1. Fate of Thrombi
Propagation: growth and spread with maintenance of physical continuity
Embolization: detachment and dislocation to other sites
Dissolution: by fibrinolysis
Organization: fibrosis and recanalization

2. Complications of Thrombi
Occlusion of blood vessels
Veins: Congestion and edema
Arteries: Ischemia and infarcts in areas supplies by the vessel
Embolization. The most serious is pulmonary embolism

3. Venous Thrombosis Mostly in superficial or deep veins of the legs
Superficial vein thrombosis lead to local edema, tenderness and infections of overlying skin
Deep vein thrombosis is more serious; it may lead to pulmonary emboli, causes edema, pain and tenderness

4. Deep Vein Thrombosis (DVT)
Stasis due to heart failure
Sedentary life style and inactivity
Conditions associated with DVT include
Cancers, pregnancy, advanced age, prolonged bed rest, post-operative, late pregnancy, and postpartum
Congenital conditions such as Factor V mutation, antithrombin III deficiency, protein C and S deficiency and defects in fibrinolysis

5. EMBOLISM
Intravascular passage of detached material distant to the site of origin leading to obstruction of the vascular lumen.
Types of emboli
Thrombi (99%)
Atherosclerotic fragments (lipid, cholesterol, calcific tissue)
Air
Fat droplets
Liquid
Tumor fragments

6. Pulmonary Thromboembolism
Etiology: Deep vein thrombosis (95%)
Small thrombi are silent (majority)
Large thrombi cause saddle emboli and lead to death or cor pulmonale
Medium size thrombi lead to pulmonary hemorrhage, but not infarcts
Recurrent emboli may cause pulmonary hypertension

7. Systemic Thromboembolism
Etiology: Intracardiac thrombi. Less commonly, aterial origin, valvular vegetations.
Affected Sites depend on the site of origin
Lower limbs (75%) and brain (10%) are affected most
Manifestations and complications depend on collateral circulation

8. Infarction
An area of ischemic necrosis caused by occlusion of either arterial supply or the venous drainage of a particular tissue
99% are caused by arterial occlusion due to thromboembolic events
Less common causes include:
Vasopasm
hemorrhage within atheroma
Twisted artery
External pressure

9. TYPES OF INFARCTS Red infarcts (hemorrhagic). White infarcts (anemic).
Septic infarcts.

10. TYPES OF INFARCTS Red infarcts occur in: White infarcts occur:
venous occlusion (eg. ovarian torsion).
loose tissue, eg. lung.
tissues with dual circulation, eg. intestine.
tissues previously congested.
reestablished flow to a site with previous arterial occlusion.
White infarcts occur:
with arterial occlusions.
in solid organs.

11. Factors influencing the development of an infarct
Nature of vascular supply.
Rate of the development of arterial occlusion.
Vulnerability of tissue to hypoxia.
Blood oxygen content.

12. Shock
Definition: Systemic hypoperfusion and reduced oxygen delivery due to either reduced cardiac output, or ineffective circulatory blood volume.
Results of shock:
hypotension.
impaired tissue perfusion.
cellular hypoxia.

13. Major types of shock Cardiogenic shock. Hypovolemic shock.
Septic shock.

14. Septic shock High mortality rate (25-75%).
Gram positive bacteria: most common cause
Gram negative bacteria produce endotoxins
Endotoxins are lipopolysaccharides (LPS).
LPS is composed of fatty acid core (lipid A) and a polysaccharide coat.
LPS binds as a complex with circulating protein to CD14 on monocytes and macrophages.

15. LPS TNF IL-6/IL-8 NO, PAF Low doses Medium doses High doses
other mediators
Low doses
Monocyte activation
Enothelial activation
Complement activation
Medium doses
Fever
Acute phase
reactants
High doses
Systemic vasodilatation
Deacreased myocardial
contractility
Endothelial injury
ARDS, thrombosis.
DIC
Local inflammation
Systemic effects
Septic shock

16. Stages of Shock Non-progressive stage: Progressive stage:
Compensatory mechanisms maintains perfusion of vital organs.
Progressive stage:
Tissue hypoperfusion with metabolic and circulatory worsening.
Irreversible stage:
Severe irreversible tissue and cellular injury.