EMBOLISM AND INFARCTION EMBOLISM AND INFARCTION

Dr.Vaishali

ObjectivesObjectives

Embolism-Defination ,types,Mechanism Embolism-Defination ,types,Mechanism C/FC/F

Infarction-Types, morphology , Infarction-Types, morphology , coagulative necrosis-gross/microscopycoagulative necrosis-gross/microscopy

Factors affecting infarctionFactors affecting infarction

Embolus- Embolus- A detached intravascular solid, liquid, or A detached intravascular solid, liquid, or gaseous mass carried by blood away from the point of gaseous mass carried by blood away from the point of originorigin

About 99% of emboli are from dislodged thrombus About 99% of emboli are from dislodged thrombus thromboembolusthromboembolus

Other rare forms of emboli:Other rare forms of emboli: - Droplets of fat, bubbles or air or nitrogen, tumor - Droplets of fat, bubbles or air or nitrogen, tumor

fragments, bits of bone marrow, foreign bodies (bullets)fragments, bits of bone marrow, foreign bodies (bullets)

- Cholesterol emboli – atherosclerotic debris - Cholesterol emboli – atherosclerotic debris

Lodge in too-small vessels Lodge in too-small vessels complete or partial vascular complete or partial vascular occlusion occlusion infarction infarction

Pulmonary Thromboembolism:Pulmonary Thromboembolism:

Thrombi from deep leg above the level of the Thrombi from deep leg above the level of the knee knee right side of heart right side of heart pulm vasculature pulm vasculature

CausesCauses

90%- Deep veins of lower extremities90%- Deep veins of lower extremities

OthersOthers

-Pelvic venous plexus-Pelvic venous plexus

-Right side of heart-Right side of heart

-Indwelling lines in systemic venous system/ -Indwelling lines in systemic venous system/ pulmonary arterypulmonary artery

Clinical features of pulmonary Clinical features of pulmonary embolismembolism

Acute pulmonary embolism Acute pulmonary embolism

-Asymptomatic -Asymptomatic

-Transient dyspnea and tachypnea -Transient dyspnea and tachypnea

-Pulmonary infarction -Pulmonary infarction

-Cardiovascular collapse & sudden death-Cardiovascular collapse & sudden death

Chronic pulmonary embolismChronic pulmonary embolism

-Usually asymptomatic-Usually asymptomatic

-Pulmonary hypertension and right-sided -Pulmonary hypertension and right-sided heart failure heart failure

Fate Fate - 60-80% pulm emboli are clinically silent 60-80% pulm emboli are clinically silent

- Cor pulmonale- if multipleCor pulmonale- if multiple

- Pulmonary haemorrhage- if in medium sized Pulmonary haemorrhage- if in medium sized arteriesarteries

- Infarction- if in end arteriolesInfarction- if in end arterioles

Systemic Thromboembolism:Systemic Thromboembolism: Emboli within arterial Emboli within arterial circulationcirculation

Most (80%) arise from intracardiac mural thrombiMost (80%) arise from intracardiac mural thrombi

Aortic aneurysms, thrombi on atherosclerotic plaques, Aortic aneurysms, thrombi on atherosclerotic plaques, or fragmentation of valvular vegetationor fragmentation of valvular vegetation

Sites for arteriolar embolization-Sites for arteriolar embolization- Lower extremities (75%) > brain (10%)>intestines> Lower extremities (75%) > brain (10%)>intestines>

kidneys> spleen >upper extremities kidneys> spleen >upper extremities

Generally cause infarction of tissues Generally cause infarction of tissues

Fat Embolism:Fat Embolism:•• 1-3 days after ≠ of long bones / soft tissue 1-3 days after ≠ of long bones / soft tissue

trauma / burnstrauma / burns

Microscopic Microscopic - Fat globules- Fat globules

Clinical presentationClinical presentation- Diffuse petechial rash in nondependent areas- Diffuse petechial rash in nondependent areas

- Sudden onset of tachypnoea, dyspnoea, - Sudden onset of tachypnoea, dyspnoea, tachycardia, neurologic symptoms – irritability, tachycardia, neurologic symptoms – irritability, can progress to comacan progress to coma

Pathogenesis of fat emboliPathogenesis of fat emboli

Both mechanical obstruction and biochemical injury Both mechanical obstruction and biochemical injury

Microemboli of neutral fat Microemboli of neutral fat ↓ ↓ Occlusion of the pulmonary and cerebral vsOcclusion of the pulmonary and cerebral vs ↓ ↓Local platelet and RBC aggregation release of FFA from Local platelet and RBC aggregation release of FFA from

the fat globulesthe fat globules ↓ ↓local toxic injury to endothelium local toxic injury to endothelium ↓ ↓

Platelet activation and recruitment of granulocytesPlatelet activation and recruitment of granulocytes

Air EmbolismAir Embolism

Gas bubbles in circulation (>100 cc of air)Gas bubbles in circulation (>100 cc of air) obstruct vascular flow & cause infarctsobstruct vascular flow & cause infarcts

CauseCause- Obstetric procedures or chest wall injuryObstetric procedures or chest wall injury

- Iatrogenic- Thoracocentesis & dialysis- Iatrogenic- Thoracocentesis & dialysis

Decompression sickness & Caisson diseasesDecompression sickness & Caisson diseases

At riskAt risk- Scuba and deep sea diversScuba and deep sea divers- underwater construction workers individuals in underwater construction workers individuals in

unpressurized aircraft in rapid ascent unpressurized aircraft in rapid ascent

MechanismMechanism

Sudden changes in atm pressure- ↑gas dissolve Sudden changes in atm pressure- ↑gas dissolve in tissues in tissues depressurize too quickly depressurize too quickly gas gas expands in tissues and bubbles out of solutionexpands in tissues and bubbles out of solution

Clinical featuresClinical featuresBends- rapid formation of gas bubbles within skeletal muscles and Bends- rapid formation of gas bubbles within skeletal muscles and

supporting tissues about joints supporting tissues about joints

Focal ischemia in tissues, including brain and heartFocal ischemia in tissues, including brain and heart

Chokes- edema, hemorrhages, emphysema may appear in lungsChokes- edema, hemorrhages, emphysema may appear in lungs

Avascular necrosis of bones due to ischemia ( Caisson disease) Avascular necrosis of bones due to ischemia ( Caisson disease)

TreatmentTreatment- Slow decompression in compression chambers- Slow decompression in compression chambers

Amniotic Fluid EmbolismAmniotic Fluid Embolism::CauseCause – –Complication of labor and the immediate postpartum Complication of labor and the immediate postpartum

period period

Clinical presentation-Clinical presentation- Sudden severe dyspnea, cyanosis, hypotensive shock Sudden severe dyspnea, cyanosis, hypotensive shock

seizures and coma seizures and coma pulm edema & DIC pulm edema & DIC

MechanismMechanism--Tear in placental membrane & rupture of uterine veins Tear in placental membrane & rupture of uterine veins

amniotic fluid and its contents enter maternal amniotic fluid and its contents enter maternal circulationcirculation

Miscellaneous pulmonary emboliMiscellaneous pulmonary emboli

Talc emboli - Granulomatous response in the Talc emboli - Granulomatous response in the lungs lungs

Cotton emboli - Cleansing of the skin prior to Cotton emboli - Cleansing of the skin prior to venipuncturevenipuncture

Schistosomiasis- Embolization of ova to the Schistosomiasis- Embolization of ova to the lungs from bladder or gutlungs from bladder or gut

Tumor emboli - Occasionally seen in lungTumor emboli - Occasionally seen in lung

INFARCTIONINFARCTIONCoagulative necrosis distal to occlusion of an Coagulative necrosis distal to occlusion of an

end- arteryend- artery

Types of infarctTypes of infarct

- Pale infarctPale infarct

- Red infarctRed infarct

- Septic infarctSeptic infarct

PALE/ WHITE PALE/ WHITE INFARCTINFARCT

UUsually due to arterial occlusionsually due to arterial occlusion

SitesSites- Heart, kidney & spleen (Solid organs)- Heart, kidney & spleen (Solid organs)

GrossGross- Wedge-shaped- Occluded vessel at apex, - Wedge-shaped- Occluded vessel at apex, periphery of organ forms the baseperiphery of organ forms the base

Initial hyperemia Initial hyperemia ▼▼ Soft, sharply delineated and light yellow Soft, sharply delineated and light yellow

with dark- with dark- red borderred border

MicroMicro- Uniform coagulative necrosis- Uniform coagulative necrosis

Solidity of tissue limits the amount of Solidity of tissue limits the amount of hemorrhage that can seep into the area of hemorrhage that can seep into the area of ischemic necrosis from adjacent capillary bedsischemic necrosis from adjacent capillary beds

Few extravasated RBCs are lysed, so white Few extravasated RBCs are lysed, so white infarcts become more pale and sharply defined infarcts become more pale and sharply defined with timewith time

Over course of a few days, it becomes more Over course of a few days, it becomes more firm and brownfirm and brown

RED INFARCTRED INFARCTHemorrhagic, usually venous occlusion but can be due Hemorrhagic, usually venous occlusion but can be due

to arterial occlusionto arterial occlusion

Sites- Organs with dual blood supply and extensive Sites- Organs with dual blood supply and extensive collateralscollaterals

LungsLungs

Small Intestine Small Intestine

BrainBrain

Gross- Sharply circumscribed, firm & dark red to purpleGross- Sharply circumscribed, firm & dark red to purple

Several days- Acute inflammatory cells infiltrate Several days- Acute inflammatory cells infiltrate the necrotic area from the viable areathe necrotic area from the viable area

Cellular debris phagocytosed by PMNs & Cellular debris phagocytosed by PMNs & macrophages- granulation tissue forms-Scarmacrophages- granulation tissue forms-Scar

SEPTIC INFARCTSEPTIC INFARCT Necrotic tissue of an infarct is seeded by Necrotic tissue of an infarct is seeded by

pyogenic bacteria and become infectedpyogenic bacteria and become infected

Pulmonary infarcts- Inhaled bacteriaPulmonary infarcts- Inhaled bacteria

Bacterial endocarditis- Emboli are infected and Bacterial endocarditis- Emboli are infected and the resultant infarcts are septicthe resultant infarcts are septic

Factors that Influence Development Factors that Influence Development of an Infarctof an Infarct

Nature of vascular supplyNature of vascular supply

Availability of alternate blood supply is most Availability of alternate blood supply is most important factorimportant factor

Rate of development of occlusionRate of development of occlusion

- Slowly developing - Slowly developing less likely to cause infarction less likely to cause infarction

Infarction in specific Infarction in specific locationslocations

Myocardial infarctionMyocardial infarction::

- Transmural / subendocardialTransmural / subendocardial

- May be pale or red depending on the extent of - May be pale or red depending on the extent of reflow of blood to infarcted areareflow of blood to infarcted area

Pulmonary infarctsPulmonary infarcts

-Only 10% of emboli elicit symptoms referable to -Only 10% of emboli elicit symptoms referable to pulmonary infarctionpulmonary infarction

Cause- CCFCause- CCF

Cerebral infarcts-Cerebral infarcts- Due to local ischemia or Due to local ischemia or generalised reduction of blood flowgeneralised reduction of blood flow

Intestinal infarcts-Intestinal infarcts- Necrosis of villous tipNecrosis of villous tip Mucosal and submucosal haemorrhagic Mucosal and submucosal haemorrhagic

necrosisnecrosis

If small – UlcerateIf small – Ulcerate

If large- StrictureIf large- Stricture

If transmural- Bowel perforation If transmural- Bowel perforation and massive bleedingand massive bleeding

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