Inflammatory Phase

With any injury comes an inflammatory phase during which repair of the damaged tissue is initiated.² Local cellular and vascular reactions are included in this wound-healing phase.³ Initial blood loss is decreased by the immediate vasoconstriction of vessels. The vasoconstrictive response may last about 5 to 10 minutes. This time frame also allows the accumulation of platelets and the formation of temporary “platelet clots” along the damaged endothelial lining of the vessels. Activation of the clotting cascade leading to the eventual formation of fibrin clots begins at this time.

The period of vasoconstriction is followed by an episode of vasodilatation and increased capillary permeability. Leukocytes, which are chemotactically recruited to the wound site, are delivered by the increased flow of blood with vasodilatation. Early battles against infection are waged at this point by neutrophils.4–7 Macrophages also migrate to the wound site to phagocytose wound debris and spent cells. Macrophages release factors important in wound repair, such as cytokines, growth factors, and collagenases.⁸ Lymphocytes also follow neutrophils into the wound site. They play an important role in the immune response because they release factors that stimulate macrophages and fibroblasts.⁹ The increased capillary permeability during inflammation can lead to the formation of local edema. Edema hinders healing by reducing the local arterial, venous, and lymphatic circulation and increases the chance of infection for the same reasons. Edema may also restrict motion, which increases the possibility of tissue fibrosis.

Exposure of injured nerves and release of chemical mediators at the wound site can produce pain. Pain often causes a patient to restrict activity because the activity may increase the pain. Decreases in appropriate activity can lead to a reduction in motion and mobility.

The inflammatory phase of healing may normally last about 2 weeks. Longer periods of inflammation are referred to as chronic inflammation.

During this phase, appropriate physical therapy interventions might include wound care, edema management, positioning, splinting, cautious passive range-of-motion exercises, active range-of-motion exercises, ambulation, and functional activities such as activities of daily living.

Proliferative Phase

Fibroblasts start converging on the wound site during inflammation, and the proliferative phase of wound healing commences with the production of collagen by these cells. Fibroblasts produce a connective tissue scaffold made up of elastin, collagen, and glycosaminoglycans. This process contributes to one of the major events during the proliferative phase of healing—rebuilding and strengthening of the wound site. Elastin is an elastic fibrous protein that provides flexibility to the wound, but it makes up only a small percentage in comparison with collagen.

Collagen is the chief protein produced by fibroblasts.¹⁰ Collagen fibrils formed by fibroblasts combine and form collagen fibers. Collagen fibers supply the preponderance of strength to the wound. The strength lies in the collagen fiber, not in the amount of collagen at the wound site,¹¹ so a patient does not need a big scar to have a strong and well-healed wound.

Ground substance (glycosaminoglycans, water, and salts) occupies the space among the elastin, collagen, vascular structures, and other cells in the healing wound.¹² The ground substance allows cell proliferation and migration and provides some cushion for the healing tissue.

Angiogenesis (the formation of new blood vessels) begins during the inflammatory phase of healing, but the majority of regrowth occurs during the proliferative healing phase.¹³ Vascular genesis is important for the distribution of nutrients and oxygen to cells at the site of healing.

Wounds that are not deep enough to destroy the epidermal basal cell layer can heal through real epidermal regeneration. In epidermal regeneration, proliferation of both epithelial cells at the margin of a wound and epidermal cells from any existing basal cell (such as those in the dermis that encompass hair follicles or sweat glands) ultimately leads to wound coverage. Deeper wounds that do not have basal cells available may still achieve wound closure with epithelium that migrates from adjacent uninjured skin. This process generally occurs only in smaller wounds.

One other concern associated with the proliferative phase of healing is wound contraction. Wounds begin to contract slightly during inflammation; however, aggressive contraction at the wound commences during the proliferative phase. Fibroblasts, particularly myofibroblasts, have contractile capability.14–16 It appears that the physiologic function of wound contraction is to decrease the surface area of the wound, but contraction takes place in wounds of all sizes. Although potentially beneficial in small wounds, contraction is more frequently the cause of decreased mobility and cosmetic change, particularly in wounds associated with joints.

Physical therapy interventions for the proliferative phase of healing may include wound care, edema management, positioning, splinting, cautious passive range-of-motion exercises, active range-of-motion exercises, ambulation, and functional activities such as activities of daily living, similar to interventions during the inflammatory phase. In addition, active assisted range-of-motion exercises, stretching, strengthening exercises, and endurance exercises may be appropriate. During this phase wounds must be handled carefully because a wound will not be as strong as normal skin.¹⁷

Maturation Phase

The maturation phase of healing is also often referred to as the remodeling phase. During the maturation phase, collagen continues to be actively deposited while it is also going through active lysis. The balance between the amount of collagen deposition by fibroblasts and the magnitude of collagen lysis influences the ultimate appearance of the scar (if scar formation occurs). If deposition exceeds lysis, either a hypertrophic scar or a keloid scar forms.18,19 Keloid scars differ from hypertrophic scars in that they extend beyond the original boundaries of the wound, they take longer to mature, and they are not associated with contracture, and there may be some biologic distinction between these types of scars.^20–22

During the maturation phase, collagen fibers are deposited in an unorganized fashion. The arrangement of these fibers, however, is influenced by stresses placed on them. For example, stretching an actively forming scar will cause the collagen fibers to align themselves along the length of the stretch and therefore become oriented in an alignment that favors mobility over restriction of movement.

The maturation phase of wound healing may last for several months. While the phase is active—that is, while collagen is being produced—the wound continues to contract with varying degrees of vitality. As the phase nears its end, wound contraction tends to diminish. Contraction during this phase is often referred to as scar contraction. If scar contraction leads to either a permanent or a semifixed positional fault at a joint, it is referred to as a scar contracture. Race, family history, depth of the wound, size of the wound, patient age, and location of the wound all appear to be factors affecting scar formation.22–25

All therapeutic interventions listed for the previous two phases may be applied to the maturation phase of healing. However, the PT or PTA can generally be more aggressive with manipulation of the wound site. Depending on circumstances, the maturation phase may also be the phase when work-hardening and work-conditioning exercises are energetically pursued. Moreover, depending on the size and location of the scar, techniques to control scar formation should be instituted.

Additional Considerations

The variables of repair and patient response to skin wounds include depth of the damage, location of the injury, size of the wound, healing time, and cause of the disruption. The depth of injury probably has the greatest impact on repair and eventual healing of a wound. For example, superficial wounds that leave a majority of the epidermal basal cells intact often heal without complication. Deeper skin damage that destroys much if not all the epidermal basal cell layer may take weeks to heal or require surgical intervention to hasten repair. Generally, the deeper the wound, the longer it takes to heal. Figure 11-2 illustrates depths of wounds and the integumentary structures involved at the varying depths.

The location of the injury can affect rehabilitation in many ways. For example, wounds on the feet can affect gait, wounds on hands can affect activities that require hand function, and wounds over any joint can lead to impairment in motion and therefore also lead to changes in strength and performance of activities of daily living. Furthermore, wounds at cosmetic sites such as the face and hands may offer psychological challenges for a patient to overcome.

The size of a wound, often measured as the percentage of total body surface area (TBSA) affected, has an effect on the extent of the physiologic response. A few of the physiologic responses that should be considered include the local inflammatory response, the basal metabolic rate, temperature control, cardiopulmonary stresses, hematopoietic reactions, and pain. For example, a large skin wound (such as an extensive burn injury) may dangerously decrease the ability of a patient to control body temperature. Also, a big wound will lead to an increased basal metabolic rate and impose extra nutritional demands on a patient that must be met to avert the protein catabolism that could lead to muscle loss. Infection is a potential problem with any open wound, and increased wound size may increase the risk of infection. As wound size increases, so does the magnitude of the physiologic response.

Wounds that require a long time to heal are associated with two primary problems. First, the risk of infection increases the longer that the wound is open. Second, a wound that takes longer than 2 to 3 weeks to heal is more likely to scar.