Infection and the chronic wound: a focus on silver.

Wound healing failure often represents the interaction of a complex series of abnormalities in the wound bed and the host’s responses to tissue injury. These may be considered the pathways to wound healing failure and are the focus of wound assessment and treatment. Factors that contribute to chronic wound healing failure include infection, any condition that produces abnormal blood flow and hypoxia, cellular failure, and trauma. Correcting one of these common pathways frequently improves the other pathways and significantly aids in wound healing. Although bacteria are present on intact skin, infection is rarely a problem because of the mechanisms that are in place to control bacteria. The outer layer of the skin, for example, provides a physical barrier to invasion. The skin’s surface is not normally conducive to bacterial growth because it has a slightly acidic pH and it secretes fatty acids and other antibacterial polypeptides. The normal flora on the skin’s surface helps prevent potentially pathogenic bacteria from becoming established. However, once this protective barrier is lost and the skin has an open wound, the subcutaneous and deeper tissues are at risk from the potential adverse effects of bacteria and other microorganisms. The presence of a wound, in essence, creates a portal of entry for these organisms. An increased bacterial burden on the surface of a wound and in wounded tissue increases the metabolic requirements of the wound and of the host’s response to that heavy bacterial load. Bacteria produce endotoxins, exotoxins, proteases, and local tissue injury. In some cases, as in gas gangrene caused by Clostridium species, bacteria produce systemic effects that are ultimately responsible for the death of the host. The presence of a bacterial burden in a wound stimulates a proinflammatory environment; the presence of bacteria induces the in-migration of monocytes, macrophages, and leukocytes—all of which initially act in an appropriate fashion but later produce a response that is exaggerated and deleterious. This is evidenced by the fact that wounds associated with a heavy bacterial burden often show healing failure. An increased bacterial burden in a wound can also affect tissue oxygen availability. Leukocytes are needed in the wound bed to kill phagocytic bacteria—by mechanisms that involve an oxydated burst and the consumption of significant amounts of molecular oxygen. In severely malperfused wounds, this increased oxygen consumption by inflammatory cells can act as a sump, ‘‘stealing’’ oxygen required for basic wound metabolism. In addition, the white blood cells’ inflammatory response—needed to kill bacteria—increases the release of damaging oxygen free radicals. The increased production of enzymes and the release of toxins can also facilitate an induced cellular failure. Bioburden may be defined as the metabolic load imposed by bacteria in the wound bed. Bacteria will compete with normal cells for available oxygen and nutrients. In addition, bacteria and bacterial products, such as endotoxins and metalloproteinases, can cause disturbances in all phases of wound healing.