Factors that interfere with wound healing may be divided by source into physical, endogenous, and exogenous categories.

Physical factors are environmental issues. Temperature affects the tensile strength of wounds. Ideal conditions allow wound healing to occur at 30°C. Decreasing the temperature to 12°C results in a 20% loss of tensile wound strength. Adequate oxygen levels are also required for appropriate wound healing. Because of vessel disruption, wounds contain lower oxygen levels than surrounding healthy tissue. Low levels of oxygen interfere with protein synthesis and fibroblast activity, causing a delay in wound healing. Oxygen levels may be compromised for many reasons, including hypovolemia, the presence of devitalized tissue, and excessively tight bandages.

Endogenous factors typically reflect the overall condition of the animal. Anemia may interfere with wound healing by creating low tissue oxygen levels. Nutrition has a significant overall effect on the body, although the ideal nutritional level for wound healing is unknown. Hypoproteinemia delays wound healing only when the total serum protein content is <2.0 g/dL. Because wound healing is a function of protein synthesis, malnutrition may alter the healing process. The addition of dl-methionine or cysteine (an important amino acid in wound repair) prevents delayed wound healing. Uremia can interfere with wound healing by slowing granulation tissue formation and inducing the synthesis of poor quality collagen. Although diabetes is a known problem with wound healing in people, it has not been demonstrated to cause a problem in animals. Obesity contributes to poor wound healing, primarily as a consequence of poor suture holding in the subcutaneous fat layers. Decreased wound perfusion may also contribute.

Exogenous factors include any external chemical that alters wound healing. Cortisone is commonly implicated in wound complications. Corticosteroids markedly inhibit capillary budding, fibroblast proliferation, and the rate of epithelialization. Similar to cortisone, vitamin E adversely affects wound healing by slowing collagen production. This effect may be reversed with vitamin A. Additional vitamin A will not improve wound healing in the absence of vitamin E or cortisone. Vitamin C is required for the hydroxylation of proline and lysine. Zinc is required for epithelial and fibroblastic proliferation; however, excessive zinc delays wound healing by inhibiting macrophage function. Radiation is detrimental to wound healing. Given 7 days before wound creation, healing is impaired. Cytotoxic drugs may also delay wound healing. Alkylating agents (eg, cyclophosphamide, melphalan) slow wound healing by blocking DNA synthesis. Though most NSAID are thought to be safe in wound healing, recent work suggests that agents selective for COX-2 inhibition may slow wound healing.

Last full review/revision March 2012 by Kevin P. Winkler, DVM, DACVS