Anterior Communicating Artery Aneurysm: Large Aneurysm, Mass Effect, Deconstructive Techniques and Coiling, Occlusion, Mass Effect Relief and Excellent Evolution
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A large anterior communicating artery (AcomA) aneurysm was treated by deconstructive techniques and intrasaccular coil occlusion in two stages. A 57-year-old woman presented with a history of chronic headaches that had been substantially aggravated in the last three weeks with associated nausea, general discomfort, slow mentation, episodes of right eye amaurosis, and even confusion. Her admission neurological evaluation also strongly suggested that she suffered seizures, although this could not be shown definitively. CT followed by MRI confirmed the presence of a large-to-giant (23 mm) AcomA aneurysm with significant perilesional edema and associated mass effect. Diagnostic cerebral angiography confirmed that the aneurysm arose from a wide neck involving the right A1-A2 junction and preferentially filled through the right internal carotid artery (ICA). It was irregularly shaped and pointed to the left side. A midsized aneurysm of the right paraophthalmic ICA was also identified. A left ICA angiogram demonstrated the presence of a patent AcomA and spontaneous crossflow. In the first-stage intervention, the right distal A1 segment was deliberately and focally occluded with coils at a point in close proximity to the aneurysm’s origin. This arterial segment is usually devoid of perforating branches. In the second procedure, performed two weeks later, the remnant of the aneurysm was embolized through an approach via the left ICA and across the AcomA. Although the patient showed rapid clinical improvement and MRI showed resolution of the mass effect, she still experienced episodic right eye visual obscuration and felt unable to return to teaching. In a third intervention, performed three years later, a flow-diverter stent was implanted across the right paraophthalmic ICA aneurysm. The patient experienced a surprising disappearance of her visual problems. This case reaffirms the validity and efficacy of deconstructive techniques in the management of selected cases of AcomA aneurysms.
KeywordsAnterior communicating artery aneurysm Deconstructive techniques Flow diversion Large aneurysm Perianeurysmal edema
Fifty-seven-year-old, female, severe headaches, right amaurosis fugax, slow mentation, diplopia
The primary goal of treatment was to protect the aneurysm from what we believed was an unstable situation of impending rupture. In the first stage, we therefore proceeded deliberately to achieve a focal occlusion of the distal right A1 segment, immediately proximal to its entrance into the aneurysm. In this way, we controlled the direct and main supply of the aneurysm (proximal control) and preserved supply to the right A2 through the left-to-right AcomA crossflow. Special attention was given to try to occlude the A1 segment at the most distal normal point possible and with the shortest endovascular coil plug. Controlled hypotension and a dual microcatheter technique were required. In the second stage intervention, the aneurysm remnant was coiled with access via the left ICA and crossing the AcomA. Near-total occlusion of the aneurysm was achieved. When visual symptoms persisted, the right paraophthalmic ICA aneurysm was treated three years later in a third intervention by flow diverter implantation in a regular fashion.
Procedure #1, 30.07.2009: diagnostic cerebral angiography and deliberate endovascular occlusion of the distal right A1
Anesthesia: local anesthesia, converted to general anesthesia; bolus of 4000 IU heparin IV, target activated clotting time (ACT): 250–320 s
Access: right femoral artery; guiding sheath: 6F Arrowsheath (Terumo); guide catheter: 6F Envoy (Cordis); microcatheters: 2x Excelsior SL10 (Stryker) for coils; microguidewire: Transend 0.014″ (Stryker)
Implants: regular and soft coils (MicroVention)
Duration: 1st–21st DSA run: 156 min; fluoroscopy time: 37 min
Procedure #2, 15.08.2009: endovascular embolization of the AcomA aneurysm remnant via the left the ICA and crossing the AcomA
Anesthesia: general anesthesia, bolus of 4000 IU heparin IV, target ACT: 250–320 s
Premedication: 1 × 100 mg ASA PO daily, starting five days before the intervention
Access: right femoral artery; guiding sheath: 6F Arrowsheath (Terumo); guide catheter: 6F Envoy (Cordis); microcatheter: Excelsior SL10 (Stryker) for coils; microguidewire: Transend 0.014″ (Stryker)
Implants: regular 18 and 10 and soft coils (MicroVention)
Duration: 1st–9th DSA run: 85 min; fluoroscopy time: 41 min
Postmedication: Dexamethasone IV (8 mg every 8 h for three days)
Procedure #3, 30.07.2012: flow-diverter implant at the supraclinoid right ICA for treatment of the ophthalmic aneurysm
Anesthesia: general anesthesia, bolus of 4000 IU heparin IV, target ACT: 250–270 s
Premedication: 1 × 100 mg ASA PO daily and 1 × 75 mg clopidogrel PO daily started five days before the procedure. Verify Now: 154 PRU
Access: right femoral artery; guiding sheath: 6F Arrowsheath (Terumo); guide catheter: Navien A+ 0.058″ (Medtronic); microcatheter: Vasco (Balt Extrusion) for flow-diverter implantation; microguidewire: Transend 0.014″ (Stryker)
Implant: flow diverter: Silk 3.5 mm / 20 mm (Balt)
Duration: 1st – 6th DSA run: 46 min; fluoroscopy time: 19 min
Postmedication: 1 × 100 mg ASA PO daily and 1 × 75 mg clopidogrel PO daily for six months, 1 × 100 mg ASA PO daily was continued for life.
Procedure #1: Uneventful, the patient was discharged after six days. However, focal seizures developed two days after the first embolization procedure. Levetiracetam 500 mg BID, was initiated, achieving good seizure control.
Procedure # 2: The patient remained sedated and ventilated for 6 h, after which she was extubated and the introducer sheath was removed. She was discharged after four days to her home.
Procedure # 3: Uneventful, the patient was discharged home after four days.
Giant intracranial aneurysms, which comprise approximately 5% of all intracranial aneurysms in most clinical series, often pose difficult and unique problems in their surgical or endovascular treatment. Aneurysms are defined as giant when their maximum diameter exceeds 2.5 cm (Gonzalez et al. 2006). This limit was selected in an arbitrary fashion but is based in part on the increased rates of morbidity and mortality with lesions over this diameter. Thus, although the definition of giant rests on aneurysm’s size, it also implies higher morbidity and mortality, with particular difficulties in management. The International Study of Unruptured Intracranial Aneurysms investigators found that the 5-year cumulative rupture rate for giant (≥25 mm) anterior circulation aneurysms (ACA, AcomA, ICA, and MCA aneurysms) was 40% (Wiebers et al. 2003). The high risk of rupture and associated morbidity and mortality necessitate treatment in most patients. In addition to the risk of subarachnoid hemorrhage (SAH), giant intracranial aneurysms often present with symptoms of mass effect or cerebral ischemia.
Prevention of hemorrhage is the primary treatment objective to be achieved for giant intracranial aneurysms that extend into the intradural space; thus, early protection should be advocated for those lesions that present with SAH. Parent artery occlusion significantly reduces flow into a giant aneurysm, which may produce thrombosis and involution in some cases. This type of treatment can be performed only when there is adequate collateral flow in the territory supplied by branches of the parent artery, and when there are no significant collateral branches between the occlusion side and the giant aneurysm, in which case parent artery occlusion would not provide lasting protection from rebleeding (Gonzalez et al. 2006).
Our patient presented with a large-to-giant aneurysm that had become symptomatic, with severe headaches secondary to the aneurysm mass and associated secondary frontal edema. Despite the lack of hemorrhage, perianeurysmal edema is considered a predictive sign of aneurysmal rupture, indicating the need for early treatment. Some authors have raised the possibility that bleb formation and enlargement of a cerebral aneurysm might be associated with an inflammatory reaction of the aneurysm wall that results in perianeurysmal edema and subsequent aneurysmal rupture (Pahl et al. 2014).
This patient presented a unique opportunity for the use of deconstructive techniques. The aneurysm was located at the A1-A2 junction, both arterial segments were relatively well-preserved and not yet incorporated into the aneurysm structure, and the lesion was predominantly supplied by one ICA with a patent AcomA complex. Our strategy consisted of diverting flow from the aneurysm by occluding the distal right A1 segment, its main and direct arterial supply. Based on neuroanatomical studies (Rosner et al. 1984), the A1 segment gives rise to an average of 6.4 (range 1–11) arteries per hemisphere, and these are divided to yield 4–49 (average 21.9) vessels as they enter the anterior perforated substance. The majority (88%) of these branches arise from the proximal half of the A1 segment. This knowledge is most relevant when deciding where and how to proceed with deliberate occlusion of A1, suggesting that occlusion should be as distal and as short as possible. In our patient, the aneurysm sustained partial thrombosis after A1 occlusion and remained partially patent, with a more indirect supply through the left ICA. This artery was then used for definitive aneurysm coiling in a second procedure performed two weeks later.
The excellent clinical and neuroradiological evolution, as demonstrated in this case, confirms the efficacy of deconstructive techniques in the management of selected anterior circulation aneurysms.
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