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Infarction in Specific Sites:
- Myocardial infarcts: Visit:
Myocardial Infarction: click here
Myocardial
infarcts are divided into two classes:
transmural
and
subendocardial
infarcts.
A transmural infarct results
from complete occlusion of a major extramural coronary artery. A
myocardial infarct is initially pale, but hemorrhage occurs with reflow
into an injured vascular bed.
Subendocardial infarction
reflects prolonged ischemia caused by partially occluding stenotic
lesions when the requirement for oxygen outstrips the supply.
- Cerebral infarcts:
Infarction of the brain may be the result
of local ischemia or of a generalized reduction in blood flow.
A generalized reduction in blood flow
resulting from systemic hypotension, as in shock, produces infarction in
the border zones between the distributions of the major cerebral
arteries.
If prolonged, severe hypotension can
cause widespread brain necrosis. The occlusion of a single vessel in the
brain - for example, after an embolus has lodged - causes ischemia and
necrosis in a well defined area.
This type of cerebral infarct may be pale
(non-hemorrhagic) or red (hemorrhagic), the latter being common with
embolic occlusions.
Infarcts in the areas supplied by small
penetrating arteries are referred to as "lacunar infarcts".
The occlusion of a large artery produces
a wide area of necrosis that may ultimately resolve as a large
fluid-filled cavity in the brain.
- Intestinal Infarct:
Visit:
GI Path Online
The earliest tissue
changes in intestinal ischemia are necrosis of the tips of the villi in
the small intestine and necrosis of the superficial mucosa in the large
intestine.
In either case more
severe ischemia leads to hemorrhagic necrosis of the submucosa and
muscularis, but not the serosa.
Small mucosal
infarcts heal in a few days, but more severe injury leads to ulceration.
These ulcers can
eventually re-epithelialize.
If the ulcers are
large they are repaired by scar tissue, a process that may lead to
strictures.
Severe transmural
necrosis may be associated with massive bleeding or perforation,
complications that often result in irreversible shock, sepsis, and
death.
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Renal Infarct:
Renal infarcts are
pyramidal in shape, with the base toward the capsule.
These pale infarcts
acquire a hemorrhagic border as granulation tissue develops.
A gray rim in early
infarcts is related to an exudate of polymorphonuclear leukocytes.
- Lung Infarct:
Visit:
Pulmonary Infarction
Inspite of the dual blood supply, from
bronchial and pulmonary vessels, pulmonary infarction is very common.
Embolus arising in any part of systemic
circulation has to pass through the lungs.
Due to dual blood supply and
free anastomosis between the pulmonary capillaries, small emboli fail to
cause any infarction in a healthy lung. But when the circulation of the
lung is slowed down associated with increased pulmonary circulatory
pressure e.g. in chronic passive venous congestion, hypostatic
congestion as seen in post-operative and post-natal period, infarction
is common. Under such condition, when branch of pulmonary artery is
blocked, force of the bronchial arteries is insufficient to supply the
obstructed area due to increased pulmonary circulatory pressure. Blood
drains into the area from all the connections and stagnate there.
Vessels in the alveolar walls give way
and blood escapes into the alveolar space as a result whole area becomes
dead and coagulated into a firm blood-filled solid, airless mass i.e. a
hemorrhagic infarct.
Big embolus blocking a big branch of
pulmonary artery causes sudden death from shock,without infarction.
Cause:
1. Embolism through pulmonary artery.
Emboli come from deep veins of legs, usually in post-operative and
post-natal period.
2. Pulmonary thrombosis, usually due to
atherosclerosis of the pulmonary artery.
Gross:
1. Usually multiple, big or small,
wedge-shaped and placed at the periphery of the lung, dark red in colour
with clean cut outline. Feels firm and cut surface is dry.
2. Overlying pleura shows patches of
fibrinous pleurisy due to irritation.
Microscopic features:
1. Alveoli are filled up with blood and
their outline is indistinct due to coagulation necrosis.
2. Pleura is congested with deposition of
fibrin.
Infarct spleen:
Cause:
1. Embolism- Example: sub-acute bacterial endocarditis.
2. Thrombosis of splenic vessels in
atherosclerosis, tropical splenomegaly, polyarteritis nodosa,
myeloproliferative disorder.
Gross:
1. Spleen is enlarged.
2. Area of infarction is usually pale,
wedge-shaped or irregular, surrounded by a zone of congestion.
3. Infarct extends up to the surface and
involves the capsule causing peri-splenitis (differs from kidney).
4. In late stage healing by fibrosis (autosplenectomy)
or abscess in case of septic thrombus.
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