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Vascular
Published in Michael Gaunt, Tjun Tang, Stewart Walsh, General Surgery Outpatient Decisions, 2018
Perform a general and vascular examination. Is one leg affected or both? In younger patients look for skin staining or soft tissue or bony overgrowth, which may suggest a vascular malformation or tumour. Examine for dilated veins and determine their pattern. Examine for the typical lipodermatosclerosis of chronic venous insufficiency. Lymphoedema starts with toes and makes them square – inability to pinch a fold of skin at the base of the second toe is known as Stemmer’s sign. It then spreads up the legs and can produce huge limbs. Chronic lymphoedematous limbs display the typical furry lichenification. Assess the mobility of the patient. Examine for the signs of a DVT or cellulitis.
Answers
Published in Thomas Hester, Iain MacGarrow, Surgical SBAs for Finals with Explanatory Answers, 2018
Haemosiderin deposition, lipodermatosclerosis, varicose eczema and ulceration are all common skin changes associated with varicose veins. Haemosiderin deposition is caused by loss of red blood cells into the tissues and consequent release of haemoglobin. Lipodermatosclerosis is the term given to skin and subcutaneous tissue changes caused by chronic venous hypertension – this is a progressive sclerosis of both skin and subcutaneous fat by fibrin deposition, tissue death and scarring.
Iliac vein stenting
Published in Sachinder Singh Hans, Alexander D Shepard, Mitchell R Weaver, Paul G Bove, Graham W Long, Endovascular and Open Vascular Reconstruction, 2017
A 67-year-old woman presented with a long-standing history of CVI of the bilateral lower extremities, including pain and swelling. Her left lower extremity was more symptomatic. The remainder of her clinical history was unremarkable, except for obstructive sleep apnea. Examination revealed an obese lady with bilateral lower extremity edema, worse on the left. There was bilateral lipodermatosclerosis involving the lower legs. Workup included venous duplex US of the lower extremities, air plethysmography, and CTV that confirmed luminal compromise of the femoro-ilio-caval segment, which was likely post-thrombotic in nature. Calf pump function was also compromised. Given her lack of improvement with conservative therapy, she was taken to the operating room for a left femoro-ilio-caval venogram, IVUS interrogation, and possible angioplasty and stenting.
Leg ulceration with histological features of pseudoxanthoma elasticum
Published in Baylor University Medical Center Proceedings, 2021
Usman Asad, Sheevam Shah, Palak Parekh
Pseudoxanthoma elasticum (PXE) is an inherited connective tissue disorder with extensive degeneration and calcification of elastic tissue, primarily in the skin, eyes, and vasculature. PXE presents as characteristic yellowish papules and plaques and retinal angioid streaks.1 Lipodermatosclerosis refers to skin induration of the lower extremities secondary to venous stasis and is often seen in patients preceding venous ulceration, which is characterized by total loss of the epidermis and partial loss of matrix structures in the upper dermis.2 In this report, we present a case of a woman who presented with ulceration and lipodermatosclerosis alongside histological features of PXE.
US budget impact of increased payer adoption of the Flexitouch advanced pneumatic compression device in lymphedema patients with advanced chronic venous insufficiency and multiple infections
Published in Journal of Medical Economics, 2018
Adam Cohen, Julia A. Gaebler, Jessica Izhakoff, Laura Gullett, Timothy Niecko, Thomas O’Donnell
The clinical literature suggests that certain sub-populations have increased risk of LE morbidity7. Patients with phlebolymphedema, a vascular condition resulting from the combined effects of LE and chronic venous insufficiency (CVI), are known to be more difficult to manage than those with LE alone, due to the involvement of the two vascular systems8. These patients often experience significant edema, lipodermatosclerosis, and skin ulceration7. Infection, typically erysipelas, cellulitis, or lymphangitis, is also a common complication of LE9. Patients who experience one episode of cellulitis have a relatively high likelihood of recurrence10.
Clinical and immunologic differences in cellulitis vs. pseudocellulitis
Published in Expert Review of Clinical Immunology, 2021
Michael Goldenberg, Henry Wang, Trent Walker, Benjamin H Kaffenberger
While associated with venous insufficiency, lipodermatosclerosis (LDS) has histologically been shown to be a panniculitis and is also referred to as sclerosing or stasis panniculitis [54]. This condition forms from the progression of venous stasis disease and results in skin ulceration [55]. During the acute phase, the condition presents as extremely tender, warm, erythematous, poorly demarcated, indurated plaques often confined to both lower legs and is often misdiagnosed as cellulitis. The chronic form develops over months and presents as hard, thick, tight, hyperpigmented, and contracted skin around the ankle, forming an “inverted champagne bottle” appearance [56]. Skin ulceration occurs in up to 13% of chronic lipodermatosclerosis cases [57]. LDS is most often found in middle-aged women [56]. Biopsies should be performed with caution in this disease [58]. The “white cell trapping theory” of pathogenesis involves leukocytes that become sequestered in the microvasculature of peripheral tissues, which release proteolytic enzymes that damage endothelial cells, leading to fibrin deposition resulting in tissue ischemia and necrosis [59, 60]. Part of this theory states that with venous stasis, the aggregability of erythrocytes increases, leading to decreased availability of complement receptor type 1 (85% of which is found on erythrocytes), which can remove antigen–antibody complexes from the circulation [61]. Thus, there is increase in inflammation, reflecting the systemic increase in interleukin (IL)-8 observed in the plasma, which increases proportionally to the degree of venous insufficiency [62]. Another theory postulates that LDS has excessive proteolytic activity by matrix metalloproteinases (MMPs) [63], which are involved with venous leg ulcer pathogenesis [64], and fibrinolytic factors of the plasminogen activation system [63]. Specifically, LDS was found to have higher levels of urokinase-type plasminogen activator and the urokinase receptor (CD87) [64]. It has also been found that LDS has high levels of transforming growth factor beta 1 adjacent to venous ulcer tissue [65], which may induce the fibrinolytic cascade and stimulate collagen production in the interstitium [66]. Studies have shown that LDS has upregulation of lysyl hydroxylase 2 in fibroblasts, providing further evidence of the profibrotic environment found in LDS [67]. Furthermore, it has been described that LDS has increased microvascular pressure and erythrocyte extravasation, which leaves fibrin bodies around the capillaries [68, 69]. With up to 20% of patients with LDS and venous ulcers being deficient in proteins C or S [70, 71], the microenvironment is ripe for microthrombosis and microinfarction [72], which leads to granulation tissue, scar formation, atrophy, and ulceration [73]. Treatment involves exercise, compression, pentoxifylline, and fibrinolytic therapy [56].