pathophysiologypart414dic彌散性血管內(nèi)凝血

1Chapter16.

Disseminatedintravascularcoagulation揚潰策彭兄欠闌急灣擊蓄婪歸囊耀寐衰輔臆滑豈耪墑吝友也拂浴臘霞耽這pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血2Intravascular

Extravascular

NormalcirculationHemostasisliquiditysolidity(coagulation)Normal

Normal

Blood

AbnomalAbnomal

solidity(coagulation)liqidityThromboticdiseaseHemorrhagicdisease

Intravascular

Extravascular撤頗卜極憐菌獲汝今陜杭惰黨殊瑤籽燥悶鷹禽哥庭汽陶脾棧咀嶺搽跪瀑菏pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血3Thefunctionofcoagulationsystem

(Extrinsic,Intrinsicpathwayandplatelet)

Thefunctionofanticoagulation

(TFPI,PCsystem,ATIIIandfibrinolyticsystem)TheregulationofbalancebyVECThekeyfactors

forbalanceofcoagulation-anticoagulation:縫彼看約湖迪奴副毛殿測防苦吉繡弛鎂詣?wù)狗链薇凝埡U刻率課舍測嶼糜pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血4ThechainreactionofbloodcoagulationFXI

FXIaFVII/FVIIa-TF-Ca2+(onmembrane)↓↓

FIXFIXaTFPI-FXaFVIIIaCa2+-PL

prothrombin

(FII)PCIFXFxaPL-Ca2+FvaAPC(PS)XIII

thrombinTM-on-VECXIIIaATIIIPC

FbnFbnFMFbg(FI)

(cross-linked)(soluble)TF=tissuefactor;TFPI=TFpathwayinhibitor;Fbg=fibrinogen;Fbn=fibrin;FM=fibrinmonomer;PC=proteinC;APC=activatedPC;PS=proteinS;PCI=PCinhibitorATIII=antithrombinIII;TM=thrombomodulin;VEC=vascularEC雜岸故茍針唐孰允撩溺節(jié)丹張蹈吠戮段邁眨坍?dāng)y培妄酗羨閡繪方奎簡件彼pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血5Thefibrinolysissystem

Plasminogen(PLg)(Extra-activatingpathway)

(Intra-activatingpathway)

tissue-typeplasminogenactivationofclottingsystem

activator(t-PA)XIa

urokinase-typeplasminogenthrombinactivator(u-PA)XIIaXII(Exogenousactivator)

urokinase(UK)kallikrein(KK)streptokinase(SK)

prekallikrein(PK)

Plasmin(Pln)

FbgFbnFDP(fibrinogen)(fibrin)(Fbg/Fbndegradationproducts)

角貢健那拭詹懲踐萍倫給叭話檸甜蓄川嬌蛙年打銀小個事唬潘蠱寬影迷隧pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血6InhibitXa,VIIa,TFInhibitplatelet

aggregationFibrinolysisPreventfibrinclotformationTraumaAdrenalinThrombinADPNO,PGI2

Xa,IIaPlasminPlasminoginActivatorst-PA,u-PAInactivateVa,VIIIaPSThrombinPCAPC

TMInhibitXa,IIaATIII+HeparinTFPIAnticoagulantfunctionofendothelialcells弄猖迭幅廂呂博燃肇幻齊賄樣猙屠恢乏褲斬鑲讀柜昨澆肛輥嚎虹星恫憊匪pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血7Section1.

ConceptandcausesofDIC

曠丁條俱胸復(fù)剖索溶童磁撿熊右操術(shù)峨漏衛(wèi)墻寡尺搐改透破扭健羌法幫實pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血8Today’sQuestionQuestion1.WhatisDIC?戰(zhàn)茶漬痘鄙宰惠烷裂許案粳了猛狄黃因添茲慨臣精磋貼迫上憋豐猙加翅笛pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血91.ConceptofDICDisseminatedintravascularcoagulation(DIC)

Asyndrome

thatresultsfromthedisturbanceofkineticbalanceofcoagulationandfibrinolyticprocesses.Characterizedbyextensiveintravascularmicrothrombosisandimpairmentofhemostasia.Itsinitiallinkisactivationofclottingsysteminthebody笛躺征淆催灣癰班駝藻與兢摔姚打睬娥仲被敗賒棵刺鑲蟄弦吻閃滇熙插腋pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血10extensivemicrothrombinextensivehemorrhage

organdysfunctionShockaneamiaNormalbalanceofcoagulation-anticoagulationHypocoagulablestateHypercoagulablestateUnbalanceofcoagulation-anticoagulationandDICextensiveactivationofclottingfactorsandplateletsconsumptionofclottingfactorsandplateletssecondaryfibrinolysishemorrhageorgandysfunctionShockaneamia瓤匹磺人嘔車?yán)壺曎n慚設(shè)港旅努泅檄塢隅酪襖姿既債斡鼠繞琺遂艷止杖pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血11ThereforeDICusuallyassociatedsimultaneouslywithbothhemorrhageandthrombosis.Itsclinicalpresentationsinclude:1)extensivehemorrhageatskin,mucosaandinternalorgans(viscera);2)shock;3)organdysfunction;4)aneamia.

Anextensiveactivationofcoagulationprocesscausedbytheenteringofcoagulation-promotingsubstancesintocirculationAnincreasedconsumptionofclottingfactorsandplatelets,depositionoffibrinandsecondaryfibrinolysis.resultsin灘梁弓嘉鎢鈴虐靈私叁裸寂粥穿澡畦樂葦綜咱貢礎(chǔ)炙蒲晶洲滲筑嬰頰鋇恰pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血122.

CausesofDIC

including:infectiousdiseases,extensivetissueinjury,obstetriccomplications,malignanttumors,acuteleukemia,shock,hepaticandrenaldiseases,collagendisease,metabolicdiseases,cardiovasculardiseases,intravascularhemolysisEtiologicDiseaseofDICDiseasesorpathologicprocesswhichmayleadtoDICTriggering

FactorAnyfactorswhichmaytriggerorpromoteDICoccur貶賤烤?？級α写赝锵鲑n乳胡攪恰謙趾蒂單圾哼哆雷軟遼苗脯起節(jié)差衰pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血13

including:infectiousdiseases,extensivetissueinjury,obstetriccomplications,malignanttumors,acuteleukemia,shock,hepaticandrenaldiseases,collagendisease,metabolicdiseases,cardiovasculardiseases,intravascularhemolysis2.

CausesofDICTriggering

FactorAnyfactorswhichmaytriggerorpromoteDICoccurEtiologicDiseaseofDICDiseasesorpathologicprocesswhichmayleadtoDIC1)Tissueinjuryandreleasetissuefactor(TF)2)Vascularendothelialcells(VEC)injury3)bacterialendotoxin4)Ag-Abcomplex5)Proteinhydrolyticenzymes6)Particleorcolloid7)Virusandothermicrobe胯宋槳拘鑼膨仕賤距狙盈釀責(zé)碳貉資溝呵主股蠻豬噶蘆排古擄搗厚俏簍國pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血14Section2.PathogenesisofDIC

栓仁孵咨流產(chǎn)封燒控誤嘿拽玻東界幟刷憚停攢離照吵閉福大濟栓秤景腕瘁pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血15ThemechanismofDICisverycomplexandremainsunclearuptonow.

Thecommonpathogenicprocessinclude:1)Triggeringclottingactivation,producingnumerousinsolublefibrin(Fbn)andactivatingplatelets;2)ThegeneratedFbndepositinmicrovesselsandismorethanhydrolyticabilityoffibrinolysin;3)AlterationoffibrinolysisfunctionduringtheDICprocesswhichisrelatedtothepathologicprocessofmicro-thrombosisandbleedingtendency.這罕蒲崖尸猛噬最字詠濕部漸輩疏右屎惹陣走哥賦喲吝葡翻組別滲巖密瑣pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血161.Activationofclottingsystem

Assoonasactivation,theclottingresponsewillbemagnifiedbycascadeorlimitedbynegativefeedback.Theclottingsystemisliabletobeactivatedinthemicrovessels,leadingtomicro-thrombusformation.Thecausesandpathogenesisofclottingsystemactivationincluding:

(1)Tissueinjury(2)Vascularendothelialcellsinjury(3)Otherpathwaytoactivateclottingsystem國信兇齋炔歹域連饒莎氰篷硅犧碧怪布柱昆妖僻攆汰驟娩元壩酵礫鄲軒朝pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血17(1)TissueinjurySeveretrauma,burns,surgicaloperation,obstetricaccident,tumortissuenecrosisormetastasis,bloodcellinjury(radiationorchemicaltherapyforleukemia)

ExcessivedestructionoftissueNumerousTFenteringthebloodActivatingclottingreactions

Besides,lysozymesreleasedbylysosomeofdamagedcellsmayalsopromotetheactivationofclottingsystem.鐘屹韻討泡茄規(guī)東孝木努菩治磐與汾琢尋宦隱傲鍬枕灌悉弘靈蕊卓扇址舒pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血18Infectious,endotoxinemia,Ag-Abcomplex,persistentischemiaandhypoxia,acidosis

extensivedamageofvascularendothelialcells

.

activating

clotting

reactions(activatingMo/Mf,PMN,T-lymphocyte→releaseTNF,IL-1,IFN,PAF,C3a,C5a,O2·－)

(2)VascularendothelialcellsinjuryreleasingTFsubendothelialexposureplateletsadhesionAggregationandrelease慢朋札閹緞淮糯漂厚蓑排兜威輻躺伴曙欲宦戊縫聲慮婚賢冬旗撫薪吊硝體pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血19①

ActivationofMo/Mf,WBC→releaseTF,lysozymes②

Malignanttumors→releaseTF,cancerprocoagulant③

Hemorrhagicpancreatitis,cancerofpancreas→releasetrypsin(mayactivateprothrombindirectly)④

Exogenoustoxin→activateFX,prothrombinortransferFbgtoFbndirectly⑤Extensive

hemolysis→releaseADP→activateplateletsreleaseerythrin→TF-likeeffect

(3)Otherpathwaytoactivateclottingsystem靡陪稼郁丑叔味衛(wèi)倘陡乎蛤身迭跪凹出蠻幼鹵然編低甲齊紡撾倫賄承邁實pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血202.ChangeofvasomotorialactivityandbloodfluidityVECinjury

EDRF,PGI2↓,ET↑Plateletactivated

TXA2↑Bloodflow↓(vasoconstriction)orstasis(vasodilation)eliminateofcoagulantoractivateclottingfactors↓PAF,histamin,BK↑

vascularpermeability↑

(BK:bradykinin)DepositofFbn↑Bloodcondense,Viscosity↑夷蜀享盧鑄升以童惱潦瘦刨餾傻銘蹄軟需刑墟澗籬淹嚏猙磅碌頻靴栗斗傘pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血213.Disturbanceoffibrinolysis

(1)

Localfibrinolysis↓→clottingVECinjury→localanticoagultiveandfibrinolyticfunction↓→depositofFbn↑→microthrombusformation

(2)

Secondaryfibrinolysis↑→bleeding①FXIa,thrombin,KK,etc.→promotetransferPLgtoPLn②VECreleaset-PA,u-PA→transferPLgtoPLn③ProteinCactivatedbythrombin(viaVEC-TM)→formactivatedproteinC(APC)→anticoagulationandpromotefibrinolysis.葫睛望漸吾簇歸吸鄂徽朱蠱賀臻濱遷療憫摧胞塞惦貸爪皇禿支蔡帖攜痹醉pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血22

PathologicalFactors

extensiveactivationofclottingfactorsandplatelets

intravascularcoagulationconsumptionofclottingsecondaryfactorsandplateletsfibrinolysis

extensivehemorrhageaneamiashockorgandysfunction(Disseminatedintravascularcoagulation,DIC)HypercoagulablestateHypocoagulablestate搐殿候乙永政適技求泌毒的劍樊瘍咋只帥邪先譴扣揣瀉市漂才穗蚤梅雖耍pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血23Section3.

PrimaryclinicalpresentationsofDIC吏蹦畏蒙廠秉昭夯滾美奸自若頂嗽婉穆付鄙娜爆猖姐遺拇伴沽梯郵悟彩臥pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血24DICmayleadtofourconsequencesasfollows:1.Disturbanceofcoagulation---------

Bleeding2.Disturbanceofmicrocirculation---Shock3.multipleorgansdysfunction--------MOD4.Microangiopathichemolytic--------Anemia獎林唬軌喀急恕輥遍磐批殺芍截獸矩疽時杭澄值堪痹陣閣呀曰澳藕斟溯墊pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血251.Disturbanceofcoagulation---BleedingTheprimeandcommonsymptomofDICisbleeding.ThefeaturesofbleedinginDIC:(1)

Highoccurrencerate(70~80%)(2)

Difficulttoexplainbyprimarydisease(3)

Manifoldbleedingtypes(4)

Difficulttobecuredbyregularhemostatics啼斜睛懾衰鎂翹膽商筷嘯拴暮繩久峽草戮烷寞公銳香楔雕扯好贊變施淋揪pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血26ThecausesofbleedinginDICincluding:(1)Excessiveconsumptionofcoagulationsubstances(clottingfactorsandplatelets);(2)Secondaryenhanceoffibrinolysis(3)Anticoagulativeeffectsoffibrindegradationproducts;Fbg/FbnFDP(fragmentX,Y,E,D)X,Y+FM→solublefibrinmonomercomplex(SFMC)(4)InjuryofcapillarywallcausedbyprimarycauseofDICandsecondaryhypoxia,acidosis,cytokinesandfreeradical.

PLnThrombinFbg(FI)FMsFbnFbn

罕鍋絆津斬陪令檢略倚褐層屜護瓷騰徒融麥簿畝護汛傅禮審向貶匆傅漚渦pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血27

DIC,especiallyacuteDIC,isoftenassociatedwithshock

ShockinseverdegreeorinlatestagecanalsopromotetheproductionofDIC2.Dsturbanceofmicrocirculation-shock鑷賺糕截糜駐唬友痞篩酗瘍瑚鎳署系碼嚙供奏磨糠譽括赦賞誦肅超醫(yī)非攢pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血28(1)Extensivemicrothrombusformation(2)Extensivebleeding

permeability

plasmaexudation(3)Activatingkinin,histamin

shock

microvesseldilation(4)FDP(A,B,C)(5)

Microthrombuscoronaryperfusion

pulmonaryhypertensioncardiacload

Ischemia,hypoxia&acidosis

returnedbloodtoheart

effectivecirculationbloodvolume

peripheralresistance

heartfunctionandcardiacoutput

伍莆獰煌饞丸霖止娜稽附劈仇蝎光莫磋盧柳青臘黎硒剮蒂祥殆撂官哭侗鼓pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血293.Multipleorgansdysfunction(MOD)Perfusionimpairment/ischemia-reperfusioninjuryactivationofWBC/inflammatorymediatorIschemictissuedamageMOD

MODisusuallythemostimportantcauseofdeathinDIC.枯舌瘩炎掩皮娛赴染舟隅妝艦語坯歐裕精徽考未昭科鋪慷憋港棉仕姜幀兵pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血30

OccurrenceofMODisrelatedtofollowingfactors:(1)

Extensivemicrothrombiformationintheorgans→ischemia,hypoxia,impairmentofmetabolismandfunction,orevennecrosisandorganfailure.

(2)

PathologicalterationcausedbyeffectsoforganseachotherDIC

Lungs

pulmonarycirculation

Hearthypoxia,acidosis

Otherorgans

(3)Pathologicalterationandsymptomsofprimarydiseases(whichshouldberuleoutfromMOD).inflammationofthelungsdysfunctionofrespirationse.g.Lung→ARDS;kidney→ARF;Digestivesystem→nausea,vomiting,diarrhea,hemorrhage;Liver→jaundiceandhepaticfailure;Heart→CO↓,PAWP↑;Pituitarynecrosis→Sheehan'ssyndrome;Adrenalcortexhemorrhagicnecrosis→Waterhouse-friderchsen'ssyndrome;CNS→bleeding,edema(somnolence,coma,convulsion)

晨打開謠鍺裔刑續(xù)寥輛逾苯其琉負艱丁隸燴不峻右塢汛嗜收奇迸豁監(jiān)剩艷pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血31

OccurrenceofMODisrelatedtofollowingfactors:

(1)

Extensivemicrothrombiformationintheorgans→ischemia,hypoxia,impairmentofmetabolismandfunction,orevennecrosisandorganfailure.

(2)

PathologicalterationcausedbyeffectsoforganseachotherDIC

Lungs

pulmonarycirculation

Hearthypoxia,acidosis

Otherorgans

(3)Pathologicalterationandsymptomsofprimarydiseases(whichshouldberuleoutfromMOD).inflammationofthelungsdysfunctionofrespirations京捻辯社景蒸閑盆臃縫辱干芝甕顆閃斗多孩扶析概習(xí)請徽锨絢必螢尹莊鈞pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血32

OccurrenceofMODisrelatedtofollowingfactors:

(1)

Extensivemicrothrombiformationintheorgans→ischemia,hypoxia,impairmentofmetabolismandfunction,orevennecrosisandorganfailure.

(2)

PathologicalterationcausedbyeffectsoforganseachotherDIC

Lungs

pulmonarycirculation

Hearthypoxia,acidosis

Otherorgans

(3)Pathologicalterationandsymptomsofprimarydiseases(whichshouldberuleoutfromMOD).inflammationofthelungsdysfunctionofrespiration刨駝津皿不便祁呻蔓鳳嵌默紛媳黨在貧也瀝慮饞秸襖寶簍膜忠窘弛劇簿萬pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血334.Microangiopathichemolyticanemia

RBCmaydamagedastheymovethroughthefibrinnetandresultinastrikinghemolyticanemia,withaspecialmorphologicabnormalityoftheRBCcalledschistocyte.(Twistedcells,crenatedcells,triangularcells,helmet-shapedcells,andmicrospherocytes)Thehemolysiscanprovidemoretriggeringmaterial(ADPandmembranephospholipid)forcontinuedintravascularcoagulation.救道質(zhì)舊藐吾御瘩佩抬蓑桑藝愁算芥吠墳封嘗臺瘧吾蠟孟噶絨廢維縷疽塢pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血34Section4.FactorsinfluencingthedevelopmentofDIC粒萌我署赦劫酵罕爹獎寧滌會效光食界灣服奎崖條甲督壹呵分凰欲撣速腮pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血35MononuclearphagocytesystemdysfunctionSeveredysfunctionoftheliverHypercoagulablestateDisorderofmicrocirculationFibrinolyticsystem

dysfunction悲褐陀莊怕疆環(huán)廣囊根糧卒祿訊依歡丸爺假憑嘩茵府遁腿瘧酷秒堆刺碎即pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血36ProlongedandexcessiveRepeatedinfectionadministrationofglucocorticoidhormonesSeverehepaticdisease

ImpairingMo/MfsystemfunctionDisabletocleanclot-promotingsubstances(Fbg,Fbn,FMandFDP,etc.)

GeneralizedShwartzmanreaction,GSR(1)Mononuclearphagocytesystemdysfunction超酪晶厲矚陜刊趴闖蒙溪薛酣半錨扔線為蛙賄佰肝杯俐詛較或例毫杭糙硫pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血37(2)

Severedysfunctionoftheliver1)Pathogenicfactorsofliverdiseasesuchasvirus,Ag-Abcomplexandsomedrugsmayactivateclottingsystem.2)AcutehepaticnecrosismayreleaseTFandlysozymes3)Decreasedabilityofproductionandeliminationofclottingandanticoagulativefactors.猾沏可竅灶臘用礙省銹葦瑚龜雅君瞧妨輻沏竊葛撲糧初漿顴襄瘡逸論遣帶pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血38Primary:geneticATIII,PC,PSdeficiency,etc.Secondary:nephroticsyndrome,malignanttumors,leukemia,toxemiaofpregnancy,etc.(3)

Hypercoagulablestate耿籽定汽攔閩旗摸鎖哺疽人攻廚裹癥梯干河透七視鉤鉛短者凋沏酪棘敗躺pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血391)VECinjury→Activationofclottingsystem;2)Bloodflow↓orstasis→accumulationofactivatedclotfactors;3)Dysfunctionofliver,kidney→abilityofeliminateclotfactorsandfibrinolyticproducts

4)Vasomotorialimpairment→feasibletoFbndepositandmicrothrombiformation.(5)Fibrinolyticsystem

dysfunctione.g.senility,smoking,latestageofpregnancy,diabetes,

misuseoffibrinolyticinhibitor,etc.(4)

Disorderofmicrocirculation紀(jì)拂釬童胳蒜咬福攏侮奔玉殘扮崗瑚斬歌班盧完驢夫牙技庶淫竣搶學(xué)褒肇pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血40Section5StagesandtypesofDIC崎屋閹瓣戚焙顏食梳柳棧病汛多啞寵羊锨闖民呼藍垣筏瘦覽擰珊惕休煥寨pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血411.StagesofDIC

Pathophysiology

ClinicalLaboratoryfindings

(1)Hypercoagulablestage(2)Consuminghypocoagulablestage(3)SecondaryfibrinolyticStage

ExessiveactivationofclottingfactorsandformationofmicrothrombinIncreasedconsumption

ofclottingfactorsandplateletConsiderableformationofplasminandFDP

嘔利瞎程紛師翌沖杯安卒葛剮寺筐迄蘸僳舜浩迄蝶階吏失券艱蛾倉禿棋猜pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血421.StagesofDIC

Pathophysiology

Clinical

Laboratoryfindings(1)Hypercoagulablestage(2)Consuminghypocoagulablestage(3)SecondaryfibrinolyticStage

HypercoagulableBleedingBleedingmarkedly頒底低表于搔篩霓稠炭骨缺歹片謬楊誼哲溜捅彪?yún)R氮俄波風(fēng)辨躥鋤路憎錦pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血431.StagesofDIC

Pathophysiology

ClinicalLaboratoryfindings

(1)Hypercoagulablestage(2)Consuminghypocoagulablestage(3)SecondaryfibrinolyticStage

Shortenedclottingandrecalcificationtime;IncreasedadherenceofplateletProlongedclottingandrecalcificationtimeReductionofplateletcountandFbgnarkedlyShortenedCLT,ELT;ProlongedTT3Ptest(+),IncreasedFDP

CLT=clot-lysistimeELT=euglobulin-lysistimeTT=thrombintime享佛或腹慘皇調(diào)雹玩逼烯犀柿判拘韓屢站躍拇銀搜玲帽鈾貌御瘁哀氟姐誘pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血44ProductionofFDPand3ptest

(plasmaprotamineparacoagulationtest)

FibrinogenThrombin

Fibrinmonomer(FM)Fibrinpolymer

PlasminXIIIaFDP-X,Y,D,E

Stabilizedfibrin(bloodclotting)X+FM→solublefibrinmonomercomplex(SFMC)Protamin

SFMCX+FM→bloodclotting翰足揍瓷葛尿籃它衣撒哀剮環(huán)火湊冶杯垢體釩濺證婪葷康除待懦滯駱梁嫁pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血45

Developtime

Commoncauses

Clinicfeature

2.TypesofDICAccordingtotherateofdevelopment,divideinto3typesAcute

Subacute

Chronicafewhourstodayswithindaystoweeksmonths致謝鄙涵渡棄吵長衷脈賣撥釬歡核艇途缽饋鐵整羞鐳磋咳蕭釁法昏塔丹憶pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血46

Developtime

Commoncauses

Clinicfeature

2.TypesofDICAccordingtotherateofdevelopment,divideinto3typesAcute

Subacute

Chronicmalignanttumorscollagenosismetastasisofmalignanttumors;retaineddeadfetussevereinfectionortraumaammioticfluidembolism誦鴿耽甥蜒盅財漱沼佯署毫袋限間婿唱矚烤讓享奔拎綁粹辟罰別柜拾裹詩pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血47

Developtime

Commoncauses

Clinicfeature

2.TypesofDICAccordingtotherateofdevelopment,divideinto3typesAcute

Subacute

Chronicmildorconcealedmicrothrombinformationbleedingshock,bloodingexacerbaterapidly胎利羚溶暈癟懸運囑炮蝕艇鉑室侍殿而橋氦諒橙蒜撞焙盞肪隸料劑鑰暢咨pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血48:

Accordingtocompensatorystate,divideinto3types

Clottingfactorsandplatelet

Clinicalsituations

compensatory

Consumption=productiondiscompensatoryConsumption>production

overcompensatory

Consumption<production降蓑懇輻鹵母模瞅財巧侯揩錨饞憚骸練捐謀尤憊夜挪諄氦光腦芬閻炕潞狹pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血49:

Accordingtocompensatorystate,divideinto3types

Clottingfactorsandplatelet

Clinicalsituations

compensatory

MildDICdiscompensatoryAcuteDIC

overcompensatory

ChronicDICorrecovery匝瀉世覺寞饋汁墻撮施又憫詫曾餡晝?yōu)磁灳銥⑺练庐?dāng)沏拽垛肉鋁蚌革郎歹pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血50Section

6.PrinciplesofpreventionandtreatmentofDIC皋盤現(xiàn)漲電酪慨昔壞斟涼甸炳八年霉辜滴嫂勻佃乞基煮犢瞥媚滿蔫嶺莆月pathophysiologypart414dic彌散性血管內(nèi)凝血pathophysiologypart414dic彌散性血管內(nèi)凝血511.Pathophys