Embolism and infarction

Luc
y Xu
 Embolism
 Embolism is the process of partial or
complete obstruction of some part of
the cardiovascular system by any mass
carried in the circulation.

Embolism Infarction
 Embolus
 The transported intravascular mass de
tached from its site of origin is called a
n embolus.
 Matter
 Solid: detached thrombi (thromboemboli)
 Liquid: fat globules, bone marrow
 Gaseous: air, other gases
 Motional pathway of embolus
 Embolus from left heart cavity or
arterial system
 Embolus from right heart cavity or
venous system
 Embolus from portal veins
 Paradoxical embolism
 Retrograde embolism
 Paradoxical embolus
 An embolus which is
carried from the
venous side of
circulation to the
arterial side or vice
versa.
 Retrograde embolus
 An embolus which travels against the
flow of blood.
 Due to increased pressure in body
cavities.
 Coughing
 Straining
 Thromboembolism
 A detached thrombus or part of
thrombus constitutes the most common
type of embolism.
 The effects depend on whether emboli
lodge in the pulmonary or systemic
circulations.
 Pulmonary thromboembolism
 Are more common in h
ospitalised or bed ridde
n patients.
 Thrombi originating fr
om large veins of low le
gs (95%)
 The pathway of pulmo
nary thromboemboli.
 Pulmonary thromboembolism
 Thrombus is large: saddle embolus
 Pulmonary thromboembolism
 Multiple emboli:
 Smaller emboli
 Impacted in a
number of vessels
 Affecting the lower
lobes of lungs.
 Consequences
 Depend on:
 Size of the occluded vessel
 The number of emboli
 The cardiovascular status of the patient
 Consequences
 Small emboli
 Clinically silent (60%-80%)
 The pulmonary circulation is
obstructed with emboli
 Sudden death
 Right ventricular failure
 Cardiovascular collapse
 Consequences
 Embolic obstruction of medium-sized a
nd terminal arteries
 Pulmonary hemorrhage
but not infarction
 Embolic obstruction of small end arteri
es and pul. congestion
 Usually result in infarction
 Systemic thromboembolism
 Most arise from intracardiac mural thr
ombi:
 Left ventricular wall infarcts
 Dilated left ventricle
 Cause infarction at the sites:
 Lower extremities
 Brain
 Internal visceral organs (spleen, kidney etc)
 Fat embolism
 Obstruction of arterioles and
capillaries by fat globules.
 Causes:
 Fracture of long bones (fatty marrow)
 Soft tissue trauma and burns
 Pathogenesis

20 μm
Pathogenesis
Pathogenesis

Pulmonary fat embolism

Pathogenesis

Osmium stain of fat

 Pathogenesis

Not obstruction of the vast pulmonary

vascular bed, but widespread obstruction of
pulmonary circulation
Pathogenesis

Fat in kidney
 Consequences
 Show no clinical findings (> 90%)
 Systemic fat embolism
 Brain
 Kidney
 Other organs:
petechiae in skin,
conjunctivae, etc.
 Gas embolism
 Air, nitrogen and other gases
 Produce bubbles within the circulation
 Obstruct the blood vessels
 Cause damages to tissue
 Air embolism
 Causes:
 Air may be sucked into veins
• Operation on head and neck
• Trauma involving the major neck veins
 Air embolism
 Usually 100-150ml of air entry is
considered fatal.
 Air emboli entry into the right heart
through pulmonary arterial trunk
 The bubbles of air in the form of froth cause
widespread vascular occlusion
 Right heart failure
Air embolism
 Decompression sickness
 When the individual decompresses
suddenly
 high atmospheric pressure to normal (diver)
 normal pressure to low (pilot)
Decompression sickness
When such an individual ascends too rapidly
The gases come out of the solution as minute bubbles
and may coalesce together to form large emboli
Especially nitrogen

O2 N2
N2 N2 N2
N2 N2
CO2 N2 N2

High atmospheric pressure

Increased amount of atmospheric
gases
 Decompression sickness effects
 Acute form:
 “The bends”:
• As the patient doubles up in bed due to acute
pain in skeletal muscles, joints, and ligments
for the rapid formation of gas bubbles.
 “The chokes”:
• Accumulation of bubbles in the lungs
 Decompression sickness effects
 Chronic form (caisson disease):
 Due to foci of ischemic necrosis throughout
body, especially the skeletal system.
 Amniotic fluid embolism
 During:
 labour
 immediate postpartum period
 Emboli:
 Contents of amniotic fluid
 Sites:
 Uterine veins
 Reach the right heart
 Amniotic fluid embolism
 Pathologic changes:
 Notable changes are seen in the lung
 Hemorrhages
 Congestion
 Edema
 Changes of ARDS
 Dilation of right side of heart
Amniotic fluid embolism

Gravid uterus Air embolism (in veins)

Amniotic fluid embolism

Squamous cells
Amniotic fluid embolism

lanugo hairs polarize

edema, congestion
hemorrhage
 Amniotic fluid embolism
 Consequences:
 Sudden death
• Severe dyspnea, cyanosis and shock
• Seizures and coma
 Survive
• DIC
• Pulmonary edema
 Infarction
 An infarction is an area of ischemic
necrosis caused by occlusion of either
the arterial supply or the venous
drainage in a particular tissue.
 Etiology
 Thrombotic or embolic events
 Almost all result from arterial occlusion
 Local vasospasm
 Expansion of atheroma
 Twisting of the vessels
 Factors that influence infarct
 the nature of the vascular supply
 the rate of development of the occlusio
n
 the vulnerability of a given tissue to hy
poxia
 the blood oxygen content
 Types of infarction
 Color
 Pale or anemic
 Red or hemorrhagic
 Age
 Recent or fresh
 Old or healed
 presence or absence of infection
 Bland or septic
 Red infarction
 With venous occlusions
 In tissues
 with dual circulation
(lung or small intestine)
 bypass circled
 loose
 previously congested
 Pale infarction
 Arterial occlusion
 Solid organs
 Heart
 Spleen
 Kidney
 Shape of infarction
 The lateral margins may be irregular
 Reflecting the pattern of vascular
supply from adjacent vessels

Different range of infarction caused by

different artery branch blocking in kidney
 Shape of infarction
 Tend to be wedge shaped

The apex pointing towards the occluded artery

Margins
red – hemorrhage / brown – hemosiderin / disappear

The wide base on the surface of the organ

 Shape of infarction
 Wedge shaped  Map shaped  Segment shaped
 Kidney  Heart  Small intestine
 Spleen
 Infarct lung
The pulmonary artery ordinarily does not HOW?
produce infarcts because lungs receive blood
supply from bronchial arteries as well.

Pulmonary artery Pulmonary vein

Bronchial artery Bronchial vein

CVC lung
When combined with left heart failure, because of the increased pressure
of pulmonary vein and pulmonary congestion, the blood flow of bronchial
circulation can not overcome the resistance of pulmonary vein.
 Infarct lung

Wedge shaped, hemorrhagic Often in the lower lobes

Infarct lung

Cut surface is dark purple

Roughly wedge shaped
Infarct lung

Coagulative necrosis of the alveolar walls

Intense alveolar capillary congestion
These place will be taken by haemosiderin,
phagocytes and granulation tissue
 Infarct kidney
 Caused by thromboemboli

The infarction is pale and the margins are red

Wedge-shaped with base resting under the
capsule and apex pointing towards the medulla
Infarct kidney

An old kidney infarct, now represented

by a large depressed fibrotic cortical scar
 Infarct kidney

Necrotic region

Inflammatory response
Infarct kidney

Coagulative necrosis
Ghosts of renal tubules and glomeruli without
intact nuclei and cytoplasmic content.
Infarct spleen

Often multiple
Pale and wedge-shaped
 Infarct brain

Cerebral infarction
The brain is an exception to these generalizations; like o
ther causes of necrosis, ischemic tissue injury in the ce
ntral nervous system results in liquefactive necrosis.
Infarct brain

Liquefactive necrosis.
 Infarct of most commonly affected organs

GROSS
LOCATION OUTCOME
APPEARANCE
Myocardium Pale Frequently fatal
Lung Hemorrhage Less commonly tatal
Brain Hemorrhage or pale Fatal if massive
Intestine Hemorrhage Frequently fatal
Not lethal unless
Kidney Pale
massive and bilateral
Spleen Pale Not lethal
Lower extremity Pale Not lethal
summary
rupture of hemorrhage
blood vessel
integrality
permeability↑ edema

artery hyperemia
much
Blood volume vein congestion

little ischemia

thrombosis

embolization
Characters of blood

infarction