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Intracranial Thrombosis: Formation or presence of a blood clot (THROMBUS) in a blood vessel within the SKULL. Intracranial thrombosis can lead to thrombotic occlusions and BRAIN INFARCTION. The majority of the thrombotic occlusions are associated with ATHEROSCLEROSIS.Thrombosis: Formation and development of a thrombus or blood clot in the blood vessel.Venous Thrombosis: The formation or presence of a blood clot (THROMBUS) within a vein.Coronary Thrombosis: Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.Sinus Thrombosis, Intracranial: Formation or presence of a blood clot (THROMBUS) in the CRANIAL SINUSES, large endothelium-lined venous channels situated within the SKULL. Intracranial sinuses, also called cranial venous sinuses, include the superior sagittal, cavernous, lateral, petrous sinuses, and many others. Cranial sinus thrombosis can lead to severe HEADACHE; SEIZURE; and other neurological defects.Carotid Artery Thrombosis: Blood clot formation in any part of the CAROTID ARTERIES. This may produce CAROTID STENOSIS or occlusion of the vessel, leading to TRANSIENT ISCHEMIC ATTACK; CEREBRAL INFARCTION; or AMAUROSIS FUGAX.Anticoagulants: Agents that prevent clotting.Sagittal Sinus Thrombosis: Formation or presence of a blood clot (THROMBUS) in the SUPERIOR SAGITTAL SINUS or the inferior sagittal sinus. Sagittal sinus thrombosis can result from infections, hematological disorders, CRANIOCEREBRAL TRAUMA; and NEUROSURGICAL PROCEDURES. Clinical features are primarily related to the increased intracranial pressure causing HEADACHE; NAUSEA; and VOMITING. Severe cases can evolve to SEIZURES or COMA.Phlebography: Radiographic visualization or recording of a vein after the injection of contrast medium.Intracranial Embolism and Thrombosis: Embolism or thrombosis involving blood vessels which supply intracranial structures. Emboli may originate from extracranial or intracranial sources. Thrombosis may occur in arterial or venous structures.Iliac Vein: A vein on either side of the body which is formed by the union of the external and internal iliac veins and passes upward to join with its fellow of the opposite side to form the inferior vena cava.Thrombophilia: A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.Femoral Vein: The vein accompanying the femoral artery in the same sheath; it is a continuation of the popliteal vein and becomes the external iliac vein.Upper Extremity Deep Vein Thrombosis: DEEP VEIN THROMBOSIS of an upper extremity vein (e.g., AXILLARY VEIN; SUBCLAVIAN VEIN; and JUGULAR VEINS). It is associated with mechanical factors (Upper Extremity Deep Vein Thrombosis, Primary) secondary to other anatomic factors (Upper Extremity Deep Vein Thrombosis, Secondary). Symptoms may include sudden onset of pain, warmth, redness, blueness, and swelling in the arm.Portal Vein: A short thick vein formed by union of the superior mesenteric vein and the splenic vein.Cerebral Veins: Veins draining the cerebrum.Heparin: A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.Factor V: Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owren's disease.Fibrinolytic Agents: Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.Hemostasis: The process which spontaneously arrests the flow of BLOOD from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements (eg. ERYTHROCYTE AGGREGATION), and the process of BLOOD COAGULATION.Heparin, Low-Molecular-Weight: Heparin fractions with a molecular weight usually between 4000 and 6000 kD. These low-molecular-weight fractions are effective antithrombotic agents. Their administration reduces the risk of hemorrhage, they have a longer half-life, and their platelet interactions are reduced in comparison to unfractionated heparin. They also provide an effective prophylaxis against postoperative major pulmonary embolism.Cavernous Sinus Thrombosis: Formation or presence of a blood clot (THROMBUS) in the CAVERNOUS SINUS of the brain. Infections of the paranasal sinuses and adjacent structures, CRANIOCEREBRAL TRAUMA, and THROMBOPHILIA are associated conditions. Clinical manifestations include dysfunction of cranial nerves III, IV, V, and VI, marked periorbital swelling, chemosis, fever, and visual loss. (From Adams et al., Principles of Neurology, 6th ed, p711)Blood Coagulation: The process of the interaction of BLOOD COAGULATION FACTORS that results in an insoluble FIBRIN clot.Antiphospholipid Syndrome: The presence of antibodies directed against phospholipids (ANTIBODIES, ANTIPHOSPHOLIPID). The condition is associated with a variety of diseases, notably systemic lupus erythematosus and other connective tissue diseases, thrombopenia, and arterial or venous thromboses. In pregnancy it can cause abortion. Of the phospholipids, the cardiolipins show markedly elevated levels of anticardiolipin antibodies (ANTIBODIES, ANTICARDIOLIPIN). Present also are high levels of lupus anticoagulant (LUPUS COAGULATION INHIBITOR).Vena Cava, Inferior: The venous trunk which receives blood from the lower extremities and from the pelvic and abdominal organs.Thromboembolism: Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.Platelet Aggregation Inhibitors: Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.Lateral Sinus Thrombosis: Formation or presence of a blood clot (THROMBUS) in the LATERAL SINUSES. This condition is often associated with ear infections (OTITIS MEDIA or MASTOIDITIS) without antibiotic treatment. In developed nations, lateral sinus thrombosis can result from CRANIOCEREBRAL TRAUMA; BRAIN NEOPLASMS; NEUROSURGICAL PROCEDURES; THROMBOPHILIA; and other conditions. Clinical features include HEADACHE; VERTIGO; and increased intracranial pressure.Bleeding Time: Duration of blood flow after skin puncture. This test is used as a measure of capillary and platelet function.Thrombectomy: Surgical removal of an obstructing clot or foreign material from a blood vessel at the point of its formation. Removal of a clot arising from a distant site is called EMBOLECTOMY.Fibrin Fibrinogen Degradation Products: Soluble protein fragments formed by the proteolytic action of plasmin on fibrin or fibrinogen. FDP and their complexes profoundly impair the hemostatic process and are a major cause of hemorrhage in intravascular coagulation and fibrinolysis.Stents: Devices that provide support for tubular structures that are being anastomosed or for body cavities during skin grafting.Protein S Deficiency: An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.Platelet Aggregation: The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.Mesenteric Veins: Veins which return blood from the intestines; the inferior mesenteric vein empties into the splenic vein, the superior mesenteric vein joins the splenic vein to form the portal vein.Subclavian Vein: The continuation of the axillary vein which follows the subclavian artery and then joins the internal jugular vein to form the brachiocephalic vein.Drug-Eluting Stents: Stents that are covered with materials that are embedded with chemicals that are gradually released into the surrounding milieu.Prothrombin: A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.Risk Factors: An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.Popliteal Vein: The vein formed by the union of the anterior and posterior tibial veins; it courses through the popliteal space and becomes the femoral vein.Jugular Veins: Veins in the neck which drain the brain, face, and neck into the brachiocephalic or subclavian veins.Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.Venous Thromboembolism: Obstruction of a vein or VEINS (embolism) by a blood clot (THROMBUS) in the blood stream.Hemorrhage: Bleeding or escape of blood from a vessel.Antibodies, Antiphospholipid: Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals.Protein C Deficiency: An absence or deficiency in PROTEIN C which leads to impaired regulation of blood coagulation. It is associated with an increased risk of severe or premature thrombosis. (Stedman's Med. Dict., 26th ed.)Cranial Sinuses: Large endothelium-lined venous channels situated between the two layers of DURA MATER, the endosteal and the meningeal layers. They are devoid of valves and are parts of the venous system of dura mater. Major cranial sinuses include a postero-superior group (such as superior sagittal, inferior sagittal, straight, transverse, and occipital) and an antero-inferior group (such as cavernous, petrosal, and basilar plexus).Activated Protein C Resistance: A hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). The activated form of Factor V (Factor Va) is more slowly degraded by activated protein C. Factor V Leiden mutation (R506Q) is the most common cause of APC resistance.Lupus Coagulation Inhibitor: An antiphospholipid antibody found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. In vitro, the antibody interferes with the conversion of prothrombin to thrombin and prolongs the partial thromboplastin time. In vivo, it exerts a procoagulant effect resulting in thrombosis mainly in the larger veins and arteries. It further causes obstetrical complications, including fetal death and spontaneous abortion, as well as a variety of hematologic and neurologic complications.Platelet Activation: A series of progressive, overlapping events, triggered by exposure of the PLATELETS to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug.Thromboplastin: Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Thrombolytic Therapy: Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.Follow-Up Studies: Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.Renal Veins: Short thick veins which return blood from the kidneys to the vena cava.Splenic Vein: Vein formed by the union (at the hilus of the spleen) of several small veins from the stomach, pancreas, spleen and mesentery.