Efficacy of a Urinary Bladder Matrix for Treating Wound Dehiscence With Hardware Exposure in a Patient With Rheumatoid Arthritis

Roger D. Bui, BSc; Kenrick Lam, MD; Vinod K. Panchbhavi, MD, FACS

Disclosures

Wounds. 2020;32(4):E27-E30. 

In This Article

Discussion

Wound dehiscence is typically managed with debridement, antibiotic therapy, and resuturing or implementing another type of wound closure device to facilitate healing by secondary intention. Negative pressure wound therapy is a treatment modality that has been a useful adjunct in the treatment of several wound types following foot and ankle surgery.[6] This negative pressure technique removes chronic edema fluid, which in turn decreases afterload to blood flow, facilitating increased perfusion of the damaged tissue and enhancing formation of granulation tissue.[6] Mendonca et al[6] ascertained NPWT use in foot and ankle surgery leads to wound closure more quickly, and, in most patients, circumvents the need for further surgery. In the present case, wound care was initially started with NPWT, but eventually NPWT was discontinued due to its inability to hold suction well because of the location of the wound.

The management of an infected, dehisced wound is one of the greatest challenges an orthopedic surgeon must face. Viol et al[5] proposed an algorithm to determine whether hardware retention was possible after wound dehiscence. They suggested that within 2 weeks of wound dehiscence, it was reasonable to retain the hardware.[5] The present authors believe their patient's prompt presentation and eventual coverage with the UBM graft made hardware retention possible.

The ideal matrix for wound healing would be amenable to cell infiltration and proliferation, while serving as a viable scaffold for the deposition of fibrous connective tissue and epithelial layer.[7] The UBM shows a bimodal growth pattern — cell infiltration on 1 surface of the scaffold and development of a monolayer of cells on the other surface. The biocompatible constitution of the UBM consists of a motley of multiple types of carbohydrates, collagens, proteins, and other components, further augmenting its clinical utility in the context of wound dehiscence.[8] The UBM product's MatriStem UBM (ACell) technology platform is based on an extracellular matrix derived from porcine bladder. The UBM is composed of an intact basement membrane and lamina propria opposing surface. A randomized controlled trial by Alvarez et al[7] comparing the effectiveness of treatment of diabetic foot ulcers with UBM plus offloading with a total contact cast (TCC) versus standard care (nonadherent dressing with TCC) revealed a significantly reduced healing time and diminished rate of ulcer occurrence. The literature documents a marked efficacy in rapid healing of severe, recalcitrant wounds that were unresponsive to conventional wound therapy.[8–10]

There is often concern about the influence of disease-modifying agents on wound healing and infection rates in surgical patients. Theoretically, the mechanism of action of tumor necrosis factor (TNF) alpha inhibitors and antimetabolites (eg, MTX) would lead to compromised wound healing. In vitro and animal studies have shown the process of wound healing can be completely arrested when inflammation or cellular proliferation are suppressed or removed from the healing cascade.[11] However, there is a paucity of clinical evidence corroborating the hindering effect MTX has on wound healing and very little evidence suggesting low-dose MTX in patients who undergo orthopedic surgery should be discontinued.[11] The clinical data on the effect of biologic TNF blockade on risk of surgical site infection are conflicting. While certain meta-analyses and observational studies have demonstrated treatment with TNF antagonists is associated with an increased risk of developing serious infection and resultant healing complication,[12–14] another national prospective observational study of 7664 anti-TNF-treated and 1354 disease-modifying anti-rheumatic drugs-treated patients with severe RA from the British Society for Rheumatology Biologics Register showed contrary results.[15] Therefore, the widely adopted discontinuation of TNF inhibitors, such as adalimumab, is often predicated on caution and experience rather than adherence to compelling literature.[16]

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