Ischemia is defined as a condition of inadequate blood supply to an area of tissue.
Infarction- Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage
Public Health Significance- Long-term exposure to other lung irritants also is a risk factor for COPD leading to IHD. Examples of other lung irritants include secondhand smoke, air pollution, and chemical fumes and dust from the environment or workplace.
3. Page 3
Mechanism
Changes occurring
Symptoms
Treatment
Infarction
Etiology
Pathogenesis
Types of Infarction
Pathologic Changes
Healing Of An Infarct
3
4. Page 4
Infarct of different organs
Pulmonary Infarct
Renal Infarct
Infarct of Spleen
Infarct Of Liver
Cerebral Infarct
Myocardial Infacrt
Public Health Significance
References
4
5. Page 5
• It is a state, when a tissue or organ has it’s arterial perfusion lowered
relative to its metabolic needs.
OR
Ischemia is defined as a condition of inadequate blood supply to an
area of tissue.
• Ischaemia [ischaem=to check and haim = blood] is inadequate
blood supply to a part of the body, even to the point of complete
deprivation.
• Is simply defined as a condition of inadequate blood supply. 5
6. Page 6
There are three harmful effects of ischemia:
Hypoxia- Oxygen deprivation. By far the most important factor
for ischemic tissue damage of very active cells. Eg. muscles
Malnutrition- blood contains glucose and amino acids that could
be metabolised by the amount of oxygen it contain, hence it is of
less importance.
Failure to remove waste products- ‘accumulation of
metabolites is the most explanatory pain in muscle ischaemia’.
6
7. Page 7
General Causes -
May be caused by inadequate cardiac output but not all tissues
are equally affected because of redistribution of avaliable blood.
Symmterical gangrene of the extremities is an occasional
manifestation.
7
8. Page 8
Local causes-
By far the most important cause of ischaemia is obstruction of
arterial flow.
Extensive venous and capillary damage also produces
ischaemia.
8
10. Page 10
• Complete obstruction by occlusive thrombosis.
• Most frequentely found in small and medium sized arteries eg:
coronary or cerebral arteries.
THROMBOSIS
10
11. Page 11
Embolism
•The effects of the embolus
are by the reflex spasm of
the arterial wall and
completed by the rapid
development of thrombus
over the embolus.
11
14. Page 14
Occlusive pressure from outside- caused by tourniquets
and tightly fitting plasters.
14
15. Page 15
Effects depend on degree of ischaemia ranging from sudden
death to no damage:
1. Ischaemia is obviated by collateral channels then there is no
effect on tissues supplied by vessels.
2. The collateral channels supply sufficient blood during
inactivity of tissue but sustain normal exercise, there may be
functional disturbances eg:angina pectoris.
15
16. Page 16
3. There may be cellular degeneration affecting the parenchyma
eg: fatty changes leading to necrosis. This is a patchy affair,
and leads to atropy accompanied by replacement fibrosis or
in central nervous system gliosis.
4. Both arterial and venous obstruction leads to circumscribed
necrosis of tissue called infarction.
16
19. Page 19
Strangulation of a hernia
obstruction at the neck of the
hernia leads to damage before
the arterial blood flow is
implicated
19
20. Page 20
Torsion of the testis- leads to haemorrhagic infarction of the organ.
20
21. Page 21
Cavernous sinus thrombosis- leads to retinal vein thrombosis and
retinal changes resulting in blindness
21
22. Page 22
Varicose veins of the legs-venous blood from the deep calf
veins are pumped by contraction of calf muscles through
communicating veins to the superficial veins. These dilate and
become varicose so that their valves become incompetent. The
high venous pressure causes distension of capillaries and
venules of the skin changing its colour to dusky blue.
22
24. Page 24
Acute leucocytoclastic vasculitis-
Affected vessels with necrosis
having their lumens occlueded by
fibrin and walls infiltered by
neutrophils showing degeneration
with karyorrhexis and clinically the
skin appears as palpable purpura.
24
25. Page 25
Frost bite-
Harmful effect of excessive cold
on the exposed body parts,
damages small blood vessels
resulting in, arteriolar spasm and
aggravation of ischaemia .
25
26. Page 26
Occlusion of fibrin-disseminated intravascular coagulation is
characterized by occlusion of small vessels by deposition of
fibrin mixed with platelets.
Occlusion of precipitated cryoglobulins- exposure of the
extremities to cold leads to vascular occlusion and hemorrhages.
26
27. Page 27
Occluision of capillaries by red cells-
Exposure of the limbs to to cold leads to haemolysis. Ischaemia
precipitated by cold is a feature of sickle cell disease, in which
chronic leg ulcers are seen. Raynaud’s syndrome may occur due
to vascular obstruction.
27
29. Page 29
Occlusion by white cells- Due to abnormal clumping of white cells
in chronic myeloid leukaemic condition infarcts may occur. Eg:
spleen
29
30. Page 30
Arteriolosclerosis-
The benign and malignant types of arteriolosclerosis can affect
small vessels in many organs; involvement of the retina and
kidney is very serious.
30
31. Page 31
Three crucial factors:
1. Speed of onset- if obstruction is sudden effect is more serious
because of less time for effective collateral circulation.
2. Extent of obstruction- complete obstruction is more serious
than partial eg : partial coronary occlusion due to
atherosclerosis is tolerated while complete obstruction causes
infarction and death.
31
32. Page 32
3. Anatomy of collateral circulation – end arteries can have
serious effects as demonstrated by steal syndrome’s eg:
obstruction of the first part of subclavian artery can cause blood
to be diverted down the vertebral artery to the arm, leading to
brain stem ischaemia.
32
33. Page 33
1. State of collateral circulation- a collateral circulation is
affected with spasm, atherosclerosis, failing to maintain a
good alternative blood supply.
2. State of oxygenation of blood- it is in respect of arterial
partial oxygen and haemoglobin level.
3. Efficiency of heart
4. Nature of affected tissue- brain and heart are more vulnerable
to ischaemia.
33
35. Page 35
There are basically two extreme effects of Ischaemia.
Absence of any damage
Sudden death
But in between there are four changes that occur
35
36. Page 36
Functional Disturbances- Angina pectoris
and intermittent claudication; both
manifested on exertion or activity.
Degeneration atrophy and replacement
fibrosis- Gradual obstruction of blood
supply
Gangrene- sudden or gradual but complete
deprivation of blood supply
Infarction- Sudden and complete
deprivation of blood supply
36
37. Page 37
Although pain is common, ischemia may occur without any
symptoms. Generally, symptoms depend on the location of the
ischemia.
37
38. Page 38
Symptoms of cardiac ischemia include:
Chest pain or pressure, which may radiate to the back, arm,
shoulder, neck, jaw or stomach
Limitations of physical abilities
Nausea with or without vomiting
Palpitations or irregular heart rhythms
Profuse sweating
Shortness of breath
38
39. Page 39
Symptoms of ischemia of the brain include:
Abnormal pupil size or non reactivity to light
Balance problems, difficulty walking, and falls
Confusion
Difficulty with memory, thinking, talking, comprehension,
writing or reading
Dizziness
Droopy eyelid
39
40. Page 40
Headache
Loss of muscle coordination
Loss of vision or changes in vision
Nausea with or without vomiting
Numbness or weakness
Paralysis
Vision problems (double vision, blurriness, loss of visual field,
sudden blindness)
Weakness (loss of strength) 40
41. Page 41
Symptoms from ischemia in other parts of the body can include:
Abdominal discomfort when eating
Bloody stool (the blood may be red, black, or tarry in texture)
Diarrhea
Leg pain with walking or climbing stairs
Nausea with or without vomiting
Non-healing sores
Pain
Skin changes 41
42. Page 42
Abnormal pupil size or nonreactivity to light
Change in level of consciousness or alertness, such as passing
out or unresponsiveness
Chest pain, chest tightness, chest pressure, palpitations
Droopy eyelid
Garbled or slurred speech or inability to speak
Hallucinations
Paralysis or inability to move a body part 42
43. Page 43
Respiratory or breathing problems such as shortness of breath
Seizure
Severe abdominal pain or headache
Sudden change in vision, loss of vision
Vomiting blood or bloody stool
43
44. Page 44
Treatment of ischemia begins with seeking regular medical care
throughout your life. Regular medical care allows a health care
professional to provide early screening tests and to promptly
evaluate symptoms and your risks for developing ischemia.
The goal of treating ischemia is to restore blood flow and
prevent further damage. Surgery may be needed to remove dead
tissue or repair injured areas. Once the initial event is managed,
treatment turns to prevention of future ischemia.
44
45. Page 45
Common treatments to reduce ischemia and restore blood flow
include:
Medications to control pain and dilate blood vessels
Medications to prevent ongoing clot formation
Medications to reduce the heart’s workload.
45
46. Page 46
Oxygen therapy
Procedures to expand blood vessels
Surgery or procedures to remove clots
Surgery to bypass blocked blood vessels
Thrombolytic drugs to dissolve clots
46
47. Page 47
Localized area of ischemic necrosis in an organ or tissue
resulting most often from reduction of arterial blood supply or
occasionally its venous drainage
47
48. Page 48
•Most Commonly - Infarcts are caused by Interruption in arterial
blood supply, called ischemic necrosis
•Less commonly - Venous obstruction can produce infarcts termed
stagnant hypoxia
48
49. Page 49
•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.
• Non occlusive circulatory insufficiency.
49
50. Page 50
Infarction usually leads to circumscribed area of coagulative
necrosis which is subsequently organized into scar tissue.
Death of cells in an area deprived of blood supply but blood
continues to seep into the devitalized area for a short time.
50
51. Page 51
OPENING OF
PERIPHERAL
ANASTOMOTIC
CHANNELS
BLOOD TRICKELS
IN THROUGH
OCCLUDED ARTERY,
AS OBSTRUSTION IS
NOT COMPLETE
INITIALLY.
VENOUS
REFLUX
51
52. Page 52
NOTE: At all the events infarcts contain a great deal of blood
and are swollen and red in colour. The red cells entering the
effected area escape through damaged capillaries and lie free
on the dead tissues. Also, a great deal of fibrin derived from
blood lie on the dead tissue.
52
53. Page 53
2. DEAD TISSUE UNDERGOES
NECROSIS
3. PROGRESSIVE AUTOLYSIS
OF NECROTIC TISSUE AND
HAEMOLYSIS OF RED CELLS.
1. DEATH OF CELLS IN AN AREA
DEPRIVED OF BLOOD SUPPLY
53
54. Page 54
4. OUTWARD DIFFUSION OF
TISSUE BREAKDOWN
PRODUCTS AND FREE
HAEMOGLOBIN INGESTED BY
MACROPHAGES
5. INFARCT IS NOW
FIRM AND DULL
YELLOW IN COLOUR
SURROUNDED BY RED ZONE
OF INFLAMMATION
6. FOLLOWED BY SHRINKAGE
OF INFARCT WHICH LATER
BECOMES WHITE
IN COLOUR 54
55. Page 55
After phase of demolition, there is slow progressive
in-growth of granulation tissue from the periphery
and eventually infarct organizes to a fibrous scar
which later undergoes hyaline changes.
55
56. Page 56
As the dead tissue undergoes necrosis in solid organs,
associated swelling of cells squeeze the blood out of infarct in
this way making it look paler.
Until necrosis is visible the ischaemic area cannot be called
infarct. Hence, human dead body is not possible to distinguish
post-mortem changes from early infarcton
Practically it takes 12-24 hours for a myocardial infarct to be
visible macroscopically recognizable.
But the first microscopic changes of necrosis can be seen only
from 6-12 hours after ischaemic episode 56
59. Page 59
BLAND : when free of bacterial contamination (infarcts of
streptococcus virdians endocarditis behave in a bland way because
organisms in the emboli are rapidly destroyed at the site of infarction)
SEPTIC : when infected (a rapid transition from the stage of
necrosis to one of suppuration resulting in large ragged abscess)
59
60. Page 60
•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. 60
61. Page 61
•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.
61
62. Page 62
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.
62
63. Page 63
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).
63
67. Page 67
Infarcts of different organs
Location Gross appearance 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
67
68. Page 68
•Embolism of the pulmonary arteries
• May occur in patients who have inadequate circulation :
Chronic lung diseases
• Congestive heart failure.
68
70. Page 70
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.
70
71. Page 71
MICROSCOPICALLY
• Characteristic histologic feature : coagulative necrosis of the
alveolar walls.
• Initially: infiltration by neutrophils and intense alveolar
capillary congestion hemosiderin, phagocytes and
granulation tissue.
71
72. Page 72
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.
72
73. Page 73
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
73
75. Page 75
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.
75
76. Page 76
•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)
76
77. Page 77
•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.
77
79. Page 79
•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
79
80. Page 80
• 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.
80
81. Page 81
•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.
81
82. Page 82
MICROSCOPICALLY
Infarcts of Zahn
occurring due to reduced portal blood flow result in atrophy of
hepatocytes and dilatation of sinusoids .
82
83. Page 83
•Local vascular occlusion
•Occasionally,
non-occlusive cause
compression of the cerebral
arteries from outside
and from hypoxic
encephalopathy.
83
84. Page 84
•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).
84
85. Page 85
•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.
85
86. Page 86
• 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.
86
87. Page 87
Compression of the cerebral arteries from outside occurs during
herniation
87
88. Page 88
• Anemic or hemorrhagic
• Affected area : soft and swollen
blurring of junction between
grey and white matter.
88
89. Page 89
•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
89
90. Page 90
Histologically –
sequential
changes
• Initially, eosinophilic neuronal necrosis and
lipid vacuolization produced by breakdown of
myelin.
• Simultaneously infiltrated by neutrophils
• After the first 2-3days, progressive invasion by
macrophages astrocytic and vascular
proliferation.
90
91. Page 91
3. macrophages clear
away the necrotic debris
by phagocytosis followed
by reactive astrocytosis, .
A hemorrhagic infarct has
some phagocytes
containing haemosiderin.
4. after 3-4 months an old
cystic infarct is formed
showing cyst transversed by
small blood vessels and has
peripheral fibrillary gliosis.
Small cavitary infarcts are
called lacunar infarcts and
are commonly found as a
complication of systemic
hypertension. 91
92. Page 92
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.
92
94. Page 94
Feature Transmural infract Subendoc
ardial
infarct
1 Definition Full-thickness, solid Inner third to
half, patchy
2 Frequency Most frequent (95%) Less frequent
3 Distribution Specific area of coronary
supply
Circumferenti
al
4 Pathogenesis > 75% coronary stenosis Hypoperfusio
n of
myocardium
5 Coronary
thrombosis
Common Rare
6 Epicarditis Common None 94
95. Page 95
•Q wave representing septal
depolarisation
•R wave representing
ventricular depolarisation
•S wave representing
depolarisation of the
Purkinje fibres
• P wave, which represents
the depolarization of the
atria
•T wave represents
the repolarization (or
recovery) of the ventricles
95
102. Page 102
•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.
102
103. Page 103
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. 103
105. Page 105
• 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.
105
106. Page 106
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%
106
108. Page 108
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.
108
109. Page 109
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.
109
110. Page 110
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.
110
112. Page 112
The immediate goal for any acute MI is to restore normal
coronary blood flow to vessels and salvage myocardium.
There are a variety of medical and medicinal therapies to treat
an MI.
112
114. Page 114
Indicated for patients with STEMI.
Should be given within 12 hours of symptom onset.
Fibrinolytics will break down clots found within the vessles
Contraindications: post op surgical patients, history of
hemorrhagic stroke, ulcer disease, pregnancy, etc.
114
115. Page 115
A diagnostic angiography which includes angioplasty and
possible stenting.
Performed by an interventional cardiologist with a cardiac
surgeon on stand by.
Percutaneous procedure through the femoral or brachial artery.
115
116. Page 116
Upon arrival to the cath lab all actue MI patients will receive:
– A bolus dose of plavix
– IV Integrelin
– Heparin dose either subcu or IV drip
– Angiomax : a DTI may be substituted for heparin and
integrelin.
116
117. Page 117
Surgical treatment where saphenous vein is harvested from the
lower leg and used to bypass the occluded vessels.
117
118. Page 118
Smoking Cessation and lifestyle modifications.
Aspirin, Beta Blockers and Clopidogrel will be indefinite.
Lipid lowering medication along with diet modifications.
118
119. Page 119
Occupational heavy lifting- It was found that people with
high amount of physical activity and those who endorse in
heavy weight lifting during their day to day physical activity
were at a high risk of IHD.
Petersen CB, Eriksen L, Tolstrup JS, Søgaard K, Grønbæk M, Holtermann A.
Occupational heavy lifting and risk of ischemic heart disease and all-cause
mortality. BMC public health. 2012 Dec 11;12(1):1070.
119
120. Page 120
COPD, or chronic obstructive pulmonary (PULL-mun-ary)
disease, is a progressive disease that makes it hard to breathe.
Most people who have COPD smoke or used to smoke.
Long-term exposure to other lung irritants also is a risk factor
for COPD leading to IHD. Examples of other lung irritants
include secondhand smoke, air pollution, and chemical fumes
and dust from the environment or workplace.
120
121. Page 121
There is a high risk of ischaemic heart disease caused by
exposure to environmental tobacco smoke or second hand
smoking.
Breathing other people's smoke is an important and avoidable
cause of ischaemic heart disease, increasing a person's risk by a
quarter.
Law M R, Morris J K, Wald N J. Environmental tobacco smoke exposure and
ischaemic heart disease: an evaluation of the evidence BMJ 1997;315 :973
121
122. Page 122
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
5. Y.M. Bhende’s - General Pathology, 5th edition
6. Edward Sheffild - Pathology in Dentistry 1st edition122
arteries may produce pulmonary infarction, though not always. This is because the lungs receive blood supply from bronchial arteries as well, and thus occlusion of pulmonary artery ordinarily does not produce infarcts.
Arrow represents wedge shaped
Later place is taken by
Found in 5%of autopsies. originating from the heart such as in
Because it draws its blood supply from under the capsule.
Pointing towards
Just as in lungs, infracts in the liver are uncommon due to dual blood supply – from portal vein and from hepatic artery. Occlusion of portal vein or its branches
Infracts of Zahn (non-ischemic infracts) produce sharply defined red-blue area in liver parenchyma.
Arterial or venous. Occasionally, it may be the result of non-occlusive cause such as compression of the cerebral arteries from outside and from hypoxic encephalopathy.
Thrombotic occlusion of the cerebral arteries is most frequently the result of atherosclerosis, and rarely, from arteries of the cranial arteries.
Thrombotic occlusion of the cerebral arteries is most frequently the result of atherosclerosis, and rarely, from arteries of the cranial arteries.
Grossly, an anemic infract becomes evident 6-12hrs after its occurrence.
Hemorrhagic infract : red and superficially resembles a hematom, it is usually a result of fragmentation of occlusive arterial emboli or venous thrombosis.lt of fragmentation of occlusive arterial emboli or venous thrombosis.
Initially, eosinophilic neuronal necrosis and lipid vacuolization produced by breakdown of myelin.
Simultaneously, the infracted area is infiltrated by neutrophils
2. After the first 2-3days, there is progressive invasion by macrophages and there is astrocytic and vascular proliferation.
3. In the following weeks to months, the macrophages clear away the necrotic debris by phagocytosis followed by reactive astrocytosis, often with little fine fibrosis.
A hemorrhagic infract has some phagocytes containing haemosiderin.
4. Ultimately, after 3-4 months and old cystic infract is formed which shows a cyst transversed by small blood vessels and has peripheral fibrillary gliosis.
Small cavitary infracts are called lacunar infracts and are commonly found as a complication of systemic hypertension.
Region of infraction depends upon the area of obstructed blood supply by one or more of three coronary arterial trunks,