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Thrombosis, embolism and infarction

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Thrombosis, embolism and infarction

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Thrombosis, embolism and infarction

  1. 1. THROMBOSIS, EMBOLISM AND INFARCTION
  2. 2. Normal Haemostasis  Process of maintaining blood in a fluid, clot – free state in normal vasculature and rapidly forming a localized haemostatic plug at the site of vascular injury  The pathologic opposite of haemostasis is thrombosis
  3. 3. Thrombosis  Formation of solid mass in circulation from the constituents of flowing blood with intact cardiovascular tree during life
  4. 4. RUDOLF VIRCHOW Coined the terms “THROMBOSIS” and “EMBOLISM”
  5. 5. Virchow Triad
  6. 6. Endothelial Injury  Main cause for thrombus formation in the heart and the arterial circulation  These are platelet – rich clots  Inflammation  Infection  Toxins from cigarette smoking  Hypercholesterolemia
  7. 7. Laminar blood flow
  8. 8. Abnormal blood flow Turbulence Stasis • Arterial thrombosis • Atherosclerotic plaque • Venous thrombosis • Aortic aneurysm • Post MI – cardiac mural thrombi • Rheumatic mitral valve stenosis • Hyperviscosity – Polycythemia vera
  9. 9. Hypercoagulability  Thrombophilia  Any disorder of blood that predisposes to thrombosis  Hypercoagulable states are associated with VENOUS THROMBOSIS
  10. 10. Hypercoagulable states GENETIC  Factor V mutation  Increased levels of factor VIII, IX, XI or Fibrinogen ACQUIRED  Prolonged bed rest or immobilization  Disseminated Cancer  Prosthetic cardiac valves  Disseminated intravascular coagulation  Oral contraceptive use  Pregnancy and post partum
  11. 11. Arterial thrombi Venous thrombi Arteries and heart veins Aorta, coronary, cerebral etc Superficial varicose veins, deep leg veins Endothelial cell injury Causes-atherosclerosis, vasculitis, trauma Venous stasis Usually mural, not occluding lumen Invariably occlusive Grey- white, friable with lines of zahn Red-blue with fibrin strands with line of zahn Grows retrogrde Grows in the direction of blood flow Meshwork of platelets, fibrin, red cells and degenerating leucocytes More enmeshed RBC s and few platelets(red or stasis thrombi)
  12. 12. Antemortem thrombus Postmortem clot Adherent to wall Not adherent to vessel wall Red in colour Fibrin with red cells and leucocytes in a haphazard network (gelatinous) Upper layer resembling chicken fat Lines of zahn present No lines of zahn – bland and non – laminated
  13. 13. Lines of zahn
  14. 14. Mural thrombi
  15. 15. Vegetations – Thrombi on heart valves
  16. 16. Arterial thrombosis
  17. 17. Fate of thrombus  Propagation  Embolization – thrombi dislodges and travels to other sites in vasculature  Dissolution – by fibrinolysis  Organisation and recanalization Older thrombi become organised by ingrowth of endothelial cells, smooth muscle cells and fibroblasts. Capillary channels reestablish continuity of lumen
  18. 18. Embolism  An embolus is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from origin.
  19. 19. Classification  Thromboembolism (most common)  Fat embolism  Air embolism  Amniotic fluid embolism
  20. 20. Pulmonary embolism Embolus lodges in the lungs (most common from deep vein thrombosis) Systemic embolism Brain, lower extremities, intestines, kidneys, spleen(arterial emboli from intracardiac mural or valvular thrombi, aortic aneurysms,
  21. 21. Pulmonary thromboembolism  Cause from venous emboli from deep leg veins  Common in hospitalised and bed ridden patients  Large thrombus gets impacted at bifurcation of pulmonary artery-saddle embolus  Multiple emboli  Paradoxical embolism
  22. 22. PULMONARY ARTERY EMBOLUS
  23. 23. Fat embolism  Obstruction of arterioles and capillaries by fat globules  Fractures of long bones  Trauma to soft tissue eg., adipose tissue Clinical features  Pulmonary insufficiency - tachypnea, dyspnea, tachycardia  Neurologic symptoms - irritability, restlessness to delirium and coma  Thrombocytopenia
  24. 24. Fat embolism
  25. 25. Air embolism  Gas bubbles within the circulation can coalesce to form frothy masses and obstruct vascular flow  Large volume of air (more than 100 cc) is necessary to produce effect in pulmonary circulation  Small volume of air trapped in coronary artery during bypass surgery  Chest wall injury  Obstetric or laproscopy procedures
  26. 26. Decompression sickness • Bends - formation of gas bubbles in skeletal muscles and joints producing pain • In lungs - edema, hemorrhages, focal atelectasis Caissons disease (chronic decompression sickness) - gas emboli in heads of femur, tibia and humeri.
  27. 27. Amniotic fluid embolism  During labour or immediate post partum period  Dyspnea, cyanosis, hypotensive shock, seizure and coma  Infusion of amniotic fluid or fetal tissue into maternal circulation via tear in placental membranes or rupture of uterine veins
  28. 28. INFARCT Def: An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. Aetiology Thrombosis or embolism Venous outflow obstruction (single outflow organs) Others : Hypotensive,local vasospasm, compression of, vessel by hematoma or tumor, torsion
  29. 29. Infarction  Tissue necrosis due to ischaemia  vascular insufficiency of any cause  usually arterial occlusion due to thrombosis/embolism  Mainly due to oxygen deficiency, but toxin accumulation & reperfusion injury may contribute  Number of determining factors  Size of vessel and size of vascular territory  Partial / total vascular occlusion  Duration of ischaemia
  30. 30. Infarct Development  Dependent on a number of factors  Nature of vascular supply  Dual supply e.g. lungs, liver  End arteries e.g. kidneys, spleen  Rate of vascular occlusion  Time for development of collateral circulation  Vulnerability to hypoxia  Neurons – 2-3mins, Myocardium – 20-30mins, Fibroblasts – hours.  Oxygen content of blood  Anaemia, cyanosis, congestive heart failure  Can result in infarction due to otherwise inconsequential blockage  Size of vessel and size of vascular territory  Partial / total vascular occlusion  Duration of ischaemia
  31. 31. Morphological Classification of infarcts  Colour-Pale/anemic/white  Red (hemorrhagic) Infarct Septic or bland
  32. 32. 2nd Year Pathology 2010 Appearance of Infarct ARTERY OCCLUSION NORMAL TISSUE INFARCTED TISSUE SURFACE FIBRINOUS EXUDATE ILL-DEFINED INFARCT BORDERS
  33. 33. Types of Infarct  Red (haemorrhagic) infarcts 1. Venous occlusion/congestion e.g. torsion 2. Loose tissues where haemorrhage can occur and blood can collect in infarcted zone e.g. lung 3. Tissues with dual blood supply e.g. lung small intestine (permitting blood flow from unobstructed vessel into infarcted zone – note flow is insufficient to rescue ischaemia) 4. Tissues that were previously congested due to sluggish venous outflow 5. When flow is re-established e.g. fragmentation of an occlusive embolus, angioplasty  White infarcts 1. arterial occlusion 2. solid tissues, where haemorrhage limited e.g. spleen, heart, kidney
  34. 34. Pale / White Infarct Ischemia following obstruction of nutrient artery or hypoperfusion of tissue  Solid organs with end-arterial circulation such as kidney, heart, spleen  Wedge shaped.occluded vessel at the apex,base at the serosal surface  Better defined with time, paler, hyperemic margins
  35. 35. 2nd Year Pathology 2010 Types of Infarct White splenic infarct
  36. 36. Microscopy  Ischemic coagulative necrosis  Demonstrable only >12-18 hrs.  Inflammation in response to necrosis  Phagocytosis of cellular debris by neutrophils & macrophages 1-2 days  Healing response  Scar tissue (brain- liquefactive necrosis)
  37. 37. Red (hemorrhagic)infarcts Sites :venous occlusion of organ with single venous outflow e.g. testicular torsion Loose tissues- e.g. lung Tissues with dual circulations: lung and gut Previously congested tissue With reperfusion of previously infarcted tissue
  38. 38. 2nd Year Pathology 2010 Types of Infarct Red pulmonary infarcts - dual pulmonary / bronchial arterial supply
  39. 39. Pulmonary infarcts  Ischemic necrosis of lung parenchyma following pulmonary embolism & lack of blood from bronchial arteries.  When blood from bronchial arteries reperfuses the ischemic area, blood leaks into the alveolar spaces  Appears triangular, red & airless.  Becomes more firm &brown with time.
  40. 40. Septic infarct  Following fragmentation of a bacterial vegetation from a heart valve or following microbes seeding a necrotic area.  Converted into an abscess  Greater inflammatory response  scarring
  41. 41. Event Sequence 1. Coagulative necrosis 2. Infiltration by neutrophils 3. Infiltration by macrophages 4. Phagocytosis of debris 5. Granulation tissue formation 6. Scar formation
  42. 42. 2nd Year Pathology 2010 Time Microscopic Features Gross Features 0 – 4 hr None None 4 – 12 hr Early coagulation necrosis (nucleus: pyknosis, cytoplasm: eosinophilia) None 12 – 24 hr Further necrosis, haemorrhage, early neutrophil infiltrate Dark mottling 1 – 3 days Marked neutrophil infiltrate and necrosis Mottled with yellow-tan necrotic centre 3 – 7 days Early phagocytosis of dead cells by macrophages (at border) Hyperaemic border, central yellow-tan softening 7 – 10 days Well-developed phagocytosis, early granulation tissue formation Maximal yellow-tan softening, depressed red-tan margins 10 – 14 days Well-developed granulation tissue, early collagen deposition Red-gray depressed infarct borders 2 – 8 wk Increased collagen deposition, decreased cellularity Grey-white scar progresses from border toward centre > 2 months Acellular collagenous scar Dense gray scar

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