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Leg ulceration in rheumatoid arthritis

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Patients with rheumatoid arthritis (RA) appear to be at increased risk of developing leg ulcers. The aetiology is not fully understood but it is likely that most are multifactorial in origin (McRorie, 2000). The mean duration of open ulceration in people with RA is five to 15 months. This compares with six months in people with leg ulceration secondary to venous insufficiency, indicating that people with RA are more resistant to treatment (Browse et al, 1988). Leg ulceration in this group is also associated with significant morbidity.

VOL: 97, ISSUE: 24, PAGE NO: 63

Michele Grange, RGN, DipMW, is specialist clinical practitioner, rheumatology

Charles Henderson, RGN, is a staff nurse, Royal National Hospital for Rheumatic Diseases NHS Trust, Bath

 

The multifactorial nature of leg ulceration in people with RA necessitates a multidisciplinary approach to care to ensure a full assessment of the patient’s needs.

The lack of evidence in support of products or approaches specifically for the management of leg ulcers in people with RA means that close liaison between team members is invaluable in ensuring that all treatment options are fully explored.

Patient history
In February 1999 Moira Smith was admitted to hospital with infected and offensive smelling ulcers on her left leg which had developed after an injury in 1996. She had lived with leg ulcers intermittently for six years. Previous treatment included skin-grafting, followed by excision of the wounds when the skin grafts failed. On this admission the ulcerated areas were painful and necrotic and had been left exposed.

Mrs Smith’s RA had proved difficult to control and she presented with abnormal blood results indicating RA flare, immobility and joint stiffness, anaemia and swollen and inflamed joints. She was also malnourished.

Holistic management
Because of the severity of Mrs Smith’s leg ulcers on admission and the difficulty in controlling her RA it was initially thought that a below-knee amputation would be necessary. However, after considerable debate and discussion with Mrs Smith the decision was taken to treat the leg ulcers. To ensure a holistic approach, doctors, rheumatology nurses and the dietitian worked together to meet her needs. She had restricted mobility due to her RA, so the multidisciplinary team also included a physiotherapist and an occupational therapist. A plastic surgeon was consulted regarding the appropriateness of further skin grafting.

Despite the possible negative impact of steroids and non-steroidal anti-inflammatory drugs on the wound-healing process the decision was taken to continue with this medication due to the unstable nature of Mrs Smith’s disease. Based on the results of a wound swab, which indicated the presence of an infection, she was started on intravenous antibiotics; oral antibiotics were required intermittently throughout her stay in hospital.

Poor oxygenation of the tissues will inhibit wound-healing and Mrs Smith was given a blood transfusion to correct her low haemoglobin. She had not been maintaining a satisfactory nutritional intake and the dietitian recommended a high protein diet.

Treatment of the ulcers
Before healing could take place sharp debridement of the ulcers was necessary to remove the devitalised tissue. Necrotic tissue can prevent wound contraction and inhibit healing (Goode, 1995; Bergstrom et al, 1994). This exposed healthy granulating tissue as well as sloughy areas. Some of the necrotic tissue had fully adhered to the underlying tissue; this was rehydrated and removed using a hydrogel covered with a non-adherent dressing pad.

After the necrotic tissue had been removed the hydrogel dressing was continued to maintain a moist wound environment. However, after two months of this treatment it became apparent that overgranulation - where granulation tissue protrudes above the level of the surrounding skin - was preventing epithelialisation. To reduce this the team decided to change the wound contact material to a polyurethane foam. Unfortunately this had to be discontinued after Mrs Smith developed a local skin reaction, and the hydrogel dressing was restarted until the inflammation and local swelling had subsided.

At this stage the ulcers were producing a moderate amount of exudate. To prevent possible saturation of the dressing and maceration of the peri-wound skin a calcium alginate fibre dressing was chosen. This was covered with a non-adherent dressing. A calcium alginate dressing can absorb 15-20 times its own weight in exudate and will provide a moist wound-healing environment if used appropriately (Thomas and Loveless, 1992).

Conclusion
Six months after admission to hospital Mrs Smith’s leg ulcers were virtually healed and she could be discharged to the community to be cared for by the district nurses.

As there is limited research into the use of wound contact materials in people with RA, treatment choices in this instance were based on general principles of wound-healing. However, the positive result achieved here illustrates how multidisciplinary involvement can ensure a thorough assessment of patient needs and a holistic approach to wound management.

In this instance multidisciplinary support and education have so far prevented Mrs Smith returning with the same problem.

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