This article provides a general approach to the assessment and treatment of poorly healing dermal wounds of the face and neck. When poor healing occurs, it can produce significant functional and cosmetic impairment. A systematic framework for treating these wounds is provided, which focuses on identifying the systemic and local factors contributing to poor healing; provides an overview of the basic tenets of wound treatment; and focuses on a general approach to preparation of the wound bed. In addition, approaching the challenge of an irradiated dermal wound and adjunctive measures to help “jump-start” a wound are discussed.
Key points
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Excellent dermal blood supply to the head and neck allow for these wounds to heal more rapidly and with fewer complications compared to wounds in other areas of the body.
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When poor healing does occur in this area, common causes are from previous irradiation, smoking, ischemia, chronic steroid use, or diabetes.
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The goal of wound treatment is to identify and remove the barriers that keep it in the delayed healing state so that the wound is able to transform into an acute healing state.
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Wounds that exhibit signs of persistent inflammation lasting more than 7 days signifies a prolonged inflammatory phase, constituting a sign of wound complication.
Introduction
Dermal wounds of the face and neck are known to heal more rapidly and with fewer complications in comparison with wounds in other areas of the body. This fact is generally attributed to the excellent blood supply and increased dermal perfusion to the head and neck. Nevertheless, when poorly healing wounds do occur they can be extremely debilitating, both functionally and cosmetically. Poorly healing wounds can lead to facial dysfunction, social stigma, dysphagia, loss of oral competence, and, at times, life-threatening exposure of major blood vessels (carotid artery). When poor healing does occur, it generally results from an underlying impediment to healing (ie, irradiation, smoking, ischemia, chronic steroid use, diabetes). Because of the impact these wounds have on patients, it is imperative that facial surgeons possess a framework for their treatment. This knowledge must be based on the basic tenets of maintaining adequate blood supply, infection control, and wound debridement. In addition, surgeons must be able to identify the local and systemic factors that contribute to poor healing, intervene on the variables that can be altered, and be familiar with the adjuvant techniques for treating recalcitrant wounds.
This review provides a general approach to assess and treat delayed and poor skin-wound healing to the face and neck. The factors that contribute to poor healing are identified, the circumstances of the particularly challenging irradiated dermal wounds are described, and recent modalities to treat refractory skin wounds are presented.
Introduction
Dermal wounds of the face and neck are known to heal more rapidly and with fewer complications in comparison with wounds in other areas of the body. This fact is generally attributed to the excellent blood supply and increased dermal perfusion to the head and neck. Nevertheless, when poorly healing wounds do occur they can be extremely debilitating, both functionally and cosmetically. Poorly healing wounds can lead to facial dysfunction, social stigma, dysphagia, loss of oral competence, and, at times, life-threatening exposure of major blood vessels (carotid artery). When poor healing does occur, it generally results from an underlying impediment to healing (ie, irradiation, smoking, ischemia, chronic steroid use, diabetes). Because of the impact these wounds have on patients, it is imperative that facial surgeons possess a framework for their treatment. This knowledge must be based on the basic tenets of maintaining adequate blood supply, infection control, and wound debridement. In addition, surgeons must be able to identify the local and systemic factors that contribute to poor healing, intervene on the variables that can be altered, and be familiar with the adjuvant techniques for treating recalcitrant wounds.
This review provides a general approach to assess and treat delayed and poor skin-wound healing to the face and neck. The factors that contribute to poor healing are identified, the circumstances of the particularly challenging irradiated dermal wounds are described, and recent modalities to treat refractory skin wounds are presented.
Phases of normal skin healing: a brief synopsis
Acute healing involves a highly complex biological cascade that requires coordination of a variety of cytokines, growth factors, structural elements, and cell types ( Fig. 1 ). This process is simplified by dividing acute healing into 4 phases: coagulative phase, inflammatory phase, proliferative phase, and remodeling phase. These phases need to occur in a well-ordered sequence. If any delay in these healing phases occurs the entire healing process will be prolonged, thus increasing the risk of developing a chronic wound. The goal of treatment of a chronic wound is to actively identify and remove the barriers that keep it in the chronic healing state. By removing the impediments of healing, the wound will be able to reengage into the acute healing phases, thus transforming the wound into an acute healing state. The overall phases of normal healing are briefly described here.
Coagulative Phase (Minutes)
The first phase of wound healing begins with a hemostatic cascade that is initiated within seconds of injury. Thrombocytes are activated by exposed collagen, and activated platelets adhere to the collagen. The extrinsic clotting cascade is activated, and a fibrin-platelet matrix is formed. This matrix not only provides clot formation but also acts as a scaffold, which concentrates growth factors. Platelets, mast cells, and fibrin-split products release factors that incite inflammation and edema.
Inflammatory Phase (2–5 Days)
As a result of platelet degranulation and cytokine cascade, capillaries vasodilate and become permeable, which results in induration and hyperemia. Circulating neutrophils are recruited by chemokines to the wound to phagocytose bacteria and other foreign-body material. Similarly, circulating monocytes appear at approximately day 3, as a result of chemokines, and transform into macrophages. Macrophages are critical in amplifying, coordinating, and sustaining the healing response, releasing numerous growth factors, cytokines, and chemokines. The wound remains in the inflammatory phase as long as bacterial burden or other inflammatory nidus is present. Data suggest that the amount of inflammation that occurs during the inflammatory phase is directly proportional to the amount of scarring that will ultimately result.
Proliferative Phase (3–14 Days)
Neovascularization, angiogenesis, and reepithelialization occur in the proliferative phase. Fibroblasts deposit disorganized type III collagen during the formation of granulation tissue. This granulating tissue replaces the fibrin-platelet matrix as the second provisional matrix for wound healing. After adequate wound-bed granulation tissue has emerged, reepithelialization initiated by keratinocytes occurs from the wound edge and adnexal structures (hair follicles, sebaceous glands, sweat glands). Myofibroblasts contract the wound.
Remodeling Phase (3 Weeks to 1 Year)
Fibroblasts and collagen matrix represent the third scaffold for dermal repair. This extracellular matrix matures as fibroblast and capillary density decreases. Extracellular matrices remodel as a result of regulated proteases, and become more similar to normal skin. The wound continues to mature and contract for up to 1 year. Type III collagen is remodeled and replaced by the stronger and more organized type I collagen. Wound strength plateaus at 80% of its original strength 3 months following injury.
Approaching delayed-healing wounds
The initial step in approaching wounds with delayed healing is to recognize the parameters contributing to its poorly healing state. The microenvironment of a normal acutely healing wound differs from a chronic poorly healing wound, as depicted in Fig. 2 . Armed with knowledge of the phases of acute healing, one should recognize that wounds that exhibit signs of persistent inflammation (redness, swelling, warmth, pain) for more than 7 days are prolonging the inflammatory phase. Prolonged inflammation is a frequent first sign of wound complications. In addition, during the proliferative phase, epithelialization should occur within 2 to 3 weeks. If epithelialization does not occur within this time span, wound healing is delayed. This clinical relevance is especially applicable to monitoring postprocedure partial-thickness wounds that have been subjected to dermabrasion, laser resurfacing, and chemical peels. In addition, the wound should be monitored closely in the postoperative period for evidence of dehiscence, malodor, necrosis, and increased exudate, as these signs also herald poor healing.
After a poorly healing wound is recognized, it is important to thoughtfully consider and identify all factors that are contributing to its delay. These factors include systemic comorbidities that affect the wound environment as well as local tissue factors , explained here in more detail.
Systemic Factors
The most frequent systemic factors that affect wound healing include conditions that impair tissue oxygenation such as cigarette smoking, anemia, chronic obstructive pulmonary disease, congestive heart failure, and vascular disease. Furthermore, common factors that impair the wound-healing cascade are chronic steroid use, hypothyroidism, malnutrition, and renal failure. A more complete list of these systemic factors is displayed in Table 1 . It is important to evaluate for these systemic comorbidities when treating a delayed-healing wound or, more importantly, before initial surgical intervention. A history and physical examination identifies most comorbid conditions. In addition, the authors recommend a laboratory workup during treatment of a chronic wound to identify any unrecognized conditions. Workup includes a complete blood count, renal panel, serum glucose, hemoglobin A1c (HbA1c), nutritional panel (albumin, prealbumin, transferrin), and thyroid-stimulating hormone (particularly for irradiated patients). A rheumatologic workup (erythrocyte sedimentation rate, rheumatoid factor, antinuclear antibodies) and testing for human immunodeficiency virus may be ordered if an immune disorder is suspected.
| Diabetes mellitus |
| Cigarette smoking |
| Anemia |
| Congestive heart failure |
| Vascular disease |
| Chronic obstructive pulmonary disease |
| Renal failure |
| Immune deficiency |
| Alcoholism |
| Prolonged steroid use |
| Hypothyroidism |
| Malnutrition |
| Malignancy |
| Medications |
Collaboration with a primary medical physician is highly desirable when treating a poorly healing wound, as every effort should be made to optimize comorbid conditions. In the authors’ experience diabetes, hypothyroidism, chronic steroid use, and malnutrition seem to be the most commonly modifiable comorbidities that impair healing. Diabetes causes vascular and neurologic impairment, which affects tissue perfusion. In addition, glycosylation impairs inflammatory and cellular processes in the healing cascade. Data suggest that diabetic patients with higher levels of HbA1c are more prone to wound complications than those with more controlled blood-sugar levels. This risk increases proportionally with each percentage point that HbA1c rises above the abnormal range (HbA1c >6.5%). Hypothyroidism impairs wound healing by inhibiting anabolic processes and reducing collagen metabolism. Chronic corticosteroid users are prone to poor healing as a result of impairment of the inflammatory phase of healing, angiogenesis, and collagen deposition. In addition to corticosteroids, a variety of other medications can impair healing and may be modifiable, as displayed in Table 2 .
| Steroids |
| Chemotherapeutic agents |
| Aspirin |
| Penicillamine |
| Cyclosporin |
| Colchicine |
| Phenylbutazone |
| Nicotine |
| Other antirheumatic drugs |
| Other vasoconstricting drugs |
Malnutrition
It has long been accepted that malnourishment leads to delayed skin healing. Like other wound impairments, recognition of malnutrition is the most important initial step in treatment. A thorough history and physical examination is accurate in predicting malnutrition 80% to 90% of the time. If the patient has muscle wasting, cachexia, a history of significant weight loss (>20% signifies severe malnutrition), or gastrointestinal malabsorption (such as history of Crohn disease or gastric bypass), malnourishment is likely. In addition to the history and physical examination, a laboratory workup can be used to evaluate signs of malnutrition such as low serum albumin (<3.0 mg/dL), prealbumin (<15 mg/dL), and transferrin (<200 mg/dL). Albumin has a half-life of 20 days and reflects long-term protein stores. Prealbumin has a shorter half-life of 3 days and can reflect response to treatment.
The best specific nutrient supplementation to address poorly healing wounds has not been universally agreed on. Protein malnutrition is the most recognized form of malnourishment. However, protein depletion rarely occurs as an isolated deficiency and most typically occurs in a globally malnourished state whereby multiple nutrients are diminished. Lipids, amino acids arginine and glutamine, vitamins A and C, and the trace element zinc all may play an important role in wound impairment.
All patients at risk for malnutrition should be treated with protein/multinutrient supplementation as early as possible before surgery. If it is predicted that a patient will not be able to eat for at least 2 weeks, enteral nutrition should be initiated. If enteral feeds cannot be initiated or tolerated, parenteral nutrition should be strongly considered. However, parenteral nutrition does carry an increased risk of sepsis, pneumonia, and other infections. The goals of supplementation are to avoid weight loss, alleviate vitamin and amino acid deficiency, and to maintain a positive nitrogen balance.
Local Tissue Factors
Whereas medical personnel are a helpful adjunct in treating systemic healing impairments, the surgeon should be an expert in clinically optimizing the healing environment of local tissue. Local tissue factors that impair healing include ischemia, venous congestion, wound dehiscence, infection, excessive exudate, desiccation, foreign bodies, irradiated tissue, and necrosis/eschar, as displayed in Table 3 . Treatment begins by assessing the physical characteristics of the wound.
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What are the wound dimensions and depth?
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Are any underlying vascular structures exposed?
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What is the moisture balance of the wound?
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Is there excessive exudate or is the wound desiccated?
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Are there significant necrotic tissues that require debriding?
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Are the wound edges healthy and epithelializing?
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Are there increased inflammatory changes?
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Is purulence present to suggest infection?
| Tissue ischemia |
| Venous insufficiency |
| Foreign body |
| Necrotic tissue |
| Dehiscence |
| Shearing forces |
| Infection |
| Excessive exudates |
Taking into account these clinical findings, the wound is classified as healing, delayed healing, or in a chronic poorly healing state. The impediments to the healing are identified and the impairments systematically treated. In the setting of infection, a wound culture is mandatory. However, in the setting of bacterial colonization a wound culture is not as relevant, because a colonized wound does not have bacterial invasion into viable tissue. A tissue biopsy is important to rule out malignancy in a chronically nonhealing ulcer, bleeding scar, or an otherwise suspicious persistent wound.
Crucial is the institution of the key tenets of local wound care: proper wound debridement, controlling infection, and maintaining adequate blood supply. These concepts culminated in a systematic approach for wound-bed preparation developed by the Wound Consensus Panel in 2003. Wound-bed preparation represents the concept that a poorly healing wound must be adequately prepared to “jump-start” it back into the acutely healing phases. This goal is achieved by methodically identifying the barriers that delay its healing to promote its endogenous healing. The tenets of wound-bed preparation are depicted in Table 4 and are represented by the acronym TIME :
Tissue
Infection/Inflammation
Moisture imbalance
Edge
| TIME Acronym | Clinical Observations | Proposed Pathophysiology | WBP Clinical Actions | Effect of WBP Actions | Clinical Outcomes |
|---|---|---|---|---|---|
| T | Tissue nonviable or deficient | Defective matrix and cell debris impair healing | Debridement (episodic or continuous)
| Restoration of wound base and functional extracellular matrix proteins | Viable wound base |
| I | Infection or inflammation | High bacterial counts or prolonged inflammation ↑ Inflammatory cytokines ↑ Protease activity ↓ Growth factor activity |
| Low bacterial counts or controlled inflammation: ↓ Inflammatory cytokines ↓ Protease activity ↑ Growth factor activity | Bacterial balance and reduced inflammation |
| M | Moisture imbalance | Desiccation slows epithelial cell migration. Excessive fluid causes maceration of wound margin | Apply moisture-balancing dressings, compression, negative pressure, or other methods of removing fluid or surgical skin coverage | Restored epithelial cell migration, desiccation avoided, edema and excessive fluid controlled, maceration avoided | Moisture balance |
| E | Edge of wound, nonadvancing or undermined | Nonmigrating keratinocytes, nonresponsive wound cells, and abnormalities in extracellular matrix, or abnormal protease activity | Reassess cause or consider corrective therapies
| Migrating keratinocytes and responsive wound cells. Restoration of appropriate protease profile | Advancing edge of wound |
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