高血压小动脉纤维素样坏死fibrinoid课件

1、脑 出 血Intracerebral hemorrhage Department of Neurology, The 2nd affiliated hospital, Harbin Medical University脑 出 血Intracerebral hemorrhConceptionIt means primary and nontraumatic intracerebral hemorrhage.Count for 20%30% in strokeHypertension is the most common underlying cause of nontraumatic intra

2、cerebral hemorrhage.ConceptionIt means primary andEtiologyHalf of the patients suffer from hypertension combined with arteriolar atherosclerosis, it is the most common cause of the disease.Others：cerebral atherosclerosis, hematopathy, cerebral amyloid angiopathy CAA , aneurysm, AVMEtiologyHalf of th

3、e patients s Pathophysiology高血压小动脉：纤维素样坏死fibrinoid necrosis、脂质透明变性hyaline fatty change、microaneurysm小动脉瘤、微夹层动脉瘤渗出exudation、破裂rupture高血压远端血管痉挛vasospasm缺氧anoxia、坏死angio-necrosis、血栓形成thrombosis斑点状出血、脑水肿brain edema融合成片(子痫) Pathophysiology高血压小动脉：纤维素样Pathophysiology 脑内动脉：壁薄、中层肌细胞及外膜结缔组织少、缺乏外弹力层随年龄增长弯曲呈螺旋状

4、出血主要部位：深穿支penetrating arteries豆纹动脉lenticulostriate artery：大脑中动脉呈直角分出，易发生粟粒状动脉瘤，为脑出血最好发部位，其外侧支称为出血动脉bleeding arteryPathophysiology 脑内动脉：壁薄、中层肌细胞及 Pathophysiology 一次出血常在30min内停止头CT动态观察：20%-40%患者24小时内血肿仍继续扩大，为活动性出血active hemorrhage或早期再出血early rebleeding多发性脑出血常继发于：hematopathy,cerebral amyloid angiopathy

5、,neoplasm,vasculitis Pathophysiology 一次出血常在30min内停 PathologyHypertensive ICH：基底节的内囊区inter capsule、壳核putamen占70%，脑叶lobe、脑干brainstem、小脑齿状核区各占10%Location of ICH：壳核（内囊、侧脑室），丘脑thalamus（第三脑室、内囊、侧脑室），脑桥pons、小脑cerebellum、蛛网膜下腔subarachnoid space、第四脑室forth ventricle PathologyHypertensive ICH：基底PathologyHypert

6、ensive ICH：cerebral penetrating artery miliary aneurysmNon Hypertensive ICH：occur in subcortical white matter without arteriosclerosisPathologyHypertensive ICH：cerePathologySwelling and congestion of hemisphere出血灶：充满血液的空腔，周围是坏死脑组织及淤点状出血性软化带、脑水肿血块溶解吞噬细胞清除含铁血黄素和坏死脑组织胶质增生（胶质瘢痕或中风囊）PathologySwelling and

7、 congestiClinical featuresage：5070 years oldsex：more male patientsseason：winter or springpast history：hypertensioninducement：activity、excitementonset：acute onsetClinical featuresage：5070 yeClinical featuresHypertensive hemorrhage occurs without warning, most commonly while the patient is awake. Head

8、ache is present in 50% of patients and may be severe, vomiting is common.Blood pressure is elevated after the hemorrhage has occurred. Thus, normal or low blood pressure in a patient with stroke makes the diagnosis of hypertensive hemorrhage unlikely, as does onset before 50 years of age. Clinical f

9、eaturesHypertensive Clinical featuresbasal ganglion hemorrhageThe two most common sites of hypertensive hemorrhage are the putamen(figure 1) and thalamus(figure 2), which are separated by the posterior limb of the internal capsule. In general, putaminal hemorrhage leads to a more severe motor defici

10、t (hemiplegia) and thalamic hemorrhage to a more marked sensory disturbance (hemianesthesia). Clinical featuresbasal gangliClinical featuresbasal ganglion hemorrhage Homonymous hemianopia may occur as a transient phenomenon after thalamic hemorrhage and is often a persistent finding in putaminal hem

11、orrhage. In large thalamic hemorrhages, the eyes may deviate downward, as in staring at the tip of the nose, because of impingement on the midbrain center for upward gaze. Clinical featuresbasal gangliClinical featuresbasal ganglion hemorrhageAphasia may occur if hemorrhage at either site exerts pre

12、ssure on the cortical language areas. Large hemorrhages may lead to consciousness disturbance, while minor hemorrhages lead to lacunar syndrome.Clinical featuresbasal gangliClinical featuresbasal ganglion hemorrhage丘脑出血thalamus hemorrhage: 丘脑膝状动脉、穿通动脉破裂，表现为三偏症状，不同于壳核之处为均等瘫、深浅感觉障碍、特征性眼征、意识障碍重、中线症状等尾状

13、核头出血caput nuclei caudati hemorrhage: 少见，仅见脑膜刺激征Clinical featuresbasal gangliClinical featurespontine hemorrhage With bleeding into the pons(figure 3), coma occurs within seconds to minutes and usually leads to death within 48 hours. Ocular findings typically include pinpoint pupils. Horizontal eyes

14、movements are absent or impaired, but vertical eye movements may be preserved. In some patients, there may be ocular bobbing.Clinical featurespontine hemoClinical featurespontine hemorrhagePatients are commonly quadriparetic or hemiplegia alternate and exhibit decerebrate posturing. Hyperthermia, re

15、spiration disorder is sometimes present. The hemorrhage usually ruptures into the forth ventricle, and rostral extension of the hemorrhage into the midbrain with resultant midposition fixed pupils is common. Clinical featurespontine hemoClinical featuresmidbrain hemorrhageMidbrain hemorrhage is rare

16、ly seen in clinic.The patients often manifest Weber syndrome.Large hemorrhages may lead to coma and flaccid paralysis.Clinical featuresmidbrain hemClinical featurescerebellar hemorrhage小脑齿状核动脉破裂The distinctive symptoms of cerebellar hemorrhage(figure 4) are severe headache, dizziness, vomiting, and

17、the inability to stand or walk, but strength in the limbs is normal.Large hemorrhages lead to coma within 12 hours in 75% of patients and within 24 hours in 90%.They may lead to compression of the brainstem.Clinical featurescerebellar hClinical featureslobar hemorrhageEtiology：AVM、Moyamoya disease、c

18、erebral amyloid angiopathy、tumorHypertensive hemorrhages also occur in subcortical white matter underlying the frontal,parietal, temporal, and occipital lobes(figure 5).Symptoms and signs vary according to the location; they can include headache, vomiting, hemiparesis, hemisensory deficits, aphasia,

19、 and visual field abnormalities.Seizures are more frequent than with hemorrhages in other locations, while coma is less so.Clinical featureslobar hemorrClinical featurescerebral ventriculus hemorrhage脉络丛plexus chorioideus动脉或室管膜下动脉破裂(figure 6)Global symptoms are obvious，but local symptoms are not.The

20、 patients may have a full recovery and a good outcome.Large hemorrhages may lead to coma, vomiting, pinpoint pupils,implies a poor outcome.Clinical featurescerebral venSupplementary findingsCT computerized tomography is chosen firstLesion:high density(hematoma) surronded by low density(edema)（figure

21、 7）Mass effect is often seen in CTSupplementary findingsCT compuSupplementary findingsMRI magnetic resonance image 急性期对幕上及小脑出血显示不如CT，对脑干出血显示优于CTICH and cerebral infarction can be distinguished by MRI 45 weeks,but CT can not distinguish themEasy to detect AVM、aneurysmComplex stagesSupplementary findi

22、ngsMRI magnSupplementary findingsDSA：to diagnose AVM、Moyamoya disease、arteritisCSF：elevated pressure,consistently bloody,but not the routine examination其他：血、尿、便常规，肝功，肾功，凝血功能，心电图等Supplementary findingsDSA：to dDiagnosisSenile patients after 50 years of agePast history of hypertensionOnset during activ

23、itySudden onset CT scanDiagnosisSenile patients afterDifferential diagnosisCerebral infarction:situation and speed of onset,blood pressure,lesion showed by CTComa due to other causes:present illness historyInjury:history of injuryNonhypertensive hemorrhage:without history of hypertensionDifferential

24、 diagnosisCerebralTreatmentmedical treatment保持安静keep quiet、卧床休息rest in bed、减少探视avoid meeting水电解质平衡keep water_electrolyte balance 和营养nutrition控制脑水肿control brain edema，降低颅内压decrease ICP:antiedema agents,e.g.mannitol控制高血压control blood pressure: antihypertensive agents or diuretic such as furosemide防治并发

25、症prevent complications:rebleeding, herniation, infectionTreatmentmedical treatment保持安Treatmentsurgical treatment时机：超早期 6-24小时Indication Contraindications术式Treatmentsurgical treatment时机Rehabilitation 尽早进行as soon as possible抗抑郁antidepressionRehabilitation 尽早进行as soon as Specific treatmentNonhypertensi

26、ve hemorrhagePoly-cerebral hemorrhage RebleedingUnstable cerebral hemorrhageSpecific treatmentNonhypertensPrognosisThe mortality in 30 days is 35%52%,half of the patients die within 2 days,due to cerebral herniation.Large hemorrhages of brainstem、thalamus 、ventricle implies a poor prognosis.Prognosi

27、sThe mortality in 30 d蛛网膜下腔出血Subarachnoid hemorrhage, SAHDepartment of Neurology, The 2nd affiliated hospital, Harbin Medical University蛛网膜下腔出血Subarachnoid hemorrhag ConceptionIt is an acute hemorrhagic cerebral vascular disease in which vessels on surface of brain and spinal cord rupture suddenly d

28、ue to many causes,blood flow into the subarachnoid space,called primary SAHSecondary SAH：hemorrhages in brain、ventricle or epidural (subdural) space rupture into subarachnoid spaceTraumatic SAHCount for 10% in stroke，for 20% in hemorrhagic stroke ConceptionIt is an acute hemoEtiologyCongenital aneur

29、ysm is most common etiologyAVM is a less frequent cause of SAHHypertensive arteriosclerosis aneurysm is the third cause of SAHMoyamoya disease is the forth causeOthers include tumor, arteritis EtiologyCongenital aneurysm is PathophysiologyCerebral artery aneurysm are most commonly congenital “berry”

30、 aneurysms, which result from developmental weakness of the vessel wall, especially at the sites of branching.AVM are most common in the middle cerebral artery distribution.Arteritis can also play an important role in the disease.Tumor invasive the vessel wall can not be overlooked. PathophysiologyC

31、erebral arterPathophysiology颅内压增高increased ICP阻塞性脑积水obstructive hydrocephalus化学性脑膜炎aseptic meningitis下丘脑功能紊乱自主神经功能紊乱dysautonimia交通性脑积水communicating hydrocephalus血管活性物质致血管痉挛vascular spasm、蛛网膜颗粒粘连、甚至脑梗死、正常颅压脑积水Pathophysiology颅内压增高increased Pathology85%90% of intracranial aneurysms locate anterior in t

32、he circle of Willis,they are mainly single,they are multiple in about 10%20% of cases,locating in the opposite site of the same vessel,called mirror aneurysm.好发于Willis环动脉分叉处破裂频度血液主要沉积在脑底部、脑池可破入脑室致脑积水蛛网膜无菌性炎症反应 Pathology85%90% of intracranClinical featuresAny age of person may suffer from SAH. The cl

33、assic (but not invariable) presentation of SAH is the sudden onset of an unusually severe generalized headache, patients often describe it as “the worst headache I ever had in my life”. The absence of the headache essentially precludes the diagnosis. Loss of consciousness is frequent, as are vomitin

34、g and neck stiffness. Symptoms may begin at any time of day and during either rest or exertion. Clinical featuresAny age of peClinical featuresThe most significant feature of the headache is that it is new. Milder but otherwise similar headaches may have occurred in the weeks prior to the acute even

35、t. These earlier headaches are probably the result of small prodromal hemorrhages (sentinel,or warning, hemorrhages) or aneurysmal stretch.Clinical featuresThe most signClinical featuresThe headache is not always severe, but the intensity of the headache may remain unchanged for several days and sub

36、side only slowly over the next 2 weeks. A recrudescent headache usually signifies recurrent bleeding.There is frequently confusion, stupor, or coma. Nuchal rigidity and other evidence of meningeal irritation are common. Meningeal irritation may induce temperature elevations to as high as 39 during t

37、he first 2 weeks. Preretinal globular subhyaloid hemorrhages (found in 20% of cases) are most suggestive of the diagnosis. Clinical featuresThe headache Clinical featuresBecause bleeding occurs mainly in the subarachnoid space in patients with aneurysmal rupture, prominent focal signs are uncommon o

38、n neurologic examination. When present, they may bear no relationship to the site of the aneurysm. An exception is oculomotor nerve palsy occurring ipsilateral to a posterior communicating artery aneurysm. Bilateral extensor plantar responses and nerve palsies are frequent in such cases. Ruptured AV

39、Ms may produce focal signs, such as hemiparesis, aphasia, or a defect of the visual fields.Clinical featuresBecause bleed Clinical featuresInducement and aura：inducement include intensive activity、exhaustion、excitement,aura can be “warning leak” and localized sign.Symptoms of SAH patients above 60 y

40、ear old are not typical：slowly onset,headache and meningeal irritation are not obvious,with severe consciousness disturbance,often accomplished with cardiac damage and other complications Clinical featuresInducement aComplicationsRecurrence of hemorrhage:Recurrence of aneurysmal hemorrhage (20% over

41、 10-14 days) is the major acute complication and roughly doubles the mortality rate. Recurrence of hemorrhage from AVM is less common in the acute period.Arterial vasospasm:Delayed arterial narrowing, termed vasospasm, occurs in vessels surrounded by subarachnoid blood and can lead to parenchymal is

42、chemia in more than one- third of cases. ComplicationsRecurrence of hemComplicationsAcute or subacute hydrocephalus:Acute or subacute hydrocephalus may develop during the first day- or after several weeks-as a result of impaired CSF absorption in the subarachnoid space. Progressive somnolence, nonfo

43、cal findings, and impaired upgaze should suggest the diagnosis.ComplicationsAcute or subacuteComplicationsSeizures: Seizures occur in fewer than 10% of cases and only following damage to the cerebral hemisphere. Others:Although inappropriate secretion of antidiuretic hormone and resultant diabetes i

44、nsidious can occur, they are uncommon.ComplicationsSeizures: Seizure Supplementary findingsCT：patients presenting with SAH are generally investigated first by CT scan(figure 8)，which will usually confirm that hemorrhage has occurred and may help to identify a focal source. 约15%患者CT仅显示脚间池少量出血，向中脑环池、外

45、侧裂池基底扩散，称非动脉瘤性SAH nA-SAHCSF:if CT scan fails to confirm the clinical diagnosis, lumber puncture is performed. The fluid is grossly bloody, the supernatant of the centrifuged CSF becomes yellow (xanthochromic), the chemical meningitis may produce pleocytosis. Supplementary findingsCT：patSupplementary

46、 findingsDSA:to detect aneurysm or AVM, it is a prerequisite to the rational planning of surgical treatment.MRI and MRA:MRI is especially useful in detecting small AVMs localized to the brainstem (an area poorly seen on CT scan).TCD：to determine CVS实验室检查：血常规、凝血功能、肝功、免疫学Supplementary findingsDSA:to d DiagnosisSymptom：the history of a sudden severe headache with confusion or obtundationSign：nuchal rigidity, a nonfocal neurologic examinationCSF：bloody spinal fluidFundus oculi：preretinal globular subhya