Thrombosis and embolism

Thrombosis Gangrene Infarction Embolism

Thrombosis inappropriate clot formation within the circulation

pathogenesis is given by Virchow’s triad endothelial injury stasis or turbulence of blood flow blood hypercoagulability

Endothelial Injury The dominant of the three Dysfunctional endothelium may elaborate greater amount of pro-coagulant factors or may synthesize lesser amount of anti-coagulant effectors. Seen commonly in HTN, trauma, radiotherapy, smoking

Hypercoagulability any alteration of the coagulation pathways that predisposes to thrombosis

Hyper-coagulable statesPrimary (Genetic) Mutations like – - Fctor V - Mutation in prothrombin gene Deficiencies like – - Antithrombin III deficiency - Protein C deficiency - Protein S deficiency   

Secondary (Acquired) Prolonged bed rest or immobilization Atrial fibrillation Tissue damage (surgery, fracture, burns) Cancer   Cardiomyopathy Hyperestrogenic states (pregnancy) Oral contraceptive use     Smoking, Obesity

Thrombi can form in Heart Arterial tree Veins

Thrombosis within arteries can lead to necrosis of tissues which it supplies Ex-thrombosis in the coronary vessels lead to myocardial infarction Thrombosis within the renal artery leads to renal infarction

Thrombosis in the viens can cause blockage of venous drainage of tissues clots formed within leg veins can ascend to block the pulmonary circulation Pulmonary embolism

Fate of a thrombus Propagation Dissolution Embolisation Organisation Recanalisation

Infarction Area of ischemic necrosis caused by occlusion of either arterial supply or the venous drainage in a particular tissue 99% infarcts are from thrombotic/embolic events and almost all are from arterial occlusion. Eg Myocardial infarction stroke gangrene of limbs due to peripheral vascular disease

Factors influencing infarction: Nature of blood supply Lungs have dual supply from pulmonary and bronchial arteries Liver has dual supply from hepatic artery and portal vein Kidney, spleen and brain have end arteries with no anastomosis Rate of occlusion: if slow, can allow for collateral formation, Tissue vulnerability to hypoxia: neural tissue is the most susceptible, dying within 3 to 4 minutes, and myocardium within 30 to 40 min Oxygen content in the blood: increased risk of infarction in anemic and cyanosed patient

Gross Morphology Infarction starts as a poorly defined wedge shaped area, with exudates and hemorrhagic area, which gets more defined by a rim of inflammation after some days. 2 types according to gross appearance

Red infarct due to venous obstruction Due to infarction of tissues with dual blood supply like intestine Due to reperfusion-restoring blood supply

White infarct Solid organs like kidney and liver with arterial occlusion

Gangrene Gangrene refers to the death of body tissue due to a lack of blood flow complicated by bacterial infection. Gangrene most commonly affects the extremities, including toes, fingers and limbs

Embolism A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin 99% of the emboli are dislodged thrombi, hence, the term THROMBOEMBOLISM Potential consequence of embolism is INFARCTION of the tissue distal to it.

Types Thromboembolism Fat embolism eg after fractures Air embolism, eg in open carotid injury,after obstetric proceedures. Amniotic fluid embolism in pregnancy

Pulmonary thromboembolism A common cause of death among hospitalized patients In greater than 95% of cases, pulmonary emboli originate from deep leg vein thrombi above the level of the knee Immobilization is a strong risk factor

What is fat embolism Describe the patho physiology of the tissue damage in fat embolism

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