INFARCTION

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DEFINITION
INFARCTION :Process of formation of an infarct.

INFARCT : An area of ischaemic necrosis, caused by occlusion of arterial

supply or impaired venous drainage within an organ or tissue.
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 CAUSES :
[Link] &/ or embolism - 99%
2. Expansion of atheroma due to Haemorrhage within plaque
3. Local vasospasm
[Link] compression of a vessel (e.g., by tumor)
[Link] of the vessels (e.g., in testicular torsion or bowel
volvulus)
6. Compression of the blood supply by edema or by entrapment
in a hernia sac, or
7. Traumatic rupture of the blood supply.
External pressure & torsion embarrassment of venous flow,
since the veins are more readily compressed than arteries
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TYPES OF INFARCT:
[Link] the basis of their color
[Link] (White)
[Link] (red)
2.(+) ce or (-) ce of bacterial contamination
[Link] infarct
[Link] infarct

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 White Infarct
 are encountered with Arterial occlusion in solid organs with end arterial
circulation eg. Heart, spleen and kidney
 solid tissues Þ deprive of its arterial circulation Þtransiently haemorrhagic, but most
become pale in a very short time.
 At the moment of vascular occlusion Þblood from anastomotic peripheral vessels
flows into the focus of injury Þ haemorrhagic appearance.
 If the tissues affected is solid Þ seepage of blood is minimal Þ R B Cs are lysed &
released Hb diffuses out or is converted to haemosiderin.
 \ In solid organ, arterial infarcts will soon (24-48 hrs) become pale. e.g. Heart,
kidney, spleen
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 Red Infarct
 are encountered with
1. venous occlusion (e.g. ovarian tosion )
2. in loose tissues ( e.g. Lung )
3. in tissues with double circulation ( e.g. lung & Small intestine)
4. in tissues previously congested
5. when flow is re-established to a site of previous arterial occlusion
and necrosis (e.g, following fragmentation of an occlusive embolus
or angioplasty of a thrombotic lesion)
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 Septic Infarct
When there is bacterial infection in the area of ischaemic necrosis
septic infarct
Due to
1- Organisms (+) t in tissues prior to development of ischaemic necrosis
e.g. infarction of lung already affected by bacterial pneumonia
2- may be brought to the area by infected blood clot.
e.g Embolization of a fragment of Bacterial vegetation from Heart

valve.
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MORPHOLOGY OF INFARCTS
Gross and Histology

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  All infarcts tend to be wedge shaped, with the apex of wedge pointing towards
focus of vascular occlusion & base of wedge at the external aspect of the organ.
 Sometimes map like patterns result from preservation of small marginal areas
of tissues which have different & unaffected sources of blood supply.
 A few hours after onset, all infarcts are poorly defined, slightly darker & firmer.
 During next 24 hours, the demarcation become better defined&color change is

Gross
more intense.
Gross
In solid organ Þ infarct – paler than normal &
{ in spongy tissues Þ infarct – red blue due to massive haemorrhage }
 In the course of several days, pale infarct become yellow white &
{ haemorrhagic infarcts – unchange.}
 Margins – better defined by narrow rim of hyperemia due to marginal
inflammatory response.
 The involved surface of organ is covered by fibrinous exudation.
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 Infarct that has occurred few hours prior to death of pt, there may be no demonstrable
cellular change since there may have been insufficient time for enzymatic degradation
of dead cells.
 If the patient live for < 12 – 18 Hrs , only H’gic suffusion may be (+)
 The characteristic cytologic change of all infarcts except those in brain is ischaemic
coagulativenecrosis : there is preservation of the basic outline of the infracted cell

Histology
which are seen as anucleate acidophilic structures. The intracellular protein are
denatured. Leuccocytic infiltration is also seen.
 { In brain, it is liquefaction necrosis. These basic may be modified by massive
Haemorrhage in Haemorrhagic infarct & bacterial suppuration in septic infarct. }
 The inflammatory exudation begins after the first few hours & become better defined
over the next few days.
 It is followed by fibroblastic reparative response beginning in the preserved margin.
 Finally, the necrotic focus is replaced by scar tissues.
 {With septic infarction, the lesion is converted to an abscess.}
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 FACTORS THAT CONDITION (GOVERN) THE
DEVELOPMENT OF AN INFARCT

Occlusion of an artery or a vein may have little or no effect or death of the tissues &
of the individual.

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 [Link] GENERAL STATUS OF BLOOD
& C V S ( HOST STATUS )
 Any systemic alteration such as Anaemia or hypoxaemia , that reduces the O2
carrying capacity of blood or velocity & volume or blood flow through the
tissues predispose to infarction
 [Link] Heart failure
 [Link] obstructive airway diseases
 [Link]
 [Link] anemia
 [Link] with abnormal Hb : carboxy Hb, Sulph Hb, Met Hb, sickle cell

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anemia prone to infarction
 2. NATURE OF VASCULAR SUPPLY

A. Double Blood Supply

e.g. LUNG & LIVER
Lung : Bronchial & pulmonary circulation
Liver : Portal & hepatic circulation
\ In individuals having normal blood & C V S – occlusion of one system, do not give rise to infarction.
But in the (+)ce of Heart failure, severe anaemia or decrease oxygenation of blood, occlusion of one system
Þ precipitate infarction
B. Parallel Arterial System
e.g. FORE ARM & BRAIN
Forearm: radial artery & ulnar artery
\ occlusion of one artery Þ do not give rise to infarction
Brain: Circle of Willis
But occlusion of one of the cerebral or cerebellar arteries Þ infarction of dependent region of brain 13
 2. NATURE OF VASCULAR SUPPLY

C. Single Arterial Supply With Rich Interarterial Anastomoses

e.g. Small intestine
Branches or superior mesenteric artery are interconnected by looping arcades - by pass focal occlusion.
But one of P° division of superior mesenteric artery or main Artery is obstructed →arcades cannot
provide compensation cause infarction.
D. Single Arterial Supply with Few Anastomoses (End Arteries)
e.g. KIDNEY
occlusion of major branches of main renal artery infarction
e.g. HEART
organ having intermediate pattern of fairly rich anastomosis & can compensate narrowing or
occlusion of 1 of 3 main trunks of coronary arterial system.

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 1. Rate of Development of Occlusion
Slowly developing occlusion is better tolerated than those
occurring suddenly, since they provide opportunity for
alternative pathways & collaterals to become activated. e.g.
HEART
2. Vulnerability of Tissue to Hypoxia
Tissues of the body vary widely in their susceptibility to hypoxia.
Neurons of Central nervous system – most sensitive to hypoxia ( 3 – 4 min )
Glial tissues – resistant to hypoxia
Myocardial cells – sensitive ( 20-30 min )
Epithelial cells of Proximal convoluted tubule - sensitive ( 3-4 Hrs )
Mesenchymal cells of body- resistant to hypoxia 15
 THANK YOU
for your attention

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