Cath Lab Digest

Continued research in the arena of diabetic foot ulcers has led to a greater understanding of the etiologies of these wounds as well as the mechanisms of healing. With this in mind, this author raises questions on wound debridement, weighs in on the impact of quorum sensing and offers insights on the roles of allografts and advanced biologic therapies.

As our understanding of the etiology of diabetic foot ulcers (DFUs) has improved, the rate of amputations has continued to decrease. The early work of Brand and colleagues identified a link among neuropathy, repetitive mechanical stress and ulcer formation, and launched the concept of total contact casting to relieve mechanical pressure.¹ Remarkably, research showed that the control of mechanical forces led to wound closure in some cases and this served as one of the first viable alternatives to amputation.²

   After identifying the link among mechanical forces, neuropathy and ulceration, the focus on healing of DFUs shifted toward the physiology of wounds. In an effort to achieve higher closure rates, clinicians began to address barriers to cellular proliferation. For many years, the debate raged on about the role of diminished blood flow in the development of DFUs as well.

   Differentiation between calcification of the intima media versus luminal blockages and the presence of basement membrane thickening was a subject of wide discussion. The argument between the impact of macroscopic and microscopic vascular disease was widely debated as well, and ultimately led to strong affiliations between vascular and podiatric surgeons.

A Closer Look At Innovations In The Treatment Of Diabetic Foot Wounds

Over the last 15 years, our understanding of wound healing has expanded. There was a realization that growth factors played a critical role in angiogenesis, mitogenesis and chemotaxis within the wound bed. This resulted in development of the first widely used, cloned, growth factor becaplermin (Regranex, Systagenix). Simultaneously, the impact of bacterial infection and colonization has led to a variety of wound dressings designed to control bacterial load. New antibiotics have also emerged in order to combat methicillin-resistant Staph aureus (MRSA) and a variety of other resistant bacteria that developed in the presence of chronic infections.

   The science of wound healing changed dramatically as both patients and clinicians realized there were alternatives to amputation. While some focused on the issues of the wound itself, others addressed the underlying bony problems. Prophylactic surgery and reconstruction of feet devastated by Charcot neuroarthropathy emerged as a new approach for managing the complex array of mechanical forces that can lead to ulceration. As our understanding of these complex deformities improved, our tools have also increased in complexity. Circular frames based on the principles of Ilizarov provided a way to reconstruct even the most severely deformed feet while allowing the clinician to evaluate and manage the foot as needed.

   Furthermore, in some cases, the patients could even remain ambulatory during the healing process. Frame designs such as the Taylor Spatial Frame (Smith and Nephew) allowed for complex readjustments over time in order to optimize the final architecture of the foot.