5. thrombosis and embolism

superficial introduction to the topic for bachelor level

1. Thrombosis And Embolism Dr. Saugat Chapagain

2. Thrombosis

3. Thrombus  a solid mass consisting of blood constituents within the blood vessel; attached to the point of origin. Thrombosis  the process of… Clot  mass of coagulated blood Haematoma  extravascular accumulation of blood clot Haemostatic plugs  normal clots to control bleeding Thrombus and Thrombosis

4. Virchow’s Triad Endothelial injury Altered blood flow (stasis/ turbulence) Hypercoagulability of blood Pathophysiology

5. Coagulation cascade

6. Vascular injury exposes subendothelial thrombogenic connective tissues (collagen, elastin, fibronectin , laminin and glycosaminoglycans ) Initial vasoconstriction to reduce blood loss. Tissue factors initiate extrinsic pathway Collagen initiate intrinsic pathway. Endothelial injury

7. Ulcerated plaque in advanced atherosclerosis. Haemodynamic stress in HTN Arterial diseases Diabetes mellitus Endogenous chemical agents (hypercholesterolemia) Exogenous chemical agents (smoking) TAO Bacterial toxins Trauma IV cannulation Radiation injury Turbulent flow of blood in aneurysm Mural thrombus following cardiac abnormality Causes of endothelial injury

8. Turbulence: unequal flow (arterial); may aggravate vascular injury as well. Stasis: slowing (venous) Blood cells and platelets migrate to periphery and pavement the endothelium Normal flow has: Central fast moving red and white blood cells. Slow moving laminar stream of platelets. Peripheral slowest moving cell-free plasma. Alteration of blood flow

9. Effects: Prevent dilution by fresh flowing blood of activated clotting factors. Disrupt laminar blood flow and bring platelets in contact of endothelium Retard the inflow of clotting factor inhibitors and permit thrombosis Promote endothelial cell activation Examples: DVT of lower limbs Mural thrombus Thrombosis in aneurism

10. Favoured by: Smoking Ageing Use of OCPs Obesity Causes: Increased coagulation factors Increased platelet count and adhesiveness Decreased levels of coagulation inhibitors Hypercoagulability

11. Primary (genetic) Deficiency of anti thrombin Deficiency of protein C or S Defects in fibrinolysis Mutation of factor V Secondary (acquired) Risk factors: Advanced age Sedentary life style Immobilization Smoking Clinical conditions leading to thrombosis: Heart diseases (MI, CHF, RHD) V ascular diseases (atherosclerosis, aneurysms, varicosities) Hypercoagulibility (polycythemia, dehydration, nephrotic syndrome) Shock Late pregnancy and puerperium drugs Factors favoring thrombosis

12. Gross: Shape and size depends on origin Arterial  white and mural (firm and pale) Venous  red and occlusive(soft, red and gelatinous) Mixed/ laminated – alt white and red layers separated by line of ZAHN . Microscopic: Lines of Zahn seen where visible Collection of cells and fibrin Morphology

13. Based on colour and components: Pale – primarily platelets Red – primarily RBCs Mixed – visible lines of zahn Based on site and mode of formation: Occlusive Mural – occurs in heart chambers/ aorta/ major arteries Based on infection: Bland – non infected Septic – infected. Types

14. Resolution – plasmin may dissolve the thrombus completely Organization – eventually covered by endothelial cells after granulation tissue formation (or calcification/ ossification) Propagation – enlargement of size may block important vessels. Thromboembolism – detachment and released into blood stream Fate of thrombus

15. Embolism

16. The process of partial or complete obstruction of some part of the CVS by any mass carried in the circulation. Commonly thromboembolism (90%) What is it?

17. Depending on matter of embolus S olid- thrombus, atheroma, malignant cell, parasites, foreign bodies. Liquid- fat globules, amniotic fluid, bone marrow Gasseous - air, other gasses Depending on infection: Bland Septic Depending on source of emboli: Cardiac emboli from left side of the heart – vegetations of endocarditis, atrial appendages Arterial – in systemic arteries of brain, spleen, kidney and intestine. Venous – in pulmonary arteries Lymphatic emboli TYPE

18. A detached thrombus or a part of thrombus. Site of lodgement : Arterial (systemic) Venous Pulmonary THROMBOEMBOLISM

19. Most common and fatal form. Occlusion of the pulmonary arterial tree. Pulmonary thrombosis (rare) ETIOLOGY More common in bed ridden patients. Causes: Thrombi originating from large veins of lower legs (popliteal, femoral and iliac) Less common sources ( varicosities of superficial veins, pelvic veins) PULMONARY THROMBOEMBOLISM

20. Detachment of thrombus  thromboembolism  drains into right atrium. Large thrombus is impacted at the bifurcation of main pulmonary artery ( saddle embolus ) or on RV or its outflow tract. If large embolus fragments  small embolus impacts in a number of vessels (esp. on lower lobes of lungs) Paradoxical embolism – passage of embolus from rt. heart to lt. heart via ASD or VSD. Pathogenesis

21. Sudden death – d/t massive pulm . Embolism . Acute cor pulmonale – RHF d/t pulmonary HTN Pulm . Infarction – obstruction of small pulm . arteries . Pulm . Haemorrhage – central pulm . Haemorrhage d/t obstruction of flow in endarteries . Resolution – 60-80 % by fibrinolysis . Pulm . HTN, chronic cor-pulmonale and pulm . Atreriosclerosis . Consequences

22. Arterial embolism Esp. originating in LV (MI, cardiomyopathy, RHD, congenital heart disease, IE, prosthetic valves) Site of origin: Heart (80%) Aorta – thrombi over ulcerated atheroma in aortic aneurysm Paradoxical – rt.  lt. in ASD or VSD Idiopathic – 10-15% Systemic thromboembolism

23. Infarction – kidney, spleen, mesentery Stroke – brain (10%) Upper and lower extremeties - peripheral vascular diseases, gangrene, etc. Effects

24. Embolism of fat globules. Obstruction by fragments of adipose tissue  fat tissue embolism. Etiology Traumatic – Trauma to bones, trauma to soft tissue Non traumatic – Burns, DM, fatty liver, pancreatitis, decompression sickness. Fat embolism

25. Mechanical obstruction – micro aggregates of fat causes obstruction of vessels. Chemmical injury – FFA causes toxic injury. Thrombocytopenia – d/t coating of fat globules with platelets. Consequences Pulmonary fat embolism Systemic fat embolism (in case of ASD/ VSD) Pathogenesis

26. Air, nitrogen and other gases, Air embolism – entry of air due to trauma, injury or surgery. Decompression sickness/ caisson’s disease, diver’s palsy or aeroembolism seen in deep sea divers. Causes: During delivery or abortion Acquired/ accidental pneumothorax Haemodialysis Accidental opening of large veins Angiography Cardiothoracic surgery / trauma Gas Embolism

27. Most serious, unpredictable and unpreventable cause of maternal mortality. Amniotic fluid may contain – epithelial squames , vernix caseosa , lanugo hair, bile from meconium and mucus s/s Sudden respiratory distress and dyspnoea Deep cyanosis CV shock Convulsions Coma Unexpected death Amniotic fluid embolism

28. Mechanical blockage of pulmonary circulation in extensive embolism Anaphylactic reaction to components DIC d/t liberation of thromboplastin Haemorrhagic manifestations d/t thrombocytopenia and afibrinogenaemia . Cause of death

29. Thank you