Infarction

• 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.
  • Embolism can result from thromboses in both arterial and venous systems.

• 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.

Appearance

• 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.

Pathogenesis

• 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.