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Compendium January 2013 (Vol 35, No 1)

Dermatologic Emergencies: Identification and Treatment

by Kathleen M. Kersey, DVM, DACVECC, Millie Rosales, DVM, DACVD, Brian K. Roberts, DVM, DACVECC

    CETEST This course is approved for 3.0 CE credits

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    Skin disease is one of the most common reasons dogs and cats are taken to the veterinarian. While many dermatologic conditions cause mild, localized signs, some, such as erythema multiforme, toxic epidermal necrolysis, cutaneous vasculitis, cutaneous drug eruptions, and thermal burns, can cause severe cutaneous signs and may have serious systemic consequences. These patients may present on an emergency basis and require intensive monitoring, diagnostics, and care. Lack of familiarity with these conditions may delay diagnosis and appropriate treatment. Pyotraumatic dermatitis may also prompt owners to seek emergency veterinary care due to the severe appearance of associated lesions.

    Skin disease is one of the primary reasons owners take a pet to the veterinarian.1 Signs often consist of pruritus and primary and secondary lesions (e.g., pustules, papules, crusting, alopecia). However, pets affected by severe diseases such as erythema multiforme (EM), toxic epidermal necrolysis (TEN), vasculitis, and cutaneous drug eruptions (CDE) may also develop systemic signs. These patients may present to the veterinarian on an emergency basis. There is little information in the veterinary literature about these dermatopathies. In addition, many veterinarians are unfamiliar with these diseases, making identification difficult and delaying treatment.

    Erythema Multiforme

    EM is an uncommon, acute, inflammatory condition of the skin and/or mucous membranes that can cause significant morbidity.2 The pathogenesis has not been fully elucidated but is proposed to be a host-specific, cell-mediated hypersensitivity reaction to various antigens.3 It has been reported in dogs secondary to administration of specific drugs (TABLE 1), infection (staphylococcal dermatitis, parvovirus), neoplasia, dietary components (beef and/or soy, chicken and/or egg), and idiopathic causes.2–8 In one review of 44 cases of EM in dogs, 10 (22.8%) were idiopathic.7 Reported causes in cats include administration of specific drugs (TABLE 1), herpesvirus infection, and application of d-limonene–based shampoo.3,9

    EM can range from mild to severe. The term erythema multiforme minor is used when ≤1 mucosal surface and <50% of total body surface area (TBSA) are affected. Erythema multiforme major is similar, but >1 mucosal surface is affected. In both forms of EM, epidermal detachment, in which the epidermis separates from the dermis, may be present and comprises <10% of TBSA.10 Lesions vary in appearance and consist of erythematous macules or papules that spread peripherally and clear centrally, producing serpiginous or annular lesions (“target lesions”). However, such lesions are not classic target lesions as described in humans, and the use of this term in veterinary EM cases is controversial. Vesicles or bullae, urticarial plaques, or a combination of lesions may also be present.3 The center of the lesion may become necrotic and slough, leaving behind erythematous erosions and ulcers7 (FIGURE 1). The most commonly involved sites in dogs include the ventrum, mucocutaneous junctions, oral cavity, pinnae, and footpads. Lesions in cats are typically ulcerative or vesiculobullous and are found on the trunk and mucocutaneous junctions.3 Some animals present with these lesions; others are evaluated for systemic signs (e.g., pyrexia, inappetence, lethargy) without obvious initial skin involvement.3 Diagnostic differentials are listed in BOX 1 .3,11 Definitive diagnosis necessitates a thorough history, physical examination, and skin biopsy. Single-cell keratinocyte apoptosis with lymphocyte satellitosis in all layers of the epidermis is characteristic of EM.3

    Key Points

    • Serpiginous or annular lesions are characteristic of erythema multiforme.
    • Successful treatment of erythema multiforme, toxic epidermal necrolysis, cutaneous vasculitis, cutaneous drug eruptions, and pyotraumatic dermatitis requires removal of the underlying cause or drug.
    • Supportive care for severe erythema multiforme, toxic epidermal necrolysis, cutaneous drug eruptions, and thermal burns consists of aggressive fluid therapy (crystalloids, colloids), antibiotics, wound management, analgesia, and nutritional support.
    • Fleas and flea-bite hypersensitivity are the most common causes of pyotraumatic dermatitis.

    Treatment is directed at removal of the underlying cause, if present (i.e., discontinue the offending drug, treat the underlying infection, and/or avoid suspect dietary antigens).7 A complete blood count and serum chemistry panel should be evaluated and may help determine the underlying cause. In severe cases and in patients with systemic signs, venous blood gases and blood lactate level should be measured. Hospitalization and intravenous (IV) fluid therapy consisting of crystalloids, colloids, and/or plasma to replace fluid, electrolytes, and proteins lost via large cutaneous defects may be required. Additional supportive care in the form of antibiotics, analgesia, nutritional support, and wound management should also be initiated in severe cases9,11 (TABLE 2). The use of immunosuppressive agents (e.g., glucocorticoids, cyclosporine, azathioprine) is controversial but may be beneficial in idiopathic cases in which they are not contraindicated (e.g., infection).3,7 A food trial with a novel or hydrolyzed protein diet should be considered in suspected idiopathic cases not responding to conventional therapy.3 Human immunoglobulin (TABLE 2) has been successful in treating refractory CDE (severe EM, TEN, Stevens-Johnson syndrome) in one cat and four dogs.12–14

    Mild cases of EM may spontaneously regress over a few weeks. Chronic, idiopathic, or relapsing cases may require lifelong therapy. Patients with widespread skin lesions or extensive oral and mucosal involvement have a poor to guarded prognosis and may die of septicemia, disseminated intravascular coagulation, or other causes.2,4,9

    Toxic Epidermal Necrolysis

    TEN is a rare mucocutaneous disorder affecting dogs, cats, and humans.15 Reported causes in dogs and cats include administration of specific drugs (TABLE 1), bacterial infections, hepatopathy, neoplasia, and idiopathy. Although the exact pathophysiology is unknown, an immunologic role is suspected.4,15

    Typically, patients initially develop systemic signs (pyrexia, lethargy, inappetence) with little dermal involvement. Early erythema is followed by vesicles, bullae, necrosis, and ulceration. Lesions may affect skin diffusely over the body, although the face and extremities are more commonly involved. Mucocutaneous junctions, mucosae (e.g., oral, gastrointestinal, rectal, conjunctival, tracheal), and footpads may also be affected. A positive Nikolsky sign (separation of the superficial layer of the epidermis from the basal layer with gentle digital pressure) and significant pain are usually present.2,4,15,16 BOX 1 lists diagnostic differentials.4,11,15 Skin biopsy is required for definitive diagnosis; histopathology reveals full-thickness coagulation necrosis of the epidermis with minimal dermal inflammation.15

    Treatment is similar to that of EM (TABLE 2) and is aimed at the underlying cause. Extensive dermal involvement results in massive fluid, electrolyte, and plasma protein losses. Supportive care akin to that for burn patients (aggressive fluid replacement, antimicrobial therapy, wound care, analgesia, nutritional support) is required.15,17 Decreased effective circulating volume is possible secondary to fluid losses, and perfusion parameters (venous blood gas, lactate, blood pressure, urine output, heart rate) should be monitored. Use of glucocorticoids is controversial. Human immunoglobulin has been used successfully.12,13 Resolution of signs may take 2 to 3 weeks if the underlying cause is corrected.15 However, the prognosis is often guarded to poor and depends on the severity of the lesions. Mortality rates in humans can be as high as 30% to 50%, with sepsis being the primary cause of death.3,4,17

    Cutaneous Vasculitis

    Vasculitis is an uncommon disorder that causes inflammation within blood vessel walls, resulting in disruption of the vessel architecture, altered blood flow, and ischemic injury to end tissues.18,19 In most cases, the proposed pathophysiology involves a type III hypersensitivity reaction with immune complex deposition along the endothelium. A type I reaction may be important during the initial stages of the disease. Activation of the complement cascade results in endothelial necrosis, thrombosis, vascular occlusion, hemorrhage, and ischemia of recipient tissues.18 The skin and visceral organs may be affected. Causes of cutaneous vasculitis include administration of specific drugs (TABLE 1), vaccines (most commonly rabies), infections (viral [feline immunodeficiency virus, feline leukemia virus, feline infectious peritonitis], rickettsial [Rocky Mountain spotted fever, ehrlichiosis, borreliosis], bacterial, parasitic [dirofilariasis]), food hypersensitivity, insect bites, and neoplasia.18–20 At least 50% of veterinary cases are idiopathic.18,20

    Cutaneous signs are variable: erosions, ulceration, crusting, palpable purpura, edema, plaques, alopecia, and necrosis.18–20 The extremities, ear tips, tail, footpads, oral mucosa, and nasal planum are commonly affected19,20 (FIGURE 2 and FIGURE 3). Systemic manifestations such as pyrexia, lethargy, anemia, gastroenteritis, glomerulonephritis, myopathy, and arthropathy may develop.18,20 Diagnostic differentials include autoimmune diseases and other dermatologic emergencies11,20 (BOX 1). Definitive diagnosis is based on skin biopsy and strong clinical suspicion.18 Early lesions (within 8 to 24 hours of onset) are the most diagnostic, as chronic lesions may only show remnant vessels with little active inflammation.19,20 A thorough history is important for assessing drug or vaccine administration and exposure to infectious agents. To evaluate for specific etiologies, a minimum database (complete blood count, serum chemistry panel, urinalysis) should be performed. Special testing for autoimmune diseases, coagulopathy, and infectious diseases (serology and DNA antigen testing) may be required.

    Therapy centers on removal or treatment of the underlying cause and immunomodulation (TABLE 2).18–20 Systemic glucocorticoids may be required for resistant or idiopathic cases. Pentoxifylline has been successful, presumably due to its hemorrheologic, immunomodulatory, antiinflammatory, and antithrombotic properties.18,21 Dapsone, sulfasalazine, tetracycline/niacinamide, cyclophosphamide, chlorambucil, and azathioprine have also been used.19,20 The prognosis depends on the extent of visceral involvement and the underlying etiology.20

    Rabies vaccine–induced vasculitis has been reported.18,20 It is characterized by a focal cutaneous vasculitis at the site of vaccination and occurs primarily in toy breed dogs with long hair growth cycles. Clinical signs include roughly annular areas of variable alopecia, hyperpigmentation, and, less commonly, scaling or erythema overlying a variably indurated dermis and subcutis. The caudal or lateral thigh, cervical region, or shoulder is typically affected. Lesions generally appear 2 to 6 months after subcutaneous administration of the vaccine and persist for months to years. Lesions may also develop at other classic vasculitis sites yet still be associated with the typical localized process.22–24 Lesions may respond to pentoxifylline therapy with up to 75% reduction in lesion size; however, they may also spontaneously resolve.20,24 Other specific vasculopathies include juvenile dermatomyositis, familial cutaneous vasculopathy of German shepherds, cutaneous and renal glomerular vasculopathy of greyhounds, proliferative arteritis of the nasal philtrum, proliferative thrombovascular necrosis of the pinnae, and solar vasculopathy.

    Cutaneous Drug Eruptions

    CDE are adverse reactions to any oral, parenteral, or topical drug.4,11 The incidence of CDE in dogs and cats out of all canine and feline dermatology cases examined at one university hospital was 2% and 1.6%, respectively.25,26 The pathogenesis may be immunologic or nonimmunologic. Immunologic reactions involve type I (immediate), II (cytotoxic), III (antigen-antibody complex), or IV (delayed) hypersensitivity. Nonimmunologic mechanisms include stimulation of complement pathways, the release of mast cell and basophil mediators, and interference with arachidonic acid metabolism.4 The most commonly implicated drugs in dogs and cats can be found in TABLE 1 , although adverse reactions to NSAIDs, fenbendazole, and carboplatin have also been reported in dogs.25–30

    CDE are manifested by variable cutaneous or mucocutaneous lesions that can mimic many other dermatopathies. Lesions may be focal, multifocal, or generalized.11 Typical eruption patterns include urticaria-angioedema, maculopapular eruptions, fixed drug reactions, exfoliative erythroderma, purpuric reactions, vesiculobullous reactions, lichenoid reactions, superficial suppurative necrolytic dermatitis, EM, and TEN. A complete description of these classifications is outside the scope of this article and may be found elsewhere.4,31 A pemphigus foliaceus-like drug reaction has also been reported.32,33 Diagnostic differentials for CDE vary based on the specific lesions present.

    Diagnosis of CDE is often difficult. Clinical signs typically develop within 1 to 3 weeks of starting the offending drug.4,31 However, CDE may develop after months or years of therapy with a particular drug or up to 3 weeks after discontinuation of a drug.4 Clinicopathologic changes reflect protein and electrolyte loss secondary to cutaneous lesions and the overall health of the patient rather than the cause of the lesions.11 Dermatohistopathology is often nonspecific (except in cases of EM and TEN) and reflects only the lesions present, but it may help rule out some diagnostic differentials. Definitive diagnosis requires rechallenge with the suspect drug to determine if clinical signs recur, but this is considered unethical by most clinicians and may have fatal consequences.4,11,31

    Primary treatment consists of discontinuation of the drug in question; cutaneous lesions typically resolve within 2 to 4 weeks after discontinuation. Lesions should be treated with topical agents (e.g., benzoyl peroxide, chlorhexidine) to help prevent secondary infection and promote healing. Supportive care (IV fluids, systemic antibiotics, nutritional support) may be warranted in more severe cases (TABLE 2). Glucocorticoid therapy is controversial but may be required in some cases to control pruritus and achieve complete resolution of cutaneous signs. The offending drug and any related drugs should be avoided in the future. The overall prognosis is good unless extensive epidermal necrosis or multiple organ involvement is present.4,11,31

    Thermal Burns

    Thermal burns are relatively uncommon in veterinary patients and occur after accidental or deliberate exposure to a heat source.34,35 Reported causes include building fires, electric heating blankets, improperly grounded electrocautery units, hot-air dryers, scalding water, automobile exhaust pipes, radiators, and malicious torture.34–36

    Burns are classified according to the depth of the burn and TBSA involved. Superficial (first-degree) burns are restricted to the epidermis and are erythematous, dry, and painful to the touch. Partial-thickness (second-degree) burns involve the epidermis and outer dermis. Depending on the depth of the burn, the skin may be black to yellow-white; hair follicles may or may not be intact; and the area may be painful to the touch or may exhibit decreased pain sensation. In full-thickness (third-degree) burns, the entire epidermis, dermis, and, potentially, underlying connective tissue, muscle, and bone are affected. Prognosis depends on the depth and extent of the burn, which may take 3 to 14 days to fully “declare” itself34,35 (FIGURE 4). TBSA affected can be estimated by using the “rule of 9s” established for human burn patients: the head and neck are approximately 9% of TBSA, each forelimb is 9%, each hindlimb is 18%, and the thorax and abdomen are each 18%.37 Severe burns covering ≥50% TBSA require intense, long-term nursing care, incur large expenses, and generally have a poor prognosis; euthanasia may be warranted.37

    Patients with severe thermal burns may present with hemodynamic compromise from hypovolemic shock. Burn wound edema can result in massive fluid and plasma protein losses during the first 12 to 24 hours due to increased vascular permeability, thus necessitating aggressive crystalloid fluid resuscitation (TABLE 2). However, patients suffering thermal burns from house fires will likely also have lung damage from smoke inhalation, and fluid therapy should be used judiciously. Specific fluid replacement formulas have been adapted from those used for human burn patients.34 After 12 to 24 hours, vascular permeability stabilizes and use of synthetic colloids may counteract the loss of plasma proteins. Oxygen supplementation should be provided as needed. If >20% TBSA is involved, significant hematologic, electrolyte, and metabolic abnormalities may develop, including anemia, hyper- or hyponatremia, hyper- or hypokalemia, and metabolic or respiratory acidosis.34,35 Clinicians should anticipate these changes and monitor and treat appropriately. Analgesia is of utmost importance, and single-agent (e.g., opioids) or combination therapy (e.g., a morphine, lidocaine, and ketamine constant-rate infusion) may be required. Burn patients are in a hypermetabolic state; early and aggressive nutritional support is required to offset protein catabolism and promote wound healing.36,37 If the patient is unable or unwilling to eat on its own, enteral (via nasogastric, esophagostomy, or gastrostomy tube) nutrition should be initiated.

    Proper wound management is imperative for preventing infection, protecting the wound, and facilitating healing. If the patient presents within 2 hours of injury, the site should be cooled with cold water or saline (37°F to 63°F) for 30 minutes to reduce heat retention and the depth of the burn. With the patient stable and sedated or anesthetized, the hair over the area should be carefully clipped, a broad-spectrum topical ointment (e.g., silver sulfadiazine, nitrofurazone) applied to the area, and a sterile occlusive dressing placed. Daily wound care consists of conservative debridement, lavage, topical therapy, and bandage replacement, typically under general anesthesia, and continues until wound closure.34,37 Healing is rapid for superficial burns and occurs through reepithelialization over approximately 7 days. In superficial partial-thickness burns, the wound may reepithelialize in 10 to 21 days with minimal scar formation. In deep partial-thickness burns, healing may occur through contraction and reepithelialization; however, because severe scarring is typical, surgical closure is recommended. Full-thickness burns often require surgical intervention in the form of skin flaps, advancement techniques, skin grafts, or vacuum-assisted closure.35

    Pyotraumatic Dermatitis

    Pyotraumatic dermatitis (acute moist dermatitis, “hot spot”) is a rapidly developing superficial to deep skin infection that occurs secondary to self-inflicted trauma from licking, chewing, or scratching.38,39 Although the condition is not life-threatening, the sudden onset, pruritic nature, and hemorrhagic appearance often provoke owners to seek veterinary care on an emergency basis. Fleas and flea-bite hypersensitivity are the most common inciting cause when patients present with caudal truncal distribution, but other ectoparasites (e.g., scabies, lice, ticks), hypersensitivity (e.g., adverse food reactions, atopic dermatitis), otitis externa, folliculitis, contact dermatitis, trauma, anal sac disease, swimming (in densely haired dogs), and a dirty, unkempt coat are additional causes.38,39 Predisposing factors for development of pyotraumatic dermatitis in dogs are a dense coat, male sex, age <4 years, fleas, and hot, humid weather.38

    Clinical signs include erythema, alopecia, and well-circumscribed, moist skin that is typically painful (FIGURE 5). Mild hemorrhage may be present secondary to self-induced trauma. Papules and pustules along the perimeter of the lesion suggest an expanding superficial pyoderma. Lesions most often appear on the trunk, tail base, lateral thigh, neck, or face. Diagnostic differentials include superficial pyoderma, dermatophytosis, and demodicosis (BOX 1), although the latter two typically do not lead to acute onset of severe pruritus at the time of lesion development. Diagnosis is based on the history, clinical signs, and cytology revealing suppurative inflammation with mixed bacteria present.39

    Treatment consists of identifying and treating the underlying cause and ensuring aggressive flea control. The lesion should be clipped and cleaned, which may require sedation depending on the location or severity of the lesion. A nonirritating, topical drying agent or astringent (e.g., 5% aluminum acetate) should be applied every 8 to 12 hours for 2 to 7 days. To control pruritus, a topical or systemic corticosteroid should be used for 5 to 10 days. Antibiotics should be initiated and continued for 1 to 4 weeks. Many studies have shown resolution of clinical signs with topical antibiotic therapy (e.g., fusidic acid, neomycin).40,41 However, systemic antibiotics (e.g., cephalosporins, potentiated penicillins, potentiated sulfonamides) should be used for lesions with cytologic evidence of infection or positive culture results that do not show improvement with topical therapy alone.38,39 An Elizabethan collar, T-shirt, or socks should be used to protect the affected area and prevent further self-induced injury.39 The prognosis is good if the underlying cause can be corrected or controlled.38


    Dermatologic emergencies are uncommon, but they may become life-threatening. In some cases, patients may present with vague systemic signs, with skin lesions developing later. Large cutaneous defects may lead to sepsis or significant plasma protein losses. Certain dermatopathies (e.g., severe EM, TEN, vasculitis, CDE, burn injuries) can cause metabolic, electrolyte, and hematologic abnormalities. Veterinarians should be aware of these conditions so that a proper diagnosis can be made and appropriate therapy instituted.

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    1. Hill PB, Lo A, Eden CA, et al. Survey of the prevalence, diagnosis and treatment of dermatological conditions in small animals in general practice. Vet Rec 2006;158:533-539.

    2. Rosenbaum MR, Kerlin RL. Erythema multiforme major and disseminated intravascular coagulation in a dog following application of a d-limonene-based insecticidal dip. J Am Vet Med Assoc 1995;207(10):1315-1319.

    3. Scott DW, Miller WH, Griffin CE, eds. Erythema multiforme. In: Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:729-740.

    4. Rosenkrantz WS. Cutaneous drug reactions. In: Griffin CE, Kwochka KW, Macdonald JM, eds. Current Veterinary Dermatology: The Science and Art of Therapy. St. Louis, MO: Mosby-Year Book;1993:154-164.

    5. Favrot C, Olivry T, Dunston SM, et al. Parvovirus infection of keratinocytes as a cause of canine erythema multiforme. Vet Pathol 2000;37:647-649.

    6. Tepper LC, Spiegel IB, Davis GJ. Diagnosis of erythema multiforme associated with thymoma in a dog and treated with thymectomy. J Am Anim Hosp Assoc 2011;47:e19-e25.

    7. Scott DW, Miller WH. Erythema multiforme in dogs and cats: literature review and case material from the Cornell University College of Veterinary Medicine (1988-96). Vet Dermatol 1999;10:297-309.

    8. Itoh T, Nibe K, Kojimoto A, et al. Erythema multiforme possibly triggered by food substances in a dog. J Vet Med Sci 2006;68:869-871.

    9. Lee JA, Budgin JB, Mauldin EA. Acute necrotizing dermatitis and septicemia after application of a d-limonene-based insecticidal shampoo in a cat. J Am Vet Med Assoc 2002;221(2):258-262.

    10. Hinn AC, Olivry T, Luther PB, et al. Erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis in the dog: clinical classification, drug exposure, and histopathological correlations. Vet Allergy Clin Immunol 1998;6:13-20.

    11. Medleau L, Hnilica KA, eds. Small Animal Dermatology: A Color Atlas and Therapeutic Guide. 2nd ed. St. Louis: Saunders; 2006:189-227.

    12. Byrne KP, Giger U. Use of human immunoglobulin for treatment of severe erythema multiforme in a cat. J Am Vet Med Assoc 2002;220(2):197-201.

    13. Trotman TK, Phillips H, Fordyce H, et al. Treatment of severe adverse cutaneous drug reactions with human intravenous immunoglobulin in two dogs. J Am Anim Hosp Assoc 2006;42:312-320.

    14. Nuttall TJ, Malham T. Successful intravenous human immunoglobulin treatment of drug-induced Stevens-Johnson syndrome in a dog. J Small Anim Pract 2004;45:357-361.

    15. Scott DW, Miller WH, Griffin CE, eds. Toxic epidermal necrolysis. In: Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia, PA: WB Saunders; 2001:740-742.

    16. Gross TL, Ihrke PJ, Walder EJ, et al, eds. Necrotizing diseases of the epidermis. In: Skin Diseases of the Dog and Cat: Clinical and Histopathologic Diagnosis. 2nd ed. Ames, IA: Blackwell; 2005:75-104.

    17. Roujeau JC, Stern RS. Severe adverse cutaneous reactions to drugs. N Engl J Med 1994;331:1272-1285.

    18. Morris DO, Beale KM. Cutaneous vasculitis and vasculopathy. Vet Clin North Am Small Anim Pract 1999;29(6):1325-1335.

    19. MacDonald JM. Nasal depigmentation. In: Griffin CE, Kwochka KW, Macdonald JM, eds. Current Veterinary Dermatology: The Science and Art of Therapy. St. Louis, MO: Mosby-Year Book; 1993:223-233.

    20. Scott DW, Miller WH, Griffin CE, eds. Vasculitis. In: Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia, PA: WB Saunders; 2001:742-756.

    21. Jasani S, Boag AK, Smith KC. Systemic vasculitis with severe cutaneous manifestation as a suspected idiosyncratic hypersensitivity reaction to fenbendazole in a cat. J Vet Intern Med 2008;22:666-670.

    22. Campbell KL, Metry CA. Variabilities of vasculitis. In: DeBoer DJ, Affolter VK, Hill PB, eds. Advances in Veterinary Dermatology. Ames, IA: Blackwell; 2010:408-416.

    23. Wilcock BP, Yager JA. Focal cutaneous vasculitis and alopecia at sites of rabies vaccination in dogs. J Am Vet Med Assoc 1986;188:1174-1177.

    24. Bensignor E. What is your diagnosis? Post-rabies-vaccination alopecia. J Small Anim Pract 1999;40:151, 189.

    25. Scott DW, Miller WH Jr. Idiosyncratic cutaneous adverse drug reactions in the dog: literature review and report of 101 cases (1990-1996). Canine Pract 1999;24:16-22.

    26. Scott DW, Miller WH Jr. Idiosyncratic cutaneous adverse drug reactions in the cat: Literature review and report of 14 cases (1990-1996). Feline Pract 1998;26:10-15.

    27. Niza MM, Félix N, Vilela CL, et al. Cutaneous and ocular adverse reactions in a dog following meloxicam administration. Vet Dermatol 2007:18:45-49.

    28. Mellor PJ, Roulois AJA, Day MJ, et al. Neutrophilic dermatitis and immune-mediated haematological disorders in a dog: suspected adverse reaction to carprofen. J Small Anim Pract 2005;46:237-242.

    29. Nuttall TJ, Burrow R, Fraser I, et al. Thrombo-ischaemic pinnal necrosis associated with fenbendazole treatment in a dog. J Small Anim Pract 2005;46:243-246.

    30. Lanore D, Sayag D. Probable cutaneous hypersensitivity to carboplatin single-agent chemotherapy in a dog. J Small Anim Pract 2010;51:654-656.

    31. Scott DW, Miller WH, Griffin CE, eds. Cutaneous adverse drug reaction. In: Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia, PA: WB Saunders; 2001:720-729.

    32. Horvath C, Neuber A, Litschauer B. Pemphigus foliaceous-like drug reaction in a 3-month-old crossbreed dog treated for juvenile cellulitis. Vet Dermatol 2007;18:353-359.

    33. White SD, Carlotti DN, Pin D, et al. Putative drug-related pemphigus foliaceus in four dogs. Vet Dermatol 2002;13:195-202.

    34. Pavletic MM, Trout NJ. Bullet, bite, and burn wounds in dogs and cats. Vet Clin North Am Small Anim Pract 2006;36(4):873-893.

    35. Garzotto CK. Thermal burn injury. In: Silverstein DC, Hooper K, eds. Small Animal Critical Care Medicine. St. Louis, MO: Saunders; 2009:683-686.

    36. Pope ER. Thermal, electrical, and chemical burns and cold injuries. In: Slatter D, ed. Textbook of Small Animal Surgery. 3rd ed. Philadelphia, PA: Saunders; 2003:356-372.

    37. Dhupa N. Burn injury. In: Wingfield WE, Raffe MR, eds. The Veterinary ICU Book. Jackson Hole, WY: Teton New Media; 2002:973-981.

    38. Holm BR, Rest JR, Seewald W. A prospective study of the clinical findings, treatment and histopathology of 44 cases of pyotraumatic dermatitis. Vet Dermatol 2004;15:369-376.

    39. Medleau L, Hnilica KA. Bacterial skin diseases. In: Small Animal Dermatology: A Color Atlas and Therapeutic Guide. 2nd ed. St. Louis, MO: Saunders; 2006:25-61.

    40. Cobb MA, Edwards HJ, Jagger TD, et al. Topical fusidic acid/betamethasone-containing gel compared to systemic therapy in the treatment of canine acute moist dermatitis. Vet J 2006;169:276-280.

    41. Schroeder H, Swan GE, Berry WL, et al. Efficacy of a topical antimicrobial-anti-inflammatory combination in the treatment of pyotraumatic dermatitis in dogs. Vet Dermatol 1996;7:163-170.

    References »

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