腦出血英文版書-intracerebralhemorrhage-lwx

1、Intracerebral HemorrhageObjectivesThe puipose of this chapter is to give an overview of intracerebral hemonhage(ICH), including etiology, mechanisms, clinical manifestation and therapies.Students are expected to master the risk factors, clinical manifestations and diagnosis of intracerebral hemorrha

2、ge, and to know the management of intracerebral hemorrhage.Key conceptsStroke refers to a sudden focal neurologic syndrome, specifically the type caused by cerebro-ascular disease.Cerebrovascular disease designates any abnonnality of the brain resulting from a pathologic process of the blood vessels

3、, including occlusion of the lumen by embolus or thrombus, niptiire of a vessel, an altered pemieability of the vessel wall, or in creased viscosity or other change in the quality of the blood flowing through the cerebral vessels.Intracerebral hemorrhage occurs when a diseased blood vessel within th

4、e brain bursts, allowing blood inside the brain. ICH is a medical emergency of highest degiee with frequent early neurological deterioration or death. The cause of ICH is usually hypertension.3.1 IntroductionStroke, with heart disease and cancer, are the most common causes of death in the world. Eve

5、ry year there are approximately 2, 000,000 cases of stroke in our countiy and intracerebral hemorrhages account fbr 20%-30% of all strokes. Reported incidence rates of ICH among Asian populations are also high er than those reported fbr whites in United States and Europe.Advancing ages and hypertens

6、ion are the most important risk factors fbr ICH, and other causes of ICH include cerebral amyloid angiopathy, vascular malfbnnations, ruptured aneurysms, coagulation disorders, use of anticoagulants and tliiombolytic agents hemonliage into a cerebral infarct, bleeding into brain tumors, and dmg abus

7、e. Cerebral amyloid angiopathy is recognized as a cause of lobar ICH in the eldeily. ICH occurs slightly more frequently among men than women.Typical symptoms of ICH include headache, focal neurologic deficits, and iinpainnent of consciousness. Most intracerebral hemonhages occur in basal ganglia, c

8、erebral lobes, cerebellum, or pons.CT scan of the head is the imaging procedure of choice in the initial evaluation of suspected ICH. Angiography should be considered fbr all patients without a clear cause of hemorrhage who are surgical candidates, particularly young, normotensive patients who are c

9、linically stable. MRI and MRA are helpfill and may obviate the need fbr contrast cerebral angiogiaphy in selected patients.Tlie treatment of acute ICH include airway protection and adequate ventilation, blood pressure control, management of increased ICP, fluid management, body temperature control,

10、surgical treatment, and so on.EtiologyHypertension: an elevation of blood pressure that may cause tiny cerebral arteries to burst.Blood thinner therapy: dmgs such as coumadiii, heparin, and warfarin are used to treat heart and stroke conditions.Arteriovenous malfbnnation(A7M): a tangle of abnonnal a

11、rteries and veins with no capillaries in between.Aiieuiysm: a bulge or weakening of an arterial wall.Head trauma: fractures to the skull and penetrating wounds, such as gunshot can damage an artery and cause bleeding.Bleeding disorders: hemophilia, sickle cell anemia, DIC, thrombocytopenia.Tumors: h

12、ighly vascular tumors such as angiomas and metastatic tumors can bleed into the brain issue.Amyloid angiopathy: a degenerative disease of the arteries.Drug usage: cocaine and other illicit drugs can cause ICH.Spontaneous: ICH by unknown causes.PathophysiologyBlood from an intracerebral hemorrhage ac

13、cumulates as a mass that can dissect tliiough and compress adjacent brain tissue, causing neuronalDysfunction. Large hematomas increase intracranial pressure. Pressure from supratentorial hematomas and the accompanying edema may cause transtentorial brain herniation, compressing the brain stem and o

14、ften causing secondaiy hemorrhages in the midbrain and pons. If the hemorrhage niptures into the ventricular system(intra-entncular hemorrhage), blood may cause acute hydrocephalus, or they can dissect into the brain stem. Cerebellar hematomas that are3 cm in diameter may cause midline shift or heni

15、iation. Herniation, midbrain or pontine hemorrhage, intraventricular hemorrhage, acute hydrocephalus, or dissection into the brain stem can impaii consciousness and cause coma and death.Clinical ManifestationsSymptoms typically begin with sudden headache, often during activity. However, headache may

16、 be mild or absent in the elderly. Loss of consciousness is common, often within seconds or a few minutes. Nausea, vomiting, delinum, and focal or generalized seizures are also common. Neurologic deficits are usually sudden and progressive. Large hemorrhages, when located in the hemispheres, cause h

17、emiparesis, when located in the posteiior fbssa, they cause cerebellar or brain stem deficits. Large hemonhages are fatal within a few days in about 1/2 of patients. In survivois, consciousness retunis and neurologic deficits gradually diminish to various degrees as the extravasated blood is resorbe

18、d. Some patients have surprisingly few neurologic deficits because hemorrhage is less destructive to brain tissue than infarction Small hemonliage may cause focal deficits without impaiimeiit of consciousness and with minimal or no headache and nausea. Small hemorrhages may mimic ischemic stroke. Cl

19、inical features vary with the site of hemorrhage.(l)Deep cerebral hemonhageTlie two most conmion sites of hypertensive liemonliage are the putamen and the thalamus, wliich are separated by the posterior limb of the intenial capsule. This segment if the intenial capsule is traversed by descending mot

20、or fibers and ascending sensoiy fibers, including the optic radiations. Pressure on these fibers from expanding lateral or medial hematoma produces a contralateral sensonmotor deficit. In general, putamiiial hemorrhage leads to a more severe motor deficit and thalamic hemorrhage to a more marked sen

21、soiy disturbance.(2) Lobar hemonhageHypertensive hemorrhages also occur in subcortical white matter underlying the frontal, parietal, temporal, and occipital lobes. Symptoms and signs vaiy according to the location, they can include headache, vomiting, hemiparesis, hemisensoiy deficits aphasia, and

22、visual field abnoniialities. Seizures are more frequent than with hemorrhages in other locations, while coma is less so.(3)Pontine hemonhageWith bleeding into the pons, coma occurs with seconds to minutes and usually leads to death witliin 48 hours. Ocular findings typically include pinpoint pupils.

23、 Horizontal eye movements are absent or impaired, but vertical eye movements may be presenxd. In some patients, there may be ocular bobbing, a bilateral downbeating exclusion of the eyes at about 5-second intervals. Patients are conunonly quadnparetic and exliibit decerebrate posturing Hyperthermia

24、is sometimes present. Tlie hemon-hage usually mptures into the fourth ventricle, and rostral extension of the hemoiThage into the midbrain with resultant niidposition fixed pupils is conunon In contrast to the classic presentation of pontine hemonliage described above, small liemonliage that spare t

25、he reticular activating system-and that are associated with less severe deficits and excellent recoveiy-also occur.) Cerebellar hemonhageTlie distinctive symptoms of cerebellar hemoiThage(headache, dizziness, vomiting, and the inability to stand or walk)begin suddenly, within minutes aftei onset of

26、bleeding. Although patients may initially be alert or only mildly confused, large hemorrhage lead to coma within 12 hours in 75% of patients and within 24 hours in 90%. When coma is present at the onset, the clinical picture is indistinguishable from that of pontine hemonhage.3. 5 Diagnostic TestsDi

27、agnostic tests help doctors detennine the source and location of the bleeding.Computed tomogiaphy(CT) scanCT is a noninvasive X-ray to teview the anatomical structures within the brain to see if there is any blood in the brain. A newer teclmology called CT angiogiaphy involves the iiijection of cont

28、rast Into the blood stream to view arteries of the brain.AngiogiamAngiogram is ail invasive procedure, where a catheter is inserted into an arteiy and passed through the blood vessels to the brain. Once thecatheter is in place, a contrast dye is iiijected into the bloodstream and X-ray images are ta

29、ken.Magnetic resonance imagiiig(MRI) scanMRI is a noninvasive test, wliich uses a magnetic field and radio-frequency waves to give a detailed view of the soft tissues of the brain. MRA(magnetic resonance angiogiam) is the same non-invasive study, except it is also an angiogram, which means it examin

30、es the blood vessels as well as the structures of the brain.If neuroimagiiig shows no hemorrhage but subarachnoid heinonliage Is suspected clinically, lumbar puncture Is necessaiy.4. 3. 6 DiagnosisICH is a medical emergency of the highest degiee with frequent early neurological deterioration or deat

31、h. Vbmiting, early change in level of consciousness and high elevation of blood pressure in a patient with acute stroke suggest ICH.CT of the head is the imaging procedure of choice in the initial evaluation if suspected ICH.Aiigiogiaphy should be considered for all patients without a clear cause of

32、 hemorrhage who are surgical candidates, particularly young, nomiotensive patients who are clinically stable.4. 3. 7 Differential DiagnosisPutamiiiat thalamic, and lobar hypertensive hemoniiages may be difficult to distinguish from cerebral infarctions. To some extent, the presence of severe headach

33、e, nausea and vomiting, and iinpainnent of consciousness are useful clues that a hemonhage may have occuiTed. CT scan identifies the underlying disorder definitively.Brainstem stroke or cerebellar infarction can mimic cerebellar hemorrhage. Wlien cerebellar hemonliage is a possibility, CT scan or MR

34、I is the most usefill diagnostic procedure, since hematomas can be quickly and accurately localized. If neither CT nor MRI is available, vertebtal angiography should be performed. The angiogram shows a cerebellar mass effect in about 85% of cases, but the procedure is time consuming. Bloody CSF will

35、 confiim the diagnosis of hemonliage, but a clear tap does not exclude the possibility of an intracerebellar liematoma-and lumbar puncture may hasten the process of herniation Lumbar puncture is therefore not advocated if a cerebellar hemon-hage is suspected.Like cerebellar hemonliage, acute penpher

36、al vestibulopathy also produces nausea, vomiting, and gait ataxia, Severe headache, impaiied consciousness, elevated blood pressure, or later age at onset, however, strongly favors cerebellar hemonliage.4. 3. 8 Treatment3. 8. 1 Supportive measuresAirway and oxygenationAlthough intubation is not requ

37、iied for all patients, airway protection and adequate ventilation are critical. Patients who exhibit a decreasing level consciousness or signs of brain stem dysfunction are candidates for aggiessive ainvay management.Blood pressure managementTlie optimal level of a patient s blood pressure should be

38、 based on individual factors such as chronic hypertension, elevated intracranial pressure(ICP) age, presumed cause of hemorrhage，and interval since onset. In general, hypertension should be treated only if mean arterial pressure is 130 mmHg or systolic BP is 180 nmiHg. Treatments of elevate blood pr

39、essure in patients with ICH are more aggressive than those for patients with ischemic stroke. Conversely, overaggressive treatment of blood pressure may decrease cei-ebral perfiision pressure and theoretically worsen brain injury, particularly in the setting of increased intracranial pressureFluid m

40、anagementTlie goal of fluid management is euvolemia. Electrolytes(sodium, potassium, calcium, and magnesium) should be checked and substituted according to nonnal values. Acidosis and alkalosis should be collected according to blood gas analysis.3.8.2 Management of increased ICPICP is considered a major contributor to mortality after ICH; thus, its control is essential. ICP may be managed tluough osmotherapy, con