| Endovascular Embolization of a de Novo True Posterior Communicating Artery Aneurysm 23 years After Surgical Clipping of an Ipsilateral Posterior Communicating Artery-internal Carotid Artery Aneurysm: A Case Report. |
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Park, Yung Ki , Chun, Hyoung Joon , Lee, Young Jun , Yi, Hyeong Joong |
1Department of Neurosurgery, Hanyang University Medical Center, Seoul, Korea. hjyi8499@hanyang.ac.kr
2Department of Neuroradiology, Hanyang University Medical Center, Seoul, Korea. |
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| Abstract |
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We describe a true posterior communicating artery (PCoA) aneurysm, which is an uncommon variant of intracranial aneurysm that was treated by endosaccular embolization. A 64-year-old woman was admitted for management of an unruptured left PCoA aneurysm. She had undergone microsurgical clipping of an ipsilateral internal carotid artery (ICA)-PCoA aneurysm 23 years prior to the current presentation. Angiography showed a saccular aneurysm 3 mm distal to the junction of the ICA and the fetal-type PCoA arising on the opposite side of the vessel to that of the previous clipping. Endovascular embolization was performed to occlude the lumen of the aneurysm while preserving the patency of the PCoA. Based on angiograms, hemodynamic stress seems to be the most feasible explanation for the de novo development of an aneurysm at the first acute bend within the PCoA in our patient. For this anatomical reason, endosaccular coil deployment was possible without the use of a balloon or stent. |
| Key Words:
Cerebral aneurysm, De novo, Endovascular embolization, Posterior communicating artery, True |
Introduction
A true posterior communicating artery (PCoA) aneurysm, arising from the PCoA several millimeters distal to the junction of the internal carotid artery (ICA) and PCoA and prior to incorporating into the posterior cerebral artery (PCA), is an uncommon variant amongst the aneurysms arising in the vicinity of the PCoA.13) In most instances, a so-called PCoA aneurysm is actually located at the junction of the ICA and the PCoA rather than in the PCoA proper. Thus, the incidence of a true PCoA aneurysm has not always been accurately reported, and the reported incidence has ranged from 0.1~2.8% of all intracranial aneurysms and it represents 4.6~11% of all the PCoA aneurysms.5)7)10)14)
In previous studies, angiograms have sometimes been insufficient to accurately identify such lesions during the preoperative period. As such, only operative exploration can render a precise diagnosis.6)13) With regard to the pathophysiology and treatment of true PCoA aneurysms, our current case has some peculiar features compared to the those of the previously reported cases; a de novo aneurysm developed and arose on the side of the ICA opposite to a previous clip placed 23 years previously and endosaccular embolization was successful while preserving the blood flow in the PCoA. We present here a brief case description and a review of the pertinent literature.
Case Report
A 64-year-old woman was referred to our department for treatment of an unruptured intracranial aneurysm. She had undergone microsurgical clipping of an unruptured ICA-PCoA aneurysm 23 years prior to the current presentation at another hospital. At that time, she had complained of left blepharoptosis and intractable, deep-seated headache. Although we could not retrieve the radiographic data related to the first aneurysm clipping, the operative notes described a large unruptured aneurysm (12x10mm) at the left ICA-PCoA junction and it projected in the posterolateral direction, along with a fetal-type PCoA. A left pterional approach was performed to obliterate the aneurysm with two straight metal Sugita clips (Fig. 1) and the patient had an uneventful postoperative course thereafter.
Upon presentation to our institution, the patient complained of headache radiating to the occipital region, intermittent tinnitus and blurred vision for the prior two months. On admission, she was alert and had a full range of higher cortical function without limb paralysis. The patient exhibited neither ptosis nor restricted eyeball movement and both pupils showed brisk light reflexes. Her past medical history included diabetes and hypothyroidism and for which medications had been provided for five years. Brain computed tomogram (CT) scans showed nonspecific postoperative changes with clip artifacts, and 3-dimensional (3-D) CT angiography showed an elongated aneurysmal dilatation (4x6mm) at the takeoff point of the left fetal-type PCoA distal and medial to the previous clip position (Fig. 2). This finding was initially believed to be aneurysm regrowth from a remnant of the clip implant, although the direction of the fundus was different from that of the previous aneurysm. On transfemoral catheter angiography, contrary to the initial speculation, the aneurysm was found to directly arise from the PCoA 3mm distal to the junction of the ICA and the PCoA (Fig. 3). Because of her medical co-morbidities and the potential hazards of an intracranial revision procedure, we selected endovascular embolization to occlude the aneurysm.
With the patient under general anesthesia and after routine preparation, the right femoral artery was punctured and a 6F shuttle catheter introducer (Cook, Bloomington, IN, USA) was advanced into the left cervical ICA. Systemic heparinization was then administered (3,000IU). Because of an apparently wide neck seen on imaging, either balloon remodeling or a stent-assisted technique was initially planned. However, traversing a microcatheter and a microguidewire into the distal PCoA toward the PCA failed due to an inner ridge between the aneurysm and the proper vascular lumen of the PCoA. We attempted to insert coils by a two-microcatheter technique, without the aid of a balloon or stent, using an Excelsior 10 microcatheter with a Synchro microguidewire (Boston Scientific, Miami, FL, USA) and an Echelon 14 microcatheter (Micro Therapeutics Inc., Irvine, CA, USA). The first coil (GDC 3D 4x8) formed an acceptable framework, and then three more coils (Axium Helix 2x8, 2 GDC US 2x4) were subsequently deployed. The final angiograms showed complete occlusion of the aneurysm while preserving patent PCoA flow (Fig. 4). The patient’s post-embolization CT scan was unremarkable, and she recovered well with immediate resolution of her tinnitus and blurred vision. The patient’s headache did not resolve until four months post-op. The one year post-embolization angiography showed a stable coil mass and patent blood flow in the PCoA flow (Fig. 5).
Discussion
Since the first clinical description of a true PCoA aneurysm by Poppen in 1950,10) only sporadic cases have been documented with respect to their surgical management. For several decades, there have been no established nomenclatures designating this subtype. Among the four types of so-called PCoA aneurysms in Krayenb?hl’s observations, only type b (fusiform aneurysms of the PCoA) and type c (saccular aneurysms of the PCoA) represent true PCoA aneurysms.5) Yoshida et al. first coined the term “true” PCoA aneurysm to describe an aneurysm originating directly from the PCoA approximately 2 to 3 mm distal to its junction with the ICA.14)
True PCoA aneurysms are infrequently reported as variants, however, their real prevalence is probably underestimated. If angiograms are not carefully assessed and particularly with 3-D reconstructions, then aneurysms in this region are easily confused with those arising from the ICA-PCoA junction. If microsurgical clipping is performed, then the exact location of the aneurysm may not be noted, that is, whether it is in the PCoA proper, because there is a specific intraoperative maxim for aneurysms in this region: do not retract the temporal lobe in order to prevent premature rupture.11) For this reason, most surgeons do not thoroughly dissect the temporal side of the ICA unless the ruptured aneurysm is secured. Once clipping is completed, the next step focuses on inspecting the anterior choroidal artery and surrounding perforating vessels as well as the oculomotor nerve. When unexpected bleeding is encountered from the presumed site of the aneurysm and this occurs despite satisfactory clip implantation, one should suspect a torn neck from an atherosclerotic ICA (neck avulsion), the presence of a dissecting or fusiform variant, extension of the aneurysm into the PCoA or a possible true PCoA aneurysm.
Efforts to identify true PCoA aneurysm variants are motivated by the difficulty of diagnosing and optimally obliterating such lesions. As stated above, angiograms are not always sensitive enough to identify true PCoA aneurysms and so the correct anatomical diagnosis can only be made at the time of exploration.6)13) When performing microsurgical clipping, clinicians must be extremely cautious not to injure the numerous perforating vessels arising directly from the PCoA, as well being cautious not to injure the oculomotor nerve when it is adherent to the aneurysm. When premature rupture occurs, temporary clipping should be attempted on at least two vessels, namely, the ICA and PCoA. If the fundus is directed laterally, then clinicians might encounter the rupture point first. Brain retraction and safe clipping should be scrupulously performed.1)9) In a previously reported meta-analyses of true PCoA aneurysms, most were saccular in nature, but the PCoA itself can be dilated, elongated or larger than normal.14) Accordingly, simultaneously obliterating the aneurysm without compromising the lumen of the PCoA is a prerequisite.
As for the pathophysiology of aneurysms arising from a non-branching arterial site, either hemodynamic stress or dissection can be a reasonable explanation. Several studies have suggested that disturbances of blood flow contribute to the formation of such true PCoA aneurysms when the vessel is acting as collateral circulation for the vertebrobasilar system, when the ipsilateral ICA is occluded or when subclavian steal occurs through an occluded contralateral subclavian artery.3)4)9) In each case, long-standing hemodynamic stress through the alternate vascular conduit is believed to result in endoluminal weakness and ultimately in aneurysm formation. When we consider that many reported aneurysms have a saccular shape and they are found 3~5mm distal to the ICA, dissection is not an appealing hypothesis for development of this particular subtype.13) Instead, some hemodynamic factors must exert their effects at the curvature of the PCoA within the carotid cistern, just before the PCoA enters the Liliequist membrane and the interpeduncular cistern.
The mechanism of the de novo aneurysm formation in the current case remains uncertain. Iatrogenic surgical trauma during the first clip placement is not a likely explanation given the long interim period of 23 years and the relative distance between the two with the fundi of the aneurysms pointing in different directions. The angiograms showed an abrupt upward curvature of the fetal-type PCoA proper at the site of the PCoA aneurysm and subsequent acute decline toward the PCA. This finding suggests that hemodynamic stress on the uppermost wall of the PCoA contributed to the formation of the aneurysm and its direction of growth with a resultant lack of cavernous sinus compression. The unidirectional hemodynamic hypothesis also explains the saccular nature of this type of aneurysm, and so this makes endosaccular embolization with detachable coil deployment the best treatment option.
Although ICA-PCoA recurrence, which was most commonly presented among the recurred aneurysms after clipping, is distinguished from the present case,12) the management for this has generally been performed with clip repositioning or placing an additional clip.2)8)12) Only one paper demonstrated that recurred ICA-PCoA aneurysm was managed with endovascular embolization.2) However, endovascular coiling was relatively easily performed in the present case because the aneurysm was not a recurrent aneurysm at the ICA-PCoA junction and instead it had newly developed distal to the primary clipping site. This case description has a major limitation in that we could not obtain the angiograms of the first operation because the first aneurysm was not clipped at our institution and most hospitals do not retain radiographic data beyond 10 years after acquisition according to their institutional guidelines. It may be possible that a true PCoA aneurysm was missed at the time of the ICA-PCoA aneurysm clipping as it is not easy to detect this type of aneurysm unless it reaches a certain size. However, this is difficult to determine as we were unable to examine the images obtained prior to and during the first procedure.
Conclusion
This case highlights the need to perform follow-up angiographic imaging in every patient following aneurysm clipping, and even in those with a long postoperative asymptomatic period. De novo aneurysms can develop at the unusual non-branching site of an enlarged PCoA proper, where blood flow causes significant stress on the acute angle of the vessel wall. In such situations, endosaccular coil embolization may be possible without the use of a balloon or stent.
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