Infarct: Definition: An infarct is a localized area of ischemic necrosis resulting from sudden and complete occlusion of its arterial blood supply without sufficient collateral circulation, (or impaired venous drainage). The process of formation of an infarct is known as infarction.

Causes of infarction: I.Arterial obstrction is the most important factor (97% of cases) Caused by:  Thrombosis on top of atherosclerosis, vasculitis  Embolism, the effects of emboli are aggravated by vasospasm  Expansion of an atheroma by hemorrhage within a plaque  External compression by e.g. tumor.

Morphology of the infarcts : It is irreversible tissue injury (necrosis), that becomes evident grossly and microscopically (light microscope) hours after cell death

Gross appearance:  Shape:  All infarcts are wedge shaped or triangle with the apex of the infarct at the occluded artery and its base on the surface of the organ (due to fan shaped distribution of blood supply). When the base is a serosal surface, it is covered by fibrinous exudates. The infarct is surrounded by hyperemia (zone of acute inflammation).  The shapes of cerebral and myocardial infarcts are irregular and determined by the distribution of the occluded vessels and the state of the collateral circulation.

Myocardial infarct

Grossly, the cerebral infarction at the upper left here demonstrates liquefactive necrosis.

On the basis of their colours  Infarcts are classified into:  1)Red (hemorrhagic) infarcts : found in:-  Tissues that have a double blood supply (lung, liver) or collateral circulation (intestine).  In loose tissue such as lung  Reperfusion of the infracted area due to:  presence of some collaterals  dissolution or fragmentation of the occluded thrombus  relief of the associated vasospasm.  Venous infarctions: interruption of venous return makes the affected tissues intensely congested and even hemorrhagic.

 2) Pale (white or anemic) infarcts:  are found as a result of arterial obstruction in solid organs e.g., heart, spleen, kidney, brain, with deficient collaterals. The continuing venous drainage of blood from the ischemic tissue accounts for the pallor of such infarcts.

 They are either: Sterile or septic  Septic infarcts are characterized by secondary bacterial infection of the necrotic tissue.  Septic infarcts occur:  When microorganisms are present in thrombus or embolus e.g., emboli of acute infective endocarditis.  When infarction occurs in a tissue (intestine) that normally contains bacteria.  When bacteria from the blood stream cause secondary infection (rare)  Infection converts the infarct into an abscess or gangrene (in the intestine). The presence or absence of microorganisms:

Regarding the age of infarct  Recent infarction: previously described.  Old infarct: scarring causes distortion and irregularities of external surface of the affected organ.

Microscopic appearance:  Coagulative necrosis (the most common)  Liquifactive necrosis (in the brain)

Fate of an infarct:  A small infarct is healed by fibrous tissue i.e. scar.  A large infarct is encapsulated by fibrous tissue capsule and undergoes dystrophic calcification.  Infection and abscess formation may complicate infarcts.  Superadded putrifaction, leads to gangrene.

II. Venous obstruction,  It is less common Caused by:  Thrombosis.  Embolism.  Compression of the vein from outside e.g., tumors,  Twisting of a pedicle of an organ e.g., testis, ovary (torsion), intestine (volvulus).  Strangulated hernia, intussusception.  In last three conditions, the venous obstruction and congestion precede the arterial obstruction.

Clinical effects and diagnosis of infarct :- Clinical effects and diagnosis of infarct :-  Abnormal function: necrosis of parenchymal cells leads to functional loss or abnormalities:-  heart failure, arrhythmia in myocardial infarct  Heamaturia in renal infarct.  Heamoptysis in pulmonary infarct  Muscle paralysis in necrosis of an area of motor cortex  Intestinal obstruction in intestinal wall necrosis (failure of peristalsis)  Systemic effects: fever, leucocytosis, ↑ ESR.  Release of contents of the necrotic cells into the blood stream and this can be used for diagnosis of cell death e.g., elevation of MB isoenzymes of creatine kinase is specific for myocardial necrosis