Hemostasis initiation

In hemostasis, there is initial vasoconstriction of the injured vessel, causing diminished blood flow distal to the injury. Then hemostasis and thrombosis share three phases ... 

Most clinicians agree that crystalloids should be the initial therapy of circulatory insufficiency. Crystalloids are preferred over colloids as initial therapy for burn patients because they are less likely to cause interstitial fluid accumulation. If volume resuscitation is suboptimal following several liters of crystalloid, colloids should be considered. Some patients may require blood products to assure maintenance of 02-carrying capacity, as well as clotting factors and platelets for blood hemostasis. 

Following injury to blood vessels, hemostasis ensures that blood loss is minimized. Initially, thrombocyte activation leads to contraction of the injured vessel and the formation of a loose clot consisting of thrombocytes (hemostasis). Slightly later, the action of the enzyme thrombin leads to the formation and deposition in the thrombus of polymeric fibrin (coagulation, blood clotting). The coagulation process is discussed here in detail. 

Hip or knee replacement surgery 30 mg every 12 hours by subcutaneous injection, with the initial dose given within 12 to 24 hours postoperatively provided hemostasis has been established. The average duration of administration is 7 to 10 days up to 14 days have been well tolerated. 

DVT prophylaxis In patients undergoing hip fracture surgery, hip replacement surgery, or knee replacement surgery, the recommended dose is 2.5 mg subcutaneously once daily. After hemostasis has been established, give the initial dose 6 to 8 hours after surgery. The usual duration of administration is 5 to 9 days. Admixture incompatibilities Do not mix fondaparinux with other injections or infusions. 

To maintain hemostasis, blood must be retained in the vasculature as fluid. At the same time, blood components must be able to respond rapidly with a clot when a vascular injury occurs. To repair a vascular injury, platelets in blood first adhere as aggregates to the endothelial cells at the affected site and form an initial blood clot. Platelets then stimulate and activate coagulation factors found in plasma to form a more stable fibrin clot. As the injury is resolved and healed, the clot is degraded. Thrombosis is a pathological event wherein a blood clot occludes a blood vessel, resulting in ischemic necrosis of the tissue fed by the blood vessel. Ischemic necrosis involves local anemia and oxygen deprivation. Thrombosis of a coronary artery may lead to myocardial infarction or unstable angina [20]. 

Clotting of blood, which protects against hemorrhage, involves the sequential initiation, interaction, and completion of several stages in hemostasis (Table 4.2). 

The platelet is central to normal hemostasis and to all thromboembolic disease. A white thrombus forms initially in high-pressure arteries by adherence of circulating platelets to areas of abnormal endothelium as described above. The growing thrombus of aggregated platelets reduces arterial flow. This localized stasis triggers fibrin formation, and a red thrombus forms around the nidal white thrombus. 

The adhesion of platelets to the subendothelial matrix via specific adhesive GPs is the initial step in primary hemostasis. Binding of platelets to the matrix results in rapid (Fig, 2) morphological conversion of platelets from flat discs to spiny spheres. 

Introduction. Cell deposition on various surfaces plays an important part in the initiation of many biological processes, such as hemostasis, thrombosis and growth of secondary tumors. It consists of two main stages (a) the conveyance of cells to the vicinity of the interacting surface, and (b) the adhesion of cells to this surface. In most of the biological systems, the main field which conveys the cells to the surface is a flow field. However, for experimental studies of the process of adhesion per se, it is convenient to use a stagnant solution in which cells are conveyed to the surface by gravity (Weiss and Harlos, 1972) or by a... 

Several investigators (9, 21, 22) have found that foreign surfaces, when exposed to blood, adsorb plasma proteins. Since platelet adhesion to the surface is the first observable event occurring in clotting on foreign surfaces, and since platelets are known to participate in hemostasis and coagulation, the indication is that platelet adhesion onto the plasma protein-coated surface plays a major role in the in vivo initiation of thrombus formation on foreign surfaces. 

In human medicine, starches with smaller average molecular weights have less profound effects on hemostasis (Treib et al 1999). This may also be the case in horses, although only one dose has been tested. In healthy horses, a 8ml/kg dose of a 10% pentastarch solution resulted in a slight decrease in the thrombin time 12 h after administration, which returned to normal after 24 h. No effect on prothrombin time or partial thromboplastin time was documented (Meister et al 1992). In healthy horses, the initial phase half-life of pentastarch is 5.6 h and the terminal phase half-life is 122 h. However, the effects on PCV, plasma total solids and plasma viscosity appear to last only 12-24 h (Meister et al 1992). In equine clinical cases, the half-life may be as short as 2h (Hermann et al 1990). Pentastarch, although available in the USA, is only approved for leukapheresis in human medicine. 

Any disorder or agent that injures the stem cells or prevents their proliferation can drastically affect the absolute platelet count. The minimal platelet count necessary for initial hemostasis is 50 000 mm If the platelet count falls below 20 000 mm a condition known as thrombocytopenia exists and the affected organism is extremely vulnerable to spontaneous bleeding episodes. Usually, thrombocytopenia due to marrow failure is also associated with reduced leukocyte and red blood cell production since chemicals or disorders that affect the megakaryocytes also impact other stem cells. This is typically determined by examining a peripheral smear of the blood or by a hematologist s bone marrow aspiration. 

The boundaries between clinical chemistry and other areas of laboratory medicine are not always distinct. In many institutions, clinical chemists initiate and direct activities, such as laboratory informatics and POCT. In some areas of the world, the term clinical chemistry has long been used to include laboratory areas such as hemostasis, thrombosis testing, immunology testing, and parts of hematology that in the United States are not considered to be part of classical clinical chemistry. 

Blood vessel walls and activated platelets play central roles in primary hemostasis. Damage to a vessel wall initiates vasoconstriction and the exposure of collagen and tissue factor to blood. This exposure initiates coagulation via the tissue factor pathway. 

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