Long Road to Wound Healing
Because all wounds are not the same, knowing the different phases of healing can result in better wound management and a smoother healing process.

By Joy Lindsay-Garvey, RN, MEd
May 9, 2005

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.

General treatment

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.

For more serious wounds, mechanical or surgical debridement is necessary. Mechanical debridement occurs when moist gauze is placed within the wound. As it dries, the necrotic tissue adheres to the gauze and is removed when the dressing is changed. Unfortunately, this type of debridement is nonselective, removing healthy as well as devitalized tissue. Surgical or sharps debridement occurs when the wound is dissected with scalpel or scissors and is the preferred method for quick debridement.

Treat the slow-to-heal wounds

In some cases, chemical enzymes, zinc wrap compression, or oxygen therapy (see sidebar, “Alternative treatments”) may be applied to hasten the healing process. A moist wound environment is also conducive to healing. And sometimes certain procedures are appropriate to certain situations. For example, if there is edema in the site of a lower extremity wound, clinicians have found success in using Unna Boot Zinc compression. Wounds do not heal in the presence of edema.

The following describes a system of wound care therapy for stage III or IV pressure ulcers and for lower extremity ulcers. Nurses should remember to begin treatment after consulting with a physician.

• Assess: Access laboratory data and medical history to determine whether the patient has diabetes, osteomyelitis, or other systemic issues. Review the patient’s medications since there are meds that will retard a patient’s healing potential, such as steroids, anticoagulants, and certain cardiac meds. Assess the patient’s ankle-brachial index (systolic ankle pressure/systolic brachial pressure) to determine PAD status if it’s a leg ulcer.
• Clean: Normal saline should be used to clean the wound. Apply warm saline compress as indicated and as tolerated. If there is MRSA, begin systemic antibiotic therapy. As per physician, apply a local antibiotic such as mupirocin (Bactroban®); cream-based antibiotics are recommended rather than those with oil bases. The many silver-based products on the market are also useful in combating infected and heavily colonized wounds.
• Debride: Irrigate to remove eschar. Use papain-urea topical (Accuzyme® or Gladase®). Cover peri-eschar tissue with papain-urea-chlorophyllin (Panafil®).
• Cover: Cover the wound with a thin hydrocellular dressing. If it’s a leg ulcer and edema is present, apply compression using an Unna Boot® with zinc oxide dressing. The compression helps to prevent further injury to the tissue by enhancing venous return.
• Reassess: Remove the dressing after four days and reassess the wound. As healing progresses, continue to apply the treatment. Change dressing every three to four days and continue treatment for 14 days. The wound should begin to show marked signs of healing, depending on the stage [status] of the wound and the patient’s underlying morbidity.

For patients with wounds on the leg, elevate the leg as often as physically possible. Nutrition should be monitored according to dietary protocol. Protocol support surface for stages III and IV wounds should include dynamic (alternating pressure), air fluidized (high air loss), or low air loss pressure devices, as appropriate.

Healing chronic wounds can be a difficult and long process. Patients should be monitored for infection and nutrition and reassessed to ensure that the care approach is successful.

Alternative treatments

There are a number of alternative treatments available for chronic wounds that do not respond to regular therapy. Three types currently in use are oxygen therapy, ultrasound treatment, and electrical stimulation.

Oxygen Therapy — Brief exposure to oxygen has been shown to improve healing rates of hard-to-heal wounds. In one study, more than two-thirds of the wounds healed when treated only with oxygen.¹ Topical oxygen treatment was delivered with an inflatable bag that adhered to the skin and fastened securely around the wound. The oxygen was administered for 90 minutes a day for four days, followed by three days of rest. This cycle was repeated for as long as the wound appeared to be healing — treatment duration lasted from 24 days to eight months.

Ultrasound Treatment — Ultrasound can be used to produce chemotaxis within the wound. This plays a role in attracting neutrophils and monocytes during the inflammatory phase of wound healing. It also stimulates fibroblasts in their production of collagen.

Electrical Stimulation — In 1994, the Agency for Health Care Policy and Research (AHCPR) issued a panel statement confirming that electrical stimulation is an acceptable complementary therapy for treating pressure ulcers. It suggested that electrical stimulation could be used successfully when combined with moist healing treatment.

An electrode covered in gel is placed on the skin near the wound or in the wound. A low-level of electricity with short pulse durations transfers energy to the wound. This current helps to attract fibroblasts and to stimulate granulation tissue growth.

— Heather Lewin, health care
editor and writer

Nutrition in wound healing

Although there is no direct cause-effect relationship between nutritional status and the development of pressure ulcers, nutrition intervention remains a major focus in prevention strategies. Poor nutritional status has been associated with an increased risk for the development of pressure ulcers. Reduced body mass index, low body weight, the inability to eat independently, reduced food intake, and low dietary intake of protein can affect the development and healing of pressure ulcers.

Protein-calorie malnutrition and deficiencies of vitamins A and C and zinc impair normal wound-healing mechanisms. If a patient who has a chronic wound also has untreated malnutrition, the healing process may be even more difficult. Protein is needed for tissue regeneration and repair. A protein deficiency can delay wound healing by exacerbating the inflammatory phase of the wound. There is also a connection between zinc and the body’s ability to synthesize protein and collagen, which is necessary for wound healing. Zinc is essential for cell division and protein synthesis.

Vitamins also play a part in wound healing. One study suggests that vitamin A can benefit wound healing by enhancing the early inflammatory phase and increasing the number of macrophages at the wound site. It also could improve the stimulation of the immune response. Vitamin C enhances neutrophil production, increases angiogenesis, acts as an antioxidant, and helps in the production of collagen.

Lymphocyte counts are also an indicator of malnourishment. A count of less than 800 indicates severe malnourishment; nutritional supplementation is suggested when the lymphocyte count is 1,800.

Patients’ nutritional needs must be assessed and treated, either by increasing intake of foods that are high in calories and protein, supplementing meals with commercially prepared oral supplements, or providing GI feedings. — Heather Lewin, health care editor and writer

Source: MacKay D, Miller AL. Nutritional support for wound healing. Altern Med Rev. 2003; 8(4):359-377.

Joy Lindsay-Garvey, RN, MEd, is a wound care specialist at Morningside House Nursing Home, Bronx, N.Y.

References

1. Wound healing, growth factors. Rosenberg L, de la Torre J. Available at: http://www.emedicine.com/plastic/topic457.htm#target3. Accessed October 19, 2004.

2. Appendix E: Managing wounds due to surgery, injury, or pressure. Milliman Care Guidelines: Inpatient and Surgical Care. 8th Edition. Available at: www.intra.ccgh.com/CareSource8th/isc/isc_ape1.htm. Accessed October 19, 2004.

3. AHCPR supported clinical practice guidelines. Executive summary. Available at: www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat2.section.4502. Accessed May 5, 2005.