2. THROMBOSIS
Thrombus – a blood clot.
Thrombosis – a pathological process whereby there is
formation of a blood clot in uninjured vasculature or
after relatively minor injury.
3. There are three main predisposing factors for
thrombus formation (Virchow’s triad):
* Damage to the endothelial lining of a blood vessel.
* Relative stasis or turbulence of blood flow.
* Increased coagulability of blood.
These predisposing factors are associated with
particular conditions or life styles
5. 1-ENDOTHELIAL DAMAGE
IN HEART AND ARTERIAL CIRCULATION
a. Endocardial injury (example MI, Valvulitis)
b. Over ulcerated plaques in the atherosclerotic
arteries
c. Hemodynamic stress: like hypertension
d. Turbulent flow over the scarred valves
e. At the sites of the traumatic or inflammatory
vascular injury
f. Hypercholesterolemia
g. Radiation or products absorbed from the Cigar
smoke.
7. 2-STASIS/TURBULENCE (contd…):
Turbulence contributes to arterial & cardiac thrombosis
by causing endothelial injury.
Stasis is major factor in development of venous thrombi.
Both stasis & turbulence
◦ Disrupt laminar flow & bring platelets into
contact with the endothelium.
◦ Prevents dilution of clotting factors inhibitors
◦ Slow down the inflow of clotting factor
inhibitors
◦ Promotes endothelial cell activation.
12. 3-INCREASED COAGULABILITY (contd…):
Primary (genetic).
Mutation in factor V (proaccelerin) gene (Leiden mutation) &
Mutation in factor II gene (prothrombin gene) .
Factor V becomes resistant to protein c inactivation
Prothrombin (II) levels elevated
Mutation in methyltetrahydrofolate gene
RARE CAUSE
Less commonly inherited deficiencies of anti-thrombin-III, protein C or
protein S.
Congenitally elevated levels of homocysteine.
13. 3-INCREASED COAGULABILITY (contd…):
Secondary (acquired)
HIGH RISK FACTORS
Stasis or vascular injury may be most important
Immobilization
Cancer
MI and atrial firillation
Tissue damage(surgery, fracture, burns)
LOWER RISK FACTORS
Cardiomyopathy
Nephrotic syndrome
Oral contraceptive
Hyper estrogenic state of pregnancy
Advancing age leading to increased platelet aggregation.
Smoking & obesity
14. Mural thrombi
Mural thrombi : When arterial
thrombi arises in heart chamber
or in aortic lumen they usually
adhere to the wall of underlying
structure and are termed mural
thrombi.
15. Arterial or cardiac thrombi:
At site of endothelial injury (e.g. atheroscelerotic plaque or
turbulence)
Grow in a retrograde direction (direction of flow- i.e.,
towards heart) from the point of attachment whereas
venous thrombi extend in direction of blood flow(i.e.,
towards the heart) .
Common sites: In descending order are coronary, cerebral &
femoral arteries.
Superimposed on atherosclerotic plaque.
Firmly adherent to injured arterial wall, gray-white &
friable.
Composed of tangled platelets, fibrin, erythrocytes &
degenerated leukocytes.
16. Morphology (contd…):
Venus thrombi or Phlebothrombosis:
Also called red or stasis thrombi.
Characteristically occur in sites of stasis.
Grow in the direction of blood flow
Almost invariably occlusive.
Prone to fragment; creating an embolus.
Most commonly (90%) affects the veins of the
lower extremities.
Differentiation from postmortem clots:
Firmer, have a point of attachment & on
transaction reveal vague strands of pale gray fibrin.
17. Morphology (contd…):
VALVULAR THROMBI:
Thrombi on heart valves are called vegetations.
Infective endocarditis - Bacterial or fungal blood born
infections leads to valve damage & thrombus formation –
results in bulky friable vegetations composed of necrotic
debris, thrombus and organisms
Non Bacterial thrombotic endocarditis (sterile vegetations on
non infected valves) in patients with hypercoagulable states
Non-infected,Verrucous-endocarditis-(Libman-Sacks
endocarditis) due to elevated levels of circulating immune
complexes
18.
19. Thrombus - Morphology
Arterial
Almost always arise
from heart
Grow in retrograde
fashion (direction of
flow)
Forms at site of
Endothelial injury(AS),
turbulence (aneurysms)
Pale/ white
Lines of Zahn
Firmly adherent to
vessel wall
From emboli Cause
infarctions (lower
extremities – 75%, Brain
(10%), Kidney, spleen)
Venous
Deep veins (popleteal
Femoral Iliac),
Antigrade (towards
heart- direction of
flow)
At site of stasis (lower
extremities)
Red / dark
No lines of Zahn
Loosely attached
(easily embolize)
Emboli cause
Pulmonary embolism (
silent in 50% of pts.)
20. Thrombus - Morphology
Venous
Loosely attached
(easily embolize)
Red/ dark
Post mortem clot
Not attached
Dark red dependant
portion & yellow
chicken fat
supernatant
21. Thrombi cause obstruction of arteries & veins.
They are possible sources of emboli.
Venus thrombosis:
Mostly occurs in superficial & deep veins of legs.
Superficial venous thrombi.
Usually in saphenous system esp. in varicosities.
Local congestion, swelling, pain & tenderness along the
course of involved vein.
Rarely embolize.
Predispose the overlying skin to infections.
22. Clinical correlations (contd…):
Venous thrombosis (contd):
Deep venous thrombosis.
In larger leg veins at or above the knee joint
(popliteal, femoral & iliac veins)
They embolize & so are clinically serious.
May cause local pain & edema.
Collateral bypass channels.
Asymptomatic in 50% of cases.
Recognized only after they have embolized.
23. Clinical correlations (contd…):
Cardiac & arterial thrombosis:
Myocardium infarction
Dyskinetic contraction of the myocardium & damage
to the adjacent endothelium leading to mural
thrombi.
Rheumatic heart disease.
Mitral valve stenosis.
Left atrial dilatation.
Atrial fibrillation
24. Clinical correlations (contd…):
Atherosclerosis.
It is a prime initiator of thrombosis related
to loss of endothelial integrity & abnormal
vascular flow.
Complication of cardiac & aortic mural thrombi
Peripheral embolization
Common sites: Brain, kidneys & spleen
30. Physiotherapy.
It is paramount that thrombosis
collaborative care programmes
include the physiotherapist to
encourage specific ambulatory
regimes. For each patient, an initial
assessment begins with discussion
and observation of the patient’s
actual and achievable ambulation
capacity:
31. Independent walking activity (achieved by
patient).
Active walking exercises (ten times hourly).
Walking activities will significantly help to
reduce deficits in venous blood flow by
activating skeletal calf muscle pumps.
It is also important to make optimum use of
the respiratory system (respiratory pumps),
to encourage specified breathing
mechanisms and to initiate collaborative
skeletal and respiratory pump exercises
