Case Report Rapport de cas Dorsal skin necrosis secondary to a solar-induced thermal burn in a brown-coated dachshund Julia P. Sumner, Cherie M. Pucheu-Haston, Natalie Fowlkes, Sandra Merchant Abstract — A 5-year-old neutered male brown dachshund dog was presented for a large dorsal cutaneous burn that occurred following direct sunlight exposure outdoors in high ambient temperatures. Although burns are quite common in dogs, full-thickness solar-induced radiation burns are less common and have not been previously reported in animals without a black hair coat. Résumé — Nécrose de la peau dorsale secondaire à une brûlure thermique induite par l’exposition au soleil chez un Dachsund à pelage brun. Un chien Dachsund brun stérilisé âgé de 5 ans a été présenté pour une grande brûlure cutanée dorsale qui s’était produite après une exposition directe au soleil à l’extérieur durant des températures élevées. Même si les brûlures sont assez courantes chez les chiens, les brûlures du troisième degré causées par l’exposition au soleil sont moins communes et n’ont pas déjà été signalées chez des animaux sans un pelage à poil noir. (Traduit par Isabelle Vallières) Can Vet J 2016;57:305–308
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olar radiation can cause skin damage in 2 distinctly different ways, either via the direct effect of radiation or due to thermal injury (1,2). Direct exposure to ultraviolet light most often causes lesions in areas that are non-pigmented or sparsely haired such as the muzzle, axillae, and ventral abdomen (1,2). Skin with higher levels of pheomelanin (yellow-red pigment) versus eumelanin (brown-black pigment) has been shown in humans to be more susceptible to DNA damage when exposed to ultraviolet radiation (3). Not only does solar radiation cause burns in these areas, but it can also predispose to the development of actinic lesions such as solar dermatitis, hemangioma, cutaneous hemangiosarcoma, actinic keratosis, and squamous cell carcinoma (2). Solar radiation is also known to cause thermal injury via thermal necrosis (1,4–6). Black skin absorbs approximately 50% more solar heat energy than unpigmented skin (1). The most accepted hypothesis is that the Department of Veterinary Clinical Sciences (Sumner, PucheuHaston, Merchant), Department of Pathobiological Sciences (Fowlkes), Louisiana State University School of Veterinary Medicine, 1909 Skip Bertman Drive, Baton Rouge, Louisiana, USA. Address all correspondence to Dr. Julia Sumner; e-mail: [email protected] Dr. Sumner’s current address is Cornell University College of Veterinary Medicine, Department of Clinical Sciences, 930 Campus Drive, Ithaca, New York 14853, USA. Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office ([email protected]) for additional copies or permission to use this material elsewhere. CVJ / VOL 57 / MARCH 2016
darkly pigmented skin of these animals acts as a “heat sink” that concentrates solar radiation energy when the animal is exposed to high ambient temperatures (4). This leads to a “dorsal thermal necrosis” that has been reported in the black spots of Dalmatians and more recently in a Vietnamese pot-bellied pig (5,6). Reports of thermal burns secondary to solar radiation are limited and confined to black-coated animals (5,6). We report a case of a full-thickness thermal burn secondary to solar-induced thermal injury occurring in a brown-coated dachshund.
Case description A 5-year-old neutered male dachshund dog was referred for treatment of a large area of dorsal skin sloughing and necrosis. The dog had been acquired from a local animal shelter approximately 14 mo before this incident. The owners administered Comfortis® (Spinosad; Elanco Animal Health, Indianapolis, Indiana, USA) and Heartgard® (Ivermectin/pyrantel; Merial, Duluth, Georgia, USA) monthly for parasite control. No other medications, supplements, or topical treatments were administered prior to presentation. The dog was vaccinated 14 mo earlier. He was fed a commercial pet food diet and had no other history of skin problems. Approximately 2 wk before presentation, the owners had left the dog outside for about 45 min while moving furniture in 30°C temperatures. He was tethered without access to shade in southwestern Louisiana. The owners noticed that he became laterally recumbent and was panting heavily, at which point they brought him inside, placed him by a fan, and started to cool him with towels soaked in cool water. The dog was inappetent for several days, and was described as hyperesthetic to touch along the dorsum. The dog appeared to recover over the next week and appeared to be doing well. Four days after the 305
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a
b Figure 1. a — Large firm coalescing nodules along the dorsum of a 5-year-old, neutered male dachshund dog 4 days after solar exposure in high ambient temperatures. b — The same dog, 11 days after solar exposure. The firm nodules previously noted along the dorsum proceeded to open and drain.
exposure, large firm coalescing nodules formed along the dog’s back (Figure 1a) and proceeded to open and drain 11 d after solar exposure (Figure 1b). The dog was seen by a veterinarian who placed him on enrofloxacin (Baytril; Bayer, Shawnee Mission, Kansas, USA), 9 mg/kg body weight (BW), PO, q24h, amoxicillin/clavulanic acid (Clavamox; Zoetis, Kalamazoo, Michigan, USA), 25 mg/kg BW, PO, q12h, and tramadol (Tramadol HCI; Amneal Pharmaceuticals LLC, Bridgewater, New Jersey, USA), 5 mg/kg BW, PO, q8h. During this period, the dog continued to have a good appetite and remained bright and responsive, but due to progression of his skin lesions, he was referred to our hospital. On presentation, the dog was bright and alert but was in severe pain upon palpation of the dorsum. He was approximately 5% dehydrated with a mildly elevated temperature of 39.8°C. A complete blood (cell) count (CBC) showed evidence of a mild lymphopenia and monocytosis with a slight left shift [WBC 12.7 3 109/L; reference range (RR): 8.0 to 14.5 3 109/L; neutrophils 8.2 3 109/L; RR: 3.0 to 11.0 3 109/L; bands 0.5 3 109/L; RR: 0 to 0.3 3 109/L; lymphocytes 0.8 3 109/L; RR: 1 to 4.8 3 109/L; and monocytes 3.2 3 109/L; RR: 0.1 to 1.4 3 109/L]. Serum chemistry showed a mild elevation in alanine aminotransferase (ALT 124 U/L; RR: 14 to 63 U/L) and a moderate elevation in aspartate aminotransferase (AST 141 U/L; RR: 2 to 38 U/L). His total protein was just above the reference range at 71 g/L (RR: 54 to 70 g/L). 306
Figure 2. On presentation to our hospital, the cutaneous abnormalities along the dorsum had progressed to a fullthickness necrosis over the entire dorsum.
The dog’s cutaneous abnormalities are shown in Figure 2. There was full-thickness skin necrosis over the entire dorsum extending from the shoulders caudally to the root of the tail to a width of about 10 cm. There was purulent material draining from beneath the eschar. Surrounding the eschar, granulation tissue and areas of re-epithelialization were noted. There was an approximately 2.5 cm 3 10 cm area of partially or completely devitalized skin on the dorsolateral right neck. The remainder of his skin, including pinnae, pads, claws, and his mucous membranes were unremarkable. The dog was placed on intravenous fluids and a fentanyl constant rate infusion (Fentanyl Citrate Injection, USP; Hospira, Lake Forest, Illinois, USA). He was then anesthetized for surgical debridement of the eschar. Areas of normal and necrotic skin were biopsied for histopathology, and the eschar was removed using sharp dissection to expose normal healthy bleeding tissue. The area was then flushed thoroughly with sterile warm saline. Following debridement, the wound was covered with a wet to dry tie-over dressing. The dog appeared much more comfortable following debridement. Dressings were changed daily following hydrotherapy and debridement of further necrotic tissue. The dog was maintained on a fentanyl patch (Duragesic; Janssen Pharmaceuticals, Titusville, New Jersey, USA), 5 mg/h transdermal for 4 d, meloxicam (Metacam; Boehringer Ingelheim, Bracknell, Berkshire, UK), 0.1 mg/kg BW, PO, q24h for 5 d, gabapentin (Neurontin; Parke-Davis, New York, New York, USA), 15 mg/kg BW, PO, q8h for 3 wk, and tramadol 4 mg/kg BW, PO, 2 to 3 times daily as needed for pain relief. The previously prescribed enrofloxacin and amoxicillin/clavulanic acid were continued for 2 wk. Surgical wound closure with the use of flaps was offered but was declined due to financial constraints. On histopathology, the skin biopsies showed diffuse necrosis and hemorrhage of the epidermis and dermis extending to the subcutis with multifocal areas of infiltration of the subcutis by low to moderate numbers of neutrophils. There was a serocellular crust, dermal fibrosis, and multifocal areas of infiltration of the panniculus by neutrophils (Figures 3a and 3b). These changes were consistent with full-thickness necrosis due to a severe burn. The dog was discharged for continuing care including daily hydrotherapy and application of bandages. Twelve weeks after presentation, the dog was doing well with almost complete resolution of the wound (Figure 4). CVJ / VOL 57 / MARCH 2016
b a
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Figure 3. Images captured with a Hamamatsu nanozoomer digital slide scanner. a — Photomicrograph of affected skin with coagulative necrosis and hemorrhage extending from the epidermis to the subcutis. There are multifocal areas of infiltration by low to moderate numbers of neutrophils in the subcutis. Hematoxylin and eosin stain (H&E) (1.25 3 objective). b — Photomicrograph of affected skin with coagulative necrosis and hemorrhage extending from the epidermis to the subcutis. H&E (2.5 3 objective).
Figure 4. Re-epithelialization and contraction of the wound with a healthy bed of granulation tissue, 12 weeks after solar-induced thermal injury.
Discussion When skin is exposed to solar radiation, energy is reflected, transmitted, or absorbed (6). Black or dark skin tends to absorb a larger amount of visible radiation which is then converted into thermal energy (6). Previous reports of solar-induced thermal necrosis have only involved black-coated animals (5,6). There are reports of solar-induced thermal burns in the human literature in women wearing black swimwear following breast reconstructive surgery (7). It is proposed that full-thickness burns occurred in these women due to the heat absorbing properties of the black clothing in conjunction with sensory deficits along the previous surgery site (7). Additionally, full-thickness burns have been described in humans with sensory abnormalities (e.g., paraplegics) who may also have defects in thermoregulation (8). A case report in the human literature describes a quadriplegic individual who sustained full-thickness burns after being exposed to intense sunlight for 2 h following a wheelchair malfunction (8). The dog herein was brown and did not have any sensory deficits that were identified. Although the lesions in this case were consistent with solar-induced thermal injury, consideration was also given as to whether any photosensitizing agents had been administered or were available to the dog. This would help explain why such a severe injury occurred in a brown-coated dog after a relatively short exposure. A careful history from the owner revealed no exposure to such agents. CVJ / VOL 57 / MARCH 2016
Similar lesions to those seen in this dog have been reported in a case series of garden hose scalding syndrome (9). These dogs (and 1 cat) sustained full-thickness dorsal thermal burns from scalding injuries after being hosed down with garden hoses that had been lying in the sun (9). The owner of our dog was questioned as to whether any such treatment had been applied, and she insisted that the dog was placed inside and cooled with a fan and wet towels. Burns tend to be classified by the depth of tissue involvement (1,4,10,11). First-degree burns involve only the epidermis, second-degree burns involve the underlying dermis, and thirddegree burns extend into the subcutaneous tissue (4,10–12). The dog in this report suffered a third-degree burn of his entire dorsum characterized on histopathology by the extension of damage into the panniculus muscle and deeper subcutis. Interestingly, the animals in the previous case reports of solar-induced thermal necrosis sustained the same level of burn severity, which may suggest some deficit in thermoregulation (5,6). The full extent of thermal burns may not be apparent until several days following exposure (1,4,5). The dog in this case had a progression from hyperesthesia immediately following the incident, to focal nodules forming along the back. This progressed to open draining wounds 12 d after exposure. This delay in skin necrosis is due to coagulation of the local vascular supply and secondary colonization with bacteria (1,4,11,12). An eschar forms and delaminates, exposing hyperdermal fat and areas of granulation tissue underneath (4,12). In this case, the eschar was surgically debrided exposing areas of epithelialization around the edges of the lesion and in small islands, which is characteristic of full-thickness burns (12). Extensive full-thickness burns can be serious and require significant intensive care (1,10–12). This can be due to electrolyte and protein imbalances and secondary bacterial infection (1,10–12). Surprisingly, several cases including this one, presented several days after the inciting injury with no need of intensive care (5,6,12). Treatment in this case focused on surgical debridement of devitalized skin, analgesia, and antimicrobial therapy in line with published recommendations (1,10–12). It 307
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is important to note, however, that the use of systemic antibiotics for treatment of full-thickness burns is controversial and may not be indicated except in cases of sepsis (12). Topical silver sulfadiazine is a well-recognized alternative to the use of systemic antimicrobials (1,12). The treatment that this dog received resulted in uncomplicated second intention healing of the wound over approximately 12 wk. CVJ
References 1. Miller WH, Griffin CE, Campbell KL. Muller and Kirk’s Small Animal Dermatology. 7th ed. St. Louis, Missouri: Elsevier, Saunders, 2013:665–684. 2. Werner A. Top 5 Sun-Induced Skin Lesions in Dogs. Clinicians Brief; 2014: June. Available from: http://www.cliniciansbrief.com/article/ top-5-sun-induced-skin-lesions-dogs Last accessed January 6, 2016. 3. Del Bino S, Bernerd F. Variations in skin colour and the biological consequences of ultraviolet radiation exposure. Br J Dermatol 2013;169 Suppl 3:33–40. 4. Gross T, Ihrke PJ, Walder EJ, Affolter VK. Skin Diseases of the Dog and Cat: Clinical and Histopathologic Diagnosis. 2nd ed. Oxford, UK: Blackwell Science, 2005:75–96.
5. Frank LA, McCormick KA, Donnell RL, Kania SA. Dorsal black skin necrosis in a Vietnamese pot-bellied pig. Vet Dermatol 2015;26:64–67, e23. 6. Hargis AM, Lewis TP. Full-thickness cutaneous burn in black-haired skin on the dorsum of the body of a Dalmatian puppy. Vet Dermatol 1999;10:39–42. 7. Alexandrides IJ, Shestak KC, Noone RB. Thermal injuries following TRAM flap breast reconstruction. Ann Plast Surg 1997;38:335–341. 8. Bull W, Priebe M, Dillig G, Dado D. Preventable wheelchair-related thermal injury. J Spinal Cord Med 2006;29:156–159. 9. Quist EM, Tanabe M, Mansell JE, Mansell JEKL, Edwards JE. A case series of thermal scald injuries in dogs exposed to hot water from garden hoses (garden hose scalding syndrome). Vet Dermatol 2012;23:162–6, e33. 10. Bohling MW. Burns. In: Tobias KM, Johnson SA, eds. Veterinary Surgery Small Animal. 1st ed. vol 2. St. Louis, Missouri: Elsevier Saunders, 2012: 1291–1302. 11. Frantz K, Byers CG. Thermal injury. Comp Contin Educ Vet 2011;33: E1–E6. 12. Pavletic MM, Trout NJ. Bullet, bite, and burn wounds in dogs and cats. Vet Clin North Am Small Anim Pract 2006;36:873–93.
Book Review Compte rendu de livre Handbook of Canine and Feline Emergency Protocols, 2nd edition McMichael M, ed. Wiley-Blackwell. Ames, Iowa, USA. 2014. 291 pp. ISBN: 9781-1185-5903-1. $69.99 USD.
T
his text has so much potential but I am left a bit confused. On the one hand, it might be useful for small animal practitioners needing quick and accurate guidance during an emergency, or it might be for actual emergency practitioners. The Introduction starts out by declaring the purpose of the Handbook as a “source of complete protocols for the most common dog and cat emergencies encountered by practicing emergency veterinarians.” And yet, either there is far too little detail for an experienced emergency veterinarian to dig into, or I get the sense that a veterinarian not seasoned in stressful emergency situations is going to be begging for more detail and guidance than this handbook offers. Certainly the protocols are accurate, as far as I, a small animal veterinarian, can tell, but they seem sparse. Everything is laid out alphabetically and is orderly and easy to follow. There is an online website included that does offer videos, additional images, formula calculations, reference guides, and review questions, but I would have preferred much of that useful informa-
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tion to be included with the written protocols. Who has time in the middle of an emergency to look up a web page? There are no appendices offering lab numbers or drug lists. Admittedly, this book is offered as a “starter protocol [source] that will be expanded, altered and personalized depending on preferences, case load and availability of the practice.” Guidelines are designed to “streamline” essentials as much as possible and “minimum database” labs are identified. Useful photographs are included for such procedures as spinal taps and abdominocentesis along with relevant radiographs such as for various pulmonary changes, pyometra, or uroliths. This is a superb handbook to grab during the initial minutes of an emergency. Protocols quickly outline what needs to be done fast. I would suggest though that the handbook be combined with other resources to add greater depth to your understanding of what processes are occurring during the emergency and how to manage the case after the initial phase. There may well be other resources available that do both aspects really well, but this text will at least get you safely to first base in a confident manner.
Reviewed by Janeen Junaid, MVSc, DVM, Certificate in Shelter Medicine, Small Animal Veterinarian, Hamilton, Ontario. CVJ / VOL 57 / MARCH 2016
S
olar radiation can cause skin damage in 2 distinctly different ways, either via the direct effect of radiation or due to thermal injury (1,2). Direct exposure to ultraviolet light most often causes lesions in areas that are non-pigmented or sparsely haired such as the muzzle, axillae, and ventral abdomen (1,2). Skin with higher levels of pheomelanin (yellow-red pigment) versus eumelanin (brown-black pigment) has been shown in humans to be more susceptible to DNA damage when exposed to ultraviolet radiation (3). Not only does solar radiation cause burns in these areas, but it can also predispose to the development of actinic lesions such as solar dermatitis, hemangioma, cutaneous hemangiosarcoma, actinic keratosis, and squamous cell carcinoma (2). Solar radiation is also known to cause thermal injury via thermal necrosis (1,4–6). Black skin absorbs approximately 50% more solar heat energy than unpigmented skin (1). The most accepted hypothesis is that the Department of Veterinary Clinical Sciences (Sumner, PucheuHaston, Merchant), Department of Pathobiological Sciences (Fowlkes), Louisiana State University School of Veterinary Medicine, 1909 Skip Bertman Drive, Baton Rouge, Louisiana, USA. Address all correspondence to Dr. Julia Sumner; e-mail: [email protected] Dr. Sumner’s current address is Cornell University College of Veterinary Medicine, Department of Clinical Sciences, 930 Campus Drive, Ithaca, New York 14853, USA. Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office ([email protected]) for additional copies or permission to use this material elsewhere. CVJ / VOL 57 / MARCH 2016
darkly pigmented skin of these animals acts as a “heat sink” that concentrates solar radiation energy when the animal is exposed to high ambient temperatures (4). This leads to a “dorsal thermal necrosis” that has been reported in the black spots of Dalmatians and more recently in a Vietnamese pot-bellied pig (5,6). Reports of thermal burns secondary to solar radiation are limited and confined to black-coated animals (5,6). We report a case of a full-thickness thermal burn secondary to solar-induced thermal injury occurring in a brown-coated dachshund.
Case description A 5-year-old neutered male dachshund dog was referred for treatment of a large area of dorsal skin sloughing and necrosis. The dog had been acquired from a local animal shelter approximately 14 mo before this incident. The owners administered Comfortis® (Spinosad; Elanco Animal Health, Indianapolis, Indiana, USA) and Heartgard® (Ivermectin/pyrantel; Merial, Duluth, Georgia, USA) monthly for parasite control. No other medications, supplements, or topical treatments were administered prior to presentation. The dog was vaccinated 14 mo earlier. He was fed a commercial pet food diet and had no other history of skin problems. Approximately 2 wk before presentation, the owners had left the dog outside for about 45 min while moving furniture in 30°C temperatures. He was tethered without access to shade in southwestern Louisiana. The owners noticed that he became laterally recumbent and was panting heavily, at which point they brought him inside, placed him by a fan, and started to cool him with towels soaked in cool water. The dog was inappetent for several days, and was described as hyperesthetic to touch along the dorsum. The dog appeared to recover over the next week and appeared to be doing well. Four days after the 305
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a
b Figure 1. a — Large firm coalescing nodules along the dorsum of a 5-year-old, neutered male dachshund dog 4 days after solar exposure in high ambient temperatures. b — The same dog, 11 days after solar exposure. The firm nodules previously noted along the dorsum proceeded to open and drain.
exposure, large firm coalescing nodules formed along the dog’s back (Figure 1a) and proceeded to open and drain 11 d after solar exposure (Figure 1b). The dog was seen by a veterinarian who placed him on enrofloxacin (Baytril; Bayer, Shawnee Mission, Kansas, USA), 9 mg/kg body weight (BW), PO, q24h, amoxicillin/clavulanic acid (Clavamox; Zoetis, Kalamazoo, Michigan, USA), 25 mg/kg BW, PO, q12h, and tramadol (Tramadol HCI; Amneal Pharmaceuticals LLC, Bridgewater, New Jersey, USA), 5 mg/kg BW, PO, q8h. During this period, the dog continued to have a good appetite and remained bright and responsive, but due to progression of his skin lesions, he was referred to our hospital. On presentation, the dog was bright and alert but was in severe pain upon palpation of the dorsum. He was approximately 5% dehydrated with a mildly elevated temperature of 39.8°C. A complete blood (cell) count (CBC) showed evidence of a mild lymphopenia and monocytosis with a slight left shift [WBC 12.7 3 109/L; reference range (RR): 8.0 to 14.5 3 109/L; neutrophils 8.2 3 109/L; RR: 3.0 to 11.0 3 109/L; bands 0.5 3 109/L; RR: 0 to 0.3 3 109/L; lymphocytes 0.8 3 109/L; RR: 1 to 4.8 3 109/L; and monocytes 3.2 3 109/L; RR: 0.1 to 1.4 3 109/L]. Serum chemistry showed a mild elevation in alanine aminotransferase (ALT 124 U/L; RR: 14 to 63 U/L) and a moderate elevation in aspartate aminotransferase (AST 141 U/L; RR: 2 to 38 U/L). His total protein was just above the reference range at 71 g/L (RR: 54 to 70 g/L). 306
Figure 2. On presentation to our hospital, the cutaneous abnormalities along the dorsum had progressed to a fullthickness necrosis over the entire dorsum.
The dog’s cutaneous abnormalities are shown in Figure 2. There was full-thickness skin necrosis over the entire dorsum extending from the shoulders caudally to the root of the tail to a width of about 10 cm. There was purulent material draining from beneath the eschar. Surrounding the eschar, granulation tissue and areas of re-epithelialization were noted. There was an approximately 2.5 cm 3 10 cm area of partially or completely devitalized skin on the dorsolateral right neck. The remainder of his skin, including pinnae, pads, claws, and his mucous membranes were unremarkable. The dog was placed on intravenous fluids and a fentanyl constant rate infusion (Fentanyl Citrate Injection, USP; Hospira, Lake Forest, Illinois, USA). He was then anesthetized for surgical debridement of the eschar. Areas of normal and necrotic skin were biopsied for histopathology, and the eschar was removed using sharp dissection to expose normal healthy bleeding tissue. The area was then flushed thoroughly with sterile warm saline. Following debridement, the wound was covered with a wet to dry tie-over dressing. The dog appeared much more comfortable following debridement. Dressings were changed daily following hydrotherapy and debridement of further necrotic tissue. The dog was maintained on a fentanyl patch (Duragesic; Janssen Pharmaceuticals, Titusville, New Jersey, USA), 5 mg/h transdermal for 4 d, meloxicam (Metacam; Boehringer Ingelheim, Bracknell, Berkshire, UK), 0.1 mg/kg BW, PO, q24h for 5 d, gabapentin (Neurontin; Parke-Davis, New York, New York, USA), 15 mg/kg BW, PO, q8h for 3 wk, and tramadol 4 mg/kg BW, PO, 2 to 3 times daily as needed for pain relief. The previously prescribed enrofloxacin and amoxicillin/clavulanic acid were continued for 2 wk. Surgical wound closure with the use of flaps was offered but was declined due to financial constraints. On histopathology, the skin biopsies showed diffuse necrosis and hemorrhage of the epidermis and dermis extending to the subcutis with multifocal areas of infiltration of the subcutis by low to moderate numbers of neutrophils. There was a serocellular crust, dermal fibrosis, and multifocal areas of infiltration of the panniculus by neutrophils (Figures 3a and 3b). These changes were consistent with full-thickness necrosis due to a severe burn. The dog was discharged for continuing care including daily hydrotherapy and application of bandages. Twelve weeks after presentation, the dog was doing well with almost complete resolution of the wound (Figure 4). CVJ / VOL 57 / MARCH 2016
b a
CA S E R E P O R T
Figure 3. Images captured with a Hamamatsu nanozoomer digital slide scanner. a — Photomicrograph of affected skin with coagulative necrosis and hemorrhage extending from the epidermis to the subcutis. There are multifocal areas of infiltration by low to moderate numbers of neutrophils in the subcutis. Hematoxylin and eosin stain (H&E) (1.25 3 objective). b — Photomicrograph of affected skin with coagulative necrosis and hemorrhage extending from the epidermis to the subcutis. H&E (2.5 3 objective).
Figure 4. Re-epithelialization and contraction of the wound with a healthy bed of granulation tissue, 12 weeks after solar-induced thermal injury.
Discussion When skin is exposed to solar radiation, energy is reflected, transmitted, or absorbed (6). Black or dark skin tends to absorb a larger amount of visible radiation which is then converted into thermal energy (6). Previous reports of solar-induced thermal necrosis have only involved black-coated animals (5,6). There are reports of solar-induced thermal burns in the human literature in women wearing black swimwear following breast reconstructive surgery (7). It is proposed that full-thickness burns occurred in these women due to the heat absorbing properties of the black clothing in conjunction with sensory deficits along the previous surgery site (7). Additionally, full-thickness burns have been described in humans with sensory abnormalities (e.g., paraplegics) who may also have defects in thermoregulation (8). A case report in the human literature describes a quadriplegic individual who sustained full-thickness burns after being exposed to intense sunlight for 2 h following a wheelchair malfunction (8). The dog herein was brown and did not have any sensory deficits that were identified. Although the lesions in this case were consistent with solar-induced thermal injury, consideration was also given as to whether any photosensitizing agents had been administered or were available to the dog. This would help explain why such a severe injury occurred in a brown-coated dog after a relatively short exposure. A careful history from the owner revealed no exposure to such agents. CVJ / VOL 57 / MARCH 2016
Similar lesions to those seen in this dog have been reported in a case series of garden hose scalding syndrome (9). These dogs (and 1 cat) sustained full-thickness dorsal thermal burns from scalding injuries after being hosed down with garden hoses that had been lying in the sun (9). The owner of our dog was questioned as to whether any such treatment had been applied, and she insisted that the dog was placed inside and cooled with a fan and wet towels. Burns tend to be classified by the depth of tissue involvement (1,4,10,11). First-degree burns involve only the epidermis, second-degree burns involve the underlying dermis, and thirddegree burns extend into the subcutaneous tissue (4,10–12). The dog in this report suffered a third-degree burn of his entire dorsum characterized on histopathology by the extension of damage into the panniculus muscle and deeper subcutis. Interestingly, the animals in the previous case reports of solar-induced thermal necrosis sustained the same level of burn severity, which may suggest some deficit in thermoregulation (5,6). The full extent of thermal burns may not be apparent until several days following exposure (1,4,5). The dog in this case had a progression from hyperesthesia immediately following the incident, to focal nodules forming along the back. This progressed to open draining wounds 12 d after exposure. This delay in skin necrosis is due to coagulation of the local vascular supply and secondary colonization with bacteria (1,4,11,12). An eschar forms and delaminates, exposing hyperdermal fat and areas of granulation tissue underneath (4,12). In this case, the eschar was surgically debrided exposing areas of epithelialization around the edges of the lesion and in small islands, which is characteristic of full-thickness burns (12). Extensive full-thickness burns can be serious and require significant intensive care (1,10–12). This can be due to electrolyte and protein imbalances and secondary bacterial infection (1,10–12). Surprisingly, several cases including this one, presented several days after the inciting injury with no need of intensive care (5,6,12). Treatment in this case focused on surgical debridement of devitalized skin, analgesia, and antimicrobial therapy in line with published recommendations (1,10–12). It 307
R A P P O R T D E CA S
is important to note, however, that the use of systemic antibiotics for treatment of full-thickness burns is controversial and may not be indicated except in cases of sepsis (12). Topical silver sulfadiazine is a well-recognized alternative to the use of systemic antimicrobials (1,12). The treatment that this dog received resulted in uncomplicated second intention healing of the wound over approximately 12 wk. CVJ
References 1. Miller WH, Griffin CE, Campbell KL. Muller and Kirk’s Small Animal Dermatology. 7th ed. St. Louis, Missouri: Elsevier, Saunders, 2013:665–684. 2. Werner A. Top 5 Sun-Induced Skin Lesions in Dogs. Clinicians Brief; 2014: June. Available from: http://www.cliniciansbrief.com/article/ top-5-sun-induced-skin-lesions-dogs Last accessed January 6, 2016. 3. Del Bino S, Bernerd F. Variations in skin colour and the biological consequences of ultraviolet radiation exposure. Br J Dermatol 2013;169 Suppl 3:33–40. 4. Gross T, Ihrke PJ, Walder EJ, Affolter VK. Skin Diseases of the Dog and Cat: Clinical and Histopathologic Diagnosis. 2nd ed. Oxford, UK: Blackwell Science, 2005:75–96.
5. Frank LA, McCormick KA, Donnell RL, Kania SA. Dorsal black skin necrosis in a Vietnamese pot-bellied pig. Vet Dermatol 2015;26:64–67, e23. 6. Hargis AM, Lewis TP. Full-thickness cutaneous burn in black-haired skin on the dorsum of the body of a Dalmatian puppy. Vet Dermatol 1999;10:39–42. 7. Alexandrides IJ, Shestak KC, Noone RB. Thermal injuries following TRAM flap breast reconstruction. Ann Plast Surg 1997;38:335–341. 8. Bull W, Priebe M, Dillig G, Dado D. Preventable wheelchair-related thermal injury. J Spinal Cord Med 2006;29:156–159. 9. Quist EM, Tanabe M, Mansell JE, Mansell JEKL, Edwards JE. A case series of thermal scald injuries in dogs exposed to hot water from garden hoses (garden hose scalding syndrome). Vet Dermatol 2012;23:162–6, e33. 10. Bohling MW. Burns. In: Tobias KM, Johnson SA, eds. Veterinary Surgery Small Animal. 1st ed. vol 2. St. Louis, Missouri: Elsevier Saunders, 2012: 1291–1302. 11. Frantz K, Byers CG. Thermal injury. Comp Contin Educ Vet 2011;33: E1–E6. 12. Pavletic MM, Trout NJ. Bullet, bite, and burn wounds in dogs and cats. Vet Clin North Am Small Anim Pract 2006;36:873–93.
Book Review Compte rendu de livre Handbook of Canine and Feline Emergency Protocols, 2nd edition McMichael M, ed. Wiley-Blackwell. Ames, Iowa, USA. 2014. 291 pp. ISBN: 9781-1185-5903-1. $69.99 USD.
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his text has so much potential but I am left a bit confused. On the one hand, it might be useful for small animal practitioners needing quick and accurate guidance during an emergency, or it might be for actual emergency practitioners. The Introduction starts out by declaring the purpose of the Handbook as a “source of complete protocols for the most common dog and cat emergencies encountered by practicing emergency veterinarians.” And yet, either there is far too little detail for an experienced emergency veterinarian to dig into, or I get the sense that a veterinarian not seasoned in stressful emergency situations is going to be begging for more detail and guidance than this handbook offers. Certainly the protocols are accurate, as far as I, a small animal veterinarian, can tell, but they seem sparse. Everything is laid out alphabetically and is orderly and easy to follow. There is an online website included that does offer videos, additional images, formula calculations, reference guides, and review questions, but I would have preferred much of that useful informa-
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tion to be included with the written protocols. Who has time in the middle of an emergency to look up a web page? There are no appendices offering lab numbers or drug lists. Admittedly, this book is offered as a “starter protocol [source] that will be expanded, altered and personalized depending on preferences, case load and availability of the practice.” Guidelines are designed to “streamline” essentials as much as possible and “minimum database” labs are identified. Useful photographs are included for such procedures as spinal taps and abdominocentesis along with relevant radiographs such as for various pulmonary changes, pyometra, or uroliths. This is a superb handbook to grab during the initial minutes of an emergency. Protocols quickly outline what needs to be done fast. I would suggest though that the handbook be combined with other resources to add greater depth to your understanding of what processes are occurring during the emergency and how to manage the case after the initial phase. There may well be other resources available that do both aspects really well, but this text will at least get you safely to first base in a confident manner.
Reviewed by Janeen Junaid, MVSc, DVM, Certificate in Shelter Medicine, Small Animal Veterinarian, Hamilton, Ontario. CVJ / VOL 57 / MARCH 2016
