The Cause of Venous Ulceration

Browse, N L; Burnand, K. G.

doi:10.1016/s0140-6736(82)90325-7

Cited by 535 publications

(207 citation statements)

References 17 publications

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“…Patients with venous ulcers have been shown repeatedly to have a prolonged eu¬ globulin lysis time and increased plasma fibrinogen levels.1 At the tissue level, excessive dermal pericapillary deposition of fibrinogen/fibrin products has been shown in skin taken from the edge of venous ulcers1 or within areas of lipodermatosclerosis,12 ie, the indurated skin associated with venous disease of the lower extremities.3 These findings have lent cre¬ dence to a unifying hypothesis for venous ulcération that was summarized byBrowse and Burnand,4 but …”

mentioning

confidence: 98%

Fibrin- and Fibrinogen-Related Antigens in Patients With Venous Disease and Venous Ulceration

Falanga

Kruskal²,

Franks³

1991

Arch Dermatol

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Abnormalities in systemic fibrinolysis have been implicated in the pathogenesis of venous ulceration. Patients with venous disease have a prolonged euglobulin lysis time and elevated plasma fibrinogen levels, yet little is known about the metabolism of fibrinogen and fibrin in such patients. In this study, we have used a technique that involves electrophoresis and densitometric analysis of captured fibrin-related antigens to measure the concentration and proportions of the individual fibrin and fibrinogen degradation products in patients with venous disease of the lower extremity. As a group, patients with venous disease had markedly elevated levels of total fibrin-related antigen and D-dimer, the terminal degradation product of cross-linked fibrin. Levels of D-monomer, the breakdown product of fibrinogen and non-cross-linked fibrin monomer, and a measure of fibrinogenolysis were normal in all patients. In patients with ulcers, the levels of D-dimer were disproportionately higher than expected from fibrin monomer levels. On an individual basis, significant elevations of D-dimer were present in six (55%) of the 11 patients with venous disease with ulcers and in three (43%) of the seven patients with venous disease without ulcers. We conclude that patients with venous disease have uniform evidence for enhanced fibrin formation, as evidenced by elevated levels of total fibrin-related antigen and D-dimer. This is regardless of whether the venous disease is accompanied by ulceration.

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mentioning

confidence: 98%

Fibrin- and Fibrinogen-Related Antigens in Patients With Venous Disease and Venous Ulceration

Falanga

Kruskal²,

Franks³

1991

Arch Dermatol

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“…Edema also decreases arterial flow to the tissue. Other theories are the oxygen diffusion block theory [15] and the physiological shunt theory [16]. Each theory suggests that lack of oxygen and nutrients for the tissues leads to the condition of lipodermatosclerosis (previously termed fat necrosis or tissue fibrosis) and also to cell death (venous ulceration).…”

Section: Discussionmentioning

confidence: 99%

Endoscopic anatomy of perforating veins in chronic venous insufficiency of the legs: “Solitary” incompetent perforating veins are often actually multiple vessels

et al. 2011

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We have already reported on the effectiveness of subfascial, endoscopic, perforating-veins surgery for chronic venous insufficiency of the legs. The incompetent perforating vein (IPV) often appears to be a single vessel, when it is actually two or more vessels. Accordingly we examined the anatomy and features of IPVS. The features of perforating veins were assessed in 173 limbs of 152 patients. In the recent 50 limbs, 1128 IPVs were subjected to complete dissection of the adventitia to confirm the number of vessels. Ninety-seven out of 110 IPVs (88.2%) had a concomitant artery. On endoscopy 128 IPVs could be classified into seven types (type N, type O, type I, type II, type III, type IV, and type V) according to the combination of arteries and veins which were presented. Type N means a normal perforator consisting of a single artery with a pair of normal veins running alongside it. Type O has the same anatomy as type N but shows reverse flow. Type I has an incompetent vein with thick walls and reverse flow, which is not accompanied by an artery. Type II is an artery associated with an incompetent vein. Type III is composed of an artery, a normal vein, and an incompetent vein. Type IV is an artery with two incompetent veins and type V contains multiple incompetent veins. When the anatomy of 128 IPVs was confirmed, 1 the number of each type was as follows: 7 type O (5%), 32 type I (25%), 1 type II (1%), 48 type III (38%), 39 type IV (30%), and 1 2 type V (1%). This is the first report on all the components of IPVs directly visualized in vivo. It has been almost impossible to predict the postoperative reversibility of IPVs after surgical ablation of superficial veins. By using our classification of IPVs, it will be possible to treat only the irreversible (true) incompetent veins and to avoid operating on arteries, normal veins, and reversibly incompetent veins. In the future, it will be necessary to devise the operative strategy according to the type of IPVs as assessed by endoscopic examination.

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“…Imaging for above-the-knee perforators was performed in the standing position while that for below-the-knee perforators was done in the sitting position. 10 The average number of incompetent perforators per lower limb was 2.7 in this series (range, [1][2][3][4] …”

Section: Methodsmentioning

confidence: 99%

“…Such venous hypertension plays a leading role in the development of venous ulceration. [1][2][3] The interruption of such incompetent perforators is an effective treatment for normalizing the ambulatory venous pressure. Traditional maneuvers to interrupt such incompetent perforators have included in this patient group, which was shown by a scanning reflux of perforators and the patent deep venous systems with or without incompetent superficial systems of the lower limb.…”

Section: Introductionmentioning

confidence: 99%

Closed Subfascial Ligation of Incompetent Perforating Veins of the Lower Extremities

et al. 2004

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The purpose of this study was to determine the effectiveness of minimally invasive surgical procedures for interrupting incompetent perforating veins of the lower limb. A closed subfascial ligation was performed in 20 patients who had incompetent perforating veins in 28 limbs as diagnosed by a clinical examination and duplex scanning. Two small transverse incisions measuring 5-10 mm in length were made on both sides of the incompetent perforating vein. Using an aneurysmal needle, a suture (polypropylene No. 1) was placed in the subfascial plane to encircle the incompetent perforating vein from all directions. Next, this suture was tied through two incisions to ligate this perforator. The mean follow-up period was 26 months. The ligation of the incompetent perforators was successful in 27 of 28 limbs and no wound complications were observed. A closed subfascial ligation of incompetent perforating veins of the lower limbs is thus considered to be easy to perform, not overly invasive, safe, and to also have very encouraging results.

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The Cause of Venous Ulceration

Cited by 535 publications

References 17 publications

Fibrin- and Fibrinogen-Related Antigens in Patients With Venous Disease and Venous Ulceration

Fibrin- and Fibrinogen-Related Antigens in Patients With Venous Disease and Venous Ulceration

Endoscopic anatomy of perforating veins in chronic venous insufficiency of the legs: “Solitary” incompetent perforating veins are often actually multiple vessels

Closed Subfascial Ligation of Incompetent Perforating Veins of the Lower Extremities

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