Abstract
Blood blister-like aneurysms of the internal carotid artery are uncommon lesions that often present with subarachnoid hemorrhage and are considered part of the spectrum of intracranial arterial dissections. Although endovascular treatment options have expanded in recent years, serious complications remain a clinical concern.
We report the case of a 42-year-old woman with a ruptured blood blister-like aneurysm arising from the anterior wall of the internal carotid artery who was treated with stent-assisted coil embolization. The initial postoperative course was uneventful and follow-up imaging showed no evidence of aneurysmal recurrence. However, the patient died 3 months after treatment. Autopsy revealed rupture of the parent artery at the opposite wall of the distal stent edge, with extravascular exposure of the stent. Histopathological examination demonstrated disruption of the internal elastic lamina extending both distal and proximal to the aneurysm, indicating that arterial dissection was more extensive than detectable by angiography.
This case suggests that multiple factors, including stent-induced vessel straightening, incomplete wall apposition, antithrombotic therapy, and pre-existing wall fragility, may contribute to delayed stent-edge rupture following stent-assisted coil embolization for blood blister-like aneurysms. Careful selection of stent type and length to adequately cover the dissected segment may be important to reduce the risk of delayed parent artery failure.
Keywords: autopsy, stent-assisted coiling, subarachnoid hemorrhage, blood blister-like aneurysm, complication
Introduction
Blood blister-like aneurysms (BBAs) are uncommon lesions that arise from non-branching sites of cerebral arteries and are most frequently observed in the internal carotid artery (ICA). They account for approximately 0.3-1% of all intracranial aneurysms.1) These aneurysms are characterized by fragile arterial walls and a high risk of rupture, often presenting as subarachnoid hemorrhage.2) In this report, we describe a patient with a ruptured BBA of the ICA who underwent stent-assisted coil (SAC) embolization but subsequently experienced a fatal delayed rupture. Autopsy findings provided insight into the underlying vascular pathology and the possible mechanism of delayed parent artery failure.
Case Report
A 42-year-old woman was transported to our hospital by ambulance after sudden onset of severe headache and nausea at home. She was alert on arrival; however, she rapidly became comatose (Glasgow Coma Scale score: E1V1M4) while in the emergency department. Non-contrast head computed tomography (CT) revealed diffuse subarachnoid hemorrhage. Head and neck CT angiography (CTA) identified a 2.2-mm aneurysmal lesion on the anterior wall of the right ICA, as well as a small aneurysm of the right middle cerebral artery (Figure 1A and B). Although the patient presented with Hunt and Kosnik grade V subarachnoid hemorrhage, the exact rupture site could not be definitively identified at that time. Given the patient's poor neurological condition, conservative management was initially selected.
Figure 1.
Preoperative images and angiographic findings.
(A) Non-contrast head CT obtained after neurological deterioration demonstrates diffuse subarachnoid hemorrhage.
(B) CT angiography shows subtle focal bulging of the anterior wall of the right internal carotid artery (white arrowhead).
(C) Lateral view of right internal carotid artery angiography demonstrates a focal bulging lesion on the anterior wall of the internal carotid artery (white arrow).
(D) Three-dimensional rotational angiography volume-rendering image of the right internal carotid artery in the oblique anteroposterior projection demonstrates the focal aneurysmal lesion on the anterior wall of the supraclinoid segment.
(E) Three-dimensional rotational angiography volume-rendering image in the oblique posteroanterior projection. The image quality is limited due to the low resolution of the older-generation angiographic system.
(F) Post-embolization lateral view of right internal carotid artery angiography shows minimal residual contrast filling at the aneurysmal neck (white arrow).
CT: computed tomography
On the following day, repeat CTA demonstrated further enlargement of the anterior wall lesion of the right ICA, supporting the diagnosis of an ICA-BBA. Because the lesion had a wide neck and shallow fundus, conventional coil embolization was considered technically infeasible. Therefore, after obtaining written informed consent from her family regarding the off-label use of a stent, SAC embolization was selected as the treatment strategy.
Endovascular treatment
The right femoral artery was accessed, and a 6-Fr long sheath was inserted. A 6-Fr guiding catheter was advanced into the right ICA using a coaxial system with a 4-Fr diagnostic catheter. Selective right ICA angiography revealed a focal bulge on the anterior wall of the supraclinoid portion of the ICA (Figure 1C). Three-dimensional rotational angiography with volume rendering also confirmed the aneurysmal lesion (Figure 1D and E). A Prowler Select Plus (Cerenovus, CA, USA) was positioned in the right middle cerebral artery, and an Excelsior SL-10 microcatheter (Stryker Neurovascular, Fremont, CA, USA) with a clockwise spiral configuration was navigated into the aneurysm using a GT 0.012-inch microguidewire (Terumo Corp., Tokyo, Japan). Because of the wide-neck morphology of the lesion, stent assistance was considered necessary to achieve stable coil placement. Clopidogrel (300 mg), aspirin (300 mg), and cilostazol (200 mg) were administered via a nasogastric tube using the simple suspension method, and approximately 1 hour was allowed to elapse. An Enterprise VRD 2 (4.5 × 14 mm; Cerenovus, CA, USA) was then partially deployed from the ICA terminal. A Target 360 ULTRA 2.5 × 3 coil (Stryker Neurovascular, Kalamazoo, MI, USA) was inserted through the SL-10 microcatheter using the semi-jail technique. After confirmation of stable coil positioning, the stent was fully deployed, followed by coil detachment. Additional coils (ED Coil ES 2 × 3 mm and 1.5 × 2 mm; Kaneka Medics, Osaka, Japan) were subsequently deployed. The Enterprise VRD was deployed from just distal to the origin of the anterior choroidal artery to the vicinity of the ophthalmic artery origin. The final angiographic result was classified as Raymond–Roy class II (neck remnant) (Figure 1F). Although a small neck remnant remained, the coil packing density was considered sufficient, and the procedure was concluded.
Postoperative course
No significant intraoperative or immediate postoperative complications were observed. However, recovery of consciousness was limited, and a tracheostomy was required 3 weeks after the procedure. Aspirin was discontinued on day 20, and dual antiplatelet therapy with clopidogrel (75 mg/day) and cilostazol (200 mg/day) was continued thereafter. Cilostazol was used as a substitute for aspirin in view of its anti-vasospastic properties during the acute phase of subarachnoid hemorrhage (Figure 2). Close follow-up imaging was difficult to perform because of the patient's persistent poor cooperation and involuntary movements, which required sedation for imaging. As a result, safe transport to the imaging suite and maintenance of a stable position could not be ensured, limiting the feasibility of repeated imaging examinations. Similarly, follow-up digital subtraction angiography (DSA) was not performed because puncture procedures and patient stability during the examination could not be adequately ensured. CTA performed on day 25 and magnetic resonance angiography performed on day 33 after onset demonstrated no residual blood flow into the aneurysm (Figure 3A and B). Serial follow-up skull radiography performed on postoperative days 53 and 103 showed no findings suggestive of aneurysm enlargement, including coil migration or separation (Figure 3C and D). On day 104 after onset, the patient developed cardiopulmonary arrest in the ward. Despite immediate resuscitative efforts, the patient could not be revived and subsequently died.
Figure 2.
Timeline of antithrombotic therapy and clinical course.
A loading dose of aspirin (300 mg), clopidogrel (300 mg), and cilostazol (200 mg) was administered on day 1 (day of stent-assisted coil embolization). Triple antithrombotic therapy was continued until day 20, after which aspirin was discontinued. Dual antithrombotic therapy with clopidogrel (75 mg/day) and cilostazol (200 mg/day) was maintained until death on day 104. Imaging follow-up time points are indicated.
ASA: acetylsalicylic acid; CLP: clopidogrel; CTA: computed tomography angiography; LD: loading dose; MRA: magnetic resonance angiography; XR: skull radiograph
Figure 3.
Postoperative imaging findings.
(A) Computed tomography angiography performed on day 25 demonstrates no residual blood flow into the aneurysm (white arrowhead).
(B) Source image of magnetic resonance angiography performed on day 33 demonstrates no residual blood flow into the aneurysm (white arrow).
(C) Lateral skull radiograph obtained on postoperative day 53 shows no findings suggestive of aneurysm enlargement, including coil migration or separation.
(D) Lateral skull radiograph obtained on postoperative day 103 demonstrates no obvious changes in coil configuration.
Autopsy results
To determine the cause of death, an autopsy was performed. Examination revealed the presence of an intracranial hematoma originating from the basal aspect of the brain parenchyma (Figure 4A and B). Notably, arterial rupture was identified not at the anterior wall where the aneurysm had arisen, but at the opposite arterial wall, with extravascular exposure of the distal end of the deployed stent (Figure 4A and C). The right ICA-BBA was sufficiently thrombosed (Figure 4B), with no evidence of recurrence and coil migration. In contrast, the small aneurysm in the M1 segment of the right middle cerebral artery remained unruptured. In addition, diffuse intimal thickening was observed throughout the major cerebral arteries, indicating atherosclerotic changes disproportionate to the patient's age.
Figure 4.
Autopsy and histopathological findings.
(A) Gross view of the right internal carotid artery reveals vascular rupture at the distal segment, with exposure of the stent through the ruptured arterial wall (black arrow). The rupture site is located on the arterial wall opposite the coil mass.
(B) Gross view of the brain from the skull base shows thrombosis of the blood blister-like aneurysm, with no evidence of coil protrusion or migration (white arrowhead).
(C) Photograph showing the resected internal carotid artery including the surrounding circle of Willis. The open arrowhead indicates the thrombosed blood blister-like aneurysm, and the black arrow indicates the distal end of the stent protruding from the vessel.
(D) Double-stained cross-sectional specimen of the internal carotid artery aneurysmal segment using α–smooth muscle actin (α-SMA) immunohistochemistry and Victoria blue staining (original magnification ×40). The area outlined by the dotted line corresponds to the aneurysmal portion and demonstrates disruption of the internal elastic lamina and loss of the smooth muscle layer. The arrow indicates extravascular exposure of the stent. Despite the limited defect of the smooth muscle layer, complete arterial wall disruption is observed, suggesting that tissue collapse was more likely caused by mechanical rupture rather than degenerative changes of the vessel wall.
(E, F) Double-stained sections combining Victoria blue staining and α-SMA immunohistochemistry of the internal carotid artery distal and proximal to the aneurysmal segment (original magnification ×40).
(E) Section distal to the rupture site demonstrates intimal injury accompanied by mural thrombus formation (black arrowhead).
(F) Section of the internal carotid artery siphon proximal to the rupture site reveals loss of continuity of the internal elastic lamina and intima, with full-thickness arterial wall disruption extending to the adventitia and associated thrombus formation beyond the vessel lumen (black arrowhead).
ICA: internal carotid artery
Histopathological examination revealed disruption of the arterial wall on the side opposite the aneurysmal segment, with loss of the adventitial structure. At the aneurysm-like bulging site itself, disruption of the internal elastic lamina and tunica media was observed (Figure 4D). In addition, disruptions of the internal elastic lamina were observed at multiple sites both distal and proximal to the aneurysm (Figure 4E and F), suggesting that arterial dissection extended beyond the regions detectable by angiography.
Discussion
BBAs of the ICA most commonly arise from the anterior wall and are widely regarded as part of the spectrum of intracranial arterial dissections.1-3) Previous pathological studies have demonstrated that many BBAs represent localized wall defects associated with disruption of the internal elastic lamina and dissection between the media and adventitia.4,5) Because these lesions often appear as subtle focal wall bulges on angiography in the acute phase, early and accurate identification remains challenging.6,7)
Despite an uneventful postoperative course with no evidence of aneurysmal recurrence, the patient died of a fatal rupture at the distal stent edge approximately 3 months after treatment. Critically, autopsy revealed that the rupture occurred at the arterial wall opposite to the original aneurysm, and histopathological examination demonstrated disruption of the internal elastic lamina extending both distal and proximal to the treated lesion (Figure 4E and F), indicating that the dissection was far more extensive than detectable by angiography.
The most important question raised by this case is why delayed rupture occurred at the arterial wall opposite to the initial rupture site, rather than at the treated aneurysm itself. We hypothesize that the following factors may have contributed synergistically to the progression of the dissection toward the distal stent edge and subsequent delayed rupture.
The Enterprise VRD is a closed-cell laser-cut stent with the highest bending stiffness among currently available intracranial stents,8) and has been reported to produce significant vessel straightening in tortuous parent arteries.9,10) In this case, the shortest available stent length (14 mm) was selected and was deployed within the tortuous ICA siphon. The combination of high bending stiffness and short stent length may have resulted in marked angular correction of the vessel curvature, concentrating mechanical stress at the stent edges. This force, applied to a pre-existing vulnerable dissected wall, may have promoted further extension of the dissection beyond the stent coverage. In vitro studies have shown that the Enterprise VRD stent has a gap ratio of 41% ± 15% between the stent and the vessel wall in curved vascular models, with kinks and malposition occurring particularly in acutely curved vessels such as the ICA siphon.11) If the stent did not tightly adhere to the opposite wall in this case, the streamlining effect may not have functioned adequately, leaving the abnormal vessel wall continuously exposed to hemodynamic stress. Additionally, the flow diversion effect of the Enterprise VRD stent is lower than that of braided stents, such as the LVIS,12) and may have been insufficient to redirect flow away from the diseased segment. However, cone-beam CT was not available in this case due to limitations of the older-generation angiographic equipment used, and the actual degree of stent apposition could not be assessed.
As described in the case presentation, triple antithrombotic therapy was initiated on day 1 and maintained until day 20, followed by dual therapy with clopidogrel and cilostazol until death on day 104 (Figure 2). It is well established that dissecting aneurysms tend to heal spontaneously over time, unlike saccular aneurysms.5) Strong antithrombotic therapy initiated on day 1, when the dissection is presumably unstable, may have disrupted the spontaneous healing process of the dissected wall opposite to the initial rupture point. This hypothesis is indirectly supported by the observation that in the wrap-and-clip method for BBAs, which preserves anterograde ICA flow without requiring antithrombotic therapy, rebleeding from the contralateral wall has not been reported to our knowledge.13) However, it should be noted that the maintenance dual antithrombotic regimen after day 20 was not excessive compared with the standard dual antiplatelet therapy commonly used for other stent-assisted coiling cases, although the specific drug combination differed from the typical aspirin–thienopyridine regimen.
Autopsy revealed diffuse intimal thickening throughout the major cerebral arteries, representing atherosclerotic changes disproportionate to the patient's age (42 years). Such pre-existing arterial wall fragility may have increased the vulnerability of the second rupture point. Furthermore, the rupture site was located at the outer curve of the tortuous ICA, where hemodynamic wall shear stress is the highest. This anatomical consideration may also explain why delayed stent-edge rupture has not been reported following stent-assisted coiling for vertebral artery dissections, which generally follow a straighter course than the ICA.
As described above, the histopathological findings suggest that the arterial dissection was more extensive than could be detected by angiography at the time of treatment. At the same time, it cannot be excluded that vessel straightening caused by stent deployment imposed additional mechanical stress on the pre-existing fragile wall, further propagating the dissection distally toward the stent edge. Therefore, the most plausible explanation for the delayed contralateral wall rupture in this case is a combination of pre-existing extensive dissection and secondary mechanical injury induced by stent placement. Notably, this mechanism of stent-associated vascular injury is not limited to BBAs; intracranial stent deployment exerts radial force and vessel straightening effects on the arterial wall, and these mechanical forces should be recognized as potential contributors to wall damage, particularly in the setting of dissecting pathology.
Various surgical and endovascular treatment strategies have been proposed for ICA-BBAs; however, no consensus has been established regarding the optimal approach.14,15) Flow diverter stents have been increasingly reported as an effective option for BBAs in recent years; however, in the setting of acute subarachnoid hemorrhage, the high metal surface coverage of flow diverters poses a significant risk of acute thrombotic complications, particularly when strong dual antiplatelet therapy must be initiated during the acute phase of hemorrhage.14) In addition, flow diverters were still investigational devices and not generally available for clinical use at the time of treatment. Therefore, SAC embolization using the Enterprise VRD was selected as a safer treatment strategy with a lower risk of thromboembolic complications, although this approach was also considered off-label. However, as discussed above, the high bending stiffness and limited wall conformability inherent to this closed-cell laser-cut stent design may have contributed to incomplete wall coverage and vessel straightening, representing a trade-off that should be considered when selecting stents for dissecting pathology in tortuous vessels. Though SAC is less invasive than open surgical procedures and carries a relatively low risk of ischemic complications, postoperative regrowth and rebleeding remain concerns.16,17) In most reported recurrent cases, rebleeding occurs from the previously treated aneurysm itself.18) In contrast, rupture occurring at the stent edge, as observed in this case, appears to be extremely rare.
Preoperative imaging techniques aimed at estimating the longitudinal extent of arterial dissection, including high-resolution vessel wall magnetic resonance imaging and combined assessment of outer and inner vessel diameters, have been reported to be useful in selected cases.19-21) However, in patients with severe neurological impairment or in emergency settings, comprehensive preoperative imaging may not be feasible. In such situations, selecting a stent of sufficient length to extend from relatively healthy vessel segments may be considered to reduce the risk of incomplete coverage of the dissected segment.16,22)
This study has several limitations. First, because the treatment was performed using an older-generation angiographic system, cone-beam CT after stent deployment was not available, and the degree of stent apposition to the vessel wall could not be evaluated. Second, although three-dimensional rotational angiography with volume rendering was obtained, the image resolution was limited due to the older-generation system, and non-subtracted images were not acquired, precluding detailed assessment of the posterior wall of the distal ICA. Third, follow-up DSA was not performed because the patient's poor neurological status precluded safe transport and positioning for the examination. Finally, the findings of this single case cannot be generalized, and it remains unclear whether the proposed mechanism would apply to other cases of BBA treated with SAC.
In summary, this case demonstrates that delayed rupture at the stent edge, rather than at the treated aneurysm itself, can occur as a rare but fatal complication of SAC embolization for ICA-BBAs. The combination of stent-induced vessel straightening, incomplete wall apposition, antithrombotic therapy, pre-existing atherosclerotic changes, and hemodynamic stress at the outer curve of the ICA may have synergistically contributed to this outcome.
Conclusions
This case underscores the importance of recognizing that arterial dissection associated with ICA-BBAs may extend beyond the angiographically visible lesion. Careful selection of stent type and length to adequately cover the potentially dissected segment, along with awareness of the mechanical effects of stent deployment on fragile vessel walls, may help reduce the risk of delayed parent artery failure.
Disclaimer
Author Ryuta Saito is one of the Editorial Board members of the Journal. This author was not involved in the peer-review or decision-making process for this paper.
Conflicts of Interest
All authors have no conflict of interest.
Informed Consent
Written informed consent for publication of this case report was obtained from the patient's family.
Submission Statement
All authors pledge that this manuscript does not contain previously published material and is not under consideration for publication elsewhere.
Acknowledgments
The authors acknowledge the use of an AI-assisted language tool for English language editing; however, all scientific content, interpretations, and clinical decisions are solely the responsibility of the authors.
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