Complex internal carotid artery (ICA) aneurysms include intracavernous, paraclinoid large/giant, dissecting and blood-blister aneurysms. Proximal parent artery occlusion (PAO) and trapping are long-practiced safe and effective option for these complex aneurysms.1 Trapping refers to both proximal and distal occlusion of parent artery including aneurysms, which is considered more reliable than proximal PAO due to without reverse flow. We hereby describe a rare case of subarachnoid hemorrhage (SAH) after trapping ICA to treat complex ICA aneurysms. The report was approved by the Ethics Committee of our institute and written informed consent was obtained from the patient.
A 21-year-old man presented initially to our hospital with diplopia, blepharoptosis in left and intractable left orbit pain for one month. Magnetic resonance imaging and cerebral angiography demonstrated a giant cavernous carotid aneurysm and a large paraclinoid aneurysm of the left ICA (Figure 1A). Balloon occlusion test (BOT) proved good tolerance and collateral flow.
One week later, the treatment was performed under general anesthesia. After completely coiling the paraclinoid aneurysm and its parent artery, the microcatheter was withdrawn to occlude the clinoid segment of the ICA. Because the portion of ICA was adjacent to the giant aneurysm, the microcatheter showed instability and the origin of ophthalmic artery was partially embolized. Then the petrous segment of ICA was occluded with two detachable balloons (Figure 1B). To put it simple, the paraclinoid aneurysm was treated by coiling the sac and its parent artery while the cavernous carotid aneurysm was treated by trapping. Two aneurysms were no longer visualized in bilateral common carotid and vertebral angiograms. No collateral flows especially retro-flow from the ophthalmic artery were visualized after trapping (Figure 1C).
The postoperative course was uneventful and orbital pain greatly released. Thirty hours after treatment, the patient suffered severe headaches and became comatose soon. CT demonstrated extensive SAH (Figure 1D and 1E). Cerebral angiography showed occlusion of the left ICA and the paraclinoid aneurysm, however, revascularization of the cavernous carotid aneurysm was seen by left external carotid artery (ECA) angiography (Figure 1F). After super-catheterizing the left internal maxillary artery with microcatheter, antegrade flow was seen from a small branch of the left internal maxillary to aneurysm and flowed out through the ophthalmic artery (Figure 1G). The small vessel was embolized with 0.8 ml Onyx, which was injected inside aneurysm till partial backflow into the feeding artery (Figure 1H). The patient discharged 29 days after the second treatment with no new neurological deficits. Six months follow-up showed obvious improvement of the diplopia and blepharoptosis. Follow-up angiography showed complete obliteration of the left ICA and complex aneurysms (Figure 1I).
Many endovascular approaches may be used to treat complex ICA aneurysms. We took into account different treatment possibilities while selecting the unique technique for the case. Stent assisted coiling technique is a relatively safe procedure; however we did not choose it due to a very high rate of recurrence for large and giant aneurysm. Total occlusion of the two aneurysms and parent artery with coil was another option; however the cost and the mass effect after embolization could be unacceptable. Flow diverter device may be an effective option; however it was not available in our market and the safety was not fully accepted.2 The fourth option, preferred in this case, was to treat the two aneurysms as one unit and exclude the lesion out of circulation by trapping. In order to evaluate the safety of trapping, both angiographic evaluation and clinical evaluation (including motor, sensitive language, and higher function testing) should be performed in a BOT. Occlusion is considered to be feasible when the delay between the venous drainage of the injected and the occluded hemisphere is less than 1.5 seconds. Balloon is inflated 30 minutes or less if angiographic results showed no delay of the circulation time. And all BOTs are performed under full heparinization. Because of the ophthalmic artery between the two aneurysms, occlusion should be done from the cavernous segment to clinoid segment of ICA to avoid collateral between ECA-ICA. Coil embolizing the paraclinoid aneurysm and the distal segment of ICA including the origin of the ophthalmic artery seemed relatively reliable. After balloon occlusion of the proximal ICA, the cavernous carotid aneurysm would decompress and shrink with diminished mass effect on the adjacent cranial nerve. We believed the option could treat the lesion thoroughly and not spend too much. Endovascular treatment is an easier and less invasive method for complex intracranial aneurysm, however, ligation by open surgery and combination with extracranial-intracranial bypass may be an alternative.
The disaster complication after trapping in our case raised questions over the reason of SAH. Because the origin of ophthalmic artery was partially embolized due to instability of microcatheter, we initially thought the ECA-ophthalmic artery-aneurysm collateral would be the reason. It was not shown in emergency angiography after SAH; however, revascularization of the cavernous carotid aneurysm was seen in ECA angiography. Micro-angiography testified a flow from a meningeal branch of internal maxillary artery to the cavernous carotid aneurysm. After circulation inside the aneurysm, the blood flowed out through the partially occluded ophthalmic artery. The angiographic findings suggested the underlying cause of the SAH was the collateral pathways: ECA-meningeal branch of internal maxillary artery-aneurysm cavity-the ophthalmic artery. In our case, the ophthalmic artery played a role of outflow tract instead of inflow tract. Furthermore, giant cavernous carotid aneurysms could cause SAH due to protruding into subarachnoid space, which has been reported by many authors.3
For giant aneurysms, revascularization with or without subsequent continued growth or rupture has been reported in the past; however, it mainly happened in posterior circulation.4 Some authors described cases of symptomatic enlargement of aneurysm after endovascular coiling and trapping. Their pathological research after resection of the lesions suggested that the role of vaso vasorum on the occluded parent artery should be considered. In our case, SAH occurred as a result of development of unusual intrinsic collateral pathways. Residual flow to the aneurysm may cause hemodynamic injury to the aneurysm wall, thus leading to rupture later. Besides the above reason, other factors, such as the congenitally weakened artery, vasculopathy in pediatric aneurysm or acute thrombosis, may contribute to the rupture.5
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