Lis Danielsen

Bacterial colonization and healing of venous leg ulcers

The aim of the study was to evaluate a possible influence of selected bacterial species on healing of venous leg ulcers. Fifty‐nine patients with venous leg ulcers were followed via frequent semiquantitative culture of bacteria from the ulcer surface and determination of the ulcer area over a period of 180 days. Occurrences of cellulitis were treated with systemic antibiotics. There was a significant difference in relative areas on days 90 and 180 when ulcers with growth of Pseudomonas aeruginosa were compared to those without (p=0.0080 and 0.0133, respectively). Ulcers with P. aeruginosa were characterized to a great extent by enlargement in contrast to those without. Ulcers with growth of Staphylococcus aureus or haemolytic streptococci healed significantly more slowly than those without when relative areas were compared on day 180 (p=0.0079 and 0.0492, respectively). Complete healing within the observation period of 180 days was observed in 10.5% of patients with P. aeruginosa and 35% of those without (p=0.0631), in 21.6% of patients with S. aureus and 62.5% of those without (p=0.0278), and in 10.5% of patients with haemolytic streptococci and 35% of those without (p = 0.0631). The initial areas of ulcers colonized with P. aeruginosa or 5. aureus were significantly larger than those without, but no significant correlation between initial areas and ulcer healing was revealed. Conclusion: Our results suggest that P. aeruginosa in venous leg ulcers can induce ulcer enlargement and/or cause a healing delay. The results also suggest a healing delay caused by 5. aureus and haemolytic streptococci. However, conclusions have to be treated with caution since P. aeruginosa was found in combination with haemolytic streptococci in 15.3% of the patients.

Ulcer bed infection

We report a case of ulcer bed infection in an enlarging venous leg ulcer without clinical signs of cellulitis in the surrounding tissues. Signs of infection in the leg ulcer were: 1) cocci‐like structures and bacteria‐like rods around vessel walls in the viable ulcer bed, 2) vasculitis‐like inflammation of deeply situated vessels of the viable tissue, 3) Pseudomonas aeruginosa‐specific antibodies in the serum (other than against exotoxin A), 4) extensive epidermolysis of normal human skin by the wound exudate in vitro, and 5) P. aeruginosa exotoxin A in the wound exudate (23 ng/ml). In an in vitro cell assay, the wound exudate was cytotoxic and rabbit antibodies to exotoxin A, but not a serine proteinase inhibitor, inhibited this cytotoxicity. P. aeruginosa exotoxin A might contribute to the pathogenesis of the ulcer enlargement. The ulcer improved after the third skin graft, probably mainly due to effective treatment with a long‐stretch compression bandage.

VENOUS LEG ULCER HEALING : A RANDOMIZED PROSPECTIVE STUDY OF LONG-STRETCH VERSUS SHORT-STRETCH COMPRESSION BANDAGES

Objective: To compare the efficacy of a long-stretch bandage with that of a short-stretch compression bandage. Design: Prospective evaluation of healing of venous leg ulcers in blindly randomized groups of patients. Setting: Bispebjerg Hospital, Copenhagen, Denmark. Patients: Forty-three patients with venous leg ulcers were included. Forty legs in 40 patients were evaluated at 1 month (34 patients), 6 months (32 patients) or 12 months (27 patients). Interventions: Both types of bandage were used at a width of 10 cm and applied using the same spiral bandaging technique. Main outcome measures: Ulcer healing and ulcer area reduction. Results: Healed ulcers after 1 month were observed in 27% of the long-stretch group and in 5% of the short-stretch group (p = 0.15); after 6 months the corresponding figures were 50% and 36% (p = 0.49) and after 12 months 71% and 30% (p = 0.06). Using life-table analysis the predicted healing rate in the long-stretch group after 12 months was 81% and for the short-stretch group 31% (p = 0.03). The mean of relative ulcer areas at 1 month was 0.45 for the long-stretch group and 0.72 for the short-stretch group (p = 0.07), at 6 months the corresponding figures were 0.81 and 0.60 (p = 0.25) and at 12 months 0.25 and 0.95 (p = 0.01). Conclusions: The present study appears to indicate a Positive influence of the elasticity of a compression bandage on venous ulcer healing.

The terminal complement complex is generated in chronic leg ulcers in the absence of protectin (CD59).

Loss of membrane complement regulators accompanied by complement activation is suggested to be involved in the pathophysiological processes leading to tissue damage in myocardial ischaemia. In the present study we have investigated whether the same phenomenon may occur in ischaemic and/or venous hypertension leg ulcers. The deposition of complement, plasma complement regulators and expression of membrane regulators were detected by immunohistochemical methods, including immunofluorescence with antibodies against C3d, the terminal complement complex (TCC), vitronectin, clusterin, decay‐accelerating factor (CD55) and protectin (CD59). Eleven frozen biopsies from ischaemic leg ulcers, 10 biopsies from venous hypertension leg ulcers, and 10 biopsies from normal skin were studied. In 9 of 11 ischaemic and in 5 of 10 venous hypertension leg ulcers, marked staining for TCC was found around the capillaries, most often at the ulcer margin. No TCC staining was found in normal skin. Staining for TCC was always accompanied by staining for clusterin and vitronectin and C3d. In normal skin, CD59 was found on the elastic fibers in the dermis, on the muscle coat, the Schwann sheath and acinar cells. Semiquantitative measurement of CD59 showed marked increased staining intensity in the endothelium in venous hypertension ulcers and diminished intensity in ischaemic ulcers compared to normal skin. No such difference could be observed for CD55. When TCC was positive in the capillary walls, weak or no staining for CD59 was found. A significantly higher ratio of TCC/CD59 was found in the ischaemic compared to venous ulcers (p=0.018). This was due to a marked difference between the ulcer margins (p=0.013). Localized areas in the venous ulcers had the same pattern as that seen in the ischaemic ulcers. Our results suggest that loss of CD59 may enhance deposition of TCC and that complement‐dependent inflammation may be an important factor in the tissue‐damaging processes seen in chronic leg ulcers.

The occurrence of pericapillary fibrin in venous hypertension and ischaemic leg ulcers: a histopathological study

Summary The presence of pericapillary fibrin and complement C3c in the ulcers of 19 patients with venous hypertension and 14 patients with ischaemic leg ulcers was investigated using histochemical and immunohistochemical techniques. There was deposition of fibrin around the capillaries in the central part of the ischaemic ulcers, and the venous hypertension ulcers, and in the non‐ulcerated skin around one of the venous hypertension ulcers and two of the ischaemic leg ulcers. The deposition of fibrin is a secondary phenomenon that occurs in the area of ulcerated skin and dose not play a major causal role in the formation of chronic leg ulcers.

The effect of sodium hydroxide and hydrochloric acid on pig dermis. A light microscopic study

In order to compare the dermal changes after exposure to direct current (d.c.) with changes after influence of acid and base influence, the skin of fully anaesthetized Danish Landrace pigs were exposed to acid and basic solutions. Biopsies were obtained immediately after and up to day 7 after the injury. Collagen fibres with increased affinity for eosin and irregular cross-striation in polarized light together with shrunken cells with dark stained nuclei were found just beneath the epidermis immediately after application of 1 N HCl. Immediately after exposure to 1 N NaOH dispersed collagen fibres showed increased eosinophilia and a fine densely spaced cross-striation in polarized light and vesicular nuclei were present within dermal cells. During the following days a narrow demarcation zone of neutrophilic granulocytes separated the zone containing abnormal collagen fibres from normal tissue below. Calcified collagen fibres were not observed and no other abnormal histochemical reactions were present. It is concluded that the morphology of acid induced lesions and base induced lesions shows resemblance to the morphology of anode and cathode lesions, respectively, but not to heat lesions. The reason for not finding depositions of calcium salts on collagen fibres in skin exposed to basic solutions could be a non-optimal pH in the tissue or that other electrochemical processes than shift in pH are necessary for the calcification process.

Cellulitis in Venous Leg Ulcers Treated with a Hydrocolloid Dressing

Objective: To evaluate the development of cellulitis in patients with venous leg ulcers in relation to colonizing or infecting microorganisms and principles of ulcer dressing. Design: Patients were prospectively randomized to either a routine leg ulcer dressing principle or hydrocolloid dressing (HCD). Setting: Tertiary care university hospital. Patients: Fifty-seven consecutive patients followed for at least 6 months. Main outcome measures: Development of cellulitis related to isolation of microorganisms and the ulcer dressing principle. Results: Development of cellulitis was only correlated to the isolation of haemolytic streptococci, predominantly belonging to Lancefield group G (2p < 0.01). Staphylococcus aureus and Pseudomonas aeruginosa did not contribute to the development of cellulitis. One infection per 198 days was found in patients treated with HCD compared with one infection per 290 days in patients treated with chlorhexidine ointment with a vehicle of carbowax polyethylene glycol (not statistically different). Conclusions: Hydrocolloid dressing treatment was safe. Cellulitis was caused by haemolytic streptococci.

The occurrence of calcium salt deposition on dermal collagen fibres following electrical injury to porcine skin

Deposition of calcium salts on collagen fibres has been shown to occur in cathode areas from 2 days to 2 months after exposure to direct current (d.c.) via contact knobs measuring 12 mm in diameter using energy level from 0.5 to 96 J and on day 7 after exposure to alternating current (a.c.) via pointed electrodes using energy level from 30 to 50 J. In order to determine the statistical relation of this histological observation to the type of energy applied 1095 biopsies from 49 pigs including biopsies from skin areas exposed to heat, 50 Hz a.c., 100 kHz a.c. and d.c. as well as from unexposed skin were examined. The specificity was 1.0 using calcium deposition as the test criterium. The sensitivity for cathode areas was found to vary from 0.52 to 1.0 depending on the biopsy technique and the number of days after exposure. Calcium salts on collagen fibres seem uniformly to be present in the cathode area from day 4 to 7, the positive test answer being depending on the biopsy technique. For 50 Hz a.c. the sensitivity using a pointed electrode was found to vary from 0.08 to 0.27 dependent on the number of days after exposure. For all other types of energy the sensitivity was 0.

Non-invasive monitoring of compression therapy: a report of three cases with venous insufficiency.

Sir, Skin oedema is believed to have a negative effect on wound healing and to contribute to skin necrosis and the development of leg ulceration (1, 2). To understand the pathologic signi® cance of oedema, it is important to be able to determine the quantity of uid content and its localization in the skin. High-frequency ultrasonography visualizes oedema as areas of reduced echogenicity in skin images (3, 4). In the post-thrombotic syndrome and lipodermatosclerosis, the drop in echogenicity is present mainly in the subepidermal region; in lymphoedema, echogenicity decreases in the entire dermis, whereas in cardiac insuf® ciency echogenicity decreases in the lower portion of the dermis (5, 6). Since the upper part of the dermis is a site of intensive metabolism (7), oedema localized in this layer might be particularly deleterious. In this study, we used high-frequency ultrasonography to quantify the reduction of dermal oedema after use of two types of compression bandages in three patients with venous insuf® ciency.