Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Wound Care Treatment & Management

  • Author: Brian J Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Zubin J Panthaki, MD, CM, FACS, FRCSC  more...
 
Updated: Mar 11, 2016
 

Medical Therapy

General treatment of nonhealing wounds

Assess the entire patient

Successful treatment of difficult wounds requires assessment of the entire patient and not just the wound. Systemic problems often impair wound healing; conversely, nonhealing wounds may herald systemic pathology.

Consider the negative effects of endocrine diseases (eg, diabetes, hypothyroidism), hematologic conditions (eg, anemia, polycythemia, myeloproliferative disorders), cardiopulmonary problems (eg, chronic obstructive pulmonary disease, congestive heart failure), GI problems that cause malnutrition and vitamin deficiencies, obesity, and peripheral vascular pathology (eg, atherosclerotic disease, chronic venous insufficiency, lymphedema).

Characterize the wound

Assess the following: (1) size and depth of involvement and the extent of undermining, (2) the appearance of the wound surface—is it necrotic or viable, (3) amount and characteristic(s) of wound exudate, and (4) status of the periwound tissues (eg, pigmented, scarred, atrophic, cellulitic).[24]

Ensure adequate oxygenation

The usual reason for inadequate tissue oxygenation is local vasoconstriction as a result of sympathetic overactivity. This may occur because of blood volume deficit, unrelieved pain, or hypothermia, especially involving the distal extent of the extremities.

Ensure adequate nutrition

Adequate nutrition is an often-overlooked requirement for normal wound healing.[25] Address protein-calorie malnutrition and deficiencies of vitamins and minerals.

Inadequate protein-calorie nutrition, even after just a few days of starvation, can impair normal wound-healing mechanisms. For healthy adults, daily nutritional requirements are approximately 1.25-1.5 g of protein per kilogram of body weight and 25-30 calories/kg. These requirements can increase, however, for patients with sizeable wounds.

Suspect malnutrition in patients with chronic illnesses, inadequate societal support, multisystemic trauma, or GI or neurologic problems that may impair oral intake. Protein deficiency occurs in approximately 25% of all hospitalized patients. Oftentimes, a thorough physical examination can reveal signs of malnutrition, such as temporal wasting, loss of subcutaneous fat, ankle/sacral edema, pronounced clavicles.

Chronic malnutrition can be diagnosed using anthropometric data to compare actual and ideal body weights and by observing low serum albumin levels. Serum prealbumin is sensitive for relatively acute malnutrition because its half-life is 2-3 days (vs 21 d for albumin). A serum prealbumin level of less than 16-17 g/dL suggests some level of malnutrition, whereas a level less than 10 g/dL suggests severe protein-calorie malnutrition.

Vitamin and mineral deficiencies also require correction. Vitamin A deficiency reduces fibronectin on the wound surface, reducing cell chemotaxis, adhesion, and tissue repair. Vitamin C is required for the hydroxylation of proline and subsequent collagen synthesis.

Vitamin E, a fat-soluble antioxidant, accumulates in cell membranes, where it protects polyunsaturated fatty acids from oxidation by free radicals, stabilizes lysosomes, and inhibits collagen synthesis. Vitamin E inhibits prostaglandin synthesis by interfering with phospholipase-A2 activity and is therefore anti-inflammatory. Vitamin E supplementation may decrease scar formation.

Zinc is a component of approximately 200 enzymes in the human body, including DNA polymerase, which is required for cell proliferation, and superoxide dismutase, which scavenges superoxide radicals produced by leukocytes during debridement.

Treat underlying infection

Issues to consider are wound infection versus colonization and osteomyelitis.[26]

A positive wound culture does not confirm a wound infection. Opportunistic microorganisms may colonize any wound. Wound exudate, which is naturally bactericidal, inhibits the spread of surface contamination from becoming a deep wound infection. However, when wound ischemia or systemic immune compromise supervenes, pathogenic microorganisms propagate until an excessive concentration of bacteria in the wound precludes healing. This heralds a true wound infection. Multidrug resistant organisms are becoming increasingly common.

Foul-smelling drainage, a spontaneously bleeding wound bed, flimsy friable tissue, increased levels of wound exudate, increasing pain, surrounding cellulitis, crepitus, necrosis, fasciitis, and regional lymphadenopathy characterize the infected wound. Fever, chills, malaise, leukocytosis, and an elevated erythrocyte sedimentation rate are common systemic manifestations of wound infection.

Wound infection requires surgical debridement and appropriate systemic antibiotic therapy. Topical antiseptics are usually avoided because they interfere with wound healing because of cytotoxicity to healing cells.

Proving the absence of osteomyelitis is often as onerous as establishing its presence. Although osteomyelitis may be associated with fevers, malaise, chronic fatigue, and limited range of motion of the affected extremity, patients often present with only a nonhealing wound or a chronic draining sinus tract overlying a bone or joint.

Plain radiographs, CT scans, radionuclide bone scans, and MRIs have a role in the workup of osteomyelitis. All too often, even a comprehensive imaging evaluation is nondiagnostic. Therefore, negative findings on radiologic workup should not deter the clinician from performing curettage of suspicious bone underlying a chronic draining wound.

Osteomyelitis is treated with surgical curettage and appropriate systemic antibiotics. Provide a wound bed that is conducive to wound healing.

Surgically debride nonvitalized tissue and with appropriate irrigation. Significant amounts of nonviable and fibropurulent tissue must be removed surgically.

Initial aggressive debridement in the operating room with the patient under local anesthesia with sedation or under regional or general anesthesia is often wise. Subsequent debridement in an outpatient setting can be performed by using topical lidocaine gel or spray anesthesia and by gentle excision using iris scissors and forceps or by scraping using a curette.

Dressing changes require clean but not necessarily sterile technique.

Remove foreign bodies

Be attentive to the possibility of foreign bodies, which may prevent healing of traumatic wounds, including road debris and retained fragments of dressing materials or suture material.

Irrigate

Gently irrigate the wound with a physiologic saline solution. If cost is a major consideration, the patient can prepare a saline solution at home by using 1 gallon of distilled water and 8 teaspoons of table salt. The solution is boiled and then cooled to room temperature before use.

If surface exudate is present, consider irrigation under pressure. An irrigation pressure of approximately 8 psi can be achieved with saline forced through a 19-gauge angiocatheter with a 35-mL syringe. Pat the wound surface with soft moist gauze; do not disrupt viable granulation tissue.

Whirlpool treatment is reserved for large and infected wounds.

Provide a moist (not wet) wound bed

After debridement, apply a moist saline dressing, an isotonic sodium chloride gel (eg, Normlgel [Scott Health Care], IntraSite gel), or a hydroactive paste (eg, DuoDerm [ConvaTec]). Optimal wound coverage requires wet-to-damp dressings, which support autolytic debridement, absorb exudate, and protect surrounding normal skin.

A polyvinyl film dressing (eg, OpSite [Smith & Nephew], Tegaderm [3M]), which is semipermeable to oxygen and moisture and impermeable to bacteria, is a good choice for wounds that are neither dry nor highly exudative.

For dry wounds, hydrocolloid dressings, such as DuoDerm or IntraSite hydrocolloid, are impermeable to oxygen, moisture, and bacteria. They maintain a moist environment, and they support autolytic debridement. They are a good choice for relatively desiccated wounds.

For exudative wounds, absorptive dressings, such as calcium alginates (eg, Kaltostat [Calgon Vestal], Curasorb [Kendall]) and hydrofiber dressings (eg, Aquacel and Aquacel-AG [Convatec]), are highly absorptive and are appropriate for exudative wounds. Alginates are available in rope form, which is useful for packing deep wounds.

For very exudative wounds, impregnated gauze dressings, such as Mesalt (Scott), are useful. Twice-daily dressing changes may be needed.

For infected wounds, use silver sulfadiazine (Silvadene) if the patient is not allergic to sulfa drugs. If the patient is allergic to sulfa, bacitracin-zinc ointment is a good alternative. An ionic-silver hydrofiber dressing (Aquacel-AG) is also a good choice.[27, 28, 29, 30, 31, 32]

For chronic and stubborn wounds, the use of Leptospermum – or Manuka honey – impregnated products may be helpful to progress towards wound closure.

Bandaging a challenging anatomic area (eg, around a heel ulcer) requires a highly conformable dressing, such as an extra-thin hydrocolloid. Securing a dressing in a highly moist challenging site (eg, around a sacrococcygeal ulcer) requires a conformable and highly adherent dressing, such as a wafer hydrocolloid.

Hydrogel sheets and nonadhesive forms are useful for securing a wound dressing when the surrounding skin is fragile.

Table 1. Characteristics and Uses of Wound-Dressing Materials (Open Table in a new window)

Category Examples Description Applications
Alginate AlgiSite, Comfeel, Curasorb, Kaltogel, Kaltostat, Sorbsan, Tegagel Alginate dressings are made of seaweed extract contains guluronic and mannuronic acids that provide tensile strength and calcium and sodium alginates, which confer an absorptive capacity. Some can leave fibers in the wound if they are not thoroughly irrigated. These dressings are secured with secondary coverage. These dressings are highly absorbent and useful for wounds have copious exudate. Alginate rope is particularly useful to pack exudative wound cavities or sinus tracts.
Hydrofiber Aquacel, Aquacel-Ag, Versiva An absorptive textile fiber pad, hydrofiber is also available as a ribbon for packing of deep wounds. This material is covered with a secondary dressing. The hydrofiber combines with wound exudate to produce a hydrophilic gel. Aquacel-Ag contains 1.2% ionic silver that has strong antimicrobial properties against many organisms, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci. Hydrofiber absorbent dressings used for exudative wounds.
Debriding agents Hypergel (hypertonic saline gel), Santyl (collagenase), Accuzyme (papain urea) Various products provide some chemical or enzymatic debridement. Debriding agents are useful for necrotic wounds as an adjunct to surgical debridement.
Foam LYOfoam, Spyrosorb, Allevyn Polyurethane foam has absorptive capacity. These dressings are useful for cleaning granulating wounds with minimal exudate.
Hydrocolloid CombiDERM, Comfeel, DuoDerm CGF Extra Thin, Granuflex, Tegasorb Hydrocolloid dressings are made of microgranular suspension of natural or synthetic polymers, such as gelatin or pectin, in an adhesive matrix. The granules change from a semihydrated state to a gel as the wound exudate is absorbed. Hydrocolloid dressings are useful for dry necrotic wounds, wounds with minimal exudate and for clean granulating wounds.
Hydrogel Aquasorb, DuoDerm, Intrasite Gel, Granugel, Normlgel, Nu-Gel, Purilon Gel, KY Jelly Hydrogel dressings are water-based or glycerin-based semipermeable hydrophilic polymers; cooling properties may decrease wound pain. These gels can lose or absorb water depending upon the state of hydration of the wound. They are secured with secondary covering. These dressings are useful for dry, sloughy, necrotic wounds (eschar).
Low-adherence dressing Mepore, Skintact, Release Low-adherence dressings are made of various materials designed to remove easily without damaging underlying skin. These dressings are useful for acute minor wounds, such as skin tears, or as a final dressing for chronic wounds that have nearly healed.
Transparent film OpSite, Skintact, Release, Tegaderm, Bioclusive Transparent films are highly conformable acrylic adhesive films with no absorptive capacity and little hydrating ability. They may be vapor permeable or perforated. These dressings are useful for clean, dry wounds with minimal exudate. They also are used to secure an underlying absorptive material, to protect high-friction areas and areas that are difficult to bandage (eg, heels) and to secure intravenous catheters.

Consider other topical agents

Topically applied platelet-derived growth factors have a modestly beneficial effect in promoting wound healing. Becaplermin gel 0.01% (Regranex), recombinant human platelet-derived growth factor (PDGF) that is produced through genetic engineering, is approved by the US Food and Drug Administration (FDA) to promote healing of diabetic foot ulcers. Regranex is contraindicated in persons with known skin cancers at the site of application. Freeze-dried, platelet-rich plasma showed promise in an animal study.[33]

Collagen comprises a significant fraction of the necrotic soft tissues in chronic wounds. The enzyme collagenase, which is derived form fermentation of Clostridium histolyticum, helps remove nonviable tissue from the surface of wounds. However, collagenase is not a substitute for an initial surgical excision of a grossly necrotic wound.

Other topical agents that have been used for wound treatment are sugar, antacids, and vitamin A&D ointment.

Avoid cytotoxic agents, such as hydrogen peroxide, povidone iodine, acetic acid, and Dakin solution (sodium hypochlorite).

Consider compression therapy

Consider the advisability of compression therapy. Compression is appropriate for ulcers caused or exacerbated by extremity edema. Compression may have to be avoided entirely in the presence of significant arterial inflow compromise.

Use support hose or elastic wraps with approximately 40-60 mm Hg of pressure in the absence of arterial disease and 20-30 mm Hg in the presence or suspicion of mild arterial insufficiency.

Manage pain

Manage wound pain by moistening dressings before removal. Consider using 2% topical lidocaine gel during wound care. (Anecdotal reports describe the use of topical morphine and diamorphine-infused gel for palliation of pressure ulcer pain in patients who are terminally ill,[34] but this use is not FDA approved.)

Treatment of specific types of wounds

Pressure ulcers

Treatment of decubitus ulcers requires prolonged surgical and nursing care.[35, 36, 37, 38] During the extended period of treatment required, the patient remains at risk for the development of new pressure ulcers at other sites.[39, 40, 41] Treatment, particularly indications for support surfaces, is based on appropriate staging of the pressure ulcer.[42, 43]

Milne et al reported the outcome of a long-term acute care hospital's program to reduce the incidence of pressure ulcers.[44] The facility used a failure mode and effects analysis to determine where improvements in care were most needed. The hospital determined that its ulcer prevalence rates, which were believed to be above average, were associated with such problems as "a lack of 1) wound care professionals, 2) methods to consistently document prevention and wound data, and 3) an interdisciplinary wound care team approach." After the hospital addressed these issues, it saw the incidence of facility-acquired pressure ulcers drop from 41% (the baseline figure) to an average of 4.2%, over a 12-month period.

Table 2. Staging Pressure Ulcers (Open Table in a new window)

Stage Definition Appearance Appropriate topical treatment Average healing time (d)
I Nonblanchable erythema of intact skin Pink skin that does not resolve when pressure is relieved; discoloration; warmth; induration DuoDerm q2-3d 14
II Partial-thickness skin loss involving epidermis and/or dermis Cracking, blistering, shallow crater, abrasion Cleanse with saline; DuoDerm/Tegaderm dressing 45
III Full-thickness skin loss into subcutaneous fatty tissues or fascia Distinct ulcer margin; deep crater (in general, 2.075 mm or deeper [the thickness of a nickel]) Debride; irrigate with saline; apply DuoDerm/Tegaderm 90
IV Full-thickness skin loss with extensive tissue involvement of underlying tissues Extensive necrosis; damage to underlying supporting structures, such as muscle, bone, tendon, or joint capsule Surgically debride; irrigate with saline (possibly under pressure); apply advanced topical dressings; consider antibiotics 120
*When the overlying skin is necrotic, the staging cannot be accurate until debridement is performed.

 

Pressure ulcers often require the following steps:

  • Debridement: The ulcer often requires surgical excision, usually down to underlying bone. In the absence of erythema, edema, fluctuance, or drainage, clean dry eschar does not need to be debrided surgically but may be softened and allowed to separate using dressings (eg, colloids, hydrogels) that provide a moist environment to encourage autolysis.
  • Topical wound care: Weeks or months of daily dressing changes are required before the wound begins granulating and appears clean enough for myocutaneous flap closure.
  • Treatment of infection: Debridement is a clean, not sterile, procedure. Frequent debridements maintain superficial colonization at acceptable levels. Swab cultures are often meaningless because they reflect only surface colonization of local infection, which does not require antibiotic treatment. In general, systemic antibiotics are not useful unless signs of progressive infection, such as bacteremia, septicemia, progressive cellulitis, or intractable osteomyelitis, are present.
  • Control of chronic wound contamination: Chronic wound contamination because of fecal incontinence can be a vexing problem in typical bedridden patients, who tend to develop sacral and ischial pressure ulcers. These types of ulcers are depicted in the images below. Initial treatment is dietary management. Foods that thicken the stool include applesauce, bananas, boiled milk, bread, cheese, creamy peanut butter, grits, oat bran, oatmeal, pasta, pretzels, rice, tapioca, and yogurt. In rare cases, fecal diversion by means of colostomy is required.
    Image of advanced sacral pressure ulcer shows the Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.
    Sacral pressure ulcer before and after flap closur Sacral pressure ulcer before and after flap closure.
    Sacral ulcer. Sacral ulcer.
  • Positioning: Patients with pressure ulcers or those at risk for a pressure ulcer should be turned in bed every 2 hours. Patients who are immobile should not be positioned directly on the trochanters; foam wedges and pillows are useful to pad pressure points, to prevent direct contact between bony prominences, and to raise their heels off the bed surface. Pressure ulcers can also be induced by shear forces if patients slide down the bed; therefore, try to use the lowest degree of elevation of the head of the bed that the patient's medical conditions allow.
  • Use of support surfaces

Support surfaces are further discussed as follows:

  • Federal regulations (Medicare Bulletin 405) dictate that patients with bedsores or those who are at risk for bedsores must be placed on an appropriate support surface.
  • Federally mandated standards of care dictate what support surfaces are allowable and provide for both civil and criminal penalties for health care entities that fail to comply.
  • Proper prevention and management of pressure ulcers in health care facilities is mandated by federal regulations (Ch IV § 483.25 (c)(1)&(2), 10/1/95), which state, "Based on the comprehensive assessment of a resident, the facility must ensure that (1) a resident who enters the facility without pressure sores does not develop pressure sores unless the individual's clinical condition demonstrates that they were unavoidable, and (2) a resident having pressure sores receives necessary treatment and services to promote healing, prevent infection and prevent new sores from developing."
  • A class I support surface is a simple pressure pad device that is required as follows:
    • For patients who cannot independently change their body position to effectively alleviate pressure
    • For patients who have any stage of pressure ulcer on the trunk or pelvis, plus impaired nutritional status, fecal or urinary incontinence, altered sensory perception, or compromised circulatory status
  • A class II support surface is a pressure-relieving device that reduces pressure over bony prominences to less than 32 mm Hg and that does so for a sustained period. A class II support surface is required as follows:
    • For patients who have multiple pressure ulcers on the trunk or pelvis that has not improved despite a comprehensive treatment, including a class I support surface for a stage II, III, or IV pressure ulcer for at least 1 month
    • For patients who have large or multiple stage III or IV pressure ulcers on the trunk or pelvis
    • For patients who have had a myocutaneous flap or skin graft procedure for a pressure ulcer on the trunk or pelvis within the past 60 days and have been on a class II or III support surface immediately before a recent discharge from a hospital or nursing facility within the past 30 days
  • A class III support surface is an advanced pressure-relieving device. A class III support surface, that is, an air-fluidized bed, may be used only for failure of a comprehensive conservative treatment plan after 30 days. (Note that an air-fluidized bed is contraindicated for any patient with associated severe pulmonary compromise because the absence of firm back support makes coughing ineffective, and the dry air thickens pulmonary secretions.) Such a conservative treatment program includes the following:
    • Education of the patient and the caregiver. A patient information page regarding pressure ulcers is available.[37]
    • Assessment by a licensed health care practitioner, at least weekly
    • Appropriate turning and positioning
    • Use of a class II support surface
    • Appropriate wound care
    • Appropriate management of incontinence
    • Appropriate nutritional management

Table 3. Support Surfaces (Open Table in a new window)

Class Type Principle Examples
I Simple Pressure-relieving pad or mat 3- to 5-inch foam mattress, gel overlay, egg-crate mattress
II Advanced Powered air* overlay for mattress with low air loss feature; nonpowered advanced pressure-reducing mattress replacement or powered air* floatation bed with or without low air loss feature Roho dry floatation mattress system, Pegasus Renaissance mattress
III Air fluidized Floatation by filtered air* flow pumped through porcelain beads Clinitron bed
*Long-term use of powered air devices is relatively contraindicated for patients with chronic obstructive lung disease, such as chronic bronchitis, emphysema, and asthma.

Additional protection is described as follows:

  • Proper off-loading for ischial ulcers: Sacral ulcers usually result from prolonged supine bed rest or from shearing forces, particularly because of the patient sliding down the bed when the head is elevated. On the other hand, ischial ulcers often result from prolonged sitting either in the head-up position in the bed or in a wheelchair. Hence, off-loading for ischial ulcer prevention and treatment requires support surfaces for sitting as well as mattress support surfaces. Sitting time must also be limited.
  • Heel protection: Pressure ulcers involving the heel regions commonly occur in patients who are bedridden, even if they are immobilized for just a few days, such as after hip surgery. A heel pressure ulcer is illustrated in the image below. Prevention and treatment of heel pressure ulcers requires off-loading. Off-loading devices are usually selected based on availability and include the following:
    Heel pressure ulcer. Heel pressure ulcer.
    See the list below:
    • Booties are simple pressure pads that surround the heel with polyester fibers, iconized fibers, or foam material.
    • Boots are made from a firm outer shell lined with pressure-relief padding. They can also provide positioning capability to help treat contractures and foot drop.
    • Pillows made from polyester and sheepskin fleece or special rubber or plastic interpose a conformable soft overlay between the heel and the mattress.
    • Suspension devices isolate the heel and transfer the weight to the lower leg. These devices also have positioning capabilities that are useful in treating contractures and foot drop.
    • Inflatable devices made from plastic sheets surround the heel and adjacent tissues.

Venous ulcers

Treatment of venous ulcers includes compression therapy, providing a moist wound environment and debridement of necrotic tissue.[45, 46] Most venous ulcers heal with these measures alone. Some require split-thickness skin grafting or application of bioengineered skin (eg, Apligraf, Dermagraft).[47] Pentoxifylline (Trental) and horse chestnut seed (available in supermarkets and health food specialty stores) have been shown to expedite healing of venous stasis ulcers. In some cases, compression therapy is inadequate to maintain healing of venous ulcers, and surgical vein stripping or ligation of venous perforators may be helpful.

A study of 98 limbs with active chronic venous ulcers revealed that all but one had venous reflux; the study also suggested that most of these patients would benefit from surgical or endovascular intervention.[48] Other studies suggested a more modest level of benefit from corrective venous surgery.[49]

Table 4. Compression Bandages for Venous Ulcers* (Open Table in a new window)

Type Description Examples
Single layer Single-layer simple tubular woven nylon/elastic bandages may be imprinted with rectangles that stretch to squares when appropriate wrapping tension (30-40 mm Hg) is applied. ACE bandage, Comperm (Conco Medical), Setopress (Seton Healthcare Group)
Three layer The layers include a padding absorption layer, a compression bandage layer, and a cohesive compression bandage. Bandages may be left in place for up to 1 week depending on wound exudate. Dyna-Flex (Johnson & Johnson)
Four layer The layers include a nonwoven wound contact layer that is permeable to wound exudate and 4 overlying bandages. Bandages may be left in place for up to 1 week depending on exudate volume. Profore (Smith & Nephew)
Impregnated wrap The porous flexible occlusive dressing is composed of stretchable gauze and a nonhardening zinc oxide paste. Unna boot (ConvaTec)
*Compression wraps are contraindicated in severe arterial compromise. Some of these products are contraindicated in patients who are allergic to latex.

Diabetic foot ulcers

The treatment of diabetic foot ulcers requires the following: (1) appropriate therapeutic footwear, (2) daily saline or similar dressings to provide a moist wound environment, (3) debridement when necessary, (4) antibiotic therapy if osteomyelitis is present, (5) optimal control of blood glucose, and (6) evaluation and correction of peripheral arterial insufficiency.[50, 51, 52, 53, 54] See also Diabetic Ulcers.

Wound coverage with cultured human cells or heterogeneic dressings and/or grafts, application of recombinant growth factors, negative pressure wound therapy, and hyperbaric oxygen treatments may also be beneficial.[18, 55, 56, 57, 58]

Lymphedema

Although lymphedema is not typically a cause of ulceration, ulcers on the extremities may fail to heal because of untreated lymphedema. Nocturnal leg elevation and elastic wraps or support hose are appropriate adjuncts to the treatment of the recalcitrant wound in an edematous extremity. For advanced and nonresponsive lymphedema, complex decongestive physiotherapy is a useful treatment option.

Next

Surgical Therapy

Methods are available to expedite healing of the clean wound. After a wound is in a steady clean state, a decision must be made about allowing it to heal by natural processes or expediting healing with a surgical procedure. Clinical experience and observation of the healing progress in the individual case dictate the appropriate treatment. Surgical options include skin grafting, application of bioengineered skin substitutes, and use of flap closures.[59]

Skin grafting

Autologous skin grafting is the criterion standard for viable coverage of partial-thickness wounds. The graft can be harvested with the patient under local anesthesia in an outpatient procedure. Meshing the graft allows wider coverage and promotes drainage of serum and blood.

Cadaveric allografting

A cadaveric skin allograft is a useful covering for relatively deep wounds after surgical excision when the wound bed does not appear appropriate for application of an autologous skin graft. The allograft is only a temporary solution

Application of bioengineered skin substitutes [53, 60, 61]

AlloDerm (LifeCell, Inc) is tissue from cadavers that is used create an acellular dermal matrix that has been freeze-dried. The collagen framework acts as a strengthening scaffold for normal tissue remodeling. Since it contains no cells or cellular components, it does not cause rejection or irritation. It can often be used for burns or full-thickness wounds.

Apligraf (Organogenesis; Novartis) is a bilayered skin substitute produced by combining bovine collagen and living cells derived from tissue-cultured human infant foreskins. One study of diabetic foot ulcers demonstrated 12-week healing rates of 39% for patients who received only standard wound care versus 56% for those who were treated by application of an Apligraf after a period of standard wound care.

Dermagraft (Smith & Nephew, Inc) is human fibroblast-derived dermal substitute manufactured by seeding dermal fibroblasts onto a 3-dimensional bioabsorbable scaffold. It has been marketed for use in the treatment of diabetic foot ulcers, venous ulcers, and pressure sores. A clinical trial showed improved healing rates in diabetic foot ulcers.

Integra (Integra Lifesciences Corp) is a dual-layered membrane system with a porous matrix that cross-links bovine tendon collagen and glycosaminoglycans. The epidermal substitute layer is made of a thin polysilicone layer that acts to control moisture. It can be used for deep partial-thickness and full-thickness burns owing to the good barrier function of the system, but operative removal of the silicone layer is required.

Oasis (Healthpoint, Ltd) is a xenogeneic acellular collagen matrix derived from porcine small intestinal submucosa in such a way that an extracellular matrix and natural growth factors remain intact. This provides a scaffold for inducing wound healing.[62] Do not use this in patients with allergies to porcine materials.

EZ Derm (Brennan Medical, Inc) is a porcine derived xenograft of collagen that has been chemically cross-linked with aldehyde to provide strength and durability. It can be used for venous stasis ulcers, diabetic ulcers, pressure ulcers, and partial-thickness burns. However, it does have the capacity to cause a potential immune response or disease transmission.

Cultured epithelial autograft (Epicel; Genzyme Tissue Repair, Cambridge, Mass) is an epidermal replacement that is grown in a tissue culture from a skin biopsy taken from the recipient and is cocultured with mouse cells. Preparation of the graft requires about 2 weeks of culture time.

Use of flap closures

Delayed primary closure of a chronic wound, as shown below, requires well-vascularized clean tissues and tension-free apposition. This usually requires undermining and mobilization of adjacent tissue planes by creating skin flaps or myocutaneous flaps.[63]

Image of advanced sacral pressure ulcer shows the Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.
Sacral pressure ulcer before and after flap closur Sacral pressure ulcer before and after flap closure.
Previous
Next

Complications

Complications of nonhealing wounds include the following:

Previous
Next

Outcome and Prognosis

The prognosis for healing of chronic wounds varies with the etiology of the wound and the general health status of the patient.

Previous
Next

Future and Controversies

The aging of the population and advances in biotechnology continue to drive the wound care industry, estimated at $10 billion globally. Besides the always-improving synthetic dressing materials, newer technologies in wound treatment include the xenogeneic tissue scaffold, bilayered human dermal substitutes, recombinant growth factors, endoscopic subfascial ligation of venous perforators, and endovascular arterial repair techniques. The use of hyperbaric oxygen therapy and electrical stimulation remain controversial.

Recent systematic reviews, although not conclusive, suggest that different debridement methods, whether they be chemical, surgical or autolytic, all result in similar results.[64] Other reviews suggest that there may be a role for negative-pressure wound therapy and hyperbaric oxygen in the management of chronic wounds and that there probably is no role for electromagnetic therapy or low-frequency ultrasound therapy based on current best evidence.[65, 66, 67, 68]

Previous
 
Contributor Information and Disclosures
Author

Brian J Daley, MD, MBA, FACS, FCCP, CNSC Professor and Program Director, Department of Surgery, Chief, Division of Trauma and Critical Care, University of Tennessee Health Science Center College of Medicine

Brian J Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies: American Association for the Surgery of Trauma, Eastern Association for the Surgery of Trauma, Southern Surgical Association, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, Tennessee Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Sneha Bhat, MD Resident Physician, Department of Surgery, University of Tennessee Health Science Center College of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Amy L Friedman, MD Professor of Surgery, Director of Transplantation, State University of New York Upstate Medical University College of Medicine, Syracuse

Amy L Friedman, MD is a member of the following medical societies: Association for Academic Surgery, International College of Surgeons, New York Academy of Sciences, Pennsylvania Medical Society, Philadelphia County Medical Society, Society of Critical Care Medicine, Association of Women Surgeons, International Liver Transplantation Society, Transplantation Society, American College of Surgeons, American Medical Association, American Medical Womens Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, American Society of Transplantation

Disclosure: Nothing to disclose.

Chief Editor

Zubin J Panthaki, MD, CM, FACS, FRCSC Professor of Clinical Surgery, Department of Surgery, Division of Plastic Surgery, Associate Professor Clinical Orthopedics, Department of Orthopedics, University of Miami, Leonard M Miller School of Medicine; Chief of Hand Surgery, University of Miami Hospital; Chief of Hand Surgery, Chief of Plastic Surgery, Miami Veterans Affairs Hospital

Zubin J Panthaki, MD, CM, FACS, FRCSC is a member of the following medical societies: American College of Surgeons, American Society for Surgery of the Hand, American Society of Plastic Surgeons, Canadian Society of Plastic Surgeons, American Council of Academic Plastic Surgeons, Miami Society of Plastic Surgeons, Medical Council of Canada, Canadian Military Engineers Association

Disclosure: Nothing to disclose.

Acknowledgements

Richard M Stillman, MD, FACS† Honorary Medical Staff, Northwest Medical Center; Former Chief of Staff and Medical Director, Wound Healing Center, Department of Surgery, Northwest Medical Center

References
  1. Cuddigan J, Berlowitz DR, Ayello EA. Pressure ulcers in America: prevalence, incidence, and implications for the future. An executive summary of the National Pressure Ulcer Advisory Panel monograph. Adv Skin Wound Care. 2001 Jul-Aug. 14 (4):208-15. [Medline]. [Full Text].

  2. Frankel H, Sperry J, Kaplan L. Risk factors for pressure ulcer development in a best practice surgical intensive care unit. Am Surg. 2007 Dec. 73(12):1215-7. [Medline].

  3. Campbell KE, Woodbury MG, Houghton PE. Heel pressure ulcers in orthopedic patients: a prospective study of incidence and risk factors in an acute care hospital. Ostomy Wound Manage. 2010 Feb. 56(2):44-54. [Medline].

  4. Horn SD, Bender SA, Ferguson ML, Smout RJ, Bergstrom N, Taler G, et al. The National Pressure Ulcer Long-Term Care Study: pressure ulcer development in long-term care residents. J Am Geriatr Soc. 2004 Mar. 52(3):359-67. [Medline].

  5. Bergstrom N, Horn SD, Smout RJ, Bender SA, Ferguson ML, Taler G, et al. The National Pressure Ulcer Long-Term Care Study: outcomes of pressure ulcer treatments in long-term care. J Am Geriatr Soc. 2005 Oct. 53(10):1721-9. [Medline].

  6. Bergstrom N. Litigation or redesign: improving pressure ulcer prevention. J Am Geriatr Soc. 2005 Sep. 53(9):1627-9. [Medline].

  7. Howard DL, Taylor YJ. Racial and gender differences in pressure ulcer development among nursing home residents in the Southeastern United States. J Women Aging. 2009 Oct. 21(4):266-78. [Medline].

  8. Horn SD, Sharkey SS, Hudak S, et al. Pressure ulcer prevention in long-term-care facilities: a pilot study implementing standardized nurse aide documentation and feedback reports. Adv Skin Wound Care. 2010 Mar. 23(3):120-31. [Medline].

  9. Abbade LP, Lastória S. Venous ulcer: epidemiology, physiopathology, diagnosis and treatment. Int J Dermatol. 2005 Jun. 44(6):449-56. [Medline].

  10. Reiber GE, Boyko EJ, Smith DG. Lower extremity foot ulcers and amputations in diabetes. Harris MI, ed. Diabetes in America. 2nd ed. Washington, DC: National Institute of Diabetes and Digestive and Kidney Diseases--National Institutes of Health; 1995.

  11. Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA. 2005 Jan 12. 293(2):217-28. [Medline].

  12. Chraibi H, Dereure O, Téot L, Guillot B. The diagnosis and treatment of carcinomas occurring at the sites of chronic pressure ulcers. J Wound Care. 2004 Nov. 13(10):447-8. [Medline].

  13. Mellemkjaer L, Holmich LR, Gridley G, Rabkin C, Olsen JH. Risks for skin and other cancers up to 25 years after burn injuries. Epidemiology. 2006 Nov. 17(6):668-73. [Medline].

  14. Alam M, Grossman ME, Schneiderman PI, Blume RS, Benvenisty AI. Surgical management of pyoderma gangrenosum: case report and review. Dermatol Surg. 2000 Nov. 26(11):1063-6. [Medline].

  15. Ehling A, Karrer S, Klebl F, Schäffler A, Müller-Ladner U. Therapeutic management of pyoderma gangrenosum. Arthritis Rheum. 2004 Oct. 50(10):3076-84. [Medline].

  16. Kang AS, McCarthy JT, Rowland C, Farley DR, van Heerden JA. Is calciphylaxis best treated surgically or medically?. Surgery. 2000 Dec. 128(6):967-71;discussion 971-2. [Medline].

  17. Ledbetter LS, Khoshnevis MR, Hsu S. Calciphylaxis. Cutis. 2000 Jul. 66(1):49-51. [Medline].

  18. Arseculeratne G, Evans AT, Morley SM. Calciphylaxis--a topical overview. J Eur Acad Dermatol Venereol. 2006 May. 20(5):493-502. [Medline].

  19. Bello YM, Phillips TJ. Necrobiosis lipoidica. Indolent plaques may signal diabetes. Postgrad Med. 2001 Mar. 109(3):93-4. [Medline].

  20. Rachline A, Lariven S, Descamps V, Grossin M, Bouvet E. Leucocytoclastic vasculitis and indinavir. Br J Dermatol. 2000 Nov. 143(5):1112-3. [Medline].

  21. Chan YC, Valenti D, Mansfield AO, Stansby G. Warfarin induced skin necrosis. Br J Surg. 2000 Mar. 87(3):266-72. [Medline].

  22. Broughton G 2nd, Janis JE, Attinger CE. Wound healing: an overview. Plast Reconstr Surg. 2006 Jun. 117(7 Suppl):1e-S-32e-S. [Medline].

  23. Jaul E. Assessment and management of pressure ulcers in the elderly: current strategies. Drugs Aging. 2010 Apr 1. 27(4):311-25. [Medline].

  24. Sarabahi S. Recent advances in topical wound care. Indian J Plast Surg. 2012 May. 45(2):379-87. [Medline]. [Full Text].

  25. Mechanick JI. Practical aspects of nutritional support for wound-healing patients. Am J Surg. 2004 Jul. 188(1A Suppl):52-6. [Medline].

  26. O'Meara SM, Cullum NA, Majid M, Sheldon TA. Systematic review of antimicrobial agents used for chronic wounds. Br J Surg. 2001 Jan. 88(1):4-21. [Medline].

  27. Bowler PG, Jones SA, Davies BJ, Coyle E. Infection control properties of some wound dressings. J Wound Care. 1999 Nov. 8(10):499-502. [Medline].

  28. Driver VR. Silver dressings in clinical practice. Ostomy Wound Manage. 2004 Sep. 50(9A Suppl):11S-15S. [Medline].

  29. Rayman G, Rayman A, Baker NR, Jurgeviciene N, Dargis V, Sulcaite R, et al. Sustained silver-releasing dressing in the treatment of diabetic foot ulcers. Br J Nurs. 2005 Jan 27-Feb 9. 14(2):109-14. [Medline].

  30. Leaper DJ. Silver dressings: their role in wound management. Int Wound J. 2006 Dec. 3(4):282-94. [Medline].

  31. Beam JW. Topical silver for infected wounds. J Athl Train. 2009 Sep-Oct. 44(5):531-3. [Medline]. [Full Text].

  32. Walker M, Parsons D. The biological fate of silver ions following the use of silver-containing wound care products - a review. Int Wound J. 2012 Nov 22. [Medline].

  33. Pietramaggiori G, Kaipainen A, Czeczuga JM, Wagner CT, Orgill DP. Freeze-dried platelet-rich plasma shows beneficial healing properties in chronic wounds. Wound Repair Regen. 2006 Sep-Oct. 14(5):573-80. [Medline].

  34. Ashfield T. The use of topical opioids to relieve pressure ulcer pain. Nurs Stand. 2005 Jul 20-26. 19(45):90-2. [Medline].

  35. Bergstrom N, Bennett MA, Carlson CE. Treatment of pressure ulcers. Clinical Practice Guideline, No. 15. Rockville, Md: US Department of Health and Human Services; 1994.

  36. Pompeo M, Baxter C. Sacral and ischial pressure ulcers: evaluation, treatment, and differentiation. Ostomy Wound Manage. 2000 Jan. 46(1):18-23. [Medline].

  37. Zeller JL, Lynm C, Glass RM. JAMA patient page. Pressure ulcers. JAMA. 2006 Aug 23. 296(8):1020. [Medline].

  38. Whitney J, Phillips L, Aslam R, Barbul A, Gottrup F, Gould L. Guidelines for the treatment of pressure ulcers. Wound Repair Regen. 2006 Nov-Dec. 14(6):663-79. [Medline].

  39. Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic review. JAMA. 2006 Aug 23. 296(8):974-84. [Medline].

  40. Wilborn D, Halfens R, Dassen T. Pressure ulcer: Prevention protocols and prevalence. J Eval Clin Pract. 2006 Dec. 12(6):630-8. [Medline].

  41. Halfens RJ. Risk assessment scales for pressure ulcers: a theoretical, methodological, and clinical perspective. Ostomy Wound Manage. 2000 Aug. 46(8):36-40, 42-4. [Medline].

  42. Dharmarajan TS, Ahmed S. The growing problem of pressure ulcers. Evaluation and management for an aging population. Postgrad Med. 2003 May. 113(5):77-8, 81-4, 88-90. [Medline].

  43. Sato M, Sanada H, Konya C, Sugama J, Nakagami G. Prognosis of stage I pressure ulcers and related factors. Int Wound J. 2006 Dec. 3(4):355-62. [Medline].

  44. Milne CT, Trigilia D, Houle TL, et al. Reducing pressure ulcer prevalence rates in the long-term acute care setting. Ostomy Wound Manage. 2009 Apr. 55(4):50-9. [Medline].

  45. Brem H, Kirsner RS, Falanga V. Protocol for the successful treatment of venous ulcers. Am J Surg. 2004 Jul. 188(1A Suppl):1-8. [Medline].

  46. Olson JM, Raugi GJ, Nguyen VQ, et al. Guideline concordant venous ulcer care predicts healing in a tertiary care Veterans Affairs Medical Center. Wound Repair Regen. 2009 Sep-Oct. 17(5):666-70. [Medline].

  47. Cavorsi J, Vicari F, Wirthlin DJ, Ennis W, Kirsner R, O'Connell SM, et al. Best-practice algorithms for the use of a bilayered living cell therapy (Apligraf) in the treatment of lower-extremity ulcers. Wound Repair Regen. 2006 Mar-Apr. 14(2):102-9. [Medline].

  48. Danielsson G, Arfvidsson B, Eklof B, Kistner RL, Masuda EM, Satoc DT. Reflux from thigh to calf, the major pathology in chronic venous ulcer disease: surgery indicated in the majority of patients. Vasc Endovascular Surg. 2004 May-Jun. 38(3):209-19. [Medline].

  49. Vowden KR, Vowden P. Preventing venous ulcer recurrence: a review. Int Wound J. 2006 Mar. 3(1):11-21. [Medline].

  50. Brem H, Sheehan P, Rosenberg HJ, Schneider JS, Boulton AJ. Evidence-based protocol for diabetic foot ulcers. Plast Reconstr Surg. 2006 Jun. 117(7 Suppl):193S-209S; discussion 210S-211S. [Medline].

  51. Eldor R, Raz I, Ben Yehuda A, Boulton AJ. New and experimental approaches to treatment of diabetic foot ulcers: a comprehensive review of emerging treatment strategies. Diabet Med. 2004 Nov. 21(11):1161-73. [Medline].

  52. Frykberg RG, Armstrong DG, Giurini J, Edwards A, Kravette M, Kravitz S, et al. Diabetic foot disorders: a clinical practice guideline. American College of Foot and Ankle Surgeons. J Foot Ankle Surg. 2000. 39(5 Suppl):S1-60. [Medline].

  53. McGuigan FX. Skin substitutes as alternatives to autografting in a wartime trauma setting. J Am Acad Orthop Surg. 2006 Oct. 14(10):S87-9.

  54. Dinh TL, Veves A. Treatment of diabetic ulcers. Dermatol Ther. 2006 Nov-Dec. 19(6):348-55. [Medline].

  55. Armstrong DG, Lavery LA. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomised controlled trial. Lancet. 2005 Nov 12. 366(9498):1704-10. [Medline].

  56. Akbari A, Moodi H, Ghiasi F, Sagheb HM, Rashidi H. Effects of vacuum-compression therapy on healing of diabetic foot ulcers: Randomized controlled trial. J Rehabil Res Dev. 2007. 44(5):631-6. [Medline].

  57. Roeckl-Wiedmann I, Bennett M, Kranke P. Systematic review of hyperbaric oxygen in the management of chronic wounds. Br J Surg. 2005 Jan. 92(1):24-32. [Medline].

  58. Yao M, Fabbi M, Hayashi H, Park N, Attala K, Gu G, et al. A retrospective cohort study evaluating efficacy in high-risk patients with chronic lower extremity ulcers treated with negative pressure wound therapy. Int Wound J. 2012 Nov 19. [Medline].

  59. Sørensen JL, Jørgensen B, Gottrup F. Surgical treatment of pressure ulcers. Am J Surg. 2004 Jul. 188(1A Suppl):42-51. [Medline].

  60. Bello YM, Falabella AF, Eaglstein WH. Tissue-engineered skin. Current status in wound healing. Am J Clin Dermatol. 2001. 2(5):305-13. [Medline].

  61. Falanga VJ. Tissue engineering in wound repair. Adv Skin Wound Care. 2000 May-Jun. 13(2 Suppl):15-9. [Medline].

  62. Srivastava A, Jennings LJ, Hanumadass M, Sethi S, DeSagun E, et al. Xenogeneic acellular dermal matrix as a dermal substitute in rats. J Burn Care Rehabil. 1999 Sep-Oct. 20(5):382-90. [Medline].

  63. Borgognone A, Anniboletti T, De Vita F, et al. Ischiatic pressure sores: our experience in coupling a split-muscle flap and a fasciocutaneous flap in a 'criss-cross' way. Spinal Cord. 2010 Mar 23. [Medline].

  64. Gethin G, Cowman S, Kolbach DN. Debridement for venous leg ulcers. Cochrane Database Syst Rev. 2015 Sep 14. 9:CD008599. [Medline].

  65. Kranke P, Bennett MH, Martyn-St James M, Schnabel A, Debus SE, Weibel S. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev. 2015 Jun 24. 6:CD004123. [Medline].

  66. Aziz Z, Cullum N. Electromagnetic therapy for treating venous leg ulcers. Cochrane Database Syst Rev. 2015 Jul 2. 7:CD002933. [Medline].

  67. Dumville JC, Land L, Evans D, Peinemann F. Negative pressure wound therapy for treating leg ulcers. Cochrane Database Syst Rev. 2015 Jul 14. 7:CD011354. [Medline].

  68. Cullum NA, Al-Kurdi D, Bell-Syer SE. Therapeutic ultrasound for venous leg ulcers. Cochrane Database Syst Rev. 2010 Jun 16. CD001180. [Medline].

 
Previous
Next
 
Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.
Sacral pressure ulcer before and after flap closure.
Chronic ulcer of medial aspect of right leg due to pyoderma gangrenosum.
Pressure ulcers of the lateral aspect of the right foot.
Basal cell cancer manifesting as a chronic leg ulcer.
Heel pressure ulcer.
Sacral ulcer.
Table 1. Characteristics and Uses of Wound-Dressing Materials
Category Examples Description Applications
Alginate AlgiSite, Comfeel, Curasorb, Kaltogel, Kaltostat, Sorbsan, Tegagel Alginate dressings are made of seaweed extract contains guluronic and mannuronic acids that provide tensile strength and calcium and sodium alginates, which confer an absorptive capacity. Some can leave fibers in the wound if they are not thoroughly irrigated. These dressings are secured with secondary coverage. These dressings are highly absorbent and useful for wounds have copious exudate. Alginate rope is particularly useful to pack exudative wound cavities or sinus tracts.
Hydrofiber Aquacel, Aquacel-Ag, Versiva An absorptive textile fiber pad, hydrofiber is also available as a ribbon for packing of deep wounds. This material is covered with a secondary dressing. The hydrofiber combines with wound exudate to produce a hydrophilic gel. Aquacel-Ag contains 1.2% ionic silver that has strong antimicrobial properties against many organisms, including methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci. Hydrofiber absorbent dressings used for exudative wounds.
Debriding agents Hypergel (hypertonic saline gel), Santyl (collagenase), Accuzyme (papain urea) Various products provide some chemical or enzymatic debridement. Debriding agents are useful for necrotic wounds as an adjunct to surgical debridement.
Foam LYOfoam, Spyrosorb, Allevyn Polyurethane foam has absorptive capacity. These dressings are useful for cleaning granulating wounds with minimal exudate.
Hydrocolloid CombiDERM, Comfeel, DuoDerm CGF Extra Thin, Granuflex, Tegasorb Hydrocolloid dressings are made of microgranular suspension of natural or synthetic polymers, such as gelatin or pectin, in an adhesive matrix. The granules change from a semihydrated state to a gel as the wound exudate is absorbed. Hydrocolloid dressings are useful for dry necrotic wounds, wounds with minimal exudate and for clean granulating wounds.
Hydrogel Aquasorb, DuoDerm, Intrasite Gel, Granugel, Normlgel, Nu-Gel, Purilon Gel, KY Jelly Hydrogel dressings are water-based or glycerin-based semipermeable hydrophilic polymers; cooling properties may decrease wound pain. These gels can lose or absorb water depending upon the state of hydration of the wound. They are secured with secondary covering. These dressings are useful for dry, sloughy, necrotic wounds (eschar).
Low-adherence dressing Mepore, Skintact, Release Low-adherence dressings are made of various materials designed to remove easily without damaging underlying skin. These dressings are useful for acute minor wounds, such as skin tears, or as a final dressing for chronic wounds that have nearly healed.
Transparent film OpSite, Skintact, Release, Tegaderm, Bioclusive Transparent films are highly conformable acrylic adhesive films with no absorptive capacity and little hydrating ability. They may be vapor permeable or perforated. These dressings are useful for clean, dry wounds with minimal exudate. They also are used to secure an underlying absorptive material, to protect high-friction areas and areas that are difficult to bandage (eg, heels) and to secure intravenous catheters.
Table 2. Staging Pressure Ulcers
Stage Definition Appearance Appropriate topical treatment Average healing time (d)
I Nonblanchable erythema of intact skin Pink skin that does not resolve when pressure is relieved; discoloration; warmth; induration DuoDerm q2-3d 14
II Partial-thickness skin loss involving epidermis and/or dermis Cracking, blistering, shallow crater, abrasion Cleanse with saline; DuoDerm/Tegaderm dressing 45
III Full-thickness skin loss into subcutaneous fatty tissues or fascia Distinct ulcer margin; deep crater (in general, 2.075 mm or deeper [the thickness of a nickel]) Debride; irrigate with saline; apply DuoDerm/Tegaderm 90
IV Full-thickness skin loss with extensive tissue involvement of underlying tissues Extensive necrosis; damage to underlying supporting structures, such as muscle, bone, tendon, or joint capsule Surgically debride; irrigate with saline (possibly under pressure); apply advanced topical dressings; consider antibiotics 120
*When the overlying skin is necrotic, the staging cannot be accurate until debridement is performed.
Table 3. Support Surfaces
Class Type Principle Examples
I Simple Pressure-relieving pad or mat 3- to 5-inch foam mattress, gel overlay, egg-crate mattress
II Advanced Powered air* overlay for mattress with low air loss feature; nonpowered advanced pressure-reducing mattress replacement or powered air* floatation bed with or without low air loss feature Roho dry floatation mattress system, Pegasus Renaissance mattress
III Air fluidized Floatation by filtered air* flow pumped through porcelain beads Clinitron bed
*Long-term use of powered air devices is relatively contraindicated for patients with chronic obstructive lung disease, such as chronic bronchitis, emphysema, and asthma.
Table 4. Compression Bandages for Venous Ulcers*
Type Description Examples
Single layer Single-layer simple tubular woven nylon/elastic bandages may be imprinted with rectangles that stretch to squares when appropriate wrapping tension (30-40 mm Hg) is applied. ACE bandage, Comperm (Conco Medical), Setopress (Seton Healthcare Group)
Three layer The layers include a padding absorption layer, a compression bandage layer, and a cohesive compression bandage. Bandages may be left in place for up to 1 week depending on wound exudate. Dyna-Flex (Johnson & Johnson)
Four layer The layers include a nonwoven wound contact layer that is permeable to wound exudate and 4 overlying bandages. Bandages may be left in place for up to 1 week depending on exudate volume. Profore (Smith & Nephew)
Impregnated wrap The porous flexible occlusive dressing is composed of stretchable gauze and a nonhardening zinc oxide paste. Unna boot (ConvaTec)
*Compression wraps are contraindicated in severe arterial compromise. Some of these products are contraindicated in patients who are allergic to latex.
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.