured aneurysm than in those with an unruptured aneurysm.²⁴ Other specific risk factors that have been described in a previous study include large aneurysms. Larger aneurysms are more likely to have residual flow within the coil mass than small aneurysms, and the greater volume of thrombus in a larger aneurysm could yield an increased risk of propagation or distal embolization.²⁶

Some reports demonstrated that stent-assisted coiling (SAC) was associated with a higher rate of thromboembolic complications than non-SAC.²⁹ However, if antiplatelets and anticoagulants are used properly, SAC is not likely to increase the possibility of thromboembolic events that are more common even in the coiling of acutely ruptured aneurysms.^{30, 31}

Vasospasm and hypercoagulability have also been proposed to explain the increased incidence of thromboembolic events, and this situation usually develops in a subarachnoid hemorrhage.³²

Although rare, clinical conditions such as heparin-induced thrombocytopenia (HIT) and antiphospholipid-antibody syndrome (APS) can also induce thromboembolic events. Potential HIT indicators during the procedure include unusual thromboembolic events and unresponsiveness to heparin, which can be explained by low activated coagulation time (ACT) levels.³³ APS is an antibody-mediated hypercoagulable state characterized by recurrent venous and arterial thromboembolic events.³⁴ Most APS patients' disease history will be well-documented, but there have been cases of practitioners performing endovascular coiling on APS patients who were either unaware they suffered from the disease or did not disclose the information to their physician.

Recognition and management

A flow defect around a coil mesh or distal emboli is usually the first angiographic evidence associated with a developing thrombus. Intraprocedural diagnosis is made by performing intermittent diagnostic angiography during the coiling procedure. The operator can see subtle radiolucency within the contrast-opacified vessels. Thrombus formation is a dynamic process, and a thrombus can vary in size and shape during the early stages of thrombotic events. When in doubt, serial imaging over time is helpful to determine possible thrombus development. In addition, neurophysiologic brain monitoring devices such as electroencephalography, somatosensory evoked potentials and/or brain stem auditory evoked potentials can provide continuous monitoring of regional electrical activity. This allows physicians to estimate regional cerebral blood flow, which in turn produces useful adjunctive information regarding clinical implications of a thromboembolic complication in a patient under general anesthesia.¹⁶

Several treatments have been used to manage periprocedural acute thromboembolism, such as: medical treatment with hypervolemia and hemodilution, increased intravenous heparin, periprocedural and postprocedural antiplatelet agents, intra-arterial thrombolysis with urokinase or tissue plasminogen activators (t-PAs), or intravenous bolus injections and continuous infusion of the glycoprotein IIb/IIIa.^35,36

Cronqvist et al. reported the results of super-selective intra-arterial fibrinolytic therapy in 19 patients for treating thromboembolic events during endovascular aneurysm treatment. They reported complete recanalization in 10 patients and partial recanalization in nine, with 14 patients eventually having good outcomes. However, three of six patients with ruptured aneurysms had intracranial bleeding complications.³⁵ The general consensus is that rescue therapy with fibrinolytic agents for intraprocedural thromboembolic events resulted in significantly more morbidity and mortality than rescue therapy with glycoprotein IIb/IIIa inhibitors.³⁷ Therefore, urokinase and tPAs are no longer considered the first choice in the treatment of thrombi during coiling of aneurysms.

Since platelets represent a primary component of acutely formed arterial thrombi, it follows that platelet inhibition is a component of management for this complication. Glycoprotein IIb/IIIa inhibitors including abciximab, eptifibatide, and tirofiban are potent antiplatelet agents that bind to the IIb/IIIa surface membrane glycoprotein receptors, preventing platelet cross-linking and aggregation. Intravenous abciximab is well described as a rescue treatment for thrombus in the context of ruptured and unruptured aneurysms.³⁸ On the other hand, intra-arterial infusion has the advantage of using a lower dosage of this drug, which potentially can lower the risk of hemorrhagic complications.^25,39 Intra-arterial abciximab can be associated with a higher rate of aneurysmal recanalization, and can also induce intracerebral hemorrhage.^40,41 Tirofiban has been used to manage acute thromboembolisms recently.⁴² Tirofiban hydrochloride monohydrate is a nonpeptide tyrosine derivative that acts as a reversible antagonist of fibrinogen, binding to the glycoprotein IIb/IIIa receptor of platelets. Its main advantage is a short half-life, which makes the drug easy to control. Even though Jeong et al. reported that intra-arterial abciximab and tirofiban exhibited similar safety and recanalization rates for the treatment of thromboembolism,⁴³ tirofiban may be safer than abciximab due to its action mechanism of reversibility.

Various mechanical thrombectomy can be performed if pharmacologic thrombolysis has failed. Cases of aspiration thrombectomy using Penumbra (Penumbra Inc., Alameda, California, USA) have been reported.⁴⁴ Mechanical rescue embolectomy using a retrievable stent can be another option for recanalization in cases in which intra-arterial tirofiban has failed or is definitely contraindicated.⁴⁵

Catheter-induced or SAH-induced vasospasm can be predictive of thromboembolic complications, and, in particular, multiple microcatheters pass through a narrow artery due to vasospasm. Verapamil, nicardipine, and nimodipine are suitable vasodilators. They also cause iatrogenic hypotension, and can be infused intra-arterially. The management of rare causes of thrombosis, such as HIT and APS, is not widely dissimilar to the treatment of general thrombosis. In the case of HIT, the thromboembolism is usually treated with glycoprotein IIb/IIIa inhibitors. With APS, treatment by anticoagulation therapy during and after the procedure is standard.

Prevention

Most neurointerventionists employ intravenous heparin as a preventive measure, often with a targeted ACT of 250–300 seconds or two times the baseline ACT, during procedures for both ruptured and unruptured aneurysms. This is considered a standard protocol for preventing procedural thromboembolic risks.

Adequate inhibition of the platelet activity, as well as anticoagulation, is a principal concern for coil embolization to prevent procedure-related thromboembolic events. Since stent-assisted coiling can reduce the rate of recanalization after coil embolization,^46,47 the use of stents has become widespread among neurointerventionists in the current era, and so preventive antiplatelets have now become a necessary regimen in the treatment of unruptured aneurysms. They have also been shown to reduce the occurrence of thromboembolic events for non-stent-assisted coiling.⁴⁸ Existing research recommends a 100∼300 mg/day dosage of aspirin and a 75 mg/day dosage of clopidogrel, administered orally 5–7 days before the coiling procedure.^48,49 However, if the patient has not followed such a regimen, a loading dose of 300–500 mg of aspirin and 300 mg of clopidogrel can be administered just before coiling, as a viable alternative.

The oral administration of antiplatelets before the coiling of unruptured cerebral aneurysms for preventing the thromboembolism is widely accepted. However, whether periprocedural antiplatelet therapy can be useful for already ruptured aneurysms is unclear. Edwards et al. showed that for patients with a ruptured aneurysm at high risk of a thromboembolic event, preventive antiplatelet therapy can significantly reduce the rate of periprocedural thromboembolic complications without leading to major systemic or intracranial hemorrhage.⁵⁰ Additional research is needed to confirm the usefulness of periprocedural antiplatelet therapy for ruptured aneurysms.

The effect of pre-treatment platelet reactivity on clinical outcomes for patients with intracranial aneurysms treated with coil embolization varies.⁵¹ This can be identified through various platelet function tests. Several point-of-care (POC) devices are commercially available, which can be used to measure platelet functions and even modify antiplatelet dosage. These include: VerifyNow (Accumetrics, San Diego, California, USA) system, multiple electrode aggregometry (Multiple analyzed, Roche diagnostics international Ltd, Rotkreuz, Switzerland), and others. These platelet function test devices are used to measure how the platelets respond to clopidogrel medication.^52,53 Recently the cut-off values of different parameters have been tested in each device.^54–56

Therefore, recognizing variability in the inhibition of platelet aggregation and the ability to measure such variability with POC testing can reduce thromboembolic events in the endovascular treatment of aneurysms. Hwang et al. reported modified antiplatelet preparation for patients with resistance to standard antiplatelet reduced the thromboembolic event occurrence in the coiling of unruptured aneurysms.⁵⁴ Building upon their findings, we have formulated a preventive antiplatelet algorithm for the coiling of unruptured aneurysms, as depicted in Figure 2.

Figure 2.

Modified preventive antiplatelet preparation for coiling of unruptured aneurysm according to platelet function test.

Flow diverter complications

It is nearly a foregone conclusion that the use of a flow diverter will become standard procedure in the future, but there are currently no standard guidelines regarding the prevention of complications related to its use, especially delayed complications related to the treatment of giant and posterior circulation aneurysms. Here, we briefly review the current academic discourse about complications related to flow diverters, drawn from published research.

Although a number of flow diverters for anatomically challenging aneurysms have seen widespread use, the pipeline embolization device (PED), in particular, has received significant attention in the recent literature and is the only product that has received Food and Drug Administration (FDA) approval.⁵⁷ The following review on the extant literature on flow diverters focuses on PED.

Delayed aneurysm rupture

Existing research documents a number of incidental cases of post-treatment aneurysmal rupture following the use of flow diverters, but there remain controversies as to the precise cause.⁵⁸ Multiple theories have been proposed that attempt to explain this phenomenon. During the healing (or cicatrization) process following flow diversion, mural thrombus formation within the aneurysm can result in inflammatory changes in the aneurysmal wall, and is a known source of protease secretion, which can weaken the aneurysmal wall.⁵⁹ The so-called ‘mural destabilization’ resulting from inflammatory interaction is a putative cause of delayed aneurysm rupture. If wall destabilization occurs before cicatrization, small changes in intra-aneurysmal pressure could potentially result in rupture. Steroids may aid in reducing the inflammatory response within an aneurysm and adjunctive coil embolization might help to stabilize thrombus formation and minimize the possibility of rupture.^59,60

Reports of early ruptures following flow diversion occurring on the same day of treatment or within a few days of the procedure are probably not attributable to an inflammatory or mural destabilization condition, since this is likely to take more than a few days or weeks to occur. Fox et al. reported that mechanical stretching can result in aneurysmal rupture.⁶⁰ In our estimation, abrupt thrombus formation in the aneurysm after flow diversion is at least partially caused by mechanical stretching. Patel et al. proposed that glycoprotein IIb/IIIa should preempt thrombus formation in aneurysms or branching vessels.⁶¹ We also postulated that glycoprotein IIb/IIIa should inhibit massive thrombus formation in the aneurysm immediately after flow diversion, avoiding acute mechanical stretching.

Intraparenchymal hemorrhage

The occurrence rate of delayed intraparenchymal hemorrhage (DIPH) is about 2–3%.^58,62 The mechanism for DIPH is not completely understood, and several hypotheses exist. Over 80% of DIPHs occurred in the vascular territory of the flow diverter, which on the surface seems to support arguments that the device and or procedure may cause parenchymal hemorrhage. However approximately 20% of DIPHs occurred in other vascular territories. This suggests that patients' variable response to dual antiplatelets could play a role in causing DIPH in non-ipsilateral vascular territories.⁵⁸ We are thus led us to believe that the antiplatelet reactivity test is gradually assuming more importance.

Other hypotheses regarding DIPH include: hemodynamic alteration from the placement of flow diverters, and hemorrhagic transformation of the ischemic lesion as induced by the flow diverter. Hu et al. suggested that the shedding of certain catheter linings may be associated with intraprocedural foreign body emboli.²⁸ The recent trend of decreasing DIPHs may be related to the evolution of flow diverter devices and the soothing of friction between the flow diverter and catheter lining.

Thromboembolic events in the flow diverter

Kallmes et al. reported the ischemic stroke rates were 4.7% (37/793) in the international retrospective study of PEDs.⁶² We argue that it is critical that neurointerventionists take note of thromboembolic events correlated to the use of the flow diverter, as some research suggests the possibility of a causal relationship with DIPH. Compared to other intracranial stent procedure, a longer period of dual antiplatelet therapy (from 7–10 days) is recommended before a flow diverter procedure. Several studies document various attempts made to prevent thromboembolic events that stem from the use of a flow diverter. These include tailored antiplatelet therapy with platelet function testing, and a new antiplatelet regimen with intra-arterial tirofiban.^56,57

Summary

Despite increasing clinical experience and technological improvements, procedural complications unfortunately still occur in the endovascular treatment of intracranial aneurysms. Management of an IAR includes prompt recognition of the hemorrhage, heparin reversal, rapid and continued occlusion of the aneurysm, control of blood pressure and intracranial pressure, and placement of ventricular drainage.

Prevention of clot formation is the best way to avoid a thromboembolic complication. However, once a thrombus is seen, immediate action is required, as an untreated clot will enlarge and the situation can worsen. And most of all, it is very important to avoid secondary complications which can cause irrevocable disaster.

Flow diverters are now an established tool for the treatment of complicated intracranial aneurysms. However, significant challenges remain in the more common use of flow diversion in neurointerventional practice. It is critical that neurointerventionists are aware of some of the potential drawbacks and complications associated with the use of flow diverters as outlined in this article.

Any neurointerventionist treating aneurysms may be confronted with these complications, regardless of skill level or technical proficiency. Therefore, the physician treating an aneurysm should keep the worst-case scenarios in mind and simulate crisis management before and during endovascular treatment.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.