When performing stenting of intracranial arterial stenosis, safety first is an issue that needs to be considered and emphasized. Now, we summarize the literature and the occurrence of complications of intracranial artery stenting in our hospital in our clinical work, in order to minimize the complications and how to deal with them in a timely and effective manner, so as to accumulate experience for further clinical work. I. Embolic events Embolic events have been reported in the literature as one of the most common complications in endoprosthetics for symptomatic carotid stenosis. Mechanical cerebral protection measures developed in recent years, including balloon protection and internal carotid filter protection techniques, have led to effective resolution of embolic events during carotid stenting. The embolic events of internal carotid artery balloon angioplasty and endoprosthesis implantation performed without embolic protection techniques were 10%. With the embolic protection technique, embolic events decreased to less than 2%.Angelini et al. performed histologic examination of the contents of the umbrella collection applied during internal carotid artery stenting and showed a debris detection rate of 83.7%, with debris composed of thrombus-like material, foam cells, and cholesterol fragments. There was only one case due to acute myocardial infarction (3%) and no cerebrovascular events during the perioperative period of 30 days after the procedure. By analogy, intracranial atherosclerotic stenosis also has the potential for embolic events (0-8.3%). However, for intracranial arterial stenting, there are no proven distal protection devices due to the fine diameter of the target vessel lumen and the long, tortuous path. Therefore, skilled and delicate operation is required to minimize the occurrence of this complication. Vasospasm During intracranial stenting, the cerebral arterial vascular wall is easily spasmed by the mechanical stimulation of the catheter, guide wire and stent delivery device. Vasospasm causes distal hemodynamics to change into a low-flow state, leading to the occurrence of distal cerebral ischemic events. Nifedipine is effective in preventing cerebral vasospasm. In addition to nifedipine, nitroglycerin or opioid may be used. The latter two may increase the incidence of hyperperfusion syndrome, so their use needs to be excluded from pseudo vasospasm. Acute occlusion The literature suggests that the main complication of previous intracranial artery balloon angioplasty is acute occlusion, with an incidence of 10-20%, usually occurring 30 minutes after balloon angioplasty. Its occurrence is associated with endothelial injury, avulsion, platelet aggregation, thrombosis, and the presence or absence of effective intraprocedural anticoagulation. Endostentoplasty is effective in preventing acute occlusion due to endothelial avulsion. Rigorous and effective preoperative antiplatelet therapy and intraoperative anticoagulation can prevent acute occlusive events. Preoperative antiplatelet drugs include Aspirin, Ticlopidine, and Clopidogrel; abroad, the potent antiplatelet drug abciximab (a platelet glycoprotein IIb/IIIa receptor antagonist for intravenous use) is also used and is considered to be more effective than oral antiplatelet drugs. . Effective postoperative anticoagulation and antiplatelet aggregation should also be emphasized after intracranial stenting. After stenting, there are different degrees of vasospasm, and the superimposition of the two can easily cause rethrombosis in a short period of time. If intraoperative vasospasm is detected, slow intravascular pumping of opioid should be used promptly. Once acute occlusion occurs, the cause of occlusion should be targeted, rapid and reasonable treatment, such as acute thrombosis requires thrombolysis, endothelial detachment requires endoprosthesis, vasospasm requires active anti-spasmodic treatment. Four, penetrating blood vessel occlusion M1 segment of the middle cerebral artery, basilar artery issued important penetrating branch vessels such as bean artery, bridge artery, and so on. Relevant basic experiments have confirmed that after stent implantation in normal blood vessels, if the wire over the small arterial vascular openings, there is no obvious hemodynamic effect on the small arterial branches. Scanning electron microscopy of specimen stents shows that the surface of stent wires is covered by endothelium and shows degenerative changes. However, endovascular stenting of stenotic vessels with atherosclerotic lesions, especially when the stent is released from the expanding balloon, is highly susceptible to displacement or dislodgement of the lesional plaque into the deep perforating openings, resulting in occlusion of the deep perforating vessels. Once acute occlusion of the penetrating branch occurs in symptomatic intracranial arterial stenosis undergoing stenting, it is difficult to obtain effective treatment due to the small diameter of the lumen and poor compensation of the side branches, and therefore prevention of the occurrence should be the main focus. Intraoperative endovascular stenting with a diameter slightly smaller than that of the target vessel, the use of low-nominal pressure stents, and the emphasis on skillful and delicate surgical operation by the operator can theoretically reduce the occurrence of perforating vessel occlusion. However, for patients with perforating TIAs in stenotic segments, the risk of luminal infarction caused by stenting is very high. Therefore, it is necessary to strictly control the indications, and it is obvious that stenting is not suitable for those whose stenotic segments are caused by plaques that simply cause perforating TIAs, and it is necessary to weigh the advantages and disadvantages for those who have both perforating TIAs and distal perfusion malfunctions. V. Hyperperperfusion syndrome Hyperperperfusion syndrome, manifested by headache, seizures, cerebral edema, and in severe cases, cerebral parenchymal or subarachnoid hemorrhage can occur. It is difficult to save a patient once a severe cerebral or subarachnoid hemorrhage occurs. The incidence of cerebral hemorrhage due to hyperperfusion syndrome ranges from 1.2% to 4.4%, which is higher than the incidence of subarachnoid hemorrhage. According to the literature, the risk factors for hyperperfusion syndrome include: (1) failure to establish good side branches in the narrow blood supply area; (2) combined hypertension; (3) simultaneous use of multiple antiplatelet drugs and combined anticoagulation therapy have increased the risk of cerebral hemorrhage. In addition, the literature suggests that stenting of the middle cerebral artery is more prone to this complication than internal carotid artery stenoplasty. Hyperperperfusion syndrome can occur anywhere from a short time to 2 weeks after hemodialysis and is associated with a temporary loss of autoregulation of dilated vessels in areas of ischemia as a result of increased blood flow. The treatment of hyperperfusion syndrome focuses on prevention and prompt recognition and resuscitation. Since the hyperperfusion phenomenon appears before the symptoms, TCD can be applied to detect the hyperperfusion phenomenon in clinical work.Once TCD monitors that the blood flow rate of the target vessel is significantly higher than that of the preoperative and intraoperative period, timely and effective treatment should be carried out. Immediate postoperative CT scan should be regarded as a routine examination. Once bleeding is detected, heparin should be discontinued and neutralized with ichthyosin, antiplatelet drugs should be discontinued and haemostatic sensitization should be used, and cranial pressure-lowering drugs should be used reasonably according to the patient’s condition (nifedipine is usually used, and pepcidin is used if necessary), and blood pressure should be controlled to be less than 110/70 mm Hg. The perioperative use of vasodilators to downregulate blood pressure in the circulation and dilate blood vessels in non-ischemic areas of the brain in the perioperative period of stent implantation can help to minimize this complication. In addition, patients with high risk factors for hyperperfusion syndrome should be alerted preoperatively. VI. Intracranial hemorrhage, including cerebral hemorrhage and arachnoid hemorrhage, is a very dangerous complication with a high mortality rate. The causes include: (1) hyperperfusion syndrome; (2) perforation caused by guidewire; (3) perforation tear; (4) vessel rupture; (5) implantation of more than one stent in the same lesion obviously increases the chance of intracranial hemorrhage. Intracranial hemorrhage caused by intracranial stent implantation can also be attributed to the special anatomical and pathophysiological characteristics of cerebral blood vessels: (1) cerebral blood vessels enter the brain parenchyma before traveling in the subarachnoid space, when it enters the brain parenchyma due to the lack of arterial peritoneum, which is mainly replaced by the perivascular membrane of the extension of the arachnoid; (2) cerebral arteries are very circuitous in their travels. Therefore, when it is difficult to pass the catheter, guidewire or stent, repeated manipulation will definitely cause damage to the endothelium. In the present study, 2 stents were implanted at the same site in 5 patients, and intracranial hemorrhage occurred in 3 of them (2 cases of cerebral hemorrhage combined with subarachnoid hemorrhage and 1 case of subarachnoid hemorrhage). The operating principle of cerebrovascular stenting should be to minimize unnecessary repeated operations to reduce complications, and in our experience, the stent is released directly without pre-dilatation. The operator should pay attention to the following two points: first, the diameter of the stent should be slightly smaller than the diameter of the normal blood vessels; second, the stent should be slowly pressurized when releasing the stent, and the pressure should not reach the normal pressure of the stent at one time, so as to allow the blood vessels to have a process of adaptation to avoid rupture of the blood vessels. Therefore, the operator must be proficient in neurointervention, fine operation, and choose the best instrumentation to prevent bleeding complications caused by operation. The treatment is the same as above. VII. Clamping/intima-media tear In the past, the incidence of arterial clamping was high when intracranial stenotic lesions were treated with PTA alone.Connors divided PTA from 1989 to 1998 into three different periods according to the techniques used. In 8 cases of early treatment, 50% had intimal tears; in 12 cases of intermediate treatment, 75% had angiographically visible intimal tears; and in 50 cases of late treatment, 14% had intimal tears. The use of stents significantly reduced the incidence of PTA clips and intimal tears. The present study demonstrated a lower incidence of clips with stenting. The literature suggests that arterial stenting can cause endothelial tears at both ends of the stent if the diameter of the stent is selected too large during the procedure or if the intraoperative stent expansion pressure is too high, resulting in arterial entrapment. After the occurrence of entrapment or intimal tear during operation, a longer stent should be selected to fully cover the entrapment or torn intima when choosing a stent. Aneurysm There are few reports of aneurysm after stenting for symptomatic intracranial stenosis, and Levy et al. reported a case of asymptomatic pseudoaneurysm at the original stenting site 6 months after stenting of the basilar artery, which was not dealt with in the literature. Theoretically, re-intervention can be considered for postoperative aneurysms or pseudoaneurysms. Studies have proved that the following changes occur in peripheral arteries and coronary arteries after stent implantation: (1) early thrombus is formed within a few days, and it will become the attachment area for subsequent cell proliferation and intimal hyperplasia; (2) a thick layer of platelet-rich thrombus is formed along the wire; (3) inflammatory cells cover the surface of the lumen of the vessel and migrate to the thrombus; (4) smooth muscle cells migrate to the nascent intima and migrate into the new intima; (5) smooth muscle cells migrate to the new intima and migrate into the new intima; and (6) the stented arteries will be stented after stent implantation; and (7) the stented arteries will have the same effect as the original stented arteries. cells migrate toward and proliferate within the neointima. Throughout this process, the extent and rate of stent-induced intimal hyperplasia were directly related to the degree of early inflammatory cell aggregation. After stent implantation, the proliferation rate, proliferation timeframe, and monocyte aggregation were higher than those after balloon dilatation alone. Restenosis can also occur in the long term after intracranial stenting.In the SSYLVIA study, the incidence of in-stent restenosis greater than 50% was 32.4% (12/37) at 6-month follow-up after intracranial stenting. Statistically significant risk factors for restenosis include: (1) postoperative residual in-stent stenosis >30%, (2) small pre-treatment vessel diameters, and (3) comorbid diabetes mellitus. It has been hypothesized that subacute or late restenosis after intracranial stenting is related to intimal hyperplasia (cell proliferation) and vascular remodeling, but there is a lack of basic research to confirm this. Noninvasive tests are the first to be considered for assessing the degree of stenosis after stent implantation. Due to the limitations of stent materials, MRA cannot be used for post-stenting follow-up. However, it has been reported in the literature that although MRA is effective in the assessment of stenosis in intracranial stenotic lesions after simple balloon dilatation, not all stenoses can be detected and the measurement of stenosis is inaccurate, and the degree of stenosis after stenting by CTA is still under investigation, and the test is limited by stent metal artifacts. Because the incidence of restenosis of Mori B-type and C-type lesions at 3 months and 1 year after stenting is 33% and 100%, respectively, some scholars believe that follow-up imaging should be performed at 3 months after stenting. In our group, one patient developed symptomatic restenosis at 6 months after surgery, with 85% stenosis, and was re-stented, with no recurrence of symptoms since the follow-up. In conclusion, the possibility of invasive angiographic review requires a comprehensive assessment of the patient’s age, medical condition, and associated risk factors for angiography, and the advantages outweigh the disadvantages. At this time, if the stenosis is only imaging stenosis and no clinical symptoms, can continue to follow up the observation; if it is symptomatic stenosis, after a comprehensive assessment, can also be re-intervention if necessary. Vasovagal reflex During stenting of the anterior group arteries, the carotid pressure receptors are stimulated by the microcatheter, microguidewire, and balloon stent delivery system to the target vessel, resulting in bradycardia and a drop in blood pressure. Similar to carotid stenoplasty, atropine can be given depending on the patient’s heart rate and blood pressure. Those with severe hypotensive responses can be dilated and pressor-boosting medications can be used, but care should be taken not to elevate blood pressure too quickly or too high to avoid hyperperfusion syndromes. Temporary cardiac priming can be used in those with bradycardia that is not improved by atropine. XI, other complications Intracranial artery stenting, like other endovascular interventions, can also occur at the puncture point of local complications, including puncture site hematoma, femoral arteriovenous fistula, pseudoaneurysm and so on. Catheter tangling, kinking, and fracture can occur during catheterization. Intraoperative fine manipulation by the operator is the key to avoid these complications. In conclusion, endovascular stenting for symptomatic intracranial atherosclerotic stenosis is a high-risk interventional operation, and recognizing the above complications and further strengthening the related research can ensure better development of this work. 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