ACUTE脑血管疾病急诊(1)

1、脑血管疾病急诊脑血管疾病急诊 丹阳市第三人民医院丹阳市第三人民医院Research on StrokeSmall Vessels, Big Problems谢谢 康康 民民The Clinical Problem Stroke ranks second after ischemic heart disease as a cause of death worldwide In the United States, where it is the third leading cause of death and the leading cause of serious long-term disa

2、bility, approximately 750,000 strokes occur annually, with an annual mortality rate exceeding 150,000.The Clinical Problem Thirty-day case fatality rates for ischemic stroke in Western societies generally range between 10 and 17%. Mortality in the first month after stroke has been reported to range

3、from 2.5% in patients with lacunar infarcts4 to 78% in patients with space-occupying hemispheric infarction.The vertebrobasilar arterial supply feeds the brain stem (medulla, pons, andmidbrain), cerebellum, occipital lobes, posterior temporal lobes, and thalamus(not visible in this view). The arteri

4、al supply consists of the extracranialand intracranial vertebral arteries, which unite to form the basilar artery,which runs midline along the ventral surface of the brain stem, feeding it withsmall, deep perforators until it merges with the circle of Willis to give off theposterior cerebral arterie

5、s. Arterial Supply of the Brain Stem, Cerebellum, Occipital Lobes, Posterior Temporal Lobes, and Thalamus.Large-Vessel and Small-Vessel Brain Disease. Axial MRI with the use of gradient-echo technique (Panel B) and fluid-attenuated inversion recovery (Panel C) highlight two prominent radiographic fe

6、atures of small-vessel brain disease: hemorrhages (Panel B, dark lesions examples shown by arrowheads) and changes in white matter (Panel C, bright lesions). The images are of a 71-year-old man with probable cerebral amyloid angiopathy.Acute Ischemic Stroke In Western societies, about 80% of strokes

7、 are caused by focal cerebral ischemia due to arterial occlusion, and the remaining 20% are caused by hemorrhages. Atherosclerosis (leading to thromboembolism or local occlusion) and cardioembolism are the leading causes of brain ischemia.PATHOPHYSIOLOGY AND TARGETSFOR INTERVENTION Ischemic brain in

8、jury is thought to result from a cascade of events fromIschemic brain injury is thought to result from a cascade of events from energy depletion to cell death. Intermediate factors include an excess of extracellular excitatory amino acids, free-radical formation, and inflammation.The ischemic penumb

9、raThe ischemic penumbra脑缺血的三种模式的图解脑缺血的三种模式的图解:中心为中心为CBF12ml/(100g.min)的梗死核心区，中间层为处于危险状的梗死核心区，中间层为处于危险状态的态的CBF为为12-20ml/(100g.min)低灌注区（缺血性半影带）外带为血低灌注区（缺血性半影带）外带为血流量减少区域流量减少区域 。CBF值为每值为每100克脑组织每分钟的血流毫升数，克脑组织每分钟的血流毫升数，正常范围是正常范围是60 80ml/（100g.min）。当）。当CGF下降至下降至20 -25 ml/（100g.min）时）时,并不出现功能丧失。并不出现功能丧失。C

10、BF进一步下降至进一步下降至10 -20 ml/（100g.min）时可造成功能丧失，但脑的结构仍保留。这种受累的）时可造成功能丧失，但脑的结构仍保留。这种受累的脑组织区域即所谓脑组织区域即所谓“缺血半影带缺血半影带”（ischemic penumbra）（朦胧）（朦胧带）。带）。缺血性半影带的概念是动态的，依赖于与其相关的其他因素，如氧合缺血性半影带的概念是动态的，依赖于与其相关的其他因素，如氧合作用、血糖、足够的作用、血糖、足够的MAP和和CPP、血管阻塞部位和侧枝循环状态以、血管阻塞部位和侧枝循环状态以及缺血时间。及缺血时间。Ischemic brain injury is though

11、t to result from a cascade of events from energydepletion to cell death.The Molecular Events Initiated in Brain Tissue by Acute Cerebral IschemiaInterruption of cerebral blood flow results in decreased energy production, which in turn causes failure of ionic pumps, mitochondrial injury, activation o

12、f leukocytes (with release of mediators of inflammation), generation of oxygen radicals, and release of excitotoxins. Increased cellular levels of sodium, chloride, and calcium ions result in stimulation of phospholipases and proteases, followed by generation and release of prostaglandins and leukot

13、rienes, breakdown of DNA and the cytoskeleton, andultimately, breakdown of the cell membrane. Alteration of geneticcomponents regulates elements of the cascade to alter thedegree of injury. AMPA denotes alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid and NMDA :N-methyl-D-aspartate. Cytotox

14、ic edema is detectable within minutes after the onset of ischemia, with a reduced apparent diffusion coefficient on diffusion-weighted imagingPrimary mechanisms of cerebral injury after SAH. Blood released in the subarachnoid space upon aneurysm rupture elevates ICP causes CBF and cerebral perfusion

15、 pressure (CPP) reductions leading to circulation arrest and ultimately cerebral ischemia. In addition, major cerebral arteries are constricted early (within an hour) after SAH and will contribute to circulation arrest and development of cerebral ischemia超早期的细胞内水肿超早期的细胞内水肿 脑组织缺血缺氧的数十分钟内-细胞内水肿常规MRI或者

16、CT上均不能显示 细胞内水肿使水的弥散受限-ADC下降-在SE-EPI成像时出现高信号。（自旋回波平面回波）-功能磁共振-弥散成像。 临床使用DWI和PWI影像技术，使处于梗死的危险组织（tissue at risk）的测量，认定为半影区。这种PWI/DWI不匹配模式可以认定。 Progression over Time (Left to Right) of the Infarct Core (Red); With Irreversible Damage at the Expense of the Ischemic Penumbra (Green).CT Scans Obtained 1 Ho

17、ur 40 Minutes after the Onset of Symptoms Suggestive of Cortical Stroke in the Territory of the Right Middle Cerebral Artery. MRI Scans Obtained 2 Days after the Onset of Ischemic Stroke in the Territory of the Right Middle Cerebral Artery. A hyperintense lesion in the temporal and frontal lobes and

18、 in the basal ganglia is shown on fluid-attenuated inversion recovery (Panel A) and diffusion weighted imaging (Panel B), corresponding to a reduced apparent diffusion coefficient (Panel C). Similar changes may be observed on diffusion-weighted imaging in the first hours after the onset of symptoms.

19、Perfusion CT Scans Obtained 1 Hour 45 Minutes after the Onset of Ischemia in the Territory of the Right Middle Cerebral Artery.A large area shows prolongation of the mean transit time (in seconds) (Panel A), and a smaller area shows a reduction in cerebral blood volume (in milliliters per 100 g) (Pa

20、nel B). These two maps suggest a large penumbra and a small infarct core (Panel C, with the penumbra shown in green and the suggested infarct core in red).脑血容量 cerebral blood volume CBV平均通过时间 mean transit time MTTCT Scan of the Brain of a Patient with Confusion, Left Hemiparesis, and Left Hemisensor

21、y Loss 50 Minutes, 3 Hours, and 25 Hours after the Onset of Stroke.For each time point, a lower (top image) and higher (bottom image) axial section is shown. The patient was treated with intravenous tPA, at a dose of 0.9 mg /kg, (200 cm per second) in the left middle and anterior cerebral arteries.

22、Angiography showed considerable vasospasm (Panel D) in the proximal segments of the left anterior arteries (arrowhead) and middle cerebral arteries (arrow). The patient underwent transluminal balloon angioplasty of the left middle cerebral artery, and direct vasodilators (papaverine and verapamil) w

23、ere infused into the left anterior cerebral artery with good resolution of the vasospasm (Panel E). The patients clinical course evolved favorably, and she was independent three months after presentation. Acute Effects of Subarachnoid Hemorrhage Cerebral vasospasm, a major cause of morbidity and mor

24、tality, refers to the intracranial vasoconstriction that may occur between 3 and 12 days after a subarachnoid hemorrhage. The cause of vasospasm is unknown;Medical Therapy nimodipine (60 mg every four hours for 21 days), which has been shown to improve the outcome after subarachnoid hemorrhage tripl

25、e-H (hypertension, hypervolemia, and hemodilution) therapy is initiated Angioplasty（Balloon angioplasty and antispasmodic agents）TREATMENT OPTIONS There are three options for treating intracranial aneurysms: observation, craniotomy with clip ligation (clipping) endovascular occlusion with the use of

26、 detachable coils (coiling)Microsurgical Clipping of an Aneurysm of the Posterior CommunicatingArtery.Panel A shows the typical skin incision (unbroken curved line) and craniotomy (dashed lines) needed to access the aneurysm.Panel B shows the applicationof the clip blade to the neck of the aneurysm.

27、Endovascular Occlusion of an Aneurysm of the Posterior Communicating Artery with Guglielmi Detachable Coils.Panel A and inset show the route of the microcatheter into the aneurysm through the right femoral artery, aorta, and left carotid artery and the beginning of the coil deployment.Panel B shows

28、the final occlusion of the aneurysm with coils.Endovascular Coiling of Ruptured Intracranial Aneurysm.Panel A shows a drawing of a platinum coil after deployment. Panel B shows cerebral angiography of a ruptured aneurysm at the basilar tip before endovascular coiling (arrow) and immediately after en

29、dovascular coiling (Panel C). Stent-Assisted Re-Coiling after Recurrence of an Aneurysm Initially Treated with Coiling.Panel A (three-dimensional rotational catheter angiogram) and Panel B (left carotid injection, two-dimensional catheter angiogram,oblique view) show an aneurysm of the posterior com

30、municating artery (Panel B, arrow). Panel C (two-dimensional catheter angiogram,lateral view) shows the successful coiling of the aneurysm (arrow); this was followed eight months later with marked coil compaction and recanalization of the aneurysm (Panel D, two-dimensional catheter angiogram, latera

31、l view). Panel E (two-dimensional catheter angiogram,lateral view) shows successful re-coiling of the aneurysm with the assistance of a stent (too small to visualize). Panel F shows the configuration used for the stent and the coil.Most Common Sites and Sources of Intracerebral HemorrhageCommon Site

32、s Intracerebral hemorrhages most commonly involve cerebral lobes, originating from penetrating cortical branches of the anterior, middle, or posterior cerebral arteries (A); basal ganglia, originating from ascending lenticulostriate branches of the middle cerebral artery (B); the thalamus, originati

33、ng from ascending thalmogeniculate branches of the posterior cerebral artery (C); the pons, originating from paramedian branches of the basilar artery (D); the cerebellum, originating from penetrating branches of the posteriorinferior, anterior inferior, or superior cerebellar arteries (E).急诊诊断和评估脑出

34、血的建议 I类 1 脑出血是急症，经常有早期持续出血和进行性恶化，严重的临床功能缺损，导致高死亡率和患病率，应及时识别和确诊 ( I类, 证据水平A)。 2 CT和磁共振都是初步影像检查的首选 ( I类, 证据水平A)；如果患者有磁共振检查的禁忌，应当查CT ( I类, 证据水平A)。 The first CT scan (Panel A) was obtained one hour after the patient presented and was followed by neurologic deterioration and expansion of the hematoma vis

35、ible on the CT scan obtained six hours after presentation (Panel B).MANAGEMENT Evaluation and Management in the Emergency Room Intensive Monitoring of Neurologic and Cardiovascular Status Mass Effect and Intracranial Hypertension Management of Blood Pressure CT可表明ICH的自然史。在90年代中期，自发性脑出血的前瞻性研究表明发病3小时内

36、患者行基线CT，复查CT发现有38的患者血肿扩大（扩大标准是血肿体积扩大33）。其中血肿扩大者中的2/3是在1小时内血肿扩大就比较明显自发性脑出血血压升高时的治疗建议自发性脑出血血压升高时的治疗建议 1 如果舒张压200 mmHg或平均动脉压150 mmHg, 要考虑用持续静脉输注积极降低血压， 血压的监测频率为每5分钟一次。 2 如果舒张压180 mmHg或平均动脉压130 mmHg，并有疑似颅内压升高的证据，要考虑监测颅内压，用间断或持续的静脉给药降低血压，以保证脑灌注压60-80 mmHg。 3 如果舒张压180 mmHg或平均动脉压130 mmHg，并且没有疑似颅内压升高的证据，要考

37、虑用间断或持续的静脉给药轻度降低血压(例如，平均动脉压110 mm Hg或目标血压为160/90 mm Hg)，每隔15分钟给病人做一次临床复查。 脑出血患者控制血压可以考虑的静脉用药脑出血患者控制血压可以考虑的静脉用药 药物 静脉团注剂量 持续输注剂量 拉贝洛尔 每15 分钟5-20 mg 2 mg/min (最大300 mg/d) 尼卡地平 NA 5-15 mg/h 艾司洛尔 静脉推注负荷量250 g/kg 25-300 gkg-1min-1 依那普利 每小时静脉推注1.25-5mg* NA 肼屈嗪 每30 分钟静脉推注5-20 mg 1.5-5gkg-1min-1 硝普钠 NA 0.1-

38、10 gkg-1min-1 硝酸甘油 NA 20-400 g/min NA：不适用。：不适用。 *因为有可能突然血压降低因为有可能突然血压降低, 依那普利的首次试验剂量应为依那普利的首次试验剂量应为0.625m手术方法的建议 I 类 1. 小脑出血3 厘米者，如神经功能继续恶化或脑干受压和/或脑室梗阻引起脑积水，应尽快手术清除出血(I 类,证据水平B)。 II 类 1. 虽然在发病后72 小时内向凝血块腔内立体定向注射尿激酶能明显减小血块和减少死亡风险，但是再出血更为常见，功能结局没有改善；因此，它的有用性还不能确定(IIb 类,证据水平B)。 2 . 尽管理论上吸引人，但用各种机械装置和/或內镜进行的微创血凝块抽吸仍然有待临床试验的进一步检验；所以，目前其有用性还不能确定 (IIb 类,证据水平B)。 3. 脑叶血块距离脑表面1cm者，可以考虑用标准开颅术清除幕上脑出血(IIb 类,证据水平B)。 手术方法的建议 III 类 1.不建议在发病后96小时内用标准开颅术常规清除幕上脑出血（III类，证据水平A）。（参考上述可能的II类例外情况，脑叶