ISCHAEMIA  AND INFARCTION<br />By,<br />Dr. R.Waduge<br />Dept. of Pathology<br />
What is ischaemia ?<br />Is a state, when a tissue or organ has it’s arterial perfusion lowered relative to its metabolic ...
What is an infarct  ?<br />An ‘infarct’  is an area of ischaemic necrosis within a tissue or organ, produced by occlusion ...
The causes of altered tissue perfusion<br />A) Arterial obstruction –<br />	Thrombosis, embolism – 99%<br />	Spasm, athero...
These causes increase tissue pressure which eventually leads to arterial obstruction. <br />e.g :- 	Mesenteric vein thromb...
Twisted testis<br />
Phlebothrombosis<br />
Strangulated umbilical hernia<br />
C) Capillary occlusion –<br />		- Vasculitis<br />		- Frost bite<br />		- DIC<br />		- Fat embolism<br />Types of infarcts...
Pale infarcts -<br />In arterial occlusion and in solid organs – heart, spleen, kidney<br />As soon as the occlusion occur...
Acute renal infarction<br />
Splenic infarction<br />
But soon the necrotic cell swell and pushes the blood out.<br />Also the red cells that have leaked out will lyse and the ...
Red or haemorrhagic infarction -<br />Occurs with –<br />Venous occlusion<br />In loose tissue – Lung<br />In tissue with ...
Several infarcts of the liver <br />
infarction produced by a medium-sized thromboembolus to the lung<br />
Infarcts may be classified as bland and septic ( infected ).<br />According to whether they are sterile or contain organis...
Cerebral abscess - There is a liquefactive center with yellow pus surrounded by a thin wall<br />
Morphology and sequelae <br />The shape of the infarct depends on area supplied by the artery.<br />Usually infarcts of lu...
Acute renal infarction<br />
In the first 12 -24 hrs infarct is not easily visible.<br />Infarct becomes better defined in 24 hrs.<br />Firm – a zone o...
In the next few days – they become pale due to breakdown of Hb and tissue products.<br />After about a week the phase of d...
Brain – the process is somewhat different.<br />The necrotic tissue undergoes rapid colliquative necrosis.<br />The macrop...
Acute cerebral infarct<br />
Acute cerebral infarction reveals marked edema (the pale areas).<br />
The nature of the vascular supply.<br />The rate of development of the occlusion.<br />The vulnerability of the tissue to ...
Neurons are very sensitive.<br />Heart cells are hard.<br />Fibroblasts are hardy. <br />Cells of proximal convoluted tubu...
The general effects of infarction - <br />Constitutional effects –<br />Fever                                           Ac...
In myocardial infarction -<br />SGOT rises from a normal level of <br /> 	( 5 – 17 IU ) to > 200 IU.<br />Creatine phospho...
The LDH begins to rise by 12 hrs, reaches a maximum at 48 hrs, returns to normal by the 11th day.<br />There are five isoe...
The effects of ischemia on various organs -<br />Heart – thrombosis and embolism are the commonest causes of arterial occl...
Coagulative necrosis<br />Heals by a scar<br />Pericarditis<br />Mural thrombosis<br />Aneurysmal dilatation<br />Rupture ...
Transmural infarction<br />
Fibrinouspericarditis<br />
Rupture of myocardium 3 weeks after  MI<br />
Nervous tissue -<br />Has a high rate of metabolism and cannot tolerate hypoxia.<br />With complete ischaemia functional c...
cerebral infarct from an arterial embolus<br />
liquefactive necrosis in a cerebral infarction <br />
Lung -<br />Pulmonary infarction ( heart failure, mitral stenosis ) <br />Embolus arising in leg veins.<br />Conical in sh...
Haemorrhagic pulmonary infarction<br />
Haemorrhagic infarction<br />
Pyeamic abscess<br />
Intestine -<br />Cause of intestinal ischaemia is a mechanical obstruction<br />Thrombosis of superior mesenteric artery.<...
Dark red to grey infarcted bowel contrasts with the pale pink normal bowel at the bottom<br />
Extremities ( limbs ) -<br />Causes –	peripheral vascular disease<br />				thrombosis<br />				spasm<br />				Raynaud’s ph...
Ulceration followed by infarction occur.<br />The infarcted area become dry, shriveled and black.<br />The dead tissue is ...
Ischemia.&.infarction
Ischemia.&.infarction
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Ischemia.&.infarction

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Ischemia.&.infarction

  1. 1. ISCHAEMIA AND INFARCTION<br />By,<br />Dr. R.Waduge<br />Dept. of Pathology<br />
  2. 2. What is ischaemia ?<br />Is a state, when a tissue or organ has it’s arterial perfusion lowered relative to its metabolic needs.<br />Is simply defined as a condition of inadequate blood supply.<br />When ischemia is severe death of tissue results. ( necrosis of cells occur)<br />
  3. 3. What is an infarct ?<br />An ‘infarct’ is an area of ischaemic necrosis within a tissue or organ, produced by occlusion of either its arterial supply or its venous drainage.<br />“Infarctive “<br />
  4. 4. The causes of altered tissue perfusion<br />A) Arterial obstruction –<br /> Thrombosis, embolism – 99%<br /> Spasm, atheroma, occlusive pressure<br />B) Venous occlusion –<br /> Extensive venous obstruction leads to an engorgement of the area drained by the vein.<br />
  5. 5. These causes increase tissue pressure which eventually leads to arterial obstruction. <br />e.g :- Mesenteric vein thrombosis<br /> Strangulation of a hernia<br /> Torsion of the testis<br /> Cavernous sinus thrombosis<br /> Ileo femoral thrombosis<br />
  6. 6. Twisted testis<br />
  7. 7. Phlebothrombosis<br />
  8. 8. Strangulated umbilical hernia<br />
  9. 9. C) Capillary occlusion –<br /> - Vasculitis<br /> - Frost bite<br /> - DIC<br /> - Fat embolism<br />Types of infarcts –<br /> Many descriptive categories<br />Pale ( Anaemic ), Red ( Haemorrhagic )<br />Bland and septic<br />Arterial and venous<br />
  10. 10. Pale infarcts -<br />In arterial occlusion and in solid organs – heart, spleen, kidney<br />As soon as the occlusion occurs blood seeps in to the affected area.<br />Venous backflow also occurs. So it’s initially – Red in colour.<br />
  11. 11. Acute renal infarction<br />
  12. 12. Splenic infarction<br />
  13. 13. But soon the necrotic cell swell and pushes the blood out.<br />Also the red cells that have leaked out will lyse and the haemoglobin diffuses out.<br />Also osmosis pulls H2O in and further increases cell swelling.<br />
  14. 14. Red or haemorrhagic infarction -<br />Occurs with –<br />Venous occlusion<br />In loose tissue – Lung<br />In tissue with a double circulation – lung / liver or tissue rich in anastomosis – Intestine <br />In previously congested tissue – lung<br />Haemorrhage in to a pale infarct<br />
  15. 15. Several infarcts of the liver <br />
  16. 16. infarction produced by a medium-sized thromboembolus to the lung<br />
  17. 17. Infarcts may be classified as bland and septic ( infected ).<br />According to whether they are sterile or contain organisms.<br />In a septic infarction abscess results in.<br />
  18. 18. Cerebral abscess - There is a liquefactive center with yellow pus surrounded by a thin wall<br />
  19. 19. Morphology and sequelae <br />The shape of the infarct depends on area supplied by the artery.<br />Usually infarcts of lung, liver, kidney and spleen occur due to blocking of end arteries, the shape is like a “wedge”.<br />The apex of the blood vessel and the base toward the surface of the organ.<br />
  20. 20. Acute renal infarction<br />
  21. 21. In the first 12 -24 hrs infarct is not easily visible.<br />Infarct becomes better defined in 24 hrs.<br />Firm – a zone of inflammation is seen.<br />The serosal surface is also inflammed – fibrinous. <br />
  22. 22. In the next few days – they become pale due to breakdown of Hb and tissue products.<br />After about a week the phase of demolition followed by fibrosis occur.<br />Then the infarct become “white”.<br />Calcification may occur.<br />Secondary infection abscess.<br />
  23. 23. Brain – the process is somewhat different.<br />The necrotic tissue undergoes rapid colliquative necrosis.<br />The macrophages engulf the debris and becomes a cyst surrounded by gliosis.<br />In the intestine – gangrene occur.<br />
  24. 24. Acute cerebral infarct<br />
  25. 25. Acute cerebral infarction reveals marked edema (the pale areas).<br />
  26. 26. The nature of the vascular supply.<br />The rate of development of the occlusion.<br />The vulnerability of the tissue to hypoxia.<br />Factors that condition the development of an infract -<br />
  27. 27. Neurons are very sensitive.<br />Heart cells are hard.<br />Fibroblasts are hardy. <br />Cells of proximal convoluted tubule are very susceptible.<br />
  28. 28. The general effects of infarction - <br />Constitutional effects –<br />Fever Acute <br />Neutrophil leucocytosis phase <br />Raised ESR response<br />In addition –<br />The necrotic tissue may release it’s enzymes in to the circulation. <br />
  29. 29. In myocardial infarction -<br />SGOT rises from a normal level of <br /> ( 5 – 17 IU ) to > 200 IU.<br />Creatine phosphokinase ( CPK ) <br />Lactate dehydrogenase ( LDH )<br />CPK rises early and returns to normal within 3 days. ( specific )<br />
  30. 30. The LDH begins to rise by 12 hrs, reaches a maximum at 48 hrs, returns to normal by the 11th day.<br />There are five isoenzyme bands of LDH in electrophoresis.<br />A fast moving LDH, is specific for heart.<br />LDH 5 – slow moving. Helpful in liver necrosis.<br />2 hrs cardiac Troponin T<br />
  31. 31.
  32. 32. The effects of ischemia on various organs -<br />Heart – thrombosis and embolism are the commonest causes of arterial occlusion.<br />Gradual occlusion <br />Angina<br />Regional infarction<br />Subendocardial infarction <br />
  33. 33. Coagulative necrosis<br />Heals by a scar<br />Pericarditis<br />Mural thrombosis<br />Aneurysmal dilatation<br />Rupture ( myomalacia cardis )<br />Arrythmias <br />
  34. 34. Transmural infarction<br />
  35. 35. Fibrinouspericarditis<br />
  36. 36. Rupture of myocardium 3 weeks after MI<br />
  37. 37.
  38. 38. Nervous tissue -<br />Has a high rate of metabolism and cannot tolerate hypoxia.<br />With complete ischaemia functional changes occur within seconds and cell death within a few minutes.<br />Causes – thrombosis of vessels and embolism from heart<br />Colliquative necrosis<br />Fits <br />
  39. 39. cerebral infarct from an arterial embolus<br />
  40. 40. liquefactive necrosis in a cerebral infarction <br />
  41. 41. Lung -<br />Pulmonary infarction ( heart failure, mitral stenosis ) <br />Embolus arising in leg veins.<br />Conical in shape. Red in colour. ( Chronic venous congestion )<br />Heamorrhagic pleural effusion is common.<br />Can get pyaemic abscesses and empyema. <br />
  42. 42. Haemorrhagic pulmonary infarction<br />
  43. 43. Haemorrhagic infarction<br />
  44. 44. Pyeamic abscess<br />
  45. 45. Intestine -<br />Cause of intestinal ischaemia is a mechanical obstruction<br />Thrombosis of superior mesenteric artery.<br />
  46. 46. Dark red to grey infarcted bowel contrasts with the pale pink normal bowel at the bottom<br />
  47. 47. Extremities ( limbs ) -<br />Causes – peripheral vascular disease<br /> thrombosis<br /> spasm<br /> Raynaud’s phenomenon<br /> DM<br />If the collateral are defective intermittent claudication occur.<br />
  48. 48. Ulceration followed by infarction occur.<br />The infarcted area become dry, shriveled and black.<br />The dead tissue is colonized by bacteria and putrefaction occur – ( wet gangrene )<br />

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