This document summarizes different types of thrombosis and embolism. It discusses thrombosis, thrombus formation, and the coagulation cascade. It also covers different causes of endothelial injury that can lead to thrombosis, including atherosclerosis, hypertension, diabetes, and smoking. Alterations in blood flow that can promote thrombosis are turbulence, stasis, and hypercoagulability. The document outlines various types of embolism including thromboembolism, fat embolism, gas embolism, and amniotic fluid embolism. It provides details on the pathogenesis, clinical manifestations, and consequences of pulmonary thromboembolism and systemic arterial embolism.

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