Deep vein thrombosis
Deep vein thrombosis often occurs in the lower extremities in the calf veins, specifically in the soleus sinusoids and valve cusps. It is prevalent when blood flow is compromised in the veins due to either intrinsic or extrinsic factors such as accident injuries and surgeries (Di Nisio, van Es & Büller, 2016). Three factors are crucial in thrombus development, according to Rudolf Virchow. These comprise, firstly, venous stasis, which obstructs the venous blood flow, thus increasing viscosity and driving to the development of microthrombi. These microthrombi are not readily removed by fluid movement past the valves when skeletal muscle pumps, causing thrombus to thrive and propagate. Secondly, the Virchow describes that the imbalance between circulating factors might lead to the hypercoagulable state in the vein, particularly in the calf veins due to an increase in circulating tissue activation factors alongside the reduction in circulating plasma antithrombin as well as fibrinolysis (Othieno, Okpo & Forster, 2018). The third factor described by Virchow is a vein or endothelial damage which can either be intrinsic or result from external trauma such as an accident or surgical trauma. Endothelial injury leads to subendothelial collagen exposure and adherence of platelets, which attracts leukocytes and transfers the tissues factor to the endothelium complicating with activated factor VII to start the coagulation cascade through the extrinsic pathway. Fibrin and red blood cells that are trapped in the clot form the major component of the venous thrombi; however, platelets contribute to a less extent.
Diagnosis
Venous thrombi are often clinically asymptomatic. Usually, they are first detected through objective methods. This is because thrombi do not fully obstruct veins, and sometimes collateral circulation provides alternatives for blood flow (Othieno, Okpo & Forster, 2018). Also, because there are many possible differential diagnoses to deep vein thrombosis, it is crucial to conduct sensitive and specific diagnostic tests to confirm such diagnoses. The test often begins with a comprehensive history taking, noting the risk factors and physical examination to generate pretest probability and effectively interpret the test (Yunxian et al., 2016. This is often done using the evidenced-based clinical prediction rule like the Wells DVT score. Patients with a low pretest probability of deep vein thrombosis will necessitate a high-sensitivity –dimer to rule out DVT. Those with high pretest probability will require compression ultrasonography, which involves sequential compression of the length of proximal veins using an ultrasound probe. Often, occlusion will be present in a healthy vein with moderate external compression; however, the affected vein will not occlude since DVT prevents occlusion of the veins. Compressive ultrasonography is preferred because of its sensitivity and specificity for DVT. Usually, contrast venography is the gold standard for diagnosing DVT, however, it is often very invasive, expensive, and less accessible, thus rarely used. Don't use plagiarised sources.Get your custom essay just from $11/page
Clinical manifestations
The signs and symptoms of deep vein thrombosis include edema (rarely do both leg swell), and dim aching pain, which often originates from the calf and appears as a cramping pain. Also, a patient may feel tenderness along the pattern of veins, discoloration, and a feeling of warmth in the affected leg. These signs are often nonspecific and vary in frequency and severity. Additionally, a patient will experience calf discomfort when dorsiflexion the ankle or knee, which regularly occurs in distal leg DVT.
Risk factors
Mayo Clinic (2020) shows that inheriting a blood clotting condition increase risk for DVT as it makes the blood clot more easily. However, this cannot cause DVT on its own unless other risk factors are involved. Additionally, external injuries such as accidents and surgeries increase the risk of blood clotting, thus will increase the probability of thrombi formation. Prolonged bed rest, as seen during hospitalization, may prevent the adequate circulation of blood as the calf muscle does not adequately contract, which may increase the risk of blood clotting. Pregnancy is another risk factor as it increases pressure in veins and pelvis, and this risk continues even six weeks post-delivery. Women having inherited blood clotting disorders are at increased risk (Di Nisio, van Es & Büller, 2016). Others include being overweight, obese, smoking, having heart disease, and cancer.
Nursing interventions
After a comprehensive assessment of the presenting signs and symptoms, the Well’s diagnostic algorithms, and establishing smart nursing diagnoses, nurses should observe the following nursing interventions. Firstly, provide comfort to the patients by elevating the affected extremity, providing graduated compression stockings, and applying some warm on the site (Yunxian et al., 2016). Graduated compression stocking (compression therapy) decreases the extent of superficial veins in the calf and increases blood flow in the deep veins. Secondly, nurses can ensure effective and tolerable positioning and exercise during bed rests. Ensure bed rest with the legs periodically elevated above the heart level while helping the patient to do tolerable leg exercises as this could enhance venous flow. Thirdly, ensure effective discharge home health education and plan to promote care transition and continuity. Educate the patient on the prescribed anticoagulants, including their purpose and the need for adherence as per the prescriptions. Also, advise the patient on activities such as leg elevation and the significance of ceasing to drink alcohol and smoking.
Treatment
Usually, the goal of treatment is to stop thrombus growth, fragmentation, recurrent thromboemboli, as well as manage post-thrombotic syndrome (Yunxian et al., 2016). The first line of treatment is blood thinners, also identified as anticoagulants, which are either be injected or taken orally. They act to reduce the blood’s capability to clot. While they do not disintegrate already formed clots, blood thinners often reduce clot’s ability to grow and lessen the risk of more blood clots. A complicated DVT or when blood thinners are not effective necessitates the administration of clot-buster, also referred to as thrombolytic, which breaks up the clots (Di Nisio, van Es & Büller, 2016). Thrombolytics are either administrated intravenously or through a catheter into the clot. Thrombolytic are rarely used unless in severe cases because they may cause serious bleedings. Patients who cannot take blood thinners are treated using filters that are administered into the large veins such as vena cava to prevent lodging of clots into the lungs after they break loose.