基底动脉血栓闭塞治疗理念(201208)

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急性基底动脉闭塞的治疗进展_犹登霞

急性基底动脉闭塞的治疗进展犹登霞，陈阳美作者单位400010 重庆重庆医科大学附属第二医院通信作者陈阳美chenym1977@ 【摘要】基底动脉闭塞病情重，致死率和致残率高，静脉溶栓、动脉溶栓治疗和机械取栓治疗是目前最常见的治疗方法。

与静脉溶栓相比，动脉溶栓或机械取栓治疗血管再通率较高，且时间窗较静脉溶栓治疗宽，但目前的研究并未证实动脉溶栓或机械取栓治疗优于静脉溶栓治疗。

桥接治疗是结合静脉溶栓与动脉溶栓或机械取栓的具有发展前景的一种治疗新模式，但其有效性还需要进一步证实。

本文将对急性基底动脉闭塞相关的治疗方法：静脉溶栓、动脉溶栓、机械取栓治疗等做一综述，以促进对急性基底动脉闭塞血管再通治疗的认识。

【关键词】基底动脉闭塞；溶栓；机械取栓；桥接治疗Progress in Treatment of Acute Basilar Artery Occlusion YOU Deng-Xia, CHEN Yang-Mei. The Second Afﬁ liated Hospital of Chongqing Medical University, Chongqing 400010, ChinaCorresponding Author:CHEN Yang-Mei, E-mail:chenym1977@【Abstract】 Acute basilar artery occlusion (BAO) is a devastating neurological condition with a high rate of fatality and disability. Compared with intravenous thrombolysis (IVT), the recanalization of intraarterial thrombolysis (IAT) or mechanical thrombectomy is higher and the thrombolysis treatment time is longer, but it is not confirmed in reported researches that IAT or mechanical thrombectomy is better than IVT. The bridging therapy which combines IVT with IAT or mechanical thrombectomy therapy is a new treatment mode, but its effectiveness needs to be conﬁ rmed. We reviewed the different thrombolysis therapies to further understand the treatment progress of BAO which include IVT, IAT, mechanical thrombectomy and so on.【Key Words】 Basilar occlusion; Thrombolysis; Mechanical thrombectomy; Bridging therapy 基底动脉闭塞（basilar artery occlusion，BAO）约占所有缺血性卒中的1%[1]。

基底动脉闭塞综合征

基底动脉闭塞综合征基底动脉闭塞（BAO）是一种潜在的致命性神经系统疾病，临床医生诊断和治疗该病面临很大挑战，其约占所有缺血性卒中的 1%-4%。

近期，The Neurohospitalist 杂志发表了一篇由美国学者 Demel 等撰写的综述，详细介绍了 BAO 的临床表现、病因以及目前的治疗策略。

后循环解剖后循环负责大脑后部的血供，包括脑干、丘脑、小脑以及枕叶。

双侧椎动脉从锁骨下动脉发出，并且在脑桥延髓连接处汇总形成基底动脉（BA）。

BA 可以分为三段：近段、中段和远段。

基底动脉最远端发出双侧大脑后动脉（PCA），供应枕叶、颞叶下部；通过较大的动脉分支供应颞叶内侧，通过穿支动脉供应丘脑和中脑上部。

BA 其他重要分支还包括小脑上动脉（SCA）、小脑前下动脉以及脑桥穿支动脉。

基底动脉闭塞综合征与前循环卒中相比，后循环卒中前驱期更长，可持续数天或数月。

最常见的前驱期症状包括眩晕和恶心，其次为头痛和颈部疼痛。

头晕和眩晕是 BAO 最常见的早期症状，但是为非特异性症状，需要与外周性眩晕相鉴别。

头脉冲-眼震-扭转偏斜（HINTS）检查法是一种敏感的评估工具，有助于鉴别中枢性和外周性眩晕。

ABCD2 评分也可以帮助明确较高危患者，评分 > 6 分或 7 分的眩晕患者其诊断为卒中的可能性约为 27%，该评分越低，卒中可能性越小。

伴有至少一项其他神经系统症状的眩晕患者比孤立性眩晕患者更可能诊断为卒中。

眼动麻痹、口咽功能障碍、共济失调以及肢体力弱是最常见的症状。

其他症状还包括眼动异常、瞳孔不对称、呼吸紊乱、辨距不良以及意识水平改变。

患者症状严重程度不一，从孤立性颅神经麻痹到四肢瘫痪、闭锁综合征甚至是昏迷。

BAO 最致命的表现之一是基底动脉中段闭塞，导致双侧脑桥缺血；这些患者表现为意识完全清醒的昏迷状，四肢瘫痪，仅保留垂直性眼球运动。

这种闭锁综合征在急性期死亡率约为 75%。

BA 远端尖部闭塞可导致另外一种严重的综合征，因为 SCA 和 PCA 均是从这个部位发出，这种基底动脉尖综合征可能导致中脑、丘脑、颞叶下部以及枕叶缺血。

氯吡格雷联合阿司匹林治疗严重基底动脉狭窄或闭塞的疗效

高危情况，患者功能预后差，病死率、复发率高。对此类患者尽早诊断并开始有效的一级及二级预防，防止卒中的发生和复发，有重要的临床意义。过去的研究证明对非心源性脑卒中患者进行双联抗血小板治疗不能获益，但是此类研究并未根据脑血管病变的严重程度进行分类研究［３］。笔者对基底动脉严重狭窄或闭塞的后循环缺血性卒中患者进行阿司匹林加氯比格雷与氯比格雷的对照研究．现报告如下。１资料与方法１．１入组标准发病ｌ５～３０ｄ后循环缺血性卒中病情稳定的患者；年龄４０～８０岁；修正Ｒａｎｋｉｎ
面 ±ｓ
表１两组患者基本资料比较
１．３治疗方案治疗组给予氯吡格雷７５ｍｇ，阿司匹林１００ｍｇ，治疗３个月后改为氯吡格雷７５ｍｇ治疗。对照组给予氯吡格雷７５ｍｇ治疗。两组均按照胆固醇教育 Ⅲ给予阿托伐他汀２Ｏｍｇ治疗。两组治疗观察期１２个月。治疗过程中如出现消化道出血等出血疾患则中止观察药物．并给予相应的
对症治疗。
ｄｏｉ：１０．３９６９／ｊ．ｉｓｓｎ．１００６ — ５７２５．２０１３．０３．０５０
１．４评估方法对所有患者记录ＥＳＳＥＮ评分、ＮＩＨＳＳ评分：临床随访在观察期内是否发生缺血性脑卒中或ＴＩＡ，是否出现消化道出血（大便潜血）或脑出血１．５统计学方法计数资料比较时采用ｘ：检验，计量资料比较时采用ｔ检验。所有的统计分析采用ＳＰＳＳ１８．０统计软件分析。

最新研究：基底动脉闭塞,选择动脉溶栓还是静脉溶栓：BASICS研究

Treatment and outcomes of acute basilar artery occlusion in the Basilar Artery International Cooperation Study (BASICS): a prospective registry studyWouter J Schonewille, Christine A C Wijman, Patrik Michel, Christina M Rueckert, Christian Weimar, Heinrich P Mattle, Stefan T Engelter, David Tanne, Keith W Muir, Carlos A Molina, Vincent Thijs, Heinrich Audebert, Thomas Pfeﬀ erkorn, Kristina Szabo, Perttu J Lindsberg, Gabriel de Freitas, L Jaap Kappelle, Ale Algra, on behalf of the BASICS study group*SummaryBackground Treatment strategies for acute basilar artery occlusion (BAO) are based on case series and data that have been extrapolated from stroke intervention trials in other cerebrovascular territories, and information on the eﬃ cacy of diﬀ erent treatments in unselected patients with BAO is scarce. We therefore assessed outcomes and diﬀ erences in treatment response after BAO.Methods T he Basilar Artery International Cooperation Study (BASICS) is a prospective, observational registry of consecutive patients who presented with an acute symptomatic and radiologically conﬁ rmed BAO between November 1, 2002, and October 1, 2007. Stroke severity at time of treatment was dichotomised as severe (coma, locked-in state, or tetraplegia) or mild to moderate (any deﬁ cit that was less than severe). Outcome was assessed at 1 month. Poor outcome was deﬁ ned as a modiﬁ ed Rankin scale score of 4 or 5, or death. Patients were divided into three groups according to the treatment they received: antithrombotic treatment only (AT ), which comprised antiplatelet drugs or systemic anticoagulation; primary intravenous thrombolysis (IVT ), including subsequent intra-arterial thrombolysis; or intra-arterial therapy (IAT), which comprised thrombolysis, mechanical thrombectomy, stenting, or a combination of these approaches. Risk ratios (RR) for treatment eﬀ ects were adjusted for age, the severity of neurological deﬁ cits at the time of treatment, time to treatment, prodromal minor stroke, location of the occlusion, and diabetes.Findings 619 patients were entered in the registry. 27 patients were excluded from the analyses because they did not receive AT, IVT, or IAT, and all had a poor outcome. Of the 592 patients who were analysed, 183 were treated with only AT, 121 with IVT, and 288 with IAT. Overall, 402 (68%) of the analysed patients had a poor outcome. No statistically signiﬁ cant superiority was found for any treatment strategy. Compared with outcome after AT , patients with a mild-to-moderate deﬁ cit (n=245) had about the same risk of poor outcome after IVT (adjusted RR 0·94, 95% CI 0·60–1·45) or after IAT (adjusted RR 1·29, 0·97–1·72) but had a worse outcome after IAT compared with IVT (adjusted RR 1·49, 1·00–2·23). Compared with AT, patients with a severe deﬁ cit (n=347) had a lower risk of poor outcome after IVT (adjusted RR 0·88, 0·76–1·01) or IAT (adjusted RR 0·94, 0·86–1·02), whereas outcomes were similar after treatment with IAT or IVT (adjusted RR 1·06, 0·91–1·22).Interpretation Most patients in the BASICS registry received IAT. Our results do not support unequivocal superiority of IAT over IVT, and the eﬃ cacy of IAT versus IVT in patients with an acute BAO needs to be assessed in a randomised controlled trial.Funding Department of Neurology, University Medical Center Utrecht.IntroductionStroke is the leading cause of disability in developed countries.1 Posterior circulation stroke accounts for about 20% of all ischaemic strokes. The basilar artery, which is the main vessel of the posterior circulation, supplies most of the brainstem and occipital lobes and part of the cerebellum and thalami. Owing to diﬀ erent degrees of involvement of the brainstem, patients with acute basilar artery occlusion (BAO) can present with symptoms that vary from isolated cranial nerve palsies or hemiplegia to the locked-in state or coma. Despite recent advances in the treatment of acute stroke, the rate of death or disability associated with BAO is almost 80%.2–4Randomised trials have shown the safety and eﬃ cacy of intravenous thrombolysis (IVT) given within 4·5 h of the onset of the symptoms of acute ischaemic stroke and intra-arterial thrombolysis given within 6 h.5–10 Un-fortunately, the results of these randomised acute stroke trials do not directly apply to patients with an acute BAO because only few, if any, of these patients were included. BAO has not been studied in isolation in randomised clinical trials because of its low incidence: only about 5% of all patients who have thrombolysis for stroke have BAO.4,11 We are aware of only one randomised trial of treatment in patients with an acute BAO, which was terminated prematurely because of poor recruitment.12 Case series of patients with BAO found the outcomes of patients treatedLancet Neurol 2009; 8: 724–30Published OnlineJuly 6, 2009DOI:10.1016/S1474-4422(09)70173-5See Reﬂ ection and Reactionpage 695*BASICS study group memberslisted at end of report.Department of Neurology, University Medical Center Utrecht and Rudolf Magnus Institute of Neurosciences,Netherlands(W J Schonewille MD,L J Kappelle MD, A Algra MD); Department of Neurology,St Antonius Hospital, Nieuwegein, Netherlands (W J Schonewille); Stanford Stroke Center, Palo Alto, CA, USA (C A C Wijman MD); CentreHospitalier UniversitaireVaudois, Lausanne, Switzerland (P Michel MD); Department of Neurology,St Elisabeth Hospital, Ravensburg, Germany(C M Rueckert MD); Departmentof Neurology, University ofDuisburg-Essen, Essen, Germany (C Weimer MD); Department of Neurology, Inselspital, University of Bern,Bern, Switzerland(H P Mattle MD); Department of Neurology, University HospitalBasel, Basel, Switzerland (S T Engelter MD); Sheba Medical Center and Tel Aviv University, Tel Aviv, Israel (D Tanne MD); Division of Clinical Neurosciences, University of Glasgow, Glasgow, UK (K W Muir MD); Department of Neurology, Hospital Val ‘d Hebron,Barcelona, Spain(C A Molina MD); Departmentof Neurology, University Hospitals Leuven and Vesalius Research Centre, VIB, Leuven, Belgium (V Thijs MD); Center for Stroke Research, CharitéUniversity Medicine Berlin,with antithrombotic therapy (AT), IVT , or intra-arterial therapy (IAT) were similar.2,13 The primary aim of the Basilar Artery International Cooperation Study (BASICS) was to obtain a better understanding of outcomes after acute BAO and to study potential diﬀ erences in treat m ent response in anticipation of a deﬁ nitive randomised controlled trial of acute treatment in these patients.MethodsPatientsBASICS was a prospective, observational, international registry of consecutive patients aged 18 years or older who presented with an acute symptomatic and radiologically conﬁ rmed BAO.14Patients were eligible for entry if theypresented with symptoms or signs attributable to disruption of the posterior circulation, and had a BAO as conﬁ rmed by CT angiography (CTA), magnetic resonance angiography (MRA), or conventional contrast angio-graphy. BAO was deﬁ ned as complete obstruction of ﬂ ow in the proximal, middle, or distal portion of the basilar artery. Patients with bilateral vertebral artery occlusions with retrograde ﬁ lling of the basilar artery were excluded. Treatments were allocated at the discretion of the treating physician. The BASICS protocol was approved by the ethics committee of the University Medical Center Utrecht, Netherlands. The requirement for additional local ethical approval diﬀ ered between participating countries and was obtained if required. Verbal or written informed consent was obtained from the patient or patient’s representative, as required by national and local guidelines. The BASICS registry opened on November 1, 2002, and closed on October 1, 2007.ProceduresDetailed data were recorded in a web-based data entry form that included information on baseline char a cter-istics, stroke risk factors, estimated time of BAO, clinical presentation, pretreatment and post-treatment imagingﬁ ndings, type and timing of treatment, neurologicaldeﬁ cits at time of treatment, complications, presumedcause of stroke, cause of death, and outcome at 1 month.Data were entered with a centre-speciﬁ c login andpassword. Deﬁ nitions of the variables collected wereincorporated in the electronic data entry form andspeciﬁ ed in a separate guideline, which was available atall participating centres.Stroke severity at time of treatment was dichotomisedas severe or mild to moderate. Patients in a coma, withtetraplegia, or in a locked-in state were classed as havinga severe stroke, whereas mild-to-moderate stroke wasdeﬁ ned as any deﬁ cit that was less than severe. Neurological deﬁ cit at the time of treatment was furtherassessed with the National Institutes of Health stroke scale (NIHSS). Estimated time of BAO was the time of onset of symptoms, as described by the patient or witness, consistent with the clinical diagnosis of BAO, on the judgment of the treating physician; if the exact time was not known, the time of onset was recorded as the last time the patient was seen by any witness before symptom onset. Transient ischaemic attack (TIA) or minor stroke in the hours or days before the index event were not counted as the time of the occlusion but were recorded under the prodromal phase. For example, the estimated time of occlusion for a patient who was admitted with an acute minor cerebellar stroke but who developed a severe deﬁ cit the next day that was consistent with the clinical diagnosis of an acute BAO was recorded as the time of the onset of the severe deﬁ cit. All pertinent data from the centres that recorded all consecutive patients were included in the registry.The primary outcome measure was poor outcome at 1 month. In view of the high risk of death and disability in patients with BAO, poor outcome was deﬁned as a modiﬁed Rankin scale (mRS) score of 4 or 5 (severe disability) or death.15 Haemorrhagic changes seen on the ﬁ rst post-treatment CT image or the occurrence of symptomatic intracranial haemorrhage at any time during the ﬁ rst month were systematically recorded as a treatment complication and, if applicable, as a cause of death. The registry did not predeﬁ ne symptomatic intracranial haemorrhage as an outcome measure, and the reporting of symptomatic intracranial haemorrhage was done entirely on the basis of each investigator’s judgment. For the primary analysis, patients were divided into three groups according to treatment: only AT (ie, received antiplatelet drugs or systemic anticoagulation); primary IVT, including subsequent IAT; or only IAT, which comprised thrombolysis, mechanical thrombectomy, stenting, or a combination of theseprocedures. These three treatment groups were deemed to represent conventional therapy before IVT was approved (AT), the current standard of care available to all patients (IVT), and the treatment available only at Campus Benjamin Franklin, Berlin, Germany(H Audebert MD); Departmentof Neurology, KlinikumGrosshadern, University of Munich, Munich, Germany(T Pfeﬀerkorn MD); Department of Neurology,UniversitätsklinikumMannheim, University of Heidelberg, Mannheim, Germany (K Szabo MD); Department of Neurology, Helsinki University CentralHospital, Program of MolecularNeurology, University of Helsinki, Helsinki, Finland (P J Lindsberg MD); Departmentof Neurology, University of Riode Janeiro, Rio de Janeiro, Brazil (G de Freitas MD); and Julius Center for Health Sciences andPrimary Care, UniversityMedical Center Utrecht, Netherlands (A Algra)Correspondence to:W J Schonewille, Department of Neurology, Mailbox G.03.228, University Medical CenterUtrecht, PO Box 85500,3508 GA Utrecht, Netherlands w.schonewille@dedicated stroke centres (IAT). Patients who received both IVT and IAT were included in the IVT group because IVT was the intended initial treatment.Statistical analysisThe target number of patients to be included in BASICS was 500, which was deemed to be suﬃ cient to answer several predetermined questions.14 Assuming that 50% of patients were being treated with IAT and about 30% with AT, a crude relative risk reduction of 23% with IAT would have a 95% CI of 2–39%. The frequency of poor outcome was compared among treatment groups with risk ratios and 95% CI. Adjusted risk ratios were calculated with Poisson regression. Adjustments are reported for only those factors that changed the crude risk ratios by more than 5%. Additionally, we report simultaneous adjustments for the three factors that had most inﬂ uence, as well as for all six factors that aﬀ ected the crude risk ratio. For the treatment comparisons that include AT, we also show the two-factor and ﬁ ve-factor adjustments because the variable time to treatment was not accurately assessed for patients treated with AT. Missing baseline data (<5% for each variable) were imputed with regression imputation for optimal adjustment for baseline diﬀerences in the assessment of treatment eﬀ ects.16 We prespeciﬁ ed separate analyses for patients with a mild-to-moderate deﬁ cit and for those with a severe deﬁ cit. Modiﬁ cation of treatment eﬀect by severity of disease and time to treatment was assessed by calculation of the p value of the treatment by eﬀ ect modiﬁ er terms in Poisson regression.Role of the funding sourceBASICS was an independent, investigator-initiated registry, and no external support was received. The corresponding author had full access to all data in the study and had ﬁnal responsibility for the decision to submit for publication.Results619 patients from 48 centres in Europe (41), South America (3), North America (2), Australia (1), and the middle east (1) were included in the registry. Participating centres and the number of patients recruited per centre are listed at the end of the paper. One centre was excluded from participation in the registry because not all pertinent data on consecutive patients were being recorded.183 patients were treated with AT, 121 with IVT, and 288 with IAT. Of the patients treated with IVT, 80 were treated with only IVT and 41 were treated with additional IAT. 179 patients in the IAT group were treated with only pharmacological thrombolysis, 79 patients were treated with pharmacological thrombolysis in con j unction with mechanical thrombectomy, and 30 were treated with only mechanical thrombectomy. 347 patients had severe deﬁ cits and 245 patients had mild-to-moderate deﬁ cits. 592 patients completed 1 month of follow-up. 27 patients were not analysed because they did not receive AT, IVT, or IAT; these patients were either comatose (n=26) or tetraplegic (n=1) at the time of presentation. 26 of these patients died, and the patient who survived (who had been comatose) had a mRs score of 5 at 1 month.Table 1 shows baseline characteristics. Patients who received IVT were more commonly treated within 3 h of a BAO than were the patients who received IAT (RR 2·38, 95% CI 1·83–3·10). The time to treatment in patients treated with only AT was not recorded accurately. PatientsFigure: Outcome at 1 month according to severity of initial disease and treatment(A) Outcome according to severity of deﬁ cit at time of treatment. (B) Outcome according to type of treatment in patients with a mild-to-moderate deﬁ cit at time of treatment. (C) Outcome according to type of treatment in patients with a severe deﬁ cit at time of treatment. Note that the treatment comparisons in panels B and C are based on crude data; table 2 shows adjusted comparisons. mRS=modiﬁ ed Rankin scale.treated with IAT more often had a severe deﬁ cit than did the patients who received AT (RR 1·58, 1·31–1·90) and the patients who received IVT (RR 1·14, 0·97–1·35). The mean NIHSS score was 10·7 (SD 7·3) in the patients with a mild-to-moderate deﬁcit and 28·0 (7·2) in the patients with a severe defecit.402 (68%) of the 592 patients who received treatment had a poor outcome at 1 month and 214 (36%) patients died. The ﬁgure shows the outcomes of patients according to the severity of their deﬁ cit and treatment modality.Table 2 shows the risk ratios for poor outcome when the three treatment modalities are compared by stroke severity, including adjustments for imbalances in baseline variables and time to treatment. After adjustment for age, NIHSS score, time to treatment, prodromal minor stroke, location of the BAO, and diabetes mellitus (6 factors), we could not show a diﬀ erence in the risks of patients with a mild-to-moderate deﬁ cit with respect to poor outcome after IVT compared with AT (RR 0·94, 95% CI 0·60–1·45) or after IAT compared with AT (RR 1·29, 0·97–1·72). There were no diﬀ erences in patients with a severe deﬁ cit, although their risk of poor outcome after IVT (RR 0·88, 0·76–1·01) or IAT (RR 0·94, 0·86–1·02) was slightly lower than their risk after AT. Adjustment for sex, the presence of prodromal symptoms, hyperlipidaemia, smoking status, and a history of peripheral artery or coronary artery disease did not inﬂ uence the treatment risk ratios. The treatment eﬀ ects of IAT versus AT were signiﬁ cantly diﬀ erent between the two strata of disease severity (p=0·03 after adjustment for 6 factors).When time to treatment was removed from the multivariable adjustment, because the accuracy of the recording of this variable was uncertain among patients treated with AT, the ﬁ ndings changed only slightly and any similarity of outcomes between the IVT and IAT treatment groups were unchanged (adjustment for two factors and ﬁ ve factors in table 2). After adjustment for ﬁve factors, patients with a severe deﬁcit had a signiﬁcantly worse outcome when treated with AT compared with those treated with IAT or IVT (RR 0·88, 95% CI 0·81–0·96)In a direct comparison of IAT with IVT (table 2), patients with a mild-to-moderate deﬁ cit had a higher risk of a poor outcome after adjustment for six factors when treated with IAT (RR 1·49, 95% CI 1·00–2·23), whereas patients with a severe deﬁ cit had similar outcomes when treated with either IAT or IVT (1·06, 0·91–1·22). The results of these comparisons were the same if a poor outcome was deﬁ ned as an mRS score of 3–5 or death; the risk ratios adjusted for six factors were 1·36 (0·96–1·93) for patients with a mild-to-moderate deﬁ cit and 1·07 (0·95–1·21) for those with a severe deﬁ cit. Table 3 shows the risk ratios for poor outcome in patients treated with IAT compared with those treated with IVT, stratiﬁ ed by time to treatment. There was no statistically signiﬁ cant diﬀerence in outcome between IVT and IAT at any time window; however, the number of patients in each stratum was small. None of the 41 patients with a severe deﬁ cit had a good outcome when treatment was started beyond 9 h after the estimated time of occlusion. Patients with a mild-to-moderate deﬁ cit had the worst outcome with IAT if the time to treatment was longer than 9 h(interaction between treatment and time to treatment p=0·09 after multivariable adjustment).72% (207) of patients treated with IAT had partial or complete recanalisation of the basilar artery (corresponding to a thrombolysis in myocardial infarction [TIMI] score of 2 or 3) at the end of the angiographic procedure. Recanalisation protected against pooroutcome after IAT (RR 0·75, 95% CI 0·66–0·85). Of the patients treated with IVT, 182 (88%) had a CTA, MRA, transcranial Doppler (TCD), or conventional angiogram hours to days after treatment, and these showed a mean overall vessel patency rate of 67%. The precise timing of recanalisation in the IVT group, however, is unknown. Basilar artery patency also protected against poor outcome in the IVT group (RR 0·67, 0·49–0·92). Symptomatic intracranial haemorrhage was more commonly reported in patients treated with IAT (39 of 288 [14%], 95% CI 10–18%) than in those treated with IVT (7 of 121[6%], 3–11%), and by fewer than 1% (1 of 183)of patients in the AT group. Intracranial haemorrhage was the cause of death in 11 (9%) of 117 patients after IAT, 3 (7%) of 41 patients treated with IVT, and 1 (2%) of 56 patients treated with AT.DiscussionThis is a prospective, international observational study of consecutive patients who presented with an acute symptomatic BAO. Although, to date, no data from a randomised controlled trial support the use of IAT for BAO, IAT was by far the most commonly used treat m ent type in our registry. Almost 50% of patients were treated with primary IAT: 56% of patients with a severe deﬁ cit and 38% of patients with a mild-to-moderate deﬁ cit. Additionally, 7% were treated with IVT followed by IAT. Our results suggest there is a diﬀ erence in the eﬃ cacy of treatment strategies in patients with an acute BAO, depending on the severity of the stroke. Patients with a mild-to-moderate deﬁ cit more often had a poor outcome if they were treated with IAT rather than with IVT. In a direct (unadjusted) comparison of IAT with IVT in these patients, the absolute increase in the risk of death or dependency associated with IAT was 20% (ﬁ gure). The better outcome in the IVT group was not attributable to the patients with a mild-to-moderate deﬁ cit who received IAT in addition to IVT, because these patients generally fared worse than those who received only IVT. Conversely, patients with a severe deﬁ cit seemed to beneﬁ t from both IVT and IAT; absolute risk of death or dependency was 19% (IVT) and 10% (IAT) lower than the risk with AT (ﬁ gure). The overall rate of death or dependency in this group was 93% in those who were treated with only AT. We found a non-signiﬁ cantly lower rate of symptomatic intracranial haemorrhage after IVT compared with after IAT, and the overall rates of haemorrhage were similar to those seen in intervention trials of anterior circulation stroke. Rates of mortality due to intracranial haemorrhage were similar after IVT or IAT.In our analyses, we used an estimated time to treatment from the onset of symptoms consistent with a clinical diagnosis of BAO, rather than the more commonly used time of onset of any symptom to treatment. Previous studies have shown that BAO is preceded by prodromal symptoms in more than 60% of patients.17,18 Most of these patients would be excluded from a potential trial that has the time of onset of any symptom to treatment as an inclusion criterion. Because the data in our registry suggest diﬀ erences in the response to diﬀ erent treatment types, we believe our results support use of the estimated time of BAO, rather than the time of onset of any symptom, to treatment as an inclusion criterion for a future randomised treatment trial in patients with an acute symptomatic BAO.Interpretation of the results from a previously published meta-analysis of 15 small case-series and from retrospectively collected data has been hampered by the use of diﬀ erent functional scales, heterogeneity in the timing of outcome assessments, and patchy recording of baseline char a cteristics.2 Another important limitation of that meta-analysis was that all the patients who were treated with IVT came from only three centres and most were from one centre. The 121 patients treated with IVT in BASICS came from 23 centres, which reduced the chance of selection bias.Our study is observational and has all the limitations of a non-randomised study. The interpretation of our results is hampered by the absence of a treatment protocol for all patients who entered the study. The reasons for clinicians to select a speciﬁ c treatment option are more complex than can be covered by the scope of a prospective registry. Multivariable analyses can never adjust completely for systematic diﬀ erences between treatment groups, which is the aim of randomisation in clinical trials. We suspect that a bias towards more aggressive treatment in patients who were thought to have a worse prognosis might have inﬂ uenced outcome in the IAT group, and that the restriction of treatment toonly AT in patients with a severe deﬁcit might have been an expression of a more palliative approach. More vigilant searching for intracranial haemorrhage in patients who received thrombolysis than in those who received AT might have exaggerated the diﬀ erences between the IVT, IAT, and AT treatment groups. Crossover to another treatment group because of clinical worsening or the absence of treatment response was not taken into account. Most patients with AT and IVT were diagnosed with BAO on the basis of only non-invasive imaging (as opposed to arterial angiography). We cannot exclude the possibility that some of these patients had a false-positive CTA or MRA, introducing a potential bias in favour of the AT and IVT groups. There might be variables that we did not measure that are relevant to outcome but are unbalanced between groups. In the design of our data entry form, we tried to take into account all factors that could aﬀ ect outcome, but we did not record possible relevant imaging or laboratory ﬁndings. Furthermore, data collection in a registry is generally not as accurate as it is in a randomised treatment trial. Nevertheless, standard neurological and functional scores and risk factor data were collected from all sites. In the analyses, we have adjusted for baseline imbalances among the treatment groups as much as possible, to help readers to interpret our data. Finally, we are of the opinion that our dataset is representative of the current practice in dedicated stroke centres around the world for patients with an acute symptomatic BAO.Our observations underscore the continued absence of a proven treatment modality for patients with an acute BAO and that current clinical practice varies widely. Furthermore, the often-held assumption that IAT is superior to IVT in patients with an acute symptomatic BAO is challenged by our observations. Therefore, we believe that a randomised controlled trial to compare IVT with IAT in patients with acute symptomatic BAO is a high priority.In the meantime, our results should encourage clinicians to treat patients who have acute symptomatic BAO and a mild-to-moderate deﬁ cit with IVT. In case of subsequent acute worsening, additional IAT can be considered. Patients who present with a severe deﬁ cit can be treated with IVT or IAT. Treatment should be initiated as soon as possible. Our data do not enable any recommendations to be made on the time window within which IVT or IAT should be used in patients with BAO. In centres that cannot provide IAT, we recommend starting IVT while the transfer of the patient to a centre that is able to provide additional IAT if needed is being arranged. Because the chance of a favourable response to therapy will probably decrease with time, the initiation of IVT should not be delayed while waiting for IAT. ContributorsWJS had the idea for the study, developed the internet database, encouraged international colleagues to contribute data to the study, analysed and interpreted the data, and wrote the ﬁ rst draft of the manuscript and the ﬁ nal report. AA and LJK supervised the design and execution of the study and contributed to subsequent versions of the manuscript. AA did the statistical analyses. CACW and PM assisted in recruitment at the participating centres, assisted in the day-to-day running of the registry, and contributed to subsequent versions of the manuscript. CW integrated the BASICS data entry form into the German Stroke Database and monitored data entry. All other authors contributed to the study by providing resources, including patients, to implement and run the study in the local centres and to obtain the required data, and by discussing the progress of the study during international meetings. All authors reviewed the study report, made comments or suggestions on the manuscript drafts, and approved the ﬁ nal version. BASICS study groupAustralia—A M Weber, G A Donnan. Belgium—V Thijs, A Peeters. Brazil—G de Freitas, A B Conforto, M Miranda-Alves, A Massaro. Finland—P Ijäs, T Bogoslovsky, P J Lindsberg. Germany—C Weimar,J Benemann, K Kraywinkel, C Haverkamp, D Michalski,K Weissenborn, M Goertler, A Kloth, A Bitsch, T Mieck, J Machetanz,P Möller, R Huber, S Kaendler, C Rueckert, H Audebert, R Müller,B Vatankhah, T Pfeﬀ erkorn,TE Mayer, K Szabo,C Disque, O Busse,C Berger, W Hacke. Israel—Y Schwammenthal,D Orion, D Tanne. Italy—M Bergui,E Pozzati. Netherlands—W J Schonewille, A Algra,L J Kappelle, G J Luijckx, P Vroomen, M D Vergouwen, Y Roos, J Stam, P Bienfait, F E de Leeuw, P de Kort, D Dippel. Spain—J Pagola, M Ribo, C Molina, A Gonzales, A Gil-Peralta. Sweden—B Norrving. Switzerland—M Arnold, U Fischer, J Gralla, H Mattle, G Schroth,P Michel, S T Engelter, S Wetzel, P Lyrer, J Gandjour, N Michael,R Baumgartner, B Tettenborn, H Hungerbuehler. UK—T Baird, K Muir. USA—C A C Wijman, A Finley Caulﬁ eld, M Lansberg, N Schwartz,C Venkatasubramanian, Z Garami, S Bogaard, F Yatzu, J Grotta. Participating centres (and number of patients at each centre) Australia—University of Melbourne (6). Belgium—University Hospital, Leuven (11); University Hospital St Luc, Brussels (10). Brazil—Hospital Quinta D’Or, Rio de Janeiro (11); University of Sao Paolo, Hospital das Clinicas (5); Federal University of Sao Paolo (2). Finland —University of Helsinki (14). Germany—(German Stroke Database [77]: University Hospital Freiburg [20]; Leipzig University [15]; University Hospital Essen [10]; Medical University Hannover [8]; University Hospital, Magdeburg [6]; University Hospital Rostock [4]; Kliniken Neuruppin [3]; Bürger Hospital, Stuttgart [3]; Heinrich Braun Krankenhaus, Zwickau [2]; Soﬁ en and Hufeland Hospital, Weimar [2]; University Hospital, Ulm [2]; Hospital Heidenheim [2]); St Elisabeth Hospital, Ravensburg (47); TEMPiS Network Bavaria (38); University of Munich (26); Universitätsklinikum Mannheim (19); Dresden University (13); Klinikum Minden (2); University of Heidelberg (2). Israel—Sheba Medical Center (19). Italy—University of Turin (5); University of Bologna (1). Netherlands—St Antonius Hospital, Nieuwegein (40); University Medical Center Utrecht (22); University Medical Center Groningen (6); Academic Medical Center, Amsterdam (5); Gelre Hospital (4); University Medical Center Nijmegen (3); St Elisabeth Hospital, Tilburg (1); Erasmus Medical Center, Rotterdam (1). Spain—Hospital Val ‘d Hebron, Barcelona (13); Hospital Virgen del Rocio, Sevilla (12). Sweden—Lund University (3). Switzerland—Inselspital, Bern (52); Centre Hospitalier Universitaire Vaudois, Lausanne (39); University Hospital, Basel (24); University Hospital Zurich (8); Kantonsspital, St Gallen (2); Kantonsspital, Aarau (2). UK—Southern General Hospital, Glasgow (23). USA—Stanford Stroke Center, Palo Alto (29); University of Texas, Houston (22).Conﬂ icts of interestWe have no conﬂ icts of interest.AcknowledgmentsWe would like to thank Louis R Caplan for his valuable support during the initiation of the registry and Mirjam Knol for statistical advice. The development of the BASICS database was supported by the Department of Neurology, University Medical Center Utrecht, Netherlands. The costs of the drugs and devices used to treat patients were covered under the costs associated with clinical care by the participating centres.。

基底动脉闭塞脑梗死健康宣教

康复计划：根据患者情况制定个性化的康复计划
04
康复效果：改善功能，提高生活质量，降低复发风险
基底动脉闭塞脑梗死的护理
生活护理
饮食护理：注意饮食清淡，多吃蔬菜水果，避免油腻食物
运动护理：适当进行运动，如散步、慢跑等，避免剧烈运动
心理护理：保持心情舒畅，避免情绪激动，保持良好的心理状态
STEP2
STEP3
STEP4
手术目的：恢复脑部供血，减轻脑梗死症状
手术方式：险：出血、感染、神经损伤等
术后护理：抗凝、抗血小板、控制血压等
康复治疗
01
康复目标：提高生活质量，恢复功能
02
康复方法：物理治疗、言语治疗、作业治疗等
03
基底动脉闭塞脑梗死的治疗
药物治疗
01
抗血小板药物：如阿司匹林、氯吡格
雷等，用于预防血栓形成
02
抗凝血药物：如华法林、肝素等，用
于预防血栓形成和溶解血栓
03
降压药物：如利尿剂、钙通道阻滞剂
等，用于控制血压，降低脑梗死风险
04
降脂药物：如他汀类药物，用于降低
胆固醇水平，预防动脉粥样硬化
手术治疗
STEP1
家庭成员应鼓励患者积极接受治疗，并帮助患者进行康
复训练。
家庭成员应关注患者的情绪变化，给予心理支持和安慰。
家庭成员应帮助患者调整生活方式，如戒烟、限酒、合
理饮食等。
谢谢
定期进行血管超声检查，了解血管弹性和血流状况
控制危险因素
控制高血压：保持血压稳定，避免剧烈波动
控制糖尿病：合理饮食，控制血糖水平
控制高血脂：减少脂肪摄入，增加运动量

基底动脉闭塞的健康宣教

04 社会支持：鼓励患者参加社会活动，建立良好的人际关系，提高心理适应能力

家庭和社会支持
家庭支持：家庭成员的关心、理解和帮助，提供心理安慰和情感支持
社会支持：社区、医疗机构、志愿者等提供的心理支持和服务，帮助患者适应和应对疾病
心理干预：心理咨询、心理治疗等专业心理支持，帮助患者调整心态，减轻心理压力
基底动脉闭塞的健康宣教
x
基底动脉闭塞的基本知识
基底动脉闭塞的健康教育
基底动脉闭塞的心理支持
基底动脉闭塞的康复和预后
基底动脉闭塞的基本知识
病因和症状
01
病因：动脉粥样硬化、高血压、糖尿病等
03
严重程度：轻度、中度、重度
02
症状：头晕、头痛、恶心、呕吐、肢体无力等
04
治疗方法：药物治疗、手术治疗、康复治疗等
社会参与：鼓励患者参与社会活动，增强自信心和自我价值感，提高生活质量
基底动脉闭塞的康复和预后
康复治疗
药物治疗：遵医嘱使用抗血小板、抗凝血等药物，控制病情
生活方式调整：戒烟限酒，保持良好的作息习惯，避免过度劳累
康复锻炼：进行适当的康复锻炼，如步行、慢跑等，提高心肺功能
定期复查：遵医嘱定期复查，监测病情变化，及时调整治疗方案
谢谢
社交支持：鼓励患者参加社交活动，增强自信心和社交能力
心理干预和治疗
01 心理干预：通过心理咨询、心理辅导等方式，帮助患者调整心态，减轻心理压力
02 心理治疗：通过药物治疗、心理疗法等方式，帮助患者缓解心理症状，提高生活质量
03 家庭支持：鼓励家庭成员参与患者的心理治疗，提供情感支持和帮助
治疗方法：药物治疗、手术治疗、康 03 复治疗等

基底动脉闭塞脑梗死疾病取栓后患者昏迷应对措施

基底动脉闭塞脑梗死取栓后患者昏迷应对应对措施急性缺血性脑血管病的治疗目标是挽救缺血半暗带，减轻原发性及继发性脑损伤。

目前被证实急性缺血性卒中早期最有效的治疗方法主要是静脉溶栓，但静脉溶栓有严格的时间窗限制，且对合并有大血管闭塞或病情严重的患者效果不佳。

《急性缺血性卒中早期治疗指南 2018》中对动脉取栓的推荐进行了大篇幅修改。

较为一致的研究结果：在经过筛选的大血管急性缺血性卒中患者中，以机械取栓为主的血管内治疗可带来明显获益。

1、发病 17 h，仍进行性加重44 岁男性，因「头晕 17 小时余，加重伴左侧肢体无力4小时余」入院。

既往高血压病史，血压控制欠佳；吸烟20余年。

患者在入院前一日（2021.02.23 22:00）上夜班时出现头晕，未予重视，（2021.02.24 11:00）头晕加重并出现左侧肢体无力、口齿不清。

于 13:00 就诊于我院急诊。

入院查体：血压：240/130 mmHg；神经系统阳性体征：嗜睡，构音不清，双侧眼球震颤明显，固视抑制试验阳性，左侧鼻唇沟浅，伸舌不能，软腭上抬无力，咽反射消失，左侧上肢及下肢肌力为 4 级，右侧上下肢肌力为 5 - 级。

指鼻试验、跟膝胫试验均为阳性；双侧病理征阳性。

NIHSS 评分为 6 分（意识 1 分，面瘫 1 分，左上肢运动 1 分，左下肢运动 1 分，共济 1 分，构音 1 分）；e-NIHSS 13 分（加眼球震颤 1 分 + 舌下神经 3 分 + 舌咽神经 3 分）；洼田饮水试验 5 级；发病前 mRS 0 分。

患者至我院急诊，急查头颅 CT 排除出血；头颈部 CTA 提示基底动脉闭塞；头颅 MRI 示：DWI 序列双侧小脑、脑干、枕叶多发梗死病灶，为后循环分布区，考虑急性基底动脉闭塞致后循环脑梗死。

图 1. 头颅 MRI 示：DWI 序列双侧小脑、脑干、枕叶多发梗死病灶图 2. 头颈 CTA 示：基底动脉闭塞基底动脉闭塞，是否积极取栓？患者发病在 24 小时内，同时存在临床症状体征与影像学不匹配，考虑存在缺血半暗带。

基底动脉闭塞的治疗方法

基底动脉闭塞的治疗方法
基底动脉闭塞是一种严重的血管疾病，需要综合治疗。

治疗方
法可以从药物治疗、介入治疗和手术治疗等多个角度来考虑。

首先，药物治疗是基底动脉闭塞的常规治疗方法之一。

这包括
抗血小板药物如阿司匹林和氯吡格雷，它们可以帮助预防血栓形成
和减少血小板聚集。

另外，脂质调节药物如他汀类药物也可以用于
控制血脂，减少动脉粥样硬化的进展。

其次，介入治疗是针对基底动脉闭塞的有效手段之一。

介入性
治疗包括经皮腔内血管成形术（PTA）和支架植入术。

在PTA中，医
生会通过导管将血管腔扩张，以改善血流通畅。

而支架植入术则是
在血管狭窄处植入支架，以维持血管通畅。

最后，对于一些严重的基底动脉闭塞病例，可能需要手术治疗。

手术治疗可以包括血管旁路手术或血管重建手术，这些手术旨在恢
复受影响的血管的正常血流。

除了上述治疗方法外，患者还应该注意生活方式的改变，包括
戒烟、控制体重、保持适当的运动和饮食习惯等。

此外，定期的随
访和监测也是治疗的重要环节，以便及时调整治疗方案。

总的来说，基底动脉闭塞的治疗方法是多方面的，需要根据患者的具体情况进行综合评估和制定个性化的治疗方案。

患者在接受治疗的过程中应该密切配合医生的指导，积极配合治疗，以达到更好的疗效。

急性基底动脉闭塞患者血管内治疗的初步临床分析

急性基底动脉闭塞患者血管内治疗的初步临床分析急性基底动脉闭塞（acute basilar artery occlusion, BAO）是一种严重的脑血管疾病，常常导致中枢神经系统功能障碍，甚至危及生命。

血管内治疗（endovascular therapy, EVT）是一种创新的治疗方法，在急性基底动脉闭塞患者中取得了一定的成功。

本文通过对急性基底动脉闭塞患者血管内治疗的初步临床分析，评估该方法的疗效和安全性，以期为临床提供参考。

据报道，急性基底动脉闭塞患者中，约有30%-40%的患者死亡，且残存者仅有少数能够恢复正常的生活。

因此，寻找一种有效的治疗方法至关重要。

EVT作为一种介入神经学的新技术，在急性基底动脉闭塞的治疗上引起了广泛关注。

研究显示，EVT可以通过内科溶栓和机械取栓两种方式进行。

内科溶栓通过静脉注射血栓溶解药物，如尿激酶等，在体内溶解血栓来恢复血液供应。

机械取栓则通过导管技术，将血栓抓取、撤除，以恢复血流。

这两种方法并不互斥，而是可以结合使用，以获得更好的疗效。

根据临床数据，EVT在急性基底动脉闭塞的治疗中具有较好的疗效和安全性。

一项研究发现，在全身溶栓治疗失败的患者中，通过EVT治疗的患者中约有50%的患者出现了重建血流、恢复神经功能的情况。

另外，EVT还可以减少脑卒中后遗症的发生，提高患者的生存率。

然而，EVT并非适用于所有急性基底动脉闭塞患者。

研究表明，EVT 治疗的适应症应根据患者的临床情况、影像学表现等进行综合评估。

一般而言，EVT适用于病情严重、症状严重的患者，以及那些未能获得满意效果的全身治疗患者。

此外，EVT也存在一定的风险和不良事件。

例如，导管操作可能导致血管损伤、血栓再栓塞等并发症。

此外，血管内治疗也需要有一支经验丰富、专业的团队来进行操作，以确保治疗的安全性和有效性。

综合以上分析，急性基底动脉闭塞患者血管内治疗通过溶栓和取栓等方式，可以较好地改善患者的预后和生活质量。

基底动脉栓塞的健康宣教

临床表现
突发性眩晕、恶心、呕吐
肢体无力、瘫痪
语言障碍、吞咽困难
意识障碍、昏迷
预防基底动脉栓塞的方法
生活方式调整
01
戒烟限酒：吸烟和过量饮酒 02
健康饮食：多吃蔬菜水果，
会增加基底动脉栓塞的风险
减少高脂肪、高胆固醇食物
的摄入
03
规律运动：每周至少进行150 04
控制体重：保持正常的体重
分钟的中等强度有氧运动，
范围，避免肥胖带来的健康
如快走、跑步、游泳等
风险
05
保持良好的心理状态：学会 06
定期体检：及时发现并控制高
缓解压力，避免焦虑、抑郁
血压、高血脂、糖尿病等疾病，
等负面情绪
降低基底动脉栓塞的风险
定期体检
01
定期进行身体检查，了解身体状况
02
及时发现并治疗高血压、高血脂、糖尿病等疾病
03
保持良好的生活习惯，如戒烟、限酒、合理饮食等
定期进行家庭急救知识培训，提高
0 7 应对突发情况的能力
基底动脉栓塞的急救措施
识别症状
突发性眩晕、恶心、呕吐言语不清、吞咽困难意识障碍、昏迷
肢体无力、麻木、瘫痪面部肌肉抽搐、嘴角歪斜
紧急处理 1 立即拨打120
急救电话
保持患者平躺，
2 头偏向一侧，防止呕吐物误吸
检查患者呼吸、
3 心跳，如有必要，进行心肺复苏
观察患者意识
4 状态，如有昏迷，保持患者呼吸道通畅
x
01
基底动脉栓塞的基本知识
02 预防基底动脉栓塞的方法
03
基底动脉栓塞的急救措施

动脉闭塞的治疗方法

动脉闭塞的治疗方法
动脉闭塞是指因动脉内壁发生粥样斑块形成，导致血管腔狭窄或完全阻塞的情况。

治疗动脉闭塞的方法包括药物治疗、介入治疗和手术治疗。

具体的治疗方案根据闭塞部位、程度和病人的整体状况而有所不同。

1.药物治疗：通常使用抗凝血药和抗血小板药物来预防血栓形成和进一步的血管阻塞。

这些药物可以减少血小板聚集和降低血液的凝血性。

2.介入治疗：介入治疗是通过导管将血管内球囊扩张、支架植入或血管成形术来恢复动脉血流。

常见的介入治疗方法包括经皮腔内血管成形术（PTA）和经皮腔内支架植入术（PCI）。

这些方法可以减少或消除血管狭窄，改善血流。

3.手术治疗：对于病情较为严重或介入治疗无效的患者，可能需要进行手术治疗。

常见的手术治疗方法包括动脉旁路移植术、动脉内膜切除术和动脉血管重建术等。

手术治疗可以重建血液供应，解除动脉闭塞。

总的来说，治疗动脉闭塞的方法需要根据个体情况进行综合考虑，早期诊断和治疗是预防并发症的关键。

患者在治疗过程中还要注意控制危险因素，如高血压、高血脂、糖尿病等，以减少闭塞的发生和复发。

一例基底动脉栓塞颅内动脉取栓血压管理个案

一例基底动脉栓塞颅内动脉取栓血压管理个案基底动脉栓塞是一种常见的脑血管疾病，常由血栓阻塞引起。

随着人们生活水平的提高和年龄的增长，这种疾病的发病率也在逐渐增加。

针对这种疾病，医学界提出了一种新的治疗方法——颅内动脉取栓。

本文将介绍一例基底动脉栓塞颅内动脉取栓血压管理个案。

个案基本信息：患者为女性，现年65岁。

患者无明显特殊基础疾病史，但有高血压和高血脂症状，服用降压和降脂药物控制血压和血脂。

患者突然出现头痛、眩晕、恶心、呕吐等症状，并出现局灶性神经系统体征。

头颅CT检查显示右侧脑梗塞影像改变，提示基底动脉栓塞。

治疗方案：经过医生详细检查和综合评估，决定给予患者颅内动脉取栓治疗。

手术前，需要进行血压管理，以减少手术风险和提高手术成功率。

血压管理的目标是将患者的收缩压维持在140-160mmHg之间。

血压管理过程：1.给予静脉输液：患者入院后立即给予静脉输注生理盐水和稀释液体，维持患者的血容量，防止低血压状态的发生。

2.药物治疗：首先，医生调整患者正在使用的抗高血压和降脂药物剂量，使其达到最佳治疗效果。

同时，给予临时抗高血压药物，如硝酸甘油和硝普钠，以快速降低患者的血压。

3.连续监测：将患者的血压进行连续监测，以了解血压的变化情况，并根据监测结果及时调整治疗方案。

监测方法包括使用无创血压监测设备、动脉插管等。

4.疼痛控制：给予患者适当的镇痛药物，以减轻患者疼痛和不适感。

同时，减少患者的紧张情绪，提供良好的治疗环境。

5.患者教育：对患者进行血压管理知识的教育，指导患者在日常生活中控制血压，遵守医生的建议和用药指导。

疗效评估：经过上述的血压管理措施后，患者的血压得到了有效的控制。

手术顺利进行，成功地取出了栓子。

术后患者的神经功能得到了较好的恢复，没有出现并发症。

结论：对于基底动脉栓塞颅内动脉取栓患者，合理的血压管理非常重要。

通过输液、药物治疗、监测和教育等措施，可以有效控制患者的血压，为手术的成功进行提供了重要的保障。

一例基底动脉栓塞颅内动脉取栓血压管理个案

一例基底动脉栓塞颅内动脉取栓血压管理个案基底动脉栓塞是指基底动脉血管内发生血栓形成导致脑灌注不足的疾病。

基底动脉栓塞通常由血栓形成或栓塞物导致，可能导致中风或其他神经功能缺陷。

针对这种病情，常用的治疗方法是颅内动脉取栓术。

在这篇文章中，我将介绍一个基底动脉栓塞颅内动脉取栓血压管理的个案。

该个案是一位65岁的男性，他于一周前突发右侧肢体乏力和言语不清的症状被紧急送往我院急诊科。

经过详细的检查和影像学评估，他被确诊为右侧大脑中动脉的栓塞。

由于颅内动脉取栓术是治疗这种病情的首选方法，他被转到我们神经外科进行手术治疗。

在术前准备阶段，我们对患者进行了详细的评估，包括病史询问、体格检查和实验室检查。

患者的既往病史中有高血压和高血脂的病史，控制得较好。

在体格检查中，我们发现患者有肢体乏力和失语的表现，但神经系统其他方面的检查结果正常。

实验室检查显示患者的血压和血脂较高，但肝肾功能正常。

术前我们与患者进行了详细的沟通，解释了手术过程和可能的并发症。

我们告诉他手术风险是很小的，但同时也提醒他可能存在出血和血栓相关的风险。

患者对手术表示同意，并签署了知情同意书。

手术当天，我们采用了经皮动脉穿刺技术对患者进行了颅内动脉取栓术。

手术过程中，我们使用导管将血栓吸出，并保持动脉通畅。

手术进行顺利，没有出现明显的并发症。

术后，患者被转到神经科进行观察和治疗。

我们密切监测他的生命体征和神经功能，以及手术区域的血流情况。

此外，我们也特别关注患者的血压管理。

在术后的血压管理中，我们采用了个体化的方法。

根据患者的病情和实验室检查结果，我们设定了目标血压范围。

考虑到患者的高血压病史，我们希望将他的血压控制在正常范围内，以减少心脑血管并发症的发生。

因此，我们开始给予患者抗高血压药物治疗，并定期调整药物剂量。

在治疗过程中，我们密切监测患者的血压，并定期进行血压测量和调整治疗方案。

在术后的观察期中，患者的血压得到了良好的控制。

他的血压保持在正常范围内，并且没有出现明显的血压波动。

基底动脉闭塞血管内治疗联合高压氧干预的疗效

［５］　刘会领，罗雁，李长平，等．Ｒｏｃｋａｌｌ、Ｂｌａｔｃｈｆｏｒｄ和ＡＩＭＳ６５评分系统在急性上消化道出血诊治中的价值［Ｊ］．天津医药，２０１７，４５（４）：４２３－４２７［６］　ＳＡＬＴＺＭＡＮＮＪＲ，ＴＡＢＡＫＹＰ，ＨＹＥＴＴＢＨ，ｅｔａｌ．Ａｓｉｍｐｌｅｒｉｃｋｓｃｏｒｅａｃｃｕｒａｔｅｌｙｐｒｅｄｉｃｔｓｉｎｈｏｓｐｉｔａｌｍｏｒｔａｌｉｔｙ，ｌｅｎｇｔｈｏｆｓｔａｙ，ａｎｄｃｏｓｔｉｎａｃｕｔｅＧＩｂｌｅｅｄｉｎｇ［Ｊ］．ＧａｓｔｒｏｉｎｔｅｓｔＥｎｄｏｓｃ，２０１１，７４（６）：１２１５－１２２４［７］　ＢＬＡＴＣＨＦＯＲＤＯ，ＭＵＲＲＡＹＷＲ，ＢＬＡＴＣＨＦＯＲＤＭ．Ａｒｉｓｋｓｗｒｅｈａｅｍｏｒｒｈａｇｅ［Ｊ］．Ｌａｎｃｅｔ，２０００，３５６（９２９８）：１３１８－１３２１．［８］　郑大伟，王承志，刘仁水，等．以改良格拉斯哥昏迷评分１５分为切换点在有创无创机械通气治疗慢性阻塞性肺疾病所致严重呼吸衰竭中的应用［Ｊ］．中华危重病急救医学，２０１１，２３（４）：２２４－２２７［９］　李伟华．非静脉曲张性上消化道出血内镜诊治回顾分析［Ｄ］．大连：大连医科大学，２０１４［１０］毛乙鸿，雷志群．不同年龄上消化道出血的病因及临床特征比较研究［Ｊ］．医学信息，２０１５，２８（９）：３１６－３１７［１１］徐国帅，吕庆，王晓欢．围手术期输血对胃癌患者影响的研究进展［Ｊ］．疑难病杂志，２０１７，１６（１０）：１０７２－１０７５［１２］ＢＵＤＩＭＩＲＩ，ＧＲＡＤＩＳＥＲＭ，ＮＩＫＯＬＩＣＭ，ｅｔａｌ．ＧｌａｓｇｏｗＢｌａｔｃｈｆｏｒｄ，ｐｒｅｅｎｄｏｓｃｏｐｉｃＲｏｃｋａｌｌａｎｄＡＩＭＳ６５ｓｃｏｒｅｓｓｈｏｗｎｏｄｉｆｆｅｒｅｎｃｅｉｎｐｒｅｄｉｃｔｉｎｇｒｅｂｌｅｅｄｉｎｇｒａｔｅａｎｄｍｏｒｔａｌｉｔｙｉｎｖａｒｉｃｅａｌｂｌｅｅｄｉｎｇ［Ｊ］．ＳｃａｎｄＪＧａｓｔｒｏｅｎｔｅｒｏｌ，２０１６，５１（１１）：１３７５－１３７９（２０１７－０７－３１收稿）基底动脉闭塞血管内治疗联合高压氧干预的疗效杨世泉　陈甲　艾瑞　魏学志　薛春梅　程晋成　陈友东基金项目：南京军区医学科技创新课题（项目编号：１５ＭＳ０５４）作者单位：２３３０１５　安徽蚌埠　中国人民解放军第１２３医院高压氧神经内科通信作者：陈友东，１６０２８０５８＠ｑｑ．ｃｏｍ［摘　要］　目的　分析血管内治疗联合高压氧干预对基底动脉闭塞的疗效。

动脉溶栓治疗基底动脉闭塞后血管再通的影响因素

动脉溶栓治疗基底动脉闭塞后血管再通的影响因素
陶华;李慎茂
【期刊名称】《中国脑血管病杂志》
【年(卷),期】2008(5)9
【摘要】基底动脉闭塞直接影响脑干的供血，并且直接累及穿支动脉，因侧支循环代偿较差，故常被视为致命性脑梗死的最主要原因。

然而，最初对于老年人群的研究认为，基底动脉闭塞属于少见疾病，而后通过全脑血管造影，发现本病并不少见。

对于基底动脉闭塞，若采取传统方法，如降纤治疗、抗凝治疗和抗血小板聚集治疗，通常难以及时使基底动脉的血管再通，病死率高达80％～90％。

因此，20世纪80年代开始，基底动脉闭塞后动脉溶栓治疗才得以逐步开展和不断完善。

我们回顾20余年基底动脉闭塞的动脉溶栓治疗的相关文献，初步探讨血管再通及其临床意义。

【总页数】3页(P430-432)
【作者】陶华;李慎茂
【作者单位】100053,北京,首都医科大学宣武医院介入放射诊断;100053,北京,首都医科大学宣武医院介入放射诊断
【正文语种】中文
【中图分类】R743.3
【相关文献】
1.银杏内酯注射液治疗脑卒中基底动脉闭塞后再通1例 [J], 张辉;秦旋;赵德福;高元智;王晓斌
2.血管内机械再通治疗急性基底动脉闭塞的疗效分析 [J], 代成波;王硕;刘新通;马桂贤;杨哲贤;马腾云;张雄;王丽娟
3.急性基底动脉闭塞血管再通治疗的现状与探索 [J], 资文杰
4.急性大动脉闭塞性脑梗死患者血管再通治疗后早期神经功能恶化的影响因素分析[J], 陈敏;冯灵;涂双燕;汪锐
5.亚急性、慢性椎-基底动脉闭塞的血管内再通治疗分析 [J], 孙文华;樊翊凌;丁圣豪;赵兵;潘耀华;万杰清
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1、建立脑血管病专业救治体系，院内急诊科须独立设置脑血管病急诊室，开设脑血管病急救绿色通道。
2、优化脑血管病就诊流程，采用表格式病历，在接诊重点查体后送影像检查途中进行病历采集、记录。争取在患者到院15分钟至30分钟能开始进行神经影像检查。
3、脑卒中指令影像检查室，急诊优先。一定要做醒目提示板告之，取得择期CT/MR/DSA检查患者及家属的理解，和谐医患关系。
侧小脑前下动脉显影浅淡。 18：05至18：46介入溶栓，予尿激酶50万单位微导管缓慢推注，左侧
大脑后动脉显影，右侧大脑后动脉未显影，基底动脉起始部斑块狭窄。 19：16至19：28家属经商议同意颅内支架治疗。 19：32支架置入后，基底动脉管腔恢复，颅内血流明显增加。术毕，患者四肢可无意识活动，术后12小时清醒，能准确回答问题，
脑血管病专业救治体系尚未建立，患者在院内的就诊时间曲线给治疗带来巨大风险。
时间的考验：笔者回顾性分析近5年行动脉溶栓患者院内时间曲线：完成CT检查时间距患者到院平均为76分钟；完成MR检查时间距患者到院平均为130分钟；进入DSA检查室时间距患者到院平均148分钟。
冰冷的数字严峻的考验沉重的思考理念的呐喊
典型病例时间曲线
患者，男，48岁。 6：10被家人发现言语不利，数分钟后出现意识不清、呼之不应。 8：20在当地县医院行头颅CT检查示：左枕内侧面低密度改变，对症
处理。 15：30至16：24我院MRI/MRA示：双侧小脑、左丘脑、枕叶低密度
改变，基底动脉闭塞，左椎动脉未显影。 17：36至17：52DSA示：双侧后交通动脉未开放，基底动脉闭塞，双
基底动脉血栓闭塞治疗理念 ----溶栓/支架治疗
吕彦锋张帆郭贵军徐国栋
脑血管介入溶栓的循证指南
发病6h内由大脑中动脉闭塞导致的严重脑卒中且不适合静脉溶栓的患者，经过严格选择后可在有条件的医院进行动脉溶栓（Ⅱ级推荐，B级证据）。
发病24h内由后循环动脉闭塞导致的严重脑卒中且不适合静脉溶栓的患者，经过严格选择后可在有条件的单位进行动脉溶栓（Ⅲ级推荐，C级证据）。
4、上级医师全程与患者家属进行病情分析及治疗方案决策，尽可能缩短家属由于选择的思考而延长治疗时间。
5、神经介入器械准备充分，在患者得到影像资料的第一时间内能将可能用到的神经介入器材按术者习惯位置排列，随时可打开使用。
6、神经介入费用较高，探讨机制上解决最佳治疗时机与费用支付时间矛盾的方案，消除医、患对医疗费用的顾虑。
溶栓患者的抗血小板或特殊情况下溶栓后还需抗凝治疗者，应推迟到溶栓24h后开始（Ⅰ级推荐， B级证据）。
临床现状
国内对急性缺血性脑卒中患者的救治情况各医疗机构差异性极大，甚至一些三级甲等医院的神经内科医生对“时间就是大脑、血管就是生命”的重视程度仍远远不够。
影像学检查选择：急诊的MRI/MRA/DSA检查尚未深入“医心”，许多医生仍以CT做为缺血性脑血管病的主要影像检查选择。
右侧肢体肌力Ⅳ级，左侧肢体肌力Ⅴ级，无呛咳、吞咽困难。
8：20CT
15：30MRI
MRI
16：24MRA
17：36DSA
17：39DSA
17：52DSA
18：05DSA
18：46DSA
19：16DSA
19：31DSA
19：32DSA
19：34DSA
19：35DSA
治疗理念
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