Acute Wounds

Clin Plastic Surg 32 (2005) 195 – 208

Acute Wounds Sai S. Ramasastry, MD, FRCS, FACS Division of Plastic Surgery, University of Illinois at Chicago, 820 South Wood Street (M/C 958), 515 CSN, Chicago, IL 60612, USA

Few if any ‘‘rules’’ govern the management of acute wounds. A basic knowledge of wound healing and a clear understanding of the potential risks and benefits of the selected therapy are paramount. This article addresses the basic concept of normal wound healing and the management of acute wounds.

Basic concepts of normal wound healing In the past several decades, we have learned a great deal about the biochemistry, molecular biology, and cell physiology of the events that lead to a healed wound (Fig. 1). The physiologic mechanisms of wound healing are similar in different tissues with slight variations. This article covers the healing of acute wounds. Wound healing is classically divided into three phases: the early, intermediate, and terminal phases (Fig. 2). The initial response to injury, whether mechanical, immunologic, thermal, or chemical, is a nonspecific inflammatory response. In all injuries that involve the skin, blood vessels are disrupted, resulting in bleeding. Immediately following injury, there is a period of vasoconstriction lasting 5 to 10 minutes, activation of platelets, and the coagulation cascade to produce hemostasis. The vasoconstriction in the early onset is mediated by catecholamines and prostaglandins. Platelets aggregate when exposed to the intravascular collagen and release adenosine diphosphate, which, in the presence of calcium, stimulates further platelet aggregation [1,2]. Platelet aggregation also

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leads to the release of cytokines, which include platelet-derived growth factor (PDGF), transforming growth factor – a (TGF-a), and transforming growth factor – b (TGF-b); these play a critical role in the later phases of wound healing. Coagulation pathways result in the production of thrombin, which catalyzes the conversion of fibrinogen to fibrin. Thrombin and fibrin contribute to hemostasis and later to other aspects of wound healing [3]. Vasoconstriction is followed by a period of vasodilatation, probably mediated by bradykinin and histamine. Thrombin contributes to the increased vascular permeability and facilitates the migration and diapedesis of leucocytes through ‘‘leaks’’ in the vascular endothelium in the zone of injury. Fibrin produces a scaffold for the migration of inflammatory and mesenchymal cells. Vasodilatation is also mediated by kinins, prostaglandins, and endothelial cell products [4,5]. Vasodilatation and cellular diapedesis lead to the characteristic physical signs of inflammation: erythema (rubor), heat (calor), pain (dolor), and edema.

Inflammatory phase The predominant initial cell type is the polymorphonuclear leucocyte, which assists in wound debridement [6]. Neutrophils, macrophages, and lymphocytes are involved in the inflammatory phase of injury (Fig. 3). Chemotaxis is the movement of an organism or cell type in response to a chemical concentration gradient. Chemotactic agents contribute to the migration of leucocytes into the extravascular space. The leucocytes phagocytose injured tissue and bacteria. Neutrophils die after phagocytos-

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plasticsurgery.theclinics.com

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COAGULATION PLATELETS

INFLAMMATION LYMPHOCYTES MACROPHAGES GRANULOCYTES

DEBRIDEMENT RESISTANCE TO INFECTION

FIBROBLASTS NEOVASCULAR GROWTH

EPITHELIUM

CONTRACTION

PROTEOGLYCANS SYNTHESIS COLLAGEN SYNTHESIS

COLLAGEN LYSIS

(REMODELING)

HEALED WOUND

Fig. 1. Schematic concept of wound healing. (From Hunt TK, Knighton DR, Thakral KK, et al. Cellular control of repair. In: Hunt TK, Heppenstall RB, Pines E, et al, editors. Soft and hard tissue repair. New York: Praeger; 1984. p. 5; with permission.)

elastases that help break down the wound matrix [11,12]. Macrophages are the primary site of cytokines that stimulate fibroblast proliferation, collagen production, and other healing processes. Macrophages are probably the most important cell in the wound healing process. Lymphocytes produce factors essential for normal wound healing [13]. They are also involved in cellular immunity and antibody production. The critical cytokines liberated are probably epidermal growth factor (EGF) and basic fibroblast

Healing Activity

ing damaged tissue and bacteria; they do not play a role in the subsequent events of healing in an uncomplicated wound (Fig. 4). Macrophages are nothing but monocytes transformed by a process mediated by serum factors and fibronectin [7 – 9]. The migration of macrophages in the wound bed is mediated by chemotactic factors. Macrophages are tremendously important in normal wound healing [10]. Macrophages phagocytose bacteria and dead tissue and secrete collagenases and

Hemostasis Inflammation

Mesenchymal Cell Migration and Proliferation, Angiogenesis, Epithelialization

1

Collagen Synthesis, Wound Remodeling Wound Contraction, Proteoglycan Synthesis

4

21

365

Days Post Wounding Fig. 2. Phases of the healing process. (From Lawrence WT. Physiology of the acute wound. Clin Plast Surg 1998;25(3):323; with permission.)

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Primary Cell Type in Wound

acute wounds

Intermediate phase

Fibroblasts

Macrophages

Neutrophils

RBC, Platelets

1

2

5

21

Days Post Wounding Fig. 3. Cellular makeup of the healing wound. RBC, red blood cells. (From Lawrence WT. Physiology of the acute wound. Clin Plast Surg 1998;25(3):327; with permission.)

Relative Numbers of Cell Types

growth factor. In the acute wound, neutrophils predominate initially, but by the third day, the macrophages predominate. What makes acute wounds become chronic? Foreign material or bacteria can cause persistent chronic inflammation. Although the acute inflammatory phase is necessary for normal wound healing, the persistence of chronic inflammation is often deleterious [14]. The persistence of neutrophils in the wound can cause release of destructive proteolytic enzymes and free radicals, which damage tissues. The oxygen free radicals lead to persistent tissue destruction. Areas of chronic inflammation can become encapsulated, leading to granuloma formation.

Platelet RBC Neutrophil

The intermediate phase of wound healing includes mesenchymal cell chemotaxis, mesenchymal cell proliferation, angiogenesis, and epithelialization. These processes are mediated by cytokines. The cytokines that are well described include PDGF, TGF-b, EGF, acidic and basic fibroblast growth factor (aFGF, bFGF), TGF-a, tumor necrosis factor (TNF), interleukin-1 (IL-1), and insulin growth factor (IGF) (Table 1). Fibroblasts are the primary mesenchymal cells involved in wound healing. They normally reside in the dermis. Undifferentiated mesenchymal cells in the area of injury may also differentiate into fibroblasts when stimulated by chemotactic factors. PDGF is chemotactic for both fibroblasts and smooth muscle cells [15,16]. Fibronectin is a primary component of extracellular matrix and is chemotactic for fibroblasts. PDGF also acts as a potent mitogenic stimulus for both fibroblasts and smooth muscle cells, augmenting the wound’s mesenchymal cell population. Mesenchymal cell proliferation can also be stimulated by TNF, IL-1, lymphokines, and IGF [17,18]. Wound angiogenesis is stimulated by high lactate levels, acidic pH, and decreased oxygen tension (pO2) in the tissue. The capillary sprouts continue to grow and interconnect, forming patent vascular loops. Cytokines primarily involved in angiogenesis include bFGF, TGF-a, TGF-b, vascular endothelial growth factor, and prostaglandins. These stimulatory cytokines diminish when the wound is completely vascularized [19 – 21].

Macrophage

Fibroblast

0 1

2

3

4

5

10

15

20

Days Post Wounding Fig. 4. Cellular phase of wound healing. Relative concentrations of various cellular components versus time in the healing wound. RBC, red blood cells. (From Lawrence WT. Wound healing biology and its application to wound management. In: O’Leary JP, Capote LR, editors. The physiologic basis of surgery. 2nd edition. Baltimore (MD): Williams and Wilkins; 1996. p. 121; with permission.)

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Table 1 Cytokine involvement in wound healing functions Healing function

Cytokine involved

Inflammatory cell migration

PDGF TGF-b TNF-a PDGF TGF-b EGF PDGF TGF-b EGF IGF TNF-a IL-1 bFGF (FGF2) aFGF (FGF1) TGF-b TGF-a EGF TNF-a VEGF IL-8 PD-ECGF EGF TGF-a KGF (FGF7) bFGF (FGF2) IGF HB-EGF PDGF TGF-b bFGF (FGF2) EGF

Fibroblast migration

Fibroblast proliferation

Angiogenesis

Epithelialization

Collagen synthesis

Abbreviations: HB-EGF, heparin-binding epidermal growth factor; IL-8, interleukin-8; KGF, keratinocyte growth factor; PD-ECGF, platelet-derived endothelial cell growth factor; VEGF, vascular endothelial growth factor. From Lawrence WT. Physiology of the acute wound. Clin Plast Surg 1998;25(3):322; with permission.

Epidermal cells constantly regenerate to provide a barrier between the external environment and the internal milieu. The process by which the epidermal cells regenerate and migrate to cover a wound is called ‘‘epithelialization.’’ This process is important in the healing of partial-thickness wounds, such as abrasions, superficial burns, and split-thickness skin graft donor sites. Epithelial cells involved in the healing of partial-thickness wounds derive from the wound edges and epithelial appendages, such as hair follicles, sweat glands, and sebaceous elements. Epithelialization in an incisional wound is rapid, usually taking 24 to 38 hours, because the cellular migration is less than a millimeter from one side of the incision to the other. However, in large wounds, such

as superficial burns and split-thickness skin graft donor sites, the process takes several weeks, depending on the size of the defect. The process of epithelialization involves cellular detachment, proliferation, and differentiation. The marginal basal cells migrate toward the center of the wound as a monolayer and exhibit contact guidance [22,23]. These cells migrate until they reach cells migrating from the opposite direction, and the migration stops by ‘‘contact inhibition.’’ The new surface epithelial cells begin to keratinize. The re-epithelialized surface has fewer basal cells and no rete pegs. The epithelium is thicker at the wound edges than in the midportion of the re-epithelialized area. Late phase of fibroplasia Fibroplasia involves the production of collagen in the wound. Collagen makes up more than 50% of the protein in scar tissue [24]. Collagen is synthesized primarily by fibroblasts, beginning 3 to 5 days after the injury. The rate of collagen synthesis increases rapidly by 3 to 4 weeks, then rapidly declines. Finally, there is a balance between the rates of collagen production and collagen destruction by collagenase. Age, tension, pressure, stress, and TGF-b affect the rate of collagen production. In human skin, type I collagen makes up 80% to 90% and type III the remaining 10% to 20%. Type III collagen is seen predominantly in the early phase of wound healing. Types II and XI are seen in cartilage, type IV in basement membranes, and type V in smooth muscle cells. Collagen consists of three polypeptide chains, each twisted into a right-hand helix. The alignment of these three chains into a triple helix is facilitated by nonhelical terminal peptide sequences. Most polypeptide chains in collagen are alpha chains. The collagen synthesis is also facilitated by hydroxylation of lysine and prolene. The hydroxylation is required for covalent crosslink formation. It requires specific enzymes for lysine and prolene and cofactors oxygen, vitamin C, a-ketoglutarate, and ferrous iron. The hydroxylation and crosslinking are prevented by deficiencies of vitamin C and oxygen and by corticosteroids, resulting in poor wound healing. The collagen molecule is synthesized into the extracellular matrix in the form of procollagen. The procollagen is converted into tropocollagen, which then aggregates into collagen fibrils. This fibrin formation is facilitated by proteoglycans in the extracellular matrix. Proteoglycans are synthesized primarily by fibroblasts and include chondroitin sulfate, dermatan sul-

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acute wounds

Wound contraction Wound contraction begins 4 to 5 days after wounding. The process involves centripetal movement of the wound edge toward the center of the wound. Maximal wound contraction continues for 12 to 15 days, as long as the wound remains open. Wound contraction progresses at an average of 0.6 to 0.75 mm per day. The tissues that have the greatest laxity demonstrate the greatest degree of wound contraction. Therefore, wounds in areas overlying bone, such as the tibia and scalp, contract very little. Wound contraction is a major contributor to the healing of full-thickness open wounds compared with incisional wounds. Wounds with square edges contract more rapidly than circular wounds. Although wound contraction is beneficial to wound healing, contraction of large open wounds across joint surfaces can lead to limitation of motion secondary to contractures. Contractures are commonly seen in burn wounds in the submental and neck areas, axillae, elbows, and other joint surfaces. The most accepted mechanism of wound contraction is attributed to myofibroblasts. Myofibroblasts were first described by Gabbiani et al [26] in 1971. Myofibroblasts most likely derive from normal fibroblasts in acute wounds and first appear on the third day after wounding. They persist in large numbers until about 21 days post-wounding. They are primarily found in the periphery of the wound. Experiments indicate that myofibroblasts pull the wound edges together in a ‘‘picture frame’’ fashion [27]. An alternative theory is that wound contraction is secondary to fibroblasts that undergo modification with stress fibers in their cytoplasm at the wound edges. Contraction is a cell-directed process that requires cell division but not collagen synthesis. PDGF and TGF-b appear to be mediators of wound contraction, whereas FGF and IGF inhibit it. Radiation and

cytotoxic drugs delay contraction by inhibiting cellular activity. Wound contraction can be detrimental in some areas, such as joint surfaces, neck, and axilla. Wound contraction can be limited by early skin grafting, fullthickness skin grafts, and splinting. Myofibroblasts disappear from the wound more frequently after a full-thickness skin graft compared with a splitthickness skin graft [28]. No pharmacologic agents inhibit wound contraction. Scar remodeling Scar remodeling is the terminal wound healing event. The collagen content of a healed wound is maximal at 21 days after injury. However, the bursting strength of the wound is only 15% that of normal skin (Fig. 5). Scar remodeling is a process to increase the wound’s bursting strength. By 6 weeks after the wounding, the wound bursting strength is 60% to 70% that of normal skin. By about 6 months, the wound bursting strength reaches a plateau at 80% of normal skin. The process of scar remodeling involves an increase in intra- and intermolecular crosslinks between collagen fibers. This increase in crosslinking is the major contributor to the increase in wound breaking strength. During this process, the quantity of type III collagen decreases as it is replaced by type I collagen. The quantity of water and glycosaminoglycans in the matrix also decreases. The scar remodeling continues over a period of 10 to 12 months. This is visible as the scar becomes less indurated, softer to the touch, and less red, assuming a color closer to the adjacent skin. Therefore, scar revision should not be undertaken for at least 6 to 8 months. The scar maturation process also involves an increase in col100%

Tensile Strength of Intact Skin

fate, heparin, heparin sulfate, keratin sulfate, and hyaluronic acid. The biologic functions of proteoglycans are not well understood. The proteoglycans can potentiate cytokines involved in angiogenesis and cellular migration. Other key components of the wound matrix are fibronectin and other attachment proteins. Fibronectin is produced by fibroblasts and epithelial cells [25]. It aids in cellular attachment, cellular migration into the wound matrix, and binding of epithelial cells to the matrix and thus contributes to epithelialization and fibroblast migration. Another component of the connective tissue is elastin. Elastin is lacking in normal scar, which hence lacks the elastic properties of normal skin.

90% 80% 70% 60% 50% 40% 30% 20% 10% 0% 10

20

30

40

50

60

Days Post Wounding Fig. 5. Tensile strength of the healing wound. (From Lawrence WT. Physiology of the acute wound. Clin Plast Surg 1998;25(3):334; with permission.)

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lagenolytic activity. The activity of collagenolytic enzymes is modulated by several tissue inhibitors of metalloproteases. Other enzymes, such as hyaluronidase, may be involved in scar remodeling [29]. Factors that impair wound healing It is important to have a clear understanding of the factors that may lead to impaired wound healing. Many factors, both local and systemic, can contribute to poor wound healing (Table 2). A diagnosis of the factors that can impair wound healing must be established so that healing conditions can be optimized by controlling the systemic factors and providing sound local wound care [30]. These factors, if not addressed early in the management of acute wounds, can lead to delayed healing or nonhealing wounds. Local ischemia and tissue hypoxia should be recognized both by history and clinical evaluation [31]. In infected wounds, the healing process is retarded or delayed by a prolonged inflammatory response. These wounds do not heal until the infection is controlled. Foreign bodies can predispose to infection, thereby delaying healing. Foreign bodies also prolong the inflammatory response. Radiation causes local tissue ischemia, and incisions in a radiated bed are slow to heal. Extrinsic or systemic factors that impair wound healing include diabetes mellitus, steroids, smoking, chemotherapeutic agents, cancer, nutritional deficiencies, liver disease, chronic renal failure, and hereditary factors. The list is by no means complete. Uncontrolled diabetes has been demonstrated to impair wound healing [32,33]. Proper control of blood sugar and prevention or aggressive treatment of infection are crucial. Steroids have been shown to affect all aspects of the wound healing process [34]. The effect of steroids on wound healing can be reTable 2 Factors that impair wound healing Intrinsic factors

Extrinsic factors

Ischemia Infection Foreign bodies Cigarette smoking Venous insufficiency Radiation fibrosis Repeated trauma Local toxins Cancer

Nutritional deficiencies Diabetes mellitus Chronic renal failure Steroids Chemotherapeutic agents Distant malignancies Old age Liver disease Other drugs Hereditary factors

From Ramasastry SS. Chronic problem wounds. Clin Plast Surg 1998;25(3):368; with permission.

versed by administration of vitamin A [35]. Smoking causes cutaneous vasoconstriction. Additionally, elevated levels of carboxyhemoglobin can adversely affect the oxygen-carrying capacity of blood [36]. Chemotherapeutic agents are more potent inhibitors of wound healing when delivered preoperatively rather than postoperatively. Therefore, any elective surgery should be planned appropriately, and chemotherapy should be deferred until after surgery [37,38].

Promoting wound healing in acute wounds Improving tissue perfusion and tissue oxygenation Adequate tissue perfusion, blood flow, and oxygen levels are requisites for wound healing [39]. Tissue perfusion is essential for the delivery of necessary nutrients, including oxygen, to the healing tissues. Oxygen is necessary for the opsonizing function of neutrophils and macrophages, the hydroxylation of prolene and lysine, and collagen synthesis [40]. Angiogenesis in an acute wound is facilitated by local wound hypoxia, which in turn causes wound hyperoxia. This hypoxia – hyperoxia cycle facilitates collagen synthesis. The rate of epithelialization is accelerated by hyperoxia and significantly slowed by hypoxia [41]. The control of bacterial population in wounds is critical for successful wound healing. The ability of leucocytes to remove bacteria depends significantly on oxygen-dependent systems [42]. In a hypoxic environment, wound infection rate increases, as may be noted in an ischemic wound. A local pO2 of 30 mm Hg or greater is required for leucocytes to kill bacteria effectively [43]. Therefore, maintaining excellent tissue perfusion and oxygen supply should reduce the risk of wound infection and facilitate wound healing. Patients undergoing cardiac and vascular procedures appear to be at a higher risk for wound complications, including infection, that are attributed to wound hypoxia [44]. Tissue perfusion also correlates with the availability of oxygen to the tissues. Tissue perfusion is affected adversely when the circulating blood volume decreases, as seen in severe hemorrhage, dialysis patients, and cases of dehydration [45,46]. It has been demonstrated that subcutaneous oxygen tensions are reduced secondary to hypovolemia, reflecting less than optimal oxygen delivery to the healing tissues. Supplemental intravenous fluids can correct this problem. Current evidence from clinical studies indicates that either colloid or crystalloid fluid replacement will support peripheral blood flow, oxygen levels, and wound healing [47]. Other factors in

acute wounds

optimizing perfusion include warming patients and maintaining the body core temperature. Regional blocks do not affect tissue perfusion, oxygenation, and wound healing [48]. The work done with epidural analgesia and anesthesia indicates that, although the time required for supplemental oxygen to reach the tissues is reduced after epidural anesthesia, regional vasodilatation and improved blood flow may be beneficial. Further studies are needed to document blood flow changes and wound healing outcomes. Supplemental oxygen Support of arterial oxygen tension is necessary to ensure that oxygen is available for transport to tissues. It has been demonstrated that supplemental oxygen increases oxygen tension peripherally, provided that perfusion is maintained [49,50]. Supplemental oxygen is indicated in the early postoperative period, particularly for patients who are likely to be at risk for wound healing problems (eg, those with longer surgical procedures, cardiovascular and abdominal surgeries, emergent surgeries, or severe infections, such as necrotizing fasciitis) [51]. Tissue oxygen levels are dependent on blood flow and adequate arterial oxygen content. Therefore, the importance of blood flow and tissue perfusion cannot be overemphasized. Studies currently in progress examine the postoperative effects of supplemental oxygen therapy on wound healing outcomes. For the moment, it appears prudent to administer supplemental oxygen at doses that correct saturation levels below 94% until patients can consistently maintain acceptable Spo2 levels. Body core temperature regulation Thermoregulation may benefit wound healing and increase resistance to infection [52]. Reduction in body temperature causes cutaneous vasoconstriction, decreased tissue perfusion, and low tissue oxygen levels. The negative effects of hypothermia on resistance to infection have recently been reported. Experimental data from animals and humans indicate that wound infection rate is significantly increased in the hypothermic state compared with the normothermic state. It is likely that the increased resistance to infection associated with normothermia is due to effects on the oxidative killing mechanisms of neutrophils and macrophages and the augmentation of immune system responses [53]. Warming of inhaled gases, use of infusion fluids, and application of body warmers are some of the methods commonly used to maintain the body core temperature, in the trauma units and during and post-surgery. Modifying the wound environment by means of local application of heat may facilitate

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wound healing. This area of increasing study has a high potential to affect wound healing. Nutrition Adequate nutritional status influences both wound healing and immune function. Cellular proliferation, phagocytosis, and the production of matrix have tremendous energy demands. Proteins, carbohydrates, and fats are required for these processes, as are vitamins and minerals. Many enzyme systems involved in wound healing are dependent on the availability of proper nutrients. The roles of ascorbic acid (vitamin C), vitamin A, copper, and zinc are well documented [54,55]. Currently, there are no well-accepted recommendations for nutritional support to influence wound healing. Most recommendations involve correcting or replacing deficiencies. Patients prone to poor nutrition include those with gastrointestinal diseases, such as Crohn’s disease, malabsorption, diarrhea, dialysis, alcoholism, cancer, and chronic illness, as well as elderly patients living alone. It is becoming increasingly clear that even mild nutritional deficiencies may impair wound healing [56]. Experimental and clinical data emphasize the need to evaluate the patient’s dietary history and nutritional status before surgical procedures, because the risk of wound healing impairment increases in the face of protein-energy malnutrition. Wounds cause variable degrees of metabolic stress, based on their size and complexity. Secretions and drains are additional sources of protein loss. Sepsis is a major source of metabolic stress. Therefore, recognition of these stress factors and provision of nutritional support are crucial to optimizing wound healing. Nutritional substrates may be particularly important during acute illnesses and metabolically stressful states. Clinically, patients who received an enteral diet supplemented with arginine, RNA, omega 3, and omega 6 fatty acids for gastrointestinal surgery had significantly fewer wound healing complications [57]. Wound healing can successfully be supported by nutrition, either by enteral or by parenteral route. Whenever the patient can eat and has no malabsorption, enteral feeding is preferred. A number of factors must be considered in selecting the preferred route: gastrointestinal function, access, length of time needed for nutritional support, number of calories required per day, and activity level.

Acute wound care The management of all acute wounds starts with a thorough history and physical examination. This

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procedure is often difficult in an emergency room setting, especially when the patient is intoxicated and combative and the treating physician is in a rush. The initial evaluation should identify all injuries and rule out associated occult injuries. The occult injuries may be life-threatening—for instance, intraabdominal trauma, injury to the brain and cervical spine, thoracic injuries, or airway injury. Patient safety comes first. The treating physician should identify the time and mechanism of injury, associated medical problems, tetanus immunization status, medications, and allergies. The basic question is whether the patient is stable or unstable and whether the patient needs resuscitation. Airway management should be prompt. Appropriate radiographs of the C-spine and CT scans of the head, chest, and abdomen help rule out occult injuries. Wound exploration can be performed in the emergency room or in the operating room, based on the location and complexity of the wound, the patient’s age, pain tolerance, associated injuries, and ability to cooperate, and the length of time required for the procedure. The basic wound healing process is the same regardless of how the wound is managed. From a clinical perspective, wound healing may be separated into primary, secondary, and tertiary or delayed primary intention. Primary wound healing follows acute closure of wounds. The healing is quick with minimal scar (eg, surgical closure of a clean laceration). Secondary wound healing occurs when the wound is allowed to heal secondarily by contraction, granulation, and epithelialization (eg, burn wounds). In tertiary healing, or the delayed primary method, a wound left open for several days is closed by bringing the edges together. Basic wound management has four components: evaluation and planning, wound preparation, wound closure, and wound dressing. Most acute wounds, with the exception of surgical wounds, are potentially contaminated. These wounds are cleaned by appropriate irrigation, debridement, trimming of the wound edges, if they are irregular, and excision in some cases. The decision to close an acute wound is based on (1) the age of the wound, (2) the degree of wound contamination, and (3) whether the wound is infected. Wounds that are often left open include human bite wounds, blast injuries, and severely contaminated or fecally contaminated wounds. Although these wounds are initially treated open, they are amenable to a delayed primary closure. In patients with severe injuries, wounds can be left open unless vital structures are exposed, such as major vessels, joints, and dura. The wound should be thoroughly irrigated with saline or antibiotic solution and dressed with

moist, absorbent gauze dressings. Injured extremities should be splinted. Wound debridement Wound debridement is the most important of the four parts of wound management. It involves sharp debridement or wound excision with a knife blade or sharp, curved scissors. More recently, ultrasound and lasers have been used for wound debridement. The direction of the wound may be changed during the debridement to coincide with the lines of skin tension and achieve a better scar. Importance should be given to both cosmesis and functional outcome (eg, in the periorbital region). Sharp debridement helps convert a dirty, contaminated wound to a clean wound, reorient lacerations, and remove devitalized tissue. Foreign bodies on the wound surface can be removed easily using a sponge, a scrub brush, or a toothbrush. Any deeply embedded dirt is removed with a sharp blade to prevent traumatic tattoos. Occasionally, fluoroscopy may be necessary to remove deeply embedded metallic foreign bodies, such as bullet or shrapnel fragments. Wound preparation The most commonly used antiseptic solutions in wound preparation are hexachlorophene (pHisoHex, Beyer Corp., Myerstown, PA) and complexed iodine solutions (Betadine, Novation Inc., Irving, TX). Any agents that are toxic to the wound should be avoided (Table 3). Wound irrigation with a 19-gauge

Table 3 Toxicity of topical agents Agent Saline Pluronic F-68 Betadine prep solution (povidone-iodine solution) Hexachlorophene solution Quaternary ammonia solution Hydrogen peroxide Betadine surgical scrub (povidone-iodine and detergent) pHisoHex (hexachlorophene and detergent) Isopropyl alcohol

Relative toxicity 0 0 1+ 2+ 3+ 6+ 8+ 8+ 10+

Saline (0) is the standard. The higher the number, the more caustic the agent. From Zurkin DD, Simon RR. Toxicity of topical agents. In: Emergency wound care — principles and practice. Rockville (MD): Aspen; 1987. p. 30; with permission.

acute wounds

needle and a 30-mL syringe provides adequate force (pressure greater than 8 psi) for an effective wound preparation. A word of caution on the use of topical antimicrobial agents is in order. Although the efficacy of topical antimicrobial agents is well documented, daily exposure to even dilute solutions of the commonly used topical agents (1% providoneiodine, 3% hydrogen peroxide, 0% – 25% acetic acid, and 0% – 5% sodium hypochlorite) may reduce wound healing and wound tensile strength [58,59].

Wound closure Superficial wounds are usually allowed to reepithelialize by providing a moist wound healing environment. Lacerations with low to moderate contamination are closed primarily after adequate debridement. Heavily contaminated wounds should be debrided, irrigated, and packed, followed by a delayed primary closure. Simple superficial lacerations are easily amenable to Steri-strip (3M Healthcare, St. Paul, MN) closure. For deeper, more complex lacerations, a layered closure is required to achieve a good cosmetic result. A tension-free closure is important and may require undermining of the wound edges. Dead space is eliminated by closing the deeper layers with absorbable sutures. Buried dermal sutures of absorbable material can align skin edges. The skin edges can be approximated with Steristrips, tissue glue, (Dermabond, Ethicon Inc., Johnson & Johnson, Somerville, NJ), or fast-absorbing gut or nonabsorbable suture. Whenever skin sutures are used, it is important to remove them as early as possible to avoid ugly stitch marks, especially in facial wounds. The location, depth, and complexity of the wound, the patient’s age, the patient’s degree of cooperation, and the presence or absence of associated injuries dictate whether one uses local or general anesthesia for the wound care. Lidocaine (Xylocaine) 0.5% to 1% with 1:100,000 epinephrine is used except in the hand. The recommended dose of lidocaine is 4 to 5 mg/kg, and the dose of lidocaine with epinephrine is 7 to 10 mg/kg. Topical anesthetics that may be used include ethylene glycol spray, lidocaine spray, lidocaine and carbacaine creams, and topical cocaine for the nose. When a soft tissue defect is too large to be closed primarily or when the primary closure results in unwanted tension and tissue distortion (eg, eyebrow, eyelid, oral commissure), either a local skin flap or a skin graft may be used. If local skin flaps are inadequate, pedicled muscle or musculocutaneous flaps

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or microvascular free flaps may be required to treat acute wounds, to cover exposed tendons, fractures, joints, dura, and major vessels, or for vascular prosthesis. Large, superficial, simple wounds are traditionally treated successfully with split-thickness skin grafts, 0.015 in. However, facial wounds often require full-thickness skin grafts to treat periorbital, perioral, and nasal areas and to prevent wound contractures and secondary deformities. The pre- and postauricular and supraclavicular regions are excellent donor sites for full-thickness skin grafts. Whenever a skin graft, skin flap, or muscle flap is planned, it is better to debride the wound and carry out dressing changes for 48 to 72 hours before the final wound coverage. This delay will help ensure that the wound has been adequately debrided and any potential infection eradicated.

Use of antibiotics Infection of traumatic wounds is related to a multitude of factors, including mechanism of injury, time elapsed since injury, wound contamination, and the presence of local or systemic factors that impair wound healing (see Table 2). All traumatic wounds are potentially contaminated, with an infection rate of 15% [60]. Infection rate is significantly reduced by thorough debridement and gentle tissue handling [61]. Research has shown that antibiotics administered preoperatively are most effective in preventing infection. Tetanus prophylaxis is key in all acute traumatic wounds (Table 4). When treating acute wounds, the decision to use antibiotic treatment is based on (1) the mechanism of injury, (2) the degree of wound contamination, (3) the patient’s delay in seeking treatment, and (4) the presence of overt signs of infection. Antibiotic treatment should not be a routine measure, especially in fresh elective surgical wounds. Systemic antibiotics should be used to treat active infections, such as cellulitis, phlebitis, and lymphangitis, grossly contaminated wounds, or active wound infection [62]. Bite wounds should be treated with antibiotics, with the choice determined by the patient’s history (Table 5).

Wound dressings No ideal wound dressing exists. The principal function of a wound dressing is to provide an optimal healing environment. The best way to expedite healing and minimize pain and discomfort is to close

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Table 4 Guidelines for tetanus prophylaxis Tetanus toxoid immunization

Wound typea

Tetanus toxoid

Tetanus immuine globulin

Three or more, the last Three or more, the last Three or more, the last Three or more, the last Three or more, the last Three or more, the last Unknown or < three Unknown or < three

Clean, minor Significant Clean, minor Significant Clean, minor Significant Clean, minor Significant

No No No Yes Yes Yes Yes Yes

No No No No No No No Yes

within 5 years within 5 years within 10 years within 10 years > 10 years > 10 years

a

Clean, minor = clean, superficial wounds. Significant = contaminated wounds, punctures, burns, frostbite, crush injuries, suturable lacerations. From Zurkin DD, Simon RR. Emergency wound care—principles and practice. Rockville (MD): Aspen; 1987. p. 28; with permission.

the wound. Once the wound is closed, the suture line can be left open to the air. Other popular measures to protect the skin closure include application of Steristrips, Band-aids, and occlusive and nonocclusive dressings. In children, pain and distress related to trauma and dressing change create a particular problem. These factors have a psychologic impact on the child and family. The beneficial effects of moist wound healing, as provided by occlusive dressings in acute wounds (surgical wounds, traumatic wounds, and burns) have been demonstrated in various studies. Regarding the use of occlusive hydrocolloid dressings in the treatment of acute wounds, evidence indicates a shorter healing time, lower frequency of infections, and greater compliance of patients, due to their minimal pain and greater ability to carry out their daily activities [63]. Data indicate that hydrocolloid dressings protect wounds equally well in adults and children and cause significantly less pain, both when in place and during removal, than do conventional absorbent

gauze dressings. Therefore, hydrocolloid dressings are excellent for treating skin-graft donor sites, dermabraded or laser-resurfaced areas, and abrasions [64]. The colloid gel produces an absorption gradient for soluble components within the exudate, thereby allowing the removal of toxic components produced by cellular and bacterial destruction. A new concept in the management of wounds is the application of negative pressure (vacuum assisted closure) therapy. It is simple to use and has many potential benefits [65], including reduction of edema, improvement in blood supply, rapid formation of granulation tissue, reduction in bacterial count, and reduction in wound size. It is an excellent technique to prepare the wound for definitive closure. Bite wounds The common bite wounds are secondary to dog, human, and cat bites. In zoo keepers, exotic animal bites are seen. All bite wounds should be thoroughly

Table 5 Choice of antimicrobials for prevention of infection in specific wounds Type of wound

Antimicrobial of choice

Adult dose (g)a

Human bite seen within 1 – 2 days

Penicillin or ampicillin (alternative: erythromycin) Dicloxacillin (alternative: erythromycin) Ampicillin (penicillin for cat bites) (alternative: tetracycline) Dicloxacillin (alternative: erythromycin)

0.5 – 1.0

Human bite older than 2 days Animal bites Other wounds

0.5 0.5 0.5 0.5 0.5 0.5

These recommendations apply only to wounds without evidence of infection at the time of examination. a Four times daily orally for 3 to 5 days. From Walton RL. Wound Care. In: Mills J, Ho MT, Trunkey DD, editors. Current emergency diagnosis and treatment. Los Altos (CA): Lange; 1985. p. 655; with permission.

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debrided and irrigated, or excised when necessary and possible. Most bite wounds can be closed after debridement. Human bite wounds are infection prone and are better treated by delayed primary closure after thorough debridement. In all bite wounds and other puncture wounds involving the hand, one should look for penetration of the joint space. Radiographs of the hand are helpful. All bite wounds should be considered tetanus prone, and appropriate tetanus prophylaxis should be administered (see Table 4). In the United States, carnivores and scavengers, including rodents, rabbits, and squirrels, are the animals most likely to transmit rabies. The decision to give antirabies prophylaxis is based on the animal and the circumstances of the bite. The rabies prophylaxis guide is shown in Tables 6 and 7. Edema control Compression therapy is an essential part of the local treatment of acute wounds in the de-

pendent areas. It is very applicable in both the upper and lower extremities, immediately following wound debridement and skin-graft procedures. Compression should be avoided whenever a local or free flap is used, because it may compromise circulation to the flap. Once the wounds are completely healed, compression garments help prevent hypertrophic scars and associated secondary deformities.

Rehabilitation and prevention Physical therapy should be involved as early as possible in managing acute wounds involving the extremities and joint surfaces. Early ambulation, early restoration of full range of motion to the involved extremity, and prevention of joint contractures are paramount. Trauma prevention by patient and family education should not be neglected. Involvement of the social services in the diagnosis and

Table 6 Rabies postexposure prophylaxis guide Animal species

Condition of animal at time of attack

Treatment of exposed persona

Domestic: dog and cat

Healthy and available for 10 days of observation Rabid or suspected rabid Unknown (escaped)

None, unless animal develops rabiesb

Wild: skunk, bat, fox, coyote, raccoon, bobcat, and other carnivores Other: livestock, rodents, and lagomorphs (rabbits and hares)

Regard as rabid unless proved negative by laboratory testse

RIGc and HDCVd Consult public health officials. If treatment is indicated, give RIGc and HDCV.d RIGc and HDCVd

Consider individually. Local and state public health officials should be consulted on questions about the need for rabies prophylaxis. Bites of squirrels, hamsters, guinea pigs, gerbils, chipmunks, rats, mice, other rodents, rabbits, and hares almost never call for antirabies prophylaxis.

These recommendations are only a guide. When applying them, take into account the species involved, the circumstances of the bite or other exposure, the vaccination status of the animal, and the presence of rabies in the region. Local or state public health officials should be consulted if questions arise about the need for rabies prophylaxis. Abbreviations: ARS, antirabies serum, equine; DEV, duck embryo vaccine; HDCV, human diploid cell rabies vaccine; RIG, rabies immune globulin. a All bites and wounds should immediately be cleansed thoroughly with soap and water. If antirabies treatment is indicated, both RIG and HDCV should be given as soon as possible, regardless of the interval from exposure. b During the usual holding period of 10 days, begin treatment with RIG and vaccine (preferably with HDCV) at first sign of rabies in a dog or cat that has bitten someone. The symptomatic animal should be killed immediately and tested. c If RIG is not available, use ARS. Do not use more than the recommended dosage. d If HDCV is not available, use DEV or other rabies vaccine. Local reactions to vaccines are common and do not contraindicate continuing treatment. Discontinue vaccine if fluorescent antibody tests of the animal are negative. e The animal should be killed and tested as soon as possible. Holding for observation is not recommended. From Walton RL. Wound Care. In: Mills J, Ho MT, Trunkey DD, editors. Current emergency diagnosis and treatment. Los Altos (CA): Lange; 1985. p. 665; with permission.

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Table 7 Rabies immunization regimens No. of 1-mL doses

Route of administration

HDCV

3

Intramuscular

DEV

3 or 4

Subcutaneous

5d

Intramuscular

23

Subcutaneous

Rabies vaccine

Postexposurec HDCV DEV

Intervals between doses

If no antibody response to primary seriesa

1 week between first and second; 2 – 3 weeks between second and thirdb 1 month between first and second; 6 – 7 months between second and thirdb or 1 week between first, second, and third; 3 months between third and fourthb

1 booster doseb

Doses to be given on days 0, 3, 7, 14, and 28 21 daily doses followed by a booster on day 31 and another on day 41b or 2 daily doses in the first 7 days, followed by 7 daily doses; then 1 booster on day 24 and another on day 34b

Additional booster dosee

2 booster dosesb 1 week apart

3 doses of HDCV at weekly intervalsb

Preexposure rabies prophylaxis for persons with special risks of exposure to rabies (eg, animal care and control personnel and selected laboratory workers) consists in immunization with either HDCV or DEV, according to the following schedule, followed by a booster dose every 2 years. Abbreviations: ARS, antirabies serum, equine; DEV, duck embryo vaccine; HDCV, human diploid cell rabies vaccine; RIG, rabies immune globulin. a If no antibody response is documented after the recommended additional booster dose(s), consult the state health department or Centers for Disease Control and Prevention. b Serum for rabies antibody testing should be collected 2 – 3 weeks after the last dose only in immunocompromised patients. c Postexposure rabies prophylaxis for persons exposed to rabies consists of the immediate, thorough cleansing of all wounds, with soap and water, administration of RIG or (if RIG is not available) ARS, and the initiation of either HDCV or DEV, according to schedule outlined. d The World Health Organization recommends a sixth dose 90 days after the first dose. e An additional booster dose should be given only to immunocompromised patients. From Walton RL. Wound Care. In: Mills J, Ho MT, Trunkey DD, editors. Current emergency diagnosis and treatment. Los Altos (CA): Lange; 1985. p. 666; with permission.

management of adult and child abuse cases is not to be ignored [65].

healing process to achieve a cosmetically pleasing and functional result.

Summary

References

The most important factors in the management of acute wounds are the history and physical examination. The goals of wound care are fivefold: avoid further tissue damage, achieve wound closure as rapidly as possible, restore function to the injured tissue, facilitate the patient’s expedient return to normal daily activities, and restore the patient’s quality of life. The treating physician must have a good understanding of the wound healing mechanism. One must rule out all associated occult injuries that may be life threatening. Proper wound assessment and management with minimal discomfort to the patient are crucial. The primary goal is to facilitate the

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