Thrombosis and antithrombotic therapy




Thrombosis


Thrombosis is the pathological process whereby platelets and fibrin interact with the vessel wall to form a haemostatic plug to cause vascular obstruction. It may be arterial, causing ischaemia, or venous, leading to stasis (Fig. 44.1). The thrombus may be subsequently lysed by fibrinolysis, organized, recanalized or embolized. Thrombosis underlies ischaemic heart, cerebrovascular and peripheral vascular diseases, venous occlusion and pulmonary embolism; it plays an important part in pre-eclampsia.



Arterial thrombosis


This occurs in relation to damaged endothelium, e.g. atherosclerotic plaques. Exposed collagen and released tissue factor cause platelet aggregation and fibrin formation (Box 44.1).






Box 44.1 Risk factors for arterial thrombosis


Hypertension


Smoking


Diabetes*


Hyperlipidaemia*


↑ Homocysteine*


Polycythaemia/thrombocythaemia


↑ Factor VIII


↑ Fibrinogen


Lupus anticoagulant


Heparin therapy (see Chapter 45)


*May be related to an inherited abnormality






Venous thrombosis


All hospital in-patients are assessed for risk of venous thromboembolism (VTE) and appropriate measures for VTE prophylaxis instituted where indicated. The most common site for deep vein thrombosis (DVT) is the leg which may be below knee or involve veins in the thigh and the iliac veins.


Factors affecting blood flow (e.g. stasis, obesity), alterations in blood constituents and damage to vascular endothelium (e.g. caused by sepsis, surgery or indwelling catheters) are important risk factors (Box 44.2). Diagnosis can be confirmed by imaging, e.g. Doppler ultrasound probe (Fig. 44.1) or, less commonly, venography. Blood tests, e.g. detection of elevated levels of d-dimers, which are derived from fibrinogen, can also be helpful, especially if recurrence is suspected.





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Jun 12, 2016 | Posted by in HEMATOLOGY | Comments Off on Thrombosis and antithrombotic therapy

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