Surgery of the Integumentary System

Chapter 16

Surgery of the Integumentary System

General Principles and Techniques

Wound Management

Surgical Anatomy

The skin is composed of epidermis, dermis, and associated adnexa. The outermost layer (i.e., epidermis) is thin but protective; it is especially thin in areas with abundant hair and slightly thicker in areas without much hair. The thickest epidermis is on the nose and footpads, where it is keratinized. The epidermis is avascular, receiving nourishment from fluid penetrating the deeper layers and from dermal capillaries. The thicker, vascular dermis lies deep to the epidermis, which it nourishes and supports. The dermis is composed of collagenous, reticular, and elastic fibers surrounded by a mucopolysaccharide ground substance. Fibroblasts, macrophages, plasma cells, and mast cells are found throughout this layer. The dermis contains blood and lymph vessels, nerves, hair follicles, glands, ducts, and smooth muscle fibers. The hypodermis, or subcutis, lies below the dermis.

Musculocutaneous vessels are the primary vessels supplying skin in human beings, apes, and swine; however, dogs and other loose-skinned animals lack musculocutaneous vessels. Musculocutaneous vessels run perpendicular to the skin’s surface, whereas vessels supplying canine and feline skin approach and travel parallel to the skin and are direct cutaneous vessels. For this reason, some human pedicle grafting techniques have limited application in dogs and cats. Terminal arteries and veins branch from direct cutaneous vessels and form subdermal (deep) plexus, cutaneous (middle) plexus, and subpapillary (superficial) plexus. The subdermal plexus supplies hair bulbs and follicles, tubular glands, the deeper portion of the gland ducts, and arrectores pilorum muscles. The cutaneous plexus supplies sebaceous glands and reinforces capillary networks around hair follicles, tubular gland ducts, and arrectores pili muscles. The subpapillary plexus lies on the outer layer of dermis, and capillary loops from this plexus project into and supply the epidermis. The capillary loop system is poorly developed in dogs and cats compared with human beings and swine, which is why canine skin does not usually blister with superficial burns.

The subdermal plexus is of major importance to skin viability. In areas where there is a panniculus muscle (cutaneous trunci, platysma, sphincter colli superficialis, sphincter colli profundus, preputialis, supramammarius muscles), the subdermal plexus lies both superficial and deep to it. Therefore, surgeons must undermine the fascial plane beneath the cutaneous musculature to preserve the integrity of the subdermal plexus. Where the panniculus is absent, such as in the extremities, the subdermal plexus runs in the deep surface of the dermis, requiring that one undermine well below the dermal surface.

Wound Healing

Wound healing is a preferred biologic process that restores tissue continuity after injury. It is a combination of physical, chemical, and cellular events that restore wounded tissue or replace it with collagen. Wound healing begins immediately after injury or incision. The four phases of wound healing are inflammation, débridement, repair, and maturation. Wound healing is dynamic; several phases occur simultaneously. The first 3 to 5 days are the lag phase of wound healing because inflammation and débridement predominate, and wounds have not gained appreciable strength. Healing is influenced by host factors, wound characteristics, and other external factors.

Stages of Wound Healing

Inflammatory Phase: Inflammation is a protective tissue response initiated by damage. This phase is characterized by increased vascular permeability, chemotaxis of circulatory cells, release of cytokines and growth factors, and cell activation (macrophages, neutrophils, lymphocytes, and fibroblasts). Hemorrhage cleans and fills wounds immediately after injury. Blood vessels constrict for 5 to 10 minutes to limit hemorrhage, but they then dilate and leak fibrinogen and clotting elements into wounds. Vasoconstriction is mediated by catecholamines, serotonin, bradykinin, and histamine. The extrinsic coagulation mechanism is activated by thromboplastin released from injured cells. Platelet aggregation and blood coagulation form a clot that ensures hemostasis and provides a scaffold for cell migration. Platelets also release potent chemoattractants and growth factors (epidermal, platelet-derived, transforming growth factors: α and β) that are necessary in later stages of wound healing (Box 16-1). Fibrin and plasma transudates fill wounds and plug lymphatics, localizing inflammation and “gluing” wound edges together. Fibronectin dimers within the clot become covalently cross-linked to fibrin and to themselves in the presence of activated factor XIII, forming a provisional extracellular matrix. This blood clot formation stabilizes the wound’s edges and provides limited wound strength. It also provides an immediate barrier to infection and fluid loss, and a substrate for early organization of the wound. Scabs form when the blood clot dries; they protect wounds, prevent further hemorrhage, and allow healing to progress beneath their surface. Inflammatory phase cells such as platelets, mast cells, and macrophages secrete growth factors or cytokines, which initiate and maintain the proliferative phase of healing. Inflammatory mediators (i.e., histamine, serotonin, proteolytic enzymes, kinins, prostaglandins, complement, lysosomal enzymes, thromboxane, and growth factors) cause inflammation that begins immediately after injury and lasts approximately 5 days. White blood cells leaking from blood vessels into wounds initiate the débridement phase.

Débridement Phase: An exudate composed of white blood cells, dead tissue, and wound fluid forms on wounds during the débridement phase. Chemoattractants encourage neutrophils and monocytes to appear in wounds (approximately 6 hours and 12 hours after injury, respectively) and initiate débridement. Neutrophils increase in number for 2 to 3 days. They prevent infection and phagocytize organisms and debris. Degenerating neutrophils release enzymes and toxic oxygen products that facilitate breakdown of bacteria, extracellular debris, and necrotic material, and they stimulate monocytes. Monocytes are essential for wound healing; neutrophils are not. Monocytes are major secretory cells synthesizing growth factors that participate in tissue formation and remodeling. Monocytes become macrophages in wounds at 24 to 48 hours. Macrophages secrete collagenases removing necrotic tissue, bacteria, and foreign material. They may coalesce and form multinucleated giant cells with phagocytic functions. Macrophages also secrete chemotactic and growth factors. Growth factors (i.e., platelet-derived growth factor, transforming growth factor-α, transforming growth factor-β, fibroblast growth factor, and interleukin-1) can initiate, maintain, and coordinate formation of granulation tissue. Chemotactic factors (i.e., complement, collagen fragments, bacterial endotoxins, and inflammatory cell products) direct macrophages to injured tissue. Macrophages also recruit mesenchymal cells, stimulate angiogenesis, and modulate matrix production in wounds. Platelets release growth factors important for fibroblastic activity. Lymphocytes appear later in the débridement phase than neutrophils and macrophages. They secrete soluble factors that may stimulate or inhibit migration and protein synthesis by other cells. However, they usually improve the rate and quality of tissue repair. Although healing is severely impaired when macrophage function is suppressed, neutropenia and lymphopenia do not inhibit healing or the development of wound tensile strength in sterile wounds.

Repair Phase: The repair phase usually begins 3 to 5 days after injury. Macrophages stimulate deoxyribonucleic acid (DNA) and fibroblast proliferation. Cytokines, in concert with extracellular matrix molecules, stimulate fibroblasts in the surrounding tissue to proliferate, express appropriate integrin receptors, and migrate into wounds. Fibroblasts are stimulated by transforming growth factor-β to produce fibronectin, which facilitates cell binding and fibroblast movement. Platelet-derived growth factor and basic fibroblast growth factor are also involved. A tissue oxygen content of approximately 20 mm Hg and slight acidity also stimulate fibroblast proliferation and collagen synthesis. Fibroblasts originate from undifferentiated mesenchymal cells in surrounding connective tissue and migrate to wounds along fibrin strands in the fibrin clot. Fibroblasts migrate into wounds just ahead of new capillary buds as the inflammatory phase subsides (2 to 3 days). They invade wounds to synthesize and deposit collagen, elastin, and proteoglycans that mature into fibrous tissue. Orientation initially is haphazard, but after 5 days tension on wounds causes fibroblasts, fibers, and capillaries to orient parallel to the incision or wound margin. Wound fibrin disappears as collagen is deposited. Collagen synthesis is associated with an early increase in wound tensile strength. As the wound matures, there is a notable increase in the ratio of type I (mature) to type III (immature) collagen. The amount of collagen reaches a maximum within 2 to 3 weeks after injury. As the collagen content of a wound increases, the number of fibroblasts and the rate of collagen synthesis decrease, marking the end of the repair stage. The fibroblastic interval of healing lasts 2 to 4 weeks, depending on the nature of the wound. Fibroblast migration and proliferation, collagen production, and capillary ingrowth are delayed if macrophages are absent.

Capillaries invade wounds behind migrating fibroblasts by the process of angiogenesis. Angiogenesis is complex, relying on interaction of extracellular matrix with cytokines that stimulate migration and proliferation of endothelial cells. Stimulus for angiogenesis probably includes macrophage production of mitogenic and chemotactic factors for endothelial cells, and low oxygen tension and increased lactic acid, which affect cytokine production. Basic fibroblast growth factor and vascular endothelial growth factor are specific angiogenic factors. Capillary buds originate from existing blood vessels with columns of capillary endothelial cells migrating toward the site of injury and uniting with other capillary buds or disrupted vessels. New capillaries increase oxygen tension in wounds, augmenting fibroplasia. Mitotic activity in adjacent mesenchymal cells increases as blood begins to flow in new capillaries. Lymphatic channels develop similar to capillary buds but more slowly. Lymphatic drainage of wounds is poor during early healing. The combination of new capillaries, fibroblasts, and fibrous tissue forms bright red, fleshy granulation tissue 3 to 5 days after injury.

Granulation tissue is formed at each wound edge at a rate of 0.4 to 1 mm/day. Unhealthy granulation tissue is white and has a high fibrous tissue content with few capillaries (Figs. 16-1 and 16-2). Granulation tissue fills defects and protects wounds. It provides a barrier to infection, a surface for epithelial migration, and a source of special fibroblasts (i.e., myofibroblasts), which are important in wound contraction. Myofibroblasts are believed to contain proteins (actin and myosin) that contribute to wound contraction. Myofibroblasts are not found in normal tissue, incised and coapted wounds, or tissue surrounding a contracting wound.

Epithelium is an important barrier to external infection and internal fluid loss. Epithelial repair involves mobilization, migration, proliferation, and differentiation of epithelial cells. Epithelialization begins almost immediately (24 to 48 hours) in sutured wounds with good edge to edge apposition because there is no defect for granulation tissue to fill (see Fig. 16-2). Epithelialization begins in open wounds when an adequate granulation bed has formed (usually 4 to 5 days). In partial-thickness skin wounds, epidermal migration over the wound surface begins almost immediately from both the wound margins and epidermal appendages, such as hair follicles and sweat glands. Epidermal cells at the margin of the wound undergo phenotypic alteration that includes retraction on intracellular monofilaments, formation of peripheral cytoplasmic actin filaments, and temporary dissolution of the desmosomes and hemidesmosomes, which release keratinocytes to migrate beneath the eschar at the junction between any remaining necrotic tissue and extracellular matrix of the viable connective tissue. The epidermal cell path of migration is determined by integrins expressed on the membranes of migrating epidermal cells. Chalone, water-soluble glycoproteins found in the epidermis, inhibits epithelial mitosis in normal tissue but is diminished in wounds, which allows epithelial cells along wound margins to divide and migrate across the granulation tissue. Other growth factors secreted by platelets, macrophages, and fibroblasts may also be involved. Increased basal cell mitotic activity occurs as early as 24 to 48 hours after wounding.

Epithelial migration is random but guided by collagen fibers. Migrating epithelial cells enlarge, flatten, and mobilize, losing their attachments to the basement membrane and other epithelial cells. Basal cells at wound edges develop microvilli and extend broad, thin pseudopodia over the exposed surface of collagen bundles. They develop intracytoplasmic microfilaments and selectively fix antiactin and antimyosin antibodies. Epithelial cells in the layers behind these altered cells migrate over them until they contact the wound surface. Cells continue to slide forward until the wound surface is covered. The migrating cells move under scabs and produce collagenase, which dissolves the base of the scab so it can be shed. Contact on all sides with other epithelial cells inhibits further cell migration (contact inhibition). Initially, new epithelium is only one cell layer thick and fragile, but it gradually thickens as additional cell layers form. After a basement membrane has been established, epithelial cells become plump, develop mitoses, and proliferate, restoring the normal, stratified, squamous epithelium architecture. Some hair follicles and sweat glands may regenerate, depending on the depth of skin damage. Epithelial migration also occurs along suture tracts, which may lead to a foreign body reaction, sterile abscess, or scarring or all of these. Epithelialization of suture tracts can be minimized by early removal of sutures. New epithelium usually is visible 4 to 5 days after injury. Epithelialization occurs faster in a moist environment than in a dry one. It will not occur over nonviable tissue. Epithelial migration is energy-dependent and related to oxygen tension. Anoxia prevents epithelial migration and mitosis, whereas hyperbaric oxygen therapy may enhance migration. Wet-dry bandages (see p. 216) débride newly formed epithelium, delaying reepithelialization.

Wound contraction reduces the size of wounds subsequent to fibroblasts, reorganizing collagen in granulation tissue and myofibroblast contraction at the wound edge. Contraction occurs simultaneously with granulation and epithelialization but is independent of epithelialization. Wound contraction involves a complex interaction of cells, extracellular matrix, and cytokines. Significant fibroblastic invasion into the wound is necessary for contraction to begin. Centripetal, full-thickness skin edges are pulled inward by contraction, and wounds may be noticeably smaller by 5 to 9 days after injury. The surrounding skin stretches (intussusceptive growth) during wound contraction, and the wound takes on a stellate appearance. Contraction progresses at a rate of approximately 0.6 to 0.8 mm/day. Wound contraction stops when wound edges meet, when tension is excessive, or when myofibroblasts are inadequate. Wound contraction is limited if skin around wounds is fixed, inelastic, or under tension, and it is inhibited if myofibroblast development or function is impaired. Contraction can also be impaired by anti-inflammatory steroids, antimicrotubular drugs, and local application of smooth muscle relaxants. If wound contraction stops before granulation tissue is covered, epithelialization may continue and cover the wound.

Maturation Phase: Wound strength increases to its maximum level because of changes in the scar during the maturation phase of wound healing. Wound maturation begins once collagen has been adequately deposited in wounds (17 to 20 days after injury) and may continue for years. The cellularity of granulation tissue is reduced as cells die. There is also a reduction in collagen content of the extracellular matrix. Collagen fibers remodel with alteration of their orientation and increased cross-linking, which improves wound strength. Fibers orient along lines of stress. Functionally oriented fibers become thicker. Type III collagen gradually decreases, and type I collagen increases. Nonfunctionally oriented collagen fibers are degraded by proteolytic enzymes (matrix metalloproteinases) secreted by macrophages, epithelial cells, endothelial cells, and fibroblasts within the extracellular matrix. The most rapid gain in wound strength occurs between 7 and 14 days after injury as collagen rapidly accumulates in the wound. Wounds gain only about 20% of their final strength in the first 3 weeks after injury. Slower increase in wound strength then occurs, but normal tissue strength is never regained in wounds; only 80% of original strength may be regained. As the number of capillaries in fibrous tissue declines, the scar becomes paler. Scars also become less cellular, flatten, and soften during maturation. Collagen synthesis and lysis occur at the same rate in maturing scars.

Moist Wound Healing

A moist wound environment allows optimal healing. Wound fluid is allowed to remain on the wound, keeping it moist. In a moist environment, débridement is hastened and selective, granulation tissue formation is promoted, and epithelialization is faster. Allowing wound fluid to remain in contact with wounds fosters autolytic débridement by endogenous enzymes that break down necrotic, but not healthy, tissue. Autolytic débridement occurs within 72 to 96 hours under an occlusive bandage. White blood cell phagocytosis decreases bacterial load and removes necrotic debris. White blood cells migrate more readily in a moist environment. Wound fluid also contains cytokines and growth factors that stimulate granulation tissue, angiogenesis, and reepithelialization. Chemotactic factors in wound fluid attract neutrophils and macrophages that secrete additional enzymes, cytokines, and growth factors. Moist wounds limit infections because more white blood cells are found in the wound, and there is improved phagocytosis and a lower pH. Scabs do not form with moist wound healing; therefore, white blood cells are not trapped in the scab, and topical medications better penetrate the wound. If the animal is receiving systemic antibiotics, wound fluids may contain antibiotics, which help prevent or control infection. Low oxygen tension under an occlusive bandage stimulates macrophage activity, fibroblast proliferation, and capillary ingrowth. The rate of epithelialization is twice as fast for wounds kept moist with occlusive dressings than for air-exposed wounds. Epithelial cells travel faster and a shorter distance for epithelialization to occur in moist environments; in air-exposed wounds, migrating epidermal cells must travel beneath a crusted scab and devitalized dermis to reach their destination. Hydrophilic, occlusive, or semiocclusive bandages help keep a wound warm and moist. Increased warmth enhances enzymatic activity. A moist wound is less painful and pruritic, tissues do not desiccate, and scar formation is less. Potential disadvantages of moist wound healing include bacterial colonization (not infection) of the wound surface, folliculitis, and maceration of the wound border.

Host Factors Affecting Wound Healing

Old animals tend to heal slowly, probably because of concurrent disease or debilitation. Malnourished animals and those with serum protein concentrations below 1.5 to 2 g/dl may have delayed wound healing and diminished wound strength. Hepatic disease may cause clotting factor deficiencies. Hyperadrenocorticism delays wound healing because of excess circulating glucocorticoids. Animals with diabetes mellitus have delayed wound healing and a predisposition to wound infections. Uremia occurring within 5 days of injury impairs healing by altering enzyme systems, biochemical pathways, and cellular metabolism. Obesity is associated with a higher incidence of postoperative wound infections in human beings. The risk of postoperative wound infection in dogs and cats also increases as the duration of anesthesia increases.

Cutaneous wounds are slower to heal in cats than dogs. Sutured wounds in cats are only half as strong as similar wounds in dogs after 7 days of healing. Cat wounds that are allowed to heal by secondary intention heal slower, produce less granulation tissue (that is more peripherally located), and heal more by contraction of wound edges than dogs (Bohling et al, 2004).

Wound Characteristics Affecting Wound Healing

Intact surfaces, such as periosteum, fascia, tendon, and nerve sheath, do not support granulation tissue; therefore, these surfaces heal slowly when exposed. Fenestration or drilling holes in exposed cortical bone may improve granulation by releasing osteogenic or other factors. Foreign material in wounds (e.g., dirt, debris, sutures, and surgical implants) can cause intense inflammatory reactions interfering with normal wound healing. Release of enzymes designed to degrade foreign bodies destroys wound matrix, prolongs inflammation, and delays the fibroblastic phase of tissue repair. Soil may contain infection, potentiating factors that inhibit antibiotics, leukocytes, and antibodies. Exposure of the wound to antiseptics delays healing and may predispose to infection. Warmth (30° C [86° F]) allows wounds to heal more quickly and with greater tensile strength than if they are at room temperature. A moist wound promotes recruitment of vital host defenses and cells, encouraging wound healing. Bandages help keep wounds warm and moist. Wounds (incisions) created with sharp surgical instruments heal faster and with less necrosis at the wound margin than those made with scissors, electroscalpels, or lasers. Wound infection interferes with the repair phase of healing. Contaminated tissues become infected if invasive bacteria multiply to 105 colony-forming units (CFU) per gram of tissue. Development of wound infection depends on the degree of tissue trauma, amount of foreign material present, delay between injury and treatment, and effectiveness of host defenses. Bacterial toxins and associated inflammatory infiltrates cause cell necrosis and vascular thrombosis. Wound exudates can separate tissue layers and further delay healing. Inflammation caused by infection further compromises vasculature, causing additional necrosis.

Healing depends on blood supply, which delivers oxygen and metabolic substrates to cells. Impairment of blood supply by trauma, tight bandages, or wound movement slows healing. Macrophages resist hypoxia, but epithelialization and fibroblastic protein synthesis are oxygen dependent. Collagen synthesis requires 20 mm Hg partial pressure of oxygen (pO2). Hyperbaric oxygen therapy increases tissue oxygen and produces more rapid gains in wound strength. Accumulation of fluid in dead space delays healing because the hypoxic fluid environment of a seroma inhibits migration of reparative cells into wounds. Fluid mechanically prevents adhesion of flaps or grafts to the wound bed.

Recruitment, proliferation, and cellular function in wound healing are controlled by growth factors; proteins synthesized and released by cells involved in wound healing. Numerous growth factors have been identified, including platelet-derived growth factor, epidermal growth factor, fibroblast growth factor, and type-transforming growth factor. Platelet-derived growth factors are found in granules, whereas macrophages must be stimulated to synthesize and release growth factors.

Fibronectins are glycoproteins critical to wound healing. They stimulate cell attachment and migration and are found in soluble form in plasma and in insoluble form in connective tissue matrix. Macrophages, endothelium, fibroblasts, and epithelium synthesize and release fibronectin. Fibronectin in the coagulum probably assists initial migration of cellular elements (macrophages and epithelium) into wounds. It binds bacterial cell wall components, collagen, actin, thrombospondin, heparan sulfate, hyaluronic acid, fibrin, cell surface receptors, and other fibronectin molecules. Fibronectin may also be important in providing an early wound-healing matrix and in interlinking cellular and matrix components during healing. Fibronectin in wounds declines as healing nears completion. Proteoglycans are also important in all phases of wound healing. The matrix during cell migration contains elevated concentrations of nonsulfated glycosaminoglycans (i.e., hyaluronate). As wound maturation progresses, more sulfated glycosaminoglycans (i.e., chondroitin sulfate and heparan sulfate) appear.

External Factors Affecting Wound Healing

Radiation therapy (see p. 262) and some drugs delay wound healing. Corticosteroids depress all phases of wound healing and increase chances of infection. Vitamin A and anabolic steroids may reverse the effects of corticosteroids on wound healing. Anti-inflammatory drugs suppress inflammation but have little effect on wound strength. Aspirin may delay blood clotting. Some chemotherapeutic drugs (e.g., cyclophosphamide, methotrexate, and doxorubicin) inhibit wound healing. Radiation therapy can profoundly inhibit wound healing, depending on dose and time of exposure relative to the time of injury. It reduces the quantity of blood vessels, affects collagen maturation, and causes increased dermal fibrosis. Therefore, chemotherapeutic drugs and radiation therapy should be avoided for 2 weeks after surgery. Vitamin A, vitamin E, and aloe vera may promote healing in irradiated wounds. Exposure to pico-tesla electromagnetic field treatment improves strength of sutured wounds and speeds contraction of open wounds in rats. Hyperbaric oxygen therapy increases dissolved oxygen in plasma, which stimulates growth of new capillaries; therefore, it may be useful for treatment of ischemic wounds. Ultrasonography and phototherapy (low-powered laser) shorten the inflammatory phase of healing and enhance release of factors that stimulate the proliferative stage of repair. Use of controlled subatmospheric pressure dressings helps remove interstitial fluid, which allows tissue decompression, helps remove tissue debris, and promotes wound healing (see p. 205).

Management of Open or Superficial Wounds

Wounds should be covered with a clean, dry bandage immediately after injury or when the animal is brought for treatment to prevent further contamination and hemorrhage (Box 16-2). Life-threatening injuries should be treated and the animal’s condition stabilized before further wound management is undertaken. When appropriate during stabilization, bandages should be removed and the wound assessed and classified as either contaminated or infected and as an abrasion, laceration, avulsion, puncture, crush, or burn wound. The “golden period” is the first 6 to 8 hours between wound contamination at injury and bacterial multiplication to greater than 105 CFU per gram of tissue. A wound is classified as infected rather than contaminated when bacterial numbers exceed 105 CFU per gram of tissue. Infected wounds often are dirty and covered with a thick, viscous exudate.

Abrasions are superficial and involve destruction of varying depths of skin by friction from blunt trauma or shearing forces. Abrasions are sensitive to pressure or touch and bleed minimally. A laceration is created by tearing, which damages skin and underlying tissue. Lacerations may be superficial or deep and have irregular edges. Avulsion wounds are characterized by the tearing of tissues from their attachments and the creation of skin flaps. Avulsion injuries on limbs with extensive skin loss are called degloving injuries. A penetrating or puncture wound is created by a missile or sharp object, such as a knife, pellet, or tooth that damages tissue. Wound depth and width vary depending on the velocity and mass of the object creating the wound. The extent of tissue damage is directly proportional to missile velocity. Pieces of hair, skin, and debris can be embedded in wounds. Crush injuries can be a combination of other types of wounds with extensive damage and contusions to skin and deeper tissue. Burns may be partial- or full-thickness skin injuries caused by heat or chemicals (see p. 257).

Wounds less than 6 to 8 hours old with minimal trauma and minimal contamination are treated by lavage, débridement, and primary closure. Generally, the sooner treatment begins, the better the prognosis. Penetrating wounds should not be primarily apposed without surgical exploration (see p. 265). Severely traumatized and contaminated wounds, wounds older than 6 to 8 hours, or infected wounds should be treated as open wounds to allow débridement and reduction of bacterial numbers. Most wounds are surgically apposed after infection has been controlled; however, some wounds heal by contraction and epithelialization (healing by secondary intention).

Often anesthesia is required for initial wound inspection and care. The objective of open wound care is to convert the open, contaminated wound into a surgically clean wound that can be closed. Aseptic technique, gentle tissue handling, and hemostasis are essential. Severely contaminated or infected wounds should be cultured after initial inspection. The area surrounding the wound should be widely clipped and prepped. The wound may be protected from clipped hair and detergents by applying a sterile, water-soluble lubricant (K-Y Jelly) or by placing saline-soaked sponges in the wound and covering with a sterile pad or towel. As an alternative, the wound may be temporarily closed with sutures, towel clamps, staples, or Michel clips. Hair may be clipped from the wound margin with scissors dipped in mineral oil to prevent hair from falling into the wound. Povidone-iodine or chlorhexidine gluconate skin scrubs are used to prepare clipped skin. The detergents in antiseptic scrubs cause irritation, toxicity, and pain in exposed tissue and may potentiate wound infection. Alcohol is very damaging to exposed tissue and should be used only on intact skin.

Initial wound management begins with removal of gross contaminants and copious lavage using a warm, balanced electrolyte solution, sterile saline, or tap water (500 to 1000 ml) (Table 16-1). Sterile isotonic saline or a balanced electrolyte solution (lactated Ringer’s solution) is the preferred lavage solution. Tap water is effective and less detrimental than distilled or sterile water, although it causes some hypotonic tissue damage (cellular and mitochondrial swelling). Wound lavage reduces bacterial numbers mechanically by loosening and flushing away bacteria and associated necrotic debris. Lavage may be facilitated by the use of noncytotoxic wound cleansers (e.g., Allclenz Wound Cleanser, Healthpoint Biotherapeutics, Fort Worth, Tex.). Generally, these cleansers are applied to loosen debris and soften necrotic tissue during bandage changes; they act as a surfactant, disrupting the ionic bonding of particles and organisms to the wound and allowing them to be easily rinsed off with saline or balanced electrolyte solutions. Lavage following application of these cleansers, however, is not necessary. Antibiotics or antiseptics (e.g., chlorhexidine or povidone-iodine; see p. 201) in the lavage solution reduce bacterial numbers; however, these agents may damage tissue. Antiseptics have little effect on bacteria in established infections. Lavaging is preferred to scrubbing the wound with sponges. Sponges inflict tissue damage that impairs the wound’s ability to resist infection and allows residual bacteria to elicit an inflammatory response.

image TABLE 16-1

Suggested Wound Cleansers

Commercial cleansers:
Surfactant breaks the bonds between foreign bodies and the wound surface
Most ionic surfactants and many nonionic surfactants have been shown to be toxic to cells, delay wound healing, and inhibit the wound’s defense mechanisms
Tap water Availability
Ease of application
Cytotoxic trace elements
Not antimicrobial
Balanced electrolyte solution:
 Lactated Ringer’s solution (LRS)
Least cytotoxic
Not antimicrobial
Normal (0.9%) solution Isotonic Slightly more acidic than LRS
Not antimicrobial
0.05% Chlorhexidine
(1 part stock solution to 40 parts sterile water or LRS) or (~25 ml stock solution per liter)
Wide antimicrobial spectrum
Good residual activity
Not inactivated by organic matter
Precipitates in electrolyte solutions
More concentrated solutions are cytotoxic and may slow granulation tissue formation
Proteus, Pseudomonas, and Candida are resistant
Corneal toxicity
0.05% Chlorhexidine with Tris EDTA Makes bacteria more susceptible to destruction by lysozymes, antiseptics, and antibiotics. Rapidly lyses P. aeruginosa, E. coli, and Proteus vulgaris
Increases antimicrobial effectiveness approximately 1000 fold.
Precipitates in electrolyte solutions
More concentrated solutions are cytotoxic and may slow granulation tissue formation
Corneal toxicity
0.1% povidone-iodine
(1 part stock to 100 parts LRS) or (~10 ml stock to 100 ml LRS)
Wide antimicrobial spectrum Inactivated by organic matter
Limited residual activity
Cytotoxic at concentrations greater than 1%
Contact hypersensitivity
Thyroid disorders if absorbed

Bacteria are effectively removed from the wound surface by high-pressure lavage. Traditionally, a 35- or 60-ml syringe and an 18-gauge needle have been thought to generate approximately 7 to 8 psi of pressure; however, it was recently shown that it generates pressures substantially higher than this (18.4 ± 9.8 psi) (Gall and Monnet, 2010). The most consistent delivery method to generate 7 to 8 psi is a 1-liter bag of fluid within a cuff pressurized to 300 mmHg (Fig. 16-3). Higher pressure (70 psi), generated by pulsatile lavage instruments (i.e., Water Pik [Teledyne], Surgilav, or Pulsavac débridement system) is more effective in reducing bacterial numbers and removing foreign debris and necrotic tissue, but it may drive bacteria and debris into loose tissue planes, damage underlying tissue, and reduce resistance to infection. Bulb syringes or fluid bottles with holes made in the cap do not generate enough pressure to remove bacteria and debris adequately.


Healing is delayed if necrotic tissue is left in the wound. Devitalized tissue is removed from the wound by débridement. Débridement involves removal of dead or damaged tissue, foreign bodies, and microorganisms that compromise local defense mechanisms and delay healing. The goal of débridement is to obtain fresh clean wound margins and wound bed for primary or delayed closure. Devitalized tissue is removed by surgical excision, autolytic mechanisms, enzymes, wet-dry bandages (see p. 216), or biosurgical methods. The extent of devitalized tissue usually is obvious within 48 hours of injury.

Surgical Débridement: Devitalized tissue should be surgically excised in layers beginning at the surface and progressing to the depths of the wound. This can be done by sharp dissection, electrosurgery, or laser. Bones, tendons, nerves, and vessels must be preserved, but bone sequestra should be removed because they may prevent complete granulation of the wound (especially with metacarpal and metatarsal degloving injuries) and predispose the wound to infection. Muscle should be débrided until it bleeds and contracts with appropriate stimuli. Extensive debridement of subcutaneous tissue should be avoided as it may delay wound healing, particularly in cats, and may place wounds at a higher risk for infection (Bohling et al, 2006). Contaminated fat should be liberally excised because it is easily devascularized and harbors bacteria, but cutaneous vessels must be spared to maintain the viability of overlying skin.

As an alternative, the entire wound can be excised en bloc if sufficient healthy tissue surrounds the wound and vital structures can be preserved. The danger of surgical débridement is removal of an excessive amount of possibly viable tissue. With penetrating wounds or punctures, it may be necessary to enlarge the wound to assess the extent of injury and allow débridement. Electrosurgery or a high-powered carbon dioxide laser can be as effective as sharp surgical débridement of devitalized tissue. They have the advantage of providing simultaneous hemostasis, which helps prevent débridement of normal tissue. Low-level laser therapy has been advocated to stimulate wound healing in chronic wounds by shortening the inflammatory phase and enhancing the release of factors that stimulate the proliferative stage of repair. Increased collagen deposition and endothelial cell, fibroblast, and myofibroblast proliferation are the most significant effects.

Surgical débridement of obviously devitalized tissue is often combined with autolytic débridement (discussed later) to remove surface contaminants and tissue of questionable viability. After surgical débridement, wounds often are treated as open wounds with hydrophilic dressings and bandages. Provision of adequate wound drainage and a viable vascular bed is important to wound healing. The wound should be closed when it appears healthy or when a bed of healthy granulation tissue has formed, unless wound closure by contraction and epithelialization is anticipated.

Enzymatic Débridement: Enzymatic débriding agents are used as an adjunct to wound lavage and surgical débridement. They are beneficial in patients that are poor anesthetic risks or when surgical débridement may damage healthy tissue necessary for reconstruction. Enzymatic agents break down necrotic tissue and liquefy coagulum and bacterial biofilm, allowing better antibiotic contact with wounds and enhanced exposure for development of cellular and humoral immunity; they do not damage living tissue if used properly. Available enzymes do not digest burned skin, necrotic bone, and connective tissue. Enzymes must remain in contact with the wound for an adequate time to produce the desired effect. Local tissue irritation may occur with enzyme use.

Granulex V aerosol spray or liquid (Bertek Pharmaceuticals, Sugarland, Texas) is an enzymatic débriding agent containing pancreatic trypsin, balsam of Peru, and castor oil. Trypsin débrides and liquefies protein, but can cause local inflammation and pyrogenic reactions; balsam of Peru stimulates capillary beds to increase wound circulation; castor oil improves epithelialization by reducing epithelial desiccation and cornification. Live yeast cell extract (some formulations of Preparation H, Whitehall Laboratories, New York, N.Y.) stimulates oxygen consumption, collagen production, and epithelialization. Collagenase-based products (Santyl, Healthpoint Biotherapeutics, Fort Worth, Tex.) are also effective for enzymatic débridement used in human wounds, specifically decubital ulcers, pressure sores, and burn wounds. Papain-based products (e.g., Accuzyme, Ziox) are also used for enzymatic debridement; however, such agents have recently been taken off market because of the concern about side effects.

Biosurgical Débridement: Maggot therapy using greenbottle fly larvae (Lucilia sericata) débrides wounds as the maggots secrete proteolytic digestive enzymes into the wound. Sterile medicinal maggots (Monarch Laboratories, LLP, Irvine, Calif.) are bred specifically for biosurgery. A single maggot may consume up to 75 mg of necrotic tissue each day. They require an optimal temperature, an oxygen supply, and a moist wound. Maggot therapy is best suited to necrotic, infected, or chronic nonhealing wounds. The maggots remove necrotic tissue, disinfect the wound, and promote granulation tissue formation. Medicinal maggots are applied to the wound at a density of five to eight per square centimeter. A hole is cut into a self-adhesive hydrocolloid dressing that matches the wound dimensions. This dressing is applied to the wound to prevent the maggots from crawling onto intact skin and to absorb wound secretions. The dressing is covered to trap the maggots in the wound, changing absorbent layers as necessary. Maggots are usually applied for two 48-hour cycles each week.


Selective use of antibiotics may help prevent or control integument infections after injury or surgery. Minimally or moderately contaminated wounds less than 6 to 8 hours old may be cleaned and closed or treated without antibiotics. Severely contaminated, crushed, or infected wounds, or wounds older than 6 to 8 hours, typically benefit from antibiotic therapy. Contaminated wounds and those with established infection should be cultured before antibiotics are given, and antibiotic selection should ultimately be based on culture and susceptibility testing. Ideally, quantitative bacterial counts should be performed before grafts or flaps are placed over granulating wounds. Reconstruction should be delayed if bacterial counts are greater than 105 CFU per gram of tissue.

Systemic antibiotics should be given if there is a high risk of bacteremia or disseminated infection. A broad-spectrum antibiotic should be administered while awaiting culture results. Antibiotic blood levels should be present at the time of surgery when antibiotics are used prophylactically for clean or clean contaminated procedures. Prophylactic antibiotics optimally are given intravenously when anesthesia is induced (see Chapter 9). Contamination occurring during surgery usually is limited to the patient’s skin flora; therefore, drugs effective against Gram-positive skin flora, especially Staphylococci spp. (see p. 92), should be selected (e.g., 22 mg/kg cefazolin given intravenously).

Topical Wound Medications

Topical Antimicrobials and Antibiotics

Antimicrobial agents and antibiotics eliminate or reduce the number of microorganisms that destroy tissue in a wound. Topical rather than systemic antibiotics are preferred for open wounds. Mildly or moderately contaminated wounds do not benefit from combined topical and systemic antibiotic therapy; however, combined therapy is advantageous in heavily contaminated wounds. Antibiotics applied within 1 to 3 hours of contamination often prevent infection. Benefits of topical drugs should outweigh their cytotoxic effects. Antibiotics used effectively as topical ointments or added to lavage solutions are penicillin, ampicillin, carbenicillin, tetracycline, kanamycin, neomycin, bacitracin, polymyxin, and cephalosporins. Once infection is established, topical and systemic antibiotics have no beneficial effect in preventing suppuration of wounds undergoing closure. Wound coagulum prevents topical antibiotics from reaching effective levels in tissues deep in the wound and also prevents systemic antibiotics from reaching superficial bacteria. These wounds must be débrided to allow antimicrobial access to bacteria.

Advantages of topical antibiotics over antiseptics in wound management include selective bacterial toxicity, efficacy in the presence of organic material, and combined efficacy with systemic antibiotics. Disadvantages include expense, narrower antimicrobial spectrum, potential for bacterial resistance, creation of “super infections,” systemic or local toxicity, hypersensitivity, and increased nosocomial infections. Antibiotic solutions are preferable to ointments and powders. Ointments liberate antibiotics slowly and may be occlusive, promoting growth of anaerobic bacteria. Powders act as foreign bodies and should not be used.

Silver Sulfadiazine: Silver sulfadiazine in a 1% water-miscible cream (Thermazene, Covidien, Mansfield, Mass.; Silvadene, King Pharmaceuticals, Bristol, Tenn.) is effective against most Gram-positive and Gram-negative bacteria and most fungi. It also serves as an antimicrobial barrier, can penetrate necrotic tissue, and enhances wound epithelialization. It is the drug of choice to treat burn wounds. In vitro toxicity to human keratinocytes and fibroblasts and inhibition of polymorphonuclear cells and lymphocytes has been shown. These wound-retardant effects of silver sulfadiazine are reversed when it is combined with aloe vera. Silver-impregnated dressings are also available (see p. 215). Ointments remain effective for up to 3 days, whereas dressings may be left in place for 7 days. Only a small amount of silver is released slowly from its molecular lattice over a sustained period, reducing cytotoxic effects of ionic silver and making it nonstaining, nonirritating, and nonsensitizing while maintaining its antimicrobial effects. These products are also hydrophilic, helping to maintain a moist wound environment and absorbing exudates.

Topical Wound-Healing Enhancers

Many topical agents have been used in the management of open wounds, some with documented benefit, others without. Unfortunately, there is a lack of well-controlled prospective studies in the veterinary literature to determine ideal agents to promote wound healing in dogs and cats.

Aloe Vera: Aloe vera gel is extracted from the aloe vera leaf and contains 75 potentially active constituents. Aloe vera has been used on burns because of its antibacterial activity against Pseudomonas aeruginosa. It also inhibits fungal growth. The antiprostaglandin and antithromboxane properties of aloe vera medications are beneficial in maintaining vascular patency and thus helping avert dermal ischemia. Aloe vera medications may also stimulate fibroblastic replication. Aloe vera has the ability to penetrate and anesthetize tissue. Acemannan, a component of aloe vera extract gel, promotes wound healing (see later discussion). It is also found in other preparations. Allantoin, another component of aloe vera extract gel, stimulates tissue repair in suppurating wounds and resistant ulcers by promoting epithelial growth. Use on full-thickness wounds is discouraged because of its anti-inflammatory effects. Aloe vera counteracts the inhibitory effects of silver sulfadiazine when the two are combined.

Acemannan: Acemannan (Carravet, Veterinary Products Laboratories, Phoenix, Ariz.; Carrasorb, Carrington Laboratories, Irving, Tex.) is available as a topical wound hydrogel or a freeze-dried gel form. It is indicated for managing superficial and deep partial-thickness burns, lacerations, dermal ulcers, abrasions, and nonhealing wounds. Acemannan is a β-(1,4) acetylated mannan derived from the aloe vera plant that enhances early stages of healing. Acemannan stimulates macrophages to secrete interleukin-1 and tumor necrosis factor alpha, which enhance fibroblast proliferation, neovascularization, epidermal growth and motility, and collagen deposition to form granulation tissue. Acemannan may also bind growth factors, prolonging their stimulating effect on formation of granulation tissue. The freeze-dried form enhances healing over exposed bone and has hydrophilic properties, which help cleanse the wound and reduce wound edema. The most effective time to begin topical application is in the early inflammatory stage of healing with daily application under a bandage, continuing into the repair stage of healing. The greatest effects are seen in the first 7 days of application. Excess granulation tissue can occur, especially with the freeze-dried form, which inhibits wound contraction.

Tripeptide-Copper Complex: Glycyl-L-histidyl-lysine tripeptide-copper complex (Iamin-Vet Skin Care Gel, Procyte, Covington, Ga.) stimulates wound healing and is a chemoattractant for mast cells, monocytes, and macrophages, which stimulate débridement, angiogenesis, collagen synthesis, and epithelialization. Enzymes involved in collagen cross-linking need copper. The best time to begin tripeptide-copper complex application is the late inflammatory and early repair phases, with treatment continuing into the later repair phase. It has been effective in accelerating wound healing in chronic, ischemic open wounds. Its greatest effect is in the first 7 days of its use. Exuberant granulation tissue may be a problem with this agent.

D-Glucose Polysaccharide (Maltodextrin NF): Maltodextrin (Intracell, Macleod Pharmaceutical, Fort Collins, Colo.) is available in a hydrophilic powder or gel form containing 1% ascorbic acid for use on contaminated and infected wounds as a wound healing stimulant. It is reported to stimulate healing by supplying glucose for cell metabolism via hydrolysis of its polysaccharide component. Its hydrophilic property draws fluid through the tissue, keeping it moist. Maltodextrin is chemotactic and pulls neutrophils, lymphocytes, and macrophages into the wound. Maltodextrin also has antibacterial and bacteriostatic properties. It reduces odor, exudates, swelling, and infection, and it may enhance early granulation tissue formation and epithelialization. After débridement and lavage, a 5- to 10-mm layer of maltodextrin is applied to the wound and covered with a bandage from the early inflammatory stage into the repair stage of healing. Daily bandage changes, lavage, and reapplication are recommended.

Honey: Honey is an old agent that has seen renewed interest. Proposed benefits include enhancing wound débridement, reducing edema and inflammation, promoting granulation tissue formation and epithelialization, and improving wound nutrition. It has a wide antibacterial effect through its enzymatic production of hydrogen peroxide from glucose, hypertonicity, low pH, inhibin content, and other unidentified components. Honey increases collagen content, accelerates collagen maturation resulting from cross-linking, and maintains optimal pH conditions for fibroblast activity. Honey contains a wide range of amino acids, vitamins, and trace elements in addition to readily assimilable sugars that stimulate tissue growth. Honey should be used early in the course of wound healing and discontinued once a healthy granulation bed is present. Honey can also be used for treating partial-thickness burns and may have greater wound healing properties than silver-based preparations (Malik et al, 2010).

Specific preparations of unpasteurized medicinal honey are recommended for wound care (Medihoney, Derma Sciences, Princeton, N.J.; Manuka Honey, Comvita WoundCare 18+, Manuka Honey USA, Orlando, Fla.). Honey is applied by impregnating sterile gauze (30 ml on 10 × 10 gauze pad), which is then positioned on the wound and covered with a thick, absorbent bandage. The wound is rebandaged one to three times a day depending on the amount of strikethrough.

Growth Factors: Application of growth factors to stimulate more rapid healing has been investigated. Application of growth factors assumes the wound is deficient in specific growth factors. Knowing which factor is deficient in what amount at what time is nearly impossible in the complex healing process. Evidence indicates that applying single growth factors to wounds is not as effective as the combination of growth factors that the body produces. Allowing these factors to remain on the wound in the wound fluid under an occlusive or semiocclusive bandage is preferred to adding exogenous growth factors. A few growth factors are available commercially including recombinant human-derived platelet-derived growth factor (Regranex, Johnson & Johnson, Arlington, Tex.), but efficacy studies in dogs and cats have yet to be performed.

Other Topical Wound Agents: Anti-inflammatory agents are often used to prevent progressive inflammatory damage; however, topical steroids may inhibit epithelialization, wound contraction, and angiogenesis. Production of exuberant granulation tissue may be reduced by one or two applications of corticosteroids. Topical anesthetics may be used to reduce the animal’s pain. Lidocaine or bupivacaine applied topically reduces traumatic and postoperative pain and may decrease the need for systemic analgesics. Hydrophilic agents cause diffusion of fluids through wound tissues to the surface or into the bandage. This dilutes the tenacious coagulum and debris on the wound surface and allows easier absorption. An organic acid combination of malic, benzoic, and salicylic acids (Derma Clens, Pfizer, New York, N.Y.) enhances fluid absorption by devitalized tissue to promote its separation from wounds. Acids do not damage underlying healthy tissue, and the 2.8 pH discourages microbial growth. Hexamethyldisiloxane acrylate copolymer (Cavilon, No Sting Barrier Film; 3M, St. Paul, Minn.) produces a uniform, transparent, colorless, fast-drying, noncytotoxic film that serves as a skin protectant type of dressing. Applied in a thin layer to clean, dry skin every third day, it allows inflammation to resolve quickly and prevents tape from causing epidermal striping and skin irritation. Hydroxyethylated amylopectin (Facilitator; Ridge Pharmaceuticals, Idexx Laboratories, Greensboro, N.C.) is a similar product used in place of a bandage on superficial lesions. This water-soluble product is placed in a thin layer (one drop spread over 2 square inches) over the wound and allowed to dry. It reduces wound drying and itching and accelerates healing. Neither of these products should be used with other topicals as they may inhibit adherence of the film to the skin.

Wound Cleansing Solutions

Wound cleansing solutions should have ideal antiseptic properties with minimal cytotoxicity. They are used primarily in the initial phases of wound management to decrease bacterial load and rid wounds of necrotic tissue and debris. Once the wound is clean, balanced electrolyte or physiologic saline solutions are ideal for cleansing it (see Table 16-1). Tap water is not an ideal wound cleanser but is acceptable to initially remove dirt and debris when there is severe contamination. Tap water’s hypotonicity causes cell swelling, which can cause significant cell destruction and delay wound healing with prolonged use. Antiseptic solutions are used early in wound management to reduce bacterial numbers and reduce chances of infection. They are contraindicated in clean wounds because all antiseptics have some cytotoxic effects and may be more damaging than beneficial to wound healing.

Commercial Wound Cleansers

Read the label carefully when selecting a commercial wound cleanser; many are a combination of agents that are contraindicated for use in wounds because of cytotoxic effects. Some ingredients to avoid include hydrogen peroxide, sodium hypochlorite, and hydrochlorous acid. The cleansing activity of many of the commercially available cleansers depends on a surfactant that breaks the bonds between foreign bodies and the wound surface. Most ionic surfactants and many nonionic surfactants are toxic to cells, delay wound healing, and inhibit the wound’s defense mechanisms. Some available commercial wound cleansers include Allclenz (Healthpoint Biotherapeutics, Fort Worth, Tex.), Sur-Clens (ConvaTec, Skillman, N.J.), Cara-Klenz (Carrington Laboratories, Irving, Tex.), and Ultra-Klenz (Carrington Laboratories, Irving, Tex.).

Chlorhexidine Diacetate

The preferred antiseptic solution for wound lavage is 0.05% chlorhexidine diacetate because of its wide spectrum of antimicrobial activity and sustained residual activity. It has antibacterial activity in the presence of blood and other organic debris, has minimal systemic absorption and toxicity, and promotes rapid healing. A 0.05% solution is created by diluting one part of stock solution with 40 parts of sterile water. Chlorhexidine forms heavy precipitates in electrolyte solutions, but this neither delays wound healing nor interferes with antibacterial activity. More potent solutions may slow the formation of granulation tissue with prolonged wound contact. Residual activity may last as long as 2 days, and effectiveness increases with repeat application. Potential drawbacks of chlorhexidine include resistance to Proteus, Pseudomonas, and Candida, and corneal toxicity.


A 1% or 0.1% povidone-iodine solution (10% stock solution diluted 1 : 10 or 1 : 100, respectively) is used frequently for wound lavage because of its wide spectrum of antimicrobial activity. Iodine compounds are active against vegetative and sporulated bacteria, fungi, viruses, protozoa, and yeasts. A 0.1% solution is recommended. This concentration kills bacteria within 15 seconds, and there is no known bacterial resistance. Povidone-iodine is a water-soluble, strongly acidic (pH 3.2) iodophor produced by combining molecular iodine with polyvinylpyrrolidone. Frequent reapplication (every 4 to 6 hours) is required when it is used as a wetting solution because residual activity lasts only 4 to 8 hours, and organic matter (i.e., blood and serous exudate) inactivates the free iodine in povidone-iodine. Iodine absorption through the skin and mucous membranes may cause excess systemic iodine concentrations and transient thyroid dysfunction. The low pH of povidone-iodine can cause or intensify metabolic acidosis when the solution is absorbed. Scrubbing wounds with povidone-iodine detergents damages tissue and potentiates infection. Contact hypersensitivities may occur in as many as 50% of dogs scrubbed with povidone-iodine compounds. Povidone-iodine at 0.5% is cytotoxic to fibroblasts.


Tris EDTA (disodium calcium salt of ethylenediamine tetraacetic acid buffered with tris [hydroxymethyl] aminomethane) added to lavage solutions increases permeability of Gram-negative bacteria to extracellular solutes and leakage of intracellular solutes. Tris-EDTA solution is prepared by adding 1.2 g of EDTA and 6.05 g of tris to 1 L of sterile water. Sodium hydroxide is used to adjust the pH of the solution to 8, and the solution is mixed and autoclaved for 15 minutes. Treated bacteria are more susceptible to destruction by lysozymes, antiseptics, and antibiotics. Tris EDTA in sterile water rapidly lyses P. aeruginosa, E. coli, and Proteus vulgaris. The addition of tris EDTA to a 0.01% chlorhexidine gluconate solution increases antimicrobial effectiveness approximately 1000-fold. Antimicrobial synergism against E. coli occurs between tris EDTA and penicillin, oxytetracycline, and chloramphenicol. Similarly, tris EDTA and gentamicin, oxytetracycline, polymyxin B, nalidixic acid, and triple sulfonamide have synergistic activity against P. vulgaris.

Other Solutions

Acetic acid at 0.25% or 0.5% occasionally is used as a lavage solution. Its antibacterial effect is achieved by lowering wound pH. Wound acidification is beneficial in wounds that contain urea-splitting organisms (e.g., Pseudomonas spp.); however, resistance to acetic acid may develop. Acetic acid is more cytotoxic to fibroblasts than bacteria. Hydrogen peroxide and Dakin’s solution should not be used as wound lavage solutions. Hydrogen peroxide, even in low concentrations, damages tissue and is a poor antiseptic. It is an effective sporicide; therefore, it may be beneficial if clostridial spores are suspected. Hydrogen peroxide dislodges bacteria and debris from wounds by effervescent action. Dakin’s solution is a 0.5% solution of sodium hypochlorite (1 : 10 dilution of laundry bleach). It releases free chlorine and oxygen into tissue, killing bacteria and liquefying necrotic tissue. However, even at half or quarter strength, Dakin’s solution is detrimental to neutrophils, fibroblasts, and endothelial cells and should not be used as a wound lavage solution.

Other Wound Treatment Methods

Experimentally, pulsed electromagnetic field treatment of open wounds enhances wound epithelialization and may promote early wound contraction without adverse effects on perfusion or tensiometric, histologic, clinicopathologic, or electroencephalographic parameters. A pulsed electromagnetic field generates complex multiform pulses of oscillating electromagnetic fields in the ultra low frequency range (0.5 to 18 Hz). Treatment for 60 minutes (magnetic field unit activated 20 minutes, deactivated 20 minutes, activated 20 minutes) was given twice daily for 21 days. A frequency of 0.5 Hz was used for the first 4 days, 3 Hz for 5 days, and 8 Hz for the last 13 days. Both ultrasonography and phototherapy delivered by low-intensity lasers shorten the inflammatory phase of healing and enhance release of factors stimulating the proliferative stage of repair. Exposure to pico-tesla electromagnetic field treatment improves the strength of sutured wounds and speeds contraction of open wounds in rats.

Assessment of Skin Viability

Skin circulation may deteriorate for 5 days after surgery because of edema and other factors. Skin viability is clinically assessed by color, warmth, pain sensation, and bleeding. Viability may also be assessed by dyes, transcutaneous oxygen or carbon dioxide, laser Doppler velocimetry, ultrasonic Doppler flow detection, and scintigraphy. Nonviable skin is black, bluish black, or white, and the area may be nonpliable, cool, and devoid of sensation. Normal skin is warm, pliable, and pink with normal capillary refill (difficult to assess) and pain sensation. Areas of questionable viability often are blue or purple, and capillary refill and sensation are poor.

Intravenous injection of vital stains fluorescein (10 mg/kg) or xylenol orange (90 mg/kg) has been used to assess vascular integrity of skin but has not been better than visual observation. Transcutaneous oxygen (pO2) or carbon dioxide (pCO2) monitoring allows immediate evaluation for ischemia but requires prolonged, quiet recumbency, and transcutaneous oxygen or carbon dioxide sensors left in place longer than 3 hours may cause superficial burns. Skin generally survives if a transcutaneous pO2 value of approximately 60 mm Hg is maintained. Transcutaneous pO2 values of 30 to 60 mm Hg may be associated with partial or complete survival. Transcutaneous pCO2 values are lower at the base of skin flaps (approximately 53 mm Hg) than at the apex (approximately 106 mm Hg), where ischemia is most apt to occur. Laser Doppler velocimetry is an indicator of capillary blood flux that may give an accurate assessment of local circulation. Probes must be placed away from major vessels to monitor relative blood flow, volume, and velocity, factors that vary with species, site, and instrumentation. Ultrasonic Doppler flow detection is a noninvasive, inexpensive means of determining blood flow and predicting viability in an area. Two sounds usually are heard with each arterial pulse, but only one sound is heard with proximal occlusion or stenosis. Areas of nonviable tissue may also be identified by evaluating the area with scintigraphy after injection of technetium 99-m methylene diphosphate.

Sep 11, 2016 | Posted by in SMALL ANIMAL | Comments Off on Surgery of the Integumentary System
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