Course Lecturer: Imon Rahman Thrombosis Course Lecturer: Imon Rahman

Thrombosis Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system. When a blood vessel is injured, the body uses platelets (thrombocytes) and fibrin to form a blood clot to prevent blood loss. Even when a blood vessel is not injured, blood clots may form in the body under certain conditions. A clot that breaks free and begins to travel around the body is known as an embolus.

Causes The composition of the blood (hypercoagulability or thrombophilia) Quality of the vessel wall (endothelial cell injury) Nature of the blood flow (stasis, turbulence)

Hypercoagulability Hypercoagulability is caused by, for example, genetic deficiencies or autoimmune disorders. Recent studies indicate that neutrophils play a pivotal role in deep venous thrombosis, mediating numerous pro-thrombotic actions

Endothelial cell injury Causes of injury to the vessel's wall include trauma, surgery, infection or turbulent flow at bifurcations. The main mechanism is exposure of tissue factor to the blood coagulation system.

Disturbed blood flow Causes of disturbed blood flow include stagnation of blood flow past the point of injury, or venous stasis which may occur in heart failure. In varicose veins or after long periods of sedentary behavior, such as sitting on a long airplane flight. Also, atrial fibrillation, causes stagnant blood in the left atrium (LA) or left atrial appendage (LAA), and can lead to a thromboembolism.

Classification Venous Thrombosis it is a phlebothrombosis is a blood clot (thrombus) that forms within a vein. Thrombosis is a term for a blood clot occurring inside a blood vessel. A classical venous thrombosis is deep vein thrombosis (DVT), which can break off (embolize), and become a life-threatening pulmonary embolism (PE). The disease process venous thromboembolism (abbreviated as VTE or DVT/PE) can refer to DVT and/or PE. An inflammatory reaction is usually present, mainly in the superficial veins and, for this reason this pathology is called most of the time thrombophlebitis. In fact, the inflammatory reaction and the white blood cells play a role in the resolution of venous clots.

Causes Venous thrombi are caused mainly by a combination of venous stasis and hypercoagulability—but to a lesser extent endothelial damage and activation. The three factors of stasis, hypercoaguability, and alterations in the blood vessel wall represent Virchow's triad, and changes to the vessel wall are the least understood. Various risk factors increase the likelhood of any one individual developing a thrombosis.

Treatment Evidence-based clinical guidelines from the American College of Chest Physicians were published in February 2012 for the treatment of VTE. Medications used to treat this condition include anticoagulants such as heparin, fondaparinux and more recently dabigatran has shown promise. Vitamin K antagonists such as warfarin are also commonly used.

Portal vein thrombosis Portal vein thrombosis is a form of venous thrombosis affecting the hepatic portal vein, which can lead to portal hypertension and reduction of the blood supply to the liver. It usually has a pathological cause such as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.

Renal vein thrombosis Renal vein thrombosis is the obstruction of the renal vein by a thrombus. This tends to lead to reduced drainage from the kidney. Anticoagulation therapy is the treatment of choice.

Jugular vein thrombosis Jugular vein thrombosis is a condition that may occur due to infection, intravenous drug use or malignancy. Jugular vein thrombosis can have a varying list of complications, including: systemic sepsis, pulmonary embolism, and papilledema. Though characterized by a sharp pain at the site of the vein, it can prove difficult to diagnose, because it can occur at random.

Embolization If a bacterial infection is present at the site of thrombosis, the thrombus may break down, spreading particles of infected material throughout the circulatory system(pyemia, septic embolus) and setting up metastatic abscesses wherever they come to rest. Without an infection, the thrombus may become detached and enter circulation as an embolus, finally lodging in and completely obstructing a blood vessel, which unless treated very quickly will lead to tissue necrosis (an infarction) in the area past the occlusion. If the occlusion is in the coronary artery, myocardial ischaemia is likely to occur, whereby cardiac myocytes cannot function properly due to lack of oxygen. This lack of oxygen is then likely to result in a myocardial infarction.

Treatment Coumarins, Vitamin K antagonists , are anticoagulants that can be taken orally to reduce thromboembolic occurrence. Where a more effective response is required, heparin can be given (by injection) concomitantly. As a side effect of any anticoagulant, the risk of bleeding is increased, so the international normalized ratio of blood is monitored. Self-monitoring and self-management are safe options for competent patients, though their practice varies. In Germany, about 20% of patients were self-managed while only 1% of U.S. patients did home self-testing.