1. Disturbances of Blood Flow- EMBOLISM
H.A. MWAKYOMA, MD

2. Disturbances of Blood Flow
Hyperemia and congestion
Hemorrhage
Ischemia
Thrombosis
Postmortem clots
Disseminated intravascular coagulation
Embolism
Infarction
Edema
Shock

3. 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 is the process by which a detached intravascular solid, liquid, or gaseous mass is carried by the blood to a site distant from its point of origin.

4. Classification of emboli
Thromboemboli –commonest: arterial,venous ,paradoxic
Air (gas )
Fat
Bone marrow
Tumour
Cholesterol
Foreign body
Amniotic fluid

5. Consequences of embolization
↓perfusion distal to embolus
Affected by collateral or dual blood supply
Possible infarction of tissue

6. Thromboemboli Most important clinically
Detached thrombi cause the commonest type of embolism
Venous-originate from veins & carried by venous system to lungs (pulmonary)
Arterial originate in large arteries, heart or 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

7. Common locations in which venous and
arterial emboli cause infarction and the anatomical routes by which they reach
these organs

8. 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”

9. Pulmonary Embolus = saddle emboli
Figure 4-17 Large embolus derived from a lower extremity deep venous thrombosis and now impacted in a pulmonary artery branch.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June :26 PM)
© 2005 Elsevier

10. 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

11. 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

13. Effects of emboli Depends on the
Collateral vascular supply of the affected tissue
The vulnerability of the tissue to ischemia
Calibre of occluded vessel

14. Fat Embolism Aetiology : TRAUMATIC CAUSES:
Definition : embolism caused by fat in the circulation
Aetiology :
TRAUMATIC CAUSES:
Trauma with multiple fractures of long bones and/or operative manipulation of fractures;
Trauma to adipose tissue or fatty liver; :

15. Fat Embolism—cont-- Acute pancreatitis. Extensive burns
NON-TRAUMATIC CAUSES
Acute pancreatitis.
Extensive burns
Diabetes mellitus
Fatty liver
Sickle cell anaemia
Decompression sickness
Inflammation of the bones and soft tissue
NB: Fat emboli tend to be small and they often cause
small infarcts adjacent to capillaries at the sites
where they lodge in.

16. Fat Embolism Pathogenesis: Mechanical theory:
Mechanical obstruction by microemboli of neutral fat +platelet &RBC aggregates
Intravascular coagulation theory:
Chemical irritation (local injury to endothelium) from release of fatty acids + platelet activation & recruitment of granulocyyes –release of free radicals,protease &ecosanoids →DIC

17. Fat emboli

18. Sites of embolization
lungs: pulmonary insufficiency
brain: restlessness, convulsions delirium, coma and sudden death
Demonstration of fat embolism
Fat globules in capillaries demonstrated in frozen sections of lung, brain .-using fat stains
Sudan dyes- Sudan black, Sudan IV or III)
Oil red O
Osmic acid

19. Clinical features Asymptomatic (up to 90% of cases)
Pulmonary insufficiency
Neurological symptoms
Anemia
Thrombocytopenia—petechial rash
Prognosis
Asymptomatic (up to 90% of cases)
Fatal in severe cases

20. Air Embolism- Gaseous 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- Decompression sickness.
Mismanaged intravenous infusions
Pathogenesis:Usually more than 150 ml of air needed to produce symptoms
Symptoms of ischemia, infarction or DIC

21. Decompression sickness
Is a specialised form of gas embolism
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

22. Amniotic Fluid Embolism
Def: Obstetrical complication with entry of amniotic fluid into uterine venous circulation
The uterine contractions that occur during childbirth can sometimes cause amniotic fluid to be driven through the placental bed into the maternal 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

23. Amniotic Fluid Embolism
Morphology:post mortem – particulate material in pulmonary arteries / thrombi in small vessels.
Pulmonary oedema,diffuse alveolar damage,systemic fibrin thrombi(DIC)

24. 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

25. Infarction Aetiology Thrombosis or embolism 99%
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

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

27. 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

28. 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)

29. 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

30. 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.

31. Examples of infarcts
Figure 4-19 Examples of infarcts. A, Hemorrhagic, roughly wedge-shaped pulmonary infarct. B, Sharply demarcated white infarct in the spleen.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 27 June :26 PM)
© 2005 Elsevier

32. In this low power view, the darker pink (eosinophilic)areas are coagulation necrosis (infarcted myocardial cells). The lighter pink areas at the left top and bottom are viable myocardium and the basophilic areas contain acute inflammatory cells entering the necrotic tissue. Note the patchy distribution of the infarcted myocardium. This patient died several days after the infarction occurred.
Iowa Histopathology Series

34. 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

35. 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: minutes
Oxygen content of blood
hemoglobin concentration and saturation