Thrombosis and embolism - PowerPoint Presentation

Slide1

Thrombosis and embolism

By Dr S

HomathySlide2

Thrombosis

Thrombosis is the formation of a solid mass (blood clot) from the constituents of blood

Platelets

Fibrin

Entrapped red cells and white cells

Within the heart or vascular system

in a

living organismSlide3

The development of a clot is life-saving when a large vessel ruptures or is severed.

However

, when a thrombus develops within the vascular system, it may be life-threateningSlide4

Thrombosis

is the consequence of inappropriate activation

( pathological) of

the processes of normal

haemostasisSlide5

Normal Haemostasis

Maintain blood in a

fluid, clot-free state

in normal vessels

Also inducing the rapid formation of a localized

haemostatic plug

at the site of injury.

Both are influenced

by

components

of the blood vessel wall

,

platelets

the

clotting sequence.Slide6

The

integrity of the blood vessel wall is crucial in normal

haemostasis

as well as in thrombosis

.Slide7

Normal

Haemostasis

Vessel injury –

brief period of arteriolar

vasoconstriction

(

neurogenic

reflex ,

endothelin

)

Endothelial injury

exposes ECM

(highly

thrombogenic

material).

Platelets adhere to endothelial cells and ECM, and are activated.Slide8

They release their secretary granules.

Platelet aggregation occurs forming haemostatic plug (

Primary

haemostasis

)

Tissue factor (produced by endothelium) activates coagulation –

formation of thrombin which act on

finbrinogen

to form fibrin (

secondary

Haemostsis

)Slide9

The process continues to form the permanent plug formed by polymerized fibrin and platelet aggregates.

At the same time tissue

plasminogen

activator (t-PA) is formed and it limits haemostatic plug.

Fibrinolysis

is also activated to limit haemostatic plug to the site of injurySlide10

Normal Endothelium

Endothelial cells are activated by injury, infection, plasma mediators and cytokines.

They have pro-thrombotic and anti-thrombotic functionsSlide11

Endothelium

The endothelial cells serve to protect against thrombi formation by

Anti-thrombotic properties:

Anti-platelet effect:

Non activated platelets do not adhere to endothelium.

PGI2, and NO (produced by endothelium) prevent platelet adhesion

Anticoagulant properties:

Heparin-like molecule activate anti-thrombin III

Thrombomodulin

binds thrombin which activate protein C (anticoagulant)

Fibrinolytic

properties:

Endothelium synthesize t-PA (

fibrinolysisSlide12

Endothelial cells also have the

procoagulant

properties

Pro-thrombotic properties:

Von

Willebrand

factor:

It enhances binding of platelets to ECM.

2.Tissue factor

Produced by endothelium, it activates extrinsic clotting pathway

Plasminogen

activator inhibitors (PAI)Slide13

Platelets

Platelets

are assigned a central role in normal

haemostasis

and thrombosis.

They

adhere to sites of endothelial injury,

aggregate

to form platelet masses

,Slide14

release granules rich in a variety of secretary products and synthesize several types of prostaglandins.

In normal

haemostasis

, platelets adhere to the severed margins of a vessel within seconds to a few minutes.

The most important stimulus to such adherence is the exposure of collagen fibrilsSlide15

Once adhered, platelets release two types of granules:

(

1) alpha granules which

contain

fibrinogen,

beta

thromboglobulin

,

cationic protein

platelet

factor 4 (

a heparin neutralizing protein

)

(

2) dense bodies, which are rich

in

serotonin,

ADP

,

ATP

ionized calciumSlide16

Initially, the platelet aggregation forms a temporary

haemostatic

plug

which

is friable and easily dislocated in rapidly flowing bloodstreams

at

this time, the clotting sequence leads to the formation of thrombin

which

is the most powerful platelet aggregator yet identifiedSlide17

Platelets :

(1) provide a temporary plug capable of controlling blood flow in small vessels in low pressure systems,

(2) initiate the development of a permanent plug composed of aggregated platelets and fibrin,

(3) release serotonin which augments vasoconstriction and

(4) contributes to the coagulation mechanism.Slide18

Coagulation system

The

coagulation system

plays a major role in normal

haemostasis

.

Maintenance

of normal fluidity of blood involves the interplay between

procoagulants

and anticoagulants

.

When

the

procoagulants

dominate and clotting is triggered inappropriately in the intact cardiovascular system

,

thrombi result

.Slide19

The critical events in blood clotting are the conversion of

prothrombin

to thrombin

the subsequent conversion of soluble fibrinogen into the stable fibrin polymerSlide20

Thrombosis

Thrombosis

is influenced by three major factors

:

VIRCHOW’S TRIAD

(1) injury to vascular endothelium,

(2) alterations in normal blood flow and

(3) alterations in the blood (

hypercoagulability

).Slide21
Slide22

Endothelial injury

Endothelial injury plays a dominant role in the formation of thrombi in

arteries and in the heart.

Once

the endothelium is damaged,

subendothelial

collagen may be exposed and

tissue

thromboplastin

,

etc., is released

and

the sequence of platelet adherence and activation of the clotting sequence

followsSlide23

Endothelial injury occurs in

myocardial infarction,

ulcerated atherosclerosis,

trauma, and

inflammatory disease of vessels.

Endothelial dysfunction is also a predisposing factor for thrombosis.

Eg

:

Hypertension,

bacterial

endotoxins

,

hypercholestrolemia

,

radiation,

cigarette smoking.Slide24

Blood Stasis and Turbulence of Flow

Turbulence enhances endothelial injury.

Stasis enhances venous thrombosis

.

Both result i

n:

Bringing platelets close to endothelium

Accumulation of clotting factors

Prevent clotting factors inhibitors

Endothelial activation

Eg

:

aortic aneurysm,

MI,

valve

stenosis

,

rheumatic heart disease,

hyperviscosity

,

sickle cell disease.Slide25

Stasis and turbulence

Distrupt

laminar flow

Prevent dilution of activated clotting factors by fresh flowing blood

Retard the inflow of clotting factor inhibitors and permits build – up of thrombi

Promote endothelial cell activationSlide26

Hypercoagulability

It is an alteration in coagulation leading to thrombosis.

Primary

: (

genetic

)

Factor V mutation

Prothrombin

mutation

Antithrombin

III deficiency

Protein C or S deficiencySlide27

Secondary

:(

acquired

)

High risk for thrombosis

Prolonged immobilization

Myocardial infarction

Tissue damage

Cancer

Prosthetic cardiac valves

DIC

Lupus anticoagulant

Low risk for thrombosis

AF

Cardiomyopathy

Sickle cell

anaemia

Nephrotic

syndrome

Contraceptive pills

SmokingSlide28

Increased

numbers of platelets,

increased

platelet stickiness,

elevated

levels of fibrinogen,

increased

generation of thrombin, etc

.,

have been identified as causing

hypercoagulability

in various clinical conditions

.Slide29

Special categories among acquired causes

1.Heparin-induced Thrombocytopenia: (

HIT

syndrom

)

When heparin is administered it induces the formation of antibodies that bind platelets and activate them.

Occurs when

unfractionated

heparin is given.

Solution – give low-molecular Wt heparin

Have anticoagulant activity

Do not interact with platelets

Prolonged serum half lifeSlide30

2.Antiphospholipid syndrome (Lupus anticoagulant):

Antibodies to

phospholipid

(

eg

.

Cardiolipin

)

In-vitro: it inhibits coagulation( inhibit assembly of

phospholipid

cpx

)

In-vivo: it induces coagulation

Approximately 20% of patients with a recent

sroke

were found to have

anticardiolipin

antibodySlide31

Morphology

Thrombi

m

ay develop in the heart, arteries, veins and capillaries.

Arterial thrombi and cardiac thrombi occur at site of endothelial injury or turbulence of flow.

Venous thrombi occur in areas of blood stasis.

Thrombi usually are attached to the underlying vessel wall (mural thrombi)Slide32

Arterial thrombi grow back(retrograde direction) to the heart.

Venous thrombi grow toward the heart.Slide33

Arterial and cardiac thrombi are firmly attached to the wall

Grossly and microscopically show

lines of

Zahn

(layers of fibrin and platelets alternate with layers of RBC and WBC.

Implies thrombosis at a site of blood flow

Venous thrombi do no show clear lamination.

Resemble coagulated blood( like clotted in test tube)Slide34

Microscopic appearance of thrombiSlide35

In the heart:

Attached to the underlying structure

Mural thrombi

common causes:

MI,

dilated

cardiomyopathy

,

arrhythmia,

myocarditis

,

valvular

disease.Slide36

In arteries:

common causes:

atherosclerosis,

aneurysm.

Arterial thrombi usually occlude the lumen,

common in

coronary,

cerebral

femoral arteries. Slide37

Deep Vein thrombosis (

phlebothrombosis

)

are almost always occlusive,

Red / stasis thrombi,

90% occur in lower extremities.

Resemble postmortem clots

Firmer , almost always have a point of attachment

Transection

reveal vague strands of pale gray fibrin Slide38

Under special circumstances thrombi may form on heart vales

.

Bacterial and fungal blood-born infection may lead to

valve damage

Development of large thrombotic masses/

vegetations ( infective

endocarditis

)Slide39

Sterile vegetations can also develop on

noninfected

valves(

NBTE

)

Hypercoagulable

states

Libman

-sacks

endocarditis

Occurs in SLESlide40

Classification of Thrombus according to

Color

Pale,

formed of platelets and fibrin

,

small, grayish white, firm and adherent

Red

, formed

of red cells and fibrin

,

dark soft and loosely attached to the vessel

Mixed

, common and has pale and red components

Presence or absence of

bacteria

Infected

or septic

Non infected

or asepticSlide41

Sites of Thrombus Formation

1.Thrombus in veins:

More common because of thin wall and slow blood flow:

Thrombophlebitis

----Septic

Phlebothrombosis

---- occurs in the veins of the calf Ms and femoral ,iliac veins------ pulmonary emboli

In the varicose veinsSlide42

2.Thrombosis in Arteries

less common than veins because of rapid flow and thick elastic wall but occur in arteries affected by:

Atheroma

,

polyarteritis

nodosa

and

thromboangitis

obliterans

(roughness of the

intima

)

Aneurysm due to stasis

Lead to

ischaemiaSlide43

3.Thrombosis in the heart

more common in the

the

left side

Mural---- occur over infarction

Vegetations---- pale over the valve

Auricular--- adherent to valve, if detach called ball thrombus

Agonal

--- red thrombi occurring in Rt. V at the time of death specially lobar pneumonia

Arterial and cardiac thrombosis possibly

embolise

to brain, kidneys, spleenSlide44

Coronary artery thrombosisSlide45

4.Thrombosis in capillaries

(very rare):

occur in acute inflammation ,sever cold and frost biteSlide46
Slide47

Fate of thrombusSlide48

1-septic

thrombus

fragmented by the

proteolytic

enzymes into septic emboli causes

pyaemic

abscesses

2-Aseptic

thrombus

its element disintegrate and form a pale red structure less mass

If

mass is small

it dissolves by

1)

.fibrinolysis(dissolution)

If

mass is large it undergoes

:Slide49

2.Propagation (progression)

3.Embolization

4.Organization and

recanalization

(inflammation and fibrosis)

Slide50

If mass is large it undergoes

Organization

:

the

thrombus is invaded by capillaries and fibroblast

change

to fibrous

mass

lead to permanent vascular occlusion

Organization

and Canalization

;

some

time capillaries dilated and allow Passage of blood through the thrombus;Slide51

Incorporation

:

the

fibrosed

thrombus shrinks from the vascular wall leaving a space which gets lined by endothelium

Dystrophic

calcification

phlebolith

Detachment

aseptic emboli--- infarctions

Propagating

thrombus-

-- due to spread of venous thrombosis Slide52
Slide53

Propagation

progressive spread of thrombosis

distally in arteries

proximally in veinsSlide54

Organisation

reparative process

ingrowth

of fibroblasts and capillaries (similar to granulation tissue)

lumen remains obstructedSlide55

Effects of thrombosis

Arterial

ischaemia

infarction

depends on site and collateral circulation

Venous

congestion

oedema

ischaemia

infarctionSlide56

Post-mortem clots( occur in cardiac chambers after death) there are two types

:

1-Red

or current jelly clot

:

occur when the components of the blood are evenly distributed throughout the clot.

This

type develops when there is rapid clotting of blood

formed

of fibrin ,red and white blood cellsSlide57

2-Yellow or chicken fat clot:

result from a settling and separation of erythrocytes from the fluid phase of the blood.

Such clots occur when postmortem clotting is delayed

which allow sedimentation

of red cells with plasma, fibrin and white cells above.

Slide58

Venous Thrombosis

Superficial:

eg

.

Saphenous

vein

Local

congesion

,

edema,

swelling,

pain,

tenderness,

ischemia,

risk of infection

Rarely

embolizeSlide59

Venous thrombosis

Thrombosis is commoner in vein than in arteries

The venous system is capacious, and of low pressure and velocity

Liable to injury

Two types of venous thrombosis

Phlebothrombosis

Due to stasis of blood in

uninflamed

veins

Usually in the calves of the legs

Thrombophlebitis

Vein wall is inflamed Slide60

Deep Vein Thrombosis

:

eg

.

Popliteal

, femoral, iliac veins.

There is a lot of collaterals so the congestion and edema are not prominent.

50% are asymptomatic

.

Most serious as it

Can

embolizeSlide61

Causes of DVTSlide62

Blood stasis

is common predisposing factor for deep vein thrombosis.

Mostly in leg veins, whenever the cardiac output is reduced

Local factors responsible for regional venous stasis Slide63

Eg.1. General conditions

a.Heart

failure,

b.Shock

due to bleeding, trauma, burn

c.low

metabolic rate

2. Local causes

a. Lack of muscular activity

b. incompetent valves

c.pressure

from outside

Also can occur in variety of

hypercoagulable

state

Eg

: pregnancy ,

cancer (Trousseau syndrome / migratory

thrombophlebitis

)Slide64

Advanced age

Bed rest

Immobilization

Increase the risk of DVT

Reduced physical activity diminishes the milking action of muscles in the lower leg and slows venous returnSlide65

Site affected

Commonly starts in the deep veins of the calf

Then spread to the posterior

tibial

vein

From here it may extend to involve the

Poplitial

, femoral and iliac veins

Even to the IVC

Iliac thrombosis is more common on left side than right ( compression of L iliac vein by the R common iliac artery)Slide66

Pathogenesis of DVT

Five stages

Primary platelet thrombosis

Following trivial

intimal

damage platelets adhere to the vein wall

Aggregate to form a pale thrombus

Stasis is paramount important

Accumulation of clotting factors and

Promote an increase in the Fibrin element-

stabilizes the mass of platelets and lea

ds to the next stage Slide67

2.Coralline thrombus

Primary platelet thrombus encourages further platelet accumulation

Which take the form of upstanding

laminae

growing across the stream

They are bent in the direction of the blood flow by the force of the stream

These

laminae

anastomose

to form an intricate structure

Resemble coralSlide68
Slide69
Slide70

This is an example of a mixed thrombus

Up to this stage it is possible for the process to ceaseSlide71

3.Occluding thrombus

Growth of the coralline thrombus progressively occludes the lumen of the vein.

Causes further stasis

Formation of more thrombus

Which completely occlude the lumen

Trails away from the coralline thrombus in the direction of the blood flow

This thrombus composed of blood clot with a smaller platelet element.

Red thrombusSlide72

4. Consecutive clot

Once the vein is occluded blood flow stops

It stops thrombosis

Can occur only in the streaming blood

Stationary column of blood beyond the occluding thrombus clots to form a consecutive clot.

Which extends up to the entrance of the next venous tributarySlide73

5. Propagated clot

Can occur by two methods

Clot when reaches the entrance of the venous tributary

Lead to the formation of another platelet and coralline thrombus

Occlusion of the

ostium

of the tributary

Then a consecutive clot will form up to the

osteum

of the next venous tributarySlide74

2.

Sometimes the column of blood above the consecutive clot is so stagnant

Forming one long cord of clotted blood

Anchored only at the site of thrombus formation

This clot retracts and lies loose in the vein except at its one point of anchorage

It can easily break off and be carried to the heart as a massive pulmonary embolus.Slide75
Slide76
Slide77

Morphology

Long propagated clot or tail

Red in

colour

With retraction- thin, pale

Loosly

attached

Head (platelet and coralline thrombus)

Is small

Firmly attached to the vein wallSlide78

Clinical features

Remarkably silent

Tenderness

Pain on passive

dorsiflexion

of the foot

(

Homans’s

sign)

Oedema

distal to the obstructed veins

All the clinical signs are unreliable

Frequently the first indication is the occurrence of pulmonary embolism.Slide79

Venous thrombosis Slide80

Specialized diagnostic procedure

Phlebography

Radioactive iodine-

labelled

fibrinogen test

Doppler ultrasound Slide81
Slide82

Complications

Massive pulmonary embolism

Smaller

pulmonary emboli, with or

withoutpulmonary

infarction

Repeated

episodes of silent

embolization

leading to a syndrome of progressive pulmonary HTSlide83

Thrombophlebitis

Inflammation of a vein wall causes damage to the endothelial lining

On

this platelets are

deposisted

Blood

flow is either normal or accelerated

Thrombosis

proceeds to complete obstruction

Thrombus

is so firmly adherent to the wall

Danger

of embolism is negligible except

pyogenic

inflammtionSlide84

DisseminatedIntravascularCoagulation

(DIC)

This condition occurs under two circumstances

Which may be found separately or in combination

The release of clotting factors into the blood stream

Extensive endothelial damageSlide85

The result is the formation of fibrin in the circulation

This produces vascular obstruction and micro-infarction

The extensive intravascular coagulation consumes the coagulation factors

Characteristic features are

Afibrinogenaemia

thrombocytopaenia

Slide86

Disseminated

IntravascularCoagulation

(

DIC

)

Refers to widespread

microthrombi

formation

in capillaries,

arterioles

venulesSlide87

Thrombi are not visible on gross inspection

Leading to circulatory insufficiency:

brain , lung, heart, kidneysSlide88

the development of the multiple thrombi

Although the

fibrinolytic

system is activated, it cannot effectively deal with the large deposits of fibrin.

As

a result, there is rapid consumption and eventually a deficiency of clotting factors,

including

fibrinogen, platelets,

prothrombin

and factor V, VII, and XSlide89

Two effects of DIC are

a sever bleeding

a deficiency of

fibrinogen,

platelets and

prothrombin

is required for the diagnosis of DIC.

Tendency to infarction

Primarily microscopic in extentSlide90

DIC

have bleeding tendencies on hemorrhagic diathesis.

Also

the widespread occlusion of the microcirculation may induce

signs

of shock,

acute

respiratory distress,

central

nervous system depression,

heart

failure or renal

failure.

Affected

tissues may not necessarily disclose the

microthrombi

because of prompt activation of the

fibrinolytic

system.Slide91

Disseminated

IntravascularCoagulation

(

DIC

)

A variety of disorders may be complicated by DIC

In

abruptio

placentae

with amniotic fluid embolism

Intrauterine retention of a dead fetus

Incompatible blood transfusion

After

Sever trauma

Fat embolism

Open-heart surgerySlide92

In the newborn after

Abruptio

placenta

Birth asphyxia

Hypothyroidism

Rhesus

immunisation

Sever infection

Purpura

fulminansSlide93

Metastatic cancers

Usually of prostate

Occationally

of the lung, pancreas stomach

Acute

leukamia

Certain vascular disorders (giant

haemangiomas

, aneurysms of aorta and other large vessels, cyanotic congenital heart disease.Slide94

Clinical features

Bleeding ,

ecchymosis

and

haemorrhage

from the body’s orifices

Thrombocytopaenia

Mild

haemolytic

anaemia

It is an emergency condition

Is treated with transfusion of fresh blood or fibrinogenSlide95

Embolism

Definition

Embolism

is the blockage of a blood vessel by detached intravascular

solid,

liquid or

gaseous mass

That is carried by the blood to a site distant from its point of origin

.

Embolus

:

An insoluble solid, liquid or gaseous mass circulating in blood streamSlide96

Virtually 99% of emboli are

thrombo

-emboli

Arterial (systemic) emboli

Venous (pulmonary) emboliSlide97

Rare forms (

non-thrombotic

)

fat

Bubbles of air / nitrogen

AS debris (cholesterol emboli)

Tumour

fragments

bits of bone marrow

Foreign bodies

Amniotic fluid embolismSlide98

Pulmonary

Thromboembolism

20-25/ 100,000 of hospital patients

95

% coming from DVT (above knee)

Depending

on the size of the embolus it may occlude

main pulmonary artery (Saddle embolus)

in small branches of vessels (multiple)

Paradoxical embolus:

cardiac embolus passing to the right side through

septal

defectSlide99

Effects

of

emboli

of Thrombotic

origin

depends

upon

Size and nature (septic or aseptic)

State of the collateral circulation in affected

organ

Aseptic produces transient ischemia if it has good collateral circulation and infarction if poor

Septic

produces

pyaemic

abscess at

the site

of impaction Slide100

Size of occluded artery

Number

of occluded arteries

Release of pro-

thrombogenic

vs

thrombolytic factors locally

Background cardiovascular statusSlide101

Pathophysiological

consequences of PE

PE

unperfused

but ventilated segment

respiratory compromise

haemodynamic

compromise

↑ resistance to pulmonary blood flowSlide102

Pulmonary

Thromboembolism

Most pulmonary emboli (60-80%) are asymptomatic because they are small.

most organized and incorporated into the vessel wall

Can also lead to right ventricular failure (

cor

pulmonale

) / sudden death.

Cardiovascular collapse occur when 60% or more of the pulmonary circulation is obstructed with emboliSlide103

Obstruction of medium- sized arteries may result

in hemorrhage, and rarely infarction

Obstruction of small vessels lead to small infarctions

Multiple emboli over time may lead to pulmonary hypertensionSlide104

Pulmonary arterial

thrombo

-embolism -

sequelae

Resorption

and resolution (asymptomatic or transient SOB)

Organisation

→ pulmonary hypertension →

cor

pulmonale

Pulmonary

infarction (

pleuritic

chest pain, cough, SOB, haemoptysis,

hypoxaemia

)

Sudden

death Slide105
Slide106
Slide107
Slide108

It is important to differentiate embolus from post-mortem clot

Post mortem clot is

Moist, shiny and gelatinous

Loosely inserted into the pulmonary trunk

Shape conforms to that of the situation where it is found

Thromboembolus

is

Dry, friable and granular

Already retracted in the leg veins

Ripple of platelets may be visible on its surface

Shape does not conform to that of its surroundings

Tightly inserted into the pulmonary tree

Removal is difficultSlide109

Clinical Features

Massive Pulmonary Embolism

Shock

Dyspnea

Apprehension

tachycardia

Sweating

Chest pain

Faintness

Cyanosis

AF

collapse

2/3 die in the first 2 hours.

It is a Medical EmergencySlide110

Dyspnea

73%

•

Pleuritc

Pain 66%

• Cough 43%

• Leg Swelling 33%

• Leg Pain 30%

•

Hemoptysis

15%

• Palpitations 12%

• Wheezing 10%

• Angina-Like pain 5

%Slide111

Differential Diagnosis

Myocardial Infarction.

Dissecting Aortic Aneurysm.

Peumothorax

.

Major Pulmonary Collapse.

Shock.

Perforating Peptic Ulcer.

Acute PancreatitisSlide112

Diagnosis of Pulmonary Embolism (PE)

Clinical picture.

Look for risk or predisposing factors for DVT

Look for ventilation-perfusion mismatch

Testing for PE.

chest radiograph

ECG

Ventilation-perfusion scanning (V/Q scanning).

Angiography

Spiral CT

D-

dimerSlide113

D-

dimer

-A marker for thrombosis and

fibrinolysis

,

can be useful in the exclusion of PE.

Specific conditions that will give positive

Ddimer

tests include

trauma, postoperative state,

malignancies.

-30% with PE will have normal D-

dimerSlide114
Slide115
Slide116

Systemic emboli

80% cardiac

2/3

rd

associated with LV wall infarction

1/4

th

– dilated left atria- in MS

On the mitral or aortic valves- infective

endocarditis

/

valvular

prosthesis

Cardiomyopathy

20% aortic

AS

Aneurysms

Valvular

vegetations

Very small fraction –paradoxical emboliSlide117

Embolization

lodging site is proportional to the degree of flow (cardiac output) that area or organ gets,

Lower extremities (75%)

brain (10%),

kidneys

splanchnic

liver Slide118

Consequence depends on the

extent of the collateral supply in the affected tissue

Tissue’s vulnerability to

ischaemia

Caliber of the vessel occludedSlide119

Effects of systemic emboli

Ischaemia

in various organs

Septic emboli according to anatomical

circumstancesproduce

Pyaemic

abscesses

Septic infarcts

mycotic

aneurysms

Spontaneous

embolistion

can occur with aortic ASSlide120
Slide121
Slide122
Slide123
Slide124

Fat Embolism

A process by which fat emboli passes into the bloodstream and lodges within a blood vessel.

Fat Embolism Syndrome (FES):

serious manifestation of fat embolism occasionally causes multi system dysfunction, the lungs are always involved and next is brainSlide125
Slide126

Causes of FES

Blunt Trauma

Long bone (Femur, tibia, pelvic) factures Slide127

Non Trauma

:

agglutination of

chylomicrons

and VLDL by high levels of plasma CRP.

disease-related

Diabetes,

acute

pancreatitis,

burns

,

SLE

,

sickle

cell crisis

drug-related

parenteral

lipid infusion

procedure-related

Orthopedic surgery, liposuctionSlide128

Pathophysiology of FES

Exact mechanism unknown, but two main hypothesis

Mechanical Hypothesis

Biochemical HypothesisSlide129

Mechanical Hypothesis

Obstruction of vessels and capillaries

Increase in

intermedullary

pressure forces fat and marrow into bloodstream

Bone marrow contents enter the venous system and lodge in the

lungs as emboliSlide130
Slide131

Smaller fat droplets may travel through the pulmonary capillaries into the systemic

circulation and hence to the brain and other organs.

Embolization

to cerebral vessels or renal vessels also leads to central nervous system and renal dysfunctionSlide132

Biochemical Hypothesis

Toxicity of free fatty acids

circulating free fatty acids directly affect

the

pneumocytes

, producing abnormalities in gas exchange

Coexisting shock,

hypovolemia

and sepsis impair liver function and augment toxic effects of free fatty acidsSlide133

hormonal changes caused by trauma and/or sepsis induce systemic release of free fatty acids as

chylomicrons

.

Acute-phase reactants, such as C-reactive proteins, cause

chylomicrons

to coalesce and create the physiologic reactions described above

.

The biochemical theory helps explain

nontraumatic

forms of fat embolism syndrome and why symptoms take 12 hours to

develope

.Slide134

Fat embolism

http://www-medlib.med.utah.edu/WebPathSlide135
Slide136

http://www-medlib.med.utah.edu/WebPathSlide137

Clinical Manifestations

Pulmonary fat embolism

Systemic fat embolism

Fat emboli enters the systemic circulation Slide138

Asymptomatic for the first 12-48 hours

Pulmonary Dysfunction

Respiratory Failure and ARDS (

tachypnea

,

dyspnea

, crackles, cyanosis)

Hypoxemia

systemic arterial hypotension, a decrease in cardiac output, and arrhythmiasSlide139

Systemic fat embolism

Fat emboli enters the systemic circulation

Lodged in the capillaries of the brain, kidney, skin and other organs

Serious event

Constitutes the

fat embolism syndrome

Lungs are certainly always involvedSlide140

In sever cases, the patient become comatose within a few hours of injury

Dies with 1-2 days

Most usually symptoms occur 24-48hours

after

injury

Fever, cyanosis, restlessness, respiratory distress, cerebral symptoms Slide141

Neurological (nonspecific)

acute confusion, headache, stupor, coma, rigidity or convulsions

If brain damage is severe, coma and death results

Dermatological

Signs

A reddish brown

petechial

rash

- helpful diagnostically

But it is not manifest until the 2

nd

or 3

rd

day

distributed to the upper body, chest, neck, upper arm,

axilla

, shoulder, oral mucous membranes and

conjunctivae

Subconjunctival

and retinal

haemorrhages

alsoSlide142

Laboratory Studies

Arterial Blood Gases (ABGs)

Urine and sputum examination

Examination of the urine may reveal fat, the test is unreliable

Haemotological

Tests

Platelet count is invariably lowered

Biochemical testsSlide143

Imagining

Chest x-ray

shows multiple flocculent shadows (snow storm appearance). picture may be complicated by infection or pulmonary edema.

CT Scan brain

may be normal or may reveal diffuse white-matter

petechial

haemorrhages

Helical CT Scan chest

may be normal as the fat droplets are lodged in capillary beds. Can detect lung contusion, acute lung injury, or ARDS may be evident.Slide144

Risk FactorsSlide145

Gaseous emboli

Air may be introduced into a systemic vein in various situations

Operations on the head and neck

Mismanaged blood transfusion

During

haemodialysis

Insufflations of the uterine tubesSlide146

Nitrogen

Enters the circulation in decompression sickness ( caisson disease)

Occurs in people who have been exposed to a high pressure

Eg

:

deep sea divers

those encased in a diving bell(caisson)

under water

tunnellers

returns to a normal atmospheric pressure too rapidlySlide147

As the pressure is reduced

Bubbles of air come out of solution from the blood and interstitial fluid

O

2

and

CO

2

are readily absorbed and removed

Inert nitrogen remains in the tissues for some time

Its presence causes mechanical damageSlide148

Clinical features

Prutitus

Severe pain around the joints and muscle(‘the bends’)

ARDS(‘the chokes’)

Involvement of nervous system

Paralysis

Confusion, seizure, coma and death

Chronic decompression syndrome

Multiple foci of bone necrosis

arthritisSlide149

Amniotic fluid embolism

Amniotic fluid containing

meconium

and

squamous

cells

may enter the uterine veins and travel to the lungs

Characterized by the sudden onset of respiratory difficulty, cyanosis and shock.Slide150