תסחיף ריאתי I: מבוא

A thrombus is a blood clot that forms within blood vessels and can block blood flow, a condition called thrombosis. An embolus forms when part of the thrombus breaks away and travels through the bloodstream. If the embolus lodges in a pulmonary artery, it causes a pulmonary embolism.

Deep vein thrombosis (DVT) is a blood clot that forms in the deep veins of the legs. In most cases, the embolus that causes pulmonary embolism originates from a thrombus in these deep leg veins. DVT and PE together are considered part of the same disease process called venous thromboembolism.

Virchow's triad includes venous stasis, hypercoagulability, and endothelial injury. Venous stasis occurs when blood flow slows due to immobility from surgery or prolonged sitting. Hypercoagulability results from conditions like antithrombin III deficiency or pregnancy. Endothelial injury may be caused by trauma or catheterization.

Venous stasis occurs when blood flow becomes stagnant due to immobility. Risk factors include prolonged bed rest after orthopedic surgery, extended plane flights, heart failure, obesity, pregnancy, and catheter use. Any condition limiting movement can slow blood circulation in the veins.

Hypercoagulability can be inherited, such as factor V Leiden or protein C/S deficiency, or acquired through malignancy, oral contraceptives, pregnancy, or inflammatory disorders. These conditions increase the tendency of blood to clot, raising the risk of thrombus formation and subsequent pulmonary embolism.

Endothelial injury damages the inner lining of blood vessels, activating clotting pathways that promote thrombus formation. Trauma, surgery, or prior thrombosis can cause this vessel wall damage. When a resulting clot dislodges and travels to the lungs, it causes pulmonary embolism.

Hospitalized and cancer patients face increased risk due to immobility, inflammation, and procoagulant states that promote blood clotting. These factors align with Virchow's triad mechanisms: reduced blood flow, increased clotting tendency, and vessel damage. Understanding these mechanisms supports early detection and prevention strategies in chronic obstructive pulmonary disease clinical contexts.