Thrombosis.pptx

thrombosis

1. Thrombosis

2. THROMBOSIS Thrombus – a blood clot. Thrombosis – a pathological process whereby there is formation of a blood clot in uninjured vasculature or after relatively minor injury .

3. Pathogenesis There are three main predisposing factors for thrombus formation ( Virchow’s triad ): * Damage to the endothelial lining of a blood vessel. * Relative stasis or turbulence of blood flow. * Increased coagulability of blood. These predisposing factors are associated with particular conditions or life styles

4. THROMBOSIS Virchow triad

5. 1- ENDOTHELIAL DAMAGE IN HEART AND ARTERIAL CIRCULATION Endocardial injury (example MI, Valvulitis ) Over ulcerated plaques in the atherosclerotic arteries Hemodynamic stress: like hypertension Turbulent flow over the scarred valves A t the sites of the traumatic or inflammatory vascular injury Hypercholesterolemia Radiation or products absorbed from the Cigar smoke.

6. 1- ENDOTHELIAL DAMAGE (Cont--) Chemical injury. Drugs. Immune reactions. Endotoxin.

7. 2-STASIS/TURBULENCE ( contd …): Turbulence contributes to arterial & cardiac thrombosis by causing endothelial injury. Stasis is major factor in development of venous thrombi. Both stasis & turbulence Disrupt laminar flow & bring platelets into contact with the endothelium. Prevents dilution of clotting factors inhibitors Slow down the inflow of clotting factor inhibitors Promotes endothelial cell activation.

8. 2-STASIS/TURBULENCE Post-operative immobility (inactive legs) and blood pooling; Post myocardial infarction (sluggish blood flow around body) Turbulence around atherosclerotic plaques or within aneurysms.

9. 3-INCREASED COAGULABILITY HYPERCOAGULABILITY: Alteration of coagulation pathways that predispose to thrombosis. Hypercoagulability can be Primary (genetic) Secondary (acquired).

10. 3-INCREASED COAGULABILITY ( contd …): Primary (genetic). Mutation in factor V ( proaccelerin ) gene (Leiden mutation) & Mutation in factor II gene ( prothrombin gene) . Factor V becomes resistant to protein c inactivation Prothrombin (II) levels elevated Mutation in methyltetrahydrofolate gene RARE CAUSE Less commonly inherited deficiencies of anti-thrombin-III, protein C or protein S. Congenitally elevated levels of homocysteine .

11. 3-INCREASED COAGULABILITY ( contd …): Secondary (acquired) HIGH RISK FACTORS Stasis or vascular injury may be most important Immobilization Cancer MI and atrial firillation Tissue damage(surgery, fracture, burns) LOWER RISK FACTORS Cardiomyopathy Nephrotic syndrome Oral contraceptive Hyper estrogenic state of pregnancy Advancing age leading to increased platelet aggregation. Smoking & obesity

12. Mural thrombi Mural thrombi : When arterial thrombi arises in heart chamber or in aortic lumen they usually adhere to the wall of underlying structure and are termed mural thrombi .

13. Morphology : Arterial or cardiac thrombi: At site of endothelial injury (e.g. atheroscelerotic plaque or turbulence) Grow in a retrograde direction (direction of flow- i.e., towards heart) from the point of attachment whereas venous thrombi extend in direction of blood flow(i.e., towards the heart) . Common sites: In descending order are coronary, cerebral & femoral arteries. Superimposed on atherosclerotic plaque. Firmly adherent to injured arterial wall, gray-white & friable. Composed of tangled platelets, fibrin, erythrocytes & degenerated leukocytes.

14. Morphology ( contd … ): Venus thrombi or Phlebothrombosis : Also called red or stasis thrombi. Characteristically occur in sites of stasis. Grow in the direction of blood flow Almost invariably occlusive. Prone to fragment; creating an embolus. Most commonly (90%) affects the veins of the lower extremities. Differentiation from postmortem clots: Firmer, have a point of attachment & on transaction reveal vague strands of pale gray fibrin .

15. Morphology ( contd … ): VALVULAR THROMBI: Thrombi on heart valves are called vegetations . Infective endocarditis - Bacterial or fungal blood born infections leads to valve damage & thrombus formation – results in bulky friable vegetations composed of necrotic debris, thrombus and organisms Non Bacterial thrombotic endocarditis (sterile vegetations on non infected valves) in patients with hypercoagulable states Non- infected,Verrucous - endocarditis - ( Libman -Sacks endocarditis ) due to elevated levels of circulating immune complexes

16. Thrombus - Morphology Arterial Almost always arise from heart Grow in retrograde fashion (direction of flow) Forms at site of Endothelial injury(AS), turbulence (aneurysms) Pale/ white Lines of Zahn Firmly adherent to vessel wall From emboli  Cause infarctions (lower extremities – 75%, Brain (10%), Kidney, spleen) Venous Deep veins ( popleteal  Femoral Iliac), Antigrade (towards heart- direction of flow) At site of stasis (lower extremities) Red / dark No lines of Zahn Loosely attached (easily embolize ) Emboli cause Pulmonary embolism ( silent in 50% of pts.)

17. Thrombus - Morphology Venous Loosely attached (easily embolize) Red/ dark Post mortem clot Not attached Dark red dependant portion & yellow chicken fat supernatant

18. Clinical correlations: Thrombi cause obstruction of arteries & veins. They are possible sources of emboli. Venus thrombosis: Mostly occurs in superficial & deep veins of legs. Superficial venous thrombi. Usually in saphenous system esp. in varicosities. Local congestion, swelling, pain & tenderness along the course of involved vein. Rarely embolize. Predispose the overlying skin to infections.

19. Clinical correlations ( contd … ): Venous thrombosis ( contd ): Deep venous thrombosis. In larger leg veins at or above the knee joint ( popliteal , femoral & iliac veins) They embolize & so are clinically serious. May cause local pain & edema. Collateral bypass channels. Asymptomatic in 50% of cases. Recognized only after they have embolized.

20. Clinical correlations ( contd … ): Cardiac & arterial thrombosis: Myocardium infarction Dyskinetic contraction of the myocardium & damage to the adjacent endothelium leading to mural thrombi. Rheumatic heart disease. Mitral valve stenosis . Left atrial dilatation. Atrial fibrillation

21. Clinical correlations ( contd … ): Atherosclerosis. It is a prime initiator of thrombosis related to loss of endothelial integrity & abnormal vascular flow. Complication of cardiac & aortic mural thrombi Peripheral embolization Common sites: Brain, kidneys & spleen

22. Fate of Thrombus: Propagation Embolization Dissolution Organization & reacanalization

23. Venous Thrombi – Clinical course

24. Thrombus: Propagation and Obstruction

25. Thrombus: Organization

26. Management Medical management Anticoagulant medicines like… Heparin given intravenously and Warfarin is given via mouth. Thrombolytic therapy. NSAID ibuprofen.

27. Physiotherapy. It is paramount that thrombosis collaborative care programmes include the physiotherapist to encourage specific ambulatory regimes. For each patient, an initial assessment begins with discussion and observation of the patient’s actual and achievable ambulation capacity:

28. Independent walking activity (achieved by patient). Active walking exercises (ten times hourly). Walking activities will significantly help to reduce deficits in venous blood flow by activating skeletal calf muscle pumps. It is also important to make optimum use of the respiratory system (respiratory pumps), to encourage specified breathing mechanisms and to initiate collaborative skeletal and respiratory pump exercises