EMBOLISM

The process of partial or complete

obstruction of some part of
cardiovascular system by any mass
carried in the circulation.

The transported intravascular mass

detached from its original is called
EMBOLUS.
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Types:
1. Depending upon the matter:
 Solid eg: thromboembolism,
atheromatous material, tumor cells.
 Liquid eg: fat globules, amniotic fluid,
bone marrow.
 Gaseous eg: air, other gases.

2. Depending upon whether infected or not:

 Bland- when sterile
 Septic- when infected
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3. Depending upon source:
 Cardiac emboli from left side of
heart.
 Arterial emboli from systemic
arteries.
 Venous emboli eg: pulmonary
arteries
 Lymphatic emboli
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4. Depending upon flow of blood:
 Paradoxical embolus or crossed
embolus: an embolus which is
carried from the venous circulation
to the arterial side or vice versa.
 Retrograde embolus: An embolus
which travels against the flow of
blood
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Thromboembolism: detached thrombus or part of
thrombus constitutes common type of embolism.
Arterial (systemic) thromboembolism:
 Causes within heart(80-85%):These are mural
thrombi in left atrium or left ventricle, vegetations
on the mitral or aortic valve, prosthetic heart
valves.
 Causes within arteries: emboli developing in relation
to atherosclerotic plaques, aortic aneurysm,
pulmonary veins & paradoxical arterial emboli from
systemic venous circulation.
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Effects of arterial emboli: depends upon
their size, site of dislodgement &
adequacy of collateral circulation.
1. Infarction: organ or affected part of
organ spleen, kidneys, brain, intestine.
2. Gangrene: following infarction in the
lower limbs.
3. Arteritis & mycotic aneurysm: from
bacterial endocarditis.
4. Myocardial infarction: following coronary
embolism.
5. Sudden death: following coronary
embolism or embolism in middle
cerebral artery.
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Venous thromboembolism: may arise
from following source.
 Thrombi in veins of lower legs.

 Thrombi in pelvic veins.

 Thrombi in veins of upper limbs.

 Thrombosis in cavernous sinus of the

brain.
 Thrombi in right of heart.
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Effect of venous embolism is
obstruction of pulmonary arterial
circulation.

Pulmonary thromboembolism:
common fatal form of venous
thromboembolism in which there is
occlusion of pulmonary arterial tree.
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Pulmonary thromboembolism
Etiology: Common in hospitalized or bed-
ridden patients.
 Thrombi originating from large veins in
lower limbs (popliteal, femoral, iliac).
 Less common, thrombi in varicosities of
superficial veins of the legs & pelvic veins.
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Pathogenesis: Thrombi detached from
any of above site produce
thromboembolism into right side of
heart.
 If thrombus is large & impacted at the
bifurcation of the main pulmonary
artery (saddle embolus) or may be
found in right ventricle or its outflow.
 Commonly, multiple emboli or a large
embolus may be fragmented into
smaller emboli & impacted in number
of vessels, affecting lower lobes.
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 Rarely, paradoxical embolism may occur
from right heart into left heart through
atrial or ventricular septal defect.
Consequences: Depend on size of
occluded vessel, number of emboli &
cardiovascular status of patient.
 Sudden death: Massive pulmonary
embolism. If death delayed then
dyspnoea, chest pain & shock.
 Acute cor pulmonale: Multiple small
emboli may obstruct- right heart failure.
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 Pulmonary infarction: obstruction of
small size arteries. Features-
fibrinous pleuritis, haemoptysis &
dyspnoea.
 Pulmonary hemorrhage: obstruction
of terminal branches (end arteries).
Features – haemoptysis, dyspnoea,
chest pain.
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 Resolution: Small pulmonary emboli

are resolved by fibrinolytic activity.
 Pulmonary HTN, Chr. Cor pulmonale &
pulmonary arteriosclerosis: Multiple
small emboli undergoing healing than
resolution.
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Systemic embolism: Arterial embolism
arising from thrombi from diseased
heart, especially left heart.
Diseases of heart:
 MI
 RHD
 Cardiomyopathy
 Congenital heart disease
 Infective endocarditis
 Prosthetic heart valves
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Consequences:
Infarction at the site of lodgment
include in descending order of
frequency, lower extremity, brain &
internal organs like brain, spleen,
kidney, intestines.
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Tumor embolism:
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Fat embolism: Obstruction of arterioles &

capillaries by fat globule. Obstruction
by adipose tissue fragments is known
as FAT TISSUE EMBOLISM.
Causes:
 Traumatic :

1. Trauma to bones

2. Trauma to soft tissue- laceration of

adipose tissue & in puerperium due to
injury to pelvic fatty tissue.
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 Non-traumatic:
1. Extensive burns
2. Diabetes mellitus
3. Fatty liver
4. Pancreatitis
5. Sickle cell anemia
6. Decompression sickness
7. Inflammation of bones & soft tissue
8. Extrinsic fat & oils introduced into
body
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Pathogenesis:
1. Mechanical theory

2. Emulsion instability theory

3. Intravascular coagulation theory

4. Toxic injury theory

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Consequences:
Pulmonary fat embolism:

Systemic fat embolism:

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Amniotic fluid embolism:
During labour & in immediate post-
partum period, the contents of
amniotic fluid may enter the uterine
veins & reach right side of heart
resulting in fatal complications.
Amniotic fluid embolus: epithelial
squames, vernix caseosa, lanugo
hair, bile from meconium & mucus.
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Clinical syndrome:
 Sudden respiratory distress & dysponea

 Deep cyanosis

 Cardiovascular shock

 Convulsions

 Coma

 Unexpected death- mechanical blockage,

anaphylactoid reaction, DIC,
haemorrhagic manifestations due to
thrombocytopenia & afibrinogenaemia.
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Gas embolism: Air, nitrogen & other gases
can produce bubbles within circulation &
obstruct the flow.
Air embolism: when air is introduced into
arterial or venous circulation.
Venous air embolism: Causes
1. Operations on head, neck, & trauma.
2. Obstetrical operations & trauma.
3. Intravenous administration of blood &
fluid.
4. Angiography.
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Effects depend upon following factors:
1. Amount of air- 100-150 ml fatal
2. Rapidity of entry.
3. Position of patient.
4. General condition of patient.

Arterial air embolism:

1. Cardiothoracic surgeries.
2. Paradoxical air embolus
3. Arteriography
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Decompression Sickness/Caisson’s disease/
Diver’s Palsy: Special form of gas embolism.
Pathogenesis: produced when the individual
decompresses suddenly, either from high
atmospheric pressure to normal level, or from
normal pressure to low atmospheric pressure.
Effects depend upon:
 Depth or altitude

 Duration of exposure to altered pressure

 Rate of ascend or descent

 General condition of the individual

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Clinical Effects:
 Acute

1. The “bends”: patient doubles in bed due

to acute pain in joints, ligaments &
tendons.
2. The “chokes”: due to accumulation of
bubbles in the lungs, resulting in acute
pulmonary distress.
3. Cerebral effects: vertigo, coma &
sometimes death.
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 Chronic
1. Avascular necrosis of bones :eg- head
femur, tibia, humerus.
2. Neurological symptoms : ischaemic necrosis
in CNS. Peraesthesias & paraplegia.
3. Lung involvement: haemorrhage, oedema,
emphysema & atelactasis. Dyspnoea, non-
productive cough & chest pain.
4. Skin manifestation: itching, patchy
erythema, cyanosis & oedema
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