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Infarction
Dr Raihan Sajid
msajid@alfaisal.edu
Embolism
Embolism
A mass of material [embolus] that can move
in the vascular system and occlude down
stream vessel
EMBOLISM
It is the process of carrying an abnormal mass (embolus)
in the blood stream to a point distant from its origin .
*An embolus is a detached intravascular solid, liquid or gaseous mass
that is carried by the blood to a site distant from its point of origin
Systemic veins
Arterial:
Heart or aorta
Paradoxic:
Pulmonary arteries
Systemic circulation
Types of embolus
Thromboembolism (the most common!
>90%)
Others
Atheromatous emboli
Amniotic fluid
Air/Gas
Fat
Foreign material (i.v. drug abusers)
Atheromatous emoboli
Due to a plaque that dislodges
Characterized by the presence of
cholesterol clefts/crystals in the
embolus
Fat embolism
Associated with trauma,
especially fractured long
bones
Characterized by
dyspnea (shortness of
breath)because of
involvement of blood
vessel of lung
demonstrated by sudan
black on special staining
Air/Gas embolism
Deep sea divers
bends due to nitrogen in joints and
muscles
Chokes due to respiratory symptoms
Chronic form Caisson disease
Also can occur during pumping of air
during laparoscopic surgery
Amniotic embolism
During parturition
presence of dead
foetal material
(squamous cells
and keratin debris)
in maternal
pulmonary
circulation
Presents with
dyspnea and DIC
Pulmonary embolism
&DVT
95% of venous thrombosis
is in the deep leg veins
the rest in deep pelvic veins
or
intra cranial venous sinuses
Systemic (arterial)
embolism
Arise in the arterial system
Effects depend on
size of the emboli,
their number
the size of the vessels
the nature of the tissue
Sources of
arterial emboli
Common sites
of infarction
as a
consequence
of arterial
emboli
Sources and
effects of
venous emboli
Infarction
Dr Raihan Sajid
msajid@alfaisal.edu
Definition
An infarct is an area of ischemic
necrosis caused by occlusion of
either the arterial supply or the
venous drainage in a particular tissue
Nearly 99% of all infarcts result from
thromboembolic events ,and almost all
result from arterial occlusion.
Red (hemorrhagic)
Infarcts are classified on the basis of their
color (reflecting the amount of
hemorrhage) and the presence or
absence of microbial infection
Red (hemorrhagic) infarcts occur
with venous occlusions (such as in ovarian
torsion and in testes)
In loose tissues (such as lung)
In tissues with dual circulations (e.g. lung and
small intestine).
MYOCARDIAL INFARCTION
Examples of
infarcts.
(A) Hemorrhagic, roughly wedge-shaped pulmonary infarct.
(B) Sharply demarcated white infarct in the spleen.
Remote
kidney
infarct, now
replaced by
a large
fibrotic
cortical
scar.
Septic infarctions
Septic infarctions may develop when
embolization occurs by
fragmentation of a bacterial
vegetation from a heart valve or
when microbes seed an area of
necrotic tissue.
Shock
Definition
Shock, or cardiovascular collapse, is
the final common pathway for a
number of potentially lethal clinical
events, including severe hemorrhage
, extensive trauma or burns, large
myocardial infarction, massive
pulmonary embolism, and microbial
sepsis.
Type of shock
Clinical example
Mechanism
Cardiogenic
Ventricular rupture
Arrhythmia
Cardiac tamponade
Pulmonary embolism
Myocardial infarction
Failure of myocardial
pump owing to
intrinsic myocardial
damage, extrinsic
pressure , or
obstruction to outflow
Hypovolemic
Hemorrhage
Fluid loss vomiting ,
diarrhea , burns , or trauma
Inadequate blood or
plasma volume
Septic
Overwhelming microbial
infections
Endotoxic shock
Gram-positive septicemia
Fungal sepsis
Peripheral vasodilation
and pooling of blood ;
endothelial activation /
injury ;
leukocyte- induced
damage ;
disseminated
intravascular
coagulation ;
Less commonly:
Neurogenic shock-in the setting of
anesthetic accident or spinal cord
injury, owing to loss of vascular tone
and peripheral pooling of blood.
Anaphylactic shock, initiated by a
generalized IgE- mediated
hypersensitivity response, is associated
with systemic vasodilatation and
increased vascular permeability
Clinical course
The clinical manifestations depend on
the precipitating insult.
In hypovolemic and cardiogenic shock,
the patient presents with hypotension;
a weak, rapid pulse; tachypnea; and
cool, clammy, cyanotic skin.
In septic shock, the skin may initially
be warm and flushed because of
peripheral vasodilation
Stages of shock
Non-progressive (compensated)
Compensatory mechanisms?
Pathogenesis
or pathogenic pathways in septic shock. Microbial products activate endothelial cells and cellular and humoral elements of the innate immune system, initiating a cascade of even
d to end-stage multiorgan failure.
Morphological changes
Changes of hypoxic injury and microthrombi in any tissue particularly in brain,
heart, lungs, kidneys, gastrointestinal
tract.
Kidneys: ATN
Lungs: Diffuse alveolar damage
Skin: Petechial hemorrhages
Thank you