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Embolism and

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

Most emboli are derived from thrombus


Most commonly pulmonary embolism from
venous thrombosis in deep leg veins(DVT)

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

ORIGIN & SITES OF EMBOLIZATION:


Venous:

Systemic veins

Arterial:

Heart or aorta

Paradoxic:

Systemic veins (through septal defect in heart or


AV shunts in lungs)
systemic circulation

Pulmonary arteries
Systemic circulation

*Retrograde: Embolus traveling against the flow of blood (metastatic deposits in


spine from carcinoma prostate due to retrograde embolism through intraspinal
veins from large thoracic & abdominal veins due to increased pressure in body
cavities: during coughing or straining)

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

Most emboli from such


sources will therefore
travel in the blood stream
and arrest in the first
vascular bed they meet . .
. in the lungs . . . hence
pulmonary embolism

Large embolus derived from a


lower extremity deep venous
thrombosis and now impacted in
a pulmonary artery branch.

Effects of pulmonary embolism


Mainly dependant on size
Small emboli may go unnoticed and lyse
May organise and cause some minor
reduction in lung function
If numerous, small emboli can cause quite
marked reduction in lung function over time
Medium sized emboli can cause significant
acute respiratory and cardiac problems
including shortness of breath, haemoptysis,
heart failure
Large emboli can cause sudden death
(saddle embolus)

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

Most commonly arise from the heart


or great vessels (eg. atheroma in
aorta)

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.

FACTORS AFFECTING INFARCTS:


Nature of the vascular supply (dual arterial supply)
Collateral circulation
Rate of development of occlusion
Duration of occlusion
Metabolic needs of the tissue/organ
Vulnerability of the tissue to hypoxia
Brain - < 3 minutes
Heart 0.5-2 hours
Kidney 2-3 hours
Skin fibroblasts - < 24 hours

Oxygen content of blood

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).

White (anemic) infarcts


White (anemic) infarcts occur
With arterial occlusions in solid organs
with end-arterial circulation (such as
heart ,spleen ,and kidney)
Solid tissues

MYOCARDIAL INFARCTION

Examples of
infarcts.
(A) Hemorrhagic, roughly wedge-shaped pulmonary infarct.
(B) Sharply demarcated white infarct in the spleen.

The dominant histologic


characteristic of infarction is
ischemic coagulative necrosis
Most infarcts are ultimately replaced
by scar tissue.
The brain is an exception to these
generalizations ; ischemic injury in
the central nervous system results in
liquefactive necrosis

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.

Gives rise to systemic hypo-perfusion


caused by reduction in:
Cardiac output
The effective circulating blood volume.

The end results are hypotension ,


followed by impaired tissue perfusion
and cellular hypoxia.

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?

(baroreceptor reflexes, release of


catecholamines, activation of renin
angiotensin axis, ADH release, generalized
sympathetic stimulation)
Progressive (organ hypoperfusion)
Irreversible (end organ failure)

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

Essential reading : Chapter 3 Robbins


Basic Pathology Ninth edition Pages 75-97

Thank you

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