THROMBOSIS

The Primary influences that predisposes to

thrombosis (virchows triad).
Endothdial Injury
Stasis or turbulences of blood.
Blood hypercoagulability.
Endothelial injury.
This the dominant influence.
By itself can lead to Thrombosis
Important in formation of Thrombus in heart
or arterial circulation.
In these two site high flow rate usually
hampers dotting by:

Preventing platelet adhesion

Dilution of coagulation factors.Endothelial
injury Endothelial contributes to Endothelial
Injury.
Thorumbus Formation in Heart Chambers.
e.g Following Myocardial Interchor.
Over Ulcerated plaque of clerosis.
Or site of traumatic or Inflammatory Vascular
Injury.
Physical injury to endothelium Exposes
subendothelial ECM(allows adhesion of platelets,
and release of tissue factor- favour coagualtion.
Note that Endothelial injury may contribute to
thrombus even when endothelium is not
completely disrupted.
Thrombus results due to inbalance between
pro- and antithrombotic effects.

Significant disruption endothelial, Functions may

occur(In Absence of endothelial cell loss)in:
Stress of hypertension.
Turbulence of blood flow.
Scarred Vulves.
Bacterial Toxin.
Ateration in normal blood flow.
Contributes to cardiac or arterial thrombosis
by: Causing endothelial injury or dysfunction.
: Causing countercurrents and pockets of
stasis
Normal Blood flow is Luminar i.e
Formed Elements as platelets flow in central axis
Separated from endothelium by slow-flowing
plasma.
Stasis and turbulence
Bring platelets into contact with endothelium.
Prevents dilution of activated clotting factors by
flesh blood.
Retards inflow of clotting factor inhibitors.
Also permits build-up of thrombi.
Stasis is a major factor in development of
venours thrombi clinical setting enter turbulence
and stasis contribules to thrombosis;
 Ulcerated atherosclerotic plaques
Exposes subendothelial ECM
Also creates a source of turbulence.

Aneurysms(abnormal aortic/arterial delations)

Causes stasis and therefore favours thrombosis

MYOCARDIAL INFARCTION
Causes endothelial injury
Non contractile myocardium brings an element of
stasis.
MITRAL Valve stenis eg 2 Rbeumatic heart
disease
Causes left anterial dilation
Profound stasis favors thrombosis.
HYPERCOAGULABILITY
Less frequent cause of thrombosis but
important
Defined as alteration in coagulation pathway
predisposing to thrombosis
Can be Primary (genetic) or Secondary
(acquired) disorder.
 Most common inherited causes are;
Mutation of factor v gene
Mutation of Prothrombin gene.
Acquired disorders leading to thrombosis
occurs in common clinical settings:
Examples
Cardiac failure or trauma;
Due to stasis
Vascular injury
Oral Contraceptives and Hyperoestrogenic
state of Pregnancy
Disseminated cancer(Release of
Procoagulant factors)
Hypercoagulabily of advance age may be due
to;
 Susceptibility to platelets aggregation
Smoking and obesity – promotes
hypercoagulability – reason unknown.

MORPHOLOGY
 Thrombi May develop anywhere in
cardiovascular system.
Are of Variable size and shape depending on
Size
Circumstances leaving to Development
Arterial or Cardiac Thrombi usually begins at
site of endothelial injury or;
At area of turbulence e.g. vessel bifurcation.
Venous thrombi characteristically occur at site
of stasis.
Arterial thrombi tends to grow in retrograde
direction.
Venous thrombi- Direction of Blood flow.
Propagating fail may not be well attached
(especially venous)
May detach causing embolus.
When arterial thrombi arise in Heart
Chambers of aortic Lumen are termed Mural
thrombi.
Common causes of Thrombi in Heart;
Abnormal myocardial contraction (arrythmias)
Dilated Myocardiapathy.
Myocaridal infarction.

Aortic thrombus
Ulcerated atherosclerotic plaque
Aneurysms

Arterial thrombi are usually occlusive the

commonest site in descending order.
Coronary arteries
Cerebral arteris
Femoral arteries

Venous Thrombosis
Almost always oculusive
Creates a long cast along vein lumen.
Because occurs in areas of stasis, there is
more emeshed erythrocytes therefore red.
Venous Thrombosis Commonly affects veins of
Lower extremites(90% of cases)
Less Community in upper limbs.
In special cases: Dura sinuses, portal vein or
hepatic veins.
Under special condations thrombi may form in
heart valves.
FATE OF THROMBUS
If Patient survives initial effects of occlusion
thrombus may undergo the following;

PROPAGATION
Thrombus may accumulate more platelets
and fibrin( Propagate) – eventual Vessel
obstruction.

Embolization
Disloge and travel to other sites of Vasculature.
Dissolution
Thrombi removed by fibronolytic activity.
Organization and recanalization.
Thrombi may induce inflammation and fibrosis
( Organization) and;
Eventually because recanalized and establish
vascular flow.
 Clinic significance
Both Arterial and venous thrombus may
cause vessel occlusion.
Venousthrombus may cause Oedema and
Congestion in various bed distal to
obstruction.
Most dramatic (grave)Conquence is
embonzation to lung – death.

Arterial thrombi may embolize.

But most important is obstruction at
critical sites.
-eg. Coronary artery leading to myocardial
infarction.

Venous thrombosis
Most occurs in superficial or deep veins of legs
Superficial thrombosis
Usually in salphenus vein(vericosity)
 Thrombi usually causes local congestion and
tenderness in affected vein.
Rarely embolizes
Impaired drainage predisposes to infection of
overlying skin from slight trauma – Vericose ulcer.
Deep vein thrombosis- grave due to embolism
Deep vein obstruction may also cause local pain
oedema and congestion
Because of collateral circualtion 50% of affected
patients may be assymptomatic.
Deep vein thrombosis may occur with stasis or
hyrercoagulabilty states
Candiac failure a common cause of venous
stasis.
Trauma, surgery, burns – reduced physical
actibity, injury to vessels, release of
procoagnatants by tissues.

Arterial thrombosis
Atherosclerosis is major contributor.
Cardiac Mural thrombus may occur in setting
to myocardial infarction.
Rheumatic heart diseases may results into
artrial mural thrombus( Mitral valve stenosis)
In addation to consequences of obstruction
may embolise Virtually to any tissue.
Primciple targets, brain, kidney, spleen (Large
volume of flow).

EMBOLISM
Defn: Detached intravascular solid, fluid or
gaseous mass that is carried by blood to distant
site from origin.
Almost all emboli represent some disloged
thrombus hence;
THROMBOEMBOLISM
Unless otherwise stated embolism reffers to
thromboembolism.
Emboa lodges in a vessel to small to allow
further passage.
May lead to partial or complete vascular
occlusion.
Consequence of occlusion is ischaemic
necrosis of distal tissue ( infarction)
Depending on site of origin may lodge
anyway in vascular tree.
Clinical consequence depends whether emboi
hodges in pulmonary or systemic circulation.

Pulmonary thromboembolism
Common in hospitalized patient.
In 95% of pulmonary embolism the origin is
thrombus in deep vein of leg.
Carried through right side of heart to
pumonary vasculature.

Depending on size;
May occlude Main Pulmonary artery.
 Impact across bifurcation(saddle embolus)
Pass into smaller branches.
Frequently there may be multiple smaller
emboli( shower from a single large mass)
In general a person with one pulmonary
embolus is at risk of having more.
Rarely embolus may pass through interatrial or
interventricular defect.
When if this happen it enters systemic
circulation( paradoxical embolism)

CLINICAL CONQUENCES.
Most pulmonary emboli(60-80%) are clinically silent
because they are small
Sudden death, right heart failure or cardivascular collapse
may occur:
When more than 60% of pulmmory circulation is
obstructed.
Embolic obstruction of medium sized arteries may result it
no pumornary haemornhage without infart.
This due to dual blood flow from bronchial
circulation.
Obstruction of small end- artery infarction of
area distal to obstruction.
Multiple emboli. Over time may cause
pumonary hypertension with right heart failure.
SYSTEMIC EMBOLISM
Emboli travelling in arterial circualtion .
Most (80%) arise from intracardiac mural
thrombi
Two third of these associated with left
ventriculary wall infarcts.
Another one quarter dilated fibrilaring left
arteria.
Remainder from;
Aortic oneurysms
Thrombi on ulceraled atheroscleerotic plaque
Valvular vegetations.
About 10-15& systemic embolism are
unknown origin.
Arterial emboli can travel wide to a variety of
sites
Major site of artterialar embolism;
Lower extremites( 75%)
Brain 10%
Lesser exlent, intestines, Spleen, upper extremities.

Consequences depends on;

Extent of collateral circulation in affected tissue.

Vulnerability of tissue to is ch aemia.

The Caliber of Vessel.

In general arterial embolism causes infarction of tissue

downstream to obstruction.