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Disseminated Disseminated Intravascular Intravascular Coagulation Coagulation Presented by Ri Presented by Ri 蕭蕭蕭 蕭蕭蕭 Jan. 29, 2007 Jan. 29, 2007

Disseminated Intravascular Coagulation Presented by Ri 蕭雅澤 Jan. 29, 2007

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  • Disseminated Intravascular CoagulationPresented by Ri Jan. 29, 2007

  • What is DICAn acquired syndrome characterized by systemic intravascular coagulationSecondary to an underlying serious illnessAlternative names: Generalized intravascular coagulationDefibrination syndromeConsumption coagulopathyComplications: thrombosis and bleeding, but bleeding is far more common

  • Coagulation systemUsually local due to anti-cloting systemDIC: systemic thrombin activationDIC much comes from the extrinic pathway

  • Anti-cloting systemAntithrombin III (AT-III) is most important since it could inactivate thrombin, XIIa, XIa, Xa, IXa and KallekreinThe action of AT-III is enhanced by heparin

  • Cause of DIC (1)Systemic inflammatory response, leading to activation of cytokine

    Release or exposure of procoagulant material into the bloodstream

    Sepsis (any microorgansim)Trauma (polytrauma, neurotrama, fat embolism)

    Cancer (Both solid tumor and hema)Obst. problemsVascular abnormality

  • Cause of DIC (2)Less common causesevere hepatic failureSnake bitesTransfusion reactionsTransplant rejectionDeficiency of protein C and protein S Although the coagulation system is activated in pre-eclampsia and HELLP syndrome, DIC only occurs in a small percentage of these Pt

  • Complications of DICAcute DICPLT, clotting factors , frbrinogen Bleeding into organs Microvascular thrombosis Digital ischemic, gangrene Renal cortical necrosis, adrenal infarctionEtiology: infection, trauma, obst. Problems, Subacute DICVenous thromboembolism (SVT, DVT, PE) Abnormal bleeding is uncommon Etiology: cancer Trousseaus syndrome

  • Diagnosis of DICS/S: (spontaneous) bleeding, ozzing at venipuncture site, digital ischemic, gangreneLabDecrease: PLT, PT, AT-III*, fibrinogen* (H=4 days)Increase: FDPs, D-dimer* (most sensitive)PB smear: fragmented RBC if microangiopathic hemolytic anemia present (about 25% of Pt)Scoring systemISTH scoring system (Taylor et al, 2000)ISTH: International Society on Thrombosis and Haemostasis

  • Differential DiagnosisLiver disease: fibrinogen(-), PLT(-,)Vit. K deficiency: fibrinogen(-), PLT(-)Sepsis: fibrinogen(-)Thrombotic thrombocytopenic purpura: fibrinogen(-), PT/PTT(-)HELLP syndrome: fibrinogen(-)

  • TreatmentTreat underlying disease!!!No specific therapy is acquired if only lab abnormality with mild clinical S/SReplacement therapy alone If etiology is rapidly reversible (obstetric cases)

  • Treatment (1)CryoprecipitateFactor 8+13, vWF, fibrinogen, fibronectinAim: Plasma fibrinogen > 150 mg/dL1U may increase fibrinogen 6-8 mg/dLFFPCoagulation factor and fibrinogen1U may increase cloting factors 4% and fibrinogen 6-8 mg/dLSFP: FFP without fibrinogenpRBC, platelet conc.

  • Treatment (2)Heparin therapyIndication: (1) Acral cyanosis (2) Serious clinical sequence and the cause is not rapidly reversibleIn other situation is controversialAntithrombin III dependent, so must check before administrationLow dose: 500-750 units per hourGoal: Fibrinogen and FDP, not PTT

  • Treatment (3)Gabexate mesilate (Foy)Serine protease inhibitorDidnt need antithrombin IIIDosage: 1-2 mg/kg/hr Clinical effect similar to heparinDrotrecogin alfa (Xigris)Recombinant human activated protein CBeneficial for DIC with sepsisEACA (with heparin)Indication: excess fibrinolysisAntithrombin IIIDidnt reduce the mortality rate

  • Xigris ICU 12-48SIRS (T/P/R, WBC)4824 < APACHE II score < 53HeparinPLT
  • Thanks for your attention!!!

    Ri teaching: 2004-12-01, 2005-01-19 Morning Meeting at Dermatology Department2004-7-20 plate 0012004-7-22 plate 0802004-7-29 plate 178