superficial introduction to the topic for bachelor level

1. Thrombosis And Embolism
Dr. Saugat Chapagain

2. Thrombosis

3.  Thrombus a solid mass consisting of blood constituents
within the blood vessel; attached to the point of origin.
 Thrombosis  the process of…
 Clot  mass of coagulated blood
 Haematoma  extravascular accumulation of blood clot
 Haemostatic plugs  normal clots to control bleeding
Thrombus and Thrombosis

4.  Virchow’s Triad
 Endothelial injury
 Altered blood flow (stasis/ turbulence)
 Hypercoagulability of blood
Pathophysiology

5. Coagulation cascade

7.  Vascular injury exposes subendothelial thrombogenic
connective tissues (collagen, elastin, fibronectin,
laminin and glycosaminoglycans)
 Initial vasoconstriction to reduce blood loss.
 Tissue factors initiate extrinsic pathway
 Collagen initiate intrinsic pathway.
Endothelial injury

8.  Ulcerated plaque in
advanced atherosclerosis.
 Haemodynamic stress in HTN
 Arterial diseases
 Diabetes mellitus
 Endogenous chemical
agents
(hypercholesterolemia)
 Exogenous chemical agents
(smoking)
 TAO
 Bacterial toxins
 Trauma
 IV cannulation
 Radiation injury
 Turbulent flow of blood in
aneurysm
 Mural thrombus following
cardiac abnormality
Causes of endothelial injury

9.  Turbulence: unequal flow (arterial); may aggravate
vascular injury as well.
 Stasis: slowing (venous)
 Blood cells and platelets migrate to periphery and
pavement the endothelium
 Normal flow has:
 Central fast moving red and white blood cells.
 Slow moving laminar stream of platelets.
 Peripheral slowest moving cell-free plasma.
Alteration of blood flow

10. Effects:
 Prevent dilution by fresh flowing blood of activated clotting
factors.
 Disrupt laminar blood flow and bring platelets in contact of
endothelium
 Retard the inflow of clotting factor inhibitors and permit
thrombosis
 Promote endothelial cell activation
Examples:
 DVT of lower limbs
 Mural thrombus
 Thrombosis in aneurism

11. Favoured by:
 Smoking
 Ageing
 Use of OCPs
 Obesity
Causes:
 Increased coagulation factors
 Increased platelet count and adhesiveness
 Decreased levels of coagulation inhibitors
Hypercoagulability

12. Primary (genetic)
 Deficiency of anti thrombin
 Deficiency of protein C or S
 Defects in fibrinolysis
 Mutation of factor V
Secondary (acquired)
 Risk factors:
 Advanced age
 Sedentary life style
 Immobilization
 Smoking
 Clinical conditions leading to
thrombosis:
 Heart diseases (MI, CHF, RHD)
 Vascular diseases
(atherosclerosis, aneurysms,
varicosities)
 Hypercoagulibility
(polycythemia, dehydration,
nephrotic syndrome)
 Shock
 Late pregnancy and puerperium
 drugs
Factors favoring thrombosis

13.  Gross:
 Shape and size depends on origin
 Arterial  white and mural (firm and pale)
 Venous  red and occlusive(soft, red and gelatinous)
 Mixed/ laminated – alt white and red layers separated by
line of ZAHN.
 Microscopic:
 Lines of Zahn seen where visible
 Collection of cells and fibrin
Morphology

14. Based on colour and components:
 Pale – primarily platelets
 Red – primarily RBCs
 Mixed – visible lines of zahn
Based on site and mode of formation:
 Occlusive
 Mural – occurs in heart chambers/ aorta/ major arteries
Based on infection:
 Bland – non infected
 Septic – infected.
Types

15.  Resolution – plasmin may dissolve the thrombus
completely
 Organization – eventually covered by endothelial cells
after granulation tissue formation (or calcification/
ossification)
 Propagation – enlargement of size may block
important vessels.
 Thromboembolism – detachment and released into
blood stream
Fate of thrombus

16. Embolism

17.  The process of partial or complete obstruction of
some part of the CVS by any mass carried in the
circulation.
 Commonly thromboembolism (90%)
What is it?

18.  Depending on matter of embolus
 Solid- thrombus, atheroma, malignant cell, parasites, foreign
bodies.
 Liquid- fat globules, amniotic fluid, bone marrow
 Gasseous- air, other gasses
 Depending on infection:
 Bland
 Septic
 Depending on source of emboli:
 Cardiac emboli from left side of the heart – vegetations of
endocarditis, atrial appendages
 Arterial – in systemic arteries of brain, spleen, kidney and
intestine.
 Venous – in pulmonary arteries
 Lymphatic emboli
TYPE

19.  A detached thrombus or a part of thrombus.
 Site of lodgement:
 Arterial (systemic)
 Venous
 Pulmonary
THROMBOEMBOLISM

20.  Most common and fatal form.
 Occlusion of the pulmonary arterial tree.
 Pulmonary thrombosis (rare)
ETIOLOGY
 More common in bed ridden patients.
Causes:
 Thrombi originating from large veins of lower legs
(popliteal, femoral and iliac)
 Less common sources ( varicosities of superficial veins,
pelvic veins)
PULMONARY THROMBOEMBOLISM

21. Detachment of thrombus  thromboembolism 
drains into right atrium.
 Large thrombus is impacted at the bifurcation of main
pulmonary artery (saddle embolus) or on RV or its
outflow tract.
 If large embolus fragments  small embolus impacts
in a number of vessels (esp. on lower lobes of lungs)
 Paradoxical embolism – passage of embolus from rt.
heart to lt. heart via ASD or VSD.
Pathogenesis

22.  Sudden death – d/t massive pulm. Embolism.
 Acute cor pulmonale – RHF d/t pulmonary HTN
 Pulm. Infarction – obstruction of small pulm. arteries.
 Pulm. Haemorrhage – central pulm. Haemorrhage d/t obstruction of
flow in endarteries.
 Resolution – 60-80 % by fibrinolysis.
 Pulm. HTN, chronic cor-pulmonale and pulm.
Atreriosclerosis.
Consequences

23.  Arterial embolism
 Esp. originating in LV (MI, cardiomyopathy, RHD,
congenital heart disease, IE, prosthetic valves)
Site of origin:
 Heart (80%)
 Aorta – thrombi over ulcerated atheroma in aortic
aneurysm
 Paradoxical – rt.  lt. in ASD or VSD
 Idiopathic – 10-15%
Systemic thromboembolism

24.  Infarction – kidney, spleen, mesentery
 Stroke – brain (10%)
 Upper and lower extremeties- peripheral vascular diseases,
gangrene, etc.
Effects

25.  Embolism of fat globules.
 Obstruction by fragments of adipose tissue  fat
tissue embolism.
Etiology
 Traumatic –
 Trauma to bones, trauma to soft tissue
 Non traumatic –
 Burns, DM, fatty liver, pancreatitis, decompression
sickness.
Fat embolism

26.  Mechanical obstruction – micro aggregates of fat
causes obstruction of vessels.
 Chemmical injury – FFA causes toxic injury.
 Thrombocytopenia – d/t coating of fat globules with
platelets.
Consequences
 Pulmonary fat embolism
 Systemic fat embolism (in case of ASD/ VSD)
Pathogenesis

27.  Air, nitrogen and other gases,
 Air embolism – entry of air due to trauma, injury or surgery.
 Decompression sickness/ caisson’s disease, diver’s palsy or
aeroembolism seen in deep sea divers.
Causes:
 During delivery or abortion
 Acquired/ accidental pneumothorax
 Haemodialysis
 Accidental opening of large veins
 Angiography
 Cardiothoracic surgery / trauma
Gas Embolism

28.  Most serious, unpredictable and unpreventable cause of
maternal mortality.
 Amniotic fluid may contain – epithelial squames, vernix caseosa,
lanugo hair, bile from meconium and mucus
s/s
 Sudden respiratory distress and dyspnoea
 Deep cyanosis
 CV shock
 Convulsions
 Coma
 Unexpected death
Amniotic fluid embolism

29.  Mechanical blockage of pulmonary circulation in
extensive embolism
 Anaphylactic reaction to components
 DIC d/t liberation of thromboplastin
 Haemorrhagic manifestations d/t thrombocytopenia
and afibrinogenaemia.
Cause of death

30. Thank you