Reference: Robbin's Basic Pathology 10th edition

1. THROMBOSIS
Mehak Naz
B.S Radiology
Submitted to : Mr. Abdul Wahid

2. OUTLINES
 Introduction
 Morphology
 Pathogenesis
 Fate of Thrombus
 Treatment

3. INTRODUCTION
 Thrombosis
 The formation or presence of a blood clot in a blood
vessel is called Thrombosis .
 It is normal for the body to produce clotting factors like
platelets and fibrin when a blood vessel is injured, to
prevent an excessive loss of blood from the body.
 If this effect is over productive it can obstruct the flow of
blood and form an embolus that moves around the blood
stream.
 Thrombus
 A thrombus is a blood clot that forms in a vessel and
remains there.

4. THROMBUS
 Development of
Thrombus
 Thrombi may develop
anywhere in the
cardiovascular system
 Within the cardiac
chambers
 On valve cusps
 Or in vessels i.e. arteries
veins or capillaries.
 Arterial or cardiac
thrombi typically arise
at the sites of
endothelial injury(e.g.
atherosclerotic plaque)
or turbulence (e.g.
bifurcation of vessels)
 Venous thrombi occurs
at the site of stasis.

5. THROMBUS
 Size and Shape
 They are of variable size
and shape
 Characteristic
 All thrombi are firmly
attached at the point of
origin.
 Growth of Thrombi
 Arterial thrombi
 Grow in retrograde
direction
 Venous thrombi
 Extends in the direction of
blood flow

6. THROMBUS
 Complication
 Embolus
 Thrombi are focally
attached to the
underlying vascular
surface and tend to
propagate toward the
heart.
 The propagating portion
of thrombus tends to be
poorly attached and
therefore prone to
fragmentation and
migration through the
blood as embolus.

7. MORPHOLOGY
 Lines of Zahn
 Mural thrombi
 Arterial thrombi
 Venous thrombi
 Postmortem clots
 Vegetation

8. LINES OF ZAHN
 Grossly and microscopically
apparent laminations of
thrombi called Lines Of
Zahn
 These represent pale
platelet and fibrin layers
alternating with darker red
cell rich layers.
 Signify that thrombus is
formed in flowing blood
 Presence can distinguish
ante mortem thrombosis
from the bland
nonlaminated clots.

9. MURAL THROMBI
 Occurs in heart chambers or in the aortic lumen
 Precursors of Cardiac Mural Thrombi
 Abnormal myocardial contraction
 Arrhythmias
 Dilated cardiomyopathy
 Myocardial infarction
 Endomyocardial injury
 Myocarditis
 Catheter trauma
 Precursors of Aortic Thrombosis
 Atherosclerotic plaque
 Aneurismal dilation

10. MURAL THROMBI

11. ARTERIAL THROMBI
 Also known as cardiac
thrombi
 Frequently occlusive
 Superimposed on an
atherosclerotic plaque or
other forms of vascular injury(
vasculitis, trauma).
 Usually begins at sites of
turbulence or endothelial
injury
 Composed of meshwork of
platelets, fibrin, red cells and
degenerating leukocytes.
 Common sites of frequency:
 Coronary>cerebral>femoral
arteries

12. VENOUS THROMBI
 Also known as phlebothrombosis
 Usually occurs at sites of stasis
 Extends in direction of blood flow
 almost invariably occlusive
 These are formed in the sluggish
venous circulation ,they tend to
contain more enmeshed RBCs
leading to the moniker red or
stasis thrombi. Venous thrombi
may not be well attached and are
prone to detachment, creating
emboli.
 The veins of lower extremities
are most commonly
affected.(90% of venous
thrombosis)

13. POSTMORTEM CLOTS
 They have two portions
 Dependent portion
 gelatinous with dark red
dependent portion where
red cells are settled,
 Upper portion
 yellow chicken fat upper
portion
 Usually not attached to
underlying wall

14. VEGETATION
 Thrombi on heart valves are
called vegetation
 Causes
 Infective endocarditis
 Can be either due to blood
borne bacteria or fungi
adhering to previously
damaged valves or can
directly cause valve damage.
 Sterile vegetation also can
develop on non infected
valves in hyper coagulable
states –non bacterial
thrombotic endocarditis
 Libman sacks endocarditis
sterile verrucuous
endocarditis occurring in
systemic lupus
erythematosus.

15. THROMBOSIS IN VESSELS
Features Arterial thrombosis Venous thrombosis
Sites Turbulence or
endothelial injury
Stasis
Occlusive Frequently Almost always
Appearance (+) lines of Zahn More enmeshed
RBC’s and platelets
Common sites of
involvement
Coronary>cerebral>fe
moral artery
Lower extremity veins
90%

16. PATHOGENESIS OF THROMBUS
 The primary
abnormalities that lead
to intravascular
thrombosis are
 Endothelial injury
 Stasis or turbulent
blood flow
 Hypercoagulability of
the blood
 These three causes are
referred as Virchow's
triad.

17. ENDOTHELIAL INJURY
 Most important factor in arterial thrombosis
 Includes thrombus formation in heart and arterial
circulation , where the high rates of blood flow
impede clot formation.
 Severe endothelial injury may triggers thrombosis
by exposing Von Willebrand factor and tissue factor.
 Inflammation and other noxious stimuli also
promote thrombosis by shifting the pattern of gene
expression in endothelium to one that is
prothrombic
 This change is sometimes refers to as endothelial
activation or dysfunction.

18. ENDOTHELIAL INJURY
MAJOR PROTHROMBIC CHANGES

19. ENDOTHELIAL INJURY
 Examples include
 Myocardial infarction
 Hemodynamic injury such as hypertension turbulent
flow over heart valves
 Endotoxins, inflammation
 Hyper cholestrolemia etc

20. ABNORMAL BLOOD FLOW
 Turbulence or chaotic blood flow contributes to arterial
and cardiac thrombosis by causing endothelial injury or
dysfunction.
 Stasis is the major factor in development of venous
thrombi.
 Normal blood flow is laminar
 Platelets are found mainly in the center of vessel lumen
 Separated from the endothelium by a slower moving layer of
plasma.
 By contrast, in stasis and turbulence;
 Promote endothelial cells activation
 Disrupt laminar flow
 Slows washout of activated clotting factors
 Impedes the inflow of clotting factors inhibitors.

21. ABNORMAL BLOOD FLOW
 Clinical manifestations
include
 aneurysm- aortic and
arterial dilation
 Acute myocardial infarction
 Rheumatic mitral valve
stenosis - results in left
arterial dilation
 Hyper viscosity syndromes
such as polycythemia Vera
– increase resistance to
flow and cause small
vessels stasis
 Sickle cell anemia – causes
vascular occlusions

22. HYPER COAGULABILITY
 Hypercoagulability refers to an abnormally high
tendency of the blood to clot, and is typically
caused by alterations in coagulation factors.
 Contributes infrequently to arterial or intracardiac
thrombosis but an important underlying risk factor
for venous thrombosis
 alteration of the coagulation pathways are divided
into two categories
 Primary genetic disorders
 Secondary acquired disorders.

23. HYPERCOAGULABILITY CAUSES

24. HYPER COAGULABILITY
 Primary genetic
disorders
 Factor V mutation
 Prothrombin mutation
 Secondary acquired
disorders
 Heparin induced
thrombocytopenia
syndrome
 Anti phospholipids
antibody syndrome

25. FATE OF THROMBUS
 If a patient survives an initial thrombotic event, during
the ensuring days to weeks the thrombus evolves
through some combination of the following four
processes
 Propagation
 Accumulate more platelets and fibrin thus result to vessel
obstruction
 Embolization
 Dislodgement and travel to other location
 Dissolution
 Result of fibrinolysis
 Organization and recanalization
 By ingrowth of endothelial cells ,smooth muscles and fibroblasts ;
reestablishment of continuity of original lumen.
 Older thrombi have extensive fibrin polymerization and tend to
become organized.

26. TREATMENT OF THROMBOSIS
 Thrombosis is most commonly treated with
anticoagulants.
 These drugs don’t breakup existing blood clots from
getting bigger and reduce your risk of developing more
clots
 Blood thinners may be taken orally or given by IV or
injected subcutaneously.
 Some examples of these drugs are;
 Warfarine and vitamin K antagonists can be taken orally
 Heparin by IV
 Streptokinase can be administered IV in emergency condition
like heart attack.
 Ultrasound-accelerated thrombolysis can also be used.

27. THANK YOU