Embolism.ppt
- 1. Embolism
- 2. Definition and Types Definition-An embolus is a detached intravascular/extravascular solid,liquid or gaseous mass that is carried by the blood to a site distant from its point of origin Varieties of emboli-intravascular-solid- fragments of thrombi (septic/aseptic), atherosclerotic debris
- 3. Types(contd.) Extravascular-Solid-Marrow fragments,decidual tissue,pancreatic tissue,tumor fragments,foreign bodies etc. Liquid-fat globules,amniotic fluid,oil Gaseous-bubbles of air,nitrogen In 99% cases,origin is dislodged thrombus
- 4. Types of Emboli Types 1)Depending on matter in the emboli 2)Depending on whether they are infected/not 3)Depending on source of emboli 4)Depending upon flow of blood,two special types of emboli 1.Paradoxical embolus 2.Retrograde embolus
- 6. Pulmonary Thromboembolism Occlusion affects large/medium sized pulmonary artery 95% pulmonary emboli arise in thrombi within large deep veins of lower limbs Pulmonary thrombosis occurs in pulmonary atherosclerosis & pulmonary hypertension Depending on size of embolus occlusion of main pulmonary artery (saddle embolus) / impact smaller arterioles-pulmonary haemorrhage/infarction
- 13. Thromboembolism
- 14. Consequences of Pulmonary Embolism Clinical significance-60-80%-clinically silent- resolution due to fibrinolysis If organized, incorporated into vascular wall With >60% obstruction-sudden death, acute cor pulmonale/cardiovascular collapse Over time,pulmonary hypertension with chronic cor pulmonale & pulmonary vascular sclerosis
- 15. Obstruction of medium sized arteries- pulmonary haemorrhage Obstruction of smaller vessels-infarction
- 16. Systemic Thromboembolism-Causes 1)Causes in the heart (80%-mural thrombus-LV infarcts, valvular disease, vegetations, cardiomyopathy) 2)Causes in the arteries(atheroma, aneurysm, fragmentation of valvular vegetation) 3)Causes in the veins-lower legs,pelvic veins,upper limb veins
- 18. Tumor Embolism
- 19. Systemic Thromboembolism- Effects Results of systemic emboli depend on- collateral vascular supply in affected tissue,tissues’ vulnerability to ischemia,caliber of vessel occluded Effects-Venous emboli-usually impact in lung,arterial emboli-infarction, gangrene, arteritis, sudden death
- 23. Major sites for arteriolar embolization are- Lower extremities,brain,intestines,kidneys,sple en,upper extremities,etc..
- 24. Fat Embolism Microscopic fat globules in circulation Fractures of long bones, trauma, extensive burns, diabetes, pancreatitis, sickle cell anemia, fatty liver Theories mechanical obstruction biochemical injury toxic injury emulsion instability theory
- 25. Fat Embolism…contd Effects-depend on size & quantity of fat globules Fat enters circulation by rupture of marrow sinusoids/venules Fat embolism syndrome Mechanical obstruction & biochemical injury Fatal in 10% cases
- 26. Fat Embolism Fat embolism with bone marrow elements in the blood vessel lumen. Hematopoietic cells and adipocytes are found (arrow).
- 28. Special stain for fat demonstration An oil red O stain for neutral fat (B) shows a globule of fat in a capillary. Several alveolar macrophages also stain, but the stain is slightly browner and in small granules. This granular pigment corresponds to the lipochrome pigment just described, which appears brown on H&E stain. Lipochrome pigment must be distinguished from the homogeneous red of fat embolism, as seen in the capillary wall.
- 29. Special stain for fat demonstration
- 30. Air Embolism Gas bubbles in circulation-vascular obstruction-distal ischaemia Causes obstetric procedures head and neck surgeries chest wall injury Maybe arterial or venous >100 ccs for clinical symptoms
- 31. Air Embolism Decompression sickness-scuba & deep sea divers Bends-painful gas bubbles in muscles & joints Chokes-Lungs Clinical significance- Focal ischaemia in brain and heart Ischaemic necrosis in heads of femurs, tibia humeri (Caisson’s disease)
- 32. Amniotic Fluid Embolism Complication of labor & immediate postpartum period-80% mortality rate Symptoms Sudden dyspnea Cyanosis hypotensive shock Pulmonary edema DIC Causes Infusion of amniotic fluid or fetal tissue into maternal circulation-tear in placental membranes or rupture of uterine veins
- 33. Amniotic Fluid Embolism Microscopy Pulmonary microcirculation shows epithelial squamous cells shed from fetal skin,lanugo hair,fat from vernix caseosa,mucin from fetal respiratory cells/GIT Marked pulmonary edema DAD Fibrin thrombi
- 35. INFARCTION
- 36. DEFINITION –it is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue
- 37. etiology-arterial /venous occlusion arterial –embolism ,thrombosis other mechanisms –local vasospasm expansion of the atheroma extrinsic compression of the vessel
- 38. entrapment in a hernia sac traumatic rupture of the blood supply twisting of the vessels eg testicular torsion or bowel volvulus compression of the blood vessel by oedema
- 39. CAUSES
- 42. INFARCTS CAUSED BY VENOUS OBSTRUCTION venous thrombosis in organs with single venous outflow channel such as testis and ovary
- 43. MORPHOLOGY classified on the basis of colour red –hemorrhagic white –anemic
- 44. classified on the basis of infection septic bland
- 45. RED INFARCTS • venous obstruction-ovarian tumour • loose tissues –lung • in tissues with dual supply –lung and small intestine • in tissues that were previously congested because of sluggish venous outflow • reperfusion
- 46. WHITE OR ANEMIC INFARCT arterial occlusion in the solid organ with end arterial circulation –heart, spleen ,kidney solidity of the tissue
- 49. MICROSCOPY ischaemic coagulative necrosis most infarcts are replaced by scar tissue ischaemic injury in brain leads to liquifactive necrosis
- 50. septic infarct embolisation of infected material
- 54. Bowel infarction
- 55. Bowel infarction
- 58. Brain infarction
- 60. Normal histology
- 63. spleen
- 64. kidney Image Description: The infarct is characterized by shadowy outlines of necrotic renal parenchyma surrounded by a zone of leukocytic infiltration and hemorrhage, appearing as a darker pink-to-orange ring around the pale necrotic area. The infarct is wedge-shaped, with the base at the capsular surface (mid upper field).
- 67. lung
- 68. Hemosiderin pigment (brown) in cells of some of the alveolar spaces, often in macrophages - signals breakdown of erythrocytes. Note absence of nuclei in cells of alveolar septa - they're dead
- 69. CLINICAL CORRELATIONS • factors that effect/ influence development of an infarct • 1.nature of vascular supply • 2.rate of development of occlusion • 3.vulnerability of a given tissue to hypoxia • 4. blood oxygen content