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What is infarction?

Infarction is the process of formation of an infarct as a result of tissue ischemia. The infarct is a localized area of ischemic necrosis caused by the occlusion of the vascular supply to the affected tissue. Mostly infarct is a coagulative type of necrosis due to sudden occlusion of arterial blood supply. If the patient lives (survives), the infarct size heals with a scar.

Types of infarcts

  • Based on color
    • Red (hemorrhagic) infarct
    • White (anemic) infarct
  • Based on age
    • Recent or fresh infarct
    • Old or healed infarct
  • Based on the presence or absence of the infection
    • Bland-when it is free of infection.
    • Septic-when it is infected.

Pathogenesis of the infarction

  • Ischemia is irreversible injury and cell death.
  • Necrosis leads to the formation of an infarct.
  • Inflammatory response at the periphery
    • Repair
    • Damaged tissue replaced by scar
  • Dystrophic calcification may occur in dead tissue.

Morphology infarction


  • Wedge-shaped infarct
    • An occluded vessel at the apex and organ periphery/surface forming the wide base.
    • Margins of
      • Acute- irregular (poorly defined) and slightly hemorrhagic
      • Later- well defined with a rim of hyperemia due to inflammation.
  • Red infarcts (hemorrhagic)
    • Seen in different conditions:
      1. Venous occlusion e.g. ovarian torsion
      2. Loose tissues e.g. lungs
      3. Tissues with dual blood supply e.g. lungs
      4. Congested tissues
      5. Reperfusion of tissue
    • Late phase- red blood cells are phagocytosed by macrophages, formation of hemosiderin pigments- firm brown color to tissue.
    • Appear as a sharply circumscribed area of necrosis and firm in consistency and dark red to purple in color.
  • White infarcts (pale or anemic)
    • Seen in solid organs with end arterial circulations of the body (e.g. heart, kidney).
    • Wedge-shaped with the occluded vessel at the apex and periphery forming the base.


  • Ischemic coagulative type of necrosis is most common but liquefactive necrosis in the brain.
  • Within 1-2 days: acute inflammatory cells along the margins.
  • Infiltration of macrophages – removal of necrotic debris.
  • In tissues composed of labile or stable cells, parenchymal regeneration at the periphery of the infarct if stromal architecture is preserved.
  • Granulation tissue formation but may replace the infarcted area which matures to form a scar.
  • Mostly infarct is replaced by scar.
  • Septic infarction: abscess formation.

Factors determining the effects of ischemia and the development of infarct

  • Anatomy of the vascular supply
    • End arterial circulation- e.g. kidney ( increased the risk of infarction)
    • Dual or parallel blood supply- e.g. liver, lungs- decrease chances of infarction
  • Rate of occlusion- slow occlusion- time for collaterals development and less chance of infarction
  • Tissue vulnerability to ischemia
    • E.g. neurons are highly sensitive to hypoxia and undergo necrosis ad damaged within 3 to 4 minutes of ischemia.
    • Myocardial cells are quite sensitive to hypoxia but less sensitive than neurons and cells damaged after 20 to 30 minutes.
  • Cardiovascular status of an individual – hypoxemia, chronic heart failure increased the risk of infarction.
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