What You Should Know About Wound Healing And Hyalofill

Start Page: 46
A 76-year-old insulin-dependent male with diabetes presented with an ulceration under his big toe (see above photo). He has a long-term history of peripheral vascular disease and previously had an amputation of the fifth toe on the same foot.
Here we see the same ulcer two weeks after the author treated it with debridement, Hyalofill, Aquacel and offloading via a Camwalker boot.
Here we see the healed ulcer of the 76-year-old insulin-dependent diabetic male, six weeks after the author began treatment.
By Alan J. Cantor, DPM

The last decade has seen a tremendous evolution in the field of advanced wound management, both as a discipline and in regard to the development of wound healing therapies. New dressings, human skin equivalents, and barometric intervention all compete for utilization in the wound healing process. While each of these options is a viable intervention, there still needs to be more recognition of how wound biology and histo-cellular function affect wound healing.
Indeed, understanding the process of healing wounds is essential for the clinician dedicated to wound medicine. Often, it is stated that understanding wound biology and physiology in the 21st century will be as mandatory as reading and writing if you wish to be a competent wound healer. It is generally accepted that the next few years will feature new agents and therapies designed and devoted to regulating specific biological and cellular functions.
It is necessary to recognize the differences between an acute wound and a chronic wound in the biological-cellular response. An acute wound is understood to be an “acute disturbance of previous intact skin by external force.”1 The acute injury, which you would see with the immunocompetent elective surgical candidate, is an injury in which you can anticipate the normal wound healing cellular response. This cellular response is the classic multi-phase response of hemostasis, inflammation, granulation, reepithelialaization and remodelling.
Early granulation has heavy inflammatory activity (due to macrophage and neutrophil proliferation), which leads to a more fragile and unstable wound. However, once you’ve resolved the inflammation, a more stable environment emerges. This allows for a matrix which permits a new epidermal layer to be formed from epithelial cells migrating from surrounding intact periwound skin. Ultimately, a new protective epidermal barrier is established over the granulation tissue.
Significantly different from the acute wound is the chronic, non-healing wound. These are the wounds you’ll see with immunosuppressed hosts (diabetics) and these wound result from “internal forces.”1 With these patients, the normal wound healing cascade is disoriented and there is a prolonged inflammatory phase.
The inability of the host to deactivate the inflammatory response creates an environment unable to organize a normal, sequential cellular response. This results in the wound’s inability to create a healthy granulating bed. Furthermore, multiple destructive byproducts are formed, obstructing the formation of a healthy wound matrix, establishing a chronic wound that is unable to organize the choreographed, orderly cellular response that you would see in an acute wound.

image description image description

Post new comment

  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.

More information about formatting options

Enter the characters shown in the image.