Because all wounds are not the same, knowing the different phases of healing can result in better wound management and a smoother healing process.
A daunting experience for any clinician is the care of chronic ulcers that have not responded to standard wound care. The presence of edema, peripheral arterial disease (PAD), and tissue ischemia are often reasons that some wounds are hard to heal. Many factors, including pH balance, nutrition, and oxygen concentration, can also contribute to the slow process healing wound.
To understand why certain methods of treatment are successful for stubborn wounds, it is imperative to understand the pathophysiology behind wound formation and wound healing and the differences between types of wounds.
How do wounds heal?
There are different types of wound closures and different phases that each wound goes through, regardless of type, during the healing process. Wounds heal by either primary, secondary, or tertiary intervention.1,2
Primary: wound closes with minimal intervention
Secondary: wound closes by contraction and reepithelialization
Tertiary: also called delayed primary closure, wound closes when there is initial debridement and suture or other method is used.
The phases of wound healing include inflammatory, proliferative, and maturation. The inflammatory phase includes the initial reaction to the injury in which a number of cells, including platelets, neutrophils, and macrophages, migrate to the site. Platelets, besides helping in clotting, act as a chemoattractant for neutrophils through a cascade effect. The neutrophils kill bacteria and aid in debridement, as do the macrophages. Macrophages are essential for wound healing because they secrete the growth factors imperative for healing.
The proliferative phase occurs when tissue reconstruction begins, including epithelialization, angiogenesis, and granulation.
The final phase is the maturation phase when wound contraction, or the inward movement of the wound’s edge, occurs. This can reduce both the amount of reepithelialization and the amount of scar tissue.
Identify the chronic wound
Pressure ulcers generally fall under the category of healing by secondary intention. The Agency for Health Care Policy and Research has established a staging system for correct assessment of pressure ulcers3:
Stage I: alterated but intact skin whose indicators may include changes in one or more of the following: skin temperature, tissue consistency, and/or sensation (pain/itching). The ulcer appears as a defined area of persistent redness in lightly pigmented skin and with persistent red, blue, or purple hues in darker skin.
Stage II: partial-thickness skin loss involving epidermis and/or dermis.
Stage III: full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.
Stage IV: full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures.
Nurses also need to take into account a number of factors when assessing a patient’s wound. According to the American Medical Directors Association, nurses should examine the patient’s general medical stability and prognosis, as well as specific comorbidities affecting wound healing, including underlying ischemia, nutrition (see sidebar, “Nutrition in wound healing”), infection, pain, and psycho behavioral factors.4
Wound healing can be complicated by various degrees of chemotaxis (also known as chemoattraction) in which cells can be attracted to chemical agents to the wound site. The concentration of different chemicals can have varied effects on the healing process. A high concentration of specific chemicals may enhance the healing process, whereas a low concentration of the same chemicals can slow the healing process.
Wounds are generally low in oxygen and pH, and high in lactate when systemic nutrition is low or when a systemic infection is present. Macrophages, attracted to a wound environment low in oxygen concentration and pH, will release lactate as well as the growth factors that help to create new tissue. But this low oxygen environment can cause a delay in wound healing since oxygen is necessary for fibroblasts to modify the collagen that heals tissues and supports new blood vessels. Oxygen is also necessary for the regulation of angiogenesis.
Increased growth factor results in “brisk angiogenesis” and the multiplication of fibroblasts at the wound margins. These fibroblasts are responsible for wound contraction, in which the edges of the wound migrate toward the wound center as healing progresses. Granulation tissue (named because it appears granular in nature), which is new, healthy growth of connective tissue, forms and also brings a rich supply of new blood vessels that help with oxygenation.
Some physiological differences in the healing of moist wounds include the modification of collagen by fibroblasts. This process enables polymerization and collagen secretion into the intracellular space in and around the wound, facilitated when oxygen is present in high concentration. This has led to the use of oxygen treatment for hard-to-heal wounds. Oxygen treatment is effective because collagen is deposited most rapidly when both lactate and oxygen concentrations are high. And the need for oxygen persists well into the healing process because, as new collagen is deposited, the old collagen is lysed.
In a moist wound environment, natural fluids in the wound containing collagen and proteoglycans form an extracellular matrix (ECM). The ECM aids in the restructuring of tissue. As the wound continues along the healing process, epithelial cells divide and then move across the basal cell layers to restore the epithelium. Basal cells continue to split until the epithelial stratification is regenerated. As the wound surface is completed, the epidermis begins to keratinize. This remodeling of the collagen matrix may continue for years, depending on the wound’s initial stage and the patient’s nutritional status, health, and age. In stage IV wounds, loss of epidermal structures, hair follicles, sweat glands, and melanocytes may be permanent.
Because various degrees of chemotaxis, the presence of edema, PAD, tissue ischemia, pH imbalances, poor nutrition, and low oxygen concentration can arrest the process of wound healing, planned, goal-oriented wound care is usually effective.
If there is eschar (slough), the wound should be debrided to facilitate healing. Inflammation, the first reaction to any change in the wound environment, is a normal response to autolytic wound debridement, in which the body’s own enzymes are used in conjunction with dressings placed on the wound. This liquefies the eschar and is painless for the patient. Biochemical debridement uses chemical enzymes such as papain-urea-chlorophyllin (Panafil®) and papain-urea topical (Gladase®) to dissolve necrotic tissue. The wound should be monitored for infection. With the completed cleansing of the wound and the maintenance of a moist wound environment, progress is usually noted.