妇产科学双语课件

ABRUPTIOPLACENTAE

DefinitionAbruptioPlacentae(placentalabruption):

prematureseparationofthenormallyimplantedplacentafromtheuterinewall.EtiologyMechanism:hemorrhageintothedeciduabasalis,leadingtoprematureplacentalseparationandfurtherbleeding.Associatedfactors:MaternalhypertensionSuddendecompressionoftheuterusMaternalcocaineusetraumaClassificationCompleteseparation:

novaginalbleedingPartialseparation:vaginalbleedingwillbeapparentMarginalseparation:vaginalbleedingwillbeapparent

diagnosisClassicclinicalpresentation:vaginalbleedingTenderuterusUterinecontractionsFetaldistressCoagulationabnormalitiesHypofibrinogenemiaIncreaseinglevelsoffibrindegradationproductsdecreasingplateletcountIncreasingprothrombintimeandpartialthromboplastintimeDecreasingotherserumclottingfactorsUltrasonography:relativelylargeretroplacentalclotsmaybedetectedPlacentalexamination

Theextentofplacentalabruptionofthematernalsurfaceoftheplacentaonwhichaclotisdetectatthetimeofdelivery.ManagementMaintainhemodynamicstabilization(

Transfusiontherapy)CrystalloidtransfusionWholebloodtherapyComponenttherapyCorrectcoagulationstatusDeliveryWhenthefetusismature,vaginaldeliveryispreferableunlessthereisevidenceoffetaldistressorhemodynamicinstability.Whenthefetusisnotmatureandplacentalabruptionislimited,observationwithclosemonitoringofbothfetalandmaternalstatus.CardiovascularComplications

GeneralConsiderationCauseofmotherdeathThe2ndcauseIncidence1%-4%GeneralConsiderationAntenatalcardiovascularchangesBloodvolumeincreaseby40%-60%Peakingat32–34weekstheexpansioninplasmavolumeisgreaterthanthatexpansionofredcellmass.CardiacoutputIncreaseby40%-50%Peakingat20-24weeksGeneralConsiderationBloodpressureDecreaseinthefirsttrimesterRisetoprepregnancylevelsinthethirdtrimesterHeartsizeVentricularchambersizeisincreasedSystolicfunctionisunchanged.GeneralConsiderationIntrapartumcardiovascularchangesFirst-stagelabor300ml–500ml↑(eachcontraction)Cardiacoutput↑(maternalpain,anxiety)Second-stagelaborLungcirculation↑(bearing-downeffortstoexpelthefetus)Venousreturn↓(afterfetusisdeliveried)Placentalcirculationislost(afterplacentaisdeliveried)GeneralConsiderationPostpartumCirculatingbloodvolume↑(Placentalcirculationislost)Circulatingbloodvolumefurther↑(mobilizationofextravascularfluidintothevascularsystem)TypesofCardiovascularComplicationCongenitalheartdisease先心:themostfrequentLefttorightshunting左向右分流型Atrialseptaldefect(ASD)房缺:mostcommonasymptomatic(mostpatients);pulmonarybloodflow↑(lesion≥2cm2)→pulmonaryhypertension→Eisenmenger’ssyndromeVentricularseptaldefect(VSD)室缺tolerated(smalllesion);leftventricularhypertrophy→pulmonaryhypertension→biventricularhypertrophyTypesofCardiovascularComplicationPatentductusarteriosus(PDA)动脉导管未闭rare(earlysurgicalrepair);hemodynamicconsequencearesimilartoVSDRighttoleftshunting右向左分流型TetralogyofFallot法洛氏四联征Pulmonarystenosis,rightventricularhypertrophy,largeventricularseptaldefectandoverridingaortathemostcommoncyanoticlesioncomplicatingpregnancyTypesofCardiovascularComplicationNon-shuntingPulmonarystenosisNotusuallyprogressiveAorticstenosisrare;itsoutcomeisbadMarfan’ssyndrome(geneticdisorder)Myxomatousdegenerationoftheheartvalves;mitralandcysticmedialnecrosis（囊性中层坏死）

oftheaorta(aneurysms动脉瘤)

deathrate:4%-50%TypesofCardiovascularComplicationRheumaticheartdiseaseMitralstenosisisthemostcommonlesion.Severelesionwithpulmonaryhypertension→pulmonaryedema→hearfailure:terminatethepregnancyHeartdiseasecausedbypreeclampsiaLeftheartfailure(increasedbloodpressureandcardiacmuscleischemia)TypesofCardiovascularComplicationPeripartumcardiomyopathyCongestivecardiomyopathy(duringthelatestageofpregnancy(3months)orwithinthefirst6monthspostpartum)AbsenceofothercausesofheartfailureItsetiolotyisuncertainManifestations:symptomscausedbyheartfailureandembolismTheriskofmaternalmortalityis30%-50%.TypesofCardiovascularComplicationMyocarditis心肌炎Manifestation:arrhythmia心律失常Sequelaeofmyocarditis心肌炎后遗症:morecommonEffectsonfetusPretermlabor,fetaldeath,fetaldistressDrugusedInheritedproblemVentricularseptaldefect(VSD):22%Marfan’ssyndrome:50%Diagnosis

EtiologydiagnosiscongenitalorrheumaticorpreeclampsiaorperipartumcardiomyopathyAnatomydiagnosisASDorVSDorPDAormitralstenosisormitralregurgitationPathophysiologydiagnosispulmonaryhypertensionorEisenmenger’ssyndromeorarrhythmiaFunctionalclassificationClass:I—IVDiagnosismoresignificantsignsHistory:palpitation(心悸),shortbreath,heartdiseaseOrthopnea(端坐呼吸),chestpain,expectorationofblood(咯血)Cyanosis紫绀,diastolicmurmur舒张期杂音ArrhythmiaEnlargementofheart(chestx-rayfilm)Echocardiogram:chamberenlarge,hypertrophy,abnormalityofvalveFunctionalclassificationofheartdiseaseNewYorkHeartAssociation(NYHA)ClassI:asymptomaticClassII:symptomswithnormalactivityClassIII:symptomswithlessthannormalactivityClassIV:symptomsatrestRevisedguidelineAccordingtotheresultofobjectivetesting(chestx-ray,EKG,echocardiogram)earlydiagnosisofheartfailurePalpitationandshortbreathwithlessthannormalactivityHR>110,R>20atrestOrthopneaatnightPersistentwetraleinlung

JudgmentofsafetyofpregnancyConceptionshouldbepreventedif:SevereheartdiseaseFunctionalclassification:classIII-IVHistoryofheartfailurePulmonaryhypertensionRighttoleftshuntingSeverearrhythmiarheumaticfever风湿热CombinedvalvediseaseAcutemyocarditisTreatment

AntenataltreatmentTerminationofpregnancy:Terminatebefore12weeks(casesnotsuitabletopregnancy)Antenatalsupervise:regularandintensiveandearly(earlypregnancy)Preventionofheartfailuresufficientrestweighcontrolpreventinginfection,correctinganemiaandarrhythmiaTreatmentTreatmentofheartfailureCardiotonic强心:digoxinVasculardilationDiuretic利尿CaesareansectionTreatmentIntrapartumtreatmentMethodofdelivery:CSFirststagecalmdown,ataractic(镇静剂),oxygensupplementSecondstageOperativevaginaldeliveryThirdstagePreventingpostpartumhemorrhagePuerperiumPreventinginfectionENDCEREBRALVASCULARDISEASE

CerebralvascularDiseaseDefinitionofterm:Thetermcerebrovasculardiseasedesignatesanyabnormalityofthebrainresultingfromapathologicprocessofthebloodvessels.Suddenlossofneurologicalfunctionisthehallmarkofcerebrovasculardisease.Cerebrovasculardiseaseisthethirdmostcommoncauseofdeathandthemostcommondisablingneurologicdisorderinwesterncivilizedcountrieswhereanincreasingproportionofpeoplesurvivetooldage.ShanghaiisenteringtheagingsocietyItsincidenceincreaseswithageandissomewhathigherinmenthaninwomen.Riskfactorsforstroke

SystolicordiastolichypertensionDiabeticsHypercholesterolemiaHeartdisease(afib)CigarettesmokingHeavyalcoholconsumptionHighhomocystineOralcontraceptiveuse

Themajortypesofcerebrovasculardisease

CerebralischaemiaandinfarctionTransientIschemicAttacksAtheroscleroticthrombosisLacunesEmbolismHemorrhageHypertensivehemorrhageRupturedaneurysmsandvascularmalformationsOther

I、CerebralischaemiaandinfarctionAnatomyandpathology

Theprincipalpathologicalprocessunderconsiderationhereistheocclusionofarteriessupplyingthebrain.ThetwointernalcarotidarteriesandthebasilararteryformtheCircleofWillisatthebaseofthebrain,whichactsasanefficientanatomoticdeviceintheeventofocclusionofarteriesproximaltoit.

AnatomyandpathologyOcclusionleadstosuddensevereischaemiaintheareaofbraintissuesuppliedbytheoccludedartery,andrecoverydependsuponrapidlysisorfragmentationoftheoccludingmaterial:

Reversalofneurologicalfunctionwithinminutesorhoursgivesrisetotheclinicalpictureofatransientischaemicattack.

AnatomyandpathologyWhentheneurologicaldeficitlastslongerthan24hours,itmaybecalledareversibleischaemicneurologicaldeficit(RIND)ifitrecoverscompletelyinafewdays,

oracompletedstrokeifthereisapersistentdeficit.

Sometimesrecoveryisveryslowandincomplete.

Neurologicalsymptomsandsigns

Thelossoffunctionthatthepatientnotices,andwhichmaybeapparentonexamination,entirelydependsontheareaofbraintissueinvolvedintheischaemicprocess.

NeurologicalsymptomsandsignsThefollowingsuggestmiddlecerebralterritory:

Dysphasia;

Dyslexia,dysgraphia,dyscalculia;

Lossofuseofcontralateralfaceandarm;

Lossoffeelingincontralateralfaceandarm.

NeurologicalsymptomsandsignsThefollowingsuggestsanteriorcerebralterritory:

Lossofuseand/orfeelinginthecontralateralleg.Thefollowingsuggestsposteriorcerebralterritory:

Developmentofacontralateralhomonymoushemianopia.NeurologicalsymptomsandsignsThefollowingsuggestsadeep-seatedlesionaffectingtheinternalcapsulewhichissuppliedbysmallperforatingbranchesofthemiddleandposteriorcerebralarteriesclosetotheirorigins:

Completelossofmotorandsensoryfunctionthroughoutthewholeofthecontralateralsideofthebodywithahomonymoushemianopia.NeurologicalsymptomsandsignsThefollowingsuggestsophthalmicarteryterritory(theophthalmicarteryarisesfromtheinternalcarotidarteryjustbelowtheCircleofWillis):

Monocularlossofvision.

NeurologicalsymptomsandsignsThefollowingsuggestvertebro-basilarterritory:

doublevision(3,4,6);

facialnumbness(5);

facialweakness(7);

vertigo(8);

dysphagia(9,10);

dysarthria(9,10,12);

ataxia;

dropattacks;

motororsensorylossinbotharmsorlegs.

1.TransientIschemicAttacks(TIA)

DefinitionoftermCurrentopinionholdsthatTIAsarebrief,reversibleepisodesoffocal,nonconvulsiveischaemicneurologicdisturbance,Consensushasbeenthattheirdurationshouldbelessthan24h.

Clinicalpicture

TransientIschaemicAttackscanreflecttheinvolvementofanycerebralartery.Thelossoffunctionentirelydependsontheinfluencedartery.

Itmaylastafewsecondsorupto12to24h,Mostofthemlast2to15min.

Thereareonlyafewattacksorseveralhundred.

Betweenattacks,theneurologicexaminationmaydisclosenoabnormalities.

Astrokemayoccurafternumerousattackshaveoccurredoveraperiodofweeksormonths.

DifferentialdiagnosisofTIAs

Transientepisodes,indistinguishablefromTIAs,areknowntooccurinpatientswithSeizure,Migraine,Transientglobalamnesia,andoccasionallyinpatientswithmultiplesclerosis,meningioma,glioblastoma,metastaticbraintumorssituatedinornearthecortex,andevenwithsubduralhematoma.

2.Cerebralthrombosis

Mostcerebrovasculardiseasecanbeattributedtoatherosclerosesandchronichypertension;untilwaysarefoundtopreventorcontrolthem,vasculardiseaseofthebrainwillcontinuetobeamajorcauseofmorbidity.

Pathogenesis

PathogenesisofIschemicneuronaldeath

Ischemia↓Excitatoryaminoacidreceptors↓

Borderzoneorpenumbra

↓Programmedcelldeath

Clinicalpicture

Ingeneral,evolutionoftheclinicalphenomenainrelationtocerebralthrombosisismorevariablethanthatofembolismandhemorrhage.Thelossoffunctionthatthepatientnotices,andwhichmaybeapparentonexamination,entirelydependsontheareaofbraintissueinvolvedintheischaemicprocess.(above)

ClinicalpictureInmorethanhalfofpatients,themainpartofthestrokeisprecededbyminorsignsoroneormoretransientattacksoffocalneurologicdysfunction.ThefinalstrokemaybeprecededbyoneortwoattacksorahundredormorebriefTIAs,andstrokemayfollowtheonsetoftheattacksbyhours,weeks,or,rarely,months.Themostoccurrenceofthethromboticstrokeisduringsleep.Thepatientawakensparalyzed.Eitherduringthenightorinthemorning.Unawareofanydifficulty,hemayariseandfallhelplesslytothefloorwiththefirststep.

ClinicalpictureAssociatedsymptoms

Seizuresaccompanytheonsetofstrokeinasmallnumberofcases(10-50%);inotherinstances,theyfollowthestrokebyweekstoyears.Thepresenceofseizuresdoesnotdefinitivelydistinguishembolicfromthromboticstrokes,butseizureattheonsetofstrokemaybemorecommonwithembolus.

ClinicalpictureAssociatedsymptomsHeadacheoccursinabout25%ofpatientswithischaemicstroke,possiblybecauseoftheacutedilationofcollateralvessels.

LaboratoryFindings

CTScanorMRI:ACTscanorMRIshouldbeobtainedroutinelytodistinguishbetweeninfarctionandhemorrhageasthecauseofstroke,toexcludeotherlesions(eg,tumor,abscess)thatcanmimicstroke,andtolocalizethelesion.CTisusuallypreferredforinitialdiagnosisbecauseitiswidelyavailableandrapidandcanreadilymakethecriticaldistinctionbetweenischaemiaandhemorrhage.LumbarPuncture:Thisshouldbeperformedinselectedcasestoexcludesubarachnoidhemorrhage.LaboratoryFindingsCerebralAngiography:

Intra-arterialangiographyisusedtoidentifyoperableextracranialcarotidlesionsinpatientswithanteriorcirculationTIAswhoaregoodsurgicalcandidates.Italsocanbeusedforintra-arterialthrombolysis(r-tPA)Magneticresonanceangiography(MRA)maydetectstenosisoflargecerebralarteries,aneurysms,andothervascularlesion,butitssensitivityisgenerallyinferiortothatofconventionalangiography.

DifferentialDiagnosis

Vasculardisordersaremistakenforischaemicstrokeincludeintracerebralhemorrhage,subduralorepiduralhematoma,andsubarachnoidhemorrhagefromruptureofananeurysmorvascularmalformation.Theseconditioncanoftenbedistinguishedbyahistoryoftraumaorofexcruciatingheadacheatonset,amoremarkeddepressionofconsciousness,orbythepresenceofneckstiffnessonexamination.TheycanbeexcludedbyCTscanorMRI.DifferentialDiagnosisDifferentialDiagnosis:Otherstructuralbrainlesionsuchastumororabscesscanalsoproducefocalcerebralsymptomsofacuteonset.Brainabscessissuggestedbyconcurrentfever,andbothabscessandtumorcanusuallybediagnosedbyCTscanorMRI.Metabolicdisturbances,particularlyhypoglycemiaandhyperosmolarnonketotichyperglycemia,maypresentinstrokelikefashion.Theserumglucoselevelshouldthereforebedeterminedinallpatientswithapparentstroke.

TreatmentofCerebralThrombosisandTransientIschemicAttacks

Thecurrenttreatmentofitmaybedividedintofourparts:ManagementintheacutephaseMeasurestorestorethecirculationandarrestthepathologicprocess1.Thrombolyticagents(t-PAonlyforcompletedstroke,w/in3~6hrs)2.Anticoagulantdrugs(Heparin,LMWH&warfarin)3.Antiplateletdrugs(AspirinorClopidogrel,DipyridamoleorTiclopidine)4.Difibrase5.Neuroprotectiveagents:barbiturates,opioidantagonistnaloxone,Manitol

TreatmentTreatmentofcerebraledemaandraisedintracranialpressureAcutesurgicalrevascularizationSurgeryforsymptomaticcarotidstenosisCarotidendarterectomy,intralumenalstents,extracranial-intracranialbypassPhysicaltherapyandrehabilitationMeasurestopreventfurtherstrokesandprogressionofvasculardisease.TreatmentSincetheprimaryobjectiveinthetreatmentofatherothromboticdiseaseisprevention,effortstocontroltheriskfactorsmustcontinue.AspirinHypotensiveagentsOversedationshouldbeavoidedSystemichypotension,severeanemiashouldbetreatedpromptlyParticularcareshouldbetakentomaintainthesystemicbloodpressure,oxygenationandintracranialbloodflowduringsurgicalprocedures,especiallyinelderlypatient.

CourseandPrognosis

Whenthepatientisseenearlyinthecerebralthrombosis,itisdifficulttogiveanaccurateprognosis.Asfortheeventualorlong-termprognosisoftheneurologicdeficit,therearemanypossibilities.Itmustbementionedthathavinghadonethromboticstroke,thepatientisatriskintheensuingmonthsandyearsofhavingastrokeatthesameoranothersite,especiallyifthereishypertensionordiabetesmellitus.

3.Embolicinfarction

Thisisoneofthemostcommoncauseofstroke.Inmostcasesofcerebralembolism,theembolicmaterialconsistsofafragmentthathasbrokenawayfromathrombuswithintheheart.Embolismduetofat,tumorcells,fibrocartilage,amnioticfluid,orairisarareoccurrenceandseldomentersintothedifferentialdiagnosisofstroke.

ClinicalPicture

Ofallstrokes,thoseduetocerebralembolismdevelopmostrapidly.

Theembolusstrikesatanytimeofthedayornight.Gettinguptogotothebathroomisatimeofdanger.

Theneurologicpicturewilldependonthearteryinvolvedandthesiteofobstruction.

ClinicalPicture

Itisimportanttorepeatthatanembolusmayproduceasevereneurologicdeficitthatisonlytemporary;symptomsdisappearastheembolusfragments.Inotherwords,embolismisacommoncauseofasingleevanescentstrokethatmayreasonablybecalledaprolongedTIA.Alsoasalreadypointedout,severalembolicangiverisetotwoorthreetransientattacksofdifferingpatternor,rarely,ofalmostidenticalpattern.

Causesofcerebralembolism:

Cardiacorigin

Noncardiacorigin

Undeterminedorigin

LaboratoryFindings

Notinfrequentlythefirstsignofmyocardialinfarctionistheoccurrenceofembolism;thereforeitisadvisablethatanECGandechocardiogrambeobtainedinallpatientswithstrokeofuncertainorigin.

ProlongedstudyofheartrhythmwithHoltermonitoringshouldbeundertaken.

LaboratoryFindings

Insome30percentofcases,cerebralembolismproducesahemorrhagicinfarction.CTscanningorMRImaybehelpfulinshowingthemoreintensehemorrhagicinfarcts,particularlyifthescanisrepeatedonthesecondorthirdday.

Courseandprognosis

Mostpatientssurvivetheinitialinsult,andinmanytheneurologicdeficitmayrecederelativelyrapidly,asindicatedabove.

Theeventualprognosisisdeterminedbytheoccurrenceoffurtheremboliandthegravityoftheunderlyingillness-cardiacfailuremyocardialinfarction,bacterialendocarditisandsoon.

Treatmentandprevention

Threephasesoftherapy:

Generalmedicalmanagementintheacutephase,

Measuresdirectedtorestoringthecirculation

Physicaltherapyandrehabilitation

Thesearemuchthesameasdescribedabovethepreventionofatherothromboticinfarction.

4.LacunarinfarctAsonemightsurmise,smallpenetratingbranchesofthecerebralarteriesmaybecomeoccluded,andtheresultinginfarctsmaybesosmallorsosituatedastocausenosymptomswhatever.Asthesoftenedtissueisremoved,itleavesasmallcavity,orlacune.

LacunarinfarctInourclinicalandpathologicmaterial,therehasalwaysbeenastrongcorrelationofthelacunarstatewithacombinationofhypertensionandatherosclerosisand,toalesserdegree,withdiabetes.

Inallthecasesoflacunarinfarction,thediagnosisdependsessentiallyontheoccurrenceofthecertainuniquestrokesyndromesoflimitedproportions.

LacunarinfarctAsmentionedabove,CTscanningislessreliablethanMRIindemonstratingthelacunes.TheEEGmaybehelpfulinanegativesense;inthecaseoflacunesintheponsortheinternalcapsule,thereisanotablediscrepancybetweentheunilateralparalysisorsensorylossandthenegligibleelectricalchangesovertheaffectedhemisphere.

LacunarinfarctRecognitionoflacunarstrokeisimportantFuturelacunarstrokecanbereducedby

treatingHTNAnticoagulationisnotindicated(Noevidence)Aspirinisalsoofuncertanty

II.IntracranialHemorrhageThisisthecommon,well-known“spontaneous”brainhemorrhage.Itisduepredominantlytochronichypertensionanddegenerativechangesincerebralarteries.Hemorrhagemayinterferewithcerebralfunctionthroughavarietyofmechanisms,includingdestructionorcompressionofbraintissueandcompressionofvascularstructures,leadingtosecondaryischaemiaandedema.IntracranialHemorrhageIntracranialhemorrhageisclassifiedbyitslocationasintracerebral,subarachnoid,subdural,orepidural,allofwhich-exceptsubduralhemorrhage-areusuallycausedbyarterialbleeding.IntracranialHemorrhageThebleedingoccurswithinbraintissue,andruptureofarterieslyinginthesubarachnoidspaceispracticallyunknownapartfromaneurysms.Theextravasationformsaroughlycircularorovalmassthatdisruptsthetissueandgrowsinvolumeasthebleedingcontinues.Adjacentbraintissueisdistortedandcompressed.Ifthehemorrhageislarge,midlinestructuresaredisplacedtotheoppositesideandreticularactivatingandrespiratorycentersarecompromised,leadingtocomaanddeath.1.IntracerebralHemorrhage

Ofallthecerebrovasculardiseases,brainhemorrhageisthemostdramatic.Ithasbeengivenitsownname,“apoplexy”.ClinicalPictureWithsmallerhemorrhages,theclinicalpictureconformsmorecloselytotheusualtemporalprofileofastroke,i.e,anabruptonsetofsymptomsthatevolvegraduallyandsteadilyoverminutes,hours,oradayortwo,dependingonthesizeoftherupturedarteryandthespeedofbleeding.Headacheandvomitingarecardinalfeatures.Verysmallhemorrhagesin“silent”regionsofthebrainmayescapeclinicaldetection.ClinicalPictureClinicalfeaturesvarywiththesiteofhemorrhage.Deepcerebralhemorrhage

Thetwomostcommonsitesofhypertensivehemorrhagearetheputamenandthethalamus,whichareseparatedbytheposteriorlimboftheinternalcapsule.Thissegmentoftheinternalcapsuleistraversedbydescendingmotorfibersandascendingsensoryfibers,includingtheopticradiations.ClinicalPictureLobarhemorrhageHypertensivehemorrhagesalsooccurinsubcorticalwhitematterunderlyingthefrontal,parietal,temporal,andoccipitallobes.Symptomsandsignsvaryaccordingtothelocation.ClinicalPicturePontinehemorrhageWithbleedingintothepons,comaoccurswithinsecondstominutesandusuallyleadstodeathwithin48hours.Ocularfindingstypicallyincludepinpointpupils.Horizontaleyemovementsareabsentorimpaired,butverticaleyemovementsmaybepreserved.CerebellarhemorrhageThedistinctivesymptomsofcerebellarhemorrhage(headache,dizziness,vomiting,andtheinabilitytostandorwalk)beginsuddenly,withinminutesafteronsetofbleeding.LaboratoryFindings

Amonglaboratorymethodsforthediagnosisofintracerebralhemorrhage,theCTscanoccupiestheforemostposition.InCTscans,freshbloodisvisualizedasawhitemassassoonasitisshed.Themasseffectandthesurroundingextrudedserumandedemaarehypodense.ByMRI,eitherinT1-or-T2weightedimages,thehemorrhageisnoteasilyvisibleinthe2or3daysafterbleeding.LaboratoryFindingsIngeneral,lumbarpunctureisilladvised,foritmayprecipitateoraggravateanimpendingshiftofcentralstructuresandherniation.Thewhitecellcountintheperipheralbloodmayrisetransientlyto15,000percubicmillimeter,ahigherfigurethaninthrombosis.DifferentialDiagnosis:

Putaminal,thalamic,andlobarhypertensivehemorrhagesmaybedifficulttodistinguishfromcerebralinfarctions.Tosomeextent,thepresenceofsevereheadache,nauseaandvomiting,andimpairmentofconsciousnessareusefulcluesthatahemorrhagemayhaveoccurred;theCTscanidentifiestheunderlyingdisorderdefinitively.CTscanorMRIisthemostusefuldiagnosticprocedure,sincehematomascanbequicklyandaccuratelylocalized.TreatmentThemanagementofpatientswithlargeintracerebralhemorrhagesandcomaincludesthemaintenanceofadequateventilation,useofcontrolledhyperventilationtoaPco2of25to30mmHg,monitoringofintracranialpressure(ICP)insomecasesanditscontrolbytheuseoftissue-dehydratingagentssuchasmannitol(osmolalitykeptat295to305mosmol/LandNaat145to150meq),andlimitingintravenousinfusionstonormalsaline.TreatmentRapidreductioninbloodpressure,inthehopeofreducingfurtherbleeding,isnotrecommended,sinceitriskscompromisingcerebralperfusionincasesofraisedintracranialpressure.Ontheotherhand,sustainedmeanbloodpressureofgreaterthan110mmHgmayexaggeratecerebraledemaandriskextensionoftheclot.Itisatapproximatelythislevelofacutehypertensionthattheuseofbeta-blockingdrugs(esmolol,labetalol)orangiotensin-convertingenzymeinhibitorydrugsisrecommended.TreatmentIncontrasttocerebralhemorrhage,thesurgicalevacuationofcerebellarhematomasisagenerallyacceptedtreatmentandisamoreurgentmatterbecauseoftheproximityofthemasstobrainstemandtheriskofabruptprogressiontocomaandrespiratoryfailure.CourseandPrognosisTheimmediateprognosisforlargeandmedium-sizecerebralclotsisgrave;some30to35percentofpatientsdiein1to30days.Eitherthehemorrhageextendsintotheventricularsystemorintracranialpressureiselevatedtolevelsthatprecludenormalperfusionofthebrain.Sometimesthehemorrhageitselfseepsintovitalcenterssuchasthehypothalamusormidbrain.CourseandPrognosisAvolumeof30mlorless,calculatedfromtheCTscan,predictedagenerallyfavorableoutcome.Inpatientswithclotsof60mlorlargerandaninitialGlasgowComaScalescoreof8orless,themortalitywas90percent.Asremarkedearlier,itisthelocationoftheclinicaleffects.2.SpontaneousSubarachnoidHemorrhageThisisthefourthmostfrequentcerebrovasculardisorderfollowingatherothrombosis,embolism,andprimaryintracerebralhemorrhage.Saccularaneurysmsarealsocalledberry”aneurysms;actuallytheytaketheformofsmall,thin-walledblistersprotrudingfromarteriesofthecircleofWillisoritsmaj