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Silver dressings: absorption and antibacterial efficacy

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VOL: 101, ISSUE: 46, PAGE NO: 45

Alan Lansdown, PhD, FRCPath, is senior lecturer in chemical pathology, Division of Investigative Sciences, Imperial College School of Medicine, London

Angela Williams, MSc, RGN, is vascular nursing specialist, Department of Vascular Surgery; Susan Chandler, RGN, is sister, Outpatients Department; Susan Benfield, RGN, is staff nurse, Outpatients Department; all three at Charing Cross Hospital, London

Sustained silver-release dressings are now well established in the management of acute and chronic wounds and burns (Lansdown, 2002). The dressings differ greatly in their total silver content, patterns of silver ion release and presumed therapeutic action (Lansdown, 2004). More detail on the dressing types has been given by Lansdown et al (2005). Exudate and wound fluid trigger the release of ‘activated’ silver ions for antibacterial action and to neutralise any toxins. The dressings liberate more silver than is required for bactericidal action (Burrell et al, 2004; Hamilton-Miller, et al, 1993).

Other than occasional references to argyria-like (bluish-black) discolorations in wounds treated with high silver-release dressings, there is no evidence that the excess silver exerts undesirable effects within the wound bed or systemically (Lansdown, 2004; Lansdown and Williams, 2004). However, there is a lack of detailed understanding on how chronic wounds respond to the excess of silver and of the local protective mechanisms to avoid silver toxicity.

The objective of the study reported here was to illustrate patterns of silver release and distribution in wound sites using non-invasive methods. We examined the bactericidal action of Acticoat 7, Actisorb Silver, Aquacel Ag, Contreet Foam and Flamazine as a feature of wound bed preparation in chronic wounds (Schultz et al, 2003).

The results of an experimental rodent study that examined the correlation between exudate absorption, silver release and silver accumulation in the wound bed are reported in the full paper in Journal of Wound Care (Lansdown et al, 2005).

Method and materials for the clinical studies involving patients

Seven patients with chronic venous ulcers of at least 30 weeks’ duration were selected. Inclusion criteria were: clinical evidence of infection, moderate to severe exudation, ankle brachial pressure indices of over 0.8 (no evidence of arterial disease), no clinical evidence of silver allergy, and patients who did not have diabetes. Patients were excluded if they were being subjected to other therapies or conditions that might influence the action of sustained silver-release dressings.

The wounds were assessed and dressings were selected by the lead vascular nurse. Secondary four-layer bandages were used and the dressings were changed every three to four days. At dressing changes, samples of wound fluid/exudate and wound scale were sampled using sterile forceps. Microbiological swabs were also taken.

Results of the clinical studies

The chronic wounds in the seven patients differed greatly in outward appearance and behaviour. There were only two adverse responses to the dressings: patients 1 and 2, given Acticoat 7 for at least 12 weeks, had darkish discolorations on the skin surface next to the wound site or in the thick, viscous, straw-coloured exudate. Acticoat 7 was selected for patients 1 and 2 because their ulcers were severely infected with copious exudate.

Accumulation of silver in the exudate varied greatly, but there was a correlation between its viscosity and the amount of silver.

The venous ulcer in patient 1 (Acticoat 7) had a copious highly viscous exudate containing blackish discolorations with very high levels of silver. After four months the Acticoat 7 (high silver) therapy was discontinued in favour of a lower silver-release product, Actisorb Silver.

After two weeks, the silver content of the wound exudate had reduced by 65 per cent. Although modest amounts of silver were measured in wound scale following the Acticoat 7 therapy, insufficient tissue was available for analysis after Actisorb Silver treatment.

Patient 3 had had a long-standing (30 years) susceptibility to chronic leg ulcers. Extensive, painful lesions on both legs had been treated for 12 weeks with Flamazine cream and four-layer bandaging. Chemical analyses of the more viscous wound exudate of the patient’s left leg showed appreciably more silver than in the watery exudate of her right leg. Ulcers on both legs remained indolent and were particularly painful, necessitating admission for topical negative therapy (TNP). Silver dressings and antimicrobial agents were not used during the 11 weeks of TNP therapy.

Wound healing for this patient improved following TNP therapy, but the ulcers were still painful. The patient returned for examination as an outpatient. Silver was still recovered from exudate 11 weeks after the start of the silver therapy, but disappeared completely over 14 weeks.

Patients 4, 5 and 6 had chronic venous ulcers of the lower leg. Their wounds varied greatly in outward appearance and behaviour but were judged to be clinically suitable for low silver-release dressings - Actisorb Silver or Aquacel Ag. The silver was absorbed by wound exudate or scale but its concentration reduced as the wounds healed.

The absorptive properties of the dressings made collection of sufficient exudate for chemical analysis difficult. However, the more viscous exudate from patient 6 contained higher levels of silver than the watery fluids from patient 5. (The silver content of the two dressings is similar, but their silver ion release patterns differ.)

The wound in patient 4 provides strong evidence that sustained silver-release dressings can provide a means of debridement. This ulcer was treated with Aquacel Ag and four-layer bandaging. When the dressings were changed at three- to four-day intervals, adherent exudate and wound debris (and presumably infected material) were gently removed with the dressing.

Patient 7 developed a chronic ulcer on his right leg five months following a skin graft. He was treated with a bland non-medicated (non-silver) dressing for four weeks before receiving Contreet Foam. The wound released small quantities of watery exudate, which was mostly absorbed into the dressing, leaving an insufficient sample for silver analysis. However, silver accumulated progressively in the wound scales following application of Contreet Foam, but it was not associated with any obvious discoloration of the skin or evidence of toxicity. Healing and re-epithelialisation progressed well within one month of starting therapy.

Wound infections

Although the lesions were treated with silver antibiotic dressings, infectious organisms were still isolated during the pre-epithelialisation phase. The nature and severity of the infections varied greatly. Importantly, re-epithelialised wounds in patients 5 and 7 did not show signs of infection when sampled after courses in Actisorb Silver and Contreet Foam therapy respectively. None of the patients received systemic antibiotics.

Discussion

Silver ion release profiles for wound dressings based on in-vitro experiments show that products currently available in Europe or the USA are of three main types (Dolmer et al, 2004):

- Products with a high silver content with a rapid silver ion release, designed for wounds with heavy exudate and bacterial colonisation;

- Products that maintain a more modest silver-release pattern, where silver ions are released over several days. These are claimed to be sufficient for moderate to severe pathogenic bacterial populations. The non-silver components of these dressings are attuned to wound bed management - exudate control, debridement of wound debris and management of the wound environment;

- Products with a low silver content, which may be sufficient for low-grade infections in chronic wounds but are more appropriately used as a barrier to infection in acute wounds, burns and surgical injuries.

In the present study, the findings for products in the first two categories illustrate that:

- None of the dressings was overtly toxic;

- All silver that was released into the wound bed was absorbed by wound exudate or debris (wound scale);

- Silver uptake by wound exudate is approximately proportional to its viscosity (protein content);

- Silver absorbed into the wound bed may be eliminated in the exudate for several weeks following the termination of silver therapy;

- The amount of silver released from dressings is closely related to the amount of moisture that is absorbed

- Sustained silver-release dressings contribute to wound-bed preparation;

- Wounds treated with silver do not attain a germ-free status, suggesting that silver-resistant organisms such as Staphylococcus aureus, Pseudomonas aeruginosa and enterococci, may contribute to indolence in healing.

Silver is commonly found in the human body at low concentrations but has no recognised physiological function. Release of high concentrations into damaged tissue does not cause toxic changes compromising wound repair. This study demonstrates that silver released into a wound bed is absorbed by exudate or dead tissue surrounding the wound cavity and is precipitated or otherwise rendered inactive.

Wound-bed preparation aims to create a conducive environment for wound healing. Present studies with a selection of silver dressings illustrate that products release silver ions at sufficient concentrations to achieve bacteriostasis without compromising patients’ health. Dressings such as Actisorb Silver, Contreet Foam and Aquacel Ag efficiently absorb exudate with wound debris, so that at dressing changes, wounds are cleansed and debrided to improve the local wound environment.

FOOTNOTE

Declaration of interest: Coloplast A/S supplied dressings and met the laboratory costs.

- A full version of this article has been published in Journal of wound Care: Lansdown, A. et al (2005) Silver absorption and antibacterial efficacy of silver dressings. Journal of Wound Care; 14: 4,155-160.

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