Ferrets: wound healing and therapy

Ferrets: wound healing and therapy

Vet Clin Exot Anim 7 (2004) 105–121 Ferrets: wound healing and therapy Anthony A. Pilny, DVM*, Laurie Hess, DVM, DABVP (Avian) Avian and Exotic Pet M...

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Vet Clin Exot Anim 7 (2004) 105–121

Ferrets: wound healing and therapy Anthony A. Pilny, DVM*, Laurie Hess, DVM, DABVP (Avian) Avian and Exotic Pet Medicine Service, The Animal Medical Center 510 East 62nd Street New York, NY 10021, USA

The anatomy of ferrets’ (Mustela putorius furo) integument is similar to that of the dog and cat. Ferrets have thick skin, especially around the head and neck, and a thick subcutis. The principles of wound management and healing in ferrets are similar to those in other domestic mammals. The following is a summary of wound healing in mammals with reference to specific cases in ferrets. Readers are referred to current small animal surgical texts for a more detailed discussion.

Wound healing A wound is a physical injury that disrupts the normal continuity of anatomic structures. Wound healing is the restoration of this continuity. Wound healing begins immediately after injury and is a dynamic process. The biologic processes of wound healing include cell regeneration, cell proliferation, collagen production, and biochemical reactions involving the hemolymphatic, cardiovascular, nervous, and endocrine systems. The four phases of wound healing are inflammation, debridement, repair, and maturation. Healing is influenced by both host factors and wound characteristics (Fig. 1).

Stages of wound healing Inflammatory phase Inflammation is a protective response initiated by wound damage. The inflammatory phase is characterized by increased vascular permeability, * Corresponding author. E-mail address: [email protected] (A.A. Pilny). 1094-9194/04/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.cvex.2003.08.002

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Fig. 1. Healing bite wound after abscessation on a ferret’s head.

chemotaxis of circulatory cells, release of cytokines and growth factors, and cell activation (macrophages, neutrophils, and fibroblasts). Hemorrhage initially cleans the wound by flushing and filling it; vessels constrict for 5 to 10 minutes and then dilate, resulting in leakage of fibrinogen and clotting factors into the wound space. Inflammatory mediators such as histamine, thromboxane, and growth factors cause inflammation for up to 5 days after injury. White blood cell leakage initiates the debridement phase. Debridement phase An exudate composed of white blood cells, dead tissue, and wound fluid forms at the injury site. Neutrophils and monocytes appear first and initiate debridement. Neutrophils phagocytize bacteria to prevent infection and release enzymes that facilitate the breakdown of necrotic material. These enzymes also stimulate monocytes to become macrophages within 24 to 48 hours. Macrophages then secrete collagenases and remove necrotic tissue, bacteria, and foreign material. They also secrete chemotactic and growth factors which can initiate, coordinate, and maintain the formation of granulation tissue. Chemotactic factors (complement, bacterial endotoxin) direct macrophages to injured tissues so that they may recruit mesenchymal cells, stimulate angiogenesis, and modulate wound matrix production. Platelets soon arrive at the wound site and release platelet growth factors important in stimulating fibroblastic activity. Lymphocytes appear later in the debridement phase and secrete soluble factors that stimulate migration and protein synthesis by other cells.

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Repair phase This phase begins 3 to 5 days after initial injury. Macrophages stimulate DNA and fibroblast proliferation. Fibroblasts migrate into wounds, ahead of new capillary buds, as the inflammatory phase subsides. They invade wounds to synthesize and deposit collagen, elastin, and proteoglycans. Wound fibrin disappears as collagen is deposited, and the wound matures into a fibrous scar. The end of the repair phase occurs as collagen content increases, and both fibroblast number and rate of collagen synthesis decrease. Maturation phase Wound strength is maximized because of changes in the scar during the maturation phase. Wound maturation begins when collagen deposition is complete (17–20 days postinjury) and may continue for several years. Normal tissue strength is never regained, but up to 80% of original strength can be achieved. Scars become less cellular, flatten, and soften during this phase.

Host factors affecting wound healing Age affects the rate of wound healing. Older animals may heal more slowly because of concurrent disease or debilitation. For instance, malnourishment and hypoproteinemia (total protein \2.0 g/dL) may delay wound healing and decrease wound strength. In addition, liver disease can result in hypoproteinemia and decreased clotting factor production, thereby slowing wound healing. In most mammals, hyperadrenocorticism may delay wound healing, because excess circulating glucocorticoids can decrease host resistance to infection. Although ferrets commonly suffer from adrenal gland disease, adrenal disorders in ferrets usually result in increased production of steroid hormones other than cortisol [1]. Thus, the cortisol-induced delay in wound healing is not seen in ferrets with adrenal disease. In humans, diabetes commonly leads to delayed wound healing from decreased leukocyte function, impaired cell adherence, and defective collagen sythesis. In animals, diabetes generally does not contribute to delaying wound healing; however, it may lead to increased risk of infection because of compromised leukocyte function. Finally, uremia impairs healing due to effects on enzyme systems and cellular metabolism. Uremia also depresses the rate of granulation tissue formation and epithelial cell division.

Wound characteristics affecting healing Factors affecting the wound’s local environment can affect the rate of healing. For example, the presence of foreign materials such as dirt, sutures,

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and debris can impair wound healing. The release of enzymes in response to foreign materials destroys wound matrix, prolongs the inflammatory phase, and delays the fibroblastic phase of tissue repair. In addition, exposure of wounds to antiseptic drugs may delay healing and predispose to infection by depressing the effects of local inflammatory mediators. Temperature can also affect healing. Warming tissues encourages wounds to heal faster by increasing circulation to affected areas. Reflex vasoconstriction caused by cooler temperatures delays wound repair. The way a wound is repaired or created can also affect how it heals. Incisions created with scalpels tend to heal faster than those created with instruments such as scissors or lasers, because sharply made incisions usually have less wound margin necrosis. Infection may profoundly delay wound healing. The development of infection depends on the amount of tissue trauma, the presence of foreign material, and the activity of host defenses. Bacteria produce collagenases that may decrease wound strength. Bacteria also can change wound pH, which may affect activity of local repair mediators. Wound exudates can further inhibit healing by separating tissue layers. Adequacy of circulation profoundly affects the rate and degree of wound healing. Healing depends on the blood supply to the injured site for the delivery of oxygen and metabolic substrates to cells. Impairment of blood supply (eg, tight bandages) slows healing. Accumulation of fluid in any dead space, such as a seroma, delays healing, because such an hypoxic fluid environment may inhibit migration of reparative cells into wounds. The recruitment, proliferation, and function of cells in wound healing is controlled by growth factors. Numerous growth factors, including epidermal growth factors, fibroblast growth factor, and platelet-derived growth factor, have been identified. Fibronectins also play an important part in wound healing. They are glycoproteins that are found in soluble form in plasma and in insoluble form in connective tissue matrix. Fibronectins stimulate cell attachment and migration and bind bacterial cell wall components, collagen, actin, fibrin, and cell surface receptors. Fibronectins may be important in providing an early wound healing matrix and interlinking cellular and matrix components during healing. Fibronectin content in wounds declines as healing nears completion. Proteoglycans are also important in all phases of wound healing. During cell migration, wound matrix contains high levels of nonsulfated glycosaminoglycans, and as wound maturation progresses, more sulfonated glycosaminoglycans (chondroitin sulfate) appear (Fig. 2).

Effects of steroid therapy on wound healing The effects of corticosteroids on wound healing are especially significant in ferrets, because many ferrets develop insulinomas or lymphoma that may

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Fig. 2. Self-inflicted wound on a ferret’s ears. Skin scrape of the aural skin revealed Demodex mites. This ferret responded to treatment with ivermectin. (Courtesy of Laura Wade.)

require palliative treatment with glucocorticoids. Through their immunosuppressive and protein catabolic effects, corticosteroids may depress all phases of wound healing and increase chances of infection. Steroids restrict the inflammatory phase of wound healing by delaying granulation tissue formation, fibroblast proliferation, and capillary budding [2]. Single-dose steroids usually do not have any significant effect on wound healing; however, in people, steroids are usually not given until 4 to 5 days postoperatively to decrease the likelihood of wound healing complications [3]. Although many ferrets receive steroids daily for the amelioration of hypoglycemia secondary to insulinomas, there have not yet been any reports regarding delayed wound healing in ferrets given steroids. Surgical procedures are commonly performed without concern on ferrets treated with steroids [4]. Acute stress or single doses of corticosteroids do not appear to effect healing. Even with high doses of steroids, wound healing will occur, although at a slower rate [5]. Radiation and certain drugs (eg, chemotherapeutics) may delay wound healing; however, no specific reports have examined the effects of these therapeutic modalities on wound healing in ferrets (Fig. 3).

Management of open or superficial wounds Wounds ideally should be covered with clean, dry, or moistened bandages to prevent further contamination. Life-threatening injuries should be treated first and the patient stabilized before further wound management is initiated. The ‘‘golden period’’ is the first 6 to 8 hours between contamination at injury and bacterial multiplication greater than 105 organisms/gram of tissue. Minimally contaminated wounds treated during this ‘‘golden period’’ are generally lavaged, debrided, and closed primarily.

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Fig. 3. A severely pruritic wound in a ferret with deep pyoderma from self-trauma. This ferret responded to treatment with pentoxyphylline and antibiotics.

The sooner the traumatized tissue is treated, the better the prognosis. Before primary closure is attempted, penetrating wounds should be explored to evaluate the extent of injury. Severely traumatized, old (>8 hours), or infected wounds should be debrided, not closed, to reduce bacterial contamination. Often these wounds are left open to heal by second intention (contraction and epithelialization). Regardless of how old a wound is, initial wound management begins with removal of gross contaminants via copious lavage with warm fluids. Lactated Ringers solution is usually the preferred lavage solution [6]. Occasionally, antiseptic drugs such as chlorhexidene or povidone–iodine are added to the lavage solution to aid in reducing bacterial numbers. However, some antiseptic drugs damage tissues and have little effect on established bacterial populations. Bacteria may be effectively removed with high-pressure lavage from a 35- or 60-mL syringe with an 18-gauge needle. Devitalized tissue may be removed through surgical excision, enzymatic debridement, or wet-dry bandaging. The extent of devitalized tissue is typically apparent within 48 hours of injury. After surgical debridement, wounds that are left open may be treated with antibiotics and wet–dry dressings. Establishing adequate wound drainage and a viable vascular bed is essential to wound healing. Wounds initially left open to heal by second intention may ultimately be closed, once adequate granulation tissue has developed. Vitamins and minerals Adequate nutrition is essential to healing. The ability of currently available commercial ferret diets to meet the specific dietary needs of

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carnivores is unknown. However, specific vitamins and minerals are known to affect wound healing. For instance, high doses of vitamin A increase inflammatory reactions. Vitamin A also stimulates fibroblasts and collagen accumulation. As a result, vitamin A may be administered to help reverse corticosteroid-induced inhibition of wound healing; however, administration of vitamin A to animals not under the influence of steroids has not been shown to alter the rate of healing [7]. Other vitamins also affect wound healing. For example, vitamin E stabilizes membranes, but high doses can impair wound healing and collagen production. In addition, vitamin C is necessary for hydroxylation of proline and lysine in collagen production. Deficiency of vitamin C may, therefore, delay wound healing. Ferrets generally do not need supplemental vitamin C, because they synthesize their own. However, ferrets with large amounts of tissue damage may benefit from supplemental vitamin C to aid in wound healing. Normal epithelial and fibroblastic proliferation requires the zincdependent enzymes DNA-polymerase and reverse transcriptase. Without adequate zinc, epithelial cells and fibroblasts migrate but cannot multiply. Thus, epithelialization cannot occur, and collagen synthesis is inadequate to hold the wound together. Zinc administration to patients with low zinc levels may help restore normal wound healing, but zinc supplemental to patients with normal zinc levels does not accelerate healing.

Topical wound medications Topical antibiotics are preferred over systemic antibiotics for the treatment of open wounds. Mildly contaminated wounds usually do not require treatment with combination systemic and topical antibiotic therapy; however, heavily contaminated wounds often do. To prevent infection, application of topical antibiotics should occur within 1 to 3 hours of wound contamination. Once infection is established in a wound, antibiotics will not inhibit wound suppuration. Wound coagulum formation then prevents topical antibiotics from reaching effective tissue levels and systemic antibiotics from reaching superficial bacteria. Thus, debridement and flushing to reduce bacterial contamination are essential to wound management.

Topical antibiotics used to treat wounds include 1. Triple antibiotic ointment (Neobacimyx)—effective against a broad spectrum of bacteria found in skin wounds. A combination of neomycin, bacitracin, and polymyxin is more effective in preventing infections than treating them. Systemic toxicosis following antibotic administration is unlikely, due to poor tissue absorption. However, efficacy of this combination topical antibiotic against Pseudomonas spp. is poor.

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2. Silver sulfadiazene, 1% cream (Silvadene)—effective against most Gram-positive and -negative bacteria and most fungi. It penetrates necrotic tissues, and is the drug of choice for treating burns. 3. Gentamicin Sulfate, 0.3% ointment (Gentak)—effective against Gramnegative bacteria such as Pseudomonas and Proteus. It is commonly used before and after grafting and in the treatment of wounds that fail to respond to therapy with triple antibiotic ointment. Caution should be taken when administering gentamicin to ferrets, as they are known to be exquisitely sensitive to the toxic effects of systemic aminoglycosides. 4. Nitrofurazone (Furacin)—has broad spectrum antimicrobial properties. It draws body fluid away from wound tissue to help dilute exudates for better absorption into bandages. However, nitrofurazone is not as efficacious in the presence of organic matter, such as excessive pus, and its application can delay epithelialization. 5. Aloe vera—most commonly used on burns for its antibacterial activity. It has antiprostaglandin and antithromboxane properties that help maintain vascular patency and prevent dermal ischemia and necrosis. Acemannan, a component of aloe vera gel, promotes wound healing and stimulates macrophages, resulting in fibroblast proliferation, epidermal growth, and collagen deposition. Acemannan may also bind growth factors, thereby prolonging their effects in promoting granulation tissue formation. Allantoin, another component of aloe vera extract, aids tissue repair by stimulating epithelial growth. Aloe vera should not be applied to full thickness wounds because of its antiinflammatory effects [8].

Systemic antibiotic therapy In general, any parenteral antibiotic used in a cat or dog to treat a wound may be used safely in a ferret. The antibiotic should be chosen based on site and degree of infection, spectrum, and bioavailability. Aminoglycosides should be used with caution in ferrets because of anecdotal reports of their increased sensitivity to these antibiotics. In general, aminoglycosides should not be used in dehydrated patients or in those with renal compromise. Culture and sensitivity is a valuable tool in the diagnosis and treatment of infection. This test will not only aid in choosing the best antibiotic but also help prevent unnecessary antibiotic treatment or treatment of resistant bacteria.

Lavage solutions Solutions used to lavage wounds include: 1. Chlorhexidene diacetate (Nolvasan Solution)—the preferred wound lavage and wetting solution due to its wide spectrum of antimicrobial

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activity and residual effects. Its antimicrobial properties are not impaired by the presence of organic material, and it has minimal systemic absorption. A dilution to 0.05% is effective in killing bacteria, and its residual activity can last up to 2 days, with increased efficacy after repeated application [9]. 2. Povidone-iodine (Betadine Solution 10%)—has a wide spectrum of activity against bacteria, fungi, viruses, and yeasts. However, organic matter (eg, exudates) inactivates the free iodine component, and scrubbing wounds with povidone–iodine detergents can impair healing by inciting tissue damage and potentiating infection. In addition, iodine absorption through mucus membranes and skin can cause transient thyroid dysfunction. 3. Tris-EDTA—added to lavage solutions significantly increases the susceptibility of bacteria to antibiotics and antiseptics. It is particularly effective in helping combat Gram-negative bacteria. Addition of TrisEDTA to 0.01% chlorhexidene increased antimicrobial effectiveness 1000-fold [10].

Analgesia Pain medication may be administered during wound treatment depending on the degree and severity of trauma and level of patient discomfort. The authors often use buprenorphine (Buprenex) intramuscularly or subcutaneously for severe pain and oral carprofen (Rimadyl) for mild to moderate pain or inflammation.

Sutures Sutures act like foreign bodies in wounds; buried sutures may increase the chance of infection by causing irritation, bacterial colonization, and tissue ischemia. The smallest gauge and amount of suture should be used to lessen the likelihood of suture-related complications. Approximating sutures are commonly used to align wound edges in anatomic apposition. Size 3-0 or 4-0 absorbable suture (PDS, polydioxanone, Ethicon Inc., Arlington, Texas) with a swaged, taper-point needle is best for closing subcutaneous and subcuticular tissues. Size 3-0 or 4-0 nonabsorbable suture (Ethilon, monofilament nylon, Ethicon Inc.) with a reverse-cutting needle is recommended in skin. Tissue adhesive can also be used to facilitate closure or hold drains. Drains Drains help evacuate infected fluids from wounds and eliminate dead space. They are most commonly used for bite wounds, lacerations, abcesses,

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and seromas. Passive drains rely on gravity for fluid removal, whereas active drains use a vacuum for fluid pull. Penrose drains (passive) are most commonly used to drain subcutaneous spaces, and active drains (JacksonPratt) are best for deep wounds. The major disadvantage of drains is the potential for retrograde contamination and worsening infection. The smallest diameter and fewest number of drains should be used. Correct placement of drains is essential. Passive drains should be secured at the dorsal aspect of the wound. In addition, to lessen the likelihood of dehiscence, they should exit through an incision at least 1 cm from the wound edge, not through the wound site itself. To decrease the chance that a patient will chew on or pull out a drain prematurely, the patient should be fitted with an elizabethan collar, and drains should be sutured to the skin. Some ferrets will not wear e-collars; however, other ferrets may tolerate small cat sized e-collars tied on with roll gauze. Individualized collars can be cut and sized from radiograph film, or avian e-collars can be adapted to fit ferrets. Most drains can be removed in 2 to 5 days or when the amount of drainage is greatly reduced. Care should be taken in removing any drains so as not to disrupt the skin-wound bed interface (Fig. 4).

Wound closure Wounds can be closed immediately after trauma occurs (primary wound closure), within 1 to 3 days after trauma when they are still infection-free (delayed primary wound closure), or after the formation of granulation tissue (secondary closure). Wounds that are left to heal by second intention contract and epithelialize without surgical closure.

Factors affecting the decision to close a wound include (Adapted from Fossum T. Surgery of the integumentary system. In: Small Animal Surgery, 2nd edition; 2002.): 1. Amount of time since injury. Wounds older than 6 to 8 hours are best treated with bandages initially. They may be closed later if they are free of infection. 2. Degree of contamination. Severe contamination requires extensive lavage and bandaging. 3. Amount of tissue damage. Severely damaged tissue in a patient with decreased host defenses (eg, immunocompromise or concurrent disease) will likely become infected and is best treated with bandaging. 4. Completeness of debridement. Wounds that have only been partially debrided or require further debridement should not be closed. 5. Status of wound vasculature. A wound with questionable blood supply should not be closed but should be evaluated to determine the extent of nonviable tissue.

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Fig. 4. Ferret receiving a blood transfusion. Ferrets lack detectable blood groups, and transfusion reactions are rare. (Courtesy of Heather Wilson.)

6. Patient’s overall health. Shocky patients and those who are at increased anesthetic risk should be treated initially with bandages. 7. Extent of tension and degree of dead space. If, in closing a wound, there is either a large amount of tension or dead space, the risk for seroma formation and infection is greater. Therefore, the wound should be bandaged and not closed primarily. 8. Location of the wound. Wounds in some anatomic locations, such as the legs and head, are too difficult to close, because there is little loose skin in these areas (Fig. 5). Delayed primary closure is best for mildly contaminated, minimally traumatized wounds or wounds older than 6 to 8 hours. Wounds are first lavaged and debrided and treated with appropriate bandages until closure. After lavage, minimally contaminated wounds that are less than 6 hours old can be closed primarily. If excessive dead space is present, Penrose drains are needed. Subcutaneous tissues should be closed with 3-0 or 4-0 buried, interrupted or continuous, approximating sutures (eg, polydioxanone). Skin edges should be apposed with subcuticular sutures or approximating skin sutures (eg, nylon). Wounds with severe contamination, infection, or tissue damage or those older than 6 to 8 hours should be left open. Most often, after lavage and exploration, debridement is necessary. Wet-to-dry bandages should be applied to continue debridement and encourage formation of granulation tissue. Wounds left to heal by second intention usually close completely, resulting in normal appearing skin, and they are often less expensive to treat than wounds that are closed surgically. The disadvantages of second intention healing include contracture with disfigurement, scarring, and incomplete healing.

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Fig. 5. Chemical burns from household bleach exposure.

Secondary closure may occur 3 to 5 days after injury, once a healthy bed of granulation tissue has formed. It is the best treatment option for severely infected or contaminated wounds or contracted wounds that have not completely closed. Secondary closure often requires resection of the granulation bed and skin margins, wound lavage, and apposition of skin edges. Instead, it is sometimes more appropriate to resect the skin margins and debride the granulation tissue surface before apposing skin. If secondary closure is not possible, a flap or graft can be placed over the defect. A bandage applied postoperatively to absorb exudates and support the wound should be changed twice daily, if there is excessive drainage, or every 3 to 4 days, if there is little or no drainage. Bandaging Bandages keep wounds clean, reduce edema and hemorrhage, decrease dead space, and minimize scar tissue formation. By keeping wounds warm, they improve healing by enhancing wound vasculature. A properly placed bandage will place pressure distal to the wound, rather than proximal, to prevent venous or lymphatic compromise. Many ferrets are intolerant of

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bandages and will require elizabethan collars to prevent removal and ingestion of bandage materials. Using the appropriate amount and size bandage material to bandage wounds is essential to avoid a tourniquet effect. Bandages should be applied smoothly to eliminate ridges or bulking that can cause discomfort and skin necrosis. Bandaged surfaces should be kept clean and dry, and owners should be taught to monitor their pets’ bandages at home for signs of swelling, odor, or discomfort. Special care should be taken in ferrets to ensure that they do not soil bandages with feces or urine. There are not only many types of bandages but also many techniques by which they may be applied. Readers are referred to small animal surgery texts for more thorough explanations of bandage types. The following is a list of the more commonly used bandages in ferrets: 1. Wet–dry. The most commonly used bandage in veterinary medicine, wet–dry bandages assist in debridement but leave viable tissues intact. The principle is that as the saline-soaked part of the bandages dries, wick action will pull exudates into the dry part of the sponge, away from the wound. Advantages to this bandage type include the ability to use antimicrobial agents in the wet part of the bandage, removal of exudates, and maintenance of patients’ comfort. The main disadvantage is that bacteria may flourish in moist environments, and tissue maceration may occur. Once granulation tissue has formed and tissue drainage is serosanguinous, a nonadherent bandage should be placed. 2. Stabilizing bandages. These bandages immobilize fractures until fixation. The Robert-Jones type is most common. These soft, heavily padded, stabilizing bandage help prevent tissue trauma during transport and handling.

Skin diseases of ferrets requiring wound management 1. Bacterial diseases: ferrets may incur bite wounds while playing, mating, or fighting, and may sustain deep puncture wounds from chewing on sharp objects. Wounds may become infected and develop into superficial or deep pyodermas, abcesses, or cellulitis. The most common organisms infecting ferret wounds are Staphylococcus and Streptococcus spp.; infection with Pastuerella and Escherichia coli may also occur [11]. Most abscesses wall off and cause few clinical signs; however, some require lancing, debridement or excision, and lavage. Drain placement may be necessary, and broad spectrum antibiotics should be administered while culture results are pending. Actinomyces, or ‘‘lumpy jaw,’’ is an uncommon condition in ferrets. This bacteria enters oral tissues via wounds to the oral mucosa or via inhalation or swallowing. Clinical signs associated with Actinomyces infection include cervical masses with sinus tracts containing thick,

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Fig. 6. Actinomyces infection in a young ferret. (Courtesy of Randy Belair.)

yellow, purulent material. Some masses are large enough to cause dyspnea. Similar signs have been seen with mandibular abscesses containing mixed Gram-negative bacteria. Surgical debridement and drainage are necessary in these cases [12] (Fig. 6). 2. Fungal diseases: systemic mycoses with skin manifestations have been infrequently reported in ferrets. Fungal infection should be considered in ferrets with persistently draining tracts or skin eruptions unresponsive to antibiotic therapy. Infection with Blastomyces dermatitidis was reported in a ferret with a persistently draining tract of the metacarpal pad that required therapy with oral ketoconazole and intravenous amphotericin B [13]. Infection with Coccidioides species in a ferret resulted in a persistent draining tract in the stifle that responded to treatment with oral ketoconazole [14]. 3. Burns/thermal injuries: burns occur when heat is applied to skin faster than tissues can dissipate it. Removal of dead tissue is essential to control sepsis and promote a viable vascular bed suitable for surgical closure, if necessary. Small burns can be excised and closed primarily. Larger burns can be left to heal by contraction and epithelialization, or they may require grafting. Second intention healing may take weeks to months, and result in scarring; therefore, skin flaps and grafts are often better options. Early wound closure lessens the likelihood of secondary infection (Fig. 7). 4. Electrical injuries: the most common cause of electrical injury in ferrets is from chewing on electrical cords. Tissue damage may be extensive due to deep penetration of the generated heat. Necrosis occurs from vascular thrombosis and release of vasoactive substances. Immediate death usually results from respiratory paralysis or ventricular fibrillation.

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Fig. 7. Severe burns from boiling water in a ferret caught in a dishwasher. (Courtesy of Jamie Morrissey.)

Fig. 8. Palate damage in a ferret that chewed an electrical cord. (Courtesy of Avery Bennett.)

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Fig. 9. Surgical repair of the wound in the palate. (Courtesy of Avery Bennett.)

Burns most often occur in the mouth (lips, gums, palate, and tongue). Pulmonary edema often occurs as a sequela. Repair of tissues should be delayed until full extent of the injury is known. Appropriate repair depends on the amount of tissue damage. Small wounds can heal by second intention, while larger injuries should be surgically repaired (Figs. 8 and 9). Summary In all species of mammals, the stages of wound healing are the same, and both host factors and wound characteristics affect how wounds heal. The basic principles of wound care in ferrets, such as lavage, bandaging, and surgical closure, are similar to those in other species; however, knowledge of ferrets’ anatomy and pathophysiology, as well as skin conditions commonly seen in ferrets, will help ensure proper wound healing.

References [1] Rosenthal KL, Peterson ME. Evaluation of plasma androgen and estrogen concentrations in ferrets with hyperadrenocorticism. J Am Vet Med Assoc 1996;209(6):1097–102. [2] Sieggreen MY. Healing of physical wounds. Nurs Clin North Am 1987;22:439. [3] Berlinger NT. Wound healing. Otolaryngol Clin North Am 1986;15:29. [4] Bennett A. Available at: http://www.vin.com/Members/SearchDB/boards/b0115000/ b0111667.htm (Accessed 12/15/02).

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[5] Johnston DE. The processes in wound healing. J Am Anim Hosp Assc 1977;13:186. [6] Buffa EA, Lubbe AM, Verstraete FJ, Swaim SF. The effects of wound lavage solutions on canine fibroblasts: an in vitro study. Vet Surg 1997;26(6):460–6. [7] Ehrlich P, Hunt TK. Effects of cortisone and vitamin A on wound healing. Ann Surg 1968;167:324. [8] Heggers JP, Kucukcelebi A, Stabenau CJ, Ko F, Broemeling LD, Robson MC, et al. Wound healing effects of aloe gel and other topical antibacterial agents on rat skin. Phytother Res 1995;9:455. [9] Lozier S, Pope E, Berg J. Effects of four preparations of 0.05% chlorhexidene diacetate on wound healing in dogs. Vet Surg 1992;21:107. [10] Ashworth CD, Nelson DR, et al. Antimicrobial potentiation of irrigation solution containing Tris EDTA. JAVMA 1990;197(11):1513–4. [11] Collins BR. Dermatologic disorders of common small non-domestic animals. In: Nesbitt GH, editor. Topics in small animal medicine: dermatology. New York: Churchill Livingstone; 1987. [12] Fox JG. Bacterial and mycoplasma diseases. In: Biology and diseases of the ferret. Philadelphia: Lea & Fehiger; 1988. [13] Lenhard A. Blastomycosis in a ferret. JAVMA 1985;186:70–2. [14] Duval-Hudelson KA. Coccidiodomycosis in three European ferrets. J Zoo Wild Med 1990;21:353–7.