Disclosure
This article discusses the management of chronic wounds. This topic is naturally diverse and far-reaching. Wound care in general and in terms of specific etiologies is considered. Frequency: Pressure ulcers occur in approximately 9% of hospitalized patients, usually during the first 2 weeks of hospitalization, and in approximately one fourth of nursing home residents. The yearly risk of pressure ulceration in patients with neurologic impairment is 5-8%, with a lifetime risk of approximately 85% and a mortality rate of 8%. The treatment of pressure ulcers in the United States is estimated to cost more than $1 billion annually. The presence of a pressure ulcer increases a nurse's workload by 50% for the patient and adds approximately $20,000 to the hospital bill. The incidence of venous ulcers in the United States is approximately 600,000 cases annually. The recurrence rate is up to 90%. According to the National Institute of Diabetes and Digestive and Kidney Diseases, an estimated 18 million Americans (6.3% of the population) are known to have diabetes, and millions more are considered to be at risk. Of those at risk, diabetes is undiagnosed in 5.2 million. Diabetic foot lesions are responsible for more hospitalizations than any other complication of diabetes. Among patients with diabetes, 15% will develop a foot ulcer, and 12-24% of those with a foot ulcer will require amputation. Indeed, diabetes is the leading cause of nontraumatic lower-extremity amputations in the United States, accounting for 60% of these amputations. Every year approximately 5% of persons with diabetes develop foot ulcers, and 1% require amputation. Diabetic peripheral neuropathy confers the greatest risk of foot ulceration; microvascular disease and suboptimal glycemic control contribute. Even with successful treatment resulting in ulcer healing, the recurrence rate in that patient population is 66% and the amputation rate rises to 12%. For excellent patient education resources, visit eMedicine's Diabetes Center. Also, see eMedicine's patient education article Diabetic Foot Care. Etiology: In general, factors that adversely affect wound healing can be remembered by using the mnemonic device DIDN'T HEAL, as follows:
Specific etiologiesArterial insufficiency See Infrainguinal Occlusive Disease. Venous insufficiency Patients with varicose veins or nonfunctional venous valves after deep vein thrombosis develop ambulatory venous hypertension, ie, distal venous pressure remains elevated despite ambulation. This constant venous hypertension seems to cause white cell and fibrin buildup, which impairs capillary blood flow or traps growth factors. Macromolecules pass into the dermis and eventually cause the hemosiderin deposition and brawny induration in the distal leg (gaiter area) characteristic of chronic venous insufficiency. Lymphedema Although not typically a cause of ulceration, extremity ulcers may fail to heal because of untreated lymphedema. Nocturnal leg elevation and elastic wraps or support hose are appropriate adjuncts to the treatment of recalcitrant wounds in edematous extremities. For advanced and nonresponsive lymphedema, complex decongestive physiotherapy is a useful treatment option. Neuropathy Sensory neuropathy involving the feet may lead to unrecognized episodes of trauma caused by ill-fitting shoes. This is compounded by motor neuropathy causing intrinsic muscle weakness and spaying of the foot on weight bearing. The result is a convex foot with a rocker-bottom appearance. Multiple fractures go unnoticed, until bone and joint deformities become marked. This is termed a Charcot foot (ie, neuropathic osteoarthropathy) and is observed most commonly in people with diabetes mellitus, affecting approximately 2% of persons with diabetes. Pressure (decubitus) ulcers Pressure (decubitus) ulcers occur because of prolonged ischemia-producing external pressure, usually to a soft tissue region overlying a bony prominence. Tissue ischemia results when external pressure exceeds capillary closing pressure (ie, 25-32 mm Hg in healthy individuals), the minimum pressure that causes collapse of the capillary when applied to a capillary bed. Shearing forces, exposure to constant moisture, and heat buildup also are major contributing factors. For example, the stratum corneum, the outer layer of skin, becomes 25 times more fragile at a relative humidity of 100% than at a relative humidity of 25% and becomes 4 times more fragile at 95°F (35°C) than at 86°F (30°C). Neoplasms Neoplasms strongly suggest malignancy in any chronic nonhealing wound, particularly if the wound appeared to occur spontaneously. Basal cell carcinoma appears smooth, pearly, and elevated above the skin surface, whereas squamous cell cancer is often somewhat erythematous and scaly and almost always occurs on sun-exposed areas. Particularly pertinent in wound care is the so-called Marjolin ulcer, a squamous cell carcinoma originating in a chronic wound such as a burn scar or sinus tract. This implies that even a wound that is decades old is not necessarily benign. Patients with Kaposi sarcoma typically present with multifocal violaceous lower extremity lesions. Patients with cutaneous lymphoma present with a single nodule or a group of papules from one to several centimeters in diameter, and these almost always occurs above the waist. Perform a biopsy of every wound suggestive of neoplasm, but remember that biopsy findings are diagnostic only if an adequate representative specimen is obtained. Radiation damage The adverse effects of prolonged or excessive electromagnetic radiation vary with the wavelength. Wavelengths of electromagnetic radiation are as follow:
Gamma radiation and x-ray exposure cause a zone of stasis, in which local blood supply is impaired by coagulative necrosis due to thrombotic occlusion of smaller arteries. Gamma and x-ray radiation also spawn ionized oxygen that adversely affects DNA. The long-term result is inhibition of regeneration of skin cells from dividing basal cells. This may cause recalcitrant painful skin ulcers. The surrounding skin is atrophic, with atrophy of hair follicles and a paucity subcutaneous fat. Ultraviolet radiation exposure, particularly ultraviolet B, causes sunburn initially and subsequently conveys a continuing risk of skin malignancy (eg, basal cell carcinoma, squamous cell carcinoma, melanoma). Excessive exposure to infrared radiation, which induces repeated or persistent skin hyperthermia of 43-47°C, may cause erythema ab igne. Patients with this skin condition present with telangiectasia, erythematous patches, and hyperpigmentation. Atheroembolism syndrome Patchy areas of ischemia involving the feet, especially in the presence of palpable pedal pulses, suggest the possibility of atheroembolism of plaque fragments from ulcerated, although nonocclusive, proximal atherosclerotic plaques or from thrombi lining the wall of an infrarenal aortic aneurysm. Pyoderma gangrenosum Pyoderma gangrenosum usually starts as a small painful papule or nodule, which is often erroneously presumed to be the result of an insect bite. The lesion enlarges, becomes ulcerated, and develops overhanging violaceous borders see Image 3. The histologic findings often are nonspecific. Associated underlying systemic problems, which occur in one half of patients with pyoderma gangrenosum, are often the best clues to the diagnosis. Examples of such systemic diseases include various arthritides, inflammatory bowel disease, hepatitis, myeloproliferative disorders, myeloma, primary biliary cirrhosis, systemic lupus erythematosus, and Sjögren syndrome. An important clue is a paradoxical response in which debridement exacerbates the wound, particularly near the areas debrided. When myofascial and osseous tissues become involved, the only choice may be surgical debridement to try to save the extremity. Sickle cell Patients with sickle cell–associated leg ulcers typically present with painful small ulcers that start as crusting nodules in the distal one third of the leg, often near the malleoli. The surrounding skin demonstrates absence of hair follicles, hyperpigmentation, and atrophy of subcutaneous fat. Radiograph findings may reveal periosteal thickening of underlying bone; true osteomyelitis is rare. Sickle cell ulcers are more common in males than in females and occur predominantly in persons aged 10-50 years. Patients with sickle cell anemia can also develop leg ulcers because of other etiologies; the physical examination should exclude arterial and venous insufficiency. Calciphylaxis Calciphylaxis is an unusual and often fatal syndrome of cutaneous necrosis that tends to develop in patients with chronic renal failure, particularly those with diabetes. The average time of onset is 3 years after the start of dialysis. The female-to-male ratio is 3:1. The initial finding of calciphylaxis may be that of livedo reticularis, followed by painful erythematous areas of thickening of the skin and subcutaneous tissues. The most common site is the thigh, though the condition may also occur in the legs or the upper extremities. Panniculitis signaling the onset of calciphylaxis may be precipitated by trauma, such as the site of an injection. Proximal painful myopathy, muscle weakness, and elevated serum creatine kinase (CK) levels may occur. Laboratory testing may demonstrate a high serum phosphate level and an elevated parathyroid hormone level. Skin biopsy reveals calcification of the arterial media and luminal stricture of small-to-medium blood vessels in the subcutaneous fat. Muscle biopsy shows patchy necrosis and atrophy. Necrobiosis lipoidica Necrobiosis lipoidica usually involves the anterior tibial areas, though it can also occur in the face, arms, and chest. Patients present with well-circumscribed, shiny, reddish-brown, oval, painless nodules or papules that have a thick shiny surface. Over several months or a year, the lesions may gradually expand and develop a waxy yellow color. Trauma may lead to infected ulcerations, and involvement of adjacent cutaneous nerves may precipitate considerable pain. Necrobiosis lipoidica is more common in women and in persons with diabetes than in others, but it may also occur in persons without diabetes and before the diagnosis of diabetes. Long-standing necrobiosis lipoidica may harbor a squamous cell carcinoma. Vasculitic wounds Vasculitic wounds tend to occur throughout the lower legs as multiple, small, painful, erythematous nodules. Scars resulting from previous vasculitic lesions may be a useful clue. Any of the disparate systemic manifestations of the diseases of cellular immunity associated with atypical skin lesions, including unexplained fevers, jaw claudication, malaise, Raynaud phenomenon, myalgias, neurologic abnormalities, and craniofacial pain syndromes, suggest the possibility of vasculitis. These lesions are rare. The differential diagnosis of wounds with these features includes other uncommon problems, such as anticoagulant-induced skin necrosis, atheroembolism syndrome (ie, trash foot), and Buerger disease. Leukocytoclastic vasculitides represent a disparate group of acquired connective tissue problems; patients present with palpable purpuric skin lesions, petechiae, and ecchymoses, usually involving the lower extremities. These syndromes include Wegener granulomatosis, Sjögren syndrome, cryoglobinemia, systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis, and hepatitis B. The common factor among these syndromes is a hypersensitivity angiitis. Skin biopsy demonstrates cuffing of the dermal microcirculation by granulocytes, which are found in diverse stages of viability, including complete cellular disintegration (ie, nuclear dust). The various disorders in this group are differentiated by clinical and serologic criteria. The presence of asymptomatic palpable purpura without thrombocytopenia suggests a drug adverse effect, such as those caused by iodides, penicillin, aspirin, chlorothiazides, oxytetracycline, isoniazid, or benzoic acid. Anticoagulant-induced skin necrosis Anticoagulant-induced skin necrosis is an unusual complication of anticoagulant therapy. It may occur with heparin or warfarin, though it is more common with warfarin. Warfarin-induced skin necrosis manifests as painful hemorrhagic skin lesions, usually in an area having abundant adipose tissue such as the thighs, abdomen, or breasts. The female-to-male ratio is 4:1. This complication is often attributable to hereditary coagulation abnormalities. Warfarin (Coumadin) depletes vitamin K–dependent coagulation factors such as protein C. Therefore, during the first several days of warfarin therapy, a period of transient hypercoagulability may occur, particularly in patients with hereditary coagulation abnormalities such as protein C deficiency or protein S deficiency, antithrombin 3 deficiency, or activated protein C resistance. Actinomycosis Actinomyces israelii is a fastidious anaerobic bacterium that is relatively common and usually nonpathogenic. In rare individuals, particularly hosts who are immunocompromised, the bacterium can become pathogenic and cause chronic, draining, painless skin ulcers and sinuses, usually in the head and neck. False-negative tissue cultures are common because the organism is often difficult to culture in vitro. However, microscopic examination of wound exudates may demonstrate characteristic sulfur granules. Actinomycosis is responsive to penicillin but requires long-term therapy. Yaws Yaws is a treponematosis caused by Treponema pertenue, which is endemic in humid regions near the equator. Approximately 3-4 weeks after exposure, a pruritic sore that resembles a raspberry (the mother yaw) develops at the site where the spirochete enters the skin. This lesion eventually opens to form an ulcer. Scratching spreads the organism and results in multiple tubercles and ulcerations elsewhere, including the hands, feet, and genitals. These ulcers may have a caseous crust. Results of serologic testing for syphilis may be positive. Treatment is with a single large dose of penicillin. Untreated yaws can erode to bone and joints and can become deforming and crippling. The lesions of pinta, caused by Treponema carateum, are similar to those of yaws, but, unlike yaws, no ulceration is present. Pinta typically begins as a papule on the dorsum of the foot or leg. The papule enlarges and becomes a pruritic plaque, which changes from a copper to gray to bluish color over time. Regional lymphadenopathy may occur. Pinta is also responsive to penicillin. Mucormycosis Mucormycosis is an acute and sometimes rapidly progressive, even fatal, fungal infection that may occur in patients who are immunocompromised, especially following a burn. The primary lesions are plaques, ulcerations and abscesses, or painful ecchymotic nodules, which may ulcerate and then become necrotic and form eschars. The diagnosis is confirmed by demonstrating fungal elements of the black discharge in KOH preparations and by culturing on standard laboratory media. Cutaneous anthrax Cutaneous anthrax results from skin exposure to Bacillus anthracis, a gram-positive bacillus. Cutaneous anthrax evolves from a pruritic papule to an ulcerated wound in 1 or 2 days and then into a black eschar over the next week or so. Associated regional lymphadenopathy may be present. Findings on special stains and cultures of the wound exudate are diagnostic. Anthrax is transmissible from specimens; therefore, so laboratory personnel should be warned in the event of clinical suspicion of this disease. Of course, appropriate public health authorities must be notified. See Anthrax for details. Pathophysiology: Phases of normal wound healingHemostatic or inflammatory phase This phase starts immediately and lasts 2-5 days. Tissue damage releases chemical mediators called cytokines (eg, transforming growth factor [TGF]-beta [interleukin-1beta]), which initiate a complex interrelated process that causes hemostasis and begins the healing process. Platelets aggregate to stem bleeding. They also release serotonin and other vasoconstrictors and activate the coagulation cascade. The result is conversion of fibrinogen into fibrin, which stabilizes the platelet plug. At that point, prostaglandins and activated complement cause vasodilation and increase capillary permeability. This allows plasma to leak into the tissue surrounding the wounded area. This is the inflammatory exudate. Monocytes and neutrophils are attracted to the site of injury. Neutrophils trap and kill bacteria immediately, while monocytes become activated macrophages, which produce growth factors and cytokines and scavenge nonviable tissue and bacteria. Angiogenic growth factors stimulate neovascularization of the wound bed. Proliferative phase This phase lasts from 2 days to 3 weeks. Macrophages recruit fibroblasts. These cells create a network of collagen fibers. When adequate oxygen and vitamin C are present, granulation tissue forms. Oxygen is incorporated by 2 amino acids, proline and lysine, which are both required for collagen chain synthesis. Vitamin C is required for the hydroxylation of proline to hydroxyproline, an amino acid found in collagen. During granulation, fibroblasts create a collagen bed to fill the defect and grow new capillaries. During contraction, myofibroblasts pull the wound edges closer together to decrease the size of the wound. During epithelialization, new epithelium migrates from the intact epidermis around the wound and can grow up to 3 cm over the granulation tissue. This process requires a moist surface. Remodeling phase This phase lasts from 3 weeks to 2 years. An organized form of collagen gradually replaces the immature, soft, gelatinous collagen. The effect is to increase the tensile strength of the healed wound, but it is <80% as strong as the original tissue. Types of wound healingFirst intention, also termed primary healing, is the healing that occurs when a clean laceration or a surgical incision is closed primarily with sutures, Steri-Strips, or skin adhesive. Second intention, also termed secondary healing, is the healing that occurs when a wound is left open to heal by granulation, contraction, and epithelialization. Delayed primary closure is a combination of the other 2 types of wound healing. It is often intentionally applied to lacerations that are not considered clean enough for primary closure. The wound is left open for 5-10 days; then, it is sutured closed to decrease the risk of wound infection. For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article Suture Care. Clinical: See Etiology.
All chronic wounds require assessment. Many heal with topical wound care; some require surgical intervention. The details vary widely with the nature of the wound. This article provides information regarding wound care in general and specific wound etiologies in particular.
Relevant Anatomy: Life is a constant battle against entropy (ie, disorder). The skin provides the primary barrier between the human protoplasm and the entropy of the external environment. Histologically, the skin is divided into the epidermis and the dermis. The epidermis consists of 5 histologic strata. From superficial to deep these layers are the (1) stratum corneum, (2) stratum lucidum, (3) stratum granulosum, (4) stratum spinosum, and (5) stratum germinativum. The keratinocyte, the preponderant epidermal cell, is generated in the stratum germinativum and eventually desquamates (sloughs) when it reaches the stratum corneum. The dermis underlies the epidermis. A dermal vascular network functions in thermoregulation and provides metabolic support for the avascular epidermis. Fibroblasts synthesize supportive and structural polymers, including ground substance, collagen, and elastin. Skin appendages include sebaceous glands, hair follicles, and sweat glands. Contraindications: See Treatment. |
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Lab Studies:
Imaging Studies:
Diagnostic Procedures:
Medical therapy: See Treatment of specific types of 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, ie, necrotic or viable; (3) amount and characteristics of wound exudate; and (4) status of the periwound tissues (eg, pigmented, scarred, atrophic, or cellulitic).
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. 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 30-35 calories/kg. Increase these requirements for those with sizable 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.
Chronic malnutrition can be diagnosed by 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 <7 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 infection
Issues to consider are wound infection versus colonization and osteomyelitis.
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 (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.
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
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. The U.S. Food and Drug Administration (FDA) has approved this agent for use in promoting the healing of diabetic foot ulcers. Regranex is contraindicated in persons with known skin cancers at the site of application. 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, but this use is not FDA approved.) Treatment of specific types of woundsSee General treatment of nonhealing wounds. Pressure ulcers Treatment of decubitus ulcers requires prolonged surgical and nursing care. During the extended period of treatment required, the patient remains at risk for the development of new pressure ulcers at other sites. Treatment, particularly indications for support surfaces, is based on appropriate staging of the pressure ulcer. Table 2. Staging Pressure Ulcers*
Table 3. Support Surfaces
Venous ulcers Treatment of venous ulcers includes compression therapy, providing a moist wound environment and debridement of necrotic tissue. Most venous ulcers heal with these measures alone. Some require split-thickness skin grafting or application of bioengineered skin (eg, Apligraf, Dermagraft). 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 recent technique for endoscopic subfascial perforator ligation appears promising. Table 4. Compression Bandages for Venous Ulcers*
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, and (5) optimal control of blood glucose. Evaluation and correction of peripheral arterial insufficiency Wound coverage with cultured human cells or heterogeneic dressings and/or grafts, application of recombinant growth factors, and hyperbaric oxygen treatments may also be beneficial. 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. 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.
Complications of nonhealing wounds include the following:
The prognosis for healing of chronic wounds varies with the etiology of the wound and the general health status of the patient.
The aging of the population and continued advances in biotechnology 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.
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