Postoperative rupture of an artery dissected from a cerebral aneurysm dome following clipping: A rare and fatal complication

Article information

J Cerebrovasc Endovasc Neurosurg. 2026;28(1):57-63

Publication date (electronic) : 2025 October 2

doi : https://doi.org/10.7461/jcen.2025.E2025.07.004

Jiwon Jung¹, Young Ha Kim^1,2,3, Pil Soo Kim^1,2,3, Jun Kyeung Ko^,1,2,3

¹Department of Neurosurgery, Pusan National University Hospital, Busan, Korea

²Biomedical Research Institute, Pusan National University Hospital, Busan, Korea

³School of Medicine, Pusan National University, Busan, Korea

Correspondence to Jun Kyeung Ko Department of Neurosurgery, Pusan National University Hospital, 179 Gudeok-ro, Seo-gu, Busan 49241, Korea Tel +82-51-240-7257 Fax +82-51-244-0282 E-mail redcheek09@naver.com

Received 2025 July 28; Revised 2025 September 1; Accepted 2025 September 13.

Abstract

INTRODUCTION

Surgical clipping remains a definitive treatment for cerebral aneurysms, particularly in cases involving multiple aneurysms. However, significant technical challenges arise when arteries are adherent to the aneurysm dome, a condition often attributed to inflammatory changes or chronic hemodynamic stress. Dissection of such vessels is occasionally necessary to achieve complete aneurysm obliteration but carries an inherent risk of arterial wall injury [3]. Although intraoperative bleeding may not be immediately evident, these subtle injuries can lead to delayed rupture, a rare yet devastating complication [5]. Here, we report a case of fatal delayed rupture of the M2 inferior division of the middle cerebral artery (MCA) following its dissection from an aneurysm dome during a clipping procedure. In accordance with our institutional policy, this case report was exempt from Institutional Review Board approval. Written informed consent for publication of clinical details and images was obtained from the patient’s legal surrogate, consistent with institutional and journal ethical standards.

CASE DESCRIPTION

A 67-year-old woman presented with three incidentally discovered unruptured intracranial aneurysms. Her initial treatment consisted of an uneventful coil embolization of a right posterior communicating artery (PCOM) aneurysm. Three months later, she was scheduled for surgical clipping of the two remaining aneurysms, located at the left anterior choroidal artery (AChA) and the bifurcation of the M2 superior division of the left MCA (Fig. 1). The prior coil embolization of the right PCOM aneurysm had been performed without stent assistance. The patient received clopidogrel monotherapy for two months post-procedure, after which antiplatelet therapy was discontinued. Consequently, no platelet function testing was performed before the clipping surgery. Preoperative laboratory tests, including platelet count and coagulation profile, were within normal limits. A left pterional approach was used to expose both aneurysms. Intraoperatively, an aneurysm was identified at the bifurcation of the M2 superior division of the left MCA. The M2 inferior division was densely adherent to the aneurysm dome, which limited visualization of the neck and posterior wall (Fig. 2). A fenestrated clip was initially applied in an attempt to preserve the adherent artery (Fig. 3). However, due to persistent poor visualization of the aneurysm neck, temporary clipping of the M1 segment became necessary. Careful dissection between the aneurysm and the M2 inferior division was then initiated using a diamond knife (Fig. 4). Temporary M1 occlusion was performed three times, with durations of 7, 8, and 4 minutes, respectively; during these periods, systolic blood pressure was maintained between 100 and 120 mmHg. After a tentative clip was placed, the dissection was completed, allowing for full visualization of the aneurysm neck, and a permanent clip was successfully applied. No reinforcement of the dissected arterial surface (e.g., with cotton, muscle wrapping, or hemostatic agents) was performed, as no vessel injury was apparent intraoperatively. The AChA aneurysm was subsequently clipped without difficulty. Intraoperative Doppler ultrasonography and indocyanine green (ICG) angiography confirmed satisfactory flow in all parent and branching arteries. Following permanent clipping of both aneurysms, meticulous hemostasis was achieved, dural and soft tissue closure proceeded in a routine fashion. Throughout the final stages of surgery, intraoperative neuromonitoring signals remained stable, there was no evidence of brain swelling, and all vital signs were within normal limits. No abnormal events suggestive of intraoperative bleeding or impending rupture were observed prior to anesthesia reversal. However, the patient failed to regain consciousness following anesthesia reversal and remained intubated. Approximately 40 minutes after the conclusion of the surgery, brain computed tomography scan revealed diffuse, thick subarachnoid hemorrhage throughout the basal cisterns and sulci (Fig. 5). A digital subtraction angiography, performed 1.5 hours postoperatively, confirmed active contrast leakage from the dissected segment of the M2 inferior division (Fig. 6). Although urgent reoperation was recommended, the family declined further intervention. The patient’s condition progressed to brain death, and she expired a few days later. A retrospective review of the surgical video revealed a remnant of arterial wall tissue—likely comprising the adventitia and a portion of media from the M2 inferior division—still attached to the aneurysm dome (Fig. 7). This finding suggested that the dissection plane may have violated the true vessel wall, leaving only a fragile tunica intima and a partial remnant of the tunica media to contain luminal pressure. It is hypothesized that this weakened vessel wall subsequently ruptured due to a transient elevation in blood pressure during anesthetic reversal.

Fig. 1.

Three-dimensional rotational angiography images of the left internal carotid artery: anteroposterior (A) and lateral (B) views. The images are reconstructed from digital subtraction angiography. Arrows indicate the aneurysm located at the bifurcation of the M2 superior division; arrowheads indicate the anterior choroidal artery aneurysm. A portion of the M2 inferior division is seen abutting the dome of the M2 superior division aneurysm.

Fig. 2.

Intraoperative microscopic view. The M2 inferior division is shown densely adherent to the dome of the M2 superior division aneurysm. An, aneurysm; br, branch; prox, proximal; Inf, inferior; Sup, superior.

Fig. 3.

A fenestrated clip is initially applied while leaving the adherent M2 inferior division intact.

Fig. 4.

Careful dissection of the M2 inferior division from the aneurysm dome using a diamond knife. An, aneurysm; Inf, inferior.

Fig. 5.

Postoperative brain computed tomography showing diffuse, thick subarachnoid hemorrhage involving the basal cisterns and sulci.

Fig. 6.

Postoperative digital subtraction angiography demonstrating diffuse vasospasm and active contrast leakage (arrowhead) from the M2 inferior division at the site of prior dissection (arrow).

Fig. 7.

During dissection with a tentative clip applied to the aneurysm neck. The arrows indicate a remnant of arterial wall tissue from the M2 inferior division attached to the aneurysm dome.

DISCUSSION

This case represents a rare but highly instructive example of delayed rupture of a dissected artery that was adherent to a cerebral aneurysm. Adhesion between aneurysms and adjacent vessels is a relatively common finding, particularly in bifurcation-type aneurysms. While complete aneurysm obliteration often necessitates the dissection of these arteries, the process carries an inherent risk of vessel wall injury [5]. In our case, the dissection was performed meticulously under temporary clipping and appeared successful, with no visible intraoperative bleeding. However, dissection can inadvertently damage the adventitia and a portion of the media, leaving only the thin tunica intima and a partial remnant of the tunica media intact. This compromised structure may initially prevent hemorrhage but renders the vessel wall fragile and susceptible to postoperative rupture under fluctuating hemodynamic stress. Although postoperative inflammation and protease activity have been implicated in delayed arterial wall rupture, these biological processes typically unfold over several days [4]. In contrast, the present case involved an immediate postoperative event, most likely precipitated by the combination of mechanical weakening from the dissection and transient hypertension during anesthetic reversal.

A critical lesson from this case is the paramount importance of inspecting the dissected arterial surface with a high index of suspicion for subtle injuries. Even in the absence of active bleeding, any visible abnormality—such as thinning, discoloration, or tissue loss—should prompt the surgeon to consider reinforcement techniques. These may include the application of hemostatic agents, wrapping with autologous muscle or synthetic material, or, in extreme cases, performing a vascular bypass. Furthermore, it is crucial to recognize that intraoperative tools like ICG and Doppler ultrasonography cannot detect all forms of arterial wall injury, especially non-transmural damage. Consequently, direct, magnified visual inspection remains an indispensable step. Our hypothesis is that the arterial wall was dissected beyond the correct anatomical plane, leading to a delamination of the adventitia and media layers. The resulting structural weakness likely culminated in a rupture under the stress of transient hypertension during anesthetic reversal. This mechanism, though rare, is plausible and must be considered in similar surgical scenarios.

From an anatomical and structural perspective, cerebral arteries differ significantly from systemic arteries. They possess a thinner tunica media and adventitia and, critically, lack an external elastic lamina, which makes them more vulnerable to mechanical manipulation and pressure fluctuations [7]. These intrinsic features may predispose cerebral vessels to injury during dissection, especially when they are inflamed or pathologically adherent to aneurysmal walls. In contrast, extracranial arteries are generally more robust and elastic, affording them greater resistance to surgical stress. In reviewing the operative video, we noted a remnant of arterial wall attached to the aneurysm dome, which we interpreted as adventitia and part of the media from the inferior M2 division. We acknowledge that the tunica intima alone is incapable of withstanding physiological intraluminal pressure, as its structural integrity depends primarily on the tunica media’s smooth muscle and elastic components. Therefore, the intraoperative finding likely represented a partial remnant of the tunica media with its overlying adventitia, while a fragile, residual intima was left covering the arterial lumen. This thin residual layer may have provided transient resistance to pressure but ultimately failed during the hemodynamic shifts of anesthetic reversal, leading to catastrophic rupture [6,8].

The choice of technique and instrumentation is crucial when dissecting vessels adherent to aneurysm domes. Sharp dissection, performed with microsurgical scissors or a diamond knife under high magnification, offers superior control compared to blunt dissection, which can cause avulsion or traction injuries. Sharp dissection is generally preferred when the adhesions are dense, fibrotic, or involve the aneurysm neck, where precise separation of tissue planes is essential. It is also indicated when the surgeon anticipates that blunt maneuvers could transmit excessive force to the fragile aneurysm wall or the adherent artery. Conversely, blunt dissection using fine suction tips, micro-dissectors, or bipolar forceps may be appropriate for loose, filmy, or primarily arachnoid adhesion, where atraumatic separation is feasible. In many cases, a hybrid approach is optimal, beginning with gentle blunt spreading to identify a plane, followed by sharp cutting of residual fibrous bands. Recognizing when to use each technique is critical, as an indiscriminate approach increases the risk of vessel injury. Key adjunctive strategies include the use of specialized micro-instruments, maintaining a clear surgical field with controlled irrigation, and utilizing temporary clipping to reduce arterial tension [1,2]. A thorough understanding of microsurgical anatomy is fundamental. Importantly, the surgeon must be prepared to abandon dissection if the risk is deemed too high, opting instead for modified clipping strategies (e.g., fenestrated clips) or, in select cases, bypass procedures. This is particularly true when critical perforators are involved, where aggressive dissection can lead to infarction or rupture [3]. Typically, the primary concern during dissection of an adherent artery is iatrogenic rupture of the aneurysm itself. However, once the aneurysm is securely clipped, this risk is eliminated, but the dissected normal artery remains vulnerable to delayed rupture. In particularly challenging cases where the artery is inseparable from the sac, a useful, albeit technically demanding, strategy is to resect the aneurysm along with the adherent portion of the branch wall and apply the clip en bloc. This may be safer than attempting to peel a fragile artery off the aneurysm. Furthermore, after a difficult dissection, it may be prudent to delay dural closure. Instead, the surgeon can perform a “challenge test” by transiently raising the patient’s blood pressure or simply observing the operative field for a period to unmask any occult bleeding from a compromised vessel. Such precautionary steps, while time-consuming, could prevent a catastrophic postoperative rupture.

Following the postoperative computed tomography and digital subtraction angiography findings, which revealed contrast leakage from the inferior M2 division, urgent reoperation was recommended. Although endovascular vessel occlusion was theoretical option, microsurgical re-operation was considered the preferred initial strategy. This approach was favored because the affected vessel was a cortical branch, and direct repair or bypass options could be explored if necessary. Endovascular occlusion, while technically feasible, would have resulted in a definite territorial infarction without the possibility of direct revascularization. These options were discussed with the patient’s family, who ultimately declined further intervention. We acknowledge that a comprehensive discussion of both surgical and endovascular strategies is essential. In retrospect, while carrying a high risk of stroke, emergent endovascular parent vessel occlusion might have offered a chance for survival.

This case underscores that for aneurysms with adherent vessels, the decision to dissect must be carefully weighed against the risk of iatrogenic vessel injury. When dissection is deemed necessary, meticulous technique and a high index of suspicion for microscopic damage are essential. Any potentially damaged vessel wall must be thoroughly inspected and, if necessary, reinforced intraoperatively to prevent fatal delayed rupture. While iatrogenic intracranial vessel injuries leading to pseudoaneurysm formation have been reported in other neurosurgical contexts, such as tumor resections, this case is distinct. The injury occurred during aneurysm clipping, specifically involving a branch artery pathologically adherent to the aneurysm dome. Unlike tumor surgery, where the primary goal is tumor removal while preserving vasculature, aneurysm clipping requires definitive exclusion of the sac, often necessitating direct and forceful manipulation of adherent vessels. This combination of aneurysm wall fragility, pathological adhesion, and the necessity of dissection creates a unique risk profile. Although recommendations for careful inspection and reinforcement are well-established, this case provides unique value by presenting definitive angiographic evidence of active rupture at the precise site of dissection. To our knowledge, an immediate postoperative rupture, directly and angiographically attributable to branch dissection during clipping, has not been previously documented in this manner. This case, therefore, highlights a specific and critical pitfall in aneurysm surgery: an adherent branch artery may pose a greater post-clipping risk of rupture than the aneurysm itself. Surgeons must remain vigilant for this complication and consider proactive reinforcement or observation strategies, even when intraoperative hemostasis appears perfect.

CONCLUSIONS

Arteries adherent to aneurysm domes pose significant challenges during clipping. Even when hemostasis is achieved and intraoperative monitoring is stable, subtle dissection-related injuries may precipitate postoperative rupture. Surgeons should consider reinforcement or prolonged observation when arterial wall integrity is uncertain. This case underscores the importance of heightened vigilance to prevent rupture immediately after clipping.

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