ischemia and infarction.pdf

CHRONIC VENOUS CONGESTION IN DIFFERENT ORGANS
INFARCTION
CAUSES OF INFARCTION
TYPES OF INFARCT
INFARCTS IN DIFFERENT ORGANS

1. Dr. Pranav N Shirbhate
(MBBS, MD, F Neuropathology, MNPSI)
Assistant Professor , Department of Pathology
Government Medical college and SuperspecialityHospital, Akola
ISCHEMIA AND INFARCTION

2. OVERVIEW
•CHRONIC VENOUS CONGESTION IN DIFFERENT ORGANS
•INFARCTION
•CAUSES OF INFARCTION
•TYPES OF INFARCT
•INFARCTS IN DIFFERENT ORGANS

3. CONGESTION
Heart failure
left sided
Back Pressure in
pulmonary vessels
CVC Lung
Right sided
Back pressure
Systemic
•CVC liver
•CVC spleen
•CVC kidney
•CVC leg veins

4. CVC LUNG
Pathogenesis
•Inability of the blood to return to left side of heart leading to stagnation
of blood in lungs
•Alveolar septa shows edema with dilated and congested capillaries
•Rupture of these capillaries lead to intra alveolar hemorrhages
•Breakdown of erythrocytes leads to release of hemoglobin which is
ingested by macrophages called heart failure cells

5. CVC LUNG
Morphology
Lungs –Heavy, Bulky and dark
brown
C/S frothy fluid, Solid with blood
Late –firm and hard –fibrous –
septa
Cut section is rusty brown (iron
deposition) –referred to as
“brown induration”

6. CVC LUNG
Microscopic picture –
Alveolar septa shows edema and fibrosis
Alveolar spaces are filled with blood cells
Hemosiderin pigment laden Macrophages
in alveolar spaces
-“ Heart failure cells”

7. CVC –LIVER
•Occurs in
•right sided C.C.F
•Hepatic vein obstruction
•Occlusion of interior vena cava
•Clinical –Tender liver
Slight enlargement

8. CVC –LIVER
•Morphology –liver enlarged with tensed
capsule
•C/S –“Nut meg” liver
Red & yellow, mottled appearance
-Congested centre lobule
-Fatty peripheral zone

9. CVC –LIVER

10. CVC –LIVER
Acute hepatic congestion
•Central vein and sinusoids are distended
•Centrilobular area is at the distal end of the hepatic blood supply, hence
centrilobularhepatocytes may undergo ischemic necrosis
•Periportalhepatocytes are better oxygenated and undergo fatty change
Chronic passive hepatic congestion
•Centrilobular region undergo necrosis and appears red brown and
depressed
•This region is surrounded by pale areas of uncongested liver with fatty
change

11. CVC –LIVER
Microscopically –centrilobular congestion and hemorrhage, hemosiderin laden macrophages and necrosis

12. CVC SPLEEN
•CVC Spleen occurs in -
• Right side C.C.F
• Portal hypertension
• Cirrhosis of liver
•Morphology-
Early stages–slight to moderate enlargement
Chronic–Progressive enlargement upto 1000gms (Normal –150gms)
Grosslyspleen is deeply congested, tense and cyanotic
Cut section –firm to gray tan –Congestive spleenomegaly

13. CVC SPLEEN
Microscopy
•Capsule –thickened
•Congestion & dilation of sinusoids
•Recent & old hemorrhages with organization of hemorrhages
•GummagandybodiesSidero-fibrotic nodules with deposition of
hemosiderin pigment and calcium salts
•hyperplasia of red pulp
•Common cause of hyper splenism

14. CVC SPLEEN

15. ISCHEMIA & INFARCTION
•Inadequate blood supply to a part of the body –ischemia
•If ischemia persists beyond permissible limits –infarction
Affects of ischemia causing deprivation of blood supply are
-Deprivation of oxygen
-Deprivation of nutrition
-Failure to remove metabolic waste which accumulate and cause damage
•Immediate effect of ischemia will be there on tissue with highest O
2requirements
and metabolic demands-Brain and Heart

16. ISCHEMIA & INFARCTION
Causes of Ischemia
•Generalized –hypovolemic shock (Cardiac failure)
•Localized -Atherosclerosis
Thrombosis
Embolism
Vasculitis
Spasm of vessels
External pressure

17. ISCHEMIA & INFARCTION
Localized causes –3 levels –
•Arterial
•Venous
•Microcirculation (arterioles, veinules, capillaries)

18. ISCHEMIA & INFARCTION
Causes of Arterial
Obstruction
Luminal occlusion
(intraluminal)
Causes in the arterial
walls (intramural)
Outside pressure on
artery (extramural)
•Thrombosis
•Embolism
•Vasospam
•Arteriosclerosis
•Polyarteritisnodosa
•Thromboangitis
obliterans
•Hypothermia
•Ergot poisoning
•Torsion
•Ligature
•Torniquet

19. ISCHEMIA & INFARCTION
Causes of Venous obstruction
Luminal occlusion
Causes in vessel wall
(intramural)
Outside pressure on
vein
•Thrombosis
•Embolism •Varicose veins of leg •Ligature
•Hematoma
•Strangulated
hernia
•Intussusception

20. ISCHEMIA & INFARCTION
Causes in microcirculation
(arterioles, veinules and capillaries)
Luminal occlusion Causes in microvascular
wall (intramural)
Outside pressure
(extramural)
Bedsores •Vasculitis –polyarteritis
nodosa, Henoch schonlein
purpura, arthusreaction
•Frostbite injuring the wall
of small vessels
•By RBC’s –sickle cell anemia
•By WBC’s –chronic myeloid
leukemia
•By precipitated cryoglobulins
•Fat embolism
•Air embolism

21. ISCHEMIA & INFARCTION
•Effect of ischemia:-
1.Functional disturbances:-
eg: angina pectoris intermittent claudication
manifested only by exertion
2. Degeneration, atrophy and replacement by fibrosis -gradual
obstruction –adaptation
3. Gangrene–sudden or gradual complete obstruction
4. Infarction

22. INFARCT
•An area of ischemic necrosis caused by either occlusion of arterial blood or
occlusion to venous drainage or both pathological process –infarction
•Non ischemic necrosis is not infarct
•Infarction differs from gangrene by absence putrefaction. Infarction is
surrounded by living tissue
•99% of infarcts –arterial occlusion -thrombosis & embolism
•Venous thrombosis –infarction –block in drainage-stagnant hypoxia

23. Factors determining severity
of ischemic injury
Anatomic patterns
General and cardiovascular status
Type of tissue affected
Rapidity of development
Degree of vascular occlusion

24. INFARCT
•Anatomic patterns
•Single arterial supply without anastomosis
•Central artery of retina
•Interlobular arteries of kidney
•Single arterial supply with rich anastomosis
•Superior mesenteric artery to small blood vessels
•Inferior mesenteric artery to distal colon
•Parallel arterial supply
•Brain by circle of Willis
•Forearm by radial and ulnar arteries
•Double blood supply
•Lungs –by bronchial circulation and pulmonary arterial branches
•Liver –by portal circulation and hepatic arterial flow

25. INFARCT
General and cardiovascular status
•Anemias
•Lowered oxygenation of blood (hypoxaemia)
•Marked coronary atherosclerosis
•Cardiac failure
•Blood loss shock

26. INFARCT
Type of tissue affected
•Mesenchymal tissues are more resistant to ischemic affect than the
parenchymal cells
•Tissues sensitive to ischemia are
•Brain (cerebral neurons)
•Myocardial cells
•Kidney ( especially epithelial cells of proximal convoluted tubules )

27. INFARCT
Rapidity of development –
•sudden vascular obstruction causes severe ischemic damage
•If develops gradually collaterals can develop and damage is less
Degree of vascular occlusion –
•complete vascular occlusion causes severe injury than partial
obstruction

28. INFARCT
Pathogenesis
Localized congestion
immediately after obstruction of the blood supply
Edema and hemorrhage
Cellular changes
Like cellular swelling, reversible changes and further
irreversible changes
Progressive proteolysis of necrotic
tissue and lysis of RBC’s
Acute inflammatory
reaction and hyperemia
Progressive in growth
of granulation tissue

29. INFARCT
Types of infarct
According to color
According to age
According to absence or
presence of infection
Pale or anemic
Arterial occlusion in compact organs(kidneys,
heart, spleen)
Red or hemorrhagic
In soft loose tissues, and in pulmarterial
obstruction or by venous occlusion in intestines
Recent or fresh
Old or healed
Bland –free of bacterial contamination
Septic –when infected

30. INFARCT
Features Red infarct White infarct
Cause •Venous occlusion •Arterialocclusion
Types of tissues affected•Loose, spongytissues eglung where
blood collects in infarcted zone
•Dual blood circulation that allows
bloodto flow from an unobstructed
parallel supply into necrotic zone
•Tissues previously congested by
venous outflow
•When flow is reestablished to a site
of previous arterial occlusion and
necrosis (egafter angioplasty)
•In solid organs
•with end arterial supply
where tissue density limits
seepage of blood from
adjoining capillary beds into
necrotic area

31. INFARCT
Morphology
•Wedge or pyramidal shape
•Base towards periphery
•Apex towards site of obstruction
•Most often peripherally situated
•Slow fibrinous exudate over serous coverings
eg: Pleura

32. INFARCT LUNG
•Cause–Embolism of Pulmonary
arteries
•Lungs also receive blood supply
from bronchial arteries
•Infarction occurs when the
person has inadequate
circulation due to chronic lung
disease and congestive cardiac
failure

33. INFARCT LUNG
Grossly –
•Shape -wedge shaped with base on the pleura
•Size –variable
•Site -most often in lower lobes
•Fibrinous pleuritic covering lung
•Cut surface –dark purple and may show the blocked vessel near the
apex of infarcted area
•Old organized and healed pulmonary infarcts appear as retracted
fibrous scars

34. INFARCT LUNG

35. INFARCT LUNG
Microscopically -
•Coagulative necrosis of the
alveolar walls
•Initially –infiltration by
neutrophils and intense alveolar
capillary congestion
•Later their place is taken by
hemosiderin, phagocytes and
granulation tissue

36. INFARCT KIDNEY
Causes
•Most common cause–thromboemboli originating from the heart
such as in mural thrombi in left atrium, myocardial infarction,
vegetative endocarditis and from aortic aneurysms
•Less commonly –renal artery atherosclerosis, arteritis and sickle
cell anemia

37. INFARCT KIDNEY
Gross –
•Often multiple and bilateral
•Type of infarct –pale or white
•Wedge shaped with base resting under the capsule and apex pointing towards
medulla
•Narrow rim of renal tissue under the capsule is spared as it draws its blood
supply from the capsular vessels
•Cut surface –in the 1
st
2 to 3 days it is red and congested but by 4
th
day it
becomes pale yellow
•At the end of one week, infarct is typically anaemicand depressed below the
surface of kidney

39. INFARCT KIDNEY
Microscopically
•Affected area shows coagulative
necrosis of renal parenchyma ( ghost
tubules and glomeruli)
•Margin of the infarct –inflammatory
reaction –initially acute but later
macrophages and fibrous tissue
predominate

40. INFARCT KIDNEY

41. INFARCT LIVER
•Infarcts in the liver are uncommon due to dual blood supply from portal vein
and hepatic artery
•Obstruction of hepatic artery or its branches caused by arteritis,
arteriosclerosis or bland/septic emboli –infarcts of liver
•Obstruction of portal vein or its branches is usually secondary to diseases like
cirrhosis, intravenous invasion of primary carcinoma of liver, carcinoma of
pancreas and pyelophlebitis
•This does not produce ischemic infarction but instead reduced blood supply to
hepatic parenchyma causes non-ischemic infarct called –infarct of zahn

42. INFARCT LIVER
Grossly –
•ischemic infarcts of the liver are usually anemic
•But may be hemorrhagic due to stuffing of site by blood from portal veins
•Infarcts of zahnproduce sharply defined red-blue area in liver parenchyma

43. INFARCT LIVER
Microscopically
•Infarcts of liver is characteristically
pale and similar to that as in
kidney or spleen
•Infarcts of zahnoccurring due to
reduced portal blood flow over
long duration result in chronic
atrophy of hepatocytes and
dilatation of sinusoids

44. INFARCT SPLEEN
•Results from occlusion of splenic artery or its branches
•Occlusion is caused most commonly by
•Thromboemboliarising in heart ( mural thrombi in left atrium,
vegetative endocarditis, myocardial infarction)
•Obstruction of microcirculationas in myeloproliferative diseases,
sickle cell anemia, arteritis, Hodgkins disease, bacterial infection

45. INFARCT SPLEEN
Grossly
•Often multiple
•Characteristically pale or
anemic and wedge shaped
with base at the
periphery and apex
pointing towards hilum

46. INFARCT SPLEEN
Microscopically
•Coagulative necrosis and inflammatory reaction is seen
•Later necrotic tissue is replaced by shrunken fibrous scar

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