There are many types of blood contacting medical devices. For example, in the area of cardiovascular treatment there are heart valves, vascular grafts and stents and in cardiac rhythm management there are pacemakers, implantable cardioverter defibrillators (ICDs) and cardiac monitors. Also, implantable catheters and ports are used for venous access and drug delivery in patients, with conditions such as cancer and systemic hypertension.
However, these devices are prone to failure, most notably due to thrombus formation. The pathological development of a thrombus presents considerable health hazards as it is not haemostasis (normal thrombus formation). A pathological thrombus is created when there is an interruption to the blood coagulation system equilibrium. This can block the flow of blood which causes numerous amounts of severe health conditions. If it separates from the wall of a vessel and embeds in the lungs, or other major organs, it can be a death-causing embolus.
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It was hypothesised by Rudolph Virchow that irregularities in three parts (Virchow’s triad) lead to the formation and spreading of thrombus. Nowadays it is achievable to measure some of the influences that increase the development of venous thromboembolism (VTE) and other cardiovascular syndromes. The Virchow’ triad suggested that the formation and proliferation of thrombus was caused by (i) blood flow, (ii) vessel wall and (iii) blood components. Irregularities in any of these three areas can lead to formation of thrombus.
Platelet aggregates and fibrin are components of thrombi that develop on medical devices that are in contact with blood. Therefore, it seems the most obvious solution to use anticoagulants and antiplatelet agents to inhibit or handle clotting. Therefore, it is crucial that haematologists comprehend the mechanisms behind clotting caused by medical devices in contact with blood and how to treat
Venous thromboembolism (VTE) is an epidemic that rain rapid in Australia and was a very big concern. The study of this sickness was a major Problem as it had affected the demographic area of Perth, Australia. The epidemic is a very big problem as VTE is connected with the trauma, surgery, and cancer and this sickness is caused while
The occlusion, caused by a haemostatic plug or thrombus is comprised of a fibrous protein called fibrin. This protein polymerises to create a tightly woven mesh, trapping platelets within the fibrin fibre meshwork, resulting in the
Now I want to talk about vascular access devices. They can be catheters as well as ports and are for repeated access. This includes central venous catheter, peripherally inserted central catheters and implanted ports. (Potter) A central venous catheter is a way to provide medications, nutrition, fluid, and blood products for a long period of time. The difference of a central venous catheter and peripheral intravenous catheter is, the central venous is usually inserted in a vein that goes directly to the heart. Also, central venous catheters
Deep vein thrombosis (DVT) is a type of cardiovascular disease. DVT is a blood clot that forms in the large deep veins in the leg or pelvis area and grows toward the heart. Including the veins in the calf and thighs, the femoral, popliteal, and iliofemoral vein are also the sites of DVT development. It is a mainly common and dangerous condition (Kesieme et al., 2011). Some DVTs may cause no pain or swelling, whereas others might be quite painful and result in a lot of swelling. Mortality is not high with prompt diagnoses and treatment for most DVTs. However some can be a threat to your life, especially the ones that develop in the deep veins as compared to the clots that develop in the visible superficial veins. Clot which forms in the deep veins is more likely to break free and travel through the veins, which is then called an embolus. When an embolus travels from the legs or pelvis area and lodges into the lung artery, the condition is known as a pulmonary embolism or PE. This is a potentially fatal condition if it is not treated immediately and can lead to death. As high as 50% of the time a DVT can progress to pulmonary embolism. Collectively, DVT and PE are known as venous thromboembolism (VTE). DVT and PE are highly preventable (Kesieme et al., 2011).
Thrombophlebitis means inflammation of a blood clot. It develops when a blood clot slows down the circulation in a vein under the skin. This usually occurs in the legs. Thrombophlebitis can affect veins in the arms or neck, but it is rare. If the affected vein is under the skin it causes superficial thrombophlebitis. If it is deep within a muscle it causes deep vein thrombus (DVT).
Venous thrombosis and arterial thrombosis are considered to be distinct pathophysiological processes due to their evident anatomical variances. With one having to deal with platelet activation while the other involving the clotting system activation, arterial thrombosis and venous thrombosis are similar yet vastly different when it comes to the processes that are performed for the body. These same processes that help the body have to be performed accordingly or the signs and symptoms begin to show. For instance, venous thrombosis can lead to Chronic Venous Insuffiency and other issues when a body part is congested. This is most commonly causes by valvular incompetence in the low-pressure superficial venous system; however, it can also be causes
FXI play a crucial role in coagulation, thromboembolism, and peripheral vascular disease mediated by venous thrombus growth in an endothelial denudated vessel and/or blood stasis. Promotion of the platelet aggregation and fibrin formation at low shear stress by the interaction of FXI and thrombin signify the role of FXI in thromboembolism [47]. Further, reduction in the thrombus formation in a denuded vessel with anti-FXI antibody indicates FXI to be a promising target in coagulation cascade to prevent thromboembolic events [47,48]. Many studies has demonstrated the reduced thrombus formation without increasing the risk of bleeding with antisense oligonucleotide (ASO) along with increased number of fluorescent platelets shed from the
As it was defined in Oxford Concise Medical Dictionary, phlebothrombosis is “an obstruction of a vein by a blood clot, without preceding inflammation of its wall. It is most common within the deep veins of the calf of the leg - deep vein thrombosis (DVT) - in contrast to thrombophlebitis, which affects superficial leg veins. Prolonged immobility, heart failure, pregnancy, injury, and surgery predispose to thrombosis by encouraging sluggish blood flow. Many of these conditions are associated with changes in the clotting factors in the blood that increase the tendency to thrombosis; these changes also occur in some women taking oral contraceptives. The affected leg may become swollen and tender. The main danger is that the clot may become detached and give rise to pulmonary
Hemostasis is the process of blood coagulation. The first thing that happens is the contraction of the smooth muscles in the blood vessel wall. next is the formation of the platelet plug, which become sticky and adhere to the defect to form a temporary plug. Formation of a blood clot then happens. The substance needed for coagulation are normally inactive in the bloodstream. some substances in clotting are ones such as, calcium ion, enzyme precursors, vitamin k, fibrinogen, calcium. After these substances are obtained then the final steps begin. First substance released from the damaged tissue and sticky platelets initiate a reaction that leads to the formation of prothrombinase. Next the prothrombinase converts prothrombin in the blood to
The precursor to thrombin is prothrombin, an inactivated protein produced in the liver. Upon injury prothrombin converts to thrombin with the purpose of catalyzing the conversion of fibrinogen to fibrin. The process changes the blood plasma soluble fibrinogen to fibrin, which is not plasma soluble. In order to do this the interaction removes two peptide chains from the ends of fibrinogen. Once this reaction is complete fibrin will begin to form a blood clot around the site of injury. While the interaction between fibrinogen is important it is not the only major
“Qualitative or quantitative abnormalities interfere with or prevent enzymatic reactions that transform clotting factors, circulating as plasma proteins into a stable fibrin clot” (Huether and McCance 544). Some defects are caused by a single factor, these would be hemophilias and von Willebrand disease and some are acquired and result from “deficient synthesis of clotting factors by the liver” which is caused by liver disease and vitamin K deficiency (Huether and McCance 544). Other abnormalities in coagulation disorders are caused by “pathologic conditions” such as a cardiovascular abnormality that alters blood flow. An example of this is thromboembolic disease where blood clots block vessels (Huether and McCance 544). Vasculitis and damage to vessels activates platelets which activates coagulation (Huether and McCance 544). Prolonged vasculitis leads to clogging of the
According to the article “Anticoagulants: A Review of the Pharmacology, Dosing, and Complications” by Mohammed Alquwaizani, Leo Buckley, Christopher Adams, John Fanikos, anticoagulants persist as the primary strategy for preventing and treating thrombosis. Hemorrhage is a principal adverse event while using anticoagulant drugs.
Because of this, the circulation is blocked and a stroke or heart attack may occur if the site of the blood clot is in one of the brain’s vessels, or the latter being in either the arteries or the heart. The purpose of anticoagulation drugs, such as Warfarin, is to thin the blood in order to delay blood clots from forming; thus, preventing a stroke or heart attack (12). Patients with mechanical valves are required to take Warfarin for the rest of their lives because thrombosis may occur when the body detects a foreign material or when the blood flow is not regulated. In our proposed modification, the metal would be covered with the individual’s own tissue; therefore, the surface of the mechanical valve would not be detected as a foreign material and the intake, as well as the cost, of Warfarin would be reduced to a certain extent. In addition, the speed of blood flow would also be regulated due to the fact that it will have to rub past the tissue covering and the surrounding areas of the improved valve’s edges would be smoothened out, so that blood will not coagulate as much.
A thrombotic embolism appears to correspond with the estrogen dosage. Estrogen/progestogen oral contraception affects blood clotting by increasing plasma fibrinogen and the activity of coagulation factors, thus making the blood more prone to clotting. The inhibitor of coagulation is usually decreased as well. Platelet activity is also enhanced with acceleration of aggregation (Bonnar, 1987). These changes that occur in the blood while taking oral contraceptives create a state of hypercoagulability. Hypercoagulable state means there is an abnormally increased shift toward blood clotting. The hypercoagulability state of the blood causes the formation of blood clots that travel to the brain or the heart
thrombus, a blood clot that forms in a vessel and remains there, and possibly cause death”