Wound Healing

Wound Healing

Edna Atwater

Penny S. Jones


Many terms are used to describe wounds. A wound may be defined as any disruption in the integrity and/or function of the skin or deeper structures that results in a structured healing pathway. A wound may be described in terms of the etiology, location, and healing response. Acute wound healing is an orderly process that occurs as interplay of specialized cells, mediators, and microbes. These events begin at the moment of wounding and end with return of integrity though not necessarily function.


A. Definition: the wound healing process is a series of events, or cascade (Table 23-1), which is dependent on specialized cells and chemical mediators. Wounds heal by one of two methods, regeneration or repair. The depth of damage will determine the type of healing that a wound will undergo. Regeneration is limited to wounds that involve the epidermis and upper layers of the dermis as well as fetal wound healing. Regeneration results in not only return of integrity but also function of the injured tissues. Wound repair is the healing process that is required for deeper wounds with more extensive tissue destruction. After the fetal period, wound repair with scar formation is due to the inflammatory process.

B. Phase I—Inflammation: upon wounding, the body’s immediate response is to achieve hemostasis followed immediately by inflammation. The goal of this phase is to control bleeding, to defend the body against invasion by the environment, and to initiate tissue repair. The clinical characteristics of this phase are the classic signs of inflammation: erythema, edema, warmth, and pain. This phase of wound healing may last for 24 to 48 hours but, in some cases, may continue for up to 2 weeks.

1. Hemostasis: upon injury, small vessels near the site constrict for 5 to 10 minutes, and both the intrinsic and extrinsic pathways of the coagulation cascade are activated. Blood is exposed to collagen in the extracellular matrix. Platelets begin to adhere and aggregate at the site of injury. At the same time, they release mediators and additional adhesive proteins, which cause more
platelets to adhere, resulting in a platelet plug. A fibrin clot is subsequently formed with the conversion of fibrinogen to fibrins. The end result, blood loss, is slowed and/or stopped.

TABLE 23-1 Wound Healing Cascade




Begins with hemostasis and release of growth factors at the time of wounding—platelets are the primary mediator in this phase.

Phagocytosis (breakdown of necrotic material)—polymorphonuclear leukocytes and macrophages are the primary mediators in this phase.


Formation of granulation tissue; wound contraction and epithelialization occur in this phase.

Fibroblasts, endothelial cells, and keratinocytes are the primary mediators in this phase.


Remodeling of scar tissue through collagen synthesis and collagen breakdown

Macrophages and fibroblasts are the primary mediators in this phase.

2. Vascular/cellular response: after brief vasoconstriction, the vessels dilate, which allows needed cells and mediators to enter the area. Platelets and mast cells secrete a multitude of mediators designed to facilitate removal of any microbes, necrotic tissue, foreign bodies, and cellular debris. The two most important mediators are platelet-derived growth factor (PDGF) and transforming growth factor beta (TGF-β). PDGF draws in and stimulates polymorphonuclear leukocytes (PMNs), including neutrophils and monocytes. Monocytes are converted to macrophages, the cellular version of garbage disposals. These cells continue the process of microbe and cellular debris removal. The end result is a clean wound that is ready to progress to the next phase. Macrophages also mediate the release of growth factors and chemoattractants that are critical to initiating the next phase of healing.

C. Phase II—Proliferative phase: this phase overlaps the inflammatory phase beginning about the 4th day postwounding and lasts for approximately 15 to 16 days. The goal of the proliferative phase of healing is to restore the barrier function of the skin. The clinical characteristics of this phase are reepithelialization, granulation, and tissue contraction.

1. Dermal reconstitution: the formation of new tissue begins 3 to 4 days after injury, which involves two processes: angiogenesis and collagen synthesis; these processes occur simultaneously and are codependent; wound contraction occurs concurrently with granulation.

a. Angiogenesis: the process of new blood vessel formation is chemically mediated by vascular endothelial growth factor A (VEGFA) and fibroblast growth factor 2 (FGF-2). As with most healing signals, it is started at the wound edge from the disrupted capillaries.

b. Collagen synthesis: TGF-β stimulates the macrophages to secrete the cytokines: FGF (fibroblast growth factor), PDGF, tumor necrosis factor alpha (TNF-α), and interleukin-1 (IL-1). TGF-β stimulates fibroblast proliferation and then migration into the fibrin clot. A complex process begins with the formation of new collagen fibers, proteoglycans, and elastin; fibroblast activity is chemically mediated by PDGF and TGF-β, as well as an acidic, low oxygen condition in the wound center. As angiogenesis proceeds, this stimulus is diminished.

2. Reepithelialization: keratinocytes are activated and begin migrating into the wound within 24 hours of injury. In deep dermal wounds, reepithelialization occurs in conjunction with collagen synthesis. Keratinocyte migration, proliferation, and reepithelialization are chemically mediated by the extracellular matrix, matrix metalloproteinase (MMPs), TGF-α, keratinocyte growth factor, and epidermal growth factor.

3. Contraction: in the later stage, macrophages cause fibroblasts to differentiate into myofibroblasts. These contractile cells pull together the wound edges, gradually reducing the size of the defect.

D. Phase III—Maturation phase: overlaps with the proliferative phase and continues for up to a year or longer after the wound has closed; TGF-β, tumor necrosis factor, and FGF-1 play a role in this phase with controlled and timely apoptosis; in full-thickness wounds, collagen is remodeled. Type III collagen is replaced by type I collagen. The goal of the maturation phase is to maximize the tensile strength of the wound and protect the scar from rupture due to mechanical stress. The tensile strength of a healed wound is always less than that of uninjured tissue. This phase is characterized clinically by raised erythematous scar tissue that gradually flattens and no longer blanches when pressure is applied.

Note: Superficial wounds do not scar; deep dermal wounds will scar.


The cells involved in the wound healing process include platelets, leukocytes, macrophages, fibroblasts, myofibroblasts, and epithelial cells (keratinocytes).

A. Platelets: the smallest cell in the blood is essential for coagulation of blood and maintenance of hemostasis. It becomes active in clot formation when blood becomes exposed to collagen after tissue injury. Platelets release PDGF and TGF-β, which assist in wound repair.

B. Leukocytes: PMNs migrate into the wound space immediately after injury. PMNs are attracted to the wound by chemoattractants produced by platelets, activated clotting factors, and fibrin. The function of these early, short-lived (approximately 4 days) cells is to provide protection from infection and remove cellular debris.

C. Macrophages: the most significant cells in wound healing. They are phagocytic cells that gradually replace leukocytes beginning approximately 4 days after wounding. Macrophages aggressively ingest bacteria and necrotic tissue, produce chemoattractants and growth factors, convert macromolecules into amino acids and sugars necessary for wound healing, and secrete lactate to stimulate collagen synthesis.

D. Fibroblasts: responsible for synthesis of collagen and other connective tissue substances during wound repair. Chemoattractants and growth factors released by platelets and macrophages stimulate fibroblasts to migrate to the wound bed beginning at the end of the inflammatory phase.

E. Myofibroblasts: fibroblasts with characteristics similar to those of smooth muscle cells. Myofibroblasts stimulate wound contraction after they migrate within the wound space.

F. Epithelial cells: keratinocytes proliferate and migrate from wound edges and intact skin appendages to reestablish an epidermal barrier. In partial-thickness (superficial) wounds, epidermal resurfacing begins within 24 hours. In deeper (full-thickness) wounds, dermal repair must take place before epithelial cells can begin to migrate.


There are three types of wound healing: primary intention, secondary intention, and tertiary or delayed primary intention.

A. Primary intention: a surgically closed wound whether closed with staples, sutures, or glue. The approximation of wound edges minimizes tissue defect and reduces the potential for infection. Typically, these wounds heal quickly with minimal scar formation.

B. Secondary intention: wound is left open and allowed to heal more slowly. They require a longer healing time for granulation tissue to fill the defect. There is higher risk for infection due to absence of protective barrier. Examples of wounds that heal by secondary intention are pressure ulcers and contaminated surgical wounds.

C. Tertiary intention: intentional delayed primary closure. Example of a wound that heals by tertiary intention is contaminated abdominal wound left open to drain following surgery and later approximated when the wound is granulating and free of infection.


Defined as those wounds caused intentionally (surgery) or by trauma (abrasion, burn, laceration). Vasculature is disrupted so hemostasis must occur. In a healthy host, healing proceeds in a timely manner.

A. Etiology.

1. Mechanical: stab wound, laceration, abrasion, blister, surgical incision, skin tear

2. Thermal: burns, including sunburn or frostbite

3. Chemical: a wound intentionally made through the use of a chemical agent (such as a chemical peel) or unintentionally by exposure to a caustic substance (including stool or urine)


Failure of the normal healing process to proceed in an orderly and timely manner can result in a chronic wound; examples include vascular ulcers, neuropathic ulcers, pressure ulcers, malignancy-related wounds (breast cancer, rectal cancer), and treatment-related wounds (IV infiltrate).

1. Vascular ulcers: may be arterial, venous, or mixed arterial and venous. Arterial ulcers are the result of impaired arterial blood flow from an underlying atherosclerotic condition or as a consequence of vasoactive medications. Venous ulcers result from edema and venous hypertension as a result of incompetent lower extremity veins.

2. Neuropathic ulcers: also known as diabetic foot ulcers, these are the result of loss of sensation to the foot (sensory neuropathy), change in the musculature (motor neuropathy), and shunting of blood and loss of the ability to sweat (autonomic neuropathy). This is often but not always precipitated by diabetes. Various medications may also cause peripheral neuropathy.

3. Pressure ulcer: a localized area of tissue necrosis due to pressure that is usually (but not always) over a bony prominence. Shear forces may also contribute to the development of the ulcer but pressure must be a significant factor.

4. Malignancy-related ulcers: may be due to the primary tumor itself or as a consequence of treatment.

5. Treatment-related ulcers: soft tissue infiltration of vasoactive and vesicant agents can result in full-thickness skin loss. Infiltration of calcium has been known to result in ulcers due to the calcium precipitation in the tissues.


Delayed healing or nonhealing is usually due to some disruption in the normal cascade of healing. Many factors can impair healing. It is imperative that these factors be recognized and addressed to augment the body’s natural ability to heal.

A. Negative factors affecting wound healing.

1. Intrinsic factors (related to patient’s general physical or mental condition)

a. Age: normal skin changes seen with aging affect the skin’s function and healing response through decreased wound contraction, decreased tensile strength, and increased metabolic response. Agerelated alterations that increase the potential for injury and impair healing include:

(1) Decreased collagen density

(2) Increased capillary fragility

(3) Decreased mechanoreceptors resulting in decreased sensory reception

(4) Decreased amount/distribution of subcutaneous fat resulting in impaired thermoregulation

(5) Reduced inflammatory response but proinflammatory environment

(6) Slower rate of neoangiogenesis and wound contraction

(7) Fewer fibroblasts and mast cells

(8) Fragmentation of elastin fibers

(9) Insufficient tensile strength (increased potential for wound dehiscence)

(10) Decreased tissue perfusion secondary to vascular disease

(11) Thinning of dermis and basement layer

(12) Increased reactive oxygen species (ROS) with decreased antioxidant activity resulting in a proinflammatory intrinsic environment and ultimately increased apoptosis and aging skin

(13) Reduced keratinocyte proliferation and turnover time

(14) Less acidic surface pH

(15) Flattening of epidermal-dermal junction and decreased adhesion

b. Nutrition: plays a vital role in all aspects of wound healing

(1) Protein: provides the structural component for tissue repair; deficiency results in decreased fibroblast proliferation, reduced collagen synthesis, decreased angiogenesis, and disrupted maturation; slow gain in tensile strength and increased incidence of wound healing abnormalities are associated with protein-energy malnutrition (PEM); PEM effects all phases of wound healing; usual recommended range of protein intake daily for wound healing is 1.25 to 1.5 g/kg but is as high as 2 g/kg/d for patient with multiple wounds in a severe catabolic state. Specific amino acids (arginine and glutamine) may have a beneficial effect, but conclusive studies are not available. Lysine and proline are also known to impact wound healing.

(2) Vitamins

(a) Vitamin A affects collagen cross-linkage, supports epithelial proliferation and migration and dermal angiogenesis, and enhances the immune system. Recommended supplementation ranges for 10,000 to 50,000 IU orally daily for 10 days.

(b) Vitamin B, especially B1, thiamine, affects enzyme activity, collagen cross-linkage, and immune response.

(c) Vitamin C is necessary for collagen synthesis, immune modulator, and antioxidant. Supplementation to 100 to 200 mg/day may be beneficial for patients with vitamin C deficiency and wounds. Caution is advised with long-term high-dose supplementation.

(d) Vitamin D accelerates wound closure, promotes reepithelialization, and improves tensile strength.

(e) Vitamin E plays a protective role in antioxidant defense.

(3) Carbohydrates: provide energy needed for wound repair; insufficient carbohydrate intake initiates body protein catabolism and increases potential for infection.

(4) Trace elements: zinc stabilizes membrane structure and function, acts as a cofactor in enzyme systems, affects immune response, and inhibits bacterial growth; copper aids in collagen linkage; iron corrects iron deficiency anemia and affects collagen synthesis; magnesium supports collagen synthesis.

c. Medical condition: underlying disease states alter the body’s normal response to healing.

(1) Diabetes: associated with vasculopathy, neuropathy, and immunopathy; greater than 100 cytologic factors associated with diabetes that impair wound healing.

(2) Hypotension: vasoconstriction promotes tissue ischemia and decreased nutrient delivery.

(3) Peripheral vascular disease (PVD): tissue perfusion is decreased resulting in hypoxia and diminished nutrients to tissue as well as impaired removal of waste products.

(4) Renal disease—the effect of uremia on wound healing in humans is not well understood; uremia does cause neuropathy and immune dysfunction.

(5) Hematopoietic abnormalities: inadequate numbers of RBCs impair oxygen transport; inadequate platelets delay the healing cascade.

(6) Gastrointestinal disease: inhibits absorption and compromises nutritional status

(7) Cardiopulmonary disease: PaO2 is decreased contributing to tissue hypoxia.

(8) Cancer: immune response is altered; risk of infection is increased.

(9) Chronic venous insufficiency: incompetent venous valves cause high-pressure venous hypertension and significant edema.

(10) Sickle cell disease: dysmorphic blood cells occlude smaller vessels, resulting in leg ulcers.

d. Infection: defined as bacterial concentrations greater than 105 organisms per gram of tissue; highly virulent organisms can cause infection at lower concentrations; important to distinguish between infection, critically colonized, and colonization. Presence of a bacterial biofilm will also delay wound healing.

(1) Signs of local and regional infection (suppressed in immunocompromised patients)

(a) Erythema

(b) Edema

(c) Induration

(d) Pain

(e) Purulent or foul-smelling drainage (depending on topical therapy, this may not be accurate)

(f) Crepitance

(g) Lymphadenopathy

(h) Delayed wound healing

(i) Pale and friable granulation tissue

(j) Wound breakdown

(2) Signs of systemic infection

(a) Fever/chills

(b) Elevation of white blood cell (neutrophil) count; increase in number of bands/segs (shift to the left)

(c) Positive blood/wound cultures

(d) Sepsis

e. Drugs: particularly important to evaluate patient’s medicines when a chronic, nonhealing wound is present; examples of drugs, which may impair healing.

(1) Corticosteroids: systemic steroids inhibit fibroblast formation and collagen synthesis; topical steroids may have varying effects on epidermal resurfacing and dermal collagen synthesis.

(2) Anticoagulants: implied effect on healing by preventing hemostasis

(3) Nonsteroidal anti-inflammatory drugs (NSAIDs): may inhibit inflammatory phase of healing

(4) Immunosuppressives: azathioprine and prednisone are associated with significant reduction in tensile strength.

(5) Chemotherapeutic agents: affect on wound healing depends on the specific drug, dose, and time of administration: increase risk of infection (due to decreased WBCs), act on any rapidly dividing cells, alter the function of fibroblasts and myofibroblasts, and impair collagen synthesis and reepithelialization

(6) Nicotine: causes vasoconstriction whether patch, gum, or lozenge. There are other studies that dispute this. They are likely better than cigarette smoking with its greater than 250 harmful chemicals but nonnicotine measures may be a better smoking cessation option for patients with wounds.

f. Hypoxia: poor tissue oxygenation slows or completely inhibits healing; this is seen in patients with cardiopulmonary disease (decreased PaO2), PVD, and diabetes; sustained tissue pressure compromises circulation leading to tissue ischemia, hypoxia, and cell death.

g. Stress: impairs healing by altering normal physiologic response; psychological stress, pain, and noise stimulate the sympathetic nervous system releasing vasoactive substances that promote vasoconstriction and alter tissue perfusion.

2. Extrinsic factors

a. Topical antimicrobials/cleansers: inappropriate use of disinfectants and antiseptics (povidone-iodine, hydrogen peroxide, acetic acid, chlorhexidine, and hypochlorite) impairs healing by having cytotoxic effects on fibroblasts.

(1) Liquid detergents: may retard healing by changing the pH of the wound bed or by cytotoxic action on fibroblasts

(2) Antiseptic cleansers (acetic acid, Dakin solution, chlorhexidine, povidone-iodine/Betadine, hydrogen peroxide): cytotoxic to fibroblasts

b. Necrotic tissue: prolongs the inflammatory phase of healing, supports microbial growth, delays epithelial cell migration, and provides a physical obstacle to wound contraction

c. Continued tissue trauma: unrelieved pressure and edema lead to progressive tissue hypoxia and cell death; friction destroys epidermal cells and alters the barrier function of the skin; shearing forces angulate blood vessels, causing localized tissue hypoxia and chronic inflammation; excessive moisture leads to tissue maceration and promotes the growth of microorganisms; wound desiccation prolongs inflammation, retards epithelial cell migration, and impairs collagen synthesis.

d. Radiation therapy: dose, frequency, and location of irradiated area in relation to the wound site will have implications for therapy; residual effects of radiation are permanent; irradiated tissue is easily damaged and slower to heal; Radiation therapy impairs healing through:

(1) Injury to fibroblasts

(2) Injury to endothelial cells

(3) Decrease in collagen production

(4) Destruction of cells in mitosis

(5) Vascular damage

(6) Increased risk of infection

(7) Apoptosis of healthy cells


A. National Pressure Ulcer Advisory Panel (NPUAP) and European Pressure Ulcer Advisory Panel (EPUAP) criteria for classification of pressure ulcer. The classification system is for pressure ulcers only and does not apply to leg ulcers or other acute or chronic wounds. The stage/category of a pressure ulcer represents the greatest depth of tissue destruction and remains constant until complete reepithelialization of the ulcer. Pressure ulcers are not backstaged. The final stage/category of a pressure ulcer cannot be determined if necrotic tissue is present and obscuring the wound base.

1. Stage/category I: intact skin with a localized area with nonblanchable redness (Figures 23-1 and 23-2). The area may be painful, firm, warmer, or cooler as compared to the surrounding skin. Stage/category I lesions may be difficult to see in more darkly pigmented skin. The use of cream may assist in distinguishing the subtle color variation due to pressure.

FIGURE 23-1. Stage I pressure ulcer on the heel. (Copyright Duke University, used with permission.)

FIGURE 23-2. Stage I pressure ulcer on the sacrum in person of color. (Copyright Duke University, used with permission.)

2. Stage/category II: partial-thickness skin loss involving the epidermis and/or dermis; clinical appearance is a shallow ulcer with a pink wound bed or may be an intact serous-filled blister/bulla (Figures 23-3 and 23-4). There is no slough or eschar. There may be devitalized dermal or epidermal tissue. These lesions are often painful due to exposed dermal nerve endings. Careful consideration required to differentiate and stage II from moisture and/or friction related skin damage.

3. Stage/category III: full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia (Figure 23-5). Actual depth of the ulcer varies with the anatomic location as some areas have a thinner layer of subcutaneous fat than others. Muscle, tendon, and bone are not exposed. There may be undermining and tunneling. Slough or eschar may also be present, but the full depth of the wound is visible.

FIGURE 23-3. Stage II pressure ulcer on the heel. (Copyright Duke University, used with permission.)

4. Stage/category IV: full-thickness skin loss with exposed muscle, bone, or supporting structures (Figure 23-6). There may be slough or eschar in the wound bed but the full depth is visible. Undermining and sinus tracts may also be associated with these ulcers.

5. Unstageable: full-thickness skin loss with the base of the wound obscured with necrotic tissue: slough or eschar (Figures 23-7 and 23-8).

6. Suspected deep tissue injury: localized area of purple or maroon intact skin or it may be a blood-filled or purple-based blister/bulla (Figures 23-9 and 23-10). As with stage/category I ulcers, these are difficult to see in darker pigmented skin. As this lesion evolves, it may be reclassified to unstageable, stage/category III or IV. It is unclear what percentage of these ulcers progress to fullthickness skin loss versus resolve without progressing to an open lesion.

FIGURE 23-4. Stage II pressure ulcer on the buttock in a person of color. (Copyright Duke University, used with permission.)

FIGURE 23-5. Stage III pressure ulcer on the sacrum. Note the absence of hair follicles in the wound base. (Copyright Duke University, used with permission.)

FIGURE 23-6. Stage IV pressure ulcer on the sacrum. If one is able to identify muscle or bone in the wound base, the ulcer is stage IV despite the amount of necrotic tissue. (Copyright Duke University, used with permission.)

FIGURE 23-7. Unstageable pressure ulcer on the heel. (Copyright Duke University, used with permission.)

FIGURE 23-8. Unstageable sacral pressure ulcer. This ulcer was very likely a suspected deep tissue injury that is evolving and is now considered unstageable. (Copyright Duke University, used with permission.)

FIGURE 23-9. Suspected deep tissue injury on the buttocks bilaterally. (Copyright Duke University, used with permission.)

FIGURE 23-10. Evolving suspected deep tissue injury in a person of color. The presence of these ulcers can be missed without close assessment of the skin tone changes. (Copyright Duke University, used with permission.)

FIGURE 23-11. Mucosal pressure ulcer related to a nasoenteric tube. (Copyright Duke University, used with permission.)

7. Mucosal: layers of tissue different are mucosal surfaces, making use of the above-described staging system problematic; these terms are used for any pressure ulcer on a mucosal surface (Figure 23-11).

B. Classification of wound by tissue depth.

1. Superficial partial thickness: involves the epidermis and upper layers of the dermis; heals primarily by reepithelialization; painful due to exposed nerve endings; examples include abrasion, burn, chemical peel, and skin tear.

2. Deep partial thickness: damage extends to the lower layers of the dermis but does not penetrate the dermis; heals by epithelialization in conjunction with varying degrees of collagen synthesis; examples include burn, dermal biopsy, and deeper skin tear.

3. Full thickness: damage extends through the epidermis and dermis into deeper structures (subcutaneous tissue, fascia, muscle, tendon, or bone); healing occurs primarily by collagen synthesis and soft tissue contraction; examples include stage III or IV pressure ulcer and open postsurgical abdominal wound.


A. Anatomic location: provides clues about wound etiology; for example, pressure ulcers commonly occur over bony prominences, venous ulcers often occur on the pretibial area of the calf; skin tears on forearms and legs.

B. Size: wound measurement is a basic parameter of assessment; a healing wound decreases in size over time; interventions should promote a gradual decrease in wound size, except following debridement when wound size can be expected to increase; assessment of size is a way to effectively evaluate efficacy of treatment.

1. Two- or three-dimensional measurement (two-dimensional measurement does not provide information regarding depth of the wound)

a. Linear measurements: measure length of the wound from 12 to 6 o’clock position with 12 o’clock being the head and 6 o’clock the feet. Measure the width at 3 to 9 o’clock position. Measuring the greatest length, width, and depth in cm or mm is not reliably reproducible between providers; gently insert cotton-tipped applicator into deepest area of wound to obtain depth measurement; as much as possible, the patient should be in the same position each time for accurate measurement of full-thickness wounds (soft tissue displacement can alter linear measures). When compared to wound tracing and digital planimetry, there was strong to modest agreement in assessing size (Figure 23-12).

b. Wound tracings: of limited value with electronic medical record; may be useful when wound margins are irregular or poorly demarcated and linear measurement is difficult; use double-layer transparent acetate and permanent marking pen to trace configuration; label clean tracing with date; mark direction of head and foot on tracing for subsequent comparisons.

c. Wound photography: used in conjunction with linear measurement and other assessment parameters; provides visual data to verify change or lack of change in linear dimensions—color of tissue and the condition of the surrounding skin. Concerns of legal issues have been noted; non-health care photos likely in legal proceedings so quality and timely health care photos would be a plus.

d. Digital planimetry: uses an acetate tracing and/or digital photography with the use of a software program to measure the wound area. Can be labor intensive, requires training for accuracy, and is more
costly than use of a disposable ruler for linear measurements. Bien, Anda, and Prokocimer found the ruler measurement to be as reliable as digital planimetry for wound measurements.

FIGURE 23-12. Wound size. (Copyright Duke University, used with permission.)

2. Volume measurement

a. Wound molds: used to assess the volume of open wounds; biocompatible molding material is poured into open wound and allowed to harden; change in size/weight of mold over time indicates progress; not practical in clinical settings.

b. Fluid instillation: cover wound with transparent film and then instill a known quantity of solution into the wound cavity, filling it to the perimeter; extract fluid with a syringe or suction and record the amount; requires serial measurements; use is limited to deep full-thickness wounds; not practical in clinical settings.

C. Undermining, tracts, or tunneling: evaluate full-thickness (stage III or IV pressure ulcers) wounds carefully for undermining/tracts; undermining most often occurs in wounds as a result of shear; sinus tracts occur generally as a result of dehiscence, infection, or a combination of neuropathy and arterial insufficiency; soft tissue tunneling is common in deep wounds; use a clock face to describe the direction of undermining, tracts, and tunnels; obtain linear measurements when possible. Use a gloved finger or cotton-tipped swab to determine the length (Figure 23-13).

D. Tissue type: accurate assessment of the wound bed leads to appropriate treatment and decreased morbidity. (Note: Viable subcutaneous tissue, fascia, muscle, tendon, and bone may also be visible at the base of deep wounds, especially after surgical debridement.) Quantify the tissue types by percentage of the wound base (Figure 23-14).

1. Epithelial tissue: regrowth of skin from wound edges or skin appendages; initially one cell layer thick, then stratifies; presents clinically as pearly pink wound margins (full-thickness wounds) or fleshy budding of the hair follicles (partial-thickness wounds)

FIGURE 23-13. Measuring amount of undermining with a cotton-tipped swab. (Copyright Duke University, used with permission.)

FIGURE 23-14. Quantifying the amount of granulation and eschar slough tissue by percentage: 20% granulation tissue, 80% slough. Quantifying the wound base using colors is acceptable: 20% pink, 20% yellow, 60% black. (Copyright Duke University, used with permission.)

2. Granulation tissue: combination of newly formed blood vessels and collagen deposited into the wound space during the proliferative phase of healing; presents clinically as fleshy granular projections of tissue; healthy granulation is moist and pink to beefy red and has a spongy texture.

3. Eschar: necrotic epidermis and dermis (full-thickness wounds only); delays wound healing by slowing epithelial cell migration and serving as a physical obstacle to wound contraction; acts as a banquet for bacterial growth; presents clinically as thick, dry leathery necrotic tissue attached to the wound surface (e.g., dry gangrene); usually black in color

4. Slough: soft, stringy necrotic tissue that may appear black, gray, yellow, or tan in color; often associated with thick drainage and increased numbers of bacteria

E. Exudate: the amount, viscosity, and color of exudate will vary with the phase of healing, amount and type of necrotic tissue present, and wound dressing.

1. Volume: volume of exudate should decrease as inflammation subsides, necrotic tissue is removed, and infection is controlled; an exception is in the immunocompromised patient where the inflammatory process may be blunted and volume of exudate is altered; volume of apparent exudate increases with use of moisture-retentive dressings for autolytic debridement, osteomyelitis, or spontaneous drainage of a soft tissue abscess; a sudden increase in the volume of exudate may signal impending wound dehiscence in primarily closed wounds; quantify volume of exudate as scant, small, moderate, large, or copious.

2. Color: the color of exudate changes as tissue repair progresses through the various phases of healing; inflammatory wound transudate is initially yellow tinged and watery (serous) as protein-rich transudate leaks from dilated blood vessels; may be blood tinged
(serosanguinous) or show evidence of fresh bleeding (sanguineous); chronic wound exudate changes color (cream, brown, gray, green) with increased proliferation of microorganisms and liquefaction of necrotic tissue.

3. Consistency: the viscosity of wound exudate changes from a watery consistency (inflammatory transudate) in acute wounds to a purulent consistency in chronic or infected wounds; change in consistency caused by accumulation of blood cells and living or dead organisms.

F. Odor: colonization or infection with certain microorganisms gives the wound a distinct odor (Pseudomonas); a pungent, strong, foul, fecal, or musty odor together with increased erythema, tenderness, and volume of exudate usually suggests infection; some moisture-retentive dressings are also associated with an unpleasant odor in the absence of infection. Quantify odor as mild, moderate, and foul.

G. Condition of periwound skin.

1. Color: assess for erythema, hypo-/hyperpigmentation, cyanosis, etc.; color changes are more difficult to assess in individuals with darker skin.

2. Intact: assess for blistering, maceration, dryness/cracking, rashes, denudation, etc.

3. Signs of active infection: a ring of erythema extending for several centimeters, induration of periwound skin

4. Directs potential topical therapy: adhesive moistureretentive dressings not indicated when surrounding skin eroded or denuded (Figure 23-15)

H. Pain response: assess and document the presence of pain or tenderness within or around the wound; may indicate infection, underlying tissue destruction, or vascular insufficiency; absence of pain may indicate nerve destruction.

I. Previous treatment: determine the previous treatment modalities; some treatments may alter wound appearance clinically or retard the healing process; for example, use of topical Neosporin may result in a well-demarcated erythematous rash around the ulcer (Figure 23-16).

FIGURE 23-16. Contact (allergic) dermatitis to topical treatment. (Copyright Duke University, used with permission.)

FIGURE 23-15. Unstageable, slough-covered ulcer on the sacrum with significant erosions on the buttocks due to moisture-associated dermatitis. (Copyright Duke University, used with permission.)

J. Infection: bacterial infection negatively affects wound healing; it may either delay the wound healing process or lead to severe morbidity or death; accurate evaluation of bacterial load in a wound is important to treatment planning. Tissue analysis for infection is gold standard but not always possible. As a swab method, the Levine method offers the most reliable and valid method.

1. Colonization: bacteria present in a wound that has not resulted in a host inflammatory response. May not delay healing.

2. Critically colonization: an imbalance between the presence of bacteria and wound immune response; often the cause of a stalled wound

3. Biofilm: are colonies of bacteria that are attached and embedded into the extracellular polymeric substance (EPS). This EPS is a coating that protects the bacteria from destruction by antimicrobials and the host immune response—essentially armor coating for the bacteria (Figure 23-17).

FIGURE 23-17. Pale wound base. There is no evidence of acute infection (foul odor, purulent drainage or surrounding edema, redness, or edema). For this nonhealing postoperative wound, the presence of a biofilm should be suspected. (Copyright Duke University, used with permission.)

K. General health assessment: assess the host—wounds do not exist in a vacuum. It is imperative to assess the status of the host and to correct/optimize any conditions recognized.

1. Age: with normal aging, there is a decrease in the inflammatory response, delayed angiogenesis, decreased collagen synthesis and degradation, slowed epithelialization, and decreased functioning of sebaceous glands; older patients are at higher risk for slow or nonhealing wounds. They are also more likely to have comorbid conditions that impair wound healing.

2. Chronic illness: assess for concomitant medical problems associated with delayed healing: diabetes, COPD, hypertension, ASHD, depression, etc.

3. Medications: assess for medications known to slow/inhibit healing: systemic corticosteroids, anticoagulants, NSAIDs, immunosuppressives, chemotherapeutic agents, and nicotine.

4. Nutritional status: healing may require an increase in calorie intake, vitamins, and trace elements; if a patient is in a state of hypoproteinemia, then healing will be negatively affected.

5. Infection: assess systemic conditions that may increase potential for infection; immune incompetence (interferes with mitosis, protein synthesis, and increases risk of infection). Infection elsewhere in the host will slow wound healing.

6. Psychosocial: assess patient’s ability/willingness to be adherent with treatment; assess hygiene; assess support systems/resources available to patient; depression and/or anxiety associated with the wound.


A. Debridement: the removal of foreign objects, damaged tissue, and cellular debris from the wound surface. The primary objectives of wound debridement are to promote timely progress along the healing continuum from inflammation to proliferation, prevent infection by removing food source for microorganisms, and correct abnormal wound repair.

1. Nonselective debridement: removes devitalized tissue from the wound but may also damage healthy tissue

a. Wet-to-dry dressings: uses saline and gauze; wet gauze is placed directly onto wound base and allowed to dry before removal; removal mechanically removes anything (health and nonhealthy tissue) that adheres to the gauze from the wound surface; painful to the patient and nonselective (can injure viable tissue); limit use to wounds that contain a large amount of soft necrotic slough or when insoluble debris is not easily removed by rinsing or cleansing; may result in gauze pieces embedded into the wound surface resulting in an increased inflammatory response (Figure 23-18).

b. Irrigation: uses water or saline to flush the wound and remove superficial nonattached cellular debris; irrigation technique may be forceful (high pressure) or gentle (low pressure); high-pressure irrigation can damage healthy tissue and is not indicated for clean, noninfected wounds, granulating wounds, or superficial wounds.

FIGURE 23-18. Gauze embedded in this venous leg ulcer will delay wound healing. (Copyright Duke University, used with permission.)

c. Hydrotherapy: whirlpool has decreased in use due to infection control issues as well as patient safety. Bedside-pulsed lavage with a single patient use device has been showed to be a safe and effective method of wound irrigation and debridement. It is indicated for debridement of wounds with loosely adherent necrotic tissue and yellow fibrinous or gelatinous exudate, to cleanse wounds of dirt and foreign contaminants; limit to wounds with extensive amounts (>50%) of necrotic tissue; very effective when paired with bedside conservative sharp debridement.

d. Surgical debridement: use of a scalpel or other instrumentation to dissect and remove necrotic tissue; technique of choice for infected wounds; prepares open wounds for closure; extensive surgical debridement may involve the sacrifice of viable tissue.

e. Topical agents: Dakin (sodium hypochlorite) solution chemically loosens/removes cellular debris; may be toxic to healthy cells and a chemical irritant to intact skin; not indicated for use on clean superficial wounds.

2. Selective debridement: selectively removes devitalized tissue from the wound without disruption or damage to healthy tissue

a. Nonionic wound cleansers, surfactants, and sterile normal saline: indicated for cleansing wounds with minimal-to-moderate amounts of slough.

b. Conservative sharp debridement: requires no anesthesia; can be done on an outpatient basis, bedside, or at home using forceps and scissors; only devitalized tissue is removed.

3. Enzymatic debridement: enzyme preparations applied topically to necrotic tissue to break down targeted substrates; products require moisture for activation; inactivated when exposed to heavy metal ions such as mercury or silver (present in some antiseptics); loose debris should be removed before application.

4. Autolytic debridement: naturally occurring enzymes produced by bacteria and macrophages in wound fluid are used to promote liquefaction of necrotic tissue; autolysis (self-digestion) is promoted by the use of moisture-retentive dressings, which trap fluid next to the wound surface.

5. Maggot therapy: medicinal maggot therapy provides selective debridement by both physical (larvae movement) and chemical (secretes and excretes digestive enzymes) means.


Base choice of product on the wound/host assessment, expected outcome of intervention, and cost of treatment.

A. Principles of wound management.

1. Reduce/eliminate causative factors.

2. Provide systemic support.

3. Remove foreign bodies/necrotic tissue.

4. Choose appropriate topical therapy.

5. Control bacterial proliferation.

6. Control drainage.

7. Curative versus palliation.

B. Goals of wound cleansing/debridement: to remove surface bacteria and other microorganisms and to hasten the removal of devitalized tissue.

C. Goals of topical therapy.

1. Create an optimum wound healing environment.

2. Manage exudate.

3. Obliterate dead space.

4. Provide insulation.

5. Protect from trauma.

D. Dressing options.

1. Semipermeable film dressing: acronyms include moisture vapor-permeable (MVP) dressings, vapor-permeable (VPM), transparent film dressings (TFDs), synthetic adhesive moisture vapor-permeable (SAM) dressings, and polyurethane films (PUFs); retains moisture in wounds with minimal exudate without macerating periwound skin; waterproof; permits oxygen and water vapor to cross the barrier; impermeable to bacteria and contaminants; maintains moist environment; promotes autolysis of necrotic tissue; provides insulation; allows for visualization of the wound; adhesive products may injure new epithelium on removal (avoid use on skin tears); indications include:

a. Superficial, partial-thickness wounds

b. Wounds with minimal necrosis or slough

c. Wounds with little or no exudate

d. Use as a secondary (cover) dressing

2. Hydrocolloid dressing: pastes or occlusive adhesive wafers composed of pectinlike material; provides moist environment; promotes autolysis and granulation; insulates wound; impermeable to bacteria and other contaminants; adhesive products may injure new epithelium on removal (avoid use on skin tears); provides moderate absorption; may be used with compression stockings/pumps, wraps, or Unna boot for:

a. Partial-thickness wounds

b. Shallow full-thickness wounds

c. Granulating full-thickness with minimal-to-moderate exudate

3. Foam dressing: wound contact surface is semipermeable or hydrophilic; outer dressing surface is hydrophobic; nonadherent; maintains moist wound environment; promotes autolytic debridement; minimal-to-moderate absorption; protects from trauma; insulates; atraumatic removal; available with and without silver; available with silicone contact layer to promote adhesion and atraumatic removal; indications include:

a. Partial-thickness wounds with minimal-to-moderate drainage

b. Full-thickness wounds with depth or dead space; use packing to fill cavity.

c. May use under compression

d. To absorb drainage around tubes (trach sites, chest tubes, gastrostomy tubes, etc.)

e. Atraumatic reduction of hypergranulation tissue (especially useful around pediatric gastrostomy tubes)

4. Calcium alginate/hydrofiber dressing: highly absorbent (can absorb 20 times its weight in wound exudate); conforms to the shape of the wound; must be covered with a secondary dressing; available with and without silver; provides a modest hemostasis effect; available in sheet and ribbon format; indications include:

a. Partial- and full-thickness wounds with moderate-toheavy exudate

b. Wounds with tunneling or sinus tracts

c. Wounds with moderate-to-small amounts of necrotic tissue

d. Infected and noninfected wounds

e. Wounds with small sanguinous ooze (e.g., tumors)

5. Biosynthetic/biologic dressing: skin substitutes; composed of tissue derived from animal or human sources; requires a secondary dressing; indicated for:

a. Full-thickness wounds

b. Noninfected wounds

6. Hydrogel dressing: water or glycerin-based amorphous gel, impregnated gauze, or sheet; promotes autolytic debridement; maintains moist environment; limited absorption of exudate; atraumatic removal; refrigerated product provides some pain relief; available with or without silver; most require a secondary dressing; indications include:

a. Partial- or full-thickness wounds

b. Deep wounds with minimal exudate

c. Wounds with varying amounts of necrosis or slough

d. Burns or tissue damaged by radiation

7. Composite dressings: combination of two or more dressing materials, moisture-retentive properties; absorptive; provides a bacterial barrier; indications include:

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Mar 9, 2021 | Posted by in NURSING | Comments Off on Wound Healing

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