Infarction

1. INFARCTION
SUNETH KAYE D. JAVELLANA

2. • An infarct is an area of ischemic necrosis caused by occlusion of
either the arterial supply (97% of cases) or venous drainage in a
particular tissue.
• Almost all infarcts result from thrombotic or embolic events; other
causes include vasospasm; extrinsic compression of a vessel by
tumor, edema, or entrapment in a hernia sac; and twisting of
vessels, such as testicular torsion or bowel volvulus.
Thrombi
Emboli
Normal vessel Vasospasm

3. • Traumatic vessel rupture is a rare cause.
• Occluded venous drainage (e.g., venous
thrombosis) most often induces congestion only
since bypass channels rapidly open to provide
outflow. Thus, infarcts due to venous thrombosis
are more likely in organs with a single venous
outflow (e.g., testis or ovary).

4. MORPHOLOGY OF AN INFARCT
• Infarcts may be either red
(hemorrhagic) or white (pale, anemic)
and may be either septic or bland.

5. MORPHOLOGY OF AN INFARCT Cont.
• Red infarcts occur in:
I. Venous occlusions (e.g., ovarian torsion)

6. II. Loose tissues (e.g., lung)

7. III. Tissues with dual circulations (e.g., lung and small
intestine)
IV. Tissues previously congested because of sluggish venous
outflow. Sites of previous occlusion and necrosis when flow is
reestablished.

8. MORPHOLOGY OF AN INFARCT Cont.
• White infarcts occur in solid organs (e.g., heart, spleen,
and kidney) with end-arterial circulations (i.e., few collaterals).
Renal Infarction
Heart Infarction

9. MORPHOLOGY OF AN INFARCT Cont.
• All infarcts tend to be wedge-shaped; the occluded vessel
marks the apex, and the organ periphery forms the base.
Lateral margins may be irregular, reflecting the pattern of
adjacent vascular supply.
• The dominant histologic feature of infarction in most tissues is
ischemic coagulative necrosis, followed temporally by an
inflammatory response (hours to days) and by a reparative
response (days to weeks) beginning in the preserved
margins. Most infarcts are ultimately replaced by scar tissue,
although (depending on the tissue) some parenchymal
regeneration may occur where the underlying stromal
architecture is spared.

10. MORPHOLOGY OF AN INFARCT Cont.
• Infarction in the central nervous system
(CNS) results in liquefactive necrosis.
• Septic infarctions occur when infected
heart valve vegetations embolize or
when microbes seed an area of necrosis;
the infarct becomes an abscess.

11. Factors that Influence Development
of an Infarct
• Anatomic pattern of vascular supply (i.e., availability of
alternative supply): Dual circulations (i.e., lung, liver) or
anastomosing circulations (i.e., radial and ulnar arteries,
circle of Willis, small intestine) protect against infarction.
Obstruction of end-arterial vessels generally causes infarction
(i.e., spleen, kidneys).
• Rate of occlusion development: Slowly developing occlusions
less often cause infarction by allowing time to develop
alternative perfusion pathways (e.g., collateral coronary
circulation).

12. Factors that Influence Development
of an Infarct Cont.
• Vulnerability to hypoxia: The susceptibility of a tissue to hypoxia
influences the likelihood of infarction.
For example:
Neurons: undergo irreversible damage
after 3 to 4 minutes of ischemia
Myocardial cells, die after only 20 to 30
minutes.
In contrast, fibroblasts within ischemic
myocardium are viable even after many
hours.

13. Factors that Influence Development of an
Infarct Cont.
• Oxygen content of blood: Anemia, cyanosis, or CHF (with
hypoxia) can cause infarction in an otherwise
inconsequential blockage.
• The partial pressure of oxygen in blood also determines
the outcome of vascular occlusion.
• Partial flow obstruction of a small vessel in an anemic or
cyanotic patient might lead to tissue infarction whereas it
would be without effect under conditions of normal
oxygen tension

14. -END-