Thrombosis is caused by Virchow's triad of endothelial injury, stasis or turbulence of blood, and hypercoagulability. Endothelial injury is the most dominant influence and can lead to thrombosis in the heart or arteries. Alterations in normal blood flow such as stasis and turbulence bring platelets into contact with the endothelium and predispose to thrombosis. Hypercoagulability, either inherited or acquired, also increases the risk of thrombosis. Thrombi may embolize, causing partial or complete occlusion of vessels and ischemic necrosis of distal tissues. Pulmonary embolism is a common complication of deep vein thrombosis in the legs. Systemic embolism usually arises from intracard

1. THROMBOSIS
The Primary influences that predisposes to
thrombosis (virchows triad).
Endothelial Injury
Stasis or turbulences of blood.
Blood hypercoagulability.
Endothelial injury.
This the most dominant influence.
By itself can lead to Thrombosis
Important in formation of Thrombus in heart
or arterial circulation.

2. In these two site high flow rate usually
hampers clotting by:
Preventing platelet adhesion
Dilution of coagulation factors.
Therefore endothelial injury contributes to;
Thrombus Formation in Heart Chambers.
Following Myocardial Infarction.
Arteries
Over Ulcerated plaque of atherosclerosis.
Or site of traumatic or Inflammatory Vascular
Injury.

3. Physical injury to endothelium Exposes
subendothelial ECM(allows adhesion of platelets,
and release of tissue factor- favouring coagulation.
Note that Endothelial injury may contribute to
thrombus even when endothelium is not
completely disrupted.
Thrombus results due to imbalance between
pro- and antithrombotic effects (dysfunction of
endothelium).
Significant disruption of endothelial Functions
may occur(In Absence of endothelial cell loss)in:

4. Stress of hypertension.
Turbulence of blood flow.
Scarred Valves.
Bacterial Toxin.
Alteration 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

5. 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
venous thrombi
 clinical setting that turbulence and stasis
contributes to thrombosis;

6.  Ulcerated atherosclerotic plaques
Exposes subendothelial ECM
Also creates a source of turbulence.
Aneurysms(abnormal aortic/arterial dilations)
Causes stasis and therefore favours thrombosis
MYOCARDIAL INFARCTION
Causes endothelial injury
Non-contractile myocardium brings an element of
stasis.

7. MITRAL Valve stenosis eg in Rheumatic heart
disease
Causes left atrial 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.

8.  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

9. Oral Contraceptives and Hyperestrogenic
state of Pregnancy
Disseminated cancer(Release of
Procoagulant factors)
Hypercoagulabily of advance age may be due
to;
 Susceptability to platelets aggregation
Smoking and obesity – promotes
hypercoagulability – reason unknown.
MORPHOLOGY

10.  Thrombi May develop anywhere in
cardiovascular system.
Are of Variable size and shape depending on
Size
Circumstances leading to their Development
Arterial or Cardiac Thrombi usually begins at
site of endothelial injury or;
At area of turbulence eg vessel bifurcation.
Venous thrombi characteristically occur at site
of stasis.

11. Arterial thrombi tends to grow in retrograde
direction.
Venous thrombi- Direction of Blood flow.
Propagating tail may not be well attached
(especially venous)
May detach causing embolus.
When arterial thrombi arise in Heart
Chambers or aortic Lumen are termed Mural
thrombi.

12. Common causes of Thrombi in Heart;
Abnormal myocardial contraction (arrythmias)
Dilated cardiomyopathy.
Myocardial infarction.
Aortic thrombus
Ulcerated atherosclerotic plaque
Aneurysms
Arterial thrombi are usually occlusive the
commonest site in descending order.

13. Coronary arteries
Cerebral arteries
Femoral arteries
Venous Thrombosis
Almost always occlusive
Creates a long cast along vein lumen.
Because they occurs in areas of stasis, there is
more emeshed erythrocytes therefore red.
Venous Thrombosis Commonly affects veins of
Lower extremities(90% of cases)

14. Less Common in upper limbs.
In special cases: Dura sinuses, portal vein or
hepatic veins.
Under special conditions thrombi may form in
heart valves.
FATE OF THROMBUS
If Patient survives initial effects of occlusion
thrombus may undergo the following;
PROPAGATION

15. Thrombus may accumulate more platelets
and fibrin( Propagate) – eventual Vessel
obstruction.
Embolization
Dislodge and travel to other sites of
Vasculature.
Dissolution
Thrombi removed by fibronolytic activity.

16. 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.
Venous thrombus may cause Oedema and
Congestion in various bed distal to
obstruction.

17. Most dramatic (grave)Conquence is
embolization 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

18. Superficial veins 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 – Varicose ulcer.
Deep vein thrombosis
Grave due to embolism
Deep vein obstruction may also cause local
pain, oedema and congestion

19. Because of collateral circulation 50% of affected
patients may be asymptomatic.
Deep vein thrombosis may occur with stasis or
hypercoagulability states
Cardiac failure a common cause of venous stasis.
Trauma, surgery, burns – reduced physical
activity, injury to vessels, release of procoagulants
by tissues.
Arterial thrombosis

20. 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 addition to consequences of obstruction
may embolize Virtually to any tissue.
Principle targets, brain, kidney, spleen (Large
volume of flow).
EMBOLISM

21. Defn: Detached intravascular solid, fluid or
gaseous mass that is carried by blood to distant
site from origin.
Almost all emboli represent some dislodged
thrombus hence;
THROMBOEMBOLISM
Unless otherwise stated embolism refers to
thromboembolism.
Emboli lodges in a vessel to small to allow
further passage.
May lead to partial or complete vascular
occlusion.

22. 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
emboli lodges in pulmonary or systemic
circulation.
Pulmonary thrombo-embolism
Common in hospitalized patient.
In 95% of pulmonary embolism the origin is
thrombus in deep vein of lower extremity.

23. Carried through right side of heart to
pulmonary 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.

24. 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 cardiovascular
collapse may occur:
When more than 60% of pulmonary circulation is
obstructed.
Embolic obstruction of medium sized arteries may
result into
 pulmonary hemorrhage without infarction.

25. 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
pulmonary hypertension with right heart failure.
SYSTEMIC EMBOLISM
Emboli travelling in arterial circulation .
Most (80%) arise from intracardiac mural
thrombi
Two third of these associated with left
ventricular wall infarcts.

26. Another one quarter dilated fibrillating left
atiria.
Remainder from;
Aortic aneurysms
Thrombi on ulcerated atherosclerotic plaque
Valvular vegetations.
About 10-15% systemic embolism are
unknown origin.
Arterial emboli can travel wide to a variety of
sites

27. Major site of arterial embolism;
Lower extremities( 75%)
Brain 10%
Lesser extent, intestines, Spleen, upper extremities.
Consequences depends on;
Extent of collateral circulation in affected tissue.
Vulnerability of tissue to ischaemia.
The Caliber of Vessel.
In general arterial embolism causes infarction of tissue
downstream to obstruction.