The Clotting Cascade in addition to DIC Coagulation Coagulation Coagulation Fibrinolytic System

The Clotting Cascade in addition to DIC Coagulation Coagulation Coagulation Fibrinolytic System

The Clotting Cascade in addition to DIC Coagulation Coagulation Coagulation Fibrinolytic System

Lee, Richard, Host has reference to this Academic Journal, PHwiki organized this Journal The Clotting Cascade in addition to DICKarim Rafaat, MDCoagulationCoagulation is a host defense system that maintains the integrity of the high pressure closed circulatory systemTo prevent excessive blood loss after injury the hemostatic systemEndothelial cellsPlateletsPlasma coagulation proteinsCoagulationImmediately after injury, primary hemostasis occursVascular constrictionPlatelet activation

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CoagulationSecondary hemostasis Stabilizes an otherwise unstable platelet plug by adding fibrin to the clot

Intrinsic PathwayVascular Surface ChangesKallikrein +HMWKHMWKCa+VIIITVIIIaVIIIa/IXaExtrinsic PathwayTissue FactorVIIa/TFCa+VTVaXa/VaCa+Ca+Common Pathway

Fibrinolytic SystemDissolves the occlusive fibrin clot Restores vessel patencyAllows normal healing of vesselPlasminogenPlasminXFibrin Split Products+ D-DimerTPA/UroAnticoagulantsSeveral natural anticoagulants existPrevents “over” coagulation Deficiencies result in prothrombotic states

ThrombomodulinProtein CProtein SActivated Protein CXXAntithrombin IIIXXTissue FactorPathway InhibitorXLaboratory Evaluation of CoagulationaPTTPt plasma incubated with surface-active powder (silica) Measures intrinsic pathway in addition to common pathwayLaboratory Evaluation of CoagulationEvaluate abnormal PTT with 1:1 mixing study

Laboratory Evaluation of CoagulationPTPt plasma incubated with source of tissue factorExtrinsic Pathway in addition to Common PathwayLaboratory Evaluation of CoagulationBoth PT/PTT elevated, typically common pathway deficiency or disease state like liver dsx/DICDisseminated Intravascular CoagulationConsumption coagulopathy, Defibrination syndromeSystemic activation of coagulationIntravascular deposition of fibrin Microvascular occlusion/thrombosis in addition to organ ischemiaThromboembolic diseaseConsumption of coagulation factors in addition to plateletsBleeding if exhausted

Disseminated Intravascular CoagulationPathophysiologyTissue factor activitation in addition to coagulationImpaired fibrinolysisDefective anticoagulation pathwaysPathophysiology of DICTissue Factor ActivationExtrinsic pathway exclusive as etiology of fibrin deposition in DICActivated by multiple pathologic statesInfection/sepsisTrauma/head traumaMalignancyVascular abnormalitiesObstetric complications

Impaired FibrinolysisBacteremia results in rapid increase in fibrinolytic activity due to endothelial cell release of plasminogen activatorsRapid decline in fibrinolytic activity due to sustained increase of plasminogen activator inhibitor, type 1PlasminogenPlasminXFibrin degredationproducts/D-DimerTPA/UrokinasePAI-1ThrombomodulinProtein CProtein SActivated Protein CXXAntithrombin IIIXXTissue FactorPathway InhibitorXDefective Anticoagulation PathwaysDefective Anticoagulation Pathways

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Clinical ManifestationsNo clinical manifestations with just abnormal labs to suggest diagnosisBleeding- 70-90%Thromboembolic- 10-40%DiagnosisInternational Society on Thrombosis in addition to Hemostasis, subcommittee on DICTreatmentTreat the underlying disease process!!!!Replace platelets, FFP, cryoprecipitate, Vitamin K

TreatmentHeparinSubacute/chronic DIC as in malignancy as more likely to have thromboembolic phenomenonAcute DIC less commonly; consider if intensive replacement therapy doesn’t alleviate bleeding/correct coags80u/kg bolus then 18u/kg/hrTreatmentRecombinant tissue pathway factor inhibitorInhibits VIIa/TF binding to factor XOPTIMIST trial 96 hr continuous infusion of rTPFI vs placebo Efficacy end point 28 day mortality Additional analysis of organ dysfunction, biomarkers of inflammation in addition to coagulationTreatmentRecombinant tissue pathway factor inhibitorOPTIMIST trial rTPFI mortality 34.2%, placebo mortality 33.9% Trend toward mortality benefit in pts with documented bloodstream infections or documented PNA

TreatmentAntithrombin IIIInhibits multiple clotting factors; most potently thrombinFirst transfused in pts with DIC in 1978 by SchipperMultiple animal studies with improved lab parameters, shortened duration of DIC, improved organ fxn, AND improved mortalityTreatmentAntithrombin IIIFourrier et al, 199335 pts septic shock, DIC44% relative risk reduction in sepsis mortalityInthorn et al, 199745 pts septic shock, DIC; co-adm with heparin gtt14% relative risk reduction in mortalitySchuster et al, 199842 pts septic shock, DIC39% relative risk reduction in mortalityTreatmentAntithrombin IIILarge phase III multinational sepsis study2314 patients worldwideNo improvement in 28 day mortality compared to placeboStudy population not as sick as they had hoped to enrollFailure to achieve target blood level of ATIIISIGNIFICANT bleeding risk if co-administer of even low dose heparin

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