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.
ASSESSING WOUNDS IN THE EPITHELIALIZATION
Periwound Skin and Wound Tissue Characteristics
Acute Proliferative
Phase Chronic Proliferative Phase Absence of Proliferative Phase Periwound skin color • Continuity with adjacent
skin
• Hemosiderin staining if recovering chronic wound
• Continuity with adjacent skin
• Paler than adjacent skin
• Hemosiderin staining
• Hemosiderin staining if chronic wound
• Halo of erythema if in chronic infl ammatory phase
• Ecchymosis Edema and
induration
• Absent • Gelatinous edema can be present, signifying trauma
• Minimal edema present Tissue temperature • Temperature can be
minimally elevated if wound is well-perfused
• Minimal change • Minimal change or coolness
Pain • Pain-free or minimal pain
• Inappropriate indicator in presence of
neuropathy
• Painful, can indicate local infl ammation; if intense, consider infection
• Minimal or absent
• Intense if infection present
Wound tissue • Shiny, bright red to pink granulation
• Sustained reduction in wound depth
• Sustained wound contraction
• Reduced size
• Covering of yellow fi brinous membrane on granulation tissue
• Livid red
• Hypergranulation
• Desiccation (dark red color)
• Poor vascularization (pale pink)
• Ecchymosis on granulation
• Necrotic tissue—stuck in chronic infl ammatory phase
• Ecchymosis on granulation infl ammation restarting
• Dull red—desiccated granulation
• Pale pink granulation
• Lacking change in wound depth
• Unsustained contraction—no reduction in size of surface area
Undermining/
tunneling
• Can be present in deep wounds
• Closes as proliferation progresses
• Can be present in deep wounds
• Fails to close or can extend
• Has potential for infection and abscess
• Can be present in deep wounds
• Fails to close or can extend
• Has potential for infection and abscess
Wound edges • Soft to fi rm
• Flexible to touch
• Rolled if full-thickness
• Change in wound shape from irregular to regular
• Reduction in size of surface area
• Drawing together
• Adherence of wound edges by end of phase
• Tight drawing together to reduce size—contracture
• Absence of continuity of wound bed and edges
• Fibrotic
• Fibrotic
• Ecchymosis on wound edge
• Unchanged size
• Rolled or jagged, irregular edges
• No change of shape—not drawing together
• Absence of continuity of wound bed and edges
Wound drainage • Serosanguineous or serous in moderate to minimal amount for wound size
• Yellow gelatinous following trauma
• Infection: viscous malodorous, red/brown, green, purulent
• Large amount
• Serous drainage, scant to minimal amounts
• Desiccated and dry Wound Healing Phase Diagnosis: Aspects of Proliferative Phase
3.9
TABLE
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Chronic Epithelialization Phase
If the edge of the wound is separated from the wound base cre- ating a gap such as shown in Figure 3.35C, the keratinocytes will still initially attempt to epithelialize the wound by migrat- ing to the periwound edge and then curling over, creating a rolled edge. Repeated cellular attempts to cross the gap result in thickening of this edge. Eventually, the cells seem to run out of reproductive capacity and become senescent as described ear- lier. Presence of thickened fi brotic wound edges is character- istic of wounds of long duration. When palpated they will feel hard, rigid, and indurated, and the wound is now in chronic epithelialization phase.
Adjacent and Periwound Tissue Assessment
The characteristics of the skin can be the same as those seen in the chronic infl ammatory and absence of infl ammatory phases. The periwound skin can show signs of ischemia, such as a pale or ashen color in the elevated position that deepens to dark purple with dependence (rubor). Pain can be constant and throbbing, or intermittent claudication during walking, if it is associated with arterial occlusive disease. The appearance of the adjacent skin is usually dry, shiny, taut, and/or hairless. These characteristics indicate the loss of hair follicles and sweat and/
or sebaceous glands, which benchmark the phase.
The wound shown in Figure 3.49 is in both the chronic epithelialization and chronic infl ammatory phases. In the same wound, the appearance of adjacent and periwound skin changed as chronicity was altered and the acute epithelializa- tion and proliferative phases were initiated.
Assessment of Wound Bed Tissue
Wound bed tissue that is hypergranulating can develop a chronic epithelialization phase because the epithelial cells can- not migrate over the hump of granulation tissue against gravity (Fig. 3.42). In this case, the granulation tissue must be trimmed back to a level even with the periwound skin for epithelializa- tion to resume.
Assessment of Wound Edges
Epithelialization of deep wounds occurs only at the edges and can involve thickening and rolling under of the edges. When the cells cannot continue to migrate across the wound, they build up an epithelial ridge along the edge of the wound, as seen in Figures 3.31A and 3.36A. Pressure ulcers typically develop a round shape when this occurs. In wounds in chronic epithelialization, the cells pile up on each other until the rolled, thickened edges become fi brotic. The wound edges need to be modifi ed and the wound bed fi lled before wound epithelializa- tion can be reinitiated. With full-thickness and deeper wounds,
CLINICAL WISDOM
Protection of Skin from Maceration
Skin barriers are products that can be used over the peri- wound skin and new scar tissue to protect them from maceration.
FIGURE 3.47 Full-thickness skin loss in the acute proliferative phase.
The wound is a full thickness venous leg ulcer. Wound edges are soft and fl exible to touch.
FIGURE 3.46 Immature keloid scar; chronic epithalialigation stage.
(Copyright © 2001, R. Scott Ward.)
CLINICAL WISDOM
Maintaining a Moist Wound Bed for Epithelialization Amorphous hydrogel dressings are useful wound mois- turizers. Along with moisture-permeable fi lms and sheet hydrogels, they provide the warm, moist, homeostatic envi- ronment that is critical for epithelialization. Avoid hydrocol- loids or other strong adhesives on new or fragile skin.
Assessment of Wound Drainage
A scant or small amount of serous or serosanguineous wound exudate is expected. The wound must be kept moist during this phase of healing, because desiccation will destroy the epithelial cells.
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1
2
B
FIGURE 3.48 A: Note beefy, red granulation tissue and island of epidermal tissue in full-thickness wound. The wound was in the acute proliferative phase on 12/28. B: Same wound as in Figure 3.47A. Note: (1) Epidermal migration from wound edges, island, and wound shape changes; (2) Progression to the acute epithelialization phase by 2/17; (3) Hyperkeratotic skin changes due to old burn wounds and poor circulation. (Copyright © C. Sussman.)
the process of healing by epithelialization at the wound edges will be arrested if (1) a large amount of wound debris inter- feres with epithelialization, or (2) the wound edges fall off into a deep wound bed with steep walls or do not adhere to the wound bed.
Hyperkeratosis (overgrowth of the horny layer of the skin) is another abnormality of the epithelialization phase. Figure 3.7 shows a wound with hyperkeratosis and the irregular shape of a heel ulcer in a 100-year-old woman. Additional photos of
hyperkeratosis and the management of the problem are shown in Chapter 12. Chronic epithelialization affects scar formation as shown in Figure 3.46. Hypertrophic and keloid scars are aber- rations of the epithelialization phase. Chapter 16 discusses scars.
Assessment of Wound Drainage
The wound can be dry with no wound drainage. Epithelial cells migrate best in a warm, moist environment; thus, if no exudates or only scant exudate is assessed, additional moisture
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FIGURE 3.49 Pyoderma gangrenosum ulcer in both chronic infl am- matory and chronic epithelialization phases. (Copyright © H. Loehne.)
1
2
FIGURE 3.50 Ischemic ulcer in chronic proliferative phase and absence of epithelialization phase. Note: (1) Punched-out ulcer appear- ance with rolled wound edges, (2) Dependent rubor. (Copyright © C. Sussman.)
may be needed to facilitate epithelialization. Wound dry- ness can be due to improper dressing selection, loss of dress- ing, dehydration of the wound or patient, or other iatrogenic conditions.
On the other hand, there may be heavy exudate from a partial-thickness ulcer that should be epithelializing, but the exudate washes out the epidermal cells faster than they can migrate and attach to the wound surface. Excessive moisture associated with certain wound products can also cause this to occur and needs to be managed.
Absence of Epithelialization Phase
Absence of the epithelialization phase can be due to many fac- tors, such as failure of the wound to fi ll with the ECM, desic- cation of the tissues, scar tissue from a prior wound that is not donating epithelial cells, or repetitive trauma to the wound edges. Figure 3-46 is an example of a wound in this phase.
Adjacent and Periwound Tissue Assessment
The color of the adjacent and periwound skin offers clues to the etiology of absence of the epithelialization phase. Absence of this phase can be related to a condition such as arterial obstructive disease (AOD). AOD limits blood supply and oxygen to the tissues and impairs the ability of the skin to repair itself. Examination of adjacent skin will reveal absence of hair, dependent rubor, and pallor on elevation. The wound will have a punched-out appearance and a very limited ring of epidermal tissue around it that does not migrate across the wound, as shown in Figure 3.50. If no prior vascular testing has been reported, further assessment of the vascular system is warranted.
Periwound skin that is dry, fl aky, macerated, or has an irreg- ular texture provides limited epidermal cells to resurface the wound. This wound will lack epithelialization activity.
Skin temperature is a refl ection of blood supply. Skin tem- perature cooler than 92°F–96°F on the torso and lower in the extremities (75°F–80°F) indicates that blood supply to the skin may be limited; warmer skin can be due to infection.
Chronic edema, which can be caused by tissue conges- tion, such as lymphedema, congestive heart failure, or venous
insuffi ciency, stretches the skin and fi lls the interstitial spaces with excess fl uid, including large protein molecules. When the capacity of the tissue to hold fl uid is exceeded, the fl uid leaks through the skin. As a result of this disease process, changes occur in the vascularity of the tissues, leading to the loss of dermal appendages and dry stasis eczema. These changes are known as lipodermatosclerosis.139 Skin changes associated with this disease process are shown in Figure 3.51A,B. Patients with lipodermatosclerosis can show absence of epithelialization phase. More information on lipodermatosclerosis is presented in Chapter 12.
Assessment of Wound Bed Tissue
As noted previously, throughout the wound healing process, the infl ammatory, proliferative, and epithelialization phases overlap. This overlapping can be seen when assessing hypo- granulation of wound bed tissue in the absence of epithelializa- tion phase: Hypogranulation occurs because of the absence of the proliferative phase. This failure to fi ll the wound bed means there will be no surface for the epidermal cells to migrate across to cover the wound.
Assessment of Wound Edges
Another intrinsic factor that causes absence of epitheliali- zation is decreased epidermal proliferation due to cellular senescence and delayed cellular migration, which are attrib- uted to aging. In this case, there is slow or absent new skin growth from the edges or islands. Absence of epithelializa- tion attributes includes dry, fl aky, hyperkeratotic skin at the wound edges. The dryness can be associated with a dry wound environment.
Assessment of Wound Drainage
Table 3.10 summarizes the fi ndings during the epithelialization phase.
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1
2 3
4
A
1 2
B
FIGURE 3.51 A: Stasis dermatitis. There is an absence of the epithelialization phase. Note evidence of: (1) Brawny edema, (2) Trophic skin changes, (3) Hemosiderin staining (hyperpigmentation), (4) Multiple shallow ulcers. B: Close-up view of same leg as in Figure 3.54A. Note evidence of (1) Edema leakage through wounds, (2) Scaling and crusting (trophic changes) due to lipodermatosclerosis.
(Copyright © B.M Bates-Jensen.)
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Periwound Skin and Wound
Tissue Characteristics Acute Epithelialization Phase
Chronic Epithelialization Phase
Absence of Epithelialization Phase
Periwound skin • Early phase has same char- acteristics as acute infl am- matory phase
• Returns to normal color for ethnicity as infl ammation subsides
• Hemosiderin staining if chronic wound
• Can be same as chronic or absence of infl ammatory phase
• Can be ischemic (pale) or ashen
• Can be purplish with dependency
• Dry, fl aky (hyperkeratotic—
can be due to desiccation or aging skin)
• Maceration: pale, wrinkled, soft, thin
• Hemosiderin staining
• Scar tissue
• Same as chronic or absence of infl ammatory phase
• Dry with hyperkeratosis or lipodermatosclerosis
Wound tissue • Even with wound edges
• Pink/red granulation
• Reduction in wound surface area
• Not connected with wound edge
• Hypergranulation
• Absence of resurfacing from edges or dermal appendages
• Hypogranulation
• Presence of scab or necrotic tissue
Undermining/tunneling • Steep walls limit migration • Steep walls limit migration • Steep walls limit migration Wound edges • New skin moves out from
wound edge and dermal appendages in irregular pattern
• Bright pink color, regardless of usual skin pigmentation
• Texture is soft to fi rm and fl exible to touch, thin
• Epithelial ridge
• Rolled under or thickened
• Dry, fl aky skin
• Rounding off of wound shape
• Fibrotic wound edge
• Rounding off of wound shape and edges
• Macerated
• Dry, fl aky skin
Wound drainage • Minimal to scant serous or serosanguineous
• Absent, dry; if hypergranula- tion, minimal/moderate
• Absent, dry Scar tissue • Thin layers of scar tissue
• Thickens over time
• Deep pink color initially;
changes to bright pink color, regardless of normal skin pigmentation
• Hypertrophic scarring
• Keloid scarring
• Hyperkeratotic scarring
• Weak, friable epithelial tissue
• Breaks or washes out Wound Healing Phase Diagnosis: Aspects of Epithelialization Phase
3.10
TABLE