Microbial Barriers

Barrier wound therapy is commonplace in the health care environment and functions to limit bacterial colonization and infection in both acute wounds and recalcitrant chronic wounds. This article reviews the nature of acute and chronic wounds and their available adjunctive barrier therapies.

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The wound healing process can be hindered easily by the bacterial bioburden with organized and dynamic polymicrobial biofilms.
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For new or acute wounds, the use of an appropriate dressing that acts as a microbial barrier is essential.
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For delayed-healing or chronic wounds, adequate sharp debridement when clinically indicated is imperative as the initial step to break the imbalanced cellular microenvironment–bioburden cycle.
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Adjunctive microbial barriers act to minimize bacterial contamination from the environment and facilitate the conversion of the chronic wound to an acute wound, which ultimately leads to a healed wound.

Key Points

Introduction

Wound care has evolved over thousands of year from an archaic therapy of honey, grease, and lint to an inconceivable use of modern health care resources. Each wound infection may cost up to $35,000 to treat, and the annual cost of pressure ulcers alone mounts to billions of dollars. In 1865, Sir Joseph Lister was the first to understand and implement an antimicrobial wound therapy. Antiseptic carbolic acid (phenol) demonstrated improved wound healing without suppuration and reduced mortality. During World War I, Alexis Carrel treated open wounds with sodium hypochlorite (Dakin solution), which aided necrotic debridement of devitalized tissue. Today the wound market is replete with innovative technological advances for wound care including technology that helps prevent infection by antimicrobial barrier therapy. This article reviews the complexities of bacteria and wound healing, the current application of antimicrobial wound therapy, and pioneering advances in wound care technology.

Wound healing

Acute Wounds

An acute wound is created by a violation in skin integrity. Acute wound healing progresses through a systematic and balanced repair process consisting of 4 phases: (1) hemostasis, (2) inflammation, (3) proliferation, and (4) remodeling.

The hemostatic phase is initiated immediately upon injury, characterized by both the intrinsic and extrinsic clotting cascades. When an injury occurs, collagen, Von Willibrand factor, and tissue factor are exposed from the subendothelium to the blood stream, acting as the inciting catalyst for the systematic repair process. A platelet plug forms, composed of platelets and fibrin. Platelets release granules containing multiple growth factors acting as a chemoattractant and thromboxane A2 acting as a potent vasoconstrictor. Transforming growth factor-beta (TGF-β) is the key growth factor released, playing a central role in wound healing.

The inflammatory phase from days 1 to 10 is characterized by an inflammatory cell wound infiltration and initiation of epithelialization occurring at 1 to 2 mm/d from wound edges. The ordered cellular influx begins with neutrophils that act as scavengers cleaning the cellular debris through phagocytosis and killing bacteria through the oxidative burst. Neutrophils secrete elastase and matrix metalloproteinases (MMPs) to degrade extracellular matrix (ECM), facilitating cellular migration. Monocytes from the blood convert to macrophages arriving at 48 hours, which are the key coordinating cells for transitioning to the proliferative phase by releasing additional growth factors and mediating angiogenesis, fibroplasia, and synthesizing nitric oxide.

From day 5, fibroblasts arrive at the wound, initiating the proliferative phase. Type 3 collagen deposition, neovascularization, and granulation tissue characterize the proliferative phase. Granulation tissue is perfused connective tissue allowing the framework for further epithelialization. Fibroblasts in the wound convert to myofibroblasts to allow wound contraction, which is the key component for healing via secondary intention. Cellular signaling for this conversion is mediated by macrophages through TGF-β. Fibroblasts also secrete MMP, which aids to facilitating cellular migration.

From day 8 through year 1, wound remodeling and maturation occur. Initial deposition of collagen is disordered, and over time remodeling of collagen at areas of increased stress allow for increased tensile strength. By week 3, type 3 collagen has been exchanged for type 1 collagen, which is the most common type of collagen in the human body. The maximal tensile strength is reached at approximately 8 weeks after injury, at 80% of its original strength. Key local wound factors to sustain a systematic repair process are listed in Box 1 .

Box 1

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