• An infarct = an area of ischemic necrosis caused by blockage of the blood supply to a tissue.
• Infarction commonly affects the heart and brain and is a major cause of illness and death.
• Other important sites include:
  • lungs
  • bowel
  • distal extremities → ischemic necrosis may produce gangrene, especially in diabetes
• The vast majority of infarctions result from:
  • arterial thrombosis, or
  • arterial embolism.
• Less common causes of arterial obstruction include:
  • vasospasm
  • hemorrhage into an atherosclerotic plaque → plaque expands and narrows the vessel
  • external compression of a vessel by:
    • tumor
    • dissecting aortic aneurysm
    • severe edema within a confined space, such as anterior tibial compartment syndrome
• Other uncommon causes include:
  • twisting of vessels → testicular torsion or bowel volvulus
  • traumatic rupture of a vessel
  • vascular entrapment within a hernia sac
• Venous thrombosis usually causes congestion rather than infarction.
• This is because collateral/bypass venous channels often open → restore venous outflow → allow arterial inflow to continue.
• Therefore, venous thrombosis usually causes infarction only when an organ has essentially a single venous outflow, such as:
  • testis
  • ovary

KEY CONCEPT

• Infarction = vascular occlusion → ischemia → tissue necrosis.
• Most infarcts are caused by arterial thrombosis or embolism.
• Arterial obstruction → infarction is common.
• Venous obstruction → usually congestion, because collateral drainage can develop.
• Venous infarction is more likely in organs with one main efferent vein.

CONCEPTUAL EXAMPLES

• Coronary artery thrombus → loss of blood supply to myocardium → myocardial infarction.
• Cerebral arterial embolus → brain ischemia → cerebral infarction.
• Testicular torsion → vessels twist → blood supply fails → testicular infarction.
• Venous thrombosis in most tissues → alternate veins drain blood → mainly congestion rather than infarction.

MORPHOLOGY

• Infarcts are classified by:
  • color → reflects the amount of hemorrhage
  • presence or absence of microbial infection
• Therefore, infarcts may be:
  • Red (hemorrhagic) or white (anemic)
  • Septic or bland
• Red infarcts occur in four main settings (Fig. 3.17A):
  • Venous occlusion
    • Example: testicular torsion
    • Blood enters but cannot drain properly → hemorrhagic infarction.
  • Tissues with dual circulation
    • Examples: lung and small intestine
    • Collateral arterial blood still enters the damaged area, but perfusion remains inadequate → red infarct.
  • Previously congested tissues
    • Slow venous outflow → blood accumulates → infarct becomes hemorrhagic.
  • Reperfusion after infarction
    • Blood flow returns after ischemic injury.
    • Example: after angioplasty opens an arterial obstruction.
    • Damaged vessels leak blood into the infarcted tissue → red infarct.

KEY CONCEPT

• Red infarct = infarction with hemorrhage.
• Think of four classic settings:
  venous blockage + dual blood supply + previous congestion + reperfusion.

CONCEPTUAL EXAMPLES

• Testicular torsion → venous drainage blocked → blood accumulates → red infarct.
• Pulmonary vessel occlusion → second blood supply still brings some blood → hemorrhagic infarct.
• Angioplasty restores flow to already damaged tissue → blood leaks into it → red reperfusion infarct.

MORPHOLOGY

• White (anemic) infarcts occur after arterial occlusion in solid organs with end-arterial circulation, especially:
  • heart
  • spleen
  • kidney (Fig. 3.17B)
• White infarcts are usually wedge-shaped:
  • apex → points toward the blocked vessel
  • base → faces the outer surface of the organ
• If the base reaches a serosal surface, a fibrinous exudate may form over it.
• In an acute infarct:
  • margins are initially poorly defined and slightly hemorrhagic
  • with time → margins become clearer
  • a narrow hyperemic rim develops because of inflammation
• Arterial infarcts in organs without dual circulation become progressively paler and more sharply defined with time.
• In contrast, organs with dual blood supply, especially the lung, usually develop hemorrhagic (red) infarcts (Fig. 3.17A).
• In hemorrhagic infarcts:
  • macrophages remove extravasated RBCs
  • heme iron → hemosiderin
  • extensive hemorrhage may eventually leave a firm brown residue
• In most tissues, the main microscopic pattern is ischemic coagulative necrosis.
• Within a few hours → inflammation begins around the infarct.
• By about 1–2 days → the inflammatory border becomes well defined.
• Later:
  • inflammation → repair
  • repair begins at the preserved margins
  • some surviving peripheral cells may regenerate if the supporting tissue framework remains intact
  • most infarcts eventually become a scar (Fig. 3.18)
• Brain is the major exception:
  • ischemic injury in the CNS → liquefactive necrosis, not coagulative necrosis.
• Septic infarcts occur when:
  • infected cardiac valve vegetations embolize, or
  • microbes infect already necrotic tissue.
• The infected infarct may become an abscess → stronger inflammatory response → healing by organization and fibrosis.

KEY CONCEPT

• White infarct → arterial blockage + solid end-arterial organ.
• Red infarct → commonly occurs in tissues with dual blood supply.
• Most infarcts → coagulative necrosis → inflammation → scar.
• Brain infarct → liquefactive necrosis.
• Septic infarct → infected infarct → abscess.

CONCEPTUAL EXAMPLES

• Coronary artery blocked → pale wedge-like myocardial infarct → white infarct.
• Pulmonary arterial blockage → blood still enters from another circulation → red infarct.
• Kidney infarct → coagulative necrosis → inflammation → fibrous scar.
• Brain ischemia → tissue softens and liquefies → liquefactive necrosis.
• Infected valve vegetation embolizes → infected infarct → abscess.

Factors That Influence Infarct Development

• Vascular occlusion may cause little effect or severe tissue necrosis, depending mainly on three factors.
• Anatomy of vascular supply:
  • The most important factor is whether the tissue has an alternative blood supply.
  • Lung → dual supply from pulmonary + bronchial arteries → pulmonary arteriole blockage usually does not cause infarction unless bronchial flow is also reduced.
  • Liver → hepatic artery + portal vein → relatively resistant to infarction.
  • Hand and forearm → radial + ulnar arteries → alternative blood flow reduces infarction risk.
  • Kidney and spleen → end-arterial circulation → arterial blockage usually causes infarction.
• Rate of occlusion:
  • Slow blockage is less likely to cause infarction because collateral vessels have time to enlarge and carry more blood.
  • Small connections normally exist between the major coronary arteries.
  • Slowly developing coronary obstruction → collateral flow may increase enough to prevent infarction, even if the original artery eventually becomes completely blocked.
• Tissue vulnerability to hypoxia:
  • Different cells tolerate loss of blood supply for different lengths of time because their metabolic needs differ.
  • Neurons → irreversible injury after only 3–4 minutes.
  • Cardiac muscle cells → die after about 20–30 minutes of ischemia.
  • Fibroblasts → may survive many hours of ischemia.

KEY CONCEPT

• Infarct development mainly depends on:
  vascular anatomy + speed of blockage + tissue sensitivity to hypoxia.
• Dual/collateral blood supply → protects against infarction.
• Slow occlusion → allows collateral circulation to develop.
• Neurons are most vulnerable, myocardium is next, and fibroblasts are much more resistant.

CONCEPTUAL EXAMPLES

• Pulmonary artery branch blocked but bronchial circulation remains intact → lung infarction may not occur.
• Renal artery blocked → no major alternative supply → kidney infarction likely.
• Coronary artery narrows slowly → collateral vessels enlarge → myocardium may remain viable.
• Brain loses blood flow → neurons can die within 3–4 minutes.