Thrombosis, venous

Prevention and treatment of venous thrombosis, PE, peripheral arterial embolism ... 

Prevention of postoperative venous thrombosis (DVT) and PE in certain patients undergoing surgical procedures, such as major abdominal surgery ... 

Ms. Jackson, age 56years, is hospitalized with a venous thrombosis. The primary health care provider orders SC heparin. In developing a care plan for Ms. Jiekson, discuss the nursing interventions that would be most important to prevent complications while administering heparin. Provide a rationale for each intervention. 

The IV solutions of plasma expanders include hetastarch (Hespan), low-molecular-weight dextran (Dextran 40), and high-molecular-weight dextran (Dextran 70, Dextran 75). Plasma expanders are used to expand plasma volume when shock is caused by bums, hemorrhage surgery, and otiier trauma and for prophylaxis of venous thrombosis and diromboembolism. When used in die treatment of shock, plasma expanders are not a substitute for whole blood or plasma, but tiiey are of value as emergency measures until die latter substances can be used. 

One meta-analysis examined the safety and efficacy of LMWH and heparinoids in 11 randomized trials of 3048 patients with acute ischemic stroke. It reported a reduction in the incidence of deep venous thrombosis (DVT) (odds ratio (OR) 0.27,... 

This category includes patients with rare causes of strokes such as nonatherosclero-tic vasculopathies, cerebral venous thrombosis, hypercoagulable states, or hematologic disorders. Two such disorders are discussed below. 

Kalbag RM, Woolf AL. Cerebral venous thrombosis. London University Press 1967. 

Ameri A, Bousser M. Cerebral venous thrombosis. Neurol Clin 1992 10 87-111. 

Einhaupl KM, Villringer A, Meister W, Mehraein S, Garner C, PeUkofer M, Haberl RL, Pfister HW, Schiedek P. Heparin treatment in sinus venous thrombosis. Lancet 1991 338 597-600. 

Bousser MG. Cerebral venous thrombosis nothing, heparin, or local thrombolysis Stroke 1999 30 481 83. 

Frey JL, Muro GJ, McDougall CG, Dean BE, Jahnke HK. Cerebral venous thrombosis combined intrathrombus rtPA and intravenous heparin. Stroke 1999 30 489 94. 

Smith AG, Cornblath WT, Deveikis JP. Local thrombolytic therapy in deep cerebral venous thrombosis. Neurology 1997 48 1613-1619. 

Holder CA, Bell DA, Lundell AL, Ulmer JL, Glazier SS. Isolated straight sinus and deep cerebral venous thrombosis successful treatment with local infusion of urokinase. J Neurosurgery 1997 86 704-707. 

Spearman MP, Jungreis CA, Wehner JJ, Gerszten PC, Welch WC. Endovascular thrombolysis in deep venous thrombosis. Am J Neuroradiol 1997 18 502-506. 

Determine a patient s relative risk (low, moderate, high, or very high) of developing venous thrombosis. 

Table 7-1).17 Venous thrombosis is uncommon in the absence of risk factors, and the effects of these risks are additive. Conversely, even in the absence of symptoms, VTE should be strongly suspected in those with multiple risk factors. 

The ACCP Conference on Antithrombotic Therapy recommended against the use of aspirin as the primary method of VTE prophylaxis.2 Antiplatelet drugs clearly reduce the risk of coronary artery and cerebrovascular events in patients with arterial disease, but aspirin produces a very modest reduction in VTE following orthopedic surgeries of the lower extremities. The relative contribution of venous stasis in the pathogenesis of venous thrombosis compared with that of platelets in arterial thrombosis likely explains the reason for this difference. 

Central PN refers to the administration of PN via a large central vein, and the catheter tip must be positioned in the vena cava. Central PN allows the infusion of a highly concentrated, hypertonic nutrient admixture. The typical osmolarity of a central PN admixture is about 1500 to 2000 mOsm/L. Central veins have much higher blood flow, and the PN admixture is diluted rapidly on infusion, so phlebitis is usually not a concern. Patients who require PN administration for longer periods of time (greater than 7 days) should receive central PN. One limitation of central PN is the need for placement of a central venous catheter and an x-ray to confirm placement of the catheter tip. Central venous catheter placement may be associated with complications, including pneumothorax, arterial injury, air embolus, venous thrombosis, infection, chylothorax, and brachial plexus injury.1,20... 

Mechanical complications of PN are related to catheter placement and the system and equipment used to administer PN. A central venous catheter must be placed by a trained professional, and risks associated with placement include pneumothorax, arterial puncture, bleeding, hematoma formation, venous thrombosis, and air embolism.1,20 Over time, the catheter may require replacement. Problems with the equipment include malfunctions of the infusion pump, intravenous tubing sets, and filters. 

A G (guanine) to A (adenine) transition in position 20210 of the prothrombin gene (prothrombin 20210 A allele) has been described that leads to increased prothrombin concentrations and, in turn, increased risk for venous thrombosis (88). This G-to-A transition that occurs in the 3 untranslated region of the gene may not be the only reason for increased prothrombin concentrations because apparently only 25% of individuals with prothrombin concentrations greater than 115% carry the prothrombin 20210 A allele (88). 

Individuals with heterozygous protein C deficiency are seven times more likely to be afflicted with venous thrombosis than normal individuals. A combination of protein C deficiency with a mutation in the factor V gene (factor V Leiden) carries a much greater risk for venous thrombosis than the presence of only one of these conditions (89). 

Collins R., Scrimgeour A., Yusuf S Peto R. Reduction in fatal pulmonary embolism and venous thrombosis by perioperative administration of subcutaneous heparin Overview of results of randomized trials in general, orthopedic, and urologic surgery. N Engl J Med 1988 318, 1162-73. 

Handeland G. F., Abildgaard U., Holm H. A Arresen E. Dose adjusted heparin treatment of deep venous thrombosis a comparison to unfractionated and low molecular weight heparin. Eur J Clin Pharmacol 1990 39, 107-12. 

Dahlback B. Resistance to activated protein C, the Arg506 to Gin mutation in the factor V gene and venous thrombosis. Functional tests and DNA based assays, pros and cons. Thromb Haemost, 1995 73,739-42. 

Poot S. R Rosendaal F. R., Reitsma P. H Bertina R. M. A common genetic variation in the 3 -untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood 1996 88,3698-703. 

Tamoxifen -nonsteroidal antiestrogen -nausea and vomiting -bowel changes (diarrhea or constipation) -headache -peripheral edema -hot flashes -endometrial carcinoma -vaginal bleeding -venous thrombosis... 

Low-molecular-weight heparin or low-dose subcutaneous unfractionated heparin (5,000 units twice daily) is recommended for prevention of deep venous thrombosis in hospitalized patients with decreased mobility due to stroke and should be used in all but the most minor strokes. 

Hypercoagulable states include malignancy activated protein C resistance deficiency of protein C, protein S, or antithrombin factor VIII or XI excess antiphospholipid antibodies and other situations. Estrogens and selective estrogen receptor modulators have been linked to venous thrombosis, perhaps due in part to increased serum clotting factor concentrations. Although a thrombus can form in any part of the venous circulation, the majority of thrombi begin in the lower extremities. Once formed, a venous... 

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