Why liquefactive necrosis in Brain ?

1. The person who asks a foolish question is a fool for 5 minutes, the one who doesn't ask a question remains a fool forever....

2. Why liquefactive necrosis in Brain ? • Because brain cells are rich in lipids and digestive hydrolytic enzymes, the brain cells are digested by their own hydrolases • The brain tissue becomes soft, liquefies, and is walled off from the healthy tissue to form cysts

3. Liquefactive necrosis can also result from bacterial infections. • Here, the hydrolases are released from the lysosomes of phagocytic neutrophils that are attracted to the infected area to kill the bacteria;

4. EMBOLISM

7. Definition Detached, intravascular, solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin

9. Usually dislodged THROMBUS (platelets + fibrin + RBC’s + degenerating WBC’s)

10. Droplets of fat • Bubbles of air / nitrogen • Cholesterol (atherosclerotic debris) • Tumour fragments • Bits of bone marrow • Foreign bodies

13. An embolism is usually thrombotic unless otherwise specifiedThromboembolism

14. Ischaemic necrosis of distal tissue ( INFARCTION )

15. TYPES • Pulmonary embolism • 2. Systemic embolism • Amniotic fluid embolism • Air embolism • Fat embolism

16. PULMONARY THROMBOEMBOLISM • Majority – clinically silent (60-80%), undergo organization • If > 60% of pulmonary circulation is obstructed => SUDDEN DEATH, RHF

18. PULMONARY EMBOLISM • More than 95% - the venous emboli arise from the deep leg vein thrombi above the level of the knee • Main pulmonary trunk • Saddle emboli • Smaller branches • Small multiple emboli

19. PULMONARY THROMBOEMBOLISM • If medium sized vessels : usually haemorrhage, no infarction • If small end arteriole : infarction • Multiple emboli : PHT with RHF

27. Causes • cardiac diseases • cancer • prolonged immobilization • Hypercoagulable states

28. Clinical significance depends on • Extent of emboli • Number of emboli • Circulatory state

29. FATE OF EMBOLI • may resolve by fibrinolysis • unresolved • pulmonary H T • pulmonary vascular sclerosis • chronic cor pulmonale • 30 % chance of developing second emboli

30. Prophylaxis: • Elevation • Elastic bandage • Early ambulation • Embolectomy • UMBRELLA filter in inferior vena cava • Thrombolysis followed by anti coagulation with monitoring

32. SYSTEMIC EMBOLISM Embolism in arterial circulation. • SOURCE : 80 – 85 % from heart • 60 -65 % from left ventricle ( intracardiac mural thrombi) • 5 – 10 % rheumatic heart disease • 5% cardiomyopathy

33. SYSTEMIC EMBOLISM • OTHER LESS COMMON SOURCES • Atherosclerotic plaques • Aortic aneurysms • Infective endocarditis • Valvular heart diseases • Paradoxical emboli from venous thrombi • UNKNOWN SOURCES 10 – 15 %

35. PARADOXICAL EMBOLISM

36. Always cause infarction • SITES : • Lower extremities 70 -75 % (gangrene) • Brain 10 % • Viscera 10 % • Upper limb 7 – 8 %

37. Factors • collateral vascular supply • tissue’s vulnerability to ischaemia • caliber of occluded vessel

38. Clinical manifestations : site and size of emboli is important femoral artery - gangrene cerebral artery (MCA) - death in hrs/ days • Treatment : anticoagulants embolectomy

39. AMNIOTIC FLUID EMBOLISM • Rare complication of labor • Major cause of maternal mortality • 86% mortality

40. AMNIOTIC FLUID EMBOLISM • Cause : Tear in placental membrane or rupture of uterine / cervical veins leading to infusion of amniotic fluid or fetal tissue into the maternal circulation

41. CLINICAL FEATURES: • Deep cyanosis • C.V.S shock • Generalized convulsions • Coma • Excessive bleeding from birth canal • DIC (due to release of thromboplastic substances)

42. AMNIOTIC FLUID EMBOLISM • The pulmonary microcirculation may contain: -squamous epithelium of fetal skin -fat from vernix caseosa -mucin from fetal respiratory and GIT -bile from meconium stained amniotic fluid

43. AMNIOTIC FLUID EMBOLISM • Investigations : • X-ray evidence in 24 – 36 hours • Pul. perfusion lung scan alb-labeled with Tec99 • Investigation of choice : pulmonary angiography

44. AIR OR GAS EMBOLISM • Bubbles of air or gas obstructing circulation • During obstetric procedures • Chest wall injury • >100 cc to produce clinical effect • Tissue damage

45. 2 types • Acute • Chronic - decompression disease Acute • “Bends” - obstruction of small vessels around joints and skeletal muscles cause patients to double up with pain • “Chokes” - respiratory and brain involvement sudden death

47. Caisson disease or decompression sickness- at risk : scuba divers, workers in offshore drilling platforms, underwater tunneling system workers

49. When air embolism is suspected at autopsy organs should be opened under water to detect escaping gas.

50. FAT EMBOLISM • Fat Emboli were first noted by F.A. Zenker in 1861 in a railroad worker with a thoraco-lumbar crush injury • The Fat Embolism Syndrome (FES) was first described by Von Bergman in 1873 in a diagnosis confirmed by post mortem examination. This patient had a fractured femur