have all been shown to significantly reduce CVI occurrence. Surgical interventions include sclerotherapy, ligation or resection of the vein, and also endovenous ablation (2017). DVT Huether and McCance state that Virchow’s triad is primarily responsible for the occurrence of DVTs. Virchow’s triad consists of venous stasis, endothelial damage, and increased coagulability. Essentially, venous stasis promotes aggregation of platelets and clotting
CVI VS DVT 3 factors in the vein affected. This collection leads to a thrombus formation, and the authors state it is often near the valve of the vein. The thrombus aggravates the surrounding tissue, leading to inflammation of the area, which further promotes growth of the thrombus. The thrombus may cause pain in the area, but is often asymptomatic if it is deep in the leg. A large enough thrombus may decrease circulation distal to its location. Similar to a CVI, this decreased circulation can lead to lower extremity edema. The authors also state that most DVTs will resolve themselves with enough time, but they warn that untreated DVTs may progress to pulmonary emboli. Additionally, even without embolization, obstructive DVTs may cause CVI and post-thrombotic syndrome. This syndrome is said to have similar symptoms as CVI (edema, pain, and ulceration). Again, similar to CVI, the authors suggest prevention as the best intervention against DVTs. Ways to prevent DVTs include walking, sequential compression devices (SCDs), and Lovenox. Ultrasound can be used to confirm DVT diagnosis along with D-dimer measurement. Newer anticoagulants such as Xarelto have been shown to have a better risk-to-benefit ratio compared to warfarin and its derivatives. In extreme cases, the patient may need thrombolytic therapy or a
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