Thrombosis, embolism, and infarction are related pathological processes involving blood clots. Thrombosis is the formation of a blood clot within a blood vessel, while embolism occurs when a piece of a clot breaks off and travels to another location. Infarction results from obstruction of blood flow by a clot, causing tissue death. The document discusses the mechanisms, types, features, and progression of thrombosis, embolism, and infarction. It also covers related topics like Virchow's triad, hypercoagulable states, fat embolism, and amniotic fluid embolism.

1. THROMBOSIS, EMBOLISM
AND INFARCTION

2. Normal Haemostasis
Process of maintaining blood in a fluid, clot – free
state in normal vasculature
and
rapidly forming a localized haemostatic plug at
the site of vascular injury
The pathologic opposite of haemostasis is
thrombosis

4. Thrombosis
Formation of solid mass in circulation from the
constituents of flowing blood with intact
cardiovascular tree during life

8. RUDOLF VIRCHOW
Coined the terms “THROMBOSIS” and
“EMBOLISM”

9. Virchow Triad

10. Endothelial Injury
Main cause for thrombus formation in the heart
and the arterial circulation
These are platelet – rich clots
Inflammation
Infection
Toxins from cigarette smoking
Hypercholesterolemia

13. Laminar blood flow

14. Abnormal blood flow
Turbulence
• Arterial thrombosis
• Atherosclerotic plaque
Stasis
• Venous thrombosis
• Aortic aneurysm
• Post MI – cardiac mural
thrombi
• Rheumatic mitral valve
stenosis
• Hyperviscosity –
Polycythemia vera

15. Hypercoagulability
Thrombophilia
Any disorder of blood that predisposes to
thrombosis
Hypercoagulable states are associated with
VENOUS THROMBOSIS

16. Hypercoagulable states
GENETIC
Factor V mutation
Increased levels of
factor VIII, IX, XI
or Fibrinogen
ACQUIRED
Prolonged bed rest or
immobilization
Disseminated Cancer
Prosthetic cardiac valves
Disseminated intravascular
coagulation
Oral contraceptive use
Pregnancy and post partum

17. Arterial thrombi Venous thrombi
Arteries and heart veins
Aorta, coronary, cerebral etc
Superficial varicose veins,
deep leg veins
Endothelial cell injury
Causes-atherosclerosis,
vasculitis, trauma
Venous stasis
Usually mural, not occluding
lumen
Invariably occlusive
Grey- white, friable with lines of
zahn
Red-blue with fibrin strands
with line of zahn
Grows retrogrde
Grows in the direction of
blood flow
Meshwork of platelets, fibrin, red
cells and degenerating
leucocytes
More enmeshed RBC s and
few platelets(red or stasis
thrombi)

18. Antemortem thrombus Postmortem clot
Adherent to wall Not adherent to vessel wall
Red in colour
Fibrin with red cells and
leucocytes in a haphazard
network (gelatinous)
Upper layer resembling
chicken fat
Lines of zahn present
No lines of zahn – bland and
non – laminated

19. Lines of zahn

20. Mural thrombi

21. Vegetations – Thrombi on heart
valves

22. Arterial thrombosis

23. Fate of thrombus
Propagation
Embolization – thrombi dislodges and travels
to other sites in vasculature
Dissolution – by fibrinolysis
Organisation and recanalization
Older thrombi become organised by
ingrowth of endothelial cells, smooth muscle
cells and fibroblasts. Capillary channels
reestablish continuity of lumen

26. Embolism
An embolus is a detached intravascular solid,
liquid or gaseous mass that is carried by the
blood to a site distant from origin.

27. Classification
Thromboembolism (most common)
Fat embolism
Air embolism
Amniotic fluid embolism

28. Pulmonary embolism
Embolus lodges in the lungs
(most common from deep vein
thrombosis)
Systemic embolism
extremities,
kidneys,
Brain, lower
intestines,
spleen(arterial emboli from
valvular
intracardiac mural or
thrombi, aortic aneurysms,
atherosclerotic plaques)

29. Pulmonary thromboembolism
Cause from venous emboli from deep leg
veins
Common in hospitalised and bed ridden
patients
Large thrombus gets impacted at bifurcation
of pulmonary artery-saddle embolus
Multiple emboli
Paradoxical embolism

30. PULMONARY ARTERY EMBOLUS

31. Fat embolism
Obstruction of arterioles and capillaries by fat
globules
Fractures of long bones
Trauma to soft tissue eg., adipose tissue
Clinical features
Pulmonary insufficiency - tachypnea, dyspnea,
tachycardia
Neurologic symptoms - irritability, restlessness to
delirium and coma
Thrombocytopenia

32. Fat embolism

33. Air embolism
Gas bubbles within the circulation can
coalesce to form frothy masses and obstruct
vascular flow
Large volume of air (more than 100 cc) is
necessary to produce effect in pulmonary
circulation
Small volume of air trapped in coronary artery
during bypass surgery
Chest wall injury
Obstetric or laproscopy procedures

34. Decompression sickness
• Bends - formation of gas
bubbles in skeletal muscles
and joints producing pain
- edema,
focal
• In lungs
hemorrhages,
atelectasis
Caissons disease (chronic
decompression sickness) -
gas emboli in heads of femur,
tibia and humeri.

35. Amniotic fluid embolism
partum
During labour or immediate post
period
Dyspnea, cyanosis, hypotensive shock,
seizure and coma
Infusion of amniotic fluid or fetal tissue into
maternal circulation via tear in placental
membranes or rupture of uterine veins

36. INFARCT
Def: An infarct is an area of ischemic necrosis
caused by occlusion of either the arterial supply
or the venous drainage in a particular tissue.
Aetiology
Thrombosis or embolism
Venous outflow obstruction (single outflow organs)
Others : Hypotensive,local vasospasm, compression of,
vessel by hematoma or tumor, torsion

37. Infarction
Tissue necrosis due to ischaemia
vascular insufficiency of any cause
usually arterial occlusion due to thrombosis/embolism
Mainly due to oxygen deficiency, but toxin
accumulation & reperfusion injury may contribute
Number of determining factors
Size of vessel and size of vascular territory
Partial / total vascular occlusion
Duration of ischaemia

38. Infarct Development
Dependent on a number of factors
Nature of vascular supply
Dual supply e.g. lungs, liver
End arteries e.g. kidneys, spleen
Rate of vascular occlusion
Time for development of collateral circulation
Vulnerability to hypoxia
Neurons – 2-3mins, Myocardium – 20-30mins, Fibroblasts – hours.
Oxygen content of blood
Anaemia, cyanosis, congestive heart failure
Can result in infarction due to otherwise inconsequential blockage
Size of vessel and size of vascular territory
Partial / total vascular occlusion
Duration of ischaemia

39. Morphological Classification of
infarcts
Colour-Pale/anemic/white
Red (hemorrhagic) Infarct
Septic or bland

40. Appearance of Infarct
ARTERY
OCCLUSION
NORMAL
TISSUE
INFARCTED
TISSUE
SURFACE
FIBRINOUS
EXUDATE
ILL-DEFINED
INFARC2nTdYear Pathology 2010
BORDERS

41. Types of Infarct
Red (haemorrhagic) infarcts
1.
2.
3.
4.
5.
Venous occlusion/congestion e.g. torsion
Loose tissues where haemorrhage can occur and blood can
collect in infarcted zone e.g. lung
Tissues with dual blood supply e.g. lung small intestine
(permitting blood flow from unobstructed vessel into infarcted
zone – note flow is insufficient to rescue ischaemia)
Tissues that were previously congested due to sluggish venous
outflow
When flow is re-established e.g. fragmentation of an occlusive
embolus, angioplasty
White infarcts
1.
2.
arterial occlusion
solid tissues, where haemorrhage limited e.g. spleen, heart,
kidney

42. Pale / White Infarct
Ischemia following obstruction of nutrient artery or
hypoperfusion of tissue
Solid organs with end-arterial circulation such as
kidney, heart, spleen
Wedge shaped.occluded vessel at the apex,base
at the serosal surface
Better defined with time, paler, hyperemic
margins

43. 2nd Year Pathology 2010
Types of Infarct
White splenic infarct

44. Microscopy
Ischemic coagulative necrosis
Demonstrable only >12-18 hrs.
Inflammation in response to necrosis
Phagocytosis of cellular debris by neutrophils &
macrophages 1-2 days
Healing response
Scar tissue (brain- liquefactive necrosis)

45. Red (hemorrhagic)infarcts
Sites :venous occlusion of organ with
single venous outflow e.g. testicular
torsion
Loose tissues- e.g. lung
Tissues with dual circulations: lung and
gut
Previously congested tissue
With reperfusion of previously infarcted
tissue

46. Types of Infarct
Red pulmonary infarcts - dual pulmonary / bronchial2andrtYeerairaPla
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47. Pulmonary infarcts
Ischemic necrosis of lung parenchyma following
pulmonary embolism & lack of blood from
bronchial arteries.
When blood from bronchial arteries reperfuses
the ischemic area, blood leaks into the alveolar
spaces
Appears triangular, red & airless.
Becomes more firm &brown with time.

48. Septic infarct
Following fragmentation of a bacterial vegetation
from a heart valve or following microbes seeding
a necrotic area.
Converted into an abscess
Greater inflammatory response
scarring

49. Event Sequence
1. Coagulative necrosis
2. Infiltration by neutrophils
3. Infiltration by macrophages
4. Phagocytosis of debris
5. Granulation tissue formation
6. Scar formation

50. 2nd Year Pathology
2010
Time Microscopic Features Gross Features
0 – 4 hr None None
4 – 12 hr Early coagulation necrosis (nucleus:
pyknosis, cytoplasm: eosinophilia)
None
12 – 24 hr Further necrosis, haemorrhage, early
neutrophil infiltrate
Dark mottling
1 – 3 days Marked neutrophil infiltrate and
necrosis
Mottled with yellow-tan
necrotic centre
3 – 7 days Early phagocytosis of dead cells by
macrophages (at border)
Hyperaemic border, central
yellow-tan softening
7 – 10 days Well-developed phagocytosis, early
granulation tissue formation
Maximal yellow-tan softening,
depressed red-tan margins
10 – 14 days Well-developed granulation tissue,
early collagen deposition
Red-gray depressed infarct
borders
2 – 8 wk Increased collagen deposition,
decreased cellularity
Grey-white scar progresses
from border toward centre
> 2 months Acellular collagenous scar Dense gray scar