There may be certain factors that may interfere with the body’s normal ability to make platelets. There is times when the
Then, antibiotics, surgery, anti-inflammatory agents, or obstetric procedures may regulate hemostasis, mainly in chronic DIC. However, in acute phase of DIC, two categories of treatment are available as follows: treatments that slow the coagulation process and therapies that substitute the coagulation factors and the missing platelets. Heparin also can be used to stop the uncontrolled stimulation of the coagulation cascade due to the antithrombotic properties. Careful monitoring of heparin is required because the heparin can worsen the bleeding. Red blood cell administration, thawed frozen plasma, and platelets transfusion may be use based on the patient
Name: Hemolytic uremic syndrome Overview: The hemolytic uremic syndrome is a condition characterized by destruction of red blood cells and kidney failure and often follows an infection of the digestive system caused by Escherichia coli, but can also occur for other reasons. The hemolytic uremic syndrome is a disease that involves two processes and two body systems: o destruction of red blood cells o kidney failure
It describes the three broad categories of factors that are thought to contribute to thrombosis, or venous thromboembolism: hypercoagulability. hemodynamic changes, and endothelial injury. As described before, hypercoagulability is the tendency to have faster and more advanced blood clotting, and venous stasis is characterized by long periods of stillness, as in airplane flights or long drives. The third is called endothelial injury.
In this process when an injury occurs to a blood vessel, causing bleeding the platelets start to stick to the injured blood vessel and release chemicals to attract other platelets. 4. Then as more platelets start sticking together they soon form a temporary clot V. The blood vessels guide blood and help the blood travels through our body.
IV bolus of unfractionated Heparin or Subcutaneous injection of low molecular weight heparin (LMWH) may be used to prevent the formation of new blood clots. Nursing consideration: Require regular monitoring of activated partial thromboplasitn time (aPTT) and needed frequent heparin dose changes (Brunner and Suddarth’s, et al, 2010: 765). Fibrinolytic therapy: This therapy is given to dissolve the thrombus in the artery and restore the blood flow. There are two fibrinolytic drugs which are streptokinase and Recombinant tissue plasminogen activators (r-TPA) which includes Alteplase, reteplase and tenecteplase (Brunner and Suddarth’s, et al, 2010: 772).
There are two types of Warfarin, one activates clotting factor and the other slows down the clotting factor. Warfarin works against the liver to produce Vitamin K, which is needed for the proteins that help blood clotting. The treatment for Warfarin is an increase of Vitamin K to help clot internal bleeding. By increasing the vitamin K it should neutralize the effects of the
The specific skills behind controlling a hemorrhage have been largely unchanged for hundreds of years. Since the first century A.D., techniques such as compression, styptics (i.e., hemostatic agents), and torsion/tourniquets have been utilized. ( Kabaroff, 2013). Since then, medicine has strived to develop the best way to improve these methods. Even through hundreds of years of research and trials, it is often found that the simplest, earliest methods remain the standard.
A treatment option for those who have suffered an ischaemic stroke is thrombolysis. As 85% of strokes are ischaemic this is a treatment option for many (Fitzpatrick and Birns,2004).The goal of thrombolysis is to disintegrate the thrombus/embolus occluding the vessel and reduce the scale of tissue damage (Fitzpatrick and Birns,2004).It is important to note that thrombolysis using ateplase should only be used to treat acute ischaemic stroke once intracranial bleeding has been ruled out by diagnostic imaging, and within 4.5hours of onset by
The major scenarios are decreased production and increased destruction of thrombocytes, or both. The major goal of diagnostic procedures should be to reveal the underlying pathologies. Examination of the bone marrow and the peripheral blood smear can be useful as well as special diagnostic tests of the assumed defect. First line therapies should target the underlying disease, however platelet transfusions may also be mandatory up to some extend. However, in case of diseases with increased platelet activation and consumption, platelet transfusion is not convenient because it may trigger a new pathologic
The exudative phase unfolds over the first 1 to 7 days after attack of lung injury. Accumulation in the alveoli of excessive fluid, protein and inflammatory cells that have move into the air spaces from the alveolar capillaries. Intrapulmonary shunt develop and blood passing cannot be oxygenated. Alveolar type I and type II cells are spoiled causing surfactant dysfunction. Alveoli become unstable and collapse and fibrotic changes take place.
The second step, sit the patient in a comfortable position with his arm fully extended while placing a clean tourniquet around the patients arm, about 3 or 4 inches above the venipuncture
Each and every tiny droplet of blood pattern is less than 1mm in
If the clot is in a deep vein, which is usually a lower extremity, they are referred to as deep vein thrombi. If the clot breaks away and travels to the lung, they are referred as a pulmonary embolism. Deep vein thrombi, and pulmonary embolisms are categorized as venous thromboembolisms (International Society on Thrombosis and Haemostasis, 2017). Although all hospitalized patients are at an increased risk of venous thromboembolism development, patients whom pose the highest risk include: patients who have cancer, had major surgery, experienced trauma, and/or are significantly immobile (The American Heart Association, 2017). Due to the nature of thromboembolism development, the risks of development have been present whenever an individual is injured or experienced decrease mobility.
4.1. Vasovagal Causes. 4.2. Orthostatic hypotension. 4.3.