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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Email: amr.aborahma@gmail.comEmail: amr.aborahma@gmail.com