Download Infarction: Definition: This is a localized area of cell necrosis in living

Infarction:
Definition: This is a localized area of cell necrosis in living organ
or tissue, resulting most
often from sudden reduction or
cessation of its arterial blood supply or occasionally its
venous drainage.
Causes of vascular obstruction:
1. Thrombosis and embolism are the usual causes.
2. Large atheromatous plaques.
3. Spasm of coronary artery.
4. Pressure on the vessels from outside e.g. by tumor, adhesion,
etc…..
5. Twisting (torsion) of the pedicle of mobile organ e.g. loop of
small intestine, ovary and tests.
Note: External pressure and torsion (causes 4 and 5) usually
interfere with venous drainage, since veins are more readily
compressible than arteries.
Types of infarctions:
- Infarction is classified according to their color
into:
1. Anemic (white or pale) or
2. Hemorrhagic (red).
- Infarction is classified according to pressure or
absence of bacteria into:
1. Septic.
2. Bland.
Pale (anemic, white) infarcts are encountered with:
1. Arterial occlusion.
2. In solid organ e.g. heart, kidney, spleen.
All infarcts, to begin with are hemorrhagic (red). This is because at
the moments of vascular occlusion, blood from anastomotic
collateral vessels, flow freely into the area of infarction.
If the tissue affected is solid, the leakage of the blood is minimal and
soon (within 1-2 days) the red blood cells lyses and the released
hemoglobin diffuses out or converted to hemosederin. The result
is rapid conversion of the red discoloration into pale one.
Hemorrhagic (red) infarcts are usually encountered with:
1. In loose tissue e.g. lung.
2. With venous occlusions.
3. In tissue having double circulation (double blood supply) or rich vascular
anastmosis.
4. In tissue that are already congested.
- The lung is an example of loose tissue that shows hemorrhagic infarction
secondary to
arterial obstruction. This is because large amount of
blood accumulates in the spongy lung
parenchyma so the infarction
remains red.
- Long segments of small intestine may show hemorrhagic infarctions due to
arterial or even
venous occlusion. This is because of rich arterial
anastmosis between many branches of the
superior mesenteric artery,
these permit continuous arterial flow to the injured area.
- Brain infarction may be pale or hemorrhagic. In the latter instance the
embolus, which
initially cause the infarction, may break into smaller
emboli and the blood from the major
artery may pour into the soft area
of Liquefactive necrosis, yielding extensive hemorrhage
into what had
been initially pale infarction.
Septic infarction may be seen in associated
with:
1. An already infected tissue.
2. Septic emboli.
3. Bactermia or septicemia.
Histological features of infarction:
1. Cross features of infarction:
Irrespective of their color (i.e. whether pale or hemorrhagic), all infarcts tend
to have wedge-shaped with the apex pointing towards the focus of vascular
occlusion. However, the exact outline of the infarct may be quite variable and
sometimes geographic (map-like) pattern occurs. The latter results from
preservation of small areas of tissue at the periphery of the infarct that have
different or unaffected sources of blood supply.
With time progression (during the next 24 hours), the infarct become more and
more demarcated from surrounding tissues, the color differences more
intense and the consistency firmer.
In solid organs the infarct appears paler than normal while in spongy tissues
the lesion is red-blue.
In the course of several days, the margins of infarcts become well defined
through the development of a narrow rim of hyperemia. This is due to the
marginal acute inflammatory response (line of demarcation).
The involved surface of the organ is usually covered by Fibrinous inflammatory
exudates (e.g. fibrinous pericarditis in myocardial infarction and Fibrinous
Pleuritis in pulmonary infarction).
2. Microscopical features of infarction:
All the infarcts except those of brain are characterized by ischemic
Coagulative necrosis of constituent cells.
If the vascular occlusion has occurred only a few hours prior to the death of
patient, there may be no demonstrable cellular changes, since there may
have been insufficient time for proteolytic enzymes to degrade dead cells.
The line of demarcation is in essence an acute inflammatory response that
surrounds the area of infarction, separating it from normal tissue. This acute
inflammation gradually invades the infarct. This is followed by a fibroblastic,
reparative response, again beginning at the margins.
Eventually the necrotic focus is gradually replaced by fibrous (scar) tissue. This
process of healing, depending on the size of infarct, may take several months.
The brains differ from other organ in that, the ischemic necrosis is of
Liquefactive type.
With septic infarction, the lesion is converted to an abscess.
Factors that influence the severity of injury resulting
from vascular occlusion:
1. General status of circulating blood and cardiovascular
system.
2. Pattern of blood supply.
3. Speed of occlusion development.
4. Susceptibility of the involved tissue to ischemia e.g.
neuron is the most sensitive and
complete anoxia
for only few minutes may result in irreversible damage.
Note:
There are four patterns of blood supply to various organ
and tissues of the body:
A. Organ with dual blood supply: e.g. lung and
liver.
So occlusion of branches of pulmonary artery is not
enough to cause infarction in the presence of normal
blood and cardiovascular system. This is because
brachial circulation prevents ischemic damage.
Similarly infarction of the liver is extremely rare,
because the portal (venous) blood flow will compensate
for any interference with hepatic arterial flow,
however, in the presence of atherosclerosis, the cardiac
failure, or sever anemia, occlusion of one system may
precipitate infarction.
B. Parallel arterial system: e.g. in the forearm and brain.
Occlusion of either the ulnar or radial artery is usually without
significant effect because the other artery will compensate.
The brain with its circle of Willis is protected from ischemic injury
resulting from occlusion at any point within the circle or in one of
the major artery supplying the circle.
C. A single arterial supply with rich inter-arterial
anastmosis: e.g. in small intestine and heart.
D. Single artery supply with no anastmosis (end- arteries):e.g.
kidneys.
The major branches of renal artery supply well-defined segments
of the kidney and occlusion of the one of these or the main artery
is almost invariably result in renal infarction.
Clinical significant of infarctions:
Cardio-vascular diseases are the most common cause of
deaths. Most of death results from myocardial and cerebral
infarction.
- Pulmonary infarction is a common complication in certain
clinical setting.
- Renal infarction unlike the above example, dose not as a
rule endangers life but is an
occasional cause of
renal failure.
- Ischemic necrosis of the lower limbs (gangrene) is a
major complication of diabetes.
Shock:
Definition: This is referring to a wide spread hypo-perfusion of cells
and tissues of the body
due to:
1. Reduction in the blood volume itself. Or
2. Reduction in cardiac output.
Or
3. Redistribution of blood within the microcirculation causing
insufficiency of effective
circulating blood volumes.
Thus in shock there is a profound circulatory failure that may result in
life-threatening hypo-perfusion of vital organs.
This widespread hypo-perfusion of shock results in:
1. Insufficient supply of oxygen and nutrients to the tissues.
2. Inadequate clearance of metabolites.
The hypoxia induces a shift from aerobic to an aerobic metabolism a by
products of latter is lactic acid with resulting drop in the PH of the
cells and sometime lactic acidosis.
At the begging, the homodynamic and metabolic disturbances induce
reversible cell injury, but if these disturbances are not corrected
rapidly the situation become worse and irreversible injury of cells
occurs that eventually leads to death of patient.
Types (classification) of shock:
1. Cardio-genic shock.
2. Hypo-volemic shock.
3. Septic shock.
4. Neurogenic shock.
5. Anaphylactic shock.
Clinical examples of these include:
Cardio-genic shock:
A. Myocardial infarction.
B. Arrhythmias.
C. Rupture of the heart.
D. Pulmonary embolism.
E. Cardiac temponade.
Hypo-volemic shock:
A. Hemorrhage: either internal or external.
B. Fluid depletion: e.g. sever continuous vomiting and/or diarrhea and extensive burns.
Septic shock: Induce by gram positive or gram negative septicemia.
Neurogenic shock: A. Anesthesia.
B. Spinal cord injury.
Anaphylactic shock: Hyper-sensitivity to drugs e.g. penicillin.
The principal mechanisms operating in these categories of shocks are as
follows:
Cardiogenic shock (pump failure): i.e. here there is reduction in cardiac
output.
This may result from myocardial damage (infarction), ventricular arrhythmia,
pressure on the heart from outside (cardiac temponade) or outflow
obstruction (pulmonary embolism).
Cardiac temponade:
Slowly developing pericardial effusion of less than 500 ml produce no effects on
cardiac function, however, rapidly developing fluid collection of as little as
200 to 300 ml may produce compression of the thin –walled atria and even
cavae and sometimes even the ventricles themselves. As a result one
prominent example of the condition that may produce potentially fatal
cardiac temponade is Hemopericardium. This may complicate:
1. Rupturing myocardial infarction.
2. Traumatic perforation.
3. Infective endocarditis.
4. Rupture aortic dissection (dissecting aneurysm) at the root of the aorta.
Hypo-volemic shock: In adequate blood or plasma volume due to loss.
Septic shock: This is caused by systemic bacterial infection, particularly with
gram-negative infection (endo-toxic shock), however it has been reported with
gram positive and fungal infections.
Endotoxins are bacterial wall lipopolysacchrides that are released when the cell
wall degraded for e.g. through the following reaction against the bacteria.
Lipopolysacchrides contains toxic fatty acids (lipid A), all the effect of septic
shock may be reproduce by injecting lipopolysacchrides alone.
At low doses, lipopolysacchrides activates macrophage and complement system
that help in eradicating the invading bacteria.
With high doses of lipopolysacchrides (as in septicemia), the syndrome of septic
shock supervenes. This is mediated through various cytokines (such as
interleukins-1 and tissue necrosis factor) and other mediator.
These at high level result in:
1. Systemic peripheral vasodilatation…………pooling of blood and hypotension.
2. Reduce myocardial contractility.
3. Wide spread endothelial injury and activation.
4. Activation of coagulation system that eventuates in DIC.
5. Cell membrane injury including endothelial cell, platelets, WBC with result
activation of
coagulation system that sometime lead to DIC.
Neurogenic shock: As due to anesthetic accident
and spinal cord injury. The loss of vascular tone
(dilatation) that leads to peripheral
vasodilatation with pooling of blood.
Anaphylactic shock: This is initiated by
generalized IGE-mediated hypersensitivity
response. The effects include wide spread
vasodilatation with pooling of blood and increase
vascular permeability that lead to decrease in
intravascular blood volume.
Stages of shock:
Shock is a progressive disorder and if not rapidly dealt
with, it will pass into deeper levels of hemodynemic and
metabolic deterioration.
The progression may be very rapid (within minutes) as in
massive hemorrhage such as that resulting from rupture of
aortic aneurysm or traumatic injury to the aorta, however
the progression is usually slow and take several hours.
So the shock progression can be divided into three stages:
1. Early (compensated) stage.
2. Progressive (decompensate) stage.
3. Irreversible stage.
1. Early (compensated) stage:
Here the compensatory mechanism operates to maintain
cardiac output and blood pressure near normal levels so
that the blood supply to vital organs remains largely
unaffected.
The compensatory mechanisms include:
A. Arteriolar constriction leading to increase in peripheral
resistance and hence elevation of blood pressure.
B. Increase heart rate to increase cardiac output.
C. Retention of fluid through:
1. Increase secretion of ADH.
2. Activation of renin-angiotensin-aldestron axis.
2. Progressive (decompensate) stage:
It occur if underlying cause is not dealt with or an
additional aggravating factors is added e.g. extensive burn
complicated by bacterial infection or hypo-volemia in the
elderly complicated with myocardial infarction. With this
stage thing will go from bad to worse because despite the
assistance of above mentioned compensatory mechanism,
there is decline in both blood pressure and cardiac output.
The consequences of this are the clinically observed increase
in respiratory rate and decrease in urine output, reflecting
pulmonary and renal hypo perfusion respectively.
The resultant hypoxias (hypoxemia) cause the cells to switch
over to anaerobic glycolysis that result in metabolic (lactic)
acidosis.
3. Irreversible stage:
Represent the point of no return i.e. even the correction
of the hemodynemic disturbance dose not stop the
progressive downwards deterioration, namely the
progressive reduction of cardiac output and blood pressure
as well as worsening of metabolic acidosis. These result in:
- Irreversible injury to the cells membrane as manifested by
paralysis of sodium-potassium and calcium pump that is
followed by gross defect in cell membrane itself, the result
is extrusion
of the cell contents to outside.
- The reduction of blood flow to vital organ such as the brain
and heart, lead to ischemic cell
deaths in these organs.
Pathological changes in shock:
These are basically in form of hypoxic injury that affects various organs and
tissues; however certain organs are much more severely affected than others.
This is due to:
1. Shunting of blood to vital organ such as brain, heart result in deprivation
of the other organs e.g. GIT, kidneys.
2. Differing cellular susceptibility to hypoxic and metabolic injury.
Shocks characterized by failure of multiple organs, ischemic and metabolic
injuries that threaten life are those of brain, heart, lung and kidneys.
However changes are also frequent in GIT, liver and adrenal.
The pathological changes may occur in any tissue but they are particularly
evident in the following:
- The brain: Show changes collectively known as Ischemic encephalopathy.
- The heart: Three types of changes occur:
1. Focal and widespread Coagulative necrosis.
2. Sub-endocardial hemorrhage.
3. Contraction bands of the cardiac muscles fibers, these appear as opaque,
transfer darkly staining area.
- Lung: The changes are those of diffuse alveolar damage and
are referred as shock lung or
acute respiratory
distress syndrome (ARDS). These changes are in essence
those of
pulmonary edema and fibrin deposition
on the alveolar walls. This syndrome is particularly
seen
in septic shock or trauma.
-Kidney: The tubules are affected principally and the changes
are those of extensive ischemic tubular injury (acute
tubular necrosis).
- Liver: It may show fatty changes and in sever cases, central
hemorrhagic necrosis (i.e. affecting the centri-lobular area).
- Intestine: May show patchy hemorrhages of mucosa
referred to as hemorrhagic enteropathy.
Note: With except of neural and myocardial loss, almost all
these tissue changes may revert to normal if the patient
survives.