coagulation assessment

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ASSESSMENT OF COAGULATION FUNCTION : 

ASSESSMENT OF COAGULATION FUNCTION PREETI

What is normal hemostasis? : 

What is normal hemostasis? comprises cellular and biochemical processes that limit blood loss resulting from injury maintain intravascular blood fluidity and promote revascularization of thrombosed vessels after injury

Principle of Hemostasis : 

Principle of Hemostasis Circulatory hemostasis is achieved by: Hemorrhage (Bleeding) Thrombosis (Clotting) Process of arresting of bleeding which includes 4 components: 1. Vascular system 2. Platelets 3. Coagulation factors 4. Fibrinolysis Three of less important factors include: complement, kinins and serine protease inhibitors

Components of hemostasis : 

Components of hemostasis Interactive

The first event….. : 

The first event….. VASOSPASM neurogenic humoral ……but can’t rely on it fully.

SO… : 

SO… Platlets play an imp role with following actions… Adhesion – [vWF] Secretion-[TxA2,ADP] Aggregation Leads to primary hemostasis

IN NEED OF…. FIBRIN : 

IN NEED OF…. FIBRIN linking of platelets in the primary plug, by fibrin converts it into a definitive clot. requires the participation of the Coagulation Cascade. known as SECONDARY HEMOSTASIS Thrombin generation: the pivotal point Result: RED CLOT

CURRENT MODEL OF HEMOSTASIS : 

CURRENT MODEL OF HEMOSTASIS

SOLDIERS….. : 

SOLDIERS…..

Slide 12: 

Endothelial damage Exposure to tissue factor Initiation of extrinsic pathway Initiate thrombin generation Activate F XII (intrinsic pathway) Amplify thrombin generation

CLOT: THE END PRODUCT OF HEMOSTASIS : 

CLOT: THE END PRODUCT OF HEMOSTASIS

Slide 14: 

ASSESSMENT

TAKE A PERSONAL HISTORY …. : 

TAKE A PERSONAL HISTORY …. Family History haemophilias follow X linked recessive inheritance up to 30% of case of haemophilia A - spontaneous mutations with no family history. Von Willebrand's disease is difficult to diagnose because of the variability in inheritance H/O surgical, traumatic events or other triggering event major surgery, a tonsillectomy or dental extractions without unusual bleeding – best possible evaluation Frequency of abnormal bleeding Duration of abnormal bleeding bleeding abnormality manifests as moderate bleeding over a prolonged period - not as bleeding at an excessive rate.

PERSONAL HISTORY …. : 

PERSONAL HISTORY …. Location of abnormal bleeding Bleeding from skin & mucous membranes - platelet disorders Bleeding in joints and muscles – haemophilias Medical Disease Liver Disease Renal Disease Haematological malignancy - leukaemia, myeloproliferative disease Vitamin K deficiency Vitamin C deficiency Solid organ malignancy - Prostate, lung, colon Medication History - aspirin, coumarin, heparin

SURGERY CAUSES AN INCREASE IN.. : 

SURGERY CAUSES AN INCREASE IN.. TISSUE FACTOR PLASMINOGEN ACTIVATOR INHIBITOR vWF ..hyper coagulable hypofibrinolytic state

These factors arise concern about hemostasis: : 

These factors arise concern about hemostasis: Surgery Immobility Infection Cancers Hypothermia Acidosis Volume expanders Extracorporeal circulation

Slide 19: 

MONITORING HEMOSTASIS : LAB TESTS

MONITORING HEMOSTASISCascade vs. Cell-based model : 

MONITORING HEMOSTASISCascade vs. Cell-based model Cell-based model Whole blood tests measure interaction of platelets, coagulation factors, and other cellular or plasma factors Factors present during clot formation- required to examine hemostasis The TEG is one such test. Cascade model Common tests (PT, aPTT, platelet counts) do not reflect the roles of cells or local vascular and tissue conditions Plasma-based assays miss - impact of platelets and platelet activation on thrombin generation. Plasma-based assays use static endpoints (e.g. fibrin formation) - miss impact of altered thrombin generation on platelet function and clot structure.

BLEEDING TIME: (DUKEŚ METHOD) : 

BLEEDING TIME: (DUKEŚ METHOD) BT = No of blots/ 2 (in min) Normal bleeding time (B.T) = 3 – 6 min measures the time taken for blood vessel constriction and platelet plug formation to occur Every 30 sec.

BLEEDING TIME: (DUKEŚ METHOD) : 

BLEEDING TIME: (DUKEŚ METHOD) Not a reliable test Great variability in results, invasive, insensitive Results vary depending on the site and depth shortened in cold weather - capillary constriction reverse is the case in hot weather. Prolonged by : lack of platelets (Thrombocytopaenia ) plt disorders (Heparin, Aspirin ) severe anaemia vWD collagen vascular disease

CLOTTING TIME: (capillary tube method) : 

CLOTTING TIME: (capillary tube method) Clean the finger with spirit - give a deep prick with a sterile lancet. Note the time (T1). Fill in two plain capillary tubes with blood. 3. Normal Clotting time (C.T) = 5 – 8 min. 4. It is increased in haemophilia. 1 2 3 4 5 6 7 8 Every 30 seconds T2

PROTHROMBIN TIME: : 

PROTHROMBIN TIME: Evaluates production of thrombin and fibrin Intrinsic Pathway Extrinsic Pathway Common Pathway CLOT PT

PROTHROMBIN TIME: : 

PROTHROMBIN TIME: Performed : At 37 °C Specimen : should be 3.8% trisodium citrate anticoagulant in a 9:1 ratio with blood Add thromboplastin Add Ca Time to fibrin strand formation measured automatically by: Photo-optical device Electromechanical device

PROTHROMBIN TIME: : 

PROTHROMBIN TIME: Normal range: 11 - 15 sec Underfilling alters the anticoagulant:blood ration of 9:1 Polycythaemia alters the anticoagulant:blood ration of 9:1 errors in the optical end point analysis by: Haemolysis Lipaemia hyperbilirubinaemia hyperproteinaemia produce

PT Prolonged??? Think of…. : 

PT Prolonged??? Think of…. Factor Deficiency Factor VII (extrinsic pathway) Common Pathway (II, V, X) Warfarin Ingestion High dose heparin Liver Dysfunction Vitamin K Deficiency Disseminated Intravascular Coagulation Lupus Anticoagulant

PT & INR: : 

PT & INR: Thromboplastin test reagents vary in sensitivity limiting the ability to compare results b/w labs International Normalized Ratio (INR) - introduced as a means of normalizing PT results among different labs Expressed as the ISI- International sensitivity index INR = (Patient's PT/ control PT)ISI

INR: : 

INR: small,portable monitor disposable test strips, do not require refrigeration Small, drop 15 μL blood sample size FDA cleared for home use Easy to use interface Uses 4 AA batteries Stores 60 test results

Activated Partial Thromboplastin Time: aPTT : 

Activated Partial Thromboplastin Time: aPTT Intrinsic Pathway Extrinsic Pathway Common Pathway CLOT APTT

aPTT: : 

aPTT: Performed : At 37 ̊ C Plasma (3.8% trisodium citrate anticoagulant in a 9:1 ratio with blood) Add kaolin/elgaic acid Phospholipid source Calcium Time the appearance of clot Normal range : 22– 35 sec Evaluates intrinsic and common pathway

aPTT Prolonged??? Think of…. : 

aPTT Prolonged??? Think of…. Heparin, direct thrombin inhibitors Factor Deficiencies – HMWK and PK – Factors XII, XI, IX, VIII (intrinsic pathway) – Common Pathway (X, V, II, I) Lupus Anticoagulant Specific Inhibitors (e.g. Factor VIII or IX inhibitors) Possible warfarin, liver dysfunction, DIC

MIXING STUDY: : 

MIXING STUDY: performed when the PT or PTT is prolonged determines etiology : factor deficiency or an inhibitor. Simple factor deficiency: mixing the patient plasma 1:1 with plasma that contains 100% of the normal factor level PT /PTT comes normal (mixing study shows correction) Inhibitor antobody presence: (factor VIII / IX) inactivates the added clotting factor from normal plasma PT/aPTT remains prolonged (fails to correct) M. commom inhibitor - nonspecific inhibitor ex. lupus anticoagulant

MIXING STUDY: : 

MIXING STUDY:

THROMBIN TIME: : 

THROMBIN TIME: Measures conversion of Fibrinogen to fibrin Performed by adding thrombin to plasma Intrinsic Pathway Extrinsic Pathway Common Pathway CLOT TT

TT IN CLINICAL STATES: : 

TT IN CLINICAL STATES: Normal < 20 sec. Shortened TT may be found in Dysfibrinogenemia Prolonged TT may be found in DIC Liver disease Hypofibrinogenemia Heparin Fibrin degradation products Lupus anticoagulant

REPTILASE TIME : : 

REPTILASE TIME : Reptilase – an enzyme found in the venom of Bothrops snakes activity similar to thrombin Unlike thrombin, resistant to inhibition by antithrombin III is added to plasma Time taken to form a clot is recorded Normal is less than 14-19 seconds Prolonged due to inhibition of Reptilase Lupus anticoagulant abnormal fibrinogen , FDP often used to exclude heparin contamination in blood sample

FIBRINOGEN LEVELS: : 

FIBRINOGEN LEVELS: Detects deficiencies of fibrinogen or the ability to convert to fibrin. Normal 200-400 mg/dL May do titers to assist in evaluation Levels decreased in: DIC - consumption of clotting factors Liver disease - decreased synthesis Massive transfusion - dilutional coagulopathy Hypofibrinogenaemia, afibrinogenaemia and dysfibrinogenaemia

FIBRINOGEN LEVELS: : 

FIBRINOGEN LEVELS: Levels increased in: Increasing age Female sex, pregnancy, oral contraception In post-menopausal women Acute phase reaction Disseminated malignancy

Euglobulin Clot Lysis Time: : 

Euglobulin Clot Lysis Time: a clot-based test of the fibrinolytic system precipitation of certain clotting factors in a complex called the euglobulin fraction contains the important fibrinolytic factors fibrinogen, PAI-1, tpa, plasminogen, and to a lesser extent alpha 2 antiplasmin also contains factor viii result less than 2 hours - increase in fibrinolysis that could correlate with bleeding Reference range – 2-6 hrs Prolonged results indicate inadequate fibrinolysis.

Activated Clotting Time : 

Activated Clotting Time measures clot formation by intrinsic and common pathways heparin and other anticoagulants prolong time to clot formation Fresh whole blood added to a tube containing negatively charged particles Time noted for the formation of a clot. Intrinsic Pathway Extrinsic Pathway Common Pathway CLOT ACT

Activated clotting time : 

Activated clotting time Type of charged particle affects the "normal" length of ACT Celite = Diatomaceous Earth: normal 100-170 sec Kaolin: normal 90-150 sec Glass particles: normal 110-190 sec None: normal 190-300 sec Used in: Cardiopulmonary bypass Hemodialysis Vascular & general surgery Good perioperative coagulation monitor : simplicity, low cost, and linear operating response at high heparin concentrations

ACTIVATED CLOTTING TIME: (ACT) : 

ACTIVATED CLOTTING TIME: (ACT) Prolonged times may be due to Heparin effect Hypothermia Platelet dysfunction Haemodilution Cardioplegic solutions Hypofibrinogenaemia Factor deficiencies

Thromboelastography: TEG : 

Thromboelastography: TEG originally described by Hartert in 1948 measures the viscoelastic properties of blood as it is induced to clot under a low shear environment resembling sluggish venous flow unique aspect of viscoelastic monitors : ability to measure the entire spectrum of clot formation from early fibrin strand generation through clot retraction and eventual fibrinolysis

The TEG (r) System: : 

The TEG (r) System: celite activated whole blood (0.36 ml) a prewarmed cuvette. suspended piston lowered into the cuvette rotation of a 4.5° arc backwards and forwards. normal clot - fast through acceleration & strengthening phase fiber strands attach to the cuvette & suspended piston Clot transmits movement onto suspended piston A “weak” clot - stretches & delays the arc movement graphically expressed as a narrow thromboelastogram A strong clot - thick thromboelastogram.

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TEG tracing: : 

TEG tracing: R: time from initiation to initial fibrin formation. (6-8 min) k: time from beginning of clot formation till amplitude of TEG reaches 20 mm (10-12 min) represents the dynamics of clot formation. alpha angle: angle b/w tline in the middle of the TEG(r) tracing and the line tangential to the developing “body” of the TEG(r) tracing normal ( > 50° ) represents the kinetics of fibrin build up and cross-linking.

TEG tracing: : 

TEG tracing: MA - (Maximum amplitude ) reflects strength of a clot dependent on no & function of platelets and interaction with fibrin. (50- 70 mm) MA60: measures rate of amplitude reduction 60 min. after MA and represents the stability of the clot.

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Slide 52: 

A -no coagulation at all - Whole blood from a heparinised patient B -normal Curve - Whole blood after the addition of heparinase

1. Small alpha angle2. Small maximal amplitude with weak clot formation Thrombocytopaenia Thrombocytopathy Hypofibrinogaemia : 

1. Small alpha angle2. Small maximal amplitude with weak clot formation Thrombocytopaenia Thrombocytopathy Hypofibrinogaemia

Application of TEG analysis : 

Application of TEG analysis .

Platelet Function Monitors: : 

Platelet Function Monitors: PFA-100 (Platlet function analyser) incorporates high-shear conditions to simulate small vessel injury in the presence of either ADP or epinephrine, both potent platelet activators Gives a single end point reading (when blood flow through the capillary ceases) as a result of plt adhesion Normal between1-3minutes effective in detecting: von Willebrand's disease aspirin-mediated platelet dysfunction Limitations : interference by thrombocytopenia and hemodilution.

Platelet Function Monitors: : 

Platelet Function Monitors: HemoSTATUS platelet function test exploits the ability of platelet activating factor (PAF) to accelerate clot formation of the kaolin-activated ACT Platelet Aggregation Testing: Born Aggregometry an agonist is added the platelets aggregate and absorb less light and so the transmission increases and this is detected by the photocell Flow Cytometry Nucleotide Assays

Platelet aggregation tests: : 

Platelet aggregation tests: Platelet Aggregation addition of an agonist (thrombin, ADP, adrenaline, collagen, ristocetin or arachnidonic acid) normally exhibits a biphasic response reversible aggregation due to the agonist followed by irreversible aggregation due to the disintegration of the platelets. Heparin induced platelet aggregation diagnosis of heparin-associated thrombocytopaenia.

THANKYOU… : 

THANKYOU…

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