Infarction

Overview
  • An infarction refers to an anatomical region of ischemic necrosis due to localized disruption of circulation.
Etiologies
  • Overview
    • Nearly all cases of infarction are due to complete or near-complete occlusion of arterial blood flow due to embolism, most typically thromboembolism. Under rare circumstances arterial flow can also be completely disrupted anatomically due to twisting closed of the arterial supply as may occur during testicular torsion or bowel volvulus. Thrombotic or anatomic disruption of venous supply generally causes congestion rather than infarction as alternate routes of venous return usually exist.
  • Risk Factors
    • Various organs are more or less prone to infarction than others. Generally, organs that have a single arterial supply are more at risk than those that have dual supplies. If the thromboembolic event occurs following a long-term, progressive stenosis of the artery then infarction is generally less severe as large numbers of alternative circulatory routes will likely have developed as a response to the chronically reduced blood flow. Additionally, some cells such as neurons and cardiomyocytes are much more sensitive to ischemia than others such as fibroblasts. Tissues which receive their blood solely from portal vessels, such as the posterior pituitary are much more prone to infarction than others as the blood they receive has a much lower oxygen tension.
Morphology
  • Overview
    • The resultant morphology of infarction largely depends on the nature of the affected organ and the circumstances of the infarction. In nearly all tissues, Ischemic Necrosis results in a pattern of coagulative necrosis except for the CNS in which it manifests as a pattern of liquifactive necrosis.
  • Pale Infarcts
    • Pale infarcts represent a lack of erythrocytes entering the ischemically injured tissue. This results when the occluded artery is the sole supply of the organ and the organ is relatively solid.
  • Red Infarcts
    • Red infarcts represent the leakage of erythrocytes into the ischemically injured tissue following arterial occlusion. This occurs if the organ possess a dual blood supply, is relatively spongey like the lung, or if the occluded artery is recanalized.
  • Sequelae
    • Whatever the initial morphology of the infarct, pale or red, an intense acute inflammatory infiltrate will begin creeping in from the edges of the infarct days after the ischemic event. Over a period of weeks, macrophages will phagocytose and recycle the dead cellular debris. Eventually, wound healing processes will be initiated that replace the necrotic tissue with a fibrotic scar.