thrombosis

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

4. THROMBOSIS
Virchow triad

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.

6. 1-ENDOTHELIAL DAMAGE (Cont--)
 Chemical injury.
 Drugs.
 Immune reactions.
 Endotoxin.

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.

9. 2-STASIS/TURBULENCE
Post-operative immobility (inactive legs) and blood
pooling;
Post myocardial infarction (sluggish blood flow
around body)
Turbulence around atherosclerotic plaques or within
aneurysms.

11. 3-INCREASED COAGULABILITY
HYPERCOAGULABILITY:
 Alteration of coagulation pathways that
predispose to thrombosis.
 Hypercoagulability can be
 Primary (genetic)
 Secondary (acquired).

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

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

25.  Propagation
 Embolization
 Dissolution
 Organization & reacanalization

26. Venous Thrombi – Clinical course

27. Thrombus: Propagation and
Obstruction

28. Thrombus: Organization

29. Management
Medical management
 Anticoagulant medicines like…
 Heparin given intravenously and
 Warfarin is given via mouth.
 Thrombolytic therapy.
 NSAID ibuprofen.

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