Use of Flow Diverters in Giant Intracranial Aneurysms and its Complications

Sir, Cerebral aneurysms are defined as giant when their diameter is ≥25 mm.[1] They represent 2%–5% of all intracranial aneurysms. They are found in all locations throughout the vasculature. In general, 34%–67% of giant intracranial aneurysms are associated with the internal carotid artery (ICA), 11%–40% with the anterior cerebral artery (ACA) and middle cerebral artery (MCA), and 13%–56% with the vertebral and basilar arteries.[2,3] The natural history of giant intracranial aneurysms is characterized by progressive growth, thrombosis, and rupture. Although giant intracranial aneurysms can be discovered incidentally, most patients develop signs and symptoms related to mass effects. Up to one-third may present with subarachnoid hemorrhage (SAH).[4] The risk of rupture (RR) of untreated, unruptured giant intracranial aneurysms (GIAs) is 8%–10% per year, with a 65%–100% mortality rate at one to five years of follow-up.[5] The treatment of ruptured or unruptured giant intracranial aneurysms is particularly challenging, with mortality rates in microsurgical clipping reported to be 6%–22%.[1,5] Endovascular approaches such as flow diverters have been used more recently as an emerging technique to treat these lesions with comparatively fewer mortality rates than microsurgery.[1] In spite of being a revolution in neurovascular surgery, there have been certain complications, both periprocedural and post-procedural. The overall complication rate is 17.0% and low mortality rate is 2.8%[6] We report a case of a GIA treated with the flow diverter and describe the treatment-related complication and its management. A 62-year-old female patient presented with complaints of intermittent headache for four months. She also had complaints of diplopia for the past four months. She was a known hypertensive for the past ten years on regular medications. Neurological examination revealed no abnormality and no extraocular deficits. Her computed tomography (CT) scan of the brain revealed hyperdense mass lesion in the right cavernous sinus [Figure 1a]. Her CT angiography of the brain axial view (b) and coronal view (c) revealed outpouching arising from the cavernous segment of right internal carotid artery suggestive of aneurysm.Figure 1: Computer tomography (CT) scan of the brain showing hyperdense mass lesion in the right cavernous sinus marked with yellow arrow (a). CT angiography of the brain axial view (b) and coronal view (c) showing outpouching arising from the cavernous segment of right internal carotid artery suggestive of aneurysm (marked with yellow arrow). Magnetic resonance imaging (MRI) of the brain showing about 19 × 19 × 12 mm size mass lesion in the right cavernous sinus, which is isointense on T1-weighted images (d), hyperintense on FLAIR images (e) and homogenously enhancing on intravenous gadolinium administration (f)Magnetic resonance imaging (MRI) of the brain revealed about a 19 × 19 × 12 mm size mass lesion in the right cavernous sinus, which was isointense on T1-weighted images [Figure 1d], hyperintense on fluid attenuated inversion recovery (FLAIR) images [Figure 1e] and homogenously enhancing on intravenous gadolinium administration [Figure 1f]. Her digital subtraction angiography (DSA) of the brain revealed two aneurysms: One was arising from cavernous segment of the right internal carotid artery of about 2.8 × 2.4 cm in size with 6-mm wide neck and another aneurysm of the right ophthalmic segment ICA of 4 × 2 mm in size with a 4-mm wide neck [Figure 2a-c]. The challenges in the procedure were the use of the flow diverter covering both the necks of the aneurysms and the deployment of the flow diverter in the complex tortuous anatomy of the cavernous segment of the ICA.Figure 2: Digital subtraction angiography (DSA) of the brain right ICA injection showing 2.4 × 2.8 cm size out pouching arising from the cavernous segment of right internal carotid artery (anteroposterior view) (a), lateral view (b), magnified lateral view (c) suggestive of giant cavernous carotid aneurysm. These images also revealed small outpouching arising from the ophthalmic segment. Lateral fluoroscopic image showing deployed flow diverter across the neck of the aneurysm with stagnation of contrast into the aneurysm (d). DSA lateral view showing hypodensity in the arterial wall suggestive of thrombosis (e, f). Post intravenous tirofiban infusion DSA anteroposterior (g) and lateral view (h) showing disappearance of thrombus and good distal flowThe patient received antiplatelet (aspirin 300 mg and clopidogrel 75 mg) medications for five days before the procedure. She underwent the procedure under general anesthesia. The right femoral artery was punctured, and an 8 French arterial short sheath was inserted. About 5000 units of heparin was given intravenously and target-activated clotting time of 250–300 was maintained throughout the procedure. Under road map guidance, 7 French neuron max was placed in the proximal right ICA and through which a 6 French navion catheter was placed in the distal internal carotid artery. Again, under roadmap guidance, a phenom microcatheter (Medtronic) advanced over 0.014 Chikai microwire (Asahi) and the lesion was crossed. A microwire was removed, and a pipeline flex shield (5 mm × 25 mm size) flow diverter (Medtronic) was placed across the neck of an aneurysm. The pipeline flex shield (Medtronic) did not get deployed at the proximal end. Multiple maneuvers were attempted, such as the advancement of a microcatheter, use of a distal intermediate catheter, and balloon dilatation, but there was no apposition against the vessel wall. So, the pipeline shield was re-sheathed and removed. Another pipeline shield device of 5 × 25 mm size was taken and successfully deployed across the neck of an aneurysm. Post-deployment run showed stagnation of the contrast material in the aneurysm with good distal flow. Also, complete wall opposition of flow diverter was confirmed [Figure 2d]. The total procedure time was around 210 minutes. While deploying the second pipeline shield device, a thrombus was noticed in the cavernous and ophthalmic segment of the ICA [Figure 2e and f]. Immediately, intravenous tirofiban 0.4 μg/kg bolus (glycoprotein IIb/IIIA [GP IIb/IIIa] Inhibitor) was given for over 30 min, and infusion was started at a rate of 0.1 μg/kg for over 12 hours. Post intravenous tirofiban injection, angiography run showed complete clearance of thrombus from the artery [Figure 2g and h]. The patient came out of anesthesia and became conscious. Her pupils were 3 mm bilaterally reacting to light with normal extraocular movements. However, she developed dense hemiplegia of the left side with hypotonia. So immediate check angiogram was done to rule out in-stent thrombosis, DSA revealed normal filling of the internal carotid artery and its branches with minimal filling in both the aneurysms. MRI brain was performed, which revealed watershed infarcts in the right frontal lobe [Figure 3a and b]. She was managed conservatively with tirofiban infusion (GP IIb/IIIa Inhibitors) for the next 12 hours. Her blood pressure was kept above 150/90 mmHg. She received oral tab aspirin of 150 mg and oral tab clopidogrel 75 mg from the next day onwards. Gradually her power on the left-sided limb improved. Within 48 hours, she regained lower limb power to grade 3/5 on the MRC (medical research council) scale. On the sixth day post procedure, the power was 4/5 in both left upper and lower limb but had a weak hand grip, and on the tenth day post procedure, power was 5/5 on the left side with a normal grip on the MRC scale. At six months follow-up, her follow-up DSA revealed complete disappearance of the aneurysms [Figure 4a and b] and she had no neurological deficit [Figure 4c].Figure 3: MRI brain diffusion weighted images showing restricted diffusion over the right frontal lobe suggestive of water shed infarct (a). Corresponding MRI brain ADC images (b)Figure 4: Follow-up DSA showing complete obliteration of the right cavernous carotid aneurysm anteroposterior view (a), lateral view (b). Clinical photograph of the patient showing good power over left-sided limbs (c)Flow diverters have revolutionized the treatment of morphologically complex wide-necked and giant intracranial aneurysms with minimal morbidity and mortality. These devices work by obstructing the blood flow from the vessel into the aneurysm and by providing a scaffold for endothelial cells to grow. These two actions isolate the aneurysm from the parent artery and eliminate the aneurysm-parent vessel interface. They also alter the flow dynamics both across and within the cerebral aneurysm, leading to thrombosis.[7,8] Multiple studies have been conducted on the use of pipeline embolization devices such as The Pipeline Embolization Device for the Intracranial Treatment of Aneurysms study (PITA study), which showed that the occlusion rate was 93% at six months.[9] Secondly, long-term results of the Buenos Aires Experience study with flow diversion showed 100% aneurysm occlusion.[10] Although flow diverters are extremely valuable in treating complex aneurysms, they carry a small yet significant risk of complications. The complications can be either periprocedural or post-procedural.[11] Periprocedural complications include thromboembolic or ischemic events, side branch occlusion, parent artery injury or rupture, incomplete expansion, and malposition or migration of flow diverting stents. Post-procedural complications include perianeurysmal edema, hemorrhage, aneurysmal rupture, and delayed parent vessel occlusion.[12] Management of thromboembolism in using a pipeline embolization device also includes its prevention. One needs to ensure preprocedural dual antiplatelet medications. Intra-procedural precautions include effective heparinization and the use of glycoprotein (GP) IIb/IIIa receptor antagonists. If a hyperacute or acute thrombus is seen intra-procedurally, intravenous antiplatelet medications, such as GP IIb/IIIa inhibitors, are a first-line approach. Conservative measures such as intravascular volume expansion and blood pressure augmentation are also used.[13,14] Cerebral watershed infarcts involve the borders of two non-anastomosing arterial systems. Pathogenesis usually involves either an embolic or hemodynamic mechanism. Symptoms vary from ipsilateral weakness to vision loss and seizures.[15] In our case, the patient developed left-sided hemiplegia, most probably due to thromboembolic complications that were definitively treated with tirofiban (GP IIb/IIIa receptor antagonists) and clopidogrel and aspirin, and the patient recovered power within ten days of the procedure. Flow diverters are a novel treatment option in managing giant intracranial aneurysms, reducing both morbidity and mortality, but it comes not without complications. Prolong procedure time can increase the risk of complications. Early detection of thrombosis and prompt treatment with GP IIb/IIIa inhibitors helps. Limited watershed infarct can bring rapid and good clinical recovery after appropriate treatment. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.