INTRODUCTION
Chronic wounds are a major cause of morbidity in the current medical landscape. An estimated $25 billion is spent annually on the treatment of chronic wounds in the United States.1 Given the ubiquity of this condition, proper and efficient treatment is important for preventing associated morbidity and mortality as well as reducing healthcare expenditures.
Wound dressings are the cornerstone of wound care, though the variety of wounds encountered in the clinical setting (Figure 1) and the multitude of dressing options make selection
of the proper dressing difficult. This review seeks to outline proper wound dressing selection to enable dermatologists to effectively hasten wound healing, prevent infection and minimize
the burden of acute and chronic wounds (Figure 2).
Phases of Wound Healing
Wound healing can be conceptually understood in three phases. During the inflammatory phase of early wound healing, a fibrin clot is formed. This clot provides an initial extracellular matrix (ECM), as well as growth factor release from platelets. These growth factors attract fibroblasts and inflammatory cells including
neutrophils to clear microbial burden and macrophages for phagocytosis and cytokine release. The balance of pro and anti-inflammatory cytokines during this period is crucial for proper wound healing and progression from the inflammatory into the proliferative phase. During the proliferative phase, a new ECM composed of type III collagen is produced by fibroblasts and an extensive network of blood vessels develops. During the maturation
phase, a definitive ECM is formed when type III collagen is replaced by type I collagen. Many of the newly formed blood vessels regress and cellular activity in the tissue returns to normal.
However, the residual tissue can take up to 1 year to regain only a fraction of the skin’s original strength (~80%).2
Assessment of a Wound
Before selection and application of a dressing, thorough wound assessment is important. Evaluation of necrosis, possibility of infection, moisture level and exudates should direct therapy. The associated co-morbidities and etiologies of some wounds (venous insufficiency, diabetic foot ulcers, nutritional deficiency, pressure ulcers) lead to tissue hypoxia, which in turn can cause tissue necrosis. Necrotic tissue impedes formation of granulation
tissue, extending the healing process. Furthermore, tissue necrosis serves as a fertile medium on which microorganisms can thrive. If there is necrotic tissue in the wound bed, it should be properly debrided, either surgically, mechanically or chemically
before the wound is dressed.
Given wounds are a breach in the skin barrier, they serve as a point of entry for bacteria and other microbes to colonize and possibly infect the wound, surrounding tissue and potentially invade systemically. While some bacterial colonization can aid wound healing by the production of proteolytic enzymes, biofilm formation can cause persistent inflammation, delaying wound healing.3,4 Furthermore, very high levels of bacteria can result in local or systemic infection. Superficial wounds can be treated with topical antibiotics or dressings impregnated with antimicrobial materials if infection is suspected. More extensive local or systemic infections may require surgical debridement and systemic antimicrobial therapy.
