Plastic surgery






The wound is a microcosm of the patient. While most wounds heal without intervention in healthy individuals, patients with systemic diseases or acute illnesses can develop non-healing wounds that require evaluation by a plastic surgeon. In general, the plastic surgeon is consulted to evaluate three types of wounds: (1) the acute wound where the final appearance may be the principal concern, (2) the wound in a patient whose medical status and/or mode of injury predisposes him or her to wound healing difficulties and the threat of a problem wound, or (3) the chronic wound refractory to past interventions.

In recent years, significant strides have been made in our overall understanding of problem wound physiology. This has led directly to clinical advances that have resulted in better treatments and overall wound care. With the staggering prevalence of chronic wounds and an ever-increasing armamentarium of wound care tools, it is imperative that the plastic surgeon maintain an updated understanding of wound healing biology and the principles of wound care. In this chapter we will focus on the basics of wound care and highlight some of the recent advances in this dynamic and expanding field.


All wounds, whether acute or chronic, should be evaluated by a physician to determine their mechanism and to outline an approach to treatment. Tetanus prophylaxis is administered when prior immunity is unknown or the most recent booster vaccine is over 5 years old. A thorough history and physical examination should be performed, with particular emphasis on any aspect that relates to the wound cause and/or persistence (e.g., comorbidities, systemic diseases, and medications). The term wound encompasses a broad range of lesions without consideration to etiology, and the list of possible etiologies is vast. Table 3.1 lists some of the major factors, both systemic and local, that can have profound effects on wound healing.

Adjunctive diagnostic tests are guided by history and physical examination of the wound. Some useful studies include laboratory tests that reflect nutritional status (albumin, prealbumin, and transferrin levels), the level of physiologic inflammation (C-reactive protein and erythrocyte sedimentation rate), and the degree of diabetes control (plasma glucose and hemoglobin A1c). In addition, patients should have a recent complete blood count and basic chemistry panel to assess for leukocytosis, anemia, and renal disease. Other useful laboratory tools include transcutaneous oxygen pressure (tcPo2) measurements, toe pressures, neurofilament testing, and ankle-brachial index (ABI) (Chapter 95). Results of these tests may direct the need for procedures such as surgical revascularization. Wound parameter documentation is also useful to monitor the progression of wound healing in an objective manner.

The main fundamentals of wound care are summarized in Table 3.2. To attain these goals, it is useful to emphasize the common causative factors that are shared by problem wounds, as opposed to isolating the differences between diverse types of wounds. With this more simplistic view, it is possible to link the majority of problem wounds to a combination of three factors: age, ischemia (including repeated episodes of ischemia–reperfusion injury), and bacterial infection. By understanding and addressing these factors, the surgeon will be able to manage most wounds.

Age and Wound Healing

Although most wounds heal without incident in aged patients, there is a slight, but consistent, decline in wound healing rates in the elderly. This decline is exacerbated when ischemia and infection are superimposed. Laboratory studies reveal a functional decline in aged fibroblasts and endothelial cells that leads to accelerated senescence, diminished growth factor production, decreased stress response to hypoxia and toxins, and a reduction in collagen and matrix production. Interestingly, aged cells share many of the same molecular derangements as those seen in diabetic patients and irradiated wound beds. Obviously age cannot be reversed; however, it should be considered an important component of wound pathology and prompt the surgeon to aggressively optimize appropriate systemic parameters in these patients (nutrition, infection, ischemia, etc.). The use of growth factors or advanced wound protocols should be considered earlier in the elderly patient.

Ischemia and Wound Healing

The role of hypoxia in wound healing is well established. In fact, local tissue hypoxia is a common characteristic of most chronic wounds. The diffusion of oxygen and nutrients from capillaries to cells is limited to a distance of 60 to 70 µm in a person breathing room air. Therefore, anything that increases tissue diffusion requirements or limits available capillary delivery systems will establish a hypoxic environment. For example, oxygen tension in wound tissues is reduced an average of 15 to 20 mm Hg (25 vs. 40 mm Hg) as a result of the damage to small vessels in periwound areas. Likewise, the tissue fibrosis commonly encountered in chronic wounds can create a significant barrier to oxygen diffusion that subsequently produces persistent tissue hypoxia and further fibrosis.

While hypoxia alone is an important component of chronic wounds, most problem wounds are characterized by repeated episodes of ischemia followed by reperfusion. The detrimental effects of ischemia–reperfusion injury have been well established in cardiac pathology and organ transplantation, but are underappreciated in cutaneous wound healing. Reperfusion injury is particularly important in lower extremity wounds, where walking and standing can lead to localized ischemia in pressure-bearing areas, or through increased edema in patients with venous stasis. Pressure relief, through sitting, rest, and foot elevation, leads to resumption of adequate tissue perfusion and a vicious cycle ensues. Repeated episodes, sometimes multiple per day, result in gradual cellular damage and a chronic milieu of persistent inflammation. Similar cycles of ischemia–reperfusion may also occur in patients with pressure sores as they shift about in bed or wheelchairs.

Surgical and nonsurgical interventions can be undertaken to maximize oxygen delivery to tissues. Examples include elevation of edematous extremities, off-loading pressure points, debridement of necrotic tissue or foreign bodies that act as a physical barrier to diffusion, pain control that reduces sympathetic constriction of peripheral vasculature associated with the “fight-or-flight” response, heating that will result in vasodilatation of cutaneous vasculature, and smoking cessation and hydration that increase oxygen delivery at the cellular level. Recent research indicates that the benefits of ensuring adequate oxygen delivery to a wound not only are restricted to established wounds but may also be useful in preventing wound complications.

Bacteria and Wound Healing

All wounds are contaminated, but excessive numbers of bacteria will interfere with wound healing. A quantitative culture of 105 bacteria per gram of tissue is usually diagnostic of infection. However, this tool is rarely used because few microbiology laboratories perform the test reliably. Furthermore, the value of 105 is relative and not universally applicable. In fact, more virulent strains of bacteria can establish systemic infections at much lower densities. The presence of diabetes, ischemia, or other comorbidities will also lower the threshold needed to establish a true infection to an unknown extent. Likewise, as more research on the physiology of bacterial biofilms is introduced, it is likely that only a fraction of the 105 bacterial count is actually necessary to establish a biofilm and create a significant barrier to wound healing.

An important mechanism by which tissue hypoxia predisposes wounds to infection is by impairing the “oxidative burst” essential to microorganismal killing by leukocytes. This enormously elevated production of oxygen-derived radicals is a self-regulated process that is important in clearing the wound off bacteria. Notably, this process of radical production, which is normally limited to the early stages of wound repair, can be aberrantly prolonged in the setting of persistent infection or inflammation (Figure 3.1). This can result in bystander damage to the body’s normal cells and in many cases characterizes the microenvironment of the indolent wound. This explains the benefit of dressings and the avoidance of foreign debris (and highlights the importance of delicate tissue handling and the proper choice of suture material) in expediting healing.

FIGURE 3.1. The normal healing milieu. A. Normal response to injury. B. Response to injury in the problem wound. ROS, reactive oxygen species; PVD, peripheral vascular disease.

Bacteria exert adverse effects on wound healing in several ways. As mentioned above, through a persistent inflammatory response, they establish an environment of free radicals, secreted toxins, and proteases that act to degrade growth factors, prevent ordered assembly of matrix proteins, and result in the creation of proteinaceous debris that constitutes a pseudoeschar. In addition, they place a significant metabolic strain (bioburden) on the wound that the host may not be able to overcome. Importantly, wound bioburden is often stratified as a prognostic indicator and to assist in management decisions. Wounds may be considered contaminated (bacteria present without proliferation), colonized (bacteria present and multiplying without overt host reaction), critically colonized (the tipping point where host response is overcome by bacterial proliferation), or infected (expanding bacterial quantity with ongoing host reaction). Critical colonization of a wound or infection is often heralded by stasis in the progression of a wound that was previously healing. In fact, if the rate of healing decreases in any wound, it should be considered infected until proven otherwise. Other signs of bioburden progression and/or overt wound infection include increasing pain in the periwound area, increased wound edema, malodorous discharge, increased drainage, or purulence.

Systemic antibiotics are unnecessary for most wounds. By definition, most wounds are open and thus adequately managed through “drainage” and proper debridements. In addition, systemic antibiotics are only delivered to adequately perfused tissues; therefore, in the setting of most problem wounds, they are ineffective. However, there are settings where systemic antibiotics are important. In general, any wound that is complicated by surrounding cellulitis should be treated with adjunctive antibiotics. As mentioned, any wound where the rate of healing decreases is considered infected. Increased pain is another indication of a worsening infection. Another sign of infection is the appearance of straw-colored “oozing” from the skin; this is actually likely evidence of an underlying Staphylococcuscellulitis or lymphangitis. Antibiotics should also be considered in wounds contaminated by oral flora or animal bites, as well as in patients with mechanical implants. In general, surface irrigation and lavage with saline may be all that is necessary for truly contaminated wounds, whereas topical antibiotics and surgical debridement are often essential management tools for overtly infected wounds.



Debridement is the single most important wound care tool to reduce bioburden and promote healing. Without adequate debridement, a wound is persistently exposed to cytotoxic stressors and competes with bacteria for scarce resources such as oxygen and nutrients. Many surgeons underappreciate the importance of adequate debridement in the management of both acute and chronic wounds.While most surgeons recognize the importance of debridement of grossly necrotic or foreign material, many still allow wounds to “heal” under a “biologic dressing” or eschar.

An eschar begins as a pseudoeschar, which is a provisional matrix of exudated serum components at the wound–air interface. If allowed to dry, the gelatinous pseudoeschar will harden to form a true eschar, or scab. Pseudoeschars and eschars may play a role in prolonging the inflammatory stage of wound healing, and hence establish an environment ripe for bacterial colonization in the compromised patient or susceptible wound bed. Likewise, the proteinaceous components of the eschar are appetizing nutrients for most bacteria. Therefore, any pseudoeschar or eschar should be debrided as it accumulates. An effective way to do this is through the proper use of dressing and debriding agents, as detailed below and in Table 3.3.

Debridement is typically considered a surgical tool, but it may also be accomplished through the use of enzymatic, mechanical, or autolytic (through host leukocyte action) means. Wound care manufacturers have produced numerous enzymatic and pro-autolytic agents. While they have been proven effective in mildly debriding wounds, their use should not supplant sharp surgical debridement as the method of choice for more heavily contaminated wounds or wounds with thicker levels of slough or eschar. Enzymatic and pro-autolytic agents work through preventing the cross-linking of exudated components and impede the bacteria-sequestering pseudoeschar and biofilms from forming. Mechanical debridement can be achieved through dressings, or newer pressurized water devices, such as the VersaJet (Smith & Nephew, Largo, FL), Waterpik (Waterpik Technologies, Fort Collins, CO), pulse-lavage, or shower spray devices. Mechanical debridement is effective at reducing bacterial counts and should be considered adjuncts to surgical debridement. Similarly, a syringe with a 20-gauge needle will generate the 15 psi necessary to lower bacterial counts in tissue.

For historical purposes, another effective means of achieving wound debridement is through the use of maggot therapy. Maggots preferentially feed on devitalized tissue and spare viable, well-perfused tissue; their secretions also target bacterial biofilms. Although they are used sparingly throughout most parts of the country, some centers utilize maggot therapy extensively.

Negative-Pressure Wound Therapy

Negative-pressure wound therapy (NPWT) has been a significant advance for the wound care practitioner. It consists of the use of a porous sponge within the wound, covered by an airtight occlusive dressing, to which a vacuum is applied. This modality has many uses and has found its way into the armamentarium of a wide array of surgical and nonsurgical specialties. It should best be thought of as an adjunct to assist in surgical closure of a problem wound. It can and has been used to completely heal a wound, but use in this manner is time-consuming, expensive, labor-intensive, and not always effective. A more practical indication is to expeditiously prepare a wound bed for surgical closure by tertiary intent.

NPWT works through multiple important mechanisms including reduction of edema and removal of wound fluid rich in deleterious enzymes, both patient and bacteria derived. In addition, the cyclic compression and relaxation of the wound tissue likely stimulates mechanotransduction pathways that result in increased growth factor release, matrix production, and cellular proliferation.

Common clinical scenarios amenable to NPWT include lymphatic leaks, venous stasis wounds, diabetic wounds, wounds with fistulae, sternal wounds, orthopedic wounds, and abdominal wounds. Likewise, NPWT is used frequently as an alternative to bolster dressings for split thickness skin grafts. Notably, by reliably encouraging granulation tissue formation and reducing wound edema, NPWT has permitted normally emergent wounds to be managed in a nonemergent fashion, allowing for medical stabilization and optimization prior to advanced reconstructive procedures. In some instances, it has even enabled avoidance of free tissue transfer.

There are several contraindications to the use of NPWT, and these include the presence of a malignancy, use on wounds characterized by ischemia, as well as inadequately debrided or badly infected wounds. There have been reports of extension of the zone of necrosis when used on ischemic wounds; for this reason, these patients should be revascularized prior to application of NPWT.

Hyperbaric Oxygen

Hyperbaric oxygen (HBO) has been shown to raise the dissolved oxygen saturation in plasma from 0.3% to nearly 7%, resulting in a four- to fivefold increase in the interstitial diffusion distance of oxygen. Historically, the initial enthusiasm to HBO led to indiscriminate and unscientific use, which created significant controversy with regard to safety and efficacy. Despite early disappointment, the use of HBO has gained increasing traction. In order to optimize results, it is important to recognize which patients benefit the most from such therapy. The use of transcutaneous oximetry has permitted evaluation of wound microcirculation, such that surgeons can accurately predict responders and nonresponders. In general, patients who demonstrate a rise in the wound tcPo2 when inspiring supplemental oxygen will benefit from HBO. Patients that will not benefit from HBO include those with normal environmental perfusion and those with ischemic limbs who require a revascularization procedure to restore adequate blood flow to the limb. It is important to note that HBO use remains largely empiric as there is a paucity of prospective randomized trials supporting its use.

Growth Factors

The first growth factor approved by the Food and Drug Administration (FDA) in the United States is platelet-derived growth factor (PDGF) or becaplermin (Regranex, Johnson & Johnson, Somerville, NJ) (Table 3.4). Although it is only FDA approved for use in the treatment of diabetic foot ulcers, is has been widely used “off-label” for the treatment of a variety of other wound types including irradiated wounds and wounds in elderly patients. Importantly, PDGF is only effective in the context of a well-prepared wound bed. Contaminated and/or infected wound beds are filled with proteases, which will rapidly degrade the protein. In addition, its use in patients with malignancy has been cautioned.

Although not growth factors per se, there has been an increase in the use of neonatal fibroblasts as a “carrier” for essential growth factors to the wound environment. Commonly used products include Apligraf (Organogenesis Inc., Canton, MA) and Dermagraft (Advanced BioHealing, Westport, CT). These products are commonly used in patients with a suboptimal wound environment, including venous stasis ulcers, diabetic wounds, and wounds in aged patients.


The rationale for using enzymatic debriding agents is that they offer a noninvasive means to selectively digest necrotic, devitalized tissue and prevent slough and eschar from accumulating (Table 3.4). Papain-based products are no longer available in the United States since they were determined by the FDA to be unapproved drugs with significant side effects. The sole enzymatic agent available for use is collagenase (Santyl, Healthpoint Ltd., Fort Worth, TX), which works by digesting necrotic collagen within wounds. Santyl is currently marketed for patients with chronic dermal ulcers and burns and is used frequently by wound care practitioners. It is important to recognize that enzymatic debridement products are not substitutes for adequate mechanical debridement; however, when properly used, they are often less traumatic to healthy surrounding tissue. In general, these products should be used in wounds with small areas of eschar or necrotic debris.


Wound care dressings (Table 3.3) can be broadly divided into seven classes: films, composites, hydrogels, hydrocolloids, alginates, foams, and absorptive dressings including NPWT.Unfortunately, within each class, there are a dizzying number of options and a paucity of prospective, randomized clinical trials that definitively prove superiority of one type versus the other. With the seemingly endless options available, it can often become overwhelming. To assist with this decision, it is best to consider the overall wound characteristics and treatment goals and match them to the appropriate dressing class.

The goal in clean wounds that are to be closed primarily, or in wounds that are granulating well, is to provide a moist healing environment to facilitate cell migration and prevent desiccation. Consequently, films can be used for incisions, and hydrogels or hydrocolloids can be used for open wounds. The amount and type of exudate that is present in the wound will determine the dressing used in wounds that have some degree of bacterial colonization. In general, hydrogels, films, and composite dressings are best for wounds with lighter amounts of exudates; hydrocolloids are used for wounds with moderate quantities; and alginates, foams, and NPWT are best used for wounds with heavier volumes of exudates. As mentioned previously, NPWT is also useful for wounds with heavy amounts of lymph drainage as a consequence of a lymphatic leak, as well as for fistulae. Wounds with large amounts of necrotic material should not be treated with dressings until a surgical debridement has been performed.

Gauze. Gauze dressings are the traditional first choice for generic wound care. The realization that the practice of moist to dry dressings for wound care is actually traumatic and proinflammatory has led to a decline in the use of these dressings in the arena of wound care. In addition, the costs associated with these dressings, particularly in personnel expenses, are high compared with modern dressings that require less frequent dressing changes. Gauze dressings are often painful to remove and are nonselective debriders that cause significant collateral damage to healthy surrounding tissue. Furthermore, many gauze dressings leave behind fine microfibers that can act as an irritant or a source of infection.

Advantages of gauze dressings include a low material expense and a readily available supply. Likewise, they may be purchased impregnated with petrolatum, iodinated compounds, or other material useful in keeping the wound bed moist. They make excellent surgical bandages and can be used in small, noncomplicated wounds or as secondary dressings. Gauze dressings remain the “gold standard” to which the FDA compares most dressings. There is no definitive evidence that other dressings will heal a wound faster than moist gauze, although they may offer other advantages.

Semiocclusive Dressings. These are sheets that are impermeable to fluids but permit the passage of small gas molecules. They are typically used in combination with gauze or other dressings and act to maintain the moisture content of clean wounds. Semiocclusive dressings are commonly used to cover and protect freshly closed incisions and skin graft donor sites and will enhance epithelialization when used this way. They should not be used in wounds known to be contaminated and wounds with moderate or higher exudate levels and should be used cautiously in patients with fragile skin prone to tearing.

Hydrogel Dressings. Hydrogel dressings are useful in maintaining a moist wound bed and rehydrating wounds to facilitate healing through autolytic debridement. Thus, they are often useful in wounds with small amounts of eschar or that are predisposed to desiccation. Their usefulness is achieved by their intrinsic moisture content and hydrophilic nature. They are usually composed of complex polysaccharides (e.g., starch). Unlike alginates and hydrocolloids, they are not dependent on the wound bed to maintain moist wound microenvironments. Yet, like the other dressings, they can absorb moderate amounts of fluid from the wound. An additional benefit is that they can be used in infected wounds. They come in various physical forms including gels, sheets, and impregnated into gauze. They are nonadhesive and therefore cause minimal pain with dressing changes. However, because of this, they usually require a secondary dressing (e.g., gauze).

Hydrocolloids. Hydrocolloids typically come in pastes, powders, or sheets that are placed within the wound and covered with a dressing to form an occlusive barrier that gels as it absorbs mild amounts of exudates. Hydrocolloids consist of gel-forming agents (typically gelatin, carboxymethyl cellulose, or pectin) that are impermeable to gases and liquids. They may be left on the wound for 3 to 5 days; during this time, they provide a moist environment that promotes cell migration and wound debridement by autolysis. However, because of their occlusive nature, they should not be used in wounds heavily colonized by bacteria, especially those with anaerobic strains. They are not highly absorbent and hence should not be used in highly exudative wounds.

Foam Dressings. Foam dressings are made of nonadhering polyurethane, which is hydrophobic, and an occlusive cover. The polyurethane is highly absorptive and acts as a wick for wound fluids, making them useful for highly exudative wounds. However, because of their high wicking ability, they are not to be used on nonexudating or minimally exudating wounds.

Alginates. Alginate dressings are derived from brown seaweed and are particularly useful in wound characterized by significant amounts of exudate. Their use permits the desired removal of exudated fluids from the wound environment and yet frees the practitioner from the burden of daily dressing changes or multiple dressing changes per day. These products should also not be used in nonexudative wounds, as they can dry out the wound bed. They come in several forms, including a rope/ribbon form that is useful for packing wounds with deep pockets. These dressings can absorb approximately 20 times their dry weight in fluid. They should be covered with a semiocclusive or gauze dressing. If the surgeon desires to use these alginate dressings on dry wounds, they should be hydrated with sterile saline prior to being placed on the wound to maintain wound moisture and permit epithelialization and autolysis. Some alginates are impregnated with silver.

Antimicrobials. Antimicrobial dressings are a generic term for a dressing that contains an antimicrobial agent. The most beneficial agent appears to be silver. Silver is ionized in the moist environment of the wound, and it is the silver ion that has biologic activity. This agent has a broad spectrum of bactericidal activity with low toxicity to human cells. Because of silver’s tri-pronged mechanism of action (cell membrane permeabilizer, inhibitor of cellular respiration, and nucleic acid denaturer), it is active against a broad range of microorganisms in vitro, including highly resistant organisms such as VRE (vancomycin-resistant enterococcus) and MRSA (methicillin-resistant Staphylococcus aureus). There are a number of silver-impregnated dressings on the market today, including Acticoat (Smith & Nephew, Largo, FL), Aquacel Ag (ConvaTec, Skillman, NJ), and Silvasorb (Medline, Mundeleine, IL). Despite the expanding incorporation of silver into many types of dressings, reliable indications for their use remain to be determined, and much of the use of silver-containing dressings is based on anecdotal experience.

Cadexomer iodine is another antimicrobial agent and is a slow-release form of iodine formulated to achieve consistent bactericidal levels within the wound bed without the wound cell damaging effects seen with the use of povidone-iodine products. Other antimicrobials include silver sulfadiazine, mafenide acetate, and preparations of sodium hypochlorite solution (Dakin’s solution).

Skin Substitutes or Human Tissue Equivalents

These were among the first tissue-engineered products applied to clinical use. As mentioned previously, besides providing wound coverage, some of these products contain living cells that are cellular factories, secreting a panoply of growth factors and other bioactive molecules that assist the wound healing cascade. One major disadvantage to their use is cost. They must be applied to meticulously clean wounds with adequate vascularity, and for certain products the site needs to be immobilized to prevent shearing and graft loss. Representative products include cultured autologous keratinocyte sheets (Epicel, Genzyme Corp, Cambridge, MA); dermal constructs such as Biobrane (Mylan Laboratories, Canonsburg, PA), Oasis (Cook Biotech, West Lafayette, IN), Integra (Integra LifeSciences Corp, Plainsboro, NJ), TransCyte (Smith & Nephew, Largo, FL), and Dermagraft (Advanced Biohealing, Westport, CT); and bilayered tissue-engineered constructs consisting of keratinocytes and fibroblasts such as OrCel (Ortec International, New York, NY), and Apligraf (Organogenesis, Canton, MA). The indications for their use are highly patient and center specific. Integra has proven especially useful for sites prone to contracture (neck and axilla) and to replenish contour in burn wounds and donor sites. In addition, it can enable coverage of tendons, bone, and surgical hardware and in select situation can obviate the need for more complex wound closures, such as flaps.

Scar Modulating Therapies. The use of silicone sheets improves the appearance of scars. This is likely the result of the increased moisture and slightly increased warmth provided by the continuous application of the silicone sheet, as this increases slightly the rate of collagenolysis. Other useful tools include steroids and pressure garments. Calcium channel blockers are used, but they are unproven, as are topical formulations of salicylic acid, an anti-inflammatory agent, although the theoretical basis underlying the use of this agent appears sound. Drugs targeting growth factors thought to be important in fibrosis are currently in clinical trials.

Common Clinical Wound Care Scenarios

The Uncomplicated Wound. Much is known about the healing rates of clean surgical incisions. The rate of healing is a direct reflection of the kinetics of collagen deposition and remodeling within the wound. When the healing cascade progresses normally, approximately 30% to 50% of the final strength of the wound is achieved in 42 days. It is for this reason that elective surgery patients are told to refrain from strenuous activity or heavy lifting for at least 6 weeks. This progression represents the expected course of healing. In patients with underlying comorbidities, including renal failure, ischemia, and steroid use, this curve is delayed and shifted to the right (see Figure 3.2). In these particular patients, postoperative instructions should be adjusted to reflect the anticipated delay in healing. Note that in healthy patients, no pharmacologic agent has been demonstrated to shift the curve to the left; that is, healing rates are for the most part maximized in healthy people. However, it may be possible to modify the quality of healing, and research on scar modulation and manipulation is currently an area of significant future promise. Below we will discuss common complicated wounds encountered by the plastic surgeon. General management plans can be found in Figure 3.3.

The Problem Wound. Problem wounds are important entities that are frequently seen by plastic surgeons. In an ideal world, these wounds would be seen by a wound care specialist as soon as possible. Unfortunately, in practice it is difficult to identify the incipient problem wound. Furthermore, not all problem wounds are actually chronic wounds. The development of biomarkers for wounds that will not heal is of tremendous importance and is an area of promising research. This also has practical importance, as many third-party reimbursement agents will not cover specialized care of wounds unless they have been present for a defined period of time. The standard definition of a chronic wound is one that has been present for 3 months but such a definition may be seized upon by insurance carriers to deny specialized care to impaired wounds. Unfortunately, this condemns the patient to months of unnecessary waiting, morbidity, and time away from work and may even worsen the outcomes in cases of threatened limb loss, for example, by allowing the progression of osteomyelitis. It is, therefore, perhaps time to redirect the conceptualization of a problem wound to de-emphasize chronicity and re-emphasize its fall off the trajectory of expected healing. The majority of problem wounds seem to share the traits of advanced age, infection, and ischemia with reperfusion injury, as described above. In addition, many problem wounds suffer from one or more unique traits that retard the healing process further, including radiation exposure and systemic comorbidities such as diabetes.

Wounds in Patients on Steroids. Wounds in patients receiving steroids are prone to infection and show decreased rates of angiogenesis, collagen deposition, and cellular proliferation. It is important to remember that steroids may exert their impairments to healing even longer after their use is discontinued. Maintenance of a clean wound with minimal bacterial colonization should be the main goal of care for these patients. In addition, experimental models of steroid-impaired healing have shown vitamin A to be a useful adjunct. The typical dose of vitamin A in patients receiving steroids is 25,000 IU daily by mouth or 200,000 IU topically three times a day.

FIGURE 3.2. The healing trajectories of a normal wound, a problem wound, and a hypothetical ideal wound are depicted. Most normal wounds heal with a slight lag phase, an exponential phase of active gain in tensile strength with active matrix deposition, and a protracted resolution phase. Note that the normal wound heals with a scar that does not achieve the tensile strength of unwounded skin (hypothetical wound curve). The curve on the right represents a problem wound curve. The exact shape of the curve is dependent on the patient and clinical scenario; however, prolongation of the lag phase, a more shallow exponential phase, and a reduction in final tensile strength are to be expected.

Wounds in Patients with Irradiated Skin (Chapter 17). Patients with irradiated wounds represent a challenging problem. The progressive endarteritis obliterans and microvascular damage, along with fibrotic interstitial changes, result in a wound marked by ischemia and cellular senescence and prone to infection. In addition, aggressive surgical debridement of these wounds often results in larger non-healing wounds. Thus, any surgical debridement should be conservative. Antimicrobial dressings capable of maintaining moist wound healing while promoting autolysis are also useful, as is the use of growth factors and even HBO therapy. In general, these wounds will often need a microvascular free flap to attain stable wound coverage.

FIGURE 3.3. A general algorithm for approaching the patient with a problem wound. After a thorough history and physical examination, appropriate adjunctive diagnostic studies are obtained. Although each wound will vary, the approach should focus on four general themes: optimization of systemic parameters, debridement, control of wound bioburden, and creation of a moist healing environment through appropriate dressings. NPWT, negative-pressure wound therapy.

The Pressure Sore Wound (Chapter 98). Pressure sores represent a common problem affecting nearly 20% of all hospitalized patients. Patients who are prone to develop pressure sores are often debilitated and elderly or suffer from some neurologic injury. Although successful healing can occur in the motivated patient, recurrence is more often the rule. The underlying etiology of these wounds is, by definition, pressure over a bony prominence. Although pressure relief is paramount in promoting healing, aggressive management of comorbidities is critical to establish an adequate healing environment. Most patients with pressure sores are malnourished and cachectic, which makes them more susceptible to wound healing deficits. As a result, they should be aggressively nourished (to an ideal albumin level > 3) and receive vitamin supplementation. Consideration should also be given to the administration of growth hormone or anabolic steroids, such as oxandrolene, as this steroid counteracts the catabolic state of these patients.

Thorough surgical debridement of nonviable tissue is important to alter the biology of the wound from its chronic state, creating a more acute wound. Given that many of these patients are debilitated or insensate, debridement at the bedside is possible. Once a thorough debridement has been performed, adjunctive wound care tools can be used to promote healing. Many of these patients may ultimately require flap reconstruction to obtain a closed wound. A frustrating aspect of the care to these patients is the high rate of recurrence despite the best efforts of the surgeon, which often is a reflection of the patient’s social situation and support system.

Muscle spasms in these patients should be controlled either medically or, in extreme cases, surgically. Dressings should be used strategically. In more superficial pressure sores (stage I or stage II), a moist, clean environment is ideal. Films or hydrogels are often useful in this situation. In deeper, more exudative pressure sores (stage II to stage IV), more absorptive dressings can be used, including hydrocolloids, alginates, or foams. Likewise, in dirty or contaminated wounds, antimicrobial dressings or Dakin’s solution can be used to help reduce bioburden.

A tremendous advance in the care of pressure sore patients has been the evolution of support surface therapies. These therapies are both pressure reducing (reduction of pressure at the ulcer site to a level that is less than that exerted by a regular surface) and pressure relieving (relief of pressure to a level less than the capillary closing pressure). These devices include air-fluidized beds, air mattresses, air flotation and water flotation devices, and low air-loss beds. The variables they control, in addition to pressure, include moisture retention, shear force, and temperature. A major drawback is their expense, which can be significant.

Wounds in Patients with Diabetes (Chapter 95). The foundation of care in the patient with diabetes is recognition that most of the ulcers seen are physiologically similar to pressure sores that have occurred in the setting of neuropathy. The neuropathic ulcer is a multietiologic lesion, with components of pressure necrosis, functional microangiopathy, and true neuropathic derangements. The term “functional microangiopathy” is preferred because, although diabetics do not have anatomic abnormalities in their arterioles and capillaries, they nevertheless do have a dysfunctional microvasculature, with impairments in vasodilatation and compensatory angiogenesis in response to ischemia. The treatment of the diabetic foot is tailored to address these varied components. Management considerations in these patients include selective debridement, tight glucose control, pressure off-loading (either through noncontact orthotics or surgically through Achilles tendon lengthening), revascularization when there is a significant arterial lesion, use of growth factors such as Regranex, and, in certain circumstances, tibial nerve decompression. Given the complexity of the derangements found in the so-called diabetic foot, and the plethora of treatment options, these patients are best served by dedicated multidisciplinary wound/limb salvage centers.

Venous Stasis Wounds. Venous stasis wounds develop in the extremities of patients with incompetent veins, which leads to a complex physiologic environment consisting of venous hypertension and relative ischemia from reduced capillary flow gradients. Compression therapy is essential for these wounds. This is true for patients who have undergone vascular surgery as for those who have not. More sophisticated and individualized compression garments have been developed. One caveat to the use of compression therapy is that this modality is contraindicated in patients with an ABI < 0.7 and should be used under close medical supervision in extremities with an ABI between 0.7 and 0.9.

Rigid compression products include the Unna boot-paste dressings and low-stretch bandages. Elastic compression dressings are more applicable for non-ambulatory patients, as they have a higher resting pressure than rigid products. Types of compression products include stockings, elastic wraps, and multilayer wraps. Use of combination dressings incorporating an elastic component and an absorptive minimally stretching component has achieved widespread acceptance as superior to the traditional Unna boot, which does not achieve optimal pressure by itself. However, when combined with elastic compression wraps, the Unna boot can be quite useful.

Compression garments should be individualized to the patient. Although ideally the pressures exerted should be between 30 and 40 mm Hg, there are situations where more or less pressure can be used. The rationale for 30 to 40 mm Hg therapy is experimental evidence showing that venous stasis ulceration is greatly increased when the ambulatory venous pressure rises above 30 mm Hg. Care should be taken not to exceed the pressure recommended for the clinical indication, as secondary ulcerations can develop. A key to the use of compression therapy is patient compliance and commitment. As treatment progresses, the extremity becomes less edematous and thus limb girth decreases. Patients must recognize when garments are not fitting appropriately and return to the clinic to be resized. Therapy should be continued for several weeks following successful closure of the wound to permit remodeling and strengthening of the neomatrix, and maintenance hosiery needs to be instituted, often for the lifetime of the patient.

Dressings are frequent adjuncts to compression therapy. The choice of dressing is dictated by the amount of drainage present. Because many compression products are worn for days at a time, the dressing chosen must be capable of absorbing high levels of exudates and transudate. When edema and bioburden are controlled, closure is often expedited by the use of tissue-engineered skin substitutes.

The indication for vascular surgical intervention remains superficial venous insufficiency with insufficiency of the perforating system. All patients with venous stasis ulcers resistant to compression therapy merit vascular studies to determine suitability for these interventions. The use of subfascial endoscopic perforator surgery is under intensive study in association with more traditional vascular approaches such as vein stripping.


Significant research is underway in the biology and tissue-engineering potential of autologous stem cells. In the future, it may be possible to augment the wound healing deficits seen in problem wound patients with the use of topical stem cells. In addition, scar modulation and manipulation therapies will likely become available to assist in minimizing the cutaneous stigmata of surgery.


Wound care is an important component of plastic surgery. As students of soft-tissue anatomy, tissue healing, and surgical reconstruction, plastic surgeons are equipped with the tools necessary to treat most wounds. Understanding the fundamental aspects behind the chronic and problem wound, strategies can be employed to alter the wound environment and tip the balance toward healing. Plastic surgeons can also judiciously intervene surgically to promptly close appropriate wounds. Basic science research and translational findings continue to advance our knowledge of wounds and assist in the development of novel treatment approaches. Unfortunately, many of the wound care products in use today are market and industry driven, with little prospective, randomized comparative studies evaluating efficacy. In addition, the concept of wound care centers has been aggressively marketed. While this concept can benefit patients, many centers are company organized and are biased in treatments delivered. In addition, these centers are often staffed by personnel with limited backgrounds in surgery and/or wound healing. The ideal wound care center is multidisciplinary, with participation of committed plastic surgeons who work closely with other team members for the benefit of the patient.

Suggested Readings

1.  Falanga V, ed. Cutaneous Wound Healing. London: Martin Dunitz; 2001.

2.  Galiano RD. Lower extremity ulcers. In: Souba W, et al., eds. ACS Surgery: Principles and Practice. Hamilton: Decker Publishing; 2008.

3.  Hess CT, ed. Clinical Guide: Wound Care. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.

4.  Hunt TK, Hopf HW. Wound healing and wound infection. What surgeons and anesthesiologists can do. Surg Clin North Am. 1997;77:587.

5.  Mustoe T. Understanding chronic wounds: a unifying hypothesis on their pathogenesis and implications for therapy. Am J Surg. 2004;187:655.

6.  Park H, Copeland C, Henry S, Barbul A. Complex wounds and their management. Surg Clin North Am. 2010;90:1181.

7.  Ramasastry SS. Acute wounds. Clin Plast Surg. 2005;32:195.

8.  Ramasastry SS. Chronic problem wounds. Clin Plast Surg. 1998;25:367.

9.  Robson MC, Steed DL, Franz MG. Wound healing: biologic features and approaches to maximize healing trajectories. Curr Probl Surg. 2001;38:72.

10.  Wu SC, Marston W, Armstrong DG. Wound care: the role of advanced wound healing technologies. J Vasc Surg. 2010;52:59S.