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Objective: The aim of this study was to assess the relationship between urinary and tissue haemosiderin in chronic leg ulcers, and its value as a diagnostic test for venous ulceration., Methods: 45 patients with chronic leg ulcers were recruited to the study (24 venous, 6 ischaemic, 6 lymphoedematous, 5 rheumatoid and 4 sickle cell). Punch biopsy of the ulcer edge was taken and early morning urine samples were collected. Positive Prussian-blue urinary haemosiderin granules were measured with a haemocytometer following Perls' staining. The percentage area of histological section staining positively with Perls' was measured using image analysis., Results: 84 urine samples and 46 ulcer biopsies were collected. Urinary haemosiderin was present in 92% of venous ulcer patients, but was absent in the ischaemic ulcer patients (p<0.0001). Significantly more urinary haemosiderin granules were detected in venous ulcer patients compared with patients who had lymphoedema (p<0.05). Tissue haemosiderin was detected in all ulcer types investigated. No correlation was found between the amounts of haemosiderin deposited in the tissue and the amount found in urine (r(2)=0.06)., Conclusions: Haemosiderin is present in the urine of most patients with venous ulcers but not in ischaemia ulcers.

Background: The aim of this study was to determine the success of excision and meshed skin grafting for chronic leg ulcers. The effects of different ulcer aetiology and ulcer size on outcome were also assessed., Methods: All patients who had excision and mesh grafting for chronic leg ulceration between January 1996 and December 2004 at St Thomas' Hospital were reviewed. Recurrence was classified as any breakdown of the ulcer during follow-up., Results: Sixty-two patients with 100 chronic leg ulcers underwent operation. Seventy-two of the ulcers were venous and the median ulcer size was 36 (range 1.5-192) cm2. Only three patients left the hospital with their ulcers unhealed, but ulcers had recurred in 28 (28 per cent) by 2 months. A further 17 ulcers recurred later, with just over half (55 per cent) remaining healed by 5 years. There was no difference between the recurrence rates of venous ulcers and ulcers of other aetiologies (P=0.980), or large (more than 10 cm2) and small ulcers (P=0.686)., Conclusion: Wide local excision and meshed skin grafting benefitted over half of these patients with refractory leg ulcers. Recurrence was most likely to occur in the first 2 months and, provided that ulcers were healed at this time, there was a low rate of further breakdown., (Copyright (c) 2006 British Journal of Surgery Society Ltd.)

Objectives: Devitalized tissue in a recalcitrant leg ulcer is common and may impede healing. The aim of this study was to evaluate the use of a non-invasive low frequency ultrasound device to debride chronic leg ulcers as an adjunct to compression bandages therapy., Methods: 19 patients with leg ulceration of at least 6 months were recruited. Low frequency ultrasound at 25kHz was delivered by a portable Sonaca--180 via a handheld probe, using normal saline as the irrigation/coupling medium. The ultrasound was applied for 10-20 seconds per probe head area onto the ulcer. Each leg underwent treatment at an interval of 2-3 weeks with compression bandages reapplied at the end of the treatment. Serial colour photographs were taken to evaluate the response at each visit., Results: Each patient received on average 5.7 treatments each ranged from 5-20 minutes depending on the ulcer size. Symptomatic relief (pain and odour reduction) was achieved in 6 patients. 7 patients achieved complete ulcer healing (mean ulcer size=4.72+/-SD 1.872cm(2)) but no response was observed in 8 patients. There were no major complications of the treatment which was relatively painless., Conclusions: The application of low frequency ultrasound debridement may heal some recalcitrant ulcers when standard compression regimens have failed. It is cheap and does not require admission. The role of simple wound cleansing requires further investigation.

Background: Both four-layer and three-layer paste bandages are widely used in the treatment of venous leg ulcers. The aim of this study was to compare the efficacy of these two bandaging regimens., Methods: The study was a prospective, randomized, open comparison of a consecutive cohort of 133 patients with venous ulcers. Participants were stratified by ulcer size into one of three groups and were randomized within each group to receive either three-layer paste or four-layer bandages. All patients were followed for 1 year. The time taken to complete ulcer healing was the primary endpoint. The time taken to apply the bandages, comfort, tolerability and cost were also assessed. Analysis was performed on the basis of intention to treat., Results: Ulcers healed completely in 51 (80 per cent) of 64 patients treated with three-layer paste bandages compared with 45 (65 per cent) of 69 patients treated with the four-layer regimen (P = 0.031). This difference developed only after 20 weeks of treatment. The median times to complete healing were 12 weeks for three-layer and 16 weeks for four-layer treatment (P = 0.040). Results of venous function tests, including half-refilling times, were similar in the two groups., Conclusion: Three-layer paste bandages were significantly more effective at healing venous ulcers than the four-layer regimen in this study., (Copyright 2003 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.)

Background: Many venous ulcers are healed by the application of external compression. It has been suggested that bandages capable of producing greater compression enhance healing. The aim of this study was to compare the time to total healing of venous ulcers in two groups of patients treated with different compression regimens in a randomized prospective trial., Methods: A total of 112 patients was studied and all were treated with a zinc-impregnated paste bandage applied directly to the ulcer. Fifty-seven patients had the paste covered by Tensopress and 55 by Elastocrepe bandages. Both groups had a tubular bandage applied over the top to retain the bandage in place. All ulcers were stratified and randomized within one of three size groups. The 'venous' aetiology of the ulcer was confirmed on completion by calf pump function tests., Results: By 26 weeks, 58 per cent of the patients treated with Tensopress and 62 per cent of those treated with Elastocrepe bandages were healed. The median healing times were 9 and 9.5 weeks respectively. Similar numbers of patients were excluded or withdrawn from both groups. Large ulcers healed significantly more slowly than small ulcers., Conclusion: There was no significant improvement in venous ulcer healing using higher compression elastic bandages.

Urokinase plasminogen activator (uPA) and tissue plasminogen activator (tPA) were assayed in biopsies from the base, edge and adjacent skin of ischaemic and venous ulcers using a functional bioimmunoassay and a standard immunoassay. Two series of 14 biopsies were examined: from seven venous and seven ischaemic ulcers in the first series, eight venous and six ischaemic in the second. It was found that tPA was detected in only four samples of ulcer edge using the bioimmunoassay and in no sample by the standard immunoassay. By contrast, uPA was detected in all but one ulcer edge biopsy and at a significantly lower median concentration in the adjacent skin (16.9 units/g) than the ulcer edge (26.1 units/g) or base (32.3 units/g) (both P < 0.01). Levels of uPA were greater in the edge and base of venous compared with ischaemic ulcers. The predominant plasminogen activator in chronic leg ulcers is uPA; this activator may play an important role in wound healing.

Eighty-five limbs in 73 patients with a healed venous ulcer were assessed by ascending and descending phlebography, foot volume plethysmography and transcutaneous oxygen measurements. Forty-four limbs had post-thrombotic changes on ascending phlebography. In 24 (28 per cent) these extended into the femoral vein, while in 20 (24 per cent) only the calf veins were involved. In the 41 limbs (48 per cent) with normal deep veins on ascending phlebography, 11 had evidence of localized incompetence of the calf communicating veins, 14 had either long saphenous incompetence, deep vein reflux to the level of the knee or below, or both of these abnormalities, and 16 limbs had no phlebographic abnormalities. However all limbs had a decreased half volume refilling time on foot volume plethysmography. Limbs with post-thrombotic changes extending into the femoral vein were associated with a significantly longer history of ulceration and more ulcer recurrences than limbs with calf vein damage (P less than 0.05 for each) and limbs with normal deep veins (P less than 0.01 for each). However, these limbs did not have lower transcutaneous oxygen ratios or longer times to achieve ulcer healing. Ascending phlebography identified a group of limbs with extensive post-thrombotic changes in which there was a higher incidence of ulcer breakdown, but this was not associated with a delay in ulcer healing.

Forty-one biopsy specimens, taken from the ulcer-bearing skin of 41 legs of 21 patients attending the varicose vein clinic, were selectively stained for fibrin with phosphotungstic acid haemotoxylin before being blindly assessed,. Layers of fibrin were found surrounding the dermal capillaries in all 26 legs with lipodermatosclerosis. None of the specimens from the 15 legs with clinically normal skin contained fibrin. There was also an increased number of dermal capillaries cut in cross section per high powered field in 24 of the 26 legs with lipodermatosclerosis compared with two of the 15 legs with normal skin (p less than 0.001). The mean reduction in foot vein pressure during exercise was significantly less in the 26 limbs with pericapillary fibrin than in the other 15 limbs (p less than 10(-6). Lipodermatosclerosis is synonymous with pericapillary fibrin deposition and is associated with, and probably secondary to, both a persistently raised venous pressure and an increase in the size of the dermal capillary bed. This extravascular deposition of fibrin probably stimulates tissue fibrosis and blocks the diffusion of oxygen to the overlying epidermis, producing cellular death and venous ulceration.

Forty-seven patients with unilateral venous ulceration have been investigated to determine if any abnormalities were present in the contralateral limbs which had not had lipodermatosclerosis or ulceration. Ascending phlebography in the non-ulcerated limbs showed post-thrombotic changes in 28 per cent and incompetent lower leg communicating veins in 19 per cent. This incidence was not significantly different to the limbs with healed ulceration (45 and 23 per cent respectively, chi 2 test, P = 0.10). Half volume refilling time measured by foot volumetry suggested that 79 per cent of the non-ulcerated limbs had evidence of deep vein incompetence or incompetent lower leg communicating veins, which was again similar to the incidence in the previously ulcerated limbs (85 per cent). Transcutaneous oxygen readings, expressed as a ratio of a reading at a standard site in the gaiter region of the leg over a reading from the upper arm, were significantly lower in non-ulcerated limbs (mean 0.84 +/- 0.26 s.d.) than in a cohort of age and sex matched controls (mean 1.02 +/- 0.14, Student's t test, P less than 0.001), and significantly higher than in previously ulcerated limbs (mean 0.68 +/- 0.31, P less than 0.01). Abnormalities in venous anatomy and function have been shown, in conjunction with evidence of reduced oxygen diffusion, through the gaiter skin before overt skin changes develop.