Infarction

pathology

1. GOOD
MORNING
DR V.VASUNDHARA
DEPARTMENT OF
CONSERVATIVE DENISTRY
AND ENDODONTICS .

2. INFARCTION
2

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

4. 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

5. 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

6. •Generally,Sudden, complete and continuous occlusion by
thrombosis or embolism
•Torsion of a vessel, e.g. in testicular torsion
•Traumatic rupture or vascular compromise by edema, e.g.
anterior compartment syndrome.
• Nonocclusive circulatory insufficiency.

7. TYPES
COLOUR
Red or hemorrhagic Pale or anemic

8. • 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.

9. 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

10. 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.

11. •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.

12. 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.

13. 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).

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

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

17. 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.

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

19. 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.

20. 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
4
th
day: centre
turns pale yellow.
1 week: typically anemic , depressed below
the surface

21. Microscopically
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.

22. 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)

23. •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.

24. •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.
MICROSCOPICALLY

25. 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.

26. •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.

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

28. CEREBRAL INFARCTION
•Local vascular occlusion
•Occasionally,
non-occlusive cause
compression of the cerebral
arteries from outside
and from hypoxic
encephalopathy.

29. •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).

30. ARTERIAL OCCLUSION
•Occlusion of the cerebral arteries by thrombi- common
•Embolic arterial occlusion is commonly derived from the
heart
mural thrombosis complicating MI
arterial fibrillation and endocarditis.

31. VENOUS OCCLUSION
• Infrequent phenomenon due to good communications
of the cerebral venous drainage.
•However in cancer, due to increased predisposition to
thrombosis, superior sagittal thrombosis may occur
leading to bilateral, parasagittal, multiple hemorrhagic
infarcts.

32. NON-OCCLUSIVE CAUSES
Compression of the cerebral arteries from outside
occurs during herniation

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

34. •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

37. 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 but more
common in elderly.

38. PREDISPOSING FACTORS FOR
CORONARY ARTHEROSCLEROSIS
Hyperlipidaemia
Hypertension
DM
Cigarette smoking etc
DOCUMENTED WELL BY AUTOPSY STUDIES
AND CORONARY ANGIOGRAPHIC STUDIES.

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

40. MECHANISM OF
MYOCARDIAL ISCHEMIA
DIMINISHED CORONARY
BLOOD FLOW
Coronary artery
disease,shock
•MYOCARDIAL
OXYGEN DEMAND
•Exercise,emotion
HYPERTROPHY OF HEART
W/O SIMULTANEOUS
INCREASE IN CORONARY
BLOOD FLOW
Hypertension,Valvular heart
disease

41. ROLE OF PLATELETS
•Rupture of atherosclerotic plaque exposes : sub
endothelial collagen to platelets which undergo
aggregation, activation & release reaction.
•These events contribute to the build up of the platelet
mass that gives rise to emboli or initiate thrombosis.

42. COMPLICATED PLAQUES
Two complications occur
Superimposed coronary thrombosis – seen in about half of the cases
of acute MI. Infusion of fibrinolysins in the first few hours of
development of acute MI in such cases restores blood flow in the
blocked vessel in majority of cases.
Intramural hemorrhage – is found in about one third of cases of acute
MI. Hemorrhage and thrombosis may occur together in some cases.

43. NON-ATHEROSCLEROTIC
CAUSES
Coronary vasospasm
Coronary ostial stenosis,
Embolism,
Thrombotic diseases,
Trauma and outside compression.

44. 1
Feature Transmural infract Subendoc
ardial
infarct
1Definition Full-thickness, solid Inner third to
half, patchy
2Frequency Most frequent (95%) Less frequent
3Distribution Specific area of coronary
supply
Circumferent
ial
4Pathogenesis > 75% coronary stenosis Hypoperfusio
n of
myocardium
5Coronary
thrombosis
Common Rare
6Epicarditis Common
None

45. LOCATION OF INFARCTS
• LV
•RV is less susceptible , due to its thin wall, having less
metabolic requirements and is thus adequately nourished
•Atrial infarcts, whenever usually accompany infarct of LV
•LA is relatively protected because it is supplied by oxygenated
blood in the left atrial chamber.

46. REGION OF INFARCTION
Area of obstructed
blood supply by one or more
of three coronary arterial
trunks in descending order:

1.Left anterior descending
coronary artery :40 to 50%
2.Right coronary artery :30 to 40%
3.Left circumflex coronary
artery:15 to 20%

47.  3 Regions of myocardial infraction.
Stenosis of the left anterior descending
coronary artery is the most common (40-
50%).
Region of infarction in the anterior part of the
left ventricle including the apex and the
anterior two-thirds of the interventricular
septum.

48. Stenosis of the right coronary artery
is the next most frequent (30-40%) .
It involves the posterior part of the
left ventricle and the posterior one-
third of the interventricular septum.

49. Stenosis of the left circumflex
coronary artery is seen least
frequently (15-20%).
Its area of involvement is the lateral
wall of the left ventricle.

50. 50
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.

51. REFERENCES
1.Robbins and Cotran - Pathologic basis of
diseases. 8
th
edition.
2. Harsh Mohan – Text book of pathology. 3
rd

edition.
3.Mc Gee, Isaacson and Wright – Oxford text
book of Pathology. Principles of Pathology
volume 1.
4.Anderson’s Pathology – 10
th
edition

52. God gave us
healing hands
..……. To heal
the wounds of the
world