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Embolism and infarction
Dr Aarathi Rau
Emboli
Definition: emboli are solid, fluid or
gaseous material carried by the blood
stream from the site of their origin or entry
into the circulation to a site distant from its
site of origin
Embolism
Classification of emboli
Thromboemboli –commonest:
arterial,venous ,paradoxic
Air (gas )
Fat
Bone marrow
Tumour
Cholesterol
Foreign body
Amniotic fluid
Consequences of embolization
↓perfusion distal to embolus
Affected by collateral or dual blood
supply
Possible infarction of tissue
Thromboemboli
Most important clinically
Venous-originate from veins & carried by
venous system to lungs (pulmonary)
Arterial originate in large arteries, heart ot
aorta ,carried by arterial blood into organs
e.g. brain, kidney, spleen (systemic)
Paradoxical originate in venous system &
cross through a heart shunt/foramen ovale
to arterial circulation
Pulmonary(Venous)
Thromboembolism
Aetiology:deep vein thrombosis
Pathogenesis: depends on the size of
embolus ,extent of embolization &
collateral circulation
Occlusion of main pulmonary artery or
main branch can cause death by
preventing blood going to the lungs
“saddle embolus”
Pulmonary Embolus
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Venous Thromboembolism (cont.)
Occlusion of the branches of
pulmonary artery .
Depending on the degree of collateral
circulation (dual blood supply of
lungs,pulmonary & bronchial)→Pulmonary
infarcts
Non occlusive thrombi “silent”
May lead to pulmonary hypertension
eventually
Systemic (Arterial)
Thromboembolism
Emboli travelling in arterial circulation
Aetio-pathogenesis
– intracardiac mural thrombi (80%)
– left atrium: dilation and fibrillation (25%)
– heart valve vegetations
– aortic mural thrombi
– paradoxical
Sites of embolization
– lower extremities (75%)
– brain (10%)
– intestine, kidney, spleen
Effects of emboli
Depends on the
Collateral vascular supply of the affected
tissue
The vulnerability of the tissue to ischemia
Calibre of occluded vessel
Fat Embolism
Definition : embolism caused by fat in the
circulation
Aetiology :trauma with multiple fractures of long
bones
Pathogenesis: Mechanical obstruction
microemboli of neutral fat +platelet &RBC
aggregates
Chemical irritation (local injury to
endothelium)from release of fatty acids
+ platelet activation & recruitment of granulocyyes
–release of free radicals,protease &ecosanoids
→DIC
Sites of embolization
lungs: pulmonary insufficiency
brain: restlessness, delirium, coma
Demonstration of fat embolism
Fat globules in capillaries demonstrated in
frozen sections of lung,brain .
Clinical features
Pulmonary insufficiency
Neurological symptoms
Anemia
Thrombocytopenia—petechial rash
Prognosis
Asymptomatic (up to 90% of cases)
Fatal in severe cases
Air Embolism
Definition :embolism caused by entry of
air bubbles into circulation
Aetiology:
Trauma: chest internal jugular vein or SVC
Obstetrical procedures
Vascular surgery
Decompression events
Pathogenesis:Usually more than 150 ml
of air needed to produce symptoms
Symptoms of ischemia, infarction or DIC
Decompression sickness
Divers (Nitrogen bubbles in decompression)
Nitrogen bubbles in blood due to rapid
decompression
Gas bubbles occlude small vessels
In joints ,bones & soft tissues “bends”
pulmonary vessels -“chokes”
Initiate DIC
Treatment -repressurise
Caisson disease - chronic decompression
sickness
Gas emboli in skeletal system → ischemic
necrosis especially in the femur,tibia,humeri
Amniotic Fluid Embolism
Def: Obstetrical complication with entry of
amniotic fluid into uterine venous circulation
Incidence: Rare but lethal in 80% cases
Pathogenesis: Amniotic fluid contains
squamous cells lanugo hair,fat, mucin
Amniotic fluid may obstruct pulmonary arteries
→ sudden death or initiate DIC
Morphology:post mortem – particulate
material in pulmonary arteries / thrombi in
small vessels.
Pulmonary oedema,diffuse alveolar
damage,systemic fibrin thrombi(DIC)
Others
Septic thromboemboli: infected thrombi
e.g. valvular vegetations in bacterial
endocarditis .infarcts become infected by
bacteria & transforms into an abscess.
Tumour emboli-don’t cause infarcts
Foreign body –IV drug users
Cholesterol –AS plaques
Infarction
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 99%
Venous outflow obstruction (single outflow
organs)
Others : Hypotensive,local vasospasm,
compression of, vessel by hematoma or
tumor, torsion
Morphological Classification of
infarcts
Colour-Pale/anemic/white
Red (hemorrhagic) Infarct
Septic or bland
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
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
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.
Examples of infarcts
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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
Clinical Correlations
Nature of blood supply
– end-artery blood supply
– dual blood supply
Rate of development of occlusion
– role of collateral circulation
Vulnerability of tissue to hypoxia
– brain: 3-4 minutes
– heart: 20-30 minutes
Oxygen content of blood
– hemoglobin concentration and saturation
MCQ’s
In which of the following conditions can a
paradoxical embolism occur?
Pulmonary stenosis
Patent ductus arteriosus
Atherosclerosis
Pulmonary infarction
In which of the following conditions can a
paradoxical embolism occur?
Pulmonary stenosis
Patent ductus arteriosus √
Atherosclerosis
Pulmonary infarction
In which organ is red infarct seen ?
kidney
Small intestine
Heart
brain
In which organ is red infarct seen
kidney
Small intestine √
Heart
brain
In which organ is pale infarct seen?
Lung
Small intestine
Kidney
brain
In which organ is pale infarct seen?
Lung
Small intestine
Kidney √
brain
In which of the following is a red infarct
seen?
Solid tissues
Following arterial occlusion
In tissues with double circulation
In previously congested tissues
In which of the following is a red infarct
seen?
Solid tissues
Following arterial occlusion
In tissues with double circulation √
In previously congested tissues √
Thank you