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Lecture for 3rd year medical students on Thrombosis

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  1. 1. Thrombosis
  2. 2. Normal haemostasis  Well regulated process  Maintain blood in a fluid, clot free state in normal vessels  Induce rapid and localized haemostatic plug at the site of vascular injury
  3. 3. Thrombosis  Formation of a solid mass  from the constituents of blood  within the vasculature (blood vessels / chambers of heart)  During life
  4. 4.  The pathologic opposite of haemostasis is thrombosis  An inappropriate activation of normal haemostatic process in uninjured vasculature or thrombotic occlusion of a blood vessel after relatively minor injury
  5. 5. Mechanism of thrombosis  Platelets adhere to endothelium forming a projecting mass  Liberation of thromboplastins from platelet aggregate leads to initiate coagulation cascade  Blood clot formation occurs
  6. 6. Pathogenesis  Three primary influences predispose to thrombus formation.  These are described as Virchow’s triad
  7. 7. Virchow’s triad There are three main factors leading to thrombosis  Damage to the endothelial cell layer of blood vessel  Changes to the flow of blood  Alteration to the constituents of blood
  8. 8. Endothelial factors  Normal vascular tree is lined by endothelial cells  Endothelium prevents elements of blood coming into contact with the subendothelial connective tissue which is highly thrombogenic.  Endothelial cell surface is resistant to thrombus formation normally  Endothelial cells can initiate both thrombogenic and antithrombogenic stimuli
  9. 9. Thrombotic and antithrombotic mechanisms  Thrombotic Thromboplastin Factor V PAF vWF  Anti-thrombotic Thrombomodulin Anti thrombin III Alpha 2 macroglobulin tPA Normally these two groups are finely balanced to prevent thrombus formation. Damage to endothelium however will favour thrombosis. Most significant in arterial thrombosis
  10. 10. Damage to the endothelium  This is of most importance in arterial thrombosis.  The endothelial cell damage could be in the form of  Endothelial cells loss  Hydrodynamic stresses causing metabolic damage eg. Prolonged Hypertension, Turbulance  Toxins and immune mediated mechanisms and radiation
  11. 11.  Endothelial cells loss  Atheromatous plaques: ulceration  Damage by surgery  Arteritis  Indwelling vascular catheters  Infusion of sclerosing chemicals  Hydrodynamic forces  Prolong hypertension  Turbulance  Toxins and immune mediated damage  Bacterial toxins  Cigarette smoke  Immune mediatd: transplant rejection, immune complex disease  Radiation
  12. 12. Regardless of the cause of endothelial damage, the end results include  Exposure of subendothelial collagen  Adherence of platelets  Exposure to tissue factor  Local depletion of prostacyclin and plasminogen activator
  13. 13. Arterial thrombosis  Seen in coronary arteries, circle of Willis, small arteries of limbs and digits.  Common in aorta due to atherom a or arteriosclerosis  Due to high pressure and rapid flow , these are often platelet variety, exception is laminated thrombus in aneurisms
  14. 14. Coronary thrombosis
  15. 15. Occlusive coronary atherosclerosis
  16. 16. Cardiac thrombosis  Thrombi of pale variety occur on the heart valves in rheumatic endocarditis  Thrombi can be seen on the surface of the infarctions  In SABE, ABE the thrombi are larger, mixed, friable and contain bacteria  In atrial fibrillation thrombi can be seen in the auricular appendage
  17. 17. Rheumatic vegetations
  18. 18. Venous thrombosis  Common due to slower flow, lower pressure with easy compressibility and eddy formation around valves  Usually start in the deep veins of the calf, frequently a propagating thrombus extending in to femoral and iliac veins  Common in patients who are immobilized
  19. 19. Sites of venous thrombosis  Leg veins:immobiliity, post surgery, hypercoagulability  Pelvic veins: pueperal sepsis,post partum, pelvic surgery,  IVC: Tumour, extension from leg  Renal vein: Tumour compression  Portal/hepatic vein: Local sepsis, tumour  Cavernous sinus: Facial sepsis  SVC:Mediastinal tumour  Axillary vein: Rucksac, surgery
  20. 20. Deep Vein thrombosis
  21. 21. Deep vein thrombosis
  22. 22. Preventing deep vein thrombosis  Patients are encouraged to move their legs regularly when confined to bed  Leg muscles are stimulated to contract during long operations using electrodes  Anticoagulants like heparin is used in patients with a risk.
  23. 23. Venous thrombosis  Abdominal operations,child birth, cardiac disease, varicose veins, inflammation may potentiate the condition.  These are attached to vein wall only in few places  Hence chances of detachment and embolism are common  Can lead to pulmonary embolism
  24. 24. Capillary thrombosis  Form when capillaries are damaged usually in acute inflammatory processes  Capillaries can be occluded by fibrin thrombi in cases of disseminated intravascular coagulation
  25. 25. Varieties of thrombosis  White: mainly platelets, mainly seen in arteries where circulation is rapid. Often non occlusive  Red: Start as small platelet aggregate, and then produces fibrin strands entrangling the blood cells  Mixed and laminated: alternate layers of red and white thrombi. Common in aneurisms.
  26. 26. Effects of thrombosis  Arterial:  Infarction  Ischaemia  No effects if there are adequate anastomoses  Venous:  Anastomoses developed frequently to by pass the obstruction
  27. 27. Collateral circulation in venous thrombosis
  28. 28. Arterial venous Risk factors Atheroma Immobility Pathogenesis Turbulant flow Damaged endothelium Stasis Hypercoagulabilit y Symptoms Sudden onset Slow onset Complications Infarction Arterial embolism Pulmonary embolism
  29. 29. Arterial & Venous thrombi  In propagation the tail builds up retrograde to the flow  Embolization is manly due to detachment of entire or almost the entire thrombus  The tail extends in the direction of flow (towards heart)  The loosely attached tail can fragment creating an embolus
  30. 30. Sequels of thrombosis  Propagation  Resolution  Organisation  Recanalisation  Incorporation  Embolism
  31. 31. Propagation of thrombus  If the rate of flow is slow as in a vein red cells are entrangled in the coagulum  In front and behind the platelet mass blood stagnates. Further formation of fibrin occurs and thrombus extends to the nearest junction  At the junction more platelets get deposited on the end of the mass. This gives the head of the thrombus a pale colour
  32. 32. Resolution  The thrombus is completely removed leading to complete recanalisation.  Occurs commonly in the small veins of the lower limb as the venous intima contains more plasminogen activator than arterial intima.  By giving streptokinase we can enhance the process of thrombolysis.  But it should be given early after thombosis as the effect is going to be less on polymerised fibrin
  33. 33. Organization  When the thrombus has formed PMNL and macrophages begin to degrade and digest fibrin  Later granulation tissue grows into the base of the thrombus and is converted into a mass of small blood vessels separated by connective tissue.  This can lead to complete block or partial block  In partial block, ultimately the thrombus shrinks and is covered by endothelial cells
  34. 34. Recanalisation  Involves production of new endothelium lined channels that convey blood through the occlusive thrombus.  Clefts are produced by shrinkage and digestion of thrombus and are lined by endothelium
  35. 35. Differences of antemortum thrombi and postmortum clots  Antemortum thrombi  Firm  Dry granular appearance  Has lines of Zahn  Has a point of attachment to wall  Post mortum clots  Cast of the vein  Rubbery gelatinous  Red current jelly/chicken fat  Not attached to vein wall
  36. 36. Antemortum / Post mortum clots Antemortum Post mortum clot clot
  37. 37. Clinical problems 1  A 65 year old female patient was admitted to accident and emergency ward with fracture of neck of R femur. Internal fixation was planned in three days time. Two days after the fracture patient complained of pain & swelling in the L calf & ankle.  What is the likely condition?  How do you proceed with the diagnosis?
  38. 38. Clinical problem 2  A 55 year old female patient who underwent debulking surgery for carcinoma of cervix. On 5 th day of operation she developed sudden chest pain with difficulty in breathing.  ECG showed classical pulmonary embolism changes  What is the likely condition?  What measures would have taken to prevent this incident.
  39. 39. Clinical problem 3  A 58 year old female patient complained of swelling & redness in the left foot. On questioning she gives history of travelling from USA 4 days back. On examination she was afebrile.  What is the likely condition?  What investigations are needed for diagnosis?  How do you prevent this?  What is the management of this patient?
  40. 40.  A 23 yr old man met with a road traffic accident and was admitted to accident service. He was found to have fractures of R femur, tibia, left femur and left radius. 24 hrs after admission he developed dyspnoea, tachycardia and restlessness. In few hours time patient progresses to a coma. He was found to have a petechial rash.  What is the likely condition?  How would you confirm the diagnosis?  Explain the pathogenesis of the signs and symptoms.