Transcutaneous oxygen tension and capillary morphologic characteristics and density in patients with chronic venous incompetence.

Uk, Franzeck; Bollinger, A; Huch, R.; Huch, A.

doi:10.1161/01.cir.70.5.806

Cited by 179 publications

(101 citation statements)

References 7 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: Pathophysiologymentioning

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: Pathophysiologymentioning

confidence: 99%

Chronic Venous Insufficiency and Venous Ulceration

Alguire

Mathes

1997

J Gen Intern Med

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“…11 P tc O 2 values % 40 mm Hg are typically considered indicative of hypoxia capable of inhibiting wound healing. 12,13 The levels near the patient's non-healing ulcers were in this range as documented in Table 1. In addition, these levels improved dramatically while breathing 100% oxygen at 1 ATA.…”

Section: Tcoms In Hbomentioning

confidence: 80%

The Use of Hyperbaric Oxygen Therapy in the Treatment of Non-healing Ulcers Secondary to Graft-versus-host Disease

Heyboer

Taylor

Morgan

et al. 2013

Journal of the American College of Clinical Wound Specialists

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We present the case of a 69 year-old gentleman with non-healing ulcers of the bilateral medial malleoli as a result of graft-versus-host disease (GvHD). The patient discussed was diagnosed with stage IV mantle cell lymphoma. Over the course of 4 years the patient was treated with autologous stem cell transplant, later reduced-intensity allogeneic stem cell transplant, and finally donor lymphocyte infusion due to recurrence. Following these therapies, the patient developed extensive GvHD that resulted in bilateral non-healing ulcers of the medial malleoli. The patient was seen in the wound care center, and his ulcers were treated with standard care that included off-loading, minor outpatient debridement, macrovascular assessment, and local moist wound healing. Despite this care, the ulcers failed to heal over a 6 month period. The patient underwent adjunctive hyperbaric oxygen therapy (HBO). He healed both ulcers within a month of completing HBO. It is our goal to discuss the pathophysiologic mechanism of non-healing wounds in the setting of GvHD and discuss the potential role of HBO in their treatment.

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“…The barrier function of the capillary wall is impaired, leading to the formation of micro-oedema, evidenced by a pericapillary ' halo '-like appearance after intravenous injection of sodium fluorescein [3,[61][62][63]. This halo, which is caused by a unique microoedema in the skin papillae, can be clearly demonstrated by capillaroscopy, especially after intravenous injection of sodium flourescein [63,64]. The oedema, which contains fibrin, proteins, and neutral polysaccharides [65], blocks the flow of nutrients between the capillaries and the skin cells and is probably the main reason for the abolished nutrition of the affected skin [63,66].…”

Section: Chronic Venous Insufficiencymentioning

confidence: 99%