Factors that influence wound healing
A number of factors can alter the rate and efficiency of healing. These can be classified in to those which act locally, and those which have systemic effects. Most of these factors have been established in studies of skin wound healing but many are likely to be of relevance to healing at other sites.
Type, size, and location of the wound
A clean, aseptic wound produced by the surgeon’s scalpel heals faster than a wound produced by blunt trauma, which exhibits abundant necrosis and irregular edges. Small blunt wounds heal faster than larger ones. Injuries in richly vascularized areas (e.g., the face) heals faster than those in poorly vascularized ones (e.g., the foot). In areas where the skin adheres to bony surfaces, as in injuries over the tibia, wound contraction and adequate apposition of the edges are difficult. Hence, such wounds heal slowly.
Wounds with impaired blood supply heal slowly. For example, the healing of leg wounds inpatients with varicose veins is prolonged. Ischemia due to pressure produces bed sores and then prevents their healing. Ischemia due to arterial obstruction, often in the lower extremities of diabetics, also prevents healing.
Wounds provide a portal of entry for microorganisms. Infection delays or prevents healing, promotes the formation of excessive granulation tissue (proud flesh), and may result in large, deforming scars.
Early motion, particularly before tensile strength has been established, subjects a wound to persistent trauma, thus preventing or retarding healing.
Prior irradiation leaves vascular lesions that interfere with blood supply and result in slow wound healing. Acutely, irradiation of a wound blocks cell proliferation, inhibits contraction, and retards the formation of granulation tissue.
Cardiovascular status, by determining the blood supply to the injured area, is important for wound healing. Poor healing attributed to old age is often due, largely, to impaired circulation.
Systemic infections delay wound healing.
Poorly controlled diabetes mellitus is associated with delayed wound healing. The risk of infection in clean wound approaches five fold the risk in non- diabetics. In diabetic patients, there can be impaired circulation secondary to arteriosclerosis and impaired sensation due to diabetic neuropathy. The impaired sensation renders the lower extremity blind to every day hazards. Hence, in diabetic patients, wounds heal the very slowly.
In protein depletion there is an impairment of granulation tissue and collagen formation, resulting in a great delay in wound healing.
Vitamin C is required for collagen synthesis and secretion. It is required in hydroxylation of proline and lysine in the process of collagen synthesis. Vitamin C deficiency (scurvy) results in grossly deficient wound healing, with a lack of vascular proliferation and collagen deposition.
Trace element deficiency
Zinc (a co-factor of several enzymes) deficiency will retard healing by preventing cell proliferation. Zinc is necessary in several DNA and RNA polymerases and transferases; hence, a deficiency state will inhibit mitosis. Proliferation of fibroblasts (fibroplasia) is, therefore, retarded.
Corticosteroids impair wound healing, an effect attributed to an inhibition of collagen synthesis. However, these hormones have many other effects, including anti-inflammatory actions and a general depression of protein synthesis. It also inhibits fibroplasia and neovascularization. Both epithelialization and contraction are impaired. It is, therefore, difficult to attribute their inhibition of wound healing to any one specific mechanism.
Thyroid hormones, androgens, estrogens and growth hormone also influence wound-healing. This effect, however, may be more due to their regulation of general metabolic status rather than to a specific modification of the healing process.