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Dr. Abdul Rehman
Embolism & Infarction
Learning Outcomes!
• Explain the causes of embolus
• Classify different forms of embolus
• Concept of infarction, classification and its morphology
• An embolus is a detached intravascular solid, liquid, or gaseous mass
that is carried by the blood to a site distant from its point oforigin
(dislodged thrombi)
• Emboli lodge in vessels too small to permit further passage, resulting in
partial or complete vascular occlusion
• Leads to tissue dysfunction and infarction
• Source of emboli: Dislodged thrombus (mainly), fat droplets, bubbles of
air or nitrogen, atherosclerotic debris (cholesterol emboli), tumor
fragments, bits of bone marrow, or amniotic fluid
EMBOLISM
Pulmonary Thromboembolism
95% of venous emboli originate from deep leg vein thrombi (DVT)
• Emboli traveling within the arterialcirculation
• Most (80%) arise from intra-cardiac muralthrombi
• Two thirds of which are associated with leftventricular infarcts
Systemic Thromboembolism
Large embolus derived from a lower
extremity deep venous thrombosis
and now impacted in a pulmonary
artery branch (Saddle Embolus)
Major sites for arteriolar embolization:
1. Lower extremities(75%)
2. Brain (10%)
3. Others: Intestines, kidneys, spleen
Systemic Thromboembolism
1- Fat Embolism
• Microscopic fat globules may be found in the circulation after fractures of
long bones (which have fatty marrow) or,rarely, in the setting of soft tissue
trauma and burns
• Symptoms include pulmonary insufficiency, thrombocytopenia, anemia
and neurological damage
Bone marrow embolus in pulmonary vessel.
The cleared vacuoles represent marrow fat
that is now impacted in a distal vessel along
with the cellular hematopoietic precursors
FatEmbolusinaglomerulus
Types of Embolus
2- AirEmbolism
• Gas bubbles within the circulation can obstruct vascular flow and can
cause distal ischemic injury
• Enter the circulation during cardiac surgery, neurosurgery, obstetric
procedures or as a consequence of chest wall injury
• Decompression sickness in scuba drivers & underwater construction
workers
• In excess of 100 cc is required to have a clinical effect
• Underlying cause is the infusion of amniotic fluid or fetal tissue into the
maternal circulation via tears in the placental membranes or rupture of
uterine veins
• Characterized by sudden severe dyspnea, cyanosis, and hypotensive shock,
followed by seizures and coma
3- Amniotic FluidEmbolism
• Definition: An infarct is an area of ischemic necrosis
• Underlying Cause: Occlusion of vascular supply to the affected tissue
• Infarction is necrosis resulting from ischemia caused by obstruction of the
blood supply to the affected area
• Pathogenesis:
Obstruction Hypoxia Reversible injury Irreversible injury
(necrosis)
Causes :
Intraluminal Intramural Extramural
- Thrombosis - Vasospasm -Tumor
- Embolism - Sclerosis - Ligation
- Atheroma - Vasculitis - Torsion
INFARCTION
INFARCTION
• Dominant histologic finding : ischemic coagulative necrosis
ischemic liquefactive necrosis (Brain)
• An inflammatory response begins to develop along the margins of
infarcts within a few hours and usually is well defined within 1 to 2 days
• Most infarcts are ultimately replaced by scar tissue
• Based on their color (reflecting the amount of hemorrhage)
1. Red (hemorrhagic) infarct 2. White (anemic) infarct
• Based on the presence or absenceof microbial infection
1. Septic infarct 2. Bland infarct
• Infarcts tend to be wedge shaped with the occluded vessel
at the apex and the organ periphery forming the base
Classification of Infarct
• Red (hemorrhagic) infarcts occur
(1) with venous occlusions (such as in ovariantorsion)
(2) With arterial occlusion in tissues with dual circulations
(lung & small intestine)
• White (anemic) infarcts occur
With arterial occlusions in solid organs with end- arterial
circulation (heart, spleen, and kidney)
• Septic infarctions may develop when embolization occurs by
fragmentation of a bacterial vegetation from a heart valve or when
microbes seed an area of necrotic tissue
➢ Factors that influence infarct development:
• Collateral blood supplies
• Rate at which an obstruction develops
• Intrinsic tissue susceptibility to ischemic injury and blood oxygenation
Types of infarct:
(A) Hemorrhagic, roughly wedge-shaped pulmonary infarct
(B) Sharply demarcated white infarct in the spleen
Remote kidney infarct replaced by a large fibrotic corticalscar

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Embolism & Infarction.pdf

  • 2. Learning Outcomes! • Explain the causes of embolus • Classify different forms of embolus • Concept of infarction, classification and its morphology
  • 3. • An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point oforigin (dislodged thrombi) • Emboli lodge in vessels too small to permit further passage, resulting in partial or complete vascular occlusion • Leads to tissue dysfunction and infarction • Source of emboli: Dislodged thrombus (mainly), fat droplets, bubbles of air or nitrogen, atherosclerotic debris (cholesterol emboli), tumor fragments, bits of bone marrow, or amniotic fluid EMBOLISM Pulmonary Thromboembolism 95% of venous emboli originate from deep leg vein thrombi (DVT) • Emboli traveling within the arterialcirculation • Most (80%) arise from intra-cardiac muralthrombi • Two thirds of which are associated with leftventricular infarcts Systemic Thromboembolism
  • 4. Large embolus derived from a lower extremity deep venous thrombosis and now impacted in a pulmonary artery branch (Saddle Embolus) Major sites for arteriolar embolization: 1. Lower extremities(75%) 2. Brain (10%) 3. Others: Intestines, kidneys, spleen Systemic Thromboembolism
  • 5. 1- Fat Embolism • Microscopic fat globules may be found in the circulation after fractures of long bones (which have fatty marrow) or,rarely, in the setting of soft tissue trauma and burns • Symptoms include pulmonary insufficiency, thrombocytopenia, anemia and neurological damage Bone marrow embolus in pulmonary vessel. The cleared vacuoles represent marrow fat that is now impacted in a distal vessel along with the cellular hematopoietic precursors FatEmbolusinaglomerulus Types of Embolus
  • 6. 2- AirEmbolism • Gas bubbles within the circulation can obstruct vascular flow and can cause distal ischemic injury • Enter the circulation during cardiac surgery, neurosurgery, obstetric procedures or as a consequence of chest wall injury • Decompression sickness in scuba drivers & underwater construction workers • In excess of 100 cc is required to have a clinical effect • Underlying cause is the infusion of amniotic fluid or fetal tissue into the maternal circulation via tears in the placental membranes or rupture of uterine veins • Characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma 3- Amniotic FluidEmbolism
  • 7. • Definition: An infarct is an area of ischemic necrosis • Underlying Cause: Occlusion of vascular supply to the affected tissue • Infarction is necrosis resulting from ischemia caused by obstruction of the blood supply to the affected area • Pathogenesis: Obstruction Hypoxia Reversible injury Irreversible injury (necrosis) Causes : Intraluminal Intramural Extramural - Thrombosis - Vasospasm -Tumor - Embolism - Sclerosis - Ligation - Atheroma - Vasculitis - Torsion INFARCTION
  • 9. • Dominant histologic finding : ischemic coagulative necrosis ischemic liquefactive necrosis (Brain) • An inflammatory response begins to develop along the margins of infarcts within a few hours and usually is well defined within 1 to 2 days • Most infarcts are ultimately replaced by scar tissue • Based on their color (reflecting the amount of hemorrhage) 1. Red (hemorrhagic) infarct 2. White (anemic) infarct • Based on the presence or absenceof microbial infection 1. Septic infarct 2. Bland infarct • Infarcts tend to be wedge shaped with the occluded vessel at the apex and the organ periphery forming the base Classification of Infarct
  • 10. • Red (hemorrhagic) infarcts occur (1) with venous occlusions (such as in ovariantorsion) (2) With arterial occlusion in tissues with dual circulations (lung & small intestine) • White (anemic) infarcts occur With arterial occlusions in solid organs with end- arterial circulation (heart, spleen, and kidney) • Septic infarctions may develop when embolization occurs by fragmentation of a bacterial vegetation from a heart valve or when microbes seed an area of necrotic tissue ➢ Factors that influence infarct development: • Collateral blood supplies • Rate at which an obstruction develops • Intrinsic tissue susceptibility to ischemic injury and blood oxygenation
  • 11. Types of infarct: (A) Hemorrhagic, roughly wedge-shaped pulmonary infarct (B) Sharply demarcated white infarct in the spleen
  • 12. Remote kidney infarct replaced by a large fibrotic corticalscar