02a surgical hemostasis
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Hemostasis in the Surgical Hemostasis in the Surgical PatientPatient
Amr AborahmaAmr Aborahma , MD , MD
Lecturer of Vascular SurgeryLecturer of Vascular Surgery
WHAT ARE YOUR EXPECTATIONS ?WHAT ARE YOUR EXPECTATIONS ?
Hemostasis in the Surgical Patient Hemostasis in the Surgical Patient Is It An Important Topic ?Is It An Important Topic ?
From your point of view !!From your point of view !!
Does All bleeding (eventually) stops ?
ClottingBleeding
Hemostasis
Under normal conditions, blood circulates Under normal conditions, blood circulates through the intact vasculature without through the intact vasculature without thrombus formation or haemorrhagethrombus formation or haemorrhage
HemostasisHemostasis
State of fluid equilibrium within the blood vessels
Vessels
Platelets
Fibrinolysis/ Inhibitors
Coagulation Proteins
HemostasisHemostasis A process which causes bleeding to stop A process which causes bleeding to stop
Primary HemostasisPrimary Hemostasis
Arteriolar vasoconstrictionArteriolar vasoconstriction
Formation of platelet plugFormation of platelet plug
Secondary HemostasisSecondary Hemostasis
Activation of coagulation cascadeActivation of coagulation cascade
Formation of permanent plugFormation of permanent plug
Constriction of vesselsConstriction of vessels
There are 2 mechanisms for vessel There are 2 mechanisms for vessel constriction:constriction:– Local smooth muscle contractile responseLocal smooth muscle contractile response
– Thromboxane AThromboxane A22 release from endothelium release from endothelium
Formation of platelet plugFormation of platelet plug
Exposure of the subendothelial layers cause platelets Exposure of the subendothelial layers cause platelets to adhere.to adhere.
They release ADP and TxAThey release ADP and TxA22, inducing further platelet , inducing further platelet
aggregation and activationaggregation and activation
Adhesion requires Adhesion requires von Willebrand factorvon Willebrand factor (vWf) from (vWf) from the subendothelial layers.the subendothelial layers.
The time taken for platelet plug to form The time taken for platelet plug to form (Bleeding Time - BT) gives a non-specific (Bleeding Time - BT) gives a non-specific indication of:indication of:
• The state of the vascular endothelium The state of the vascular endothelium • The number of platelets in the circulation The number of platelets in the circulation • The platelets are functioning correctly (can The platelets are functioning correctly (can
release granules and produce pseudopodia) release granules and produce pseudopodia) • Demonstrates the presence of vWF Demonstrates the presence of vWF
Coagulation FactorsCoagulation FactorsFactor IFactor I FibrinogenFibrinogenFactor IIFactor II ProthrombinProthrombinFactor IIIFactor III Tissue ThromboplastinTissue ThromboplastinFactor IVFactor IV Calcium IonsCalcium IonsFactor VFactor V Labile Factor, ProaccelerinLabile Factor, ProaccelerinFactor VIIFactor VII Stable Factor, ProconvertinStable Factor, ProconvertinFactor VIIIFactor VIII Antihemophilic FactorAntihemophilic FactorFactor IXFactor IX Christmas FactorChristmas FactorFactor XFactor X Stuart-Prower FactorStuart-Prower FactorFactor XIFactor XI Plasma Thromboplastin AntecedentPlasma Thromboplastin AntecedentFactor XIIFactor XII Hageman FactorHageman FactorFactor XIIIFactor XIII Fibrin Stabilizing FactorFibrin Stabilizing Factor
All coagulation factors are made in the All coagulation factors are made in the liver, except for vWFliver, except for vWF
Clotting cascadeClotting cascadeIntrinsic Pathway Intrinsic Pathway – All factors occur from All factors occur from withinwithin the circulation the circulation– in vivoin vivo, the pathway is triggered by exposure of "contact factors" , the pathway is triggered by exposure of "contact factors"
to collagen or basement membrane at the site of injury or a to collagen or basement membrane at the site of injury or a foreign substance such as a prosthetic deviceforeign substance such as a prosthetic device
Extrinsic Pathway Extrinsic Pathway – Requires tissue thromboplastin to be released from damaged Requires tissue thromboplastin to be released from damaged
cells (outside the circulation)cells (outside the circulation)
Both pathways lead to the activation of prothrombin Both pathways lead to the activation of prothrombin (factor II)(factor II) Final common pathway converts fibrinogen to fibrinFinal common pathway converts fibrinogen to fibrin
Clotting cascadeClotting cascade
Natural inhibitors of the coagulation cascadeNatural inhibitors of the coagulation cascade
ThrombomodulinThrombomodulin
Antithrombin IIIAntithrombin III
Tissue factor pathway inhibitorTissue factor pathway inhibitor
Protein CProtein C
Protein SProtein S
Which is moving?Which is moving?
Natural inhibitors of the coagulation cascadeNatural inhibitors of the coagulation cascade
Antithrombin III is a large protease inhibitor that inhibits Antithrombin III is a large protease inhibitor that inhibits thrombin and factors IXa, Xa, XIa, and XIIa but does not thrombin and factors IXa, Xa, XIa, and XIIa but does not inhibit thrombin within clotsinhibit thrombin within clots
Heparin accelerates the reaction time of Heparin accelerates the reaction time of
antithrombin III 1000 foldantithrombin III 1000 fold
Natural inhibitors of the coagulation cascadeNatural inhibitors of the coagulation cascade
Protein C and Protein SProtein C and Protein S Vitamin K-dependent serine proteases synthesized Vitamin K-dependent serine proteases synthesized in the liver in the liver Circulate as inactive forms (zymogens)Circulate as inactive forms (zymogens) Protein C Protein C
inhibits the activity of factors Va and inhibits the activity of factors Va and VIIIaVIIIa Protein S Protein S
cofactor that potentiates the action of cofactor that potentiates the action of Protein CProtein C
Take A Break !!!Take A Break !!!Watch this video Watch this video
Defects of HemostasisDefects of Hemostasis
Congenital disordersCongenital disorders Hemophilia A,BHemophilia A,B von Willebrand diseasevon Willebrand disease
Acquired disordersAcquired disorders Hepatic disordersHepatic disorders DICDIC Vitamin K defeciencyVitamin K defeciency Anticoagulants Anticoagulants Massive blood transfusionMassive blood transfusion Platelet disordersPlatelet disorders
Eckman et al. Ann Intern Med Vol 138, Eckman et al. Ann Intern Med Vol 138, No 5No 5
Preoperative screening for bleeding riskPreoperative screening for bleeding risk
Complete history and physicalComplete history and physical
Preoperative screening for bleeding riskPreoperative screening for bleeding risk
Incidence of a significant hereditary deficiency of a Incidence of a significant hereditary deficiency of a coagulation factor is low (1 per 10,000-40,000)coagulation factor is low (1 per 10,000-40,000)
approximately 1/3 of these are asymptomaticapproximately 1/3 of these are asymptomatic
Acquired deficiencies of factors should be suspected in the Acquired deficiencies of factors should be suspected in the presence of advance hepatic disease, malabsorption, or presence of advance hepatic disease, malabsorption, or malnutritionmalnutrition
Hemostasis Screening TestsHemostasis Screening Tests
• Bleeding Time• Clotting Time1. Platelet Count2.2. PTPT3.3. APTTAPTT4.4. TTTT5.5. Euglobulin Clot Lysis TimeEuglobulin Clot Lysis Time6.6. D = DimerD = Dimer
-Vascular -Platelet-Coagulation factors-Fibrinolysis
Clinical testing and preoperative screeningClinical testing and preoperative screening
Prothrombin time (PT)Prothrombin time (PT)
measure extrinsic and common pathwaysmeasure extrinsic and common pathways
affected by low concentrations of fibrinogen, prothrombin affected by low concentrations of fibrinogen, prothrombin and factors II, V, VII, Xand factors II, V, VII, X
Activated partial thomboplastin time (aPTT)Activated partial thomboplastin time (aPTT)
measures intrinsic and common pathwaysmeasures intrinsic and common pathways
deficiencies in all clotting factors except factors VII and deficiencies in all clotting factors except factors VII and XIII may prolong the aPTTXIII may prolong the aPTT
Surgical hemostasisSurgical hemostasis
Stopping the bleedingStopping the bleeding
Direct pressure.Direct pressure.
More direct pressure. Pack. Pack. Pack.More direct pressure. Pack. Pack. Pack.
Electrocautery.Electrocautery.
Ligate vesselLigate vessel
MethylcelluloseMethylcellulose
GelfoamGelfoam– AbsorbableAbsorbable– Liquefies in 2-5 Liquefies in 2-5
daysdays– Serves as a Serves as a
scaffold for scaffold for coagulationcoagulation
Oxidized regenerated celluloseOxidized regenerated cellulose
SurgicelSurgicel– Binds platelets and chemically precipitates Binds platelets and chemically precipitates
fibrinfibrin
Microfibrillar collagenMicrofibrillar collagen
Decellularized bovine sourceDecellularized bovine source
Stimulates latelet adhesionStimulates latelet adhesion
Stops venous oozeStops venous ooze
Absorbed in 90 daysAbsorbed in 90 days
Thrombin + Gelfoam + CaClThrombin + Gelfoam + CaCl
Thrombin for cleavage/activationThrombin for cleavage/activation
Gelfoam as matrixGelfoam as matrix
Very useful in vascular surgeryVery useful in vascular surgery
Fibrin glueFibrin glue
TiseelTiseel
FDA approved in 1998FDA approved in 1998
Concentrated fibrinogen and f VIIIConcentrated fibrinogen and f VIII
Thrombin and calciumThrombin and calcium
Aprotinin to prevent clot dissolutionAprotinin to prevent clot dissolution
Takes time to prepareTakes time to prepare
Good for diffuse oozing, needle punctures, Good for diffuse oozing, needle punctures, parenchymal injuriesparenchymal injuries
Questions
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