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 emboliNumber of emboliCirculatory 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 disease5% cardiomyopathy
SYSTEMIC EMBOLISM
OTHER LESS COMMON SOURCESAtherosclerotic plaquesAortic aneurysms Infective endocarditisValvular heart diseasesParadoxical 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 cyanosisC.V.S shockGeneralized convulsionsComaExcessive bleeding from birth canalDIC (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 circulationDuring obstetric proceduresChest wall injury>100 cc to produce clinical effectTissue damage
2 types AcuteChronic - 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 bonesSignificant soft tissue traumaDiabetes mellitusPancreatitis
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 petechiaeMental confusionGlobules of fat in urine
FAT EMBOLISM
Morphologyconfirmed at autopsyslices of lung squeezed under
salinefat 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