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. The images below depict a sacral pressure ulcer.
 View Image | Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture. |
Pressure ulcers are a commonly encountered condition in both acutely hospitalized and long-term institutionalized patients. They are estimated to occur in approximately 9% of hospitalized patients, usually during the first 2 weeks of hospitalization. This is in spite of adopting methods to reduce the development of pressure ulcers, such as repositioning, cushioning bony prominences, and using specialized mattresses. In high-risk hospitalized patient populations, the prevalence of pressure sores is even higher, with studies quoting incidence rates as high as 38%.[1] One study found that even with the use of a pressure-reducing bed and early nutritional support, 3% of patients in a surgical intensive care unit who were in the study developed pressure ulcers.[2] The annual 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%.
In another prospective study, Campbell et al determined the incidence of heel pressure ulcers in 150 orthopedic patients. The cohort consisted of patients who were admitted to an acute care hospital either for elective orthopedic surgery or for the treatment of a fractured hip. The incidence of heel pressure ulcers in all patients was 13.3%, and the incidence in patients with hip fractures was higher than that of elective surgery patients (16% vs 13%, respectively). However, patients with hip fractures in whom pillows and rolled sheets were used to relieve heel pressure had a significantly lower ulcer rate than did the other hip fracture patients. When all patients in the study were taken into account, the presence of respiratory disease was the only factor significantly associated with the development of pressure ulcers.[3]
The prevalence of pressure ulcers among patients residing in long-term care facilities has been reported as anywhere from 2.3-28% and has been an increasingly common reason for litigation.[4, 5, 6, 7, 8] The presence of a pressure ulcer increases a nurse's workload for that patient by 50% and adds approximately $20,000 to the hospital bill. The treatment of pressure ulcers in the United States is estimated to cost more than $1 billion annually.
Venous ulcers make up 70% of chronic lower extremity ulcers.[9] 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 most recent Centers for Disease Prevention National Diabetes Statistics Report, an estimated 29 million Americans (9% 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 8.1 million individuals. Diabetic foot lesions are one of the most frequent causes of hospitalization secondary to a 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.[10] Diabetic peripheral neuropathy confers the greatest risk of foot ulceration; microvascular disease and suboptimal glycemic control also contribute to this total. Even with successful treatment and ulcer healing, the recurrence rate in that patient population is 66% and the amputation rate rises to 12%.[11]
In general, factors that adversely affect wound healing can be remembered by using the mnemonic device DIDN'T HEAL, as follows:
Arterial insufficiency
See Infrainguinal Occlusive Disease.
Venous insufficiency
Patients with varicose veins or nonfunctional venous valves after deep vein thrombosis develop ambulatory venous hypertension, that is, 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 splaying 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% when compared with a relative humidity of 25%, and it 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 appears to have occurred spontaneously.[12]
Basal cell carcinoma appears smooth, pearly, and elevated above the skin surface, as illustrated in the image below, 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.[13] 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.
View Image | Basal cell cancer manifesting as a chronic leg ulcer. |
It is recommended to perform a biopsy of most wounds suggestive of a neoplasm. However, it is important to 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 follows:
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 the 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, scaling, 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, as shown in the image below.
View Image | Chronic ulcer of medial aspect of right leg due to pyoderma gangrenosum. |
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.[14, 15]
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.[16, 17]
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.[18]
Necrobiosis lipoidica
Necrobiosis lipoidica, a necrotizing skin lesion characterized by collagen degeneration and a granulomatous response, 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. The exact cause is unknown. 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.[19] 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, cryoglobulinemia, systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis, and hepatitis B. The common factor among these syndromes is a hypersensitivity angiitis.[20]
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.[21] It can occur with the use of 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.[21]
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, 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.
The phases of normal wound healing can be described as follows:
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.
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 of 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.
This phase lasts from 3 weeks to 2 years.[22] 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 less than 80% as strong as the original tissue.
First 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 aforementioned types of wound healing. It is often intentionally applied to lacerations that are not considered clean enough for immediate primary closure. The wound is left open for 5-10 days; then, it is sutured closed to decrease the risk of wound infection. Improved blood flow at the wound edges, which develops increasingly over the first few days, is another benefit of this style of wound healing and can be associated with progressive increases in resistance to infections.
All chronic wounds require assessment.[23] Many heal with topical wound care; some require surgical intervention. The details vary widely with the nature of the wound, and often a combination of management strategies is required, along with constant reassessment of wound progression. This article provides information regarding wound care in general and specific wound etiologies in particular.
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.
For more information about the relevant anatomy, see Skin Anatomy.
The prognosis for healing of chronic wounds varies with the etiology of the wound and the general health status of the patient.
The Wound Healing Society often uses the mnemonic device TIME, which is a comprehensive description of the key elements associated with impaired wound healing, as follows:
Complications of nonhealing wounds include the following:
The following tests may be useful to identify factors associated with wound development or those that can slow wound healing:
Additional studies that may play a role in evaluating specific wound etiologies include vascular laboratory studies (eg, plethysmography, pulse-volume recordings [PVRs]) to assess the hemodynamic significance of arterial occlusive disease.
Plain radiography, CT, and MRI may help in looking for underlying osseous abnormalities (including osteomyelitis), proximity of the wound to hardware, or foreign bodies.
Vascular ultrasonography may be indicated to evaluate for aneurysmal disease, arterial-occlusive disease, or deep venous occlusion.
In cases in which plain radiography or MRI are not diagnostic, bone scanning may be needed to evaluate for osteomyelitis. Technetium Tc 99m–labeled WBC scanning (Ceretec) has high specificity and sensitivity for osteomyelitis. However, it requires 24 hours for completion and it lacks anatomic detail.
Perform a biopsy of every suspicious wound, but remember that biopsy results are diagnostic only if an adequate representative specimen is obtained.
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).[29]
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.[30] 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.[31]
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.[32, 33, 34, 35, 36, 37]
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
 View Table | See Table |
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.[38]
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,[39] but this use is not FDA approved.)
Pressure ulcers
Treatment of decubitus ulcers requires prolonged surgical and nursing care.[40, 41, 42, 43] During the extended period of treatment required, the patient remains at risk for the development of new pressure ulcers at other sites.[44, 45, 46] Treatment, particularly indications for support surfaces, is based on appropriate staging of the pressure ulcer.[47, 48]
Milne et al reported the outcome of a long-term acute care hospital's program to reduce the incidence of pressure ulcers.[49] 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
View Table | See Table |
Pressure ulcers often require the following steps:
View Image | Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture. |
View Image | Sacral pressure ulcer before and after flap closure. |
View Image | Sacral ulcer. |
Support surfaces are further discussed as follows:
Table 3. Support Surfaces
View Table | See Table |
Additional protection is described as follows:
View Image | Heel pressure ulcer. |
Venous ulcers
Treatment of venous ulcers includes compression therapy, providing a moist wound environment and debridement of necrotic tissue.[50, 51] Most venous ulcers heal with these measures alone. Some require split-thickness skin grafting or application of bioengineered skin (eg, Apligraf, Dermagraft).[52] 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.[53] Other studies suggested a more modest level of benefit from corrective venous surgery.[54]
Table 4. Compression Bandages for Venous Ulcers*
View Table | See Table |
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.[55, 56, 57, 58, 59] 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, 60, 61, 62, 63]
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.
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.[64]
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.
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 [58, 65, 66]
AlloDerm (Allergan, 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.[67] 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.
EpiFix (MiMedex, Inc) is a relatively new matrix scaffold used in wound healing. It is composed of dehydrated human amnion/chorion membrane (dHACM). EpiFix is a bioactive tissue matrix allograft, and the dHACM preserves and contains multiple extracellular matrix proteins, cytokines, growth factors, and other specialty proteins.
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.[68]
View Image | Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture. |
View Image | Sacral pressure ulcer before and after flap closure. |
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.[24] 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.[25, 26, 27, 28]
Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.
Pressure ulcers of the lateral aspect of the right foot.
Basal cell cancer manifesting as a chronic leg ulcer.
Chronic ulcer of medial aspect of right leg due to pyoderma gangrenosum.
Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.
Sacral pressure ulcer before and after flap closure.
Sacral ulcer.
Heel pressure ulcer.
Image of advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.
Sacral pressure ulcer before and after flap closure.
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.
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.
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.
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* flotation bed with or without low air loss feature Roho dry floatation mattress system, Pegasus Renaissance mattress III Air fluidized Flotation 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.
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.
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