1. An infarction is an area of ischemic necrosis in an organ resulting from reduced blood supply, usually due to arterial obstruction. 2. The main causes of infarction are thromboembolism and atherosclerosis, which interrupt arterial blood flow. This leads to localized tissue death from coagulative necrosis. 3. Pathologically, infarcts appear pale and wedge-shaped, with inflammation at the borders and eventual scar formation. Location and outcomes vary by organ, such as potentially lethal myocardial infarction or non-lethal splenic infarction.

1. INFARCTION
2
Dr.Abhinav golla
Assistant Professor
Consultant Pathologist
Aadhya Medicure Pathlas

2. CONTENTS
Definition
Etiology
Types
Pathogenesis
Pathologic changes
Infarcts of different organs
References

3. DEFINITION
Localized area of ischemic necrosis in an
organ or tissue resulting most often from
reduction of arterial blood supply or
occasionally its venous
drainage………………….ROBBINS

4. ETIOLOGY
•Most Commonly,Infarcts are caused by Interruption in
arterial blood supply, called ischemic necrosis
•Less commonly,Venous obstruction can produce infarcts
termed stagnant hypoxia

12. • Depending on Age
a.Recent or fresh.
b.Old or healed.
•Presence or absence of infection.
a.Bland – when free of bacterial contamination
b.Septic – when infected.

13. PATHOGENESIS
Localized hyperemia
Edema and hemorrhage
Cellular changes
Progressive proteolysis of necrotic tissue and lysis of red cells
An acute inflammatory reaction and hyperaemia
Blood pigments liberated by hemolysis
Progressive ingrowth of granulation tissue

14. PATHOLOGIC
CHANGES
•Grossly, infarcts of solid organs -wedge-shaped
• apex -pointing towards occluded
artery wide base - on the surface of the
organ.
•Infarcts due to arterial occlusion -pale
venous obstruction - hemorrhagic.
•Most infarcts become pale later as the red cell are lysed
but pulmonary infarcts never become pale due to
extensive amount of blood.

15. •Cerebral infarcts : poorly defined with central
softening (encephalomalacia).
•Recent infarcts : slightly elevated over the surface
•Old infarcts : shrunken , depressed under the surface
of the organ.

16. Microscopically
•The pathognomic cytologic change in all infarcts is
coagulative (ischaemic) necrosis of the affected area
of tissue or organ.
•In cerebral infarcts- characteristic
liquefactive necrosis.

17. At periphery of an infarct, inflammatory reaction is
noted.
Initially neutrophils predominate ,later macrophages and
fibroblasts appear.
Eventually, necrotic area is replaced by fibrous scar
tissue, may show dystrophic calcification.
In cerebral infarcts, the liquefactive necrosis is followed
by gliosis i.e. replacement by microglial cells distended
by fatty material (gitter cells).

18. INFARCTS OF DIFFERENT
ORGANS
Location Gross
appearanc
e
Outcome
1 Myocardial infraction Pale Frequently lethal
2 Pulmonary infraction Hemorrhagic Less commonly
fatal
3 Cerebral infraction Hemorrhagic &
Pale
Fatal if massive
4 Intestinal infraction Hemorrhagic Frequently lethal
5 Renal infraction Pale Not lethal unless
massive &
bilateral
6 Infract spleen Pale Not lethal
7 Infract liver Pale Not lethal
8 Infracts of lower extremity Pale Not lethal

19. LUNG
INFARCTION
•Embolism of the pulmonary arteries
• May occur in patients who have inadequate circulation :
Chronic lung diseases
• Congestive heart failure.

21. GROSS:
pulmonary infarcts : wedge-shaped
Base on the pleura,
hemorrhagic, variable in size
lower lobes.
Cut surface : dark purple
Shows blocked vessel near the apex of the infarcted area.
Old organized and healed pulmonary infarcts appear as
retracted fibrous scars.

22. Microscopically
•Characteristic histologic feature : coagulative
necrosis of the alveolar walls.
•Initially: infiltration by neutrophils and intense
alveolar capillary congestion hemosiderin,
phagocytes and granulation tissue.

23. KIDNEY INFARCTION
Renal infarcts are Common
caused by Thromboemboli
most commonly originating from heart
such as mural thrombi in the left atrium ,MI,Vegetative
endocarditis
Less commonly
renal artery atherosclerosis,
arteritis
sickle cell anemia.

24. Grossly:multiple and bilateral
Characteristically:wedge shape
Base - under capsule
Apex-pointing towards medulla
Narrow rim of preserved renal tissue is spared
Cut surface in first 2 to 3 days : red and congested
4th day: centre
turns pale yellow.
1 week: typically anemic , depressed below
the surface

25. Microscopi
cally
 Characteristic:
 affected area shows coagulative
necrosis of renal parenchyma i.e. ghosts of
renal tubules and glomeruli without
intact nuclei and cytoplasmic content.
 The margin of the infarct shows
inflammatory reaction – initially acute but
later macrophages and fibrous tissue
predominate.

26. INFARCT SPLEEN
•Common site for infarcts
•It results from Occlusion of one of the splenic arteries or
its branches.
Most common cause : thromboemboli arising in heart
(eg.mural thrombi in the left atrium
vegetative endocarditis
myocarditis
myocardial infarction)

27. •Less frequently by obstruction of microcirculation (e.g.
in myeloproliferative diseases, sickle cell anemia,
arteritis, Hodgkin's disease, bacterial infections).
•Grossly, splenic infarcts are often multiple.
•Characteristically pale or anemic, wedge-shaped
•
•
base - at the periphery
apex -pointing towards hilum.

28. •Features are similar to those found in anemic infarcts in
kidney.
•Coagulative necrosis and inflammatory reaction are
seen.
•Later, the necrotic tissues is replaced by shrunken
fibrous scar.
M
ICROSCOPI
CALLY

29. INFARCT LIVER
• Uncommon
• Dual blood supply
•Obstruction of the portal vein is usually secondary
to other diseases : Hepatic cirrhosis,
IV invasion of primary CA of liver,
CA of pancreas
•Generally does not produce ischemic infarction
but instead reduced blood supply to hepatic
parenchyma causes non-ischemic infarct called
infarct of Zahn.

30. •Obstruction of the hepatic artery or its branches:
arteritis, arterio-sclerosis, bland or septic emboli.
•Grossly, anemic but sometimes hemorrhagic due to
stuffing of the site by blood from the portal vein.
•Infarcts of Zahn (non-ischemic infarcts) produce sharply
defined red-blue area in liver parenchyma.

31. Microscopically
Infarcts of Zahn occurring due to reduced portal blood
flow result in atrophy of hepatocytes and dilatation
of sinusoids .

32. CEREBRAL INFARCTION
•Local vascular occlusion
•Occasionally,
non-occlusive cause
compression of the cerebral
arteries.

33. •Clinically, the signs and symptoms depend upon the
region infarcted.
•In general, the focal neurologic deficit termed stroke, is
present.
•However, significant atherosclerotic cerebrovascular
disease may produce transient ischemic attacks
(TIA).

34. PATHOLOGIC CHANGES
• Anemic or hemorrhagic
• Affected area : soft and swollen
blurring of junction between grey
and white matter.

35. •Within 2-3days, the infarct undergoes softening and
degeneration.
• Central liquefaction with peripheral firm glial reaction
• thickened leptomeninges, forming a cystic infarct.
•Hemorrhagic infarct : red and superficially resembles a
hematoma

36. MYOCARDIAL INFARCTION
Most Important consequence of coronary
artery disease
Patient may die within first few hours of the
onset while remainder suffer from effects of
cardiac function
INCIDENCE:Occurs at all age butmore
common inelderly.

37. PREDISPOSINGFACTORSFOR
CORONARY ARTHEROSCLEROSIS
Hyperlipidaemia
Hypertension
DM
Cigarette smoking etc
DOCUMENTED WELL BY AUTOPSY
STUDIES AND CORONARY
ANGIOGRAPHIC STUDIES.

38. ETIOPATHOGENESIS
1.Mechanism of myocardial ischemia
2.Role of platelets
3.Complicated plaques
4.Non – atherosclerotic causes
5.Transmural versus subendocardial infarcts

39. MECHANISM OF
MYOCARDIAL ISCHEMIA
DIMINISHEDCORONARY
BLOOD FLOW
Coronary artery
disease,shock
• MYOCARDIAL
OXYGEN DEMAND
•Exercise,emotion
HYPERTROPHY OF HEART
W/O SIMULTANEOUS
INCREASE INCORONARY
BLOOD FLOW
Hypertension,Valvular heart
disease

40. 1
Feature Transmuralinfract Subendoc
ardial
infarct
1 Definition Full-thickness, solid Inner third to
half, patchy
2 Frequency Most frequent (95%) Less frequent
3 Distribution Specific area ofcoronary
supply
Circumferent
ial
4 Pathogenesis >75%coronarystenosis Hypoperfusio
n of
myocardium
5 Coronary
thrombosis
Common Rare
6 Epicarditis Common None

42. Microscopically
The changes are similar in both transmural and
subendocardial infracts.
There is ischemic coagulative necrosis of the
myocardium which eventually heals by fibrosis.
However, sequential microscopic changes are
observed.
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43. REFERENCES
1.Robbins and Cotran - Pathologic basis of
diseases. 8th edition.
2. Harsh Mohan – Text book of pathology. 3rd
edition.
3.Mc Gee, Isaacson and Wright – Oxford text
book of Pathology. Principles of Pathology
volume 1.
4.Anderson’s Pathology – 10th edition

44. ..……. To heal
the wounds of the
world