Tuesday, May 3, 2011

INFARCTION:
The word "infarction" comes from the Latin "infarcire" meaning "to plug up or cram."
An infarction is the formation of an infarct, that is, an area of tissue death (ischemic necrosis) due to a local lack of oxygen caused by obstruction of the tissue's BLOOD SUPPLY  i.e Arterial supply or Venous drainage.

CAUSES OF INFARCTION:
ARTERIAL CAUSES: 
The supplying ARTERY
 may be blocked by an obstruction (e.g. an arterial embolus, thrombus, or atherosclerotic plaque)
may be mechanically compressed (e.g. tumor, volvulus, or hernia)
ruptured by trauma (e.g. atherosclerosis or vasculitides)
vasoconstricted (e.g. cocaine vasoconstriction leading to myocardial infarction)
 
venous causes:
§Occluded venous drainage (e.g. venous thrombosis) can cause infarction but more often induce congestion only (due to rapid blood flow through collaterals).
§ Infarcts due to venous thrombosis are  more likely in organs with single venous outflow, such as testis or ovary.
 
INFARCT MORPHOLOGY:
Morphologically, the necrotic tissue of an infarct swells, and the infracted area often protrudes above  the surface of the organ.
As an infarct ages it undergoes fibrosis, reduces in size, and ultimately shrinks below the surface of the organ.


CLASSIFICATION OF INFARCTION
Classified according to colour and the presence or absence of infection
 1. WHITE INFARCT OR ANEMIC INFARCT
2. RED INFARCT OR HEMORRHAGIC INFARCT.

Red  OR Hemorrhagic infarct occurs:
- In venous occlusion ( Example: ovarian torsion)
In loose tissues (such as lungs, placenta)
-  In tissues with dual circulation (Example: lungs and small intestine)
In tissues previously congested because of sluggish venous outflow.
At a site of previous occlusion and necrosis when flow is re-established i.e repurfusion  injury


White infarctions (anemic infarcts) affect solid organs with end arterial circulation such as the
spleen , kidneys and Heart.
wherein the solidity of the tissue  substantially limits the amount of nutrients (blood/oxygen/glucose/fuel) that can flow from adjoining capillaries into  the area of  ischemic necrosis

 
SEPTIC INFARCTION:
An area of necrosis resulting from vascular obstruction caused by emboli consisting of clumps of bacteria or infected material.
E.G: infected cardiac valve
In these cases the infarct is converted into an abscess and Abscess slowly organize to SCAR.


 
Pathogenesis and pathology of red infract:
-Arterial obstruction causes fall of distal blood pressure to capillary pressure with dilation of capillaries causing injury due to anoxia.  This is the commonest cause.
-
-Blood from the veins accumulates in the dilated and injured capillaries with outpouring of fluid and RBC into the surrounding tissue.
-
-Thus, the area becomes red, engorged and even hemorrhagic with venous blood, hence the term RED infarction


  white infarct pathology:
 > Atherosclerotic  plaque is injured, ulcerates, or is ruptured
> leading to  platelet aggregation, fibrin deposition, spasm (clot formation and  occlusion)
> cells robbed of O2 begin relying on anaerobic glycolysis
 > after 10 seconds, fuel is depleted and cells become stunned
 > stunned cells unable to participate in contraction
 reversible if O2 supply is restored
 > if O2 is not restored then INFARCTION (MI) occurs
  and in this cells become necrotic




Gross features:  
-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.
e.g This is a recent spleen infarct, showing the classic triangular or wedge shape and the distinctly pale appearance. The reaction zone here is not too apparent, because it is obscured by marked sinusoidal hyperemia




Factors that influence development of an infarct:
1. Pattern of vascular supply:
§ Organs with dual circulation (lung, liver) or anastomosing circulation (radial and ulnar arteries, circle of Willis, small intestine) are protected against infarction.
§ Organs supplied with end arteries (spleen, kidneys) usually develop infarct after occlusion of the arterial supply.    
§
2. Rate of development of occlusion:
Slowly developing occlusions less often cause infarction by providing time to develop alternate perfusion pathways.
 (Example: collateral coronary circulation).

3.  Changes due to hypoxia:
§ Neurons undergo irreversible damage after 3 to 4 minutes of ischemia
§ myocardial cells die only after 20 to 30 minutes.
§ In contrast, fibroblasts within ischemic myocardium are viable even after many hours.
4. Oxygen content of blood:
Anemia, cyanosis, or congestive heart failure (with hypoxia) may cause infarction.