The person who asks a foolish
question is a fool for 5 minutes,
the one who doesn't ask a
question remains a fool forever....
Why liquefactive necrosis in Brain ?
• Because brain cells are rich in lipids and
digestive hydrolytic enzymes, the brain
cells are digested by their own hydrolases
• The brain tissue becomes soft, liquefies,
and is walled off from the healthy tissue to
form cysts
• Liquefactive necrosis can also result from
bacterial infections.
• Here, the hydrolases are released from
the lysosomes of phagocytic neutrophils
that are attracted to the infected area to kill
the bacteria;
EMBOLISM
Definition
Detached, intravascular,
solid, liquid or gaseous mass that
is carried by the blood to a site
distant from its point of origin
• Usually dislodged THROMBUS
(platelets + fibrin + RBC’s +
degenerating WBC’s)
•
•
•
•
•
•
Droplets of fat
Bubbles of air / nitrogen
Cholesterol (atherosclerotic debris)
Tumour fragments
Bits of bone marrow
Foreign bodies
An embolism is usually thrombotic unless
otherwise specified
Thromboembolism
Ischaemic necrosis of distal tissue
( INFARCTION )
TYPES
1. Pulmonary embolism
2. Systemic embolism
• Amniotic fluid embolism
• Air embolism
• Fat embolism
PULMONARY THROMBOEMBOLISM
Majority – clinically silent (60-80%),
undergo organization
If > 60% of pulmonary circulation is
obstructed => SUDDEN DEATH, RHF
PULMONARY EMBOLISM
 More than 95% - the venous emboli arise from the
deep leg vein thrombi above the level of the knee
 Main pulmonary trunk
 Saddle emboli
 Smaller branches
 Small multiple emboli
PULMONARY THROMBOEMBOLISM
If medium sized vessels : usually
haemorrhage, no infarction
If small end arteriole : infarction
Multiple emboli : PHT with RHF
Causes
 cardiac diseases
 cancer
 prolonged immobilization
Hypercoagulable states
Clinical significance depends on
Extent of emboli
Number of emboli
Circulatory state
FATE OF EMBOLI
 may resolve by fibrinolysis
 unresolved




pulmonary H T
pulmonary vascular sclerosis
chronic cor pulmonale
30 % chance of developing second
emboli
 Prophylaxis:
 Elevation
 Elastic bandage
 Early ambulation
 Embolectomy
 UMBRELLA filter in inferior vena cava
Thrombolysis followed by anti coagulation
with monitoring
SYSTEMIC EMBOLISM
Embolism in arterial circulation.
 SOURCE : 80 – 85 % from heart
 60 -65 % from left ventricle ( intracardiac
mural thrombi)
 5 – 10 % rheumatic heart disease
 5% cardiomyopathy
SYSTEMIC EMBOLISM
 OTHER LESS COMMON SOURCES
 Atherosclerotic plaques
 Aortic aneurysms
 Infective endocarditis
 Valvular heart diseases
 Paradoxical emboli from venous thrombi
 UNKNOWN SOURCES 10 – 15 %
PARADOXICAL
EMBOLISM
 Always cause infarction
 SITES :
Lower extremities 70 -75 % (gangrene)
Brain 10 %
Viscera 10 %
Upper limb 7 – 8 %
Factors



collateral vascular supply
tissue’s vulnerability to ischaemia
caliber of occluded vessel
Clinical manifestations : site and size of
emboli is important
femoral artery - gangrene
cerebral artery (MCA) - death in hrs/ days
Treatment :
anticoagulants
embolectomy
AMNIOTIC FLUID EMBOLISM
 Rare complication of labor
 Major cause of maternal mortality
 86% mortality
AMNIOTIC FLUID EMBOLISM
Cause : Tear in placental membrane or
rupture of uterine / cervical veins leading
to infusion of amniotic fluid or fetal tissue
into the maternal circulation
CLINICAL FEATURES:
Deep cyanosis
C.V.S shock
Generalized convulsions
Coma
Excessive bleeding from birth canal
DIC (due to release of thromboplastic
substances)
AMNIOTIC FLUID EMBOLISM
 The pulmonary microcirculation may contain:
-squamous epithelium of fetal skin
-fat from vernix caseosa
-mucin from fetal respiratory and GIT
-bile from meconium stained amniotic fluid
AMNIOTIC FLUID EMBOLISM
 Investigations :
 X-ray evidence in 24 – 36 hours
 Pul. perfusion lung scan alb-labeled with Tec99
 Investigation of choice : pulmonary angiography
AIR OR GAS EMBOLISM
Bubbles of air or gas obstructing circulation
During obstetric procedures
Chest wall injury
>100 cc to produce clinical effect
Tissue damage
 2 types
Acute
Chronic - decompression disease
Acute
 “Bends” - obstruction of small vessels
around joints and skeletal muscles cause
patients to double up with pain
 “Chokes” - respiratory and brain
involvement sudden death
Caisson disease or decompression
sickness
- at risk :
scuba divers, workers in offshore drilling
platforms, underwater tunneling system
workers
When air embolism is suspected at
autopsy organs should be opened under
water to detect escaping gas.
FAT EMBOLISM
 Fat Emboli were first noted by F.A. Zenker in
1861 in a railroad worker with a thoraco-lumbar
crush injury
 The Fat Embolism Syndrome (FES) was first
described by Von Bergman in 1873 in a
diagnosis confirmed by post mortem
examination. This patient had a fractured femur
FAT EMBOLISM
Causes:
Fracture of long bones
Significant soft tissue trauma
Diabetes mellitus
Pancreatitis
FAT EMBOLISM
Clinical Manifestations ( by 1 to 3 days )
 Pulmonary Insufficiency, Anaemia,
Thrombocytopenia ( a diffuse petechial
rash in non-dependent areas in 20-50% cases )
Conjunctival petechiae
Mental confusion
Globules of fat in urine
FAT EMBOLISM
Morphology
confirmed at autopsy
slices of lung squeezed under
saline
fat globules floating on surface
 Mechanism of injury
Mechanical : microemboli of neutral
fat block the pulmonary and
cerebral microvasculature
Biochemical injury to micro vessels .
Release of free fatty acids from the
fat globules - toxic endothelial
injury and activation of coagulation
system
 Microscopic
 Demonstration of fat with frozen
sections and fat staining
(Alcohol in paraffin section dissolves fat)
 Fat stains – Oil red “O”
Sudan black
Air Embolism Practicals
Apr 3rd Friday 9.50 to 12.00 am
Third Floor Laboratory Building
Both Batches