Presentation on theme: "脑 出 血 Intracerebral hemorrhage Department of Neurology, The 2nd affiliated hospital, Harbin Medical University."— Presentation transcript:
脑 出 血 Intracerebral hemorrhage Department of Neurology, The 2nd affiliated hospital, Harbin Medical University
Conception It means primary and nontraumatic intracerebral hemorrhage. Count for 20%~30% in stroke Hypertension is the most common underlying cause of nontraumatic intracerebral hemorrhage.
Etiology Half 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, AVM
Pathology Hypertensive 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%基底节的内囊区壳核 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丘脑小脑
Pathology Hypertensive ICH ： cerebral penetrating artery miliary aneurysm Non Hypertensive ICH ： occur in subcortical white matter without arteriosclerosis
Pathology Swelling 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）
Clinical features age ： 50~70 years old sex ： more male patients season ： winter or spring past history ： hypertension inducement ： activity 、 excitement onset ： acute onset
Clinical features Hypertensive hemorrhage occurs without warning, most commonly while the patient is awake. Headache 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 features basal ganglion hemorrhage The 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. putamen(figure 1) thalamus(figure 2) In general, putaminal hemorrhage leads to a more severe motor deficit (hemiplegia) and thalamic hemorrhage to a more marked sensory disturbance (hemianesthesia).
Clinical features basal ganglion hemorrhage Homonymous hemianopia may occur as a transient phenomenon after thalamic hemorrhage and is often a persistent finding in putaminal hemorrhage. 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 features basal ganglion hemorrhage Aphasia may occur if hemorrhage at either site exerts pressure on the cortical language areas. Large hemorrhages may lead to consciousness disturbance, while minor hemorrhages lead to lacunar syndrome.
Clinical features basal ganglion hemorrhage 丘脑出血 thalamus hemorrhage: 丘脑出血 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 尾状核头出血 caput nuclei caudati hemorrhage: 少见，仅见脑膜刺激征
Clinical features pontine hemorrhage With bleeding into the pons(figure 3), coma occurs within seconds to minutes and usually leads to death within 48 hours.pons(figure 3) Ocular findings typically include pinpoint pupils. Horizontal eyes movements are absent or impaired, but vertical eye movements may be preserved. In some patients, there may be ocular bobbing.
Clinical features pontine hemorrhage Patients are commonly quadriparetic or hemiplegia alternate and exhibit decerebrate posturing. Hyperthermia, respiration 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 features midbrain hemorrhage Midbrain hemorrhage is rarely seen in clinic. The patients often manifest Weber syndrome. Large hemorrhages may lead to coma and flaccid paralysis.
Clinical features cerebellar hemorrhage 小脑齿状核动脉破裂 The distinctive symptoms of cerebellar hemorrhage(figure 4) are severe headache, dizziness, vomiting, and the inability to stand or walk, but strength in the limbs is normal.cerebellar hemorrhage(figure 4) 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 features lobar hemorrhage Etiology ： AVM 、 Moyamoya disease 、 cerebral amyloid angiopathy 、 tumor Hypertensive hemorrhages also occur in subcortical white matter underlying the frontal,parietal, temporal, and occipital lobes(figure 5).(figure 5) Symptoms and signs vary according to the location; they can include headache, vomiting, hemiparesis, hemisensory deficits, aphasia, and visual field abnormalities. Seizures are more frequent than with hemorrhages in other locations, while coma is less so.
Clinical features cerebral ventriculus hemorrhage 脉络丛 plexus chorioideus 动脉或室管膜下动 脉破裂 (figure 6) (figure 6) Global symptoms are obvious ， but local symptoms are not. The patients may have a full recovery and a good outcome. Large hemorrhages may lead to coma, vomiting, pinpoint pupils,implies a poor outcome.
Supplementary findings CT computerized tomography is chosen first Lesion:high density(hematoma) surronded by low density(edema) （ figure 7 ） （ figure 7 ） Mass effect is often seen in CT
Supplementary findings MRI 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 CT ICH and cerebral infarction can be distinguished by MRI 4~5 weeks,but CT can not distinguish them Easy to detect AVM 、 aneurysm Complex stages
Supplementary findings DSA ： to diagnose AVM 、 Moyamoya disease 、 arteritis CSF ： 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
Diagnosis Senile patients after 50 years of age Past history of hypertension Onset during activity Sudden onset CT scan
Differential diagnosis Cerebral infarction:situation and speed of onset,blood pressure,lesion showed by CT Coma due to other causes:present illness history Injury:history of injury Nonhypertensive hemorrhage:without history of hypertension
Treatment medical 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 防治并发症 prevent complications:rebleeding, herniation, infection
Prognosis The 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.
蛛网膜下腔出血 Subarachnoid hemorrhage, SAH Department of Neurology, The 2nd affiliated hospital, Harbin Medical University
Conception It is an acute hemorrhagic cerebral vascular disease in which vessels on surface of brain and spinal cord rupture suddenly due to many causes,blood flow into the subarachnoid space,called primary SAH Secondary SAH ： hemorrhages in brain 、 ventricle or epidural (subdural) space rupture into subarachnoid space Traumatic SAH Count for 10% in stroke ， for 20% in hemorrhagic stroke
Etiology Congenital aneurysm is most common etiology AVM is a less frequent cause of SAH Hypertensive arteriosclerosis aneurysm is the third cause of SAH Moyamoya disease is the forth cause Others include tumor, arteritis
Pathophysiology Cerebral artery aneurysm are most commonly congenital “berry” 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.
Pathology 85%~90% of intracranial aneurysms locate anterior in the 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
Clinical features Any age of person may suffer from SAH. The classic (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 vomiting and neck stiffness. Symptoms may begin at any time of day and during either rest or exertion.
Clinical features The 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 event. These earlier headaches are probably the result of small prodromal hemorrhages (sentinel,or warning, hemorrhages) or aneurysmal stretch.
Clinical features The headache is not always severe, but the intensity of the headache may remain unchanged for several days and subside 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 the first 2 weeks. Preretinal globular subhyaloid hemorrhages (found in 20% of cases) are most suggestive of the diagnosis.
Clinical features Because bleeding occurs mainly in the subarachnoid space in patients with aneurysmal rupture, prominent focal signs are uncommon on 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 ⅵ nerve palsies are frequent in such cases. Ruptured AVMs may produce focal signs, such as hemiparesis, aphasia, or a defect of the visual fields.
Clinical features Inducement and aura ： inducement include intensive activity 、 exhaustion 、 excitement,aura can be “warning leak” and localized sign. Symptoms of SAH patients above 60 year 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
Complications Recurrence of hemorrhage:Recurrence of aneurysmal hemorrhage (20% over 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 ischemia in more than one- third of cases.
Complications Acute 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, nonfocal findings, and impaired upgaze should suggest the diagnosis.
Complications Seizures: 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 insidious can occur, they are uncommon.
Supplementary findings CT ： 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、 外侧裂池基底扩散，称非动脉瘤性 SAH nA- SAH(figure 8) CSF: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 findings DSA:to detect aneurysm or AVM, it is a prerequisite to the rational planning of surgical treatment.aneurysm 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
Diagnosis Symptom ： the history of a sudden severe headache with confusion or obtundation Sign ： nuchal rigidity, a nonfocal neurologic examination CSF ： bloody spinal fluid Fundus oculi ： preretinal globular subhyaloid hemorrhages CT findings
Differential diagnosis Hypertensive intracranial hemorrhage ： there are prominent focal findings. Intracranial infection:it is excluded by the CSF examination. Tumor stroke or metastasis:they can be distinguished from SAH by evidence of tumor. Non-typical SAH
Principle of treatment 控制继续出血 control active hemorrhage 防治迟发性 CVS prevent tardive CVS 去除病因 eliminate etiology 防止复发 prevent recurrence
Treatment medical treatment 一般处理 general treatment ： absolute bed rest 4~6 weeks,preventing elevation of arterial or intracranial pressure(mild sedation, analgesics),but nA-SAH is an exception. 降颅压 decrease ICP ： antiedema agents eg.mannitol or surgical decompression 防治再出血 prevent recurrence ： PAMBA 防治迟发 CVS prevent tardive CVS ： calcium channel antagonist drug e.g. nimodipine CSF 置换 CSF exchange ： it can remove red cells,since the procedure may be accomplished with some complications, it should be used carefully.
Treatment surgical treatment Opportunity of operation ： 24~72 hours after hemorrhage Subject to operation 术式 血管内介入治疗、 γ- 刀治疗
Prognosis The probability of survival following aneurysmal rupture is related to the patient s state of consciousness and the elapsed time since the hemorrhage. Hunt grade ： grade Ⅰ ~ Ⅱ have a good outcome,grade Ⅳ ~ Ⅴ have a poor one,grade Ⅲ have a moderate one. Main cause of death ： including recurrence of hemorrhage 、 tardive CVS Main commemorstive sign ： may be cognitive impairment