Deep Venous Thrombosis: Pathophysiology and Treatment

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Introduction

This is the formation of a blood clot in the body, usually in the deep veins. They mainly occur in the vessels of the lower limb (Office of the Surgeon General, 2008). Thrombophlebitis occurs when the vein swells and becomes inflamed. This condition is fatal and the most lethal effect of thrombosis. The clot partially or fully blocks the vein. This causes tenderness, redness, sores, and swelling. Half of the individuals affected by deep venous thrombosis are asymptomatic (Office of the Surgeon General, 2008). At times, the clot breaks off and may be lodged in the lung causing pulmonary embolism. It is due to the blockage of the pulmonary arteries or their branches, thus limiting the perfusion of the lungs. Pulmonary embolisms estimated to occur in a third of the cases of deep venous thrombosis (Office of the Surgeon General, 2008).

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900,000 people are estimated to be affected by deep venous thrombosis (DVT) in the United States. At least 60,000 deaths are due to the condition or related complications such as pulmonary embolism. A third of the cases will have a recurrence in 10 years. Eight percent of the United States population is estimated to have inherited thrombophilia which predisposes them to the development of the condition (“Data and Statistics on Venous Thromboembolism,” 2018).

Pathophysiology

During the initial process, the clot is composed of platelets and fibrin. Erythrocytes become lodged in the clot as it moves with the flow of the blood. Inflammation may develop depending on the infiltration of granulocytes into the surrounding walls of the vessel. The development of a clot is dependent on the following factors: hypercoagulability, vascular damage, and stasis. Any condition that encourages these factors is linked with the development of deep venous thrombosis (Mazzolai et al., 2017, p. 4210).

Clinical situations linked with stasis include orthopedic surgery, trauma (resulting in fractures), immobilization following severe disease such as myocardial infarction. Vascular damage occurs with inflammation of the blood vessel in Behçet’s disease, thromboangiitis obliterans, and homocystinuria (Fauci et al., 2005, p.1491). Hypercoagulability occurs in conditions such as Factor V Leiden mutation, antithrombin deficiency, hyperhomocysteinemia, disseminated intravascular coagulation, and systemic lupus erythematosus (Fauci et al., 2005, p.1491).

Physical Assessment and Examination

As stated previously, DVT causes swelling, warmth, redness, and tenderness of the affected limb. Hence, when the condition is suspected in an individual, the involved limb should be inspected for redness. The physician should also palpate it, checking for warmth and tenderness. The circumference of each leg at 10 centimeters below the tibial tuberosity should be measured. A difference of more than one cm between the legs is indicative of DVT (Fauci et al., 2005, p.1491). Visibly distended veins may also be observed. To observe these features, the limb should be exposed adequately from the groin to the toes.

The physical assessment of individuals suspected of DVT is incomplete without assessing for the development of its most serious complication, pulmonary embolism. Due to this risk, movement of the leg should be minimized during the physical examination as the clot can become dislodged. The patient is assessed for signs of respiratory distress such as the use of accessory muscles of breathing, tachypnea, dyspnea, or indrawing of the intercostal muscles (Fauci et al., 2005, p.1491). The physician should also auscultate the individual’s chest, listening for crepitations that signify lung edema which results from the embolism. In these patients, they will also have tachycardia (a heartbeat greater than 100 beats per minute).

Treatment Plan and Patient Education

In suspected cases of DVT, the diagnosis has to be confirmed. D-dimer tests can be done initially. Their levels are usually elevated. When this test is positive and used together with clinical diagnosis, the sensitivity is 80 percent. Diagnosis can also be confirmed using a Doppler ultrasound whose sensitivity is 70 percent. Compression ultrasound is used in most centers. In suspected pulmonary embolism, a computed tomography scan of the chest is necessary to rule it out (Fauci et al., 2005, p.1492).

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The major goal of treatment is to prevent pulmonary embolism. All patients with clots in the thigh must undergo treatment. During admission, the individual is given low molecular weight heparins and warfarin. The heparin is stopped once the internationalized normalized ratio (INR) is within the therapeutic range, usually 2 to 3. Apixaban can also be used initially at 10 milligrams for the first week and five milligrams twice a day for the remainder of the treatment period (Mazzolai et al., 2017, 4211). Six weeks of treatment is recommended for patients with clots in the leg, where a risk factor was not identified. Recurrent thrombosis indicates lifetime anticoagulation.

Supportive treatment is also important. Bedrest is indicated with the elevation of the affected leg. Warm compresses are also applied. Patients at high risk of recurrent thrombosis wear elastic support stockings. The patients should be advised against taking no-steroidal anti-inflammatory drugs during treatment as it may mask the development of clot extension (Fauci et al., 2005, p.1492). They are also taught the risk factors to enable their change of lifestyles.

Follow-up

This is done to avoid recurrence and prevent complications of treatment. Compliance is also assessed during these visits. Conditions such as renal failure, pregnancy, and weight changes warrant an adjustment of the dose (Mazzolai et al., 2017, p.4214).

References

  1. Data and Statistics on Venous Thromboembolism. (2018). Web.
  2. Fauci, A., Braunwald, E., Kasper., D., Hauser, S., Longo, D., & Jameson, J. et al. (2005). Harrison’s principles of internal medicine (16th ed., pp. 1491-1493). New York, NY: McGraw-Hill.
  3. Mazzolai, L., Aboyans, V., Ageno, W., Agnelli, G., Alatri, A., & Bauersachs, R. et al. (2017). Diagnosis and management of acute deep vein thrombosis: a joint consensus document from the European Society of Cardiology working groups of aorta and peripheral vascular diseases and pulmonary circulation and right ventricular function. European Heart Journal, 39(47), 4208-4218. doi: 10.1093/eurheartj/ehx003
  4. Office of the Surgeon General. (2008). The Surgeon General’s call to action to prevent deep vein thrombosis and pulmonary embolism. Rockville, MD: U.S. Public Health Service.

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NursingBird. (2021, December 27). Deep Venous Thrombosis: Pathophysiology and Treatment. Retrieved from https://nursingbird.com/deep-venous-thrombosis-pathophysiology-and-treatment/

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NursingBird. (2021, December 27). Deep Venous Thrombosis: Pathophysiology and Treatment. https://nursingbird.com/deep-venous-thrombosis-pathophysiology-and-treatment/

Work Cited

"Deep Venous Thrombosis: Pathophysiology and Treatment." NursingBird, 27 Dec. 2021, nursingbird.com/deep-venous-thrombosis-pathophysiology-and-treatment/.

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NursingBird. (2021) 'Deep Venous Thrombosis: Pathophysiology and Treatment'. 27 December.

References

NursingBird. 2021. "Deep Venous Thrombosis: Pathophysiology and Treatment." December 27, 2021. https://nursingbird.com/deep-venous-thrombosis-pathophysiology-and-treatment/.

1. NursingBird. "Deep Venous Thrombosis: Pathophysiology and Treatment." December 27, 2021. https://nursingbird.com/deep-venous-thrombosis-pathophysiology-and-treatment/.


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NursingBird. "Deep Venous Thrombosis: Pathophysiology and Treatment." December 27, 2021. https://nursingbird.com/deep-venous-thrombosis-pathophysiology-and-treatment/.