Microcirculatory Aspects of Venous Ulceration

Butler, C.M.; Smith, Phillip D.

doi:10.1111/j.1524-4725.1994.tb03220.x

Cited by 23 publications

(8 citation statements)

References 38 publications

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“…10,33 Sustained hypertension at the capillary level is associated with many morphologic changes including elongation and dilation of the capillary bed, increased surface area of the endothelium, increased type IV collagen in the basement membrane, and the formation of a pericapillary fibrin cuff. 12,[34][35][36][37] These abnormal capillaries are more permeable to large molecules, including fibrinogen, 38 and it has been hypothesized that leaked fibrinogen is converted to fibrin in the pericapillary space. 37,38 Other studies have shown that the fibrinolytic activity of blood and tissues is deficient in patients with lipodermatosclerosis, resulting in a decreased clearance of fibrin.…”

Section: Epidemiology and Natural Historymentioning

confidence: 99%

Chronic Venous Insufficiency and Venous Ulceration

Alguire

Mathes

1997

J Gen Intern Med

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OBJECTIVE:To review and summarize the literature on the normal venous circulation of the leg, and the epidemiology, pathophysiology, and treatment of chronic venous insufficiency (CVI).DATA SOURCES: English-language articles identified through a MEDLINE search using the terms venous insufficiency or varicose ulcer and epidemiology, pathophysiology, diagnosis, and clinical trial (pt), and selected cross-references. STUDY SELECTION:Articles on epidemiology, pathophysiology, and treatment of CVI. Randomized, controlled studies were specifically sought for treatment efficacy. DATA EXTRACTION:Data were manually extracted from selected studies and reviews; emphasis was placed on information relevant to the general internist. pproximately 5 million people in the United States exhibit some evidence of chronic venous insufficiency (CVI) and between 400,000 and 500,000 of these individuals have or will develop a venous leg ulcer. 1-3 The signs of CVI include engorgement of the cutaneous veins and dependent edema in mildly affected patients to pigmentation, dermatitis, and ulceration in the more severe cases. Although most patients are asymptomatic, others have leg heaviness and aching or recurrent and recalcitrant leg ulcers punctuated by bouts of cellulitis. These more severe cases are associated with recurrent hospitalization, high health-care costs, and disability. 4,5 Venous insufficiency with trophic skin changes or ulceration is a frustrating problem, which many physicians approach with a sense of ennui. This may be due to the chronic and remitting nature of the problem, the need for lifestyle modification, inconvenient therapies, and contradictory information regarding medical and surgical management. Nevertheless, CVI, including ulceration, is a manageable problem. The purpose of this review is to present the normal anatomy and physiology of the venous circulation and to summarize the epidemiology, pathophysiology, and treatment of CVI. DATA SYNTHESIS: METHODSA MEDLINE search for relevant English-language articles published between 1966 and 1996 was completed using the following MeSH terms: venous insufficiency or varicose ulcer and epidemiology, pathophysiology, diagnosis, and clinical trial (pt). When selecting articles on treatment, randomized, controlled trials were reviewed whenever possible. Emphasis was placed on reviewing articles with clinical relevance for internal medicine physicians. ANATOMY AND NORMAL PHYSIOLOGYVenous blood from the skin and subcutaneous fat is collected in a system of superficial venules and veins that drain toward the deep venous system underneath the fascia via three major pathways: (1) through the long or short saphenous veins, which join the deep system at the saphenofemoral and saphenopopliteal junctions; (2) through the perforating veins originating from the long or short saphenous veins or their branches; or (3) directly into the deep venous system or bypass the deep system entirely and enter the pelvis. 6 Deep veins are categorized as either intramuscular or intermuscular; o...

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Section: Epidemiology and Natural Historymentioning

confidence: 99%

Chronic Venous Insufficiency and Venous Ulceration

Alguire

Mathes

1997

J Gen Intern Med

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“…It is estimated that the Health Service in the United Kingdom spends £600 million per annum 4 on man-agement of this problem, 4 which amounts to nearly 2% of the total health-care expenditure.Among volunteers without venous disease, leukocyte sequestration in the lower limb and white blood cell activation have been produced by means of experimental venous hypertension lasting 30 minutes. 5 At the same time various endothelial factors are released, suggesting that this stimulus is enough to produce minor endothelial injury. Among patients with venous disease, plasma levels of neutrophil elastase and lactoferrin (a secondary granule enzyme) also are elevated, confirming the presence of a chronic inflammatory state.…”

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confidence: 99%

Increased plasma vascular endothelial growth factor among patients with chronic venous disease

Shoab¹,

Scurr²,

Coleridge-Smith³

1998

Journal of Vascular Surgery

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Skin damage in the presence of chronic venous disease is partially mediated through leukocytes. The endothelium is activated and exhibits proliferation in the skin. Up-regulation of vascular endothelial growth factor (VEGF) expression in the skin of patients with chronic venous disease has been demonstrated with immunohistologic techniques. Abnormal VEGF expression can have local deleterious effects. The aim of this study was to determine whether patients with chronic venous disease have elevated plasma levels of VEGF. We conducted a prospective study with 30 patients with varicose veins of clinical, etiologic, anatomic, and pathologic class C3 (normal skin, n = 15) and C4 (trophic skin changes, n = 15) and 25 control subjects with no clinical evidence of venous or arterial disease of the lower limb. Blood samples were collected from a foot vein of each subject before and after a period of experimental venous hypertension produced by means of standing. Assay of VEGF protein was performed with a sandwich enzyme-linked immunosorbent assay. Plasma VEGF level was elevated in both groups of patients with venous disease compared with the control group. The median VEGF levels among patients were 81 pg/mL (interquartile range [IQR] 56 to 122) supine and 98 pg/mL (IQR 63 to 153) after standing for 30 minutes. Median VEGF levels among control subjects were 52 pg/mL (IQR 35 to 71) lying supine and 60 pg/mL (IQR 39 to 105) after standing for 30 minutes. Experimental venous hypertension caused a small rise in VEGF levels among the patients but not the control subjects. Further studies are required to determine whether increased VEGF expression contributes to tissue injury in chronic venous disease.

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“…Silver in ionized form applied in Textus bioactive® dressing is constantly released in small concentrations to the wound. It stimulates production of the growth fac-tors, cytokines and metaloproteinases by macrophages, fibroblasts and keratinocytes in the wound and accelerates the process of proliferation (6,14,15,18,19).…”

Section: Discussionmentioning

confidence: 99%

Leg venous ulcer healing process after application of membranous dressing with silver ions

Kucharzewski¹,

Wilemska-Kucharzewska²,

Kózka³

et al. 2013

Phlebologie

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SummaryAim: To assess the efficiency of application of new membranous dressing with silver ions in patients with chronic venous ulceration.Methods: 58 patients were divided randomly into two groups. In group A (n=30) mean ulcer surface area was 8.52 cm2, in group B (n=28) mean wound surface area was 8.29 cm2. In group A membranous dressings with silver ions (Textus Bioactiv® by Biocell GmbH, Germany) were used. In group B hydrocolloid dressing Unna’s boot was applied. All dressings were changed every 7 days until the wound was completely healed. Changes in wound area were calculated and the speed of healing process was measured every week with healing per day index (cm2/day).Results: After 7 weeks ulcers healed in all patients of group A. Ulcers in group B healed after 16 weeks of treatment.Conclusion: On the basis of this outcome the authors concluded that application of membranous dressing with silver ions speeds up the process of treating chronic lower leg ulceration.

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Microcirculatory Aspects of Venous Ulceration

Abstract: Inflammatory mechanisms play a significant role in the pathogenesis of venous disease but the exact mechanisms producing venous ulceration remain to be elucidated.

Cited by 23 publications

References 38 publications

Chronic Venous Insufficiency and Venous Ulceration

Chronic Venous Insufficiency and Venous Ulceration

Increased plasma vascular endothelial growth factor among patients with chronic venous disease

Leg venous ulcer healing process after application of membranous dressing with silver ions

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