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  • The term "infarction" is used to describe the formation of a segmental or localised area of ischemic necrosis in a tissue or organ following occlusion of the blood supply in the absence of an adequate collateral circulation.
  • In domestic animals, infarcts are most commonly the result of embolic arteriolar impaction.
  • Infarctions may differ in nature.
    • The may be:
      • Bland
      • Infected
        • Low virulence organisms.
      • Septic
        • Virulent organisms, often with toxins.
      • Neoplastic.
        • Neoplastic infarction is often the precursor to metastatic tumour growth.


  • Grossly, infacts appear as pale or red “wedges” .
    • Shape can often be more irregular.
  • Redness depends on:
    • The relative blood content.
      • I.e. whether haemorrhage or adjacent venous engorgementis involved.
    • Whether there is co-existing inflammation/ infection.


  • The kidney is taken as an example of pathogenesis of an infarct.
    • The events outlined below assume comeplete obstruction of a functional end-arteriole by a bland embolus.

  1. The first stage is occlusion of a functional end-arteriole, in this example at the cortico-medullary junction.
    • This results in wedge-shaped area of cortical ischemia within the first 12 hours.
  2. Following occlusion, there is stasis of blood, hypoxia, leakage from capillaries and venules, and dilatation of vascular anastomoses.
    • Blood becomes trapped in the affected area, leading to reddening of the wedge.
    • This is exacerbated by hypoxic degeneration of capillaries, plasma leakage and swelling.
    • Occurs 12-24 hours.
  3. The wedge undergoes coagulative necrosis.
    • There is RBC haemolysis.
    • Cells at the periphery swell and break down to due upset in osmotic pressure.
      • There is also capillary congestion, haemorrhage and neutrophil infiltration at the periphery.
    • The squeezing effect tends to make the wedge become paler.
    • Occurs 24-36 hours.
  4. There is an inflammatory and demolition phase.
    • There is increased infiltration of polymorphs and macrophages in the peripheral zone.
      • The peripheral zone becomes more congested.
    • 36-72 hours.
  5. A healing phase follows.
    • Initially, macrophages and chronic inflammatory cells are present.
    • Later, there is granulation/ fibrous tissue replacement.
    • This phase may last up to 7-10 days or longer, depending on the nature of the lesion.

Infarction in Specific Organs

  • Organs and tissues with good alternative blood supplies or less-dense parenchyma tend to accomodate congestion, haemolysis, oedema and inflammation better.
    • For example, lung, liver, spleen and intestine.
    • Infarcts tend to be red but are less wedge-shaped and softer than in the kidney.
    • Infarcts in these organs are less common because of good collateral blood supplies.
  • In the brain, infarction in cerebral arterioles leads to colliquative necrosis.
    • Microglia are activated.
      • Some microglia phagocytose spilled myelin and become foamy Gitter cells.