2010自发性脑出血指南汇总
自发性脑出血诊疗指南 ppt课件
外科治疗
➢ ICH患者外科手术治疗作用仍有争议。 ➢ 早期手术可以解除血肿的占位效应、降低颅内
压、减少周围脑组织的中毒反应。 ➢ 外科手术的指征可简单理解为（能让病人从外
科治疗中获益）：中青年ICH患者，血肿较大， 脑疝风险高，不适宜保守治疗者。
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幕上血肿开颅手术
➢ 对于大多数幕上 ICH 患者而言，手术的有效性尚不明 确（Ⅱb 类推荐， A 级证据；较上一版指南有修订）
➢ 使用立体定向设备进行微创血肿清除术，单用 内镜或与溶栓药物联用，这些方式的疗效尚不 明确（Ⅱb 类推荐， B 级证据；较上一版指 南有修订）。
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你会选择怎么样的治疗方案呢？
➢ A：硬通道引流 ➢ B：软通道引流 ➢ C：内镜血肿清除 ➢ D：小骨窗血肿清除 ➢ E：骨瓣开颅血肿清除 ➢ F：血肿清除并去骨瓣减压 ➢ G：保守治疗 ➢ H：其他治疗方式
➢ 如果可能的话，康复应该尽早开始并于出院后在 社区继续进行，形成良好协作的项目以实现早期 出院和以家庭为基础的康复来促进恢复（Ⅱa 类 推荐， B 级证据；同上一版指南）。
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➢ 手术清除脑干血肿对很多病例是有害的。
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脑出血去骨瓣减压术
➢ 伴有以下情况的幕上 ICH 患者可采用去骨瓣 减压术联合或不联合血肿清除术治疗以减少死 亡率：昏迷（GCS＜8分）、显著中线移位的大 面积血肿、ICP 升高且药物治疗无效（IIb 类 推荐，C 级证据；新增推荐内容）；
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微创外科治疗
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维生素K拮抗剂相关性脑出血
➢ 停用VKA，使用PCCs（凝血酶原复合物）比使用 FFP（冰冻新鲜血浆）并发症更少，纠正INR更为 迅速，作为首选考虑（ Ⅱb类推荐，B级证据 ）； 并静脉应用维生素K（Ⅰ类证据，C级推荐）。
2010脑出血指南
ISSN: 1524-4628Copyright © 2010 American Heart Association. All rights reserved. Print ISSN: 0039-2499. OnlineStroke is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX 72514DOI: 10.1161/STR.0b013e3181ec611bpublished online Jul 22, 2010; Stroke Cardiovascular Nursingand on behalf of the American Heart Association Stroke Council and Council onMacdonald, Steven R. Messé, Pamela H. Mitchell, Magdy Selim, Rafael J. Tamargo Loch P. Broderick, E. Sander Connolly, Jr, Steven M. Greenberg, James N. Huang, R. Lewis B. Morgenstern, J. Claude Hemphill, III, Craig Anderson, Kyra Becker, JosephAssociation/American Stroke Association Guideline for Healthcare Professionals From the American HeartGuidelines for the Management of Spontaneous Intracerebral Hemorrhage. A located on the World Wide Web at:The online version of this article, along with updated information and services, is/reprints Reprints: Information about reprints can be found online atjournalpermissions@ 410-528-8550. E-mail:Fax:Kluwer Health, 351 West Camden Street, Baltimore, MD 21202-2436. Phone: 410-528-4050. Permissions: Permissions & Rights Desk, Lippincott Williams & Wilkins, a division of Wolters/subscriptions/Subscriptions: Information about subscribing to Stroke is online atGuidelines for the Management of SpontaneousIntracerebral HemorrhageA Guideline for Healthcare Professionals From the American HeartAssociation/American Stroke AssociationThe American Academy of Neurology affirms the value of this guideline as an educationaltool for neurologists.The American Association of Neurological Surgeons and the Congress of Neurological Surgeons have reviewed this document and affirm its educational content.Lewis B.Morgenstern,MD,FAHA,FAAN,Chair;J.Claude Hemphill III,MD,MAS,FAAN,Vice-Chair;Craig Anderson,MBBS,PhD,FRACP;Kyra Becker,MD;Joseph P.Broderick,MD,FAHA;E.Sander Connolly,Jr,MD,FAHA; Steven M.Greenberg,MD,PhD,FAHA,FAAN;James N.Huang,MD;R.Loch Macdonald,MD,PhD;Steven R.Messé,MD,FAHA;Pamela H.Mitchell,RN,PhD,FAHA,FAAN;Magdy Selim,MD,PhD,FAHA;Rafael J.Tamargo,MD;on behalf of the American Heart AssociationStroke Council and Council on Cardiovascular NursingPurpose—The aim of this guideline is to present current and comprehensive recommendations for the diagnosis and treatment of acute spontaneous intracerebral hemorrhage.Methods—A formal literature search of MEDLINE was performed.Data were synthesized with the use of evidence tables.Writing committee members met by teleconference to discuss data-derived recommendations.The American Heart Association Stroke Council’s Levels of Evidence grading algorithm was used to grade each recommendation.Prerelease review of the draft guideline was performed by6expert peer reviewers and by the members of the Stroke Council Scientific Statements Oversight Committee and Stroke Council Leadership Committee.It is intended that this guideline be fully updated in3years’time.Results—Evidence-based guidelines are presented for the care of patients presenting with intracerebral hemorrhage.The focus was subdivided into diagnosis,hemostasis,blood pressure management,inpatient and nursing management, preventing medical comorbidities,surgical treatment,outcome prediction,rehabilitation,prevention of recurrence,and future considerations.Conclusions—Intracerebral hemorrhage is a serious medical condition for which outcome can be impacted by early, aggressive care.The guidelines offer a framework for goal-directed treatment of the patient with intracerebral hemorrhage.(Stroke.2010;41:00-00.)Key Words:AHA Scientific StatementsⅢintracerebral hemorrhageⅢtreatmentⅢdiagnosisⅢintracranial pressureⅢhydrocephalusⅢsurgeryThe American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal,professional,or business interest of a member of the writing panel.Specifically,all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest. This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on May19,2010.A copy of the statement is available at /presenter.jhtml?identifierϭ3003999by selecting either the“topic list”link or the“chronological list”link(No.KB-0044).To purchase additional reprints,call843-216-2533or e-mail kelle.ramsay@.The American Heart Association requests that this document be cited as follows:Morgenstern LB,Hemphill JC3rd,Anderson C,Becker K,Broderick JP,Connolly ES Jr,Greenberg SM,Huang JN,Macdonald RL,MesséSR,Mitchell PH,Selim M,Tamargo RJ;on behalf of the American Heart Association Stroke Council and Council on Cardiovascular Nursing.Guidelines for the management of spontaneous intracerebral hemorrhage:a guideline for healthcare professionals from the American Heart Association/American Stroke Association.Stroke.2010;41:●●●–●●●.Expert peer review of AHA Scientific Statements is conducted at the AHA National Center.For more on AHA statements and guidelines development, visit /presenter.jhtml?identifierϭ3023366.Permissions:Multiple copies,modification,alteration,enhancement,and/or distribution of this document are not permitted without the express permission of the American Heart Association.Instructions for obtaining permission are located at /presenter.jhtml? identifierϭ4431.A link to the“Permission Request Form”appears on the right side of the page.©2010American Heart Association,Inc.Stroke is available at DOI:10.1161/STR.0b013e3181ec611bS pontaneous,nontraumatic intracerebral hemorrhage(ICH) is a significant cause of morbidity and mortality throughout the world.Although much has been made of the lack of a specific targeted therapy,much less is written about the success and goals of aggressive medical and surgical care for this disease.Recent population-based studies suggest that most patients present with small ICHs that are readily survivable with good medical care.1This suggests that excellent medical care likely has a potent,direct impact on ICH morbidity and mortality now,even before a specific therapy is found.Indeed,as discussed later,the overall aggressiveness of ICH care is directly related to mortality from this disease.2One of the purposes of this guideline,therefore,is to remind clinicians of the impor-tance of their care in determining ICH outcome and to provide an evidence-based framework for that care.In order to make this review brief and readily useful to practicing clinicians,the reader is referred elsewhere for the details of ICH epidemiology.1,3,4Similarly,there are many ongoing clinical studies throughout the world related to this disease.The reader is encouraged to consider referring patients to these important efforts,which can be found at /trials/.We will not discuss on-going studies because we cannot cover them all;the focus of this statement is on currently available therapies.Finally,a recent guideline on pediatric stroke was published5that obviates the need to repeat the issues of pediatric ICH here. The last ICH Guidelines were published in2007,6and this current article serves to update those guidelines.As such, differences from former recommendations are specified in the current work.The writing group met by phone to determine subcategories to evaluate.These included emergency diagnosis and assessment of ICH and its causes;hemostasis,blood pressure(BP);intracranial pressure(ICP)/fever/glucose/ seizures/hydrocephalus;iron;ICP monitors/tissue oxygenation; clot removal;intraventricular hemorrhage(IVH);withdrawal of technological support;prevention of recurrent ICH;nursing care;rehab/recovery;future considerations.Each subcategory was led by an author with1or2additional authors making contributions.Full MEDLINE searches were done of all English-language articles regarding relevant human disease treatment.Drafts of summaries and recommendations were circulated to the whole writing group for feedback.A conference call was held to discuss controversial issues.Sections were revised and merged by the Chair.The resulting draft was sent to the whole writing group for ments were incor-porated by the Vice Chair and Chair,and the entire committee was asked to approve the final draft.Changes to the document were made by the Chair and Vice Chair in response to peer review,and the document was again sent to the entire writing group for suggested changes and approval.Recommendations follow the American Heart Association Stroke Council’s methods of classifying the level of certainty of the treatment effect and the class of evidence(Tables1and2).All Class I recommendations are listed in Table3.Emergency Diagnosis and Assessment of ICHand Its CausesICH is a medical emergency.Rapid diagnosis and attentive management of patients with ICH is crucial because early deterioration is common in the first few hours after ICH onset.More than20%of patients will experience a decrease in the Glasgow Coma Scale(GCS)score ofՆ2points between the prehospital emergency medical services assess-ment and the initial evaluation in the emergency department (ED).7Among those patients with prehospital neurological decline,the GCS score decreases by an average of6points and the mortality rate isϾ75%.Further,within the first hour of presentation to a hospital,15%of patients demonstrate a decrease in the GCS score ofՆ2points.8The risk for early neurological deterioration and the high rate of poor long-term outcomes underscores the need for aggressive early management.Prehospital ManagementThe primary objective in the prehospital setting is to provide ventilatory and cardiovascular support and to transport the patient to the closest facility prepared to care for patients with acute stroke (see ED Management section that follows).Secondary priorities for emergency medical services providers include obtaining a focused history regarding the timing of symptom onset(or the time the patient was last normal)and information about medical history, medication,and drug use.Finally,emergency medical services providers should provide advance notice to the ED of the impending arrival of a potential stroke patient so that critical pathways can be initiated and consulting services can be alerted.Advance notice by emergency medical services has been demonstrated to significantly shorten time to computed tomography(CT)scanning in the ED.9 ED ManagementIt is of the utmost importance that every ED be prepared to treat patients with ICH or have a plan for rapid transfer to a tertiary care center.The crucial resources necessary to man-age patients with ICH include neurology,neuroradiology, neurosurgery,and critical care facilities including adequately trained nurses and physicians.In the ED,appropriate consul-tative services should be contacted as quickly as possible and the clinical evaluation should be performed efficiently,with physicians and nurses working in parallel.Table4describes the integral components of the history,physical examination, and diagnostic studies that should be obtained in the ED. For patients with ICH,emergency management may in-clude neurosurgical interventions for hematoma evacuation, external ventricular drainage or invasive monitoring and treatment of ICP,BP management,intubation,and reversal of coagulopathy.Although many centers have critical pathways developed for the treatment of acute ischemic stroke,few have protocols for the management of ICH.18Such pathways may allow for more efficient,standardized,and integrated management of critically ill patients with ICH. NeuroimagingThe abrupt onset of focal neurological symptoms is presumed to be vascular in origin until proven otherwise.However,it is impossible to know whether symptoms are due to ischemia or hemorrhage based on clinical characteristics alone.Vomiting, systolic BPϾ220mm Hg,severe headache,coma or decreased level of consciousness,and progression over minutes or hours all suggest ICH,although none of these findings are specific;2Stroke September2010neuroimaging is thus mandatory.19CT and magnetic resonance imaging(MRI)are both reasonable for initial evaluation.CT is very sensitive for identifying acute hemorrhage and is consid-ered the gold standard;gradient echo and T2*susceptibility-weighted MRI are as sensitive as CT for detection of acute blood and are more sensitive for identification of prior hemorrhage.20,21 Time,cost,proximity to the ED,patient tolerance,clinical status, and MRI availability may,however,preclude emergent MRI in a sizeable proportion of cases.22The high rate of early neurological deterioration after ICH is in part related to active bleeding that may proceed for hours after symptom onset.The earlier time from symptom onset to first neuroimage,the more likely subsequent neuroimages will demonstrate hematoma expansion.15,23,24Among patients undergoing head CT within3hours of ICH onset,28%to 38%have hematoma expansion of greater than one third on follow-up CT.8,25Hematoma expansion is predictive of clinical deterioration and increased morbidity and mortali-ty.8,10,15,25As such,identifying patients at risk for hematoma expansion is an active area of research.CT angiography and contrast-enhanced CT may identify patients at high risk of ICH expansion based on the presence of contrast extravasa-tion within the hematoma.26–30MRI/angiogram/venogram and CT angiogram/venogram are reasonably sensitive at identifying secondary causes of hemorrhage,including arte-riovenous malformations,tumors,moyamoya,and cerebral vein thrombosis.31–33A catheter angiogram may be consid-ered if clinical suspicion is high or noninvasive studies are suggestive of an underlying vascular cause.Clinical suspicion of a secondary cause of ICH may include a prodrome of headache,neurological,or constitutional symptoms.Radio-logical suspicions of secondary causes of ICH should beTable1.Applying Classification of Recommendations and Level ofEvidence*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations,such as sex,age,history of diabetes,history of prior myocardial infarction,history of heart failure,and prior aspirin use.A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials.Even though randomized trials are not available,there may be a very clear clinical consensus that a particular test or therapy is useful or effective.†In2003,the ACCF/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when writing recommendations.All guideline recommendations have been written in full sentences that express a complete thought,such that a recommendation,even if separated and presented apart from the rest of the document(including headings above sets of recommendations),would still convey the full intent of the recommendation.It is hoped that this will increase readers’comprehension of the guidelines and will allow queries at the individual recommendation level.Morgenstern et al Intracerebral Hemorrhage Guideline3invoked by the presence of subarachnoid hemorrhage,un-usual(noncircular)hematoma shape,the presence of edema out of proportion to the early time an ICH is first imaged,an unusual location for hemorrhage,and the presence of other abnormal structures in the brain like a mass.An MR or CT venogram should be performed if hemorrhage location,rela-tive edema volume,or abnormal signal in the cerebral sinuses on routine neuroimaging suggest cerebral vein thrombosis. In summary,ICH is a medical emergency,characterized by high morbidity and mortality,which should be promptly diagnosed and aggressively managed.Hematoma expansion and early deteriora-tion are common within the first few hours after onset. Recommendations1.Rapid neuroimaging with CT or MRI is recommendedto distinguish ischemic stroke from ICH(Class I;Level of Evidence:A).(Unchanged from the previous guideline) 2.CT angiography and contrast-enhanced CT may beconsidered to help identify patients at risk for hema-toma expansion(Class IIb;Level of Evidence:B),and CT angiography,CT venography,contrast-enhanced CT,contrast-enhanced MRI,magnetic resonance an-giography,and magnetic resonance venography can beuseful to evaluate for underlying structural lesions, including vascular malformations and tumors when there is clinical or radiological suspicion(Class IIa;Level of Evidence:B).(New recommendation)Medical Treatment for ICH Hemostasis/Antiplatelets/Deep VeinThrombosis ProphylaxisUnderlying hemostatic abnormalities can contribute to ICH. Patients at risk include those on oral anticoagulants(OACs), those with acquired or congenital coagulation factor deficien-cies,and those with qualitative or quantitative platelet abnormal-ities.Patients undergoing treatment with OACs constitute12% to14%of patients with ICH,34,35and with increased use of warfarin,the proportion appears to be increasing.36Recognition of an underlying coagulopathy thus provides an opportunity to target correction in the treatment strategy.For patients with a coagulation factor deficiency and thrombocytopenia,replace-ment of the appropriate factor or platelets is indicated.For patients being treated with OACs who have life-threatening bleeding,such as intracranial hemorrhage,the general recommen-dation is to correct the international normalized ratio(INR)as rapidly as possible.37,38Infusions of vitamin K and fresh-frozen plasma(FFP)have historically been recommended,but more recently,prothrombin complex concentrates(PCCs)and recom-binant factor VIIa(rFVIIa)have emerged as potential therapies. Vitamin K remains an adjunct to more rapidly acting initial therapy for life-threatening OAC-associated hemorrhage be-cause even when given intravenously,it requires hours to correct the INR.39–41The efficacy of FFP is limited by risk of allergic and infectious transfusion reactions,processing time,and the volume required for correction.Likelihood of INR correction at 24hours was linked to time to FFP administration in1study, although17%of patients still did not have an INRՅ1.4at this time,suggesting that FFP administered in this manner may be insufficient for rapid correction of coagulopathy.42PCCs are plasma-derived factor concentrates primarily used to treat factor IX deficiency.Because PCCs also contain factors II,VII,and X in addition to IX,they are increasingly recommended for warfarin reversal.PCCs have the advan-tages of rapid reconstitution and administration,having high concentrations of coagulation factors in small volumes,and processing to inactivate infectious agents.Though different PCC preparations differ in relative amounts of factors(with VII the most likely to be low),several studies have shown that PCCs can rapidly normalize INR(within minutes)in patients taking OACs(reviewed in43–45).Nonrandomized retrospective reviews and a small case-control study have shown more rapid correction of INR with vitamin K and PCC than vitamin K and FFP,but have not revealed a difference in clinical outcome.46–48One randomized trial compared the use of a PCC(Konyne)to supplement FFP versus FFP alone in patients with OAC-related ICH,finding that those who received PCC had significantly shorter time to INR correction and received less volume of FFP.Although there was no difference in outcome,those who received FFP also had more adverse events,primarily attributable to fluid overload.49 Although PCCs may theoretically increase the risk of throm-botic complications,this risk appears relatively low.43De-Table2.Definition of Classes and Levels of Evidence Used in American Heart Association Stroke Council Recommendations Class I Conditions for which there is evidence forand/or general agreement that theprocedure or treatment is useful andeffectiveClass II Conditions for which there is conflictingevidence and/or a divergence ofopinion about the usefulness/efficacyof a procedure or treatmentClass IIa The weight of evidence or opinion is infavor of the procedure or treatment Class IIb Usefulness/efficacy is less wellestablished by evidence or opinion Class III Conditions for which there is evidenceand/or general agreement that theprocedure or treatment is notuseful/effective and in some casesmay be harmfulTherapeutic recommendationsLevel of Evidence A Data derived from multiple randomizedclinical trials or meta-analysesLevel of Evidence B Data derived from a single randomizedtrial or nonrandomized studiesLevel of Evidence C Consensus opinion of experts,casestudies,or standard of care Diagnostic recommendationsLevel of Evidence A Data derived from multiple prospectivecohort studies using a referencestandard applied by a maskedevaluatorLevel of Evidence B Data derived from a single grade A study,or one or more case-control studies,orstudies using a reference standardapplied by an unmasked evaluator Level of Evidence C Consensus opinion of experts4Stroke September2010spite the lack of large,well-controlled,randomized trials, PCCs are being increasingly recommended as an option in guidelines promulgated for warfarin reversal in the setting of OAC-associated life-threatening or intracranial hemor-rhages.37,38,50–52Table5provides a list of several products for factor replacement in warfarin reversal that are commer-cially available in the United States at the present time. rFVIIa,licensed to treat hemophilia patients with high titer inhibitors or congenital factor VII deficiency,has garnered attention as a potential treatment for spontaneous and OAC-associated ICH.Although rFVIIa can rapidly normalize INR in the setting of OAC-associated ICH,53–57it does not replenish all of the vitamin K–dependent factors and there-fore may not restore thrombin generation as well as PCCs.58 In light of the limited data,a recent American Society of Hematology evidence-based review recommended against routine use of rFVIIa for warfarin reversal.59rFVIIa has also been tested in patients with non-OAC ICH.A phase2randomized trial showed that treatment with rFVIIa within4hours after ICH onset limited hematoma growth and improved clinical outcomes relative to placebo, though with increased frequency of thromboembolic events (7%versus2%).60A subsequent phase3study comparing placebo with20g/kg and80g/kg of rFVIIa failed to show differences in clinical outcome,despite confirming the ability of both doses to diminish hematoma enlargement.61Although overall serious thromboembolic adverse events were similar, the higher rFVIIa(80g/kg)group had significantly more arterial events than the placebo group.The authors noted imbalances in the treatment groups,particularly the greater number of patients with IVH in the higher-dose rFVIIa group.60It remains to be determined whether rFVIIa will benefit a particular subset of patients with ICH,but currently its benefits in ICH patients,whether or not they are under-going treatment with OACs,remain unproven.Studies of the effect of prior antiplatelet agent use or platelet dysfunction on ICH hematoma growth and outcome have found conflicting results.Reported antiplatelet agent use was not associated with hematoma expansion or clinical outcome in the placebo group of an ICH neuroprotective study.62However,others have suggested that platelet dys-function as measured by platelet function assays may be associated with hematoma expansion and clinical out-come.63,64The utility and safety of platelet transfusion orTable3.Class I RecommendationsRecommendations Class/Level of EvidenceEmergency diagnosis and assessment of ICH and its causes Rapid neuroimaging with CT or MRI is recommended to distinguishischemic stroke from ICH.(Unchanged from the previousguideline)Class I,Level AMedical treatment for ICH Patients with a severe coagulation factor deficiency or severethrombocytopenia should receive appropriate factor replacementtherapy or platelets,respectively.(New recommendation)Class I,Level CHemostasis/antiplatelets/DVT prophylaxis Patients with ICH whose INR is elevated due to OAC should havetheir warfarin withheld,receive therapy to replace vitaminK–dependent factors and correct the INR,and receiveintravenous vitamin K.(Revised from the previous guideline)Class I,Level CPatients with ICH should have intermittent pneumatic compressionfor prevention of venous thromboembolism in addition to elasticstockings.(Unchanged from the previous guideline)Class I,Level BInpatient management and prevention ofsecondary brain injuryGeneral monitoring Initial monitoring and management of ICH patients should takeplace in an intensive care unit,preferably one with physicianand nursing neuroscience intensive care expertise.(Unchangedfrom the previous guideline)Class I,Level B Management of glucose Glucose should be monitored and normoglycemia is recommended Class I,Level CSeizures and antiepileptic drugs Patients with clinical seizures should be treated with antiepilepticdrugs.(Revised from previous guideline)Patients with a change in mental status who are found to haveelectrographic seizures on EEG should be treated withantiepileptic drugs Class I,Level A Class I,Level CProcedures/surgery—clot removal Patients with cerebellar hemorrhage who are deterioratingneurologically or who have brainstem compression and/orhydrocephalus from ventricular obstruction should undergosurgical removal of the hemorrhage as soon as possible.(Revised from the previous guideline)Class I,Level BPrevention of recurrent ICH After the acute ICH,absent medical contraindications,BP shouldbe well controlled,particularly for patients with ICH locationtypical of hypertensive vasculopathy.(New recommendation)Class I,Level ACT indicates computed tomography;MRI,magnetic resonance imaging;DVT,deep vein thrombosis;INR,international normalized ratio;OAC,oral anticoagulants; and EEG,electroencephalogram.Morgenstern et al Intracerebral Hemorrhage Guideline5other agents in patients with a normal platelet count,but use of antiplatelet agents or platelet dysfunction,is not known.Patients with ICH have a high risk of thromboembolic disease.65Women and African Americans appear to be at greater risk.65–67Intermittent pneumatic compression combined with elastic stockings has been shown by a randomized trial to be superior to elastic stockings alone in reducing occurrence of asymptomatic deep vein thrombosis after ICH (4.7%versus 15.9%).68Graduated compression stockings alone are ineffec-tive in preventing deep vein thrombosis.69Less clear,however,is the role of adding anticoagulation to pneumatic compression.Two small randomized studies found no difference in deep vein throm-bosis incidence,and no increase in bleeding,in patients given low-dose subcutaneous heparin initiated at day 4or at day 10after ICH.70,71An uncontrolled study of treatment initiated on day 2found a reduction in thromboembolic disease without increased rebleeding.70Recommendations1.Patients with a severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate fac-tor replacement therapy or platelets,respectively (Class I;Level of Evidence:C).(New recommendation)2.Patients with ICH whose INR is elevated due to OACs should have their warfarin withheld,receive therapy to replace vitamin K–dependent factors and correct the INR,and receive intravenous vitamin K (Class I;Level of Evidence:C).PCCs have not shown improved outcome compared with FFP but may have fewer complications compared with FFP and are reasonable to consider as an alternative to FFP (Class IIa;Level of Evidence:B).rFVIIa does not replace all clotting factors,and although the INR may be lowered,clotting may not be restored in vivo;therefore,rFVIIa is not routinely recommended as a sole agent for OAC re-versal in ICH (Class III;Level of Evidence:C).(Revised from the previous guideline).3.Although rFVIIa can limit the extent of hematoma expansion in noncoagulopathic ICH patients,thereTable 4.Integral Components of the History,PhysicalExamination,and Work-Up of the Patient With ICH in the EDCommentsHistoryTime of symptom onset (or time the patient was last normal)Initial symptoms and progression of symptoms Vascular risk factors Hypertension,diabetes,hypercholesterolemia,and smoking MedicationsAnticoagulants,antiplatelet agents,decongestants,antihypertensivemedications,stimulants (including diet pills),sympathomimeticsRecent trauma or surgeryCarotid endarterectomy or carotid stenting in particular,as ICH may be related to hyperperfusion after such procedures DementiaAssociated with amyloid angiopathy Alcohol or illicit drug useCocaine and other sympathomimetic drugs are associated with ICH,stimulants Seizures Liver diseaseMay be associated with coagulopathy Cancer and hematologic disorders May be associated with coagulopathyPhysical examination Vital signsFever is associated with early neurologic deterioration 10Higher initial blood pressure is associated with early neurologic deterioration and increased mortality 11A general physicalexamination focusing on the head,heart,lungs,abdomen,and extremities A thorough but time-urgent neurologic examinationA structured examination such as the National Institutes of Health Stroke Scale can be completed in minutes and provides a quantification that allows easy communication of the severity of the event to other caregivers.GCS score is similarly well known and easily computed,and the initial GCS score is a strong predictor of long-term outcome.12,13These can be supplemented as needed Serum and urine tests Complete blood count,electrolytes,blood urea nitrogen and creatinine,and glucoseHigher creatinine is associated with hematoma expansion.Higher serum glucose is associated with hematoma expansion and worse outcome(although there are no data to suggest that normalization improves outcome)11,14Prothrombin time or INR and an activated partial thromboplastin timeWarfarin-related hemorrhages are associated with an increased hematoma volume,greater risk ofexpansion,and increased morbidity and mortality 15–17(Continued )Table 4.ContinuedCommentsToxicology screen in young or middle-aged patients to detect cocaine and other sympathomimetic drugs of abuseCocaine and other sympathomimetic drugs are associated with ICHUrinalysis and urine culture and a pregnancy test in a woman of childbearing age Other routine tests ECGTo assess for active coronary ischemia or prior cardiac injury that may indicate poor cardiac function and to obtain a baseline in the event ofcardiopulmonary issues during hospitalization Chest radiograph NeuroimagingAs described in the textGCS indicates Glasgow Coma Scale;ECG,electrocardiogram.6Stroke September 2010。
2010年美国脑出血诊治指南精要(中文版)
2010 年美国脑出血诊治指南精要丁香园站友脑壳译急诊诊断与评估：推荐迅速行CT 或MRI 以鉴别缺血性卒中和脑出血（I 类A 级证据）。
可行CTA 和增强CT 以帮助确定高危患者血肿扩大，CTA、CTV、增强CT、增强MRI、MRA 和MRV 有助于评估潜在的结构损害，包括血管畸形和肿瘤（若临床怀疑或影像学怀疑）（IIa 类 B 级证据）。
脑出血的药物治疗：患有严重凝血因子缺乏或血小板减少的患者需接受适当的凝血因子或血小板替代治疗（I 类 C 级证据）。
由口服抗凝血药（OAC）导致INR 升高的脑出血患者需停止服用华法林，给予维生素K 依赖性因子替代治疗并纠正INR，同时静脉给予维生素K（I 类C 级证据）。
与新鲜冰冻血浆（FFP）相比，凝血酶原复合体浓缩物（PCC）并未提高患者预后，但患者并发症可能比使用FFP 者少，因此有理由将PCC作为FFP 的替代物（IIa 类 B 级证据）。
重组因子VIIa（rFVIIa）不能替代所有凝血因子，尽管其可能使INR 降低，但体内凝血功能可能尚未得到恢复，因此，对于需要逆转OAC 的脑出血患者来说，不建议常规将rFVIIa 作为唯一的药物（III 类 C 级证据）虽然对无凝血病的患者来说rFVIIa 可限制血肿体积增大，但血栓栓塞风险却有增加，并且对患者无选择地使用rFVIIa 并未获得明确的临床益处。
因此，不推荐对患者无选择地使用rFVIIa（III 类 A 级证据）。
在做出任何推荐使用rFVIIa 的决定之前，需进行进一步研究，以确定对筛选后的患者使用rFVIIa是否能够获益。
给予有抗血小板治疗史的脑出血患者输注血小板，其作用尚不明确，尚需深入研究（IIb 类 B 级证据）。
为预防脑出血患者静脉血栓栓塞，需给予间歇气压疗法并穿戴弹力袜（I 类B 级证据）对于脑出血发生后1-4 天无法活动的患者，在确认出血停止后，可考虑给予低剂量低分子肝素或普通肝素皮下注射以预防静脉血栓栓塞。
自发性脑出血管理指南解读
◦ CT灌注成像证实数小时内降压至 140mmHg以下不影响血肿周围血流灌注。
◦ 发病30min内用尼卡地平降压的实验发现 血压控制在135mmHg以下转归最好 （160mmHg以下）
◦ 400余例中国人的实验证实发病6h内血压 降低至140mmHg以下是安全的。
◦ 没有关于血压220mmHg以上患者及需要 手术患者的强化降压研究
四、操作、手术
1、ICP检测和治疗 2、IVH相关的操作与手术 3、血肿清除术
ICP检测和治疗
1. 脑室引流治疗脑积水是合理的，尤 其在意识水平降低的患者中11a B
2. GCS≤8分，有小脑幕切迹疝临床证 据或伴有严重的IVH、脑积水患者可 考虑ICP检测和治疗。维持CCP在 50~70mmHg可能是合理的11b C
4. 癫痫发作；
查体
1. 生命体征 2. 头、心、肺、腹、四肢为重点的
全身查体。 3. 神经系统查体，包括GCS、
NIHSS、GOS
化验
血常规 生化：电解质、血尿素氮、肌酐、血糖
（转归）心脏特异性肌钙蛋白（转归） 凝血酶原时间、部分凝血活酶时间（华法
令相关） 尿液化验与培养，育龄妇女做妊娠试验 可卡因和拟交感神经药物毒理学检查
3. ICH患者不应使用糖皮质激素治疗 ICP升高III B
脑室出血IVH
IVH是ICH死亡率从20%升高至 51%
早期VP分流，三脑室造瘘和腰大 池引流
◦ 腰大池分流增加引流管置入时间，减 少需要永久分流可能
VC+尿激酶
血肿清除术
血肿清除术的理论基础是通过减轻 占位效应或血液产物的细胞毒性来 预防脑疝形成、降低ICP以及减轻 水肿对周围组织的病理生理学影响。
2010年美国心脏病协会自发性颅内出血指南
AHA/ASA 自发性颅内出血管理指南—美国心脏病协会/ 美国中风协会专业医学指南译者：wxhsin2 美国神经病学会证实该指南适用于神经科医师培训，美国神经外科医师协会和美国神经外科医师代表大会审阅了该指南并肯定了该指南的内容。
Lewis B. Morgenstern, MD, FAHA, FAAN, Chair;J. Claude Hemphill III, MD, MAS, FAAN, Vice-Chair; Craig Anderson, MBBS, PhD, FRACP; Kyra Becker, MD; Joseph P. Broderick, MD, FAHA; E. Sander Connolly, Jr,MD, FAHA;Steven M. Greenberg, MD, PhD, FAHA, FAAN; James N. Huang, MD; R. Loch Macdonald, MD, PhD;Steven R. Mess, MD, FAHA; Pamela H. Mitchell, RN, PhD, FAHA, FAAN;Magdy Selim, MD, PhD, FAHA; Rafael J. Tamargo, MD;本指南代表美国心脏协会、中风协会及心血管护理协会的观点。
目的：本指南旨在提供目前急性自发性颅内出血的诊断和治疗建议。
方法：本指南基于MEDLINE 检索的结果，使用证据列表( evidence tables)来合成数据，写作组成员通过远程会议来讨论基于研究数据的推荐意见，并使用美国心脏协会中风分会的证据分级法则对推荐意见进行分级，本指南由 6 位审核专家及中风分会科学指南监督委员会和中风分会指导委员会全体成员审阅，并将于 3 年内完整更新。
结果：本指南旨在为颅内出血病人的管理提供基于研究数据的建议，本指南包括以下几个部分：诊断，止血方法，血压管理，住院病人护理，并发症预防，手术治疗，预后评估，康复，复发的预防及出院后注意事项。
脑出血诊疗指南(临床诊疗指南)
脑出血诊疗指南(临床诊疗指南)【概述】脑出血是指原发于脑实质内的出血，故称为自发性脑出血；高血压性小动脉硬化和破裂是本病最常见的原因，故也称作高血压性脑出血。
脑淀粉样血管病、动静脉畸形、动脉瘤、血液病、凝血功能异常、脑动脉炎、药物滥用，以及肿瘤和脑梗死为其他的脑内出血原因。
自发性脑出血的出血部位以壳核最多见，其次为丘脑、尾状核、半球白质、脑桥、小脑和脑室等。
【临床表现】1、一般症状1)急性起病并出现局灶性神经功能缺损，一般可于数小时内达高峰。
个别患者因继续出血和血肿扩大，临床症状进行性加重，持续时间6～12小时。
2)除小量脑出血外，大部分患者均有不同程度的意识障碍。
意识障碍的程度是判断病情轻重和预后的重要指标。
3)头痛和呕吐是脑出血最常见的症状，通常为颅内压增高的表现。
4)血压增高是脑出血常见的原因与伴发病。
血压增高和心跳及脉搏缓慢同时存在，往往是颅压增高的重要指征。
5)脑出血者可出现癫痫发作，癫痫发作多为局灶性和继发性全身发作。
以脑叶出血和深部出血最多见。
2、局灶症状和体征：局灶症状与血肿的部位相关，但定位诊断的准确性不如神经影像结果。
1)壳核出血：常见，多为外侧豆纹动脉破裂所致。
血肿可局限于壳核本身，也可扩延累及周围脑组织。
血肿向内压迫内囊出现典型的临床表现，为对侧偏瘫、偏身感觉障碍和偏盲。
急性期伴有两眼向病灶侧凝视，血肿位于优势半球可出现失语。
2)丘脑出血：若血肿较大，按血肿扩展的方向不同而出现不同的临床综合征：向外扩张侵及内囊，向内破入脑室，向下侵及下丘脑和中脑背侧，以及向上扩张侵及顶叶白质，因而出现各自相应的症状和体征。
但临床常见的临床表现以多寡为序有：轻偏瘫或偏瘫、半身感觉缺失、上凝视麻痹、瞳孔异常(瞳孔缩小和对光反射消失)、失语、疾病感缺失、眼球向病灶侧凝视(与壳核出血同)、偏盲和缄默。
3)尾状核出血：多见于尾状核头部，易破入脑室，临床表现多为急性发病的头痛、呕吐、颈僵直等脑膜刺激征，并伴有一定程度的意识障碍、短暂性近记忆力障碍，临床上难与蛛网膜下腔出血鉴别。
脑出血2010指南
• rFVIIa[p10] does not replace all clotting factors,
• •
and although the INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is not routinely recommended as a sole agent for OAC reversal in ICH (Class III; Level of Evidence: C). (Revised from the previous guideline). 重组凝血因子VII并不能替代所有的凝结因子；虽 然INR可能会被降低，但是体内的血凝块并不能 消除。所以，并不推荐把rFvlla作为脑出血病人 OAC逆转的唯一药剂。（由先前指南修订）
• 四、Inpatient Management[p14] and
Prevention of Secondary Brain Injury Recommendations • 关于住院病人的处理治疗和预防二次脑损 伤的建议
• 1. Initial monitoring and management of ICH
三、Blood Pressure Recommendations（有关血压方 面的建议）
• 1. Until ongoing clinical trials of BP intervention for ICH
are completed, physicians must manage BP on the basis of the present incomplete efficacy evidence.Current suggested recommendations for target BP in various situations are listed in Table 6 and may be considered (Class IIb; Level of Evidence: C). (Unchangedfrom the previous guideline) 在正在进行的脑出血病人血压干预临床试验完成之前，医 师必须依据目前不完善的循证医学证据的基础，来适当控 制血压。目前，对于不同情况下所推荐的血压处理方法， 请见表6，值得借鉴。（与先前的指南并无差异）
自发性颅内出血诊疗指南
自发性颅内出血诊疗指南【病因】1、脑血管畸形(1)脑动静脉畸形是儿童时期的常见原因之一，可分为先天性、感染性与外伤性；(2)毛细血管扩张、海绵状血管瘤、软脑膜静脉及毛细血管的畸形、脑底异常血管网(moyamoya病)等。
2、血液病(1)血友病患儿中2.2%～7.4%发生(2)小儿特发性血小板减少性紫癜10%(3)白血病、再生障碍性贫血、溶血性贫血、弥漫性血管内凝血、凝血障碍等血液病，以及抗凝疗法的并发症，均可发生。
3、颅内其他原因包括颅脑外伤，颅内肿瘤，脑动脉炎，中毒性脑病等。
4、颅外其他原因包括维生素k缺乏症，维生素c缺乏症，肝病，高血压，感染或结缔组织病等其他各种原因所致的脑内血肿。
5、新生儿颅内出血原因新生儿颅内出血(neonatal intracranial hemorrhage，nich)(1)产伤(2)缺氧其中在＜34孕周、出生体重＜1500g的未成熟儿高达40%～50%。
6.其他尚有部分小儿的原因不明。
【临床表现】1、脑出血2、原发性蛛网膜下腔出血(subdural hemorrhage) 小儿蛛网膜下腔出血比成人少见。
因动脉瘤、动静脉畸形等血管异常所致者以6岁以上年长儿较多见，且有随年龄增长而逐渐增多的趋势。
常起病急剧，主要表现为血液刺激或容量增加所致的脑膜刺激征和颅内高压征，如颈项强直、剧烈头痛、喷射性呕吐等。
半数以上病例出现意识障碍、面色苍白和惊厥发作。
病初2～3天内常有发热。
大脑凸面血管破裂所致的蛛网膜下腔出血，若病变部位靠近额叶、颞叶时，常可出现明显的精神症状，可表现为胡言乱语、自言自语、模仿语言和摸空动作等。
可伴发血肿或脑梗死而出现局灶性神经体征，如肢体瘫痪、脑神经异常等。
眼底检查可见玻璃体下出血。
3、硬膜下出血(subdural hemorrhage) 婴幼儿多见。
通常分为小脑幕上和小脑幕下两种类型，前者最常见，多因大脑表面的细小桥静脉撕裂出血所致；后者多由于小脑幕撕裂所致。
脑出血和脑卒中疾病指南
自发性脑出血治疗指南(AHA/ASA2015版)2015年版美国心脏协会／美国卒中协会自发性脑出血治疗指南已于近期发表在Stroke杂志上。
该版指南在多个方面较原指南做出更新，现将新增的推荐内容作以简介。
一、脑出血急诊诊断与评估在对脑出血病人做初步评估时需要进行基线严重度评分（I级推荐，B级证据）。
二、脑出血的内科治疗1. 新指南加入了新型抗凝药相关脑出血的治疗推荐，指出对于使用达比加群、利伐沙班或阿哌沙班等药物引起脑出血的患者，VIII因子旁路活性抑制剂（FEIBA）、凝血酶原复合物浓缩物（PCC）或重组活化VII因子（rFVIIa）可用作个体化治疗。
在2小时内服用标准剂量上述药物的患者可使用活性炭。
达比加群相关脑出血可考虑血液透析（IIb级推荐，C级证据）。
2. 硫酸鱼精蛋白可用于使用肝素的急性脑出血患者（IIb级推荐，C级证据）。
3. 脑出血患者并发系统性深静脉血栓或肺栓塞时可全身使用抗凝或放置下腔静脉滤网（II a级推荐，C级证据）。
两者选择需考虑以下因素，包括出血时间、血肿稳定性、出血病因及病人一般状况（IIa级推荐，C级证据）。
三、血压与脑出血预后新指南去除了原指南上不同情况的血压目标值，将收缩压以220 mmHg分界，指出收缩压在150 mmHg至220 mmHg的脑出血患者，如无禁忌，将收缩压快速降至140 mmHg是安全的（I 级推荐，A级证据），且对神经功能改善有益（IIa级推荐，B级证据）。
对于收缩压大于2 20 mmHg的脑出血患者可使用连续静脉药物积极降压，并给予常规血压监测（IIb级推荐，C 级证据）。
四、院内管理和继发性脑损伤的预防指南新增内科并发症处理的内容：1. 所有脑出血病人给予口服药前均需按照正规流程评估吞咽功能以减少肺部感染风险（I 级推荐，B级证据）。
2. 脑出血后需应用心电图和心肌酶检测系统筛查心肌缺血或梗死（IIa级推荐，C级证据）。
五、操作/手术1. 皮质类固醇激素不应用于治疗脑出血后颅内压升高（III级推荐，B级证据）。
自发性脑出血管理指南
止血和凝血障碍、抗血小板药、深 静脉血栓的预防
• ③ 对于正在接受达比加群、利伐沙班或阿哌沙班治疗的ICH患者，是 否给予或给予哪种治疗[包括VIII因子旁路活性抑制剂（FEIBA）、其 他PCC类或rFVIIa]需要根据患者情况而定，进行个体化管理。当患者 接受达比加群、利伐沙班或阿哌沙班治疗2 h内时，可考虑给予活性 炭（activated charcoal）。接受达比加群治疗的患者，可考虑进行血 液透析治疗。（2b、C、新）
• ① 对于合并重度凝血因子缺乏或重度血小板减少的患者，应分别给予 适当的代替治疗或补充血小板。（1、C）
• ② 对于服用维生素K拮抗剂（VKA）的ICH患者，若国际标准化比值 （INR）升高，此时应停用VKA、接受维生素K依赖性凝血因子 （vitamin K–dependent factors），纠正IRN，并静脉给予维生素K。 （1、C、修改）
• 与新鲜冰冻血浆（FFP）相比，凝血酶原复合物（PCC）具有并发症 少、纠正INR速度更快的优点，可考虑使用PCC。（2b、B、修改）
• 重组凝血因子FVIIa（rFVIIa）尽管可以降低INR，但并不能代替所有 的凝血因子发挥作用，因此不能使所有的凝血异常均恢复正常，不推 荐其用于ICH患者。（3、C、修改）
自发性脑出血管理指南
在全世界范围内，自发性、非创伤性脑出
血（ICH）一直是人群高并发症发病率和高
死亡率的重要原因之一。基于人群的研究 显示，良好的临床管理可有效降低ICH相关 的并发症发病率和死亡率。AHA/ASA联合 发布的2015年最新指南，旨在对2010年指 南进行更新，提供ICH临床管理的最新证据 和推荐，同时提醒临床医师重视ICH的治疗。 在该指南中，推荐强度从高到低依次为：1 （利>>>弊）、2a（利>>弊）、2b（利≥ 弊）、3级（无益或有害），证据质量等级 从高到低依次为：A、B、C。
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血压的管理
► 1.根据目前完成的关于ICH血压干预的研究结论，临床医生 必须基于目前尚不完全的证据来控制血压，目前推荐的不同 情况下的降压目标见表六，仅供参考（Ⅱb C）。 2.收缩压150-220mmHg的住院患者，快速降压至140mmHg 可能是安全的（Ⅱa B）。 表六.高血压的ICH患者降压推荐意见 1.SBP>200mmHg或MAP>150mmHg,建议持续静脉应用降 压药物快速降压，测血压，5min/次。 2.SBP>180mmHg或MAP>130mmHg，且可能存在颅内高压， 可考虑监测颅内压，并间断或持续静脉应用降压药物以降压， 保持脑灌注压不低于60mmHg. 3.SBP>180mmHg或MAP>130mmHg,且没有颅内高压的证 据，可考虑间断或持续应用降压药物温和降压（如可降压至 160/90mmHg或MAP至110mmHg），监测血压，15min/次
► 3. 尽管对于凝血机制正常的ICH患者，rFVIIa可以限制血肿扩大，但是证据表明在不筛选 病例的情况下，应用rFVIIa会增加血栓形成的风险，且缺乏增加临床收益的证据，因此， 在不筛选病例的条件下，不推荐应用rFVIIa（Ⅲ A）。在作出推荐应用rFVIIa的意见之前， 需要进一步研究是否应用rFVIIa会使特定的人群获益。
手术策略
► 1.对于大多数ICH患者而言，手术的作用尚不确定。（Ⅱb C） （新推荐） 2.小脑出血伴神经功能恶化、脑干受压和/或脑室梗阻致脑积 水者应尽快手术清除血肿。（Ⅰ B）（根据前版修订） 不推荐以脑室引流作为该组患者的初始治疗。（Ⅲ C）（新 推荐） 3.脑叶出血超过30ml且血肿距皮层表面1cm以内者，可考虑 开颅清除幕上血肿。（Ⅱb B）（根据前版修订） 4.把立体定向设备或内镜单用，或与溶栓药物联用，以微创 的方式清除血肿，其效果尚不确定，目前正处于研究阶段。 （Ⅱb B）（新推荐） 5.尽管理论上来看有效，但是没有明确的证据表明超早期清 除幕上血肿可以改善临床预后或降低死亡率。早期开颅清除 血肿可能增加再出血的风险，从而产生负面作用。（Ⅲ B）
癫痫
►2.抽搐的患者应该应用抗癫痫药物（Ⅰ A）， ►持续EEG监测可能被用于障碍超过脑损伤程
度的ICH患者（Ⅱa B）， ►意识障碍、精神状态改变且EEG捕捉到癫痫
样放电的患者可应用抗癫痫药物（Ⅰ C）。 ►不建议预防性应用抗癫痫药物（Ⅲ B）。
ICH患者急诊室病史、查体及诊治要点
►
1. 病史： 发病时间或最后被发现正常的时间 初发症状及症状变化 危险因素 高血压、糖尿病、高脂血症、吸烟 服用药物史 抗凝药，抗血小板药，减充血药，降压药，stimulants（包括促进消化的 药物） 拟交感类药物 痴呆 淀粉样脑血管病相关痴呆 酒精及其它不良嗜好 可卡因及其它拟交感类药物抽搐 肝脏疾病 可能与凝血异常相关 肿瘤与血液系统疾病 可能与凝血异常相关 2. 查体 生命体征 发热与早期神经疾病进展有关，血压较高与早期病情进展及死亡率 增高相关 全身查体，以头，心、肺、四肢为重点 系统的快速神经系统专科查体 结构化的评估，比如国立中风健康量表可以在数分钟内 完成，并提供医护人员沟通病情严重程度的重要定量指标，GCS评分也被广泛熟知并 容易计算，且最初的GCS评分是预测长期临床预后的重要依据；这些必要时均可采用。 3. 实验室检查 血细胞计数、电解质，血尿素氮，肌酐、血糖 血肌酐升高与血肿扩大 相关，血糖升高与血肿扩大及较差的临床预后相关（尽管没有证据表明控制血糖正常 可以改善临床预后） 凝血酶原时间，INR，APTT 华法林相关的血肿与更大的血肿体积、更高的血肿扩大风 险、更高的致残率和致死率相关。 对于中青年患者行毒物筛查是否存在可卡因或其它拟交感类药物滥用 可卡因和其它拟 交感类药物与ICH相关 育龄妇女尿常规、尿培养及尿妊娠试验 4. 其它检查 ECG 评估是否存在可能导致心功能恶化的活动的心肌缺血或基础心脏损 害，获得住院期间心肺事件发生后的基线资料 胸片
► 1. 合并严重凝血因子缺乏或严重血小板减少的患者应该分别给予适当补充凝血因子或血小 板（Ⅰ C）。
► 2. INR升高的OACs相关ICH患者，应停用华法林，补充维生素K依赖的凝血因子，并静脉 应用维生素K（Ⅰ C）；PCCs与FFP相比，临床预后无明显差异，但并发症少；可以作为 FFP之外的替代选择（Ⅱa B）。rFVIIa并不能纠正全部的凝血异常，尽管可以降低INR，从 而不能完全使机体恢复正常的血栓形成机制。因此，不推荐常规应用rFVIIa（Ⅲ C）。
ICH的诊治 止血/抗血小板/预防深静脉血栓形成
潜在的凝血异常，如口服抗凝药物有凝血因子缺乏或血小板减少症的患者， 纠正这些异常都是必须的。
► 总体的建议是以最快的速度纠正INR； ► 维生素K联合 凝血酶原复合物及 重组凝血因子VIIa ► 患者24小时后INR降至≤1.4。
► 输注血小板的效果和安全性尚未可知。
自发性脑出血指南
2010
本指南包括以下几个部分：
► 诊断, ► 止血方法, ► 血压管理, ► 住院病人护理管理, ► 并发症预防, ► 手术治疗, ► 预后评估, ► 康复, ► 复发的预防 ► 出院后注意事项。
ICH的急诊诊断和评估及病因
►ICH 发生后在最初几小时内病情进展非常常 见；院前急诊医疗评估与急诊室评估对比发 现,超过20%的患者在此过程中Glasgow昏迷 评分（GCS）将下降超过2分,在上述患；另外,在进入医院的第一个小时 内,15%的患者GCS下降超过2分；从而早期 神经功能进一步减退和较差的长期预后的比 率降低了强力医学干预的必要性。
► 4. 曾经应用抗血小板药物治疗的ICH 患者，输血小板的有效性并不清楚，需要进一步研究 （is considered investigational）（Ⅱb B）。
► 5. ICH患者可行气压动力治疗联合应用弹力袜来防止深静脉血栓形成（Ⅰ B）。 ► 6. 症状发生1-4天后活动较少的患者，在证据表明出血停止的条件下，可应用小剂量低分