Like the infl ammatory phase, the proliferative phase can be described with three aspects: acute, chronic, or absent.
• The acute proliferative phase is the active biologic process of proliferation, including extracellular matrix (ECM) synthesis, granulation tissue formation and degradation, and wound contraction.
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Periwound Skin and Wound
Tissue Characteristics Acute Infl ammatory Phase Chronic Infl ammatory Phase Absence of Infl ammatory Phase Periwound skin color • Unblanchable erythema
in light-skinned patients
• Discoloration or deepen- ing of normal color in darkly pigmented patients
• Ecchymosis (purplish bruising)
• Halo of erythema or darkening
• Hemosiderin (rust-brown) staining
• Hemosiderin staining
• Ecchymosis
• Pale or ashen skin color
• Absence of erythema or darkening
• Hemosiderin staining
• Ecchymosis
Edema and induration • Firmness
• Taut, shiny skin
• Localized swelling
• Consolidation (hardness) between adjacent tissues
• Gelatinous edema may be seen on wound tissue
• Minimal fi rmness
• Absent
• May feel boggy
Tissue temperature • Elevated initially, decreases as infl amma- tion progresses
• Minimal change or coolness • Minimal change or coolness
Pain • Present; wound is tender
and painful unless neu- ropathy is present
• Minimal pain unless arterial etiology or infection, then can have intense pain
• Minimal or no pain unless arterial etiology, then can have intense pain
Wound tissue • Blister with clear or bloody fl uid
• Shallow or deep crater with red to pink color
• Red muscle
• White, shiny fascia
• Yellow reticular layer of dermis with granulation buds
• Necrotic; varies in color from yellow to brown to black
• Necrotic tissue covering full or partial surface area
• Soft or hard necrotic tissue
• Yellow fi brin or slough
• Portion of wound can have granulation tissue
• Can also appear as clean, pale pink
• Covered with hard, dry eschar
• Necrotic; varies in color from yel- low to brown to black
• Scab
Undermining/tunneling • Can be present in deep wounds
• Has potential for infection and abscess
• Can be present in deep wounds
• Has potential for infection and abscess
• Can be present in deep wounds
• Has potential for infection and abscess
Wound edges • Diffuse, indistinct; can still be demarcating from healthy tissues
• Distinct; edges can be rolled or thickened
• Is not continuous with wound bed if deep wound cavity
• Has distinct, well-defi ned wound edges
• Can be attached to necrotic tissue
Wound drainage • Serous or serosanguineous • Infection
• Viscous
• Malodor
• Pus (yellow, tan, gray, or green)
• Moderate to large amount
• Scant or dry Wound Healing Phase Diagnosis: Aspects of Infl ammatory Phase
3.8
TABLE
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• The chronic proliferative phase is characterized by a wound that is stuck in the proliferative phase, hyperproliferating, or not progressing to the next phase of epithelialization and remodeling.
• Absence of the proliferative phase is characterized by a wound bed that lacks signs of ECM development or is not contract- ing (see Fig. 3.35A).
Assessment of each of these three aspects of the prolifera- tive phase is described next, using the same four categories of wound attributes discussed for the infl ammatory phase: adja- cent and periwound tissue, wound bed tissue, wound edges, and wound drainage.
Acute Proliferative Phase
Signs of acute proliferation indicate a healthy response and normal healing. They are also benchmarks against which to evaluate impaired responses.
Adjacent and Periwound Tissue Assessment
During the acute proliferative phase, periwound skin regains color and contour symmetry with that of adjacent skin (i.e., edema is resolved). With recovering chronic wounds, however, you will likely see hemosiderin staining (pigmenta- tion) around the wound margins (Fig. 3.41B). Ecchymosis should be resolved. Skin turgor is normal and is not stretched or taut because the edema and induration are resolved (absent).
Firmness is absent or minimal.
Periwound skin temperature, when palpated or measured with an LCD skin thermometer, is the same as the adjacent skin or slightly elevated, due to the enhanced perfusion of tissues and higher metabolic activities associated with heal- ing. A temperature gradient of 4°F or greater indicates infl ammation and possible infection, and further evaluation is needed.
Minimal pain is experienced during this phase. Pain may be entirely absent in patients with neuropathy. Sudden onset of pain suggests possible infection.
As previously described, wound undermining and tunneling occurs following debridement of the skin and subcutaneous tissue (Fig. 3.33). The extent of undermining or tunneling is a measure of the total soft tissue involved in the wound.
Tunneling may be unobservable from the surface and yet have a great extent, as shown in Figure 3.16A,B of the same wound.
In the proliferative phase, undermining and tunneling close as the tissues reestablish continuity during the laying down of the collagen matrix and granulation tissue (Fig. 3.41A,B).
Reduction of the extent of undermining/tunneling is a measure of the progression of proliferation and reduced overall wound size. Record fi ndings of undermining and tunneling as part of the tissue assessment. If the tunneling extends beyond approxi- mately 15 cm, notify the physician. Chapter 4 describes how to measure undermining/tunneling and calculate the extent of the overall wound.
Wound Bed Assessment
Granulation tissue develops during this phase. Granulation buds are clearly seen in Figure 3.41B. Wounds that have a bowl- shaped cavity will fi ll with ECM and granulation tissue during the acute proliferative phase to create a surface across which epidermal cells can migrate. Notice in these photos how the cavity is fi lling to create a level surface with the adjacent skin.
The acute proliferative phase, which overlaps with the late infl ammatory phase, starts when the wound bed tissue begins to show red or pink granulation buds. The collagen matrix is laid down and is infi ltrated by and supports the growing capil- lary bed, giving it a red color. Reduced depth in a full- thickness wound is a measure of proliferation activity. The collagen matrix does not replace the structures or functions of the tissues
2 3
4 1
A
1
2
B
FIGURE 3.41 A: Chronic infl ammatory phase. Note: (1) Yellow, stringy slough; (2) Edema; (3) Skin color changes (red), erythema; (4) Rib bone noted in superior ulcer. Wound severity diagnosis: Impaired integumentary integrity secondary to skin involvement extending into fascia, muscle, and bone (Stage IV pressure ulcer). B: Same wound as in Figure 3.35A.
Note: (1) Softening of the rolled epidermal ridge edge around granulation base, (2) Brown hemosiderin staining (hemo- siderosis). Wound healing phase: acute proliferative phase. (Copyright © C. Sussman.)
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Chronic Proliferative Phase
Chronic proliferation develops when tissue integrity is not rees- tablished in a timely fashion.
Adjacent and Periwound Tissue Assessment
In the chronic proliferative phase, the color of the skin at the wound edges can blanch or begin to draw together very tightly (Fig. 3.35D). Gelatinous edema can be present, signifying an episode of trauma.
Compared with the temperature of the adjacent skin, peri- wound skin during the chronic proliferative phase can be cool or mildly elevated. There may be signs of intense pain, indicating that the wound has been traumatized and is undergoing another episode of acute infl ammation, or infection may be present.
Tunneling can extend a long distance, presenting an oppor- tunity for infection to travel up the fascial plane. Tissues in the tunnel can be necrotic. Tunneling can become a sinus tract, a cavity, or channel underlying a wound that involves an area larger than the visible surface of the wound (Fig. 3.16A,B). An abscess can form in the tunnel or sinus tract.70 When under- mining/tunneling persists in a proliferating wound and the assessment fi ndings include a black hole that has no reachable bottom, the wound requires urgent medical management.
Wound Bed Tissue Assessment
Wound bed tissue in the chronic proliferative phase is com- monly caused by infection. The presence of infection may be indicated by a livid red surface color (Fig. 3.36A) or rep- resent a change from healthy red to pale pink. An example is Figure 3.25B, which was progressing through the proliferative phase. Seven days later, it had attributes of infection, prolifera- tion had ceased, and the wound was in the chronic prolifera- tive phase and the change was attributed to infection (Fig. 3.43).
Other features of infection that can be observed in granulating wounds include superfi cial bridging, friable tissue, bleeding on contact, pain in the wound, and a delay in healing. There are two stages in the proliferative phase when the granulation tissue can show these characteristics of infection: approximately 10 days postoperatively and at the end stage of healing, when the wound has progressed satisfactorily, but then becomes indolent.129
Other factors that can contribute to chronic proliferation include poor vascular supply, desiccation, hemorrhage, and hypergranulation (Fig. 3.34). Poor vascular supply is indicated by pale pink, blanched to dull, and dusky red granulation tissue.
Desiccated granulation tissue is dark, dull, and garnet red as seen in Figure 3.3. Hemorrhage can result from trauma to the fragile tissues, such as from pressure. Hemorrhaging of the granulation tissue vessels causes acute infl ammation in the area and pro- motes scarring. The surface on the granulation tissue looks like a purple bruise. In Figure 3.44, note the small hemorrhagic area at the center of the wound, indicating rupture of blood vessels.
An imbalance of collagen synthesis and degradation can allow the collagen to proliferate unchecked, creating a hump of granulation tissue called “hypergranulation.” When hyper- granulation tissue overfl ows the wound bed, the epithelial cells cannot “climb the hill” of granulation tissue against gravity; the result is that the epithelialization process is halted. It is as if the proliferative “switch” is stuck and won’t turn off, leaving the wound in a chronic proliferative phase. In this state, the tissue is predisposed to infection (Fig. 3.42).
that occupied the cavity prior to injury; rather, this is scar tissue. The prevailing opinion is that this deep red color indi- cates a healthy, healing wound. Figure 3.36B is such a wound.
A contrary opinion is presented shortly.
Another feature that has been reported to appear during the acute proliferative phase of healing in a number of patients is the development of a yellow, fi brinous membrane on the sur- face of the granulation tissue. When removal of this membrane has been attempted, it has recurred within a few days. Wounds that develop this yellow membrane appear to be less susceptible to infection and heal in a normal fashion. It is important to rec- ognize this membrane during examination and avoid unneces- sarily disrupting it.129
Assessment of Wound Edges
The wound edges are soft to fi rm and fl exible to touch. Edges will roll in full-thickness wounds, but when the wound tissue fi lls the cavity to a point even with the edge of the wound, the edges will fl atten, and epithelialization and contraction will continue together (Fig 3.31B,C and 3.41B). At this point, the wound acquires a distinctive wound shape or “picture frame.”
The cells that control the movement of the picture frame, the myofi broblasts, are located beneath the wound edge. The cells are contractile and will move forward, drawing the wound together, as in the drawing together of purse strings, shrinking the size of the open area measurably. The shape that the wound now assumes predicts the resulting speed of contraction. Linear wounds contract rapidly. Square or rectangular wounds con- tract at a moderate pace. Circular wounds contract slowly.
Wound contraction is a major activity of the acute prolifera- tive phase of healing. Contraction reduces the areas that need to close by epithelialization. Contraction in areas such as the glu- teals and abdomen is typically uncomplicated, but contracture is troublesome in areas such as the head, neck, and hand. Drawing together too tightly in those areas will cause a defect or contrac- ture that can impair function and cosmesis. Wounds that would have a poor outcome if allowed to close by contraction warrant surgical intervention at the start of the proliferative phase.133 Assessment of Wound Drainage
During the acute proliferative phase, the wound drainage is sero- sanguineous and of moderate to minimal quantity and odor.
FIGURE 3.42 Hypergranulation tissue; chronic proliferative phase. (Copy- right © B.M. Bates-Jensen.)
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3
1 9/24
FIGURE 3.43 Chronic proliferative phase with attributes of infection.
Note: (1) Hemorrhagic area of trauma; (2) Hypopigmentation;
(3) Dull, pink granulation tissue. (Copyright © B.M. Bates-Jensen.)
FIGURE 3.44 Wound is in chronic proliferative phase. Note: (1) Trauma to granulation tissue caused hemorrhagic spot that may go on to necrose, (2) Hemosiderin staining from prior bleeding surrounds ulcer. (Copyright © C. Sussman.)
Assessment of Wound Edges
One sign that a wound is in the chronic proliferative phase is when wound edges roll in and become hard and fi brotic, inhib- iting further wound contraction. Figure 3.35C is an example of rolled fi brotic edges. Wounds of different pathogeneses develop this problem, including pressure ulcers and venous ulcers. This is apparently due to imbalances in the wound biochemistry that controls tissue deposition and degradation during the prolif- erative phase. Another area of research suggests that impaired senescent cells are present in specifi c cellular patterns in the edges of nonhealing wound that are different from those of healing wounds and the true “healing edge” of the wound lies further away from the wound edge than traditionally thought.
The true “healing edge” is the wound margin where cells capa- ble of migration and wound healing are found. Scientists are developing tools, like bar coding scanners, that can be used to identify the healing wound margins and thus guide wound debridement and improve healing outcomes.137
Assessment of Wound Drainage
Chronic proliferative exudate can be a yellow, gelatinous, vis- cous material on the wound granulation base, which indicates the wound has been traumatized. This appearance should not be confused with residue from wound dressings, such as amor- phous hydrogels, or hydrocolloids or treatments, such as anti- microbial ointments.
An infected wound in chronic proliferation can have a malodorous, viscous, reddish-brown, green, or gray exudate.
Figure 3.36A shows an apparently clean wound; however, the wound dressing shows signs of moderate to large amounts of sanguineous and purulent, reddish-brown exudate. This is a benchmark of the chronic proliferative phase and the wound needs treatment to recover.
Absence of Proliferative Phase
The absence of proliferation may be caused by interference in the healing cascade due to one or more of the following factors.
Adjacent and Periwound Tissue Assessment
The presence of hemosiderin staining or a halo of erythema surrounding the wound signifi es a wound that is also in the chronic infl ammatory phase. The skin can show signs of ecchy- mosis. Edema and pain are minimal or absent. Temperature is the same as adjacent skin, or coolness is present signifying poor perfusion.
Wound Bed Tissue Assessment
A wound in the absence of proliferative phase is either not pro- ducing granulation tissue or not contracting (Fig. 3.35A). The wound bed tissue can appear dry, dull red, and desiccated, like
CLINICAL WISDOM
Management of Hypergranulation
Because hypergranulation inhibits the reepithelialization of the wound surface, it must be prevented or controlled.
Methods for preventing and controlling hypergranulation include the following:
1. Cauterization, by applying silver nitrate sticks to the sur- face, will necrose the superfi cial granulation tissue, which can then be wiped off.
2. Excess hypergranulation tissue can be trimmed by rub- bing with a gauze sponge or snipping with scissors. This can trigger a new infl ammatory cascade.
3. The application of hypertonic saline is a nontoxic method of reducing hypergranulation (see Chapter 20).
4. The application or avoidance of certain wound dressings:
silicone gel dressings have preventative potential,134 and polyurethane foam-type dressings reduce hypergranu- lation.135 Occlusive moisture-retentive dressings appear to enhance the development of hypergranulation136 (see Chapter 20).
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soft and thin to touch, making it very susceptible to trauma, such as from pressure.
Assessment of Wound Bed Tissue and Wound Edges
Within hours of wounding, epithelial cells start migrating toward the center from the wound edges to cover the defect with new skin. The wound edges must be adhered to the wound base for epithelial cell migration to cover the wound. Gradually, the epithelium spreads across the wound bed, as shown in Figure 3.31A–D. The migrating tissue is connected to the adjacent skin and pulls it along to cover the opening.133
The new skin will be bright pink, regardless of normal pigmentation, and may never regain the melanin factors that color skin (Fig. 3.45). New skin is formed as a very thin sheet, and it takes several weeks for it to thicken. If the wound is less than full-thickness, islands of pink epithelium can appear in the wound bed from migrating cells donated by the der- mal appendages, hair follicles, and sweat glands. Cells from these islands and edges spread out and cover the open area.
Figure 3.48A shows a wound with an island of epithelium.
Figure 3.48B shows the migration of the epithelium across the wound from the edges and island. Notice how the edges of the new epithelium are jagged.
Full-thickness wounds lose these island contributors, and they never regenerate.138 Full-thickness wounds begin to epithelialize when the edges are attached and even with the wound so that there are no sides or walls, and the epithelial cells can migrate from the edge across the wound surface. Edges are soft to fi rm and fl exible to touch, as shown in Figure 3.47. This wound went on to heal by epithelialization from the wound edges.
Wounds can bypass this phase of repair if it is necessary to place a skin graft or muscle fl ap to close the wound. Large wounds and wounds in areas where contraction will be harm- ful or will simply take too long to cover the wound can benefi t from surgical repair. The wound shown in Figure 3.51B was closed at that time by a split-thickness skin graft to speed the repair process.
dried raw meat, or it can contain pale pink granulation tissue (see Figure 3.2). There is no change in wound depth in a 2- to 4-week time frame. Wounds that are simultaneously in the chronic infl ammatory phase or absence of infl ammatory phase often have a surface appearance of necrotic tissue and/or hem- orrhage/ecchymosis. Any signs of ecchymosis signify a restart of the infl ammatory process within the wound. The chronic infl am- matory phase and absence of the proliferative phase can both be used as wound healing diagnoses for the same wound. The prog- nosis would be for the wound to progress to the acute prolifera- tive phase. The medical history and systems review should guide you to investigate the reasons behind the impairments to the pro- liferation process.
Assessment of Wound Edges
Wound edges can be rolled or jagged, and the wound shape is irregular. The wound does not change shape, signifying lack of wound contraction. Deep wounds can lack continuity of wound bed and edges. The wound does not reduce in size.
Assessment of Wound Drainage
Wounds lack exudate or have scant serous exudate. The wound in Figure 3.36D is in the chronic infl ammatory phase and has absence of a proliferative phase. Note the scant amount of serous exudate on the wound dressing. Treatment interventions should be reviewed to determine why the wound lacks moisture. Table 3.9 summarizes the fi ndings during the proliferative phase.