Deep Vein Thrombosis and Thromboembolism - Coursework Example

SECTION A Deep vein thrombosis (DVT) and thromboembolism is commonly seen in sedentary and bedridden individuals (Bloch & Hoffer, 2004). Other conditions associated with an increased risk for DVT include: long airplane or car trips (lasting more then four hours), stroke, acute myocardial infarction, sepsis, nephrotic syndrome, ulcerative colitis, systemic lupus erythematosis, polycythemia rubra vera, thrombocytosis, heparin-induced thrombocytopenia, IV drug abuse, disorders of plasminogen activation, inherited disorders of coagulation/fibrinolysis (Schreiber, 2005), elderly individuals, obesity, prior history of DVT, venous stasis, local compression on the veins, and acute factors like severe dehydration (Guirguis, 2000). DVT also can occur from iatrogenic injury of the femoral veins (Wood, 2000; Joynt, 2000), malignancy (pancreas, lung, ovary, testes, urinary tract, breast and stomach), after major surgery (orthopedic, thoracic, abdominal and genitourinary procedures), following trauma (fractures of spine, pelvis, femur, tibia and spinal cord), burns, pregnancy and the postpartum period, estrogen use, hypercoagulable states (deficiencies of protein C, protein S, fibrinogen, factor V, factor VIII, factor IX, factor XI, prothrombin, and antiphospholipid antibodies), venulitis (thromboangitis obliterans, Behcets disease, and homocystinuria) (Creager & Dzau, 1998), end-stage renal disease and congestive cardiac failure (Casserly, 2000). Thrombogenesis is a finely balanced process between coagulation and fibrinolytic pathways. The interaction between plasminogen activators (e.g. tissue plasminogen activator) and inhibitors that modulate this activity (e.g. plasminogen activator inhibitor, PAI-1) influences the fibrinolytic system. Plasma fibrinogen determines plasma viscosity, blood flow, affects platelet aggregation, blood viscosity, interacts with plasminogen binding and along with thrombi, mediates the final steps in clot formation. The levels of fibrinogen associates directly with age, obesity, smoking, diabetes and LDL-C and inversely with HDL-C, alcohol use, physical activity and exercise level. Increased fibrinogen is also associated with many different forms of vascular and inflammatory disease. Impaired fibrinolysis, as demonstrated by the elevated levels of plasminogen activator, is seen in obese patients, and explains the increased risk of thrombosis and other vascular disease in the obese (Chung & Lip, 2004). Virchow’s classical triad of factors that lead to the development of thrombosis (thrombogenesis) are: abnormalities of blood vessel wall, abnormalities of blood constituents (hypercoagulability), and abnormalities of blood flow (venous stasis and turbulence) (Chung & Lip, 2004). As a result of prolonged immobilization due to surgery, long distance travel or lesser physical activity in elderly individuals etc, there is an absence of the normal rhythmic contraction of leg muscles, which leads to venous stasis. Cardiac failure also causes sluggish venous circulation and venous stasis (Robbins & Kumar, 1987). Venous stasis in turn causes venous hypertension (which can be worsened if there is history of venous reflux, varicose veins, or prior DVT) and leads to clot formation (Bloch & Hoffer, 2004). The formation of an occlusive clot worsens the process of venous stasis and hypertension. Obstruction of the deep venous system by clots results in the shunting of blood flow to superficial veins through the perforating veins. Extension of a clot to the iliac veins can cause sudden, massive swelling of the leg (phlegmasia cerulea dolens), and in severe cases can progress to obstruct the arterial inflow as well (phlegmasia alba dolens). Hume (1970) has documented that the origin of venous thrombi is usually in the recesses behind the valve cusps in the deep veins of the lower leg. According to the order of frequency, the following veins of the lower extremities are affected: deep calf, femoral, popliteal, and iliac veins (Robbins & Kumar, 1987). In a minority of cases, DVT arises from the ileofemoral system as a result of direct vessel wall injury during hip surgery or catheter-induced damage. In the majority of cases, calf vein thrombi dissolve completely without therapy. However, in approximately 20% of cases, the thrombus propagates proximally before embolizing. In five to ten days after the thrombus formation, the process of adherence and organization of the venous thrombus begins. If this process has not been already fully established, the non-adherent, disorganized thrombus may propagate and/or embolize (Schreiber, 2005.) There is some controversy as to whether isolated calf vein thrombi carries a limited risk of pulmonary embolism or not. While some studies suggest that isolated calf vein thrombi are small and the embolization of such thrombi do not cause significant morbidity or mortality, other studies reveal that isolated calf vein thrombi do embolize with rapid propagation proximally, causing fatal pulmonary embolism (Schreiber, 2005.) The end-result of the propagation and organization of the venous thrombus is usually destruction of the venous valves, producing different degrees of venous outflow obstruction, and ultimately in the development of chronic venous insufficiency. Even with anticoagulation therapy, less than 10% of patients have spontaneous lysis and complete recanalization of established proximal DVT (Schreiber, 2005.) Hypercoagulability can be defined as an alteration of the blood or specifically the clotting mechanism that predisposes to thrombosis. Some of the hypercoagulable states include deficiencies of protein C, protein S, fibrinogen, factor V, factor VIII, factor IX, factor XI, prothrombin, and antiphospholipid antibodies. Users of oral contraceptives have an increased concentration of plasma fibrinogen, prothrombin and factors VII, VIII, and X. A sudden hypercoagulable state occurs in diffuse intravascular coagulopathy due to infection and heparin-induced thrombocytopenia. Many drugs can also induce a hypercoagulable state (Bloch & Hoffer, 2004). Trauma, surgery and burns are conditions, which are associated with prolonged immobilization, injury to vessels, release of procoagulant substances from tissues and reduced t-PA activity, any of which can lead to thrombosis (Robbins & Kumar, 1987). In patients with disseminated cancer, the secretion of thrombogenic factors or the absorption of procoagulant products from necrotic tumor cells have been proposed as the mechanism of thrombosis. Venous thrombi have a rich admixture of erythrocytes, and hence known as red, coagualative or stasis thrombi (Robbins & Kumar, 1987). Initially, the thrombus is composed mainly of platelets and fibrin. Later on, the red blood cells become interspersed within fibrin. The inflammatory response in the vessel wall may be minimal or characterized by granulocyte infiltration, endothelial loss and edema (Creager & Dzau, 1998.) SECTION B In patients with suspected DVT, the clinical assessment might be difficult because of the nonspecific and vague nature of the physical findings (Schreiber, 2005). Vigilant nursing care is therefore very essential, not just because of the risk of further embolic episodes, but also because of the potential serious complications of treatment (Reid, 1999.) The various differential diagnoses of pulmonary embolism should be carefully considered with any patient suspected to have pulmonary embolism (PE). These conditions include pneumonia, asthma, anemia, angina pectoris, myocardial infarction, congestive cardiac failure, pericarditis, primary pulmonary hypertension, rib fracture, pneumothorax, costochondritis, aortic stenosis, shock, and myocarditis. All patients suspected of PE must be stratified according to risk, ideally with a criteria-validated clinical decision rule (Sharma, 2006.) General nursing interventions that are aimed at reducing the risk of complications and keep the patient comfortable include: adequate intake of fluid and dietary fiber, ankle and leg exercises, elastic compression stockings to aid venous return, logrolling, coughing, deep breathing, and meticulous skin care (Nursing, 2003.) The investigations, which are to be performed include: arterial blood gas study (ABGs), plasma D-dimer ELISA test (this is positive in only 30% of patients. Therefore, the D-dimer test alone is not routinely recommended at present). Chest radiography shows the Westermark sign, which is a dilatation of pulmonary vessels and a sharp cutoff. The other signs in a chest X-ray are: atelectasis, small pleural effusion, and an elevated diaphragm. (Sharma, 2006.) Ventilation-perfusion (V/Q) scanning of the lungs are reliable indicators for PE and normal or near-normal scans can reliably exclude PE, but there is much support for replacing V/Q scanning with spiral CT ( Costello & Gupta, 2001.) Noninvasive tests for lower extremity DVT might help to evaluate patients who have nondiagnostic V/Q scan patterns. (Sharma, 2006.) Color-flow Doppler imaging and compression ultrasonography have a high sensitivity (89-100%) and specificity (89-100%) for detection of proximal DVT in symptomatic patients. (Sharma, 2006.) Spiral CT scanning (helical CT scan) helps to view the main, lobar, and segmental pulmonary emboli, and has sensitivity greater than 90% (Sharma, 2006). The high accuracy of spiral CT makes it the first-line investigation for pulmonary embolism. In addition, spiral CT also provides an alternative diagnosis in a high percentage of patients (Goodman, 2000.) Combined spiral CT scan for the detection of pulmonary embolism as well as deep venous thrombosis, further identifies emboli in the deep venous system of the lower limbs or the pelvic veins. Pulmonary angiography, even if false negative, helps to exclude clinically relevant PE. Magnetic resonance imaging (sensitivity of 85% and specificity of 96%) can identify central, lobar, and segmental emboli. One study (Kluge et al., 2006) prospectively assessed whether it is feasible and better to do combined MRI examinations (thoracic MRI for suspected pulmonary embolism (PE) and MR venography for DVT). The study was able to detect 17% more cases of thromboembolism when compared with separate examinations. Echocardiography is less accurate in the diagnosis of PE. Central PE may be identified by transesophageal echocardiography. Electrocardiographic studies are not very useful. The finding in an electrocardiogram includes tachycardia and nonspecific ST-T wave abnormalities, which however, are neither sensitive nor specific. A S1-Q3-T3 pattern is a classic finding of right-heart strain, but this is observed in only 20% of patients with pulmonary embolism. The medical care of pulmonary embolism includes, immediate, full anticoagulation therapy, which should not be delayed by diagnostic investigations. Initial anticoagulation is performed with intravenous heparin, which prevents additional thrombus formation and permits endogenous mechanisms to lyse the clot that has already formed. However, heparin does not directly dissolve thrombus that already exists. Simultaneous oral anticoagulation is also started with warfarin. Heparin is discontinued after a therapeutic dose of warfarin is established, and warfarin therapy is maintained subsequently. Heparin is started after major active bleeding has been excluded and after rectal examination with testing for occult blood. An initial bolus of 5000 to 10,000 units is followed by a continuous infusion of 1000 to 1500 u/h. The heparin dose is further adjusted to maintain an aPTT that is at least twice the control value (Creager & Dzau, 1998.) Low molecular weight heparins (LMWHs) have many distinct advantages over unfractionated heparin. They have a greater bioavailability, can be administered subcutaneously, has a longer duration of anticoagulant effect, has a lower prevalence of complications and is less expensive (Chen, et al., 2005.) Warfarin is initiated at a dose of 7.5 to 10 mg, and reduced after several days. The target INR should be 3.0. The duration of anticoagulation for PE is for one year. (Creager & Dzau, 1998.) The indications for thrombolytic therapy include: patients who are hemodynamically unstable, have right-heart strain, and high-risk patients with underlying poor cardiopulmonary reserve. Thrombolysis dissolves much of the pulmonary thrombus, and prevents the continuous release of serotonin and other neurohumoral factors, which aggravate pulmonary hypertension, and thereby decreases the likelihood of recurrent PE (Creager & Dzau, 1998.) However, the role of thrombolytic therapy in the management of acute PE is controversial, since clinical trials have not demonstrated reduced mortality rates or early resolution of symptoms when compared to heparin (Nielsen, et al., 1995.) Thrombolytic regimens include 100 mg of recombinant tissue-plasminogen activators, alteplase (t-PA) and reteplase (r-PA), along with urokinase and streptokinase (Sharma, 2006.) Surgical management of PE includes inferior vena cava (IVC) interruption by the insertion of an IVC filter. The indications for IVC filter are: patients with an absolute contraindication to anticoagulant therapy, and patients with massive PE in whom recurrent embolism will be fatal. Filters may be permanent (e.g. Greenfield), temporary (e.g. Antheor, Gunther) or retrievable (e.g. Gunther Tulip) (Brenner, et al., 2001.) Compression stockings, which provide a compression of 30-40 mm Hg gradient, are a safe and effective method to prevent venous thromboembolism in patients who are at high risk when heparin therapy is not desirable or is contraindicated. The traditional belief that it is ideal to restrict patients with acute deep vein thrombosis in bed for several days, has been disproved by clinical studies, which have shown that there is a good clinical outcome with walking exercises and good compression (Partsch, 2005.) ************************************************************************************************** References Bloch, RD & Hoffer, EK (2004). Deep venous thrombosis, lower extremity. Retrieved from e medicine Brenner C, Molloy M, McEniff N (2001). Use of inferior vena cava filters in thromboembolic disease two case reports with a literature review. Ir Med J. 2001 Oct;94(9):267-8. Casserly LF, Reddy SM, Dember LM (2000). Venous thromboembolism in end-stage renal disease. Am J Kidney Dis 2000 Aug; 36(2): 405-11. Creager, MA, Dzau, VJ (1998). Harrison’s principles of internal medicine, 1998, 14th edition, vol 1, pp.1403-4). Chung, I & Lip, GYH (2004). Virchow’s triad revisited: Blood constituents. Pathophysiol Haemost Thromb 2003/2004; 33: 449-454. Chen LY, Ying KJ, Hong WJ, Zhou P (2005). Comparison of low-molecular-weight- heparin and unfractionated heparin for acute PTE. J Zhejiang Univ Sci B. 2005 Dec;6(12):1195. Costello, P& Gupta, KB (2001). Pulmonary embolism: imaging modalities--V/Q scan, spiral (helical) CT, and MRI. Semin Vasc Med. 2001 Nov;1(2):155-64. Goodman, PC (2000). Spiral CT for pulmonary embolism. Semin Respir Crit Care Med. 2000;21(6):503-10. Guirguis, N, Budisavljevic, MN, Self, S (2000). Acute renal artery and vein thrombosis after renal transplant, associated with a short partial thromboplastin time and factor V Leiden mutation. Ann Clin Lab Sci 2000 Jan; 30(1): 75-8. Hume (1970). Venous Thrombosis in Pulmonary Embolism. Cambridge, Harvard University Press, p.25. Joynt, GM, Kew, J, Gomersall, CD (2000). Deep venous thrombosis caused by femoral venous catheters in critically ill adult patients. Chest 2000 Jan; 117(1): 178-83. Kluge, A, Mueller C, Strunk ,J, Lange, U, Bachmann, G (2006). Experience in 207 combined MRI examinations for acute pulmonary embolism and deep vein thrombosis. AJR Am J Roentgenol. 2006 Jun;186(6):1686-96. Nielsen, HK, Lassen, JF, Ravn, HB, Husted, SE (1995). Anticoagulant and thrombolytic therapy in deep venous thrombosis and pulmonary embolism. Ugeskr Laeger. 1995 May15;157(20):2835-40. Nursing (2003).  Managing pelvic fractures: Treatment and nursing care. Partsch, H (2005). Ambulation and compression after deep vein thrombosis: dispelling myths. Semin Vasc Surg. 2005 Sep;18(3):148-52. Robbins, SL & Kumar, V (1987). Fluid and Hemodynamic Derangements. Basic Pathology, 4th edition, W.B. Saunders Company, 1987. p.70-72. Reid, E (1999). Pulmonary embolism: an overview of treatment and nursing issues. British Journal of Nursing, Vol. 8, Iss. 20, 11 Nov 1999, pp. 1373–1378. Schreiber, D (2005). Deep Venous Thrombosis and Thrombophlebitis. Retrieved from e medicine < http://www.emedicine.com/emerg/topic122.htm> Sharma, S (2006). Pulmonary Embolism. Retrieved from e medicine Wood, KE, Reedy, JS, Pozniak, MA (2000). Phlegmasia cerulea dolens with compartment syndrome: a complication of femoral vein catheterization. Crit Care Med 2000 May;28(5): 1626-30 Read More