Why liquefactive necrosis in Brain ?

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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