Thrombophilia physical examination: Difference between revisions
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*[[Warfarin_necrosis|Warfarin skin necrosis]] | *[[Warfarin_necrosis|Warfarin skin necrosis]] | ||
*[[Livedo reticularis]] | *[[Livedo reticularis]] | ||
*Thrombophilia and Chronic Venous Ulcers: Chronic venous reflux and venous hypertension promote inflammation and skin changes of the lower extremity that predispose the skin to ulceration. Lymphatic destruction, excessive colloid filtration resulting in regional edema, fibrin deposition, a diffusion barrier to oxygen, and infiltration of lymphocytes and neutrophils have all been shown to occur in the setting of elevated lower extremity venous pressure. Compression therapy is the mainstay of treatment for CVUs with up to 96% of ulcers healing.25 The current CHEST guidelines based on randomized control trials show a significant benefit to the use of 30 mmhg-40 mmhg compression stockings for at least 2 years in decreasing progression of venous disease after an episode of DVT. Surgical correction of venous reflux does not seem to aid in ulcer healing of primary CVUs; however, it does seem to reduce ulcer recurrence rates. Other treatments, identified by the CHEST guidelines, showing some benefit in the healing of venous ulcers are pentoxifylline and rutosides.17 There is currently no evidence for modifying these recommendations in patients with thrombophilia. | |||
*Thrombophilia and Varicose Veins: | |||
*Thrombophilia and Superficial Venous Thrombosis: | |||
==References== | ==References== |
Revision as of 19:06, 13 February 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Asiri Ediriwickrema, M.D., M.H.S. [2]
Overview
Physical examination of patients with thrombophilia is usually remarkable for signs of deep venous thrombosis, pulmonary thrombosis, renal vein thrombosis, cerebral vein thrombosis, superficial vein thrombosis, arterial thrombosis, portal hypertension, which can be sign of portal vein thrombosis, warfarin skin necrosis, or livedo reticularis.[1][2][3]
Physical Examination
Physical examination of patients with thrombophilia is usually remarkable for:[1][2][3]
- Signs of deep venous thrombosis, pulmonary thrombosis, renal vein thrombosis, cerebral vein thrombosis, superficial vein thrombosis, or arterial thrombosis
- Portal hypertension, which can be a sign of portal vein thrombosis
- Warfarin skin necrosis
- Livedo reticularis
- Thrombophilia and Chronic Venous Ulcers: Chronic venous reflux and venous hypertension promote inflammation and skin changes of the lower extremity that predispose the skin to ulceration. Lymphatic destruction, excessive colloid filtration resulting in regional edema, fibrin deposition, a diffusion barrier to oxygen, and infiltration of lymphocytes and neutrophils have all been shown to occur in the setting of elevated lower extremity venous pressure. Compression therapy is the mainstay of treatment for CVUs with up to 96% of ulcers healing.25 The current CHEST guidelines based on randomized control trials show a significant benefit to the use of 30 mmhg-40 mmhg compression stockings for at least 2 years in decreasing progression of venous disease after an episode of DVT. Surgical correction of venous reflux does not seem to aid in ulcer healing of primary CVUs; however, it does seem to reduce ulcer recurrence rates. Other treatments, identified by the CHEST guidelines, showing some benefit in the healing of venous ulcers are pentoxifylline and rutosides.17 There is currently no evidence for modifying these recommendations in patients with thrombophilia.
- Thrombophilia and Varicose Veins:
- Thrombophilia and Superficial Venous Thrombosis:
References
- ↑ 1.0 1.1 DeLoughery TG. Hemostasis and Thrombosis: Springer International Publishing; 2014.
- ↑ 2.0 2.1 Cohoon KP, Heit JA (2014). "Inherited and secondary thrombophilia". Circulation. 129 (2): 254–7. doi:10.1161/CIRCULATIONAHA.113.001943. PMC 3979345. PMID 24421360.
- ↑ 3.0 3.1 Seligsohn U, Lubetsky A (2001). "Genetic susceptibility to venous thrombosis". N Engl J Med. 344 (16): 1222–31. doi:10.1056/NEJM200104193441607. PMID 11309638.