T H RO M B O S I S , EMBOLISM

AND INFARCTION
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
Thrombosis
⚫ Formation of solid mass in circulation from the
constituents of flowing blood with intact
cardiovascular tree during life
 RUDOLF

VIRCHOW
Coined the terms “THROMBOSIS” and
“EMBOLISM”
Virchow Triad
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
Laminar blood flow
 Abnormal blood flow

Turbulence Stasis
• Venous thrombosis
• Arterial thrombosis • Aortic aneurysm
• Atherosclerotic plaque • Post MI – cardiac mural
thrombi
• Rheumatic mitral valve
stenosis
• Hyperviscosity –
Polycythemia vera
Hypercoagulability
⚫ Thrombophilia
⚫ Any disorder of blood predisposes to
that
thrombosis
⚫ Hypercoagulable states are associated
with VENOUS THROMBOSIS
 Hypercoagulable states
GENETIC ACQUIRED

⚫ Factor V mutation ⚫ Prolonged bed rest or

⚫ Increased levels of
immobilization
factor VIII, IX, ⚫ Disseminated Cancer
XI or Fibrinogen ⚫ Prosthetic cardiac
valves
⚫ Disseminated intravascular
coagulation
⚫ Oral contraceptive use
⚫ Pregnancy and post partum
 Arterial thrombi Venous thrombi
Arteries and heart veins
Superficial varicose veins,
Aorta, coronary, cerebral etc
deep leg veins
Endothelial cell injury
Causes-atherosclerosis, Venous stasis
vasculitis, trauma
Usually mural, not occluding
Invariably occlusive
lumen
Grey- white, friable with lines of Red-blue with fibrin strands
zahn with line of zahn
Grows in the direction of
Grows retrogrde
blood flow
Meshwork of platelets, fibrin, red More enmeshed RBC s and
cells and degenerating leucocytes few platelets(red or stasis
thrombi)
 Antemortem thrombus Postmortem clot
Adherent to wall Not adherent to vessel wall

Fibrin with red cells and

leucocytes in a haphazard
Red in colour network (gelatinous) Upper
layer resembling chicken fat

No lines of zahn – bland and

Lines of zahn present non – laminated
Lines of zahn
Mural thrombi
Vegetations – Thrombi on heart
valves
Arterial thrombosis
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
Embolism
⚫ An embolus is a detached intravascular solid,
liquid or gaseous mass that is carried by the blood
to a site distant from origin.
Classification
⚫ Thromboembolism (most common)
⚫ Fat embolism
⚫ Air embolism
⚫ Amniotic fluid embolism
Pulmonary embolism
Embolus lodges in the lungs
(most common from deep vein
thrombosis)

Systemic embolism
Brain, lower extremities,
intestines, kidneys,
spleen(arterial emboli from
intracardiac mural or
thrombi, aortic aneurysms,
valvular
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
PULMONARY ARTERY
EMBOLUS
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
Fat embolism
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
Decompression sickness
• Bends - formation of gas
bubbles in skeletal muscles and
joints producing pain
• In lungs -
hemorrhages, ede
atelectasis ma,
Caissons disease (chronic focal
decompression sickness) - gas
emboli in heads of femur, tibia
and humeri.
Amniotic fluid embolism
⚫ During labour or immediate partum
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
 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
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
 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
Morphological Classification of
infarcts
⚫ Colour-Pale/anemic/white
⚫ Red (hemorrhagic) Infarct

Septic or bland
Appearance of Infarct

NORMAL
TISSUE

ARTERY SURFACE
INFARCTE
FIBRINOUS
D
EXUDATE
TISSUE
OCCLUSION

ILL-DEFINED
INFARC2nTd Year Pathology
2010
 Types of Infarct
⚫ Red (haemorrhagic) infarcts
1. Venous occlusion/congestion e.g. torsion
2. Loose tissues where haemorrhage can occur and blood can
collect in infarcted zone e.g. lung
3. 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)
4. Tissues that were previously congested due to sluggish venous
outflow
5. When flow is re-established e.g. fragmentation of an occlusive
embolus, angioplasty

⚫ White infarcts
1. arterial occlusion
2. solid tissues, where haemorrhage limited e.g. spleen, heart,
kidney
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
Types of Infarct

2nd Year Pathology 2010

White splenic infarct
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)
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
 Types of Infarct

Red pulmonary infarcts - dual pulmonary / bronchial2andrtYeerairaPl

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