Endovascular Embolization of Ruptured Infundibular Dilation of Posterior Communicating Artery: A Case Report

1. Introduction

ID of the PCo-A refers to funnel-shaped widenings with a diameter less than 3 mm at the junction of the posterior communicating artery and the internal carotid artery [1–3]. ID of the PCo-A was regarded as normal anatomical variants with a low risk of rupture [4]. However, with increasing reports of ruptured ID of the PCo-A, bleeding is also found to occur in cases of ID of the PCo-A. Aggressive treatment (i.e., surgical clipping) is preferred for most patients presenting with hemorrhage [2–6], but little is known about the endovascular treatment of this condition. We report a case of ruptured ID of the PCo-A successfully treated by endovascular embolization.

2. Case Presentation

A 35-year-old man was admitted with sudden onset of headache and vomiting. At admission, he was in relatively good condition. Hunt-Hess scale was grade III, and the GCS score was 13 at presentation. A CT scan of the head revealed SAH mainly in the right suprasellar cistern with a Fisher grade of 3 (Figure 1(a)). Dehydration therapy was performed immediately. Nine hours after the onset of symptoms, the patient lapsed into a coma; Hunt-Hess grade progressed to IV, and the GCS score deteriorated to 8. A repeated head CT examination revealed rebleeding, acute hydrocephalus, hematocele at bilateral posterior horns of the lateral ventricle, and a Fisher grade of 4 (Figure 1(b)). A CTA was performed together with a CT and revealed a conical expansion of the infundibulum at the origin of the right posterior communicating artery with a diameter of less than 3 mm. The thin right posterior communicating artery arose from the apex of the infundibulum. In addition, no aneurysm was noted in angiography (arrow in Figures 1(c) and 1(d)). DSA and 3-D reconstruction were then performed, and these findings were similar to those seen in the CTA (arrow in Figures 1(e), 1(f), and 1(g)). After these imagings, conservative treatments including dehydration therapy were administered to allow the reabsorption of SAH. Nimodipine was given for antivasospasm treatment. In the meantime, lumbar drainage was performed to drain bloody cerebrospinal fluid.

After 20 days of conservative treatment, the patient’s condition got better, and he could follow simple commands. A repeated head CT showed that SAH was reabsorbed, and the size of the ventricles became normal (Figure 1(h)). DSA was performed again and yielded the same result as the previous one (arrow in Figure 1(i)). Thus, ruptured ID of the PCo-A was diagnosed, and we planned to perform coil embolization. Because of the wide neck of the ID, stent-assisted occlusion was required. As a result, clopidogrel and aspirin were administrated orally for one week.

At day 27 after the bleed, endovascular coil embolization was performed under general anesthesia. The right femoral artery was punctured using the Seldinger technique to introduce a vascular sheath. Heparin was administered. Vertebral angiography with carotid compression was performed before vascular embolization so as to observe the blood supply to the posterior circulation of the ID of the PCo-A. The result showed that blood flow reversed into the internal carotid artery through the posterior communicating artery (Figures 2(a) and 2(b)). Subsequently, endovascular embolization of the ID of the PCo-A was conducted. After a suitable working angle was selected, a Neuroform3 stent (4.0 mm  ×  20 mm) was successfully released using an Echelon-14 microcatheter and Transend-300 microguidewire to completely cover the neck of the ID of the PCo-A. Subsequently, an Echelon-10 microcatheter was delivered into the ID of the PCo-A using Transend-300 microguidewire through the stent mesh. After angiography, a HydroCoil 10 coil (2 mm  ×  2 cm, MicroVention, Aliso Viejo, Calif) was released into the ID of the PCo-A. However, the coil was not detached due to the unfavorable location (Figure 2(c)). The left femoral artery was punctured for introduction of a vascular sheath, and then an Echelon-10 microcatheter was placed into the PCo-A ID using a Transend-300 microguidewire via the posterior communicating artery (Figure 2(d)). Four HydroCoil 10 coils were sequentially released (2 mm  ×  2 cm, 2 mm  ×  2 cm, 2 mm  ×1 cm, 2 mm  ×  1 cm) to fill the ID of the PCo-A (Figure 2(e)). No enhancement of the ID of the PCo-A was shown in the angiography of anterior or posterior circulation, and leakage of the contrast agent did not occur (Figures 2(f) and 2(g)). The coil placed in the internal carotid artery was detached (Figure 2(h)). After catheters and sheaths were removed, the procedure was completed.

Postoperative course was uneventful. The patient was treated with clopidogrel and aspirin. During a 1-year followup, the patient recovered well and could care for himself. His GOS score was 4, and SAH did not recur. The follow-up DSA showed no signs of ID of the PCo-A (Figures 3(a) and 3(b)).

3. Discussion

ID of the PCo-A is not a rare clinical entity. However, the prevalence of it on carotid angiography ranges from 5% to 17% [6–9] or even higher, as shown in other studies [10, 11]. The natural history of ID of the PCo-A remains unclear; it is generally recognized as an anatomical variant resulting from incomplete retrogression of vessels during embryonic development. ID of the PCo-A usually does not rupture or bleed [6, 8]. However, a number of studies have reported fatal SAH caused by ID of the PCo-A rupture or its progression to aneurysms [3, 4]. Hemorrhage due to the rupture of the ID of the PCo-A is surgically treated (i.e., surgical clipping) to prevent disastrous consequences due to rebleeding [5, 6, 8, 12–20]. In most IDs of the PCo-A, PCo-A is not well developed and has few perforating branches; so, the origin of the ID of the PCo-A is clipped in an orientation parallel to the internal carotid artery to prevent rebleeding [12–18].

However, in our patient, although the right PCo-A was underdeveloped, neurosurgical clipping treatment was not selected, and stent-assisted endovascular coil embolization was performed using a combined approach of anterior and posterior circulation. This approach was considered because we found that the ID of the PCo-A had a wide junction with the internal carotid artery, making full clipping quite difficult similar to wide-necked aneurysms [21]. Moreover, a previous study has shown that the bleeding points in the ruptured ID of the PCo-A were mostly located at the distal side of the ID, close to the internal carotid artery [22]. Under such circumstances, blood could still flow into the inside of the ID along the PCo-A even when the origin of the ID is clipped.

In the current study, enhancement of the PCo-A was not revealed in the DSA of posterior circulation, but it appeared in the angiography of the compressed internal carotid artery. Blood flowed reversely into the internal carotid artery (Figure 2(b)) indicating the possibility of rebleeding if the neck of the ID was clipped and the ruptured bleeding point was left untreated. However, clipping the bleeding points of the ID of the PCo-A might result in new bleeding sites near the previous ones, due to the continuous impact of blood flow; there is also the probability that the ID of the PCo-A will progress to an aneurysm [22, 23]. Therefore, at least 2 aneurysm clips are needed for isolation of the ID of the PCo-A in order to prevent rebleeding. It is difficult to place two aneurysm clips because of the narrow operating space around the posterior communicating artery. On the contrary, stent-assisted coil embolization by means of endovascular approach is relatively safe in comparison to neurosurgical clipping. Therefore, we preferred to perform endovascular treatment.

Although the patient experienced two SAH episodes in this study, the CTA on admission and first the DSA did not reveal the aneurysm but a conical expansion of the infundibulum at the origin of the right posterior communicating artery. At that time, ruptured ID of PCo-A could not be confirmed because profound SAH might have resulted in vasospasms that hide a very small aneurysm. In addition, the condition of the patient was critical. If we had attempted to treat the expansion of the infundibulum, disastrous result might have occurred or the aneurysm might have been missed. The better alternative was to wait until the blood was reabsorbed. After 20 days of conservative treatment, the repeated CT revealed reabsorption of blood along with an improvement in the condition of the patient. The DSA was performed and confirmed the diagnosis of ruptured ID of the PCo-A. Endovascular treatment lead to a good outcome. The follow-up DSA did not show the recurrence of ID of the PCo-A.

To date, no report on endovascular intervention treatment for ruptured ID of the PCo-A is available. We made an attempt to provide a new strategy for its treatment. While considering endovascular embolization for eligible patients with ID of the PCo-A, the following two factors need to be taken into account. First, the ipsilateral internal carotid artery needs to be compressed when conducting vertebral angiography so as to fully assess the hemodynamic status of the ID of the PCo-A. Therefore, rupture due to incomplete filling and blood supply from the posterior circulation can be prevented. Second, stent-assisted embolization is required because of the wide neck of the ID of the PCo-A. When full blocking is not possible through the internal carotid artery of the anterior circulation alone, it is preferable to carry out the blocking through the combined approach of anterior and posterior (via the posterior communicating artery) circulation.

4. Conclusion

Stent-assisted endovascular coil embolization through a combined approach of anterior and posterior circulation provides a new strategy for treatment of hemorrhage due to rupture of the ID of the PCo-A.