Small cerebral aneurysms at non-branching sites are typically thought to have thrombus-formed pseudoaneurysms or extremely weak aneurysm walls. Trapping with bypass has been regarded as the treatment of choice due to the high risk and difficulty of conventional clipping and coil embolization. This study aims to investigate a case of high-flow bypass trapping for a ruptured aneurysm in the middle cerebral artery (MCA) at non-branching sites. In this study, subarachnoid hemorrhage was found on CT, and a small aneurysm was found on CT angiography (CTA) at the MCA M1 segment’s non-branching site. In addition, a pseudoaneurysm was strongly suggested by the intraoperative digital subtraction angiography (DSA) results. It was determined that the aneurysm was a pseudoaneurysm located over the actual aneurysm sac’s rupture site. Although coil embolization was carried out, the treatment had to be stopped because the aneurysm disappeared completely during the procedure. However, according to the results of the magnetic resonance angiography, the aneurysm resurfaced on day five and grew in size. As a result, the patient was cured on day 15 after trapping with high-flow bypass. Trapping with high-flow bypass was thought to be the safest and most reliable first treatment option for pseudoaneurysms at non-branching MCA sites due to the unusual and noteworthy course of this case.
An aneurysm of the anterior wall of the internal carotid artery (ICA) is typical of small cerebral aneurysms that occur at non-branching sites. The aneurysm’s wall is extremely fragile or takes the form of a pseudoaneurysm caused by a thrombus [1]. Conventional clipping and coil embolization are risky and difficult because of the disease, so trapping with bypass has been considered the preferred treatment [2]. However, the etiology of the aneurysm and the most effective treatment strategy have not yet been determined, but flow diverters (FD) have recently been widely used in the chronic phase of aneurysm treatment [3]. In this study, we talk about our experience treating a patient with a ruptured aneurysm in the middle cerebral artery (MCA) at non-branching locations. Based on the specific imaging findings and clinical course of the aneurysm, we describe its etiology and treatment.
The patient, a 58-year-old woman, was admitted to the hospital after experiencing a sudden headache and loss of consciousness. According to the Glasgow Coma Scale E3V4M5, she presented to the hospital with slurred consciousness but no neurological deficits. A subarachnoid hemorrhage (SAH) was seen on the head CT (Figure 1A), and a small 2-mm aneurysm was seen on the CT angiography (Figure 1B) of the right MCA. The aneurysm was saccular in shape and could have been an aneurysm at the bifurcation with a perforating branch, despite the fact that it was small and non-branching, indicating a dissecting lesion. As a result, assuming embolization, digital subtraction angiography (DSA) was carried out under general anesthesia. With a 2.8-mm maximum diameter aneurysm visible at the non-branching segment of the right M1 (Figures 1C, 1D), delayed contrast and congestion findings suggested a pseudoaneurysm with an irregular wall and a maximum diameter of 8 mm, which was suspected to have undergone a significant shape change in a short period of time. We guessed that the aneurysm was a pseudoaneurysm over the break site of the genuine aneurysm sac and chose to perform snaking just on the genuine aneurysm part to forestall rebleeding in the intense stage.
Endovascular procedure A trans-femoral approach was used to insert a 6 Fr guiding sheath catheter (Axcelguide, Medikit, Tokyo, Japan) into the right ICA; A microcatheter (Headway 17, MicroVention, Inc., Aliso Viejo, CA) was carefully positioned at the base of the aneurysm after a 3.4 Fr intermediate catheter (TACTICS, Technorat Corporation, Aichi, Japan) was directed to the ICA’s siphon. A SMART COIL complex extra soft 2.5 mm x 6 cm (Penumbra, Alameda, CA) that was smaller than the aneurysm’s true component was used for the first coil. SHOURYU HR 4-7 (Kaneka Medix, Osaka, Japan) was utilized to initiate balloon-assisted embolization (Figure 2A). However, embolization was difficult because the coil dynamics were distorted during the aneurysm sac framing, which was determined to be a true component; As a result, the coil was retrieved temporarily. Following that, the confirmatory imaging findings (Figure 2B) revealed that the aneurysm had completely vanished, necessitating the end of the treatment. Figure 2C shows that postoperative CT showed no evidence of an expanding hemorrhage.
Clinical course No antiplatelet therapy or fasudil was given to treat cerebral vasospasm during the acute phase. On day two, DSA revealed no aneurysm, while on day five, magnetic resonance angiography revealed a recurrence (Figure 3B). In addition, a larger aneurysm was detected by DSA on day 14 (Figure 3C), and high-flow bypass trapping was used on day 15.
Craniotomy procedure After the external carotid artery M2 was anastomized with a left radial artery graft, a right frontotemporal craniotomy was performed. The ICA bifurcation was temporarily blocked, and trapping was done after confirming the presence of perforating branches in the M1 segment both before and after the aneurysm neck in a flow reversal condition. From that point onward, the ICA was opened and the treatment was finished. Due to brain swelling and the pseudoaneurysm’s firmly attached position to the frontal lobe, it was extremely challenging to open the Sylvian fissure during the intraoperative procedure. Figure 4A shows that the pseudoaneurysm looked like a very fragile blood clot. The absence of branching at the aneurysm’s origin (Figures 4B-4D) suggests that it was a non-branching aneurysm.
Course of treatment following surgery The patient received a single antithrombotic medication the day after the procedure, and an MRI revealed no new signs of cerebral infarction. On day 14, there was no aneurysm and good patency of the bypass was observed in DSA (Figure 5A). Despite the absence of neurological deficits, the patient was admitted to the hospital with a Modified Rankin Scale score of 1 (rehabilitation for the impairment with long-term bed rest). One year after treatment, DSA revealed no aneurysm recurrence and excellent bypass patency (Figure 5B).
Conversation
This study introduced two significant discoveries. In the first place, what had all the earmarks of being a non-spreading saccular aneurysm in the M1 that was viewed as the reason for SAH might have been a pseudoaneurysm. Second, it has been demonstrated that trapping with high-flow bypass is the safest and most reliable treatment option.
DSA demonstrated that the aneurysm was not an obvious branching aneurysm but rather a continuous aneurysm with an irregular wall typical of a saccular aneurysm. Additionally, contrast delay and congestion were observed throughout the entire aneurysm, indicating that the pathophysiology was distinct from that of a normal saccular aneurysm [4]. Pseudoaneurysms, which arise from a minor tear in the internal elastic lamina, have been linked pathologically to non-branching aneurysms. In addition, it has been reported that half of the pseudoaneurysms found to be the cause of SAH and formed in the main artery for anterior circulation other than the ICA had normal vessel lacerations on imaging, indicating that the aneurysm itself was caused by a thrombus [1].
On the other hand, pathological findings and the formation of pseudoaneurysms at the saccular aneurysm’s rupture site rather than in the main artery wall have been reported in numerous studies. Despite the fact that the aneurysm was located at a non-branching site on CTA in our case, its sac-like morphology and lack of wall irregularity suggest that it could be mistaken for a typical saccular aneurysm. However, the DSA results suggested that the aneurysm was actually a pseudoaneurysm that had formed over the saccular aneurysm’s rupture site. As a result, we concluded that coil embolization was an option for treating the saccular component. In point of fact, embolization was extremely challenging, and it’s possible that some of the parts we thought were true saccular aneurysms were actually pseudoaneurysms created by a thrombus. The distorted motion of the framing coil into the component that we determined to be the true aneurysmal component can be inferred from the images, but it is difficult to determine the extent of the aneurysm’s rupture hole and the boundary with the pseudoaneurysm. Even though numerous studies have reported cases of aneurysms losing their visualization for a brief period of time due to various external factors [5], in our case, mechanical stimulation by temporary coil insertion and blood flow interruption with balloon assistance may have promoted the pseudoaneurysm’s rapid thrombosis. This is due to the fact that the entire aneurysm lost its visualization following coil retrieval. Due to the presence of intracranial hypertension and hematoma, it is difficult to determine whether it was a branching aneurysm on DSA imaging; however, the possibility that it was a branching aneurysm of the M1 segment perforating branch cannot be ruled out. In any case, the imaging findings and clinical course were one of a kind, so it was important to think about treatment options because the main cause might be a pseudoaneurysm, even though it might look like a saccular aneurysm.
For the pseudoaneurysm in our non-branching M1 segment, trapping with high-flow bypass was the safest and most reliable treatment option. Because their walls are made of very fragile thrombi and they bleed easily, pseudoaneurysms generally require more careful treatment [1]. Trapping with bypass has been regarded as the standard treatment for an aneurysm of the anterior wall of the ICA up until this point, and there has been no determination of an effective treatment strategy for pseudoaneurysms. Conventional neck clipping has been linked to a high rate of fatal rebleeding during the procedure [6]; endovascular coiling, on the other hand, has been linked to re-enlargement and rebleeding, resulting in insufficient prophylactic effect [7]. Both of these procedures are known to be risky procedures. Many studies in recent years have shown that FD has positive outcomes [8], but these studies are not currently available in Japan because insurance does not cover the acute stage. However, the same poor outcomes have been reported with conventional clipping and coiling for lesions in the proximal site of the MCA [9], so the treatment strategy for pseudoaneurysms other than ICA is dependent on the location of the aneurysm and the condition of the bleeding hole. The risk of perforating branch infarction occurring prior to and following M1 trapping as a complication should guide the choice of trapping with bypass in M1 lesions. Consequently, using a high-flow bypass to maintain blood flow in the perforating branch is essential to maximize retrograde blood flow. Coil embolization was our choice for the acute treatment of a suspected pseudoaneurysm, with early rebleeding prevention taking precedence over the possibility of recurrence. In the event of a recurrence, we made the decision to conduct re-treatment and conduct frequent postoperative examinations. The difficult and early abandonment of coil embolization into the thrombus’s pseudoaneurysm necessitated high-flow bypass trapping with favorable clinical outcomes. We believe that trapping with high-flow bypass may be the safer and more reliable procedure when the preoperative imaging results indicate a pseudoaneurysm of the M1 segment.
Conclusions The preoperative examination of SAH frequently reveals the presence of aneurysms at non-branching sites other than the ICA. Neurosurgeons should be aware, based on the findings of this study, that even a small cerebral aneurysm that appears to be a saccular aneurysm at non-branching M1 sites may actually be a very vulnerable pseudoaneurysm. We believe that the most effective treatment for pseudoaneurysms at MCA non-branching sites is high-flow bypass trapping. In the future, additional case reports on the condition will be necessary to establish the standard of care.
