June 2018   |   Volume 16   |   Issue 6

Nasal Planum Disease in Dogs

in this issue

in this issue

Top 5 Lip Depigmentation Causes in Dogs

Cutaneous & Renal Glomerular Vasculopathy in a Springer Spaniel

Quiz: White Blood Cell Evaluation in Blood Films

Acute Respiratory Distress in a Brachycephalic Dog

Which Drugs Can Be Used Concurrently with Trazodone During & After Tibial Plateau-Leveling Osteotomy?

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Nasal Planum Disease in Dogs

Darren Berger, DVM, DACVD, Iowa State University

Dermatology

|Peer Reviewed

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Nasal Planum Disease in Dogs

Many pet owners believe a dog’s nose is an indicator of health status and will thus seek veterinary care for any change in coloration or texture or if lesions develop. Following is a discussion of the more common and breed-specific conditions that present with lesions primarily affecting the nasal planum.

Noninflammatory Depigmenting Conditions

Idiopathic Nasal Depigmentation

Idiopathic nasal depigmentation occurs when a nasal planum that was pigmented at birth later loses its color. The condition may wax and wane, but only the nose is affected, with no changes in the nasal planum architecture (ie, the cobblestone-like appearance is preserved [Figure 1]). Other noninflammatory depigmenting conditions include snow nose and Dudley nose. Snow nose is a seasonal decrease in nasal pigmentation commonly observed in Arctic breeds and retrievers.1 Dogs with Dudley nose have no nasal pigmentation and are generally affected from birth. Both are cosmetic defects and do not warrant further investigation or therapy.

Idiopathic nasal depigmentation in a 6-year-old neutered male Labrador retriever. Depigmentation is confined to the nasal planum. The cobblestone-like architecture is preserved.
Idiopathic nasal depigmentation in a 6-year-old neutered male Labrador retriever. Depigmentation is confined to the nasal planum. The cobblestone-like architecture is preserved.

FIGURE 1 Idiopathic nasal depigmentation in a 6-year-old neutered male Labrador retriever. Depigmentation is confined to the nasal planum. The cobblestone-like architecture is preserved.

FIGURE 1 Idiopathic nasal depigmentation in a 6-year-old neutered male Labrador retriever. Depigmentation is confined to the nasal planum. The cobblestone-like architecture is preserved.

Vitiligo

Vitiligo is a rare acquired disease associated with melanocyte destruction that results in hair and skin depigmentation over several months. The exact pathogenesis is unknown but is thought to be multifactorial, with a hereditary predisposition observed in Belgian Tervuren dogs, rottweilers, and old English sheepdogs.1 Vitiligo is characterized by symmetric macular or patchy leukoderma and leukotrichia that commonly affect multiple areas simultaneously, including the nasal planum (Figure 2). Vitiligo is considered a cosmetic disease in dogs with no consistently successful intervention reported, although spontaneous resolution has been observed.1

Patchy nasal depigmentation caused by vitiligo in a 7-year-old neutered male crossbreed dog
Patchy nasal depigmentation caused by vitiligo in a 7-year-old neutered male crossbreed dog

FIGURE 2 Patchy nasal depigmentation caused by vitiligo in a 7-year-old neutered male crossbreed dog

FIGURE 2 Patchy nasal depigmentation caused by vitiligo in a 7-year-old neutered male crossbreed dog

Hyperkeratotic Conditions

Nasal parakeratosis of Labrador retrievers is a familial dermatosis characterized by the accumulation of adherent keratin debris along the dorsal nasal planum with secondary crusting, fissures, erosions, and depigmentation (Figure 3). It typically becomes apparent at an early age (ie, 6-12 months). Lesions may wax and wane but are limited to the nasal planum. Although this is an incurable, lifelong condition, prognosis is good, and early management with frequent application of softening agents (eg, petroleum jelly, propylene glycol) may help prevent severe fissuring.

Significant thick adherent crusting and early fissure formation due to hereditary nasal parakeratosis in a 5-year-old neutered male chocolate Labrador retriever. Image courtesy of A. Kirby, Animal Dermatology Clinic
Significant thick adherent crusting and early fissure formation due to hereditary nasal parakeratosis in a 5-year-old neutered male chocolate Labrador retriever. Image courtesy of A. Kirby, Animal Dermatology Clinic

FIGURE 3 Significant thick adherent crusting and early fissure formation due to hereditary nasal parakeratosis in a 5-year-old neutered male chocolate Labrador retriever. Image courtesy of A. Kirby, Animal Dermatology Clinic

FIGURE 3 Significant thick adherent crusting and early fissure formation due to hereditary nasal parakeratosis in a 5-year-old neutered male chocolate Labrador retriever. Image courtesy of A. Kirby, Animal Dermatology Clinic

Nasodigital hyperkeratosis can affect the nose and/or foot pads and is commonly encountered as a congenital hereditary disorder or age-related change. The condition is characterized by an accumulation of thickened, hard, dry keratin along the dorsal nasal planum and edges of the foot pads (Figure 4). This condition may be observed in any breed but is more commonly encountered in cocker spaniels, boxers, and bulldogs. This abnormal accumulation of keratin may lead to pain and discomfort if secondary erosions, ulceration, or fissures develop. Prognosis is good, and treatment should be focused on softening and removing excess keratin. A recent investigation showed daily use of a natural skin-restorative balm to be helpful in managing this condition.2

Idiopathic nasal hyperkeratosis in a 10-year-old spayed American cocker spaniel. Excessive keratin can be seen forming frond- or finger-like projections without signs of inflammation.
Idiopathic nasal hyperkeratosis in a 10-year-old spayed American cocker spaniel. Excessive keratin can be seen forming frond- or finger-like projections without signs of inflammation.

FIGURE 4 Idiopathic nasal hyperkeratosis in a 10-year-old spayed American cocker spaniel. Excessive keratin can be seen forming frond- or finger-like projections without signs of inflammation.

FIGURE 4 Idiopathic nasal hyperkeratosis in a 10-year-old spayed American cocker spaniel. Excessive keratin can be seen forming frond- or finger-like projections without signs of inflammation.

Infectious Diseases

Mucocutaneous Pyoderma

Mucocutaneous pyoderma is a bacterial infection that affects the mucocutaneous junctions and nasal planum. Similar to superficial bacterial folliculitis, the infection is normally secondary to an underlying condition (eg, allergic hypersensitivity, endocrinopathy). Lesions may be symmetric and characterized by erythema, crusting, erosions, depigmentation, and discomfort (Figure 5) and are most commonly found along the lip margins (especially the commissures) and nasal planum. Treatment consists of systemic administration of a first-tier antimicrobial (ie, cephalexin, clindamycin, amoxicillin–clavulanic acid) for a minimum of 3 weeks.3 Prognosis is good if the underlying condition can be identified and managed.

Symmetric nasal depigmentation and crusting in a 7-year-old spayed Maltese with mucocutaneous pyoderma
Symmetric nasal depigmentation and crusting in a 7-year-old spayed Maltese with mucocutaneous pyoderma

FIGURE 5 Symmetric nasal depigmentation and crusting in a 7-year-old spayed Maltese with mucocutaneous pyoderma

FIGURE 5 Symmetric nasal depigmentation and crusting in a 7-year-old spayed Maltese with mucocutaneous pyoderma

Dermatophytosis

Dermatophytosis (ie, ringworm) may mimic an autoimmune condition such as pemphigus foliaceus, with the nasal planum and/or face solely affected; however, this presentation is uncommon and is typically seen with infections caused by Trichophyton mentagrophytes, which is acquired from direct or indirect contact with rodents. Dermatophytosis is typically characterized by crusting and depigmentation of the nasal planum, along with folliculitis and furunculosis of facial skin when affected (Figure 6). Treatment should include systemic administration of a triazole derivative or terbinafine. Prognosis is good if the point source can be eliminated to prevent recurrence.

Nasal depigmentation and mild crusting secondary to dermatophytosis as a result of an infection with Trichophyton mentagrophytes in a 3-year-old neutered male Saint Bernard. Image courtesy of J.O. Noxon, Iowa State University
Nasal depigmentation and mild crusting secondary to dermatophytosis as a result of an infection with Trichophyton mentagrophytes in a 3-year-old neutered male Saint Bernard. Image courtesy of J.O. Noxon, Iowa State University

FIGURE 6 Nasal depigmentation and mild crusting secondary to dermatophytosis as a result of an infection with Trichophyton mentagrophytes in a 3-year-old neutered male Saint Bernard. Image courtesy of J.O. Noxon, Iowa State University

FIGURE 6 Nasal depigmentation and mild crusting secondary to dermatophytosis as a result of an infection with Trichophyton mentagrophytes in a 3-year-old neutered male Saint Bernard. Image courtesy of J.O. Noxon, Iowa State University

Deep Mycotic Infections

Deep mycotic infections (eg, blastomycosis, histoplasmosis) may also present with lesions initially confined to the nasal planum. Depigmentation, swelling, ulceration, and destruction or deformation of the nasal planum are typically present (Figure 7). These conditions have a geographic distribution within the United States, where the infective spores are acquired from the environment via inhalation or inoculation. Prognosis varies from poor to guarded, as many cases have systemic involvement at the time of diagnosis and require extended antifungal treatment regimens with a high occurrence of disease relapse.

Depigmentation, swelling, and ulceration of the right alar fold and nasal planum secondary to an infection with Blastomyces dermatitidis in a 2-year-old neutered male Labrador retriever
Depigmentation, swelling, and ulceration of the right alar fold and nasal planum secondary to an infection with Blastomyces dermatitidis in a 2-year-old neutered male Labrador retriever

FIGURE 7 Depigmentation, swelling, and ulceration of the right alar fold and nasal planum secondary to an infection with Blastomyces dermatitidis in a 2-year-old neutered male Labrador retriever

FIGURE 7 Depigmentation, swelling, and ulceration of the right alar fold and nasal planum secondary to an infection with Blastomyces dermatitidis in a 2-year-old neutered male Labrador retriever

Autoimmune Conditions

Pemphigus Foliaceus

Pemphigus foliaceus in dogs occurs as a result of autoantibodies produced against a keratinocyte adhesion molecule that causes cells to detach from one another in the outer layers of the epidermis.4 The disease typically occurs in middle-aged animals, with breed predispositions observed in Akitas, chow chows, Doberman pinchers, dachshunds, and cocker spaniels. The cause of pemphigus foliaceus is idiopathic in most cases, but cases that occur secondary to drug reactions (eg, antimicrobials, topical preventives) or vaccination or as sequelae to a systemic inflammatory condition have been reported.

Lesions consist of pustules, crusts, erosions, and depigmentation and are commonly found along the nasal planum, on the inner aspect of the ears, and on the foot pads (Figure 8).5 Treatment typically involves systemic immunosuppressive medications tapered to the lowest dose required to control disease. Care should be taken not to taper medications too soon or too quickly, as this can lead to clinical relapses and subsequently overall greater cumulative doses. Prognosis varies from guarded to poor and is primarily dependent on the patient’s ability to tolerate the medications.

Nasal depigmentation, ulceration, and crusting as a result of pemphigus foliaceus in an 8-year-old spayed Labrador retriever
Nasal depigmentation, ulceration, and crusting as a result of pemphigus foliaceus in an 8-year-old spayed Labrador retriever

FIGURE 8 Nasal depigmentation, ulceration, and crusting as a result of pemphigus foliaceus in an 8-year-old spayed Labrador retriever

FIGURE 8 Nasal depigmentation, ulceration, and crusting as a result of pemphigus foliaceus in an 8-year-old spayed Labrador retriever

Discoid Lupus Erythematosus

Discoid lupus erythematosus is a relatively benign condition. Although the exact pathogenesis of the disease is not known, it is known to be photoaggravated. The nasal planum is the primary location affected, but lesions may also be noted at the periocular, foot pad, perianal, and ear regions. Lesions consist of erythema, depigmentation, loss of the normal nasal planum architecture, erosions, ulceration, and crusting beginning along the dorsal portion of the nasal planum (Figure 9). Treatment protocols vary, with prognosis being fair to good. A key to therapeutic success is limiting or protecting the patient from excessive UV light exposure.

Erythema, depigmentation, loss of nasal architecture, and ulceration along the dorsal aspect of the nasal planum in a 4-year-old spayed Pembroke Welsh corgi with discoid lupus erythematosus
Erythema, depigmentation, loss of nasal architecture, and ulceration along the dorsal aspect of the nasal planum in a 4-year-old spayed Pembroke Welsh corgi with discoid lupus erythematosus

FIGURE 9 Erythema, depigmentation, loss of nasal architecture, and ulceration along the dorsal aspect of the nasal planum in a 4-year-old spayed Pembroke Welsh corgi with discoid lupus erythematosus

FIGURE 9 Erythema, depigmentation, loss of nasal architecture, and ulceration along the dorsal aspect of the nasal planum in a 4-year-old spayed Pembroke Welsh corgi with discoid lupus erythematosus

Uveodermatologic Syndrome

Uveodermatologic syndrome is the result of an autoimmune process directed against components of melanocytes. Although the condition may be seen in multiple breeds, it is most commonly reported in Akitas, in which a genetic basis has been proposed.6 The disease process results in granulomatous panuveitis and leukoderma, which may progress to severe crusting and ulcerations (Figure 10); of note, leukoderma may be present in multiple locations and not limited to the nasal planum. Overall, prognosis is fair, and therapy should be primarily focused on the eyes to prevent ocular complications.

Marked crusting, depigmentation, and ulceration of the nasal planum in a 4-year-old neutered male Akita with uveodermatologic syndrome
Marked crusting, depigmentation, and ulceration of the nasal planum in a 4-year-old neutered male Akita with uveodermatologic syndrome

FIGURE 10 Marked crusting, depigmentation, and ulceration of the nasal planum in a 4-year-old neutered male Akita with uveodermatologic syndrome

FIGURE 10 Marked crusting, depigmentation, and ulceration of the nasal planum in a 4-year-old neutered male Akita with uveodermatologic syndrome

Dermal Arteritis

Dermal arteritis of the nasal philtrum is a rare condition most commonly seen in Saint Bernards and characterized by a distinct linear or circular ulcer on the central portion of the nasal planum along the philtrum (Figure 11). The condition can cause recurrent bleeding episodes, which may require immediate intervention. The exact etiology and whether a genetic basis exists are unknown.7 Prognosis is fair, with topical tacrolimus providing an alternative to systemic treatment options.7 Lifelong treatment is required, and permanent scarring in the lesion area is likely.

Significant ulceration of the nasal planum along the nasal philtrum in a 6-year-old neutered male bloodhound with dermal arteritis of the nasal philtrum. Image courtesy of A. Diesel, Texas A&M University
Significant ulceration of the nasal planum along the nasal philtrum in a 6-year-old neutered male bloodhound with dermal arteritis of the nasal philtrum. Image courtesy of A. Diesel, Texas A&M University

FIGURE 11 Significant ulceration of the nasal planum along the nasal philtrum in a 6-year-old neutered male bloodhound with dermal arteritis of the nasal philtrum. Image courtesy of A. Diesel, Texas A&M University

FIGURE 11 Significant ulceration of the nasal planum along the nasal philtrum in a 6-year-old neutered male bloodhound with dermal arteritis of the nasal philtrum. Image courtesy of A. Diesel, Texas A&M University

Neoplastic/Infiltrative Conditions

Cutaneous epitheliotropic lymphoma is an uncommon malignancy seen in older dogs. Although the exact etiology is unknown, an association with atopy has been suggested.8 Nasal planum lesions are common, along with depigmentation of mucocutaneous junctions, pronounced erythema, and scaling (Figure 12). Treatment protocols typically involve lomustine +/- radiation therapy; prognosis is poor, with a median survival time of 6 months following diagnosis.9

Nasal planum crusting and depigmentation secondary to epitheliotropic lymphoma in an 8-year-old neutered male English bulldog
Nasal planum crusting and depigmentation secondary to epitheliotropic lymphoma in an 8-year-old neutered male English bulldog

FIGURE 12 Nasal planum crusting and depigmentation secondary to epitheliotropic lymphoma in an 8-year-old neutered male English bulldog

FIGURE 12 Nasal planum crusting and depigmentation secondary to epitheliotropic lymphoma in an 8-year-old neutered male English bulldog

Conclusion

Most conditions that affect the nasal planum will present with clinical similarities. Appropriate diagnosis of nasal planum disease requires understanding the conditions that can occur, understanding patient signalment, and ruling out mucocutaneous pyoderma as a primary differential. Once the noninflammatory depigmenting, hyperkeratotic, and infectious conditions have been ruled out, biopsy is typically required for definitive diagnosis. Because it is beyond the scope of this article to thoroughly cover all therapy options for the presented conditions, readers are encouraged to consult additional references (see Suggested Reading) for a more complete discussion regarding disease-specific therapeutic considerations.

References & Suggested Reading

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Diagnosing Nasal Planum Disease in Dogs

Darren Berger, DVM, DACVD, Iowa State University

Dermatology

|Peer Reviewed

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Diagnosing Nasal Planum Disease in Dogs
Clinician's Brief
Clinician's Brief
Clinician's Brief
Clinician's Brief
*Labrador retrievers may also be affected by this condition. For a discussion of differences in presentation, see our article, Nasal Planum Disease in Dogs, as well as Suggested Reading below.

UV = ultraviolet

Suggested Reading

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Cutaneous & Renal Glomerular Vasculopathy in a Springer Spaniel

Florence Vessières, DMV, MRCVS, Anderson Moores Veterinary Specialists, Hampshire, United Kingdom

David Walker, BVetMed (Hons), DACVIM (Small Animal), DECVIM-CA, MRCVS, Anderson Moores Veterinary Specialists, Hampshire, United Kingdom

Internal Medicine

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Cutaneous & Renal Glomerular Vasculopathy in a Springer Spaniel

Figure 1 Digits IV and V of the right pelvic limb with interdigital ulceration

Molly, a 2-year-old, 40-lb (18-kg) spayed springer spaniel living in the United Kingdom, was presented for a 4-day history of progressive, multifocal, ulcerative skin lesions and a 24-hour history of lethargy, anorexia, and vomiting. The skin lesions initially affected only the right pelvic limb; however, the day before presentation, additional ulcers developed over both inguinal areas, the lips, and the nasal planum. Molly was up-to-date on vaccinations and received monthly imidacloprid and moxidectin topical parasite prevention.

Physical Examination

Mucous membranes were slightly dry, and clinical dehydration was assessed at approximately 6%. Examination showed interdigital ulceration and soft tissue swelling of digits IV and V on the right pelvic limb (Figure 1), superficial erosion of the skin in the inguinal area, and multiple erosions and ulcers over the rostral aspect of the upper and lower lips and nasal planum (Figure 2). No other abnormalities were noted.

Multiple erosions and ulcers are present over the rostral aspect of the patient’s upper and lower lips and nasal planum.
Multiple erosions and ulcers are present over the rostral aspect of the patient’s upper and lower lips and nasal planum.

Figure 2 Multiple erosions and ulcers are present over the rostral aspect of the patient’s upper and lower lips and nasal planum.

Figure 2 Multiple erosions and ulcers are present over the rostral aspect of the patient’s upper and lower lips and nasal planum.

Diagnostics

Systolic blood pressure measured by Doppler ultrasonography was persistently increased (195 mm Hg; range, 100-150 mm Hg). CBC showed thrombocytopenia (platelet count, 50 × 103/µL [50 x 109/L] ; range, 150-500 × 103/µL [150-500 x 109/L]), and serum chemistry profile revealed hypoalbuminemia, hyperbilirubinemia, and azotemia. International Renal Interest Society (IRIS) grade III acute kidney injury (AKI) was suspected (Table).1 Basal cortisol concentration (4.4 μg/dL [121 nm/L]; normal, >2 μg/dL [>55 nmol/L]) was within normal limits, making glucocorticoid-deficient hypoadrenocorticism unlikely. PCR for Leptospira spp in a single blood sample was negative. Antinuclear antibody test results were not suggestive of systemic lupus erythematosus.

TABLE

Serum Chemistry Profile Results

Analyte Result Reference Range
Albumin 2.0 g/dL (20 g/L) 2.5-4.0 g/dL (25-40 g/L)
Bilirubin 0.88 mg/dL (15.1 µmol/L) <0.58 mg/dL (<9.9 µmol/L)
Blood urea nitrogen 112 mg/dL (40 mmol/L) 8.4-25.2 mg/dL (3.9 mmol/L)
Creatinine 4.0 mg/dL (354 µmol/L) 0.7-1.4 mg/dL (62-124 µmol/L)

 

Urine specific gravity was 1.025; urinalysis was otherwise unremarkable. Urine protein:creatinine ratio was elevated at 2.5 (normal, <0.4). Urine culture was negative. A urinary catheter was placed to monitor urinary output and adjust fluid therapy accordingly as part of standard management of AKI. 

No significant findings were identified on abdominal ultrasonography or radiography of the thorax, abdomen, and limbs. Skin biopsy samples were not obtained because of concerns regarding the effects of sedation on renal perfusion.

Presumptive Diagnosis

Skin lesions and clinical abnormalities were suggestive of cutaneous and renal glomerular vasculopathy (CRGV). Differential diagnoses included leptospirosis, pyelonephritis, intoxication (eg, grape, ethylene glycol), immune-complex glomerulonephritis, and previous or current renal hypoperfusion (eg, prerenal azotemia), although these conditions are not typically associated with ulcerative skin lesions. A concurrent or associated dermatologic condition (eg, immune-mediated vasculitis, chemical burn) could not be excluded but was considered less likely.

Treatment

Standard AKI and supportive treatments were initiated (see Treatment at a Glance), including amlodipine (0.1 mg/kg PO q24h initially, then increased to 0.1 mg/kg PO q12h in the absence of clinical response), maropitant (1 mg/kg SC q24h), omeprazole (1 mg/kg PO q12h), and methadone (0.2 mg/kg IV q4h). Antibiotic therapy (ampicillin [15 mg/kg IV q8h]) was initiated to manage secondary infection of skin lesions, pending PCR for Leptospira spp and urinalysis results.

Crystalloid fluid therapy (ie, lactated Ringer’s solution) was initiated at 12.75 mL/kg/hr   to provide maintenance fluid therapy and correct 6% dehydration. Urine output measurement after 6 hours of fluid therapy demonstrated urine production of 0.4 mL/kg/hr (normal, >1 mL/kg/hr). Fluid therapy rate was adjusted to match the dog’s urine output and avoid volume overload. A furosemide bolus  (1 mg/kg IV) was administered, and furosemide (0.5 mg/kg/hr CRI) was started; urine output remained <0.5 mL/kg/hr over the next 6 hours.

TREATMENT AT A GLANCE

  • Fluid therapy (typically over 4-6 hours to allow accurate assessment of urine output) should aim first to correct suspected hypovolemia (rare) and/or dehydration. Once the fluid deficit has been corrected, urine output should be monitored, and the fluid rate should be adjusted to match urine production and avoid volume overload.7 
  • Systemic hypertension should be managed with amlodipine (or hydralazine if immediate control is necessary). ACE inhibitors may reduce glomerular filtration rate and are contraindicated in these cases.7 
  • CRGV skin lesions tend to heal spontaneously over days to weeks with appropriate management, including broad-spectrum antibiotic therapy, if indicated, and appropriate wound management.7

Outcome

Eighteen hours after admission, serum chemistry profile showed worsening azotemia with a creatinine concentration of 7.7 mg/dL (681 µmol/L) (IRIS Grade IV oligoanuric AKI). The patient was obtunded. Several options were discussed with the owner, including use of mannitol and/or fenoldopam to promote diuresis, referral for therapeutic plasma exchange and/or continuous renal replacement therapy, and euthanasia. Therapeutic plasma exchange has been used in humans with conditions similar to CRGV.2,3 After consideration, Molly was euthanized. Postmortem examination disclosed renal and cutaneous lesions consistent with thrombotic microangiopathy, including fibrinoid necrosis of the glomerular arterioles with frequent vessels occluded by thrombi and concurrent evidence of tubular necrosis and cutaneous coagulative necrosis with rare intravascular thrombi. The presence of these lesions with Molly’s clinical signs and progression confirmed CRGV.4

The Take-Home

CRGV is an uncommon disease of unknown cause and is also referred to as Alabama rot in reference to a North American disease of unknown origin that is characterized by similar histopathologic lesions.5 CRGV has been reported in greyhounds in North America5 and a Great Dane in Germany.6 

Until 2012, few (<5) cases had been reported in Europe. Since then, more than 150 cases in the United Kingdom, including one in Northern Ireland, have been confirmed by postmortem examination in nongreyhound breeds; 30 of these cases were reported in 2018, making CRGV a rare condition. Although a definitive cause has not yet been identified, research investigating environmental and genetic causes (mainly complement system dysfunction) is ongoing.

Ulcerated, vasculitis-like skin lesions of the extremities, ventrum, face, and tongue are typically reported first.4 Some dogs develop skin lesions and azotemia; others develop skin lesions only and do not become azotemic, although the percentage of dogs that develop skin lesions only is unknown due to the lack of gold standard testing antemortem and the lack of specificity of the skin lesions. The average time from onset of skin lesions to development of azotemia is 3 days (range, 1-10 days).4 Once AKI is present, prognosis is poor, with a mortality rate of 85%.5 Dogs that do not develop azotemia have an excellent prognosis, provided that wounds are adequately managed with standard local care and systemic antibiotic therapy. Thus far, there have been no reports of CRGV recurrence in a dog that survived the disease or of CRGV transmission between dogs. CRGV does not appear to be zoonotic, although standard precautions should be followed (eg, wearing gloves and a protective apron) until more is known about the disease etiology.

AKI = acute kidney injury, CRGV = cutaneous and renal glomerular vasculopathy, IRIS = International Renal Interest Society

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Quiz: White Blood Cell Evaluation in Blood Films

Lisa M. Pohlman, DVM, MS, DACVP, Kansas State University

Clinical Pathology

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Quiz: White Blood Cell Evaluation in Blood Films

Numeric and morphologic evaluation of WBCs are essential components of the CBC.

Automated in-house hematology analyzers can aid in the numeric portion of the assessment, but no hematology analyzers are able to identify morphologic abnormalities in the cells. Toxic changes, left shifts (regenerative or degenerative), neoplastic cells in circulation, parasites, and inclusions are among the important findings that require blood film evaluation. In addition, even when all CBC values are within the reference interval, abnormalities may still be detected on the blood film. The following images and their interpretations focus on WBC morphology.

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References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Research Note: Insights into Liver Regeneration

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The hepatic progenitor cell (HPC) niche is a histologic location and functional unit that is important in maintaining and regulating HPCs, cells that can differentiate into cholangiocytes or hepatocytes. HPCs are activated only when the regenerative capacity of all mature cell lines in the diseased liver is exhausted. In this study of feline lymphocytic cholangitis (LC), authors found immunohistochemical markers were expressed in more cells or expressed more intensely in livers of cats with LC (n = 12) than in normal cat livers (n = 2). This suggests the HPC niche is remodeled and activated in cats suffering from LC and may guide options for new treatments focusing on regeneration.

Source

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

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Research Note: Ki67 as Prognostic Factor inDogs with B-Cell Lymphoma

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Diffuse large B-cell lymphoma (DLBCL) is the most common type of lymphoma in dogs and humans. DLBCL has an aggressive and heterogeneous biologic course. Ki67 is an important marker of cell proliferation in humans with DLBCL. Mitotic index (MI) is another important indicator. Lymph node samples (n = 29) from dogs with DLBCL treated with a 19-week CHOP protocol were evaluated for Ki67 immunostaining and MI values. This study showed that Ki67 immunostaining on biopsy specimens was associated with shorter survival times in dogs with DLBCL. MI was not a prognostic factor, according to this study.

Source

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

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Esophagitis in Cats with Stomatitis

Michael Jennings, VMD, DAVDC, Veterinary Specialty & Emergency Center, Greater Philadelphia, Pennsylvania

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Esophagitis in Cats with Stomatitis

In the Literature

Kouki MI, Papadimitriou SA, Psalla D, Kolokotronis A, Rallis TS. Chronic gingivostomatitis with esophagitis in cats. J Vet Intern Med. 2017;31(6):1673-1679.


FROM THE PAGE …

Feline chronic gingivostomatitis (FCG) can be frustrating to owners who want to know why their cat is affected and clinicians wondering why some patients respond to treatment whereas others do not. Interest levels are raised when new studies describe possible comorbidities that might play a role in this disease; however, it is important to remember to interpret these reports critically.

In this study, physical, oral, and endoscopic examinations were performed on 58 cats with clinical signs of stomatitis and 12 healthy control cats. A significant majority (57/58) of cats with stomatitis had concurrent esophagitis. It was concluded that cats with FCG should undergo endoscopy and, if inflammation is noted, be treated for esophagitis because it may aggravate the FCG. However, none of the cats with FCG showed signs specific to esophageal disease, and endoscopic examination to evaluate whether esophagitis responded after treatment was performed in only 3 of the 57 cats. 

In addition, the study authors stated that current FCG treatment options are unrewarding due to the multifactorial nature of the disease, suggesting that there are few effective treatment options for FCG. However, 2 studies that have investigated prognosis with surgical extractions—the recognized standard of care1—have found that approximately 70% to 80% of cats will respond to full or partial mouth extractions, whereas only 5% to 6% of cats are refractory to treatment.2,3

The finding that cats with FCG may have concurrent esophagitis is interesting. However, there does not appear to be enough evidence of a relationship to warrant focusing on esophagitis.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Extraction of all teeth/tooth roots in areas of inflammation should be performed in all cats with FCG as a first-line definitive treatment.

 

2

Cats with FCG have severe oral inflammation and often show signs of oral pain. Medicating these patients can be challenging, and the decision to prescribe additional oral medications should be carefully considered.

3

Referral to a veterinary dental specialist is recommended for refractory cases.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Parvovirus Myocarditis in Young Dogs

Ashley E. Jones, DVM, DACVIM (Cardiology), Veterinary Specialty Center, Buffalo Grove, Illinois

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Parvovirus Myocarditis in Young Dogs

In the Literature

Ford J, McEndaffer L, Renshaw R, Molesan A, Kelly K. Parvovirus infection is associated with myocarditis and myocardial fibrosis in young dogs. Vet Pathol. 2017;54(6):964-971.


FROM THE PAGE …

Canine parvovirus is typically caused by canine parvovirus type 2, a single-stranded, nonenveloped DNA virus. Dogs 6 weeks to 6 months of age are at the highest risk for infection; however, infection can occur earlier. Puppies infected within 2 weeks of birth are at a high risk for the virus invading the cardiac myocytes, which can result in fatal necrotizing myocarditis. Some dogs will survive the acute infection but may later develop heart failure secondary to lymphocytic myocarditis and fibrosis. Although parvovirus infection has been less commonly seen since the development of a vaccine, the authors of this study hypothesized that parvoviral infection of myocardial cells is underrecognized as a cause of cardiac damage in dogs younger than 2 years. 

This retrospective study examined tissue archives of dogs 2 years of age or younger from June 2007 to November 2015. Forty dogs with a diagnosis of myocardial necrosis, inflammation, or fibrosis were identified, along with 41 age-matched controls. Histopathology of the samples was graded based on severity of myocardial necrosis, inflammation, and fibrosis on a scale of 0 to 3, with 0 indicating normal tissue and 3 being most severe (≥25% area of total tissue affected). In addition, PCR and reverse transcription quantitative PCR (RT-qPCR) were used to identify parvoviral DNA in the tissue samples. Immunohistochemistry and in situ hybridization (ISH) were performed on any case or control sample that tested positive with PCR or RT-qPCR.    PCR identified parvoviral DNA in 12/40 cases and 2/41 controls; RT-qPCR identified the same cases. Immunohistochemistry identified parvoviral material in 7/12 positive PCR cases, whereas ISH signal was detectable in 9 of these 12 cases. Immunohistochemistry and ISH were negative in both PCR-positive control cases.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Parvoviral myocardial infection appears to be a more common cause of myocardial damage in young dogs than previously thought, despite widespread vaccination.

 

2

PCR-based detection of canine parvovirus type 2 is a reliable, inexpensive, and rapid method to presumptively identify parvoviral myocarditis; ISH can provide an alternative for diagnosis, with higher sensitivity than immunohistochemistry.

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Patch Testing for Canine Adverse Food Reactions

Alison Diesel, DVM, DACVD, Texas A&M University

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Patch Testing for Canine Adverse Food Reactions

In the Literature

Johansen C, Mariani C, Mueller RS. Evaluation of canine adverse food reactions by patch testing with single proteins, single carbohydrates and commercial foods. Vet Dermatol. 2017;28(5):473-e109.


FROM THE PAGE …

Although less common than flea allergy and atopic dermatitis, cutaneous adverse food reaction (CAFR) is an important differential to consider in pruritic patients without parasites or infection. This is especially true when clinical signs, either strictly cutaneous and/or GI, are present in very young animals.1 Elimination diet trials using either home-prepared or commercially available novel protein–carbohydrate diets or hydrolyzed protein sources are key to accurate diagnosis.

In this prospective, cross-sectional study, 25 client-owned dogs with confirmed CAFR underwent patch testing with various proteins (raw and cooked), carbohydrates, and commercial dry food diets. All dogs had previously undergone elimination diet trials with rechallenge to confirm CAFR. Individual ingredient provocations identified ingredients that led to positive responses (ie, increased pruritus of ≥3 points on a validated scale). Protected chambers containing various individual food allergens and commercial dry diets were then affixed to the dogs for 48 hours for patch testing; positive and negative reactions were recorded.

Patch testing sensitivity was found to be 100%, 70%, and 22.2% for proteins, carbohydrates, and commercial dry diets, respectively. Negative predictive values were 100%, 79%, and 72% for proteins, carbohydrates, and commercial diets, respectively. Positive predictive values were 75% for proteins and 74% for carbohydrates. 

The authors concluded that patch testing may be helpful in identifying suitable protein sources for elimination diets. Carbohydrate patch test results were not as reliable as those for protein. Testing with commercial dry dog food did not appear to be useful.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

No available laboratory test (either serum-based or intradermal) reliably diagnoses CAFR. This holds true for patch testing as well, confirmed by the findings of this study. Elimination diet trials remain the gold standard for diagnosing CAFR in companion animals.

2

An elimination diet trial of at least 8 weeks’ duration is recommended for CAFR diagnosis in dogs and cats.2

 

3

Careful and complete diet history is imperative for choosing a novel protein for consideration in an elimination diet trial. Cross-reactivity of closely related protein sources should be considered.1 In addition, hydrolyzed versions of proteins to which a patient is allergic can manifest via pruritic flares.3

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Which Drugs Can Be Used Concurrently with Trazodone During & After Tibial Plateau-Leveling Osteotomy?

Which Drugs Can Be Used Concurrently with Trazodone During & After Tibial Plateau-Leveling Osteotomy?

Taly Reyes, BS, LVMT, VTS (Anesthesia & Analgesia) , University of Tennessee

Carrie Davis, DVM, DACVAA, University of Tennessee

Karen M. Tobias, DVM, MS, DACVS, University of Tennessee

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Which Drugs Can Be Used Concurrently with Trazodone During & After Tibial Plateau-Leveling Osteotomy?

Sirius, a 9-year-old neutered male Labrador retriever, is presented for surgical management of a right cranial cruciate ligament rupture. He has had previously identified episodes of anorexia, nausea, and anxiety. In addition, he has been treated with oral acepromazine for storm phobia intermittently for the past 2 years and currently receives oral amitriptyline for separation anxiety. He also has a history of atopic dermatitis, for which he receives hydroxyzine. He is currently on monthly heartworm and flea prevention. Physical examination is within normal limits except for right stifle swelling and pain. Thoracic radiography, CBC, serum chemistry profile, and urinalysis findings are within normal limits. Sirius will undergo anesthetic induction for tibial plateau-leveling osteotomy. The surgeon has prescribed trazodone during the procedure, and drug administration will be continued at home to facilitate exercise restriction and decrease anxiety.

Which of the following drugs would be appropriate to use concurrently with trazodone in this patient?

Based on the information provided, how would you grade the following drugs and why?

Do Not Use Proceed with Caution Safe

The following represents the best responses based on drug metabolism, pharmacokinetics, species, diagnostic differentials, clinical and laboratory data, and other pertinent findings.

Acepromazine

Correct ResponseCautionAcepromazine is a phenothiazine tranquilizer that antagonizes dopaminergic receptors, resulting in the desired goal of sedation. However, acepromazine antagonizes other receptors, including α1-adrenergic receptors, leading to the undesirable effects of vasodilation.1 Caution is thus indicated because trazodone is an α1-adrenergic antagonist (see Mechanism of Action).

Although use of acepromazine is of minimal risk to this otherwise healthy patient, when the drug is used in combination with trazodone, lower doses of acepromazine should be recommended to lessen the likelihood of hypotension during surgery.2

Hydromorphone

Correct ResponseSafeHydromorphone, a pure µ-opioid agonist used for analgesia, should be safe to administer concurrently with trazodone.

Propofol

Correct ResponseSafePropofol is a γ-aminobutyric acid (GABA)-A neurotransmitter receptor agonist commonly used as a sedative and induction agent. Although propofol may induce vasodilation, it is metabolized quickly and thus should be safe to administer concurrently with trazodone.

Isoflurane

Correct ResponseSafeIsoflurane is the most common inhalation agent used for maintenance of anesthesia in veterinary medicine. This drug has effects on GABA receptors, N-methyl-d-aspartate receptors, and glycine receptors. Isoflurane causes dose-dependent hypotension; however, because of its low lipid solubility, it is metabolized quickly and thus should be safe to administer to orthopedic surgical patients concurrently with trazodone.

Cefazolin

Correct ResponseSafeCefazolin, a β-lactam antibiotic that leads to bacterial cell lysis, should be safe to administer concurrently with trazodone.

Ketoconazole

Correct ResponseCautionKetoconazole is an antifungal drug that also inhibits cytochrome P450 3A (CYP3A) metabolism of multiple drugs, including trazodone. By inhibiting this enzyme pathway, there is potential to increase trazodone plasma concentrations, which could result in serotonin syndrome. Therefore, CYP3A-inhibitor drugs should be used with caution in dogs receiving trazodone. Other CYP3A inhibitors commonly used in dogs include erythromycin, clarithromycin, and itraconazole.

Maropitant

Correct ResponseSafeMaropitant, a neurokinin-1 receptor antagonist, is commonly prescribed for its antiemetic effect in the perioperative period. Because it works on a different receptor than does trazodone, maropitant is considered safe to use concurrently.

Mirtazapine

Correct ResponseCautionMirtazapine is primarily used as an appetite stimulant and antiemetic. It is important to recognize that mirtazapine antagonizes several receptors, including serotonin receptor subtypes, with resultant increased serotonin levels. Because of the risk for serotonin syndrome, mirtazapine should be used with caution in dogs receiving trazodone.3,4

Hydroxyzine

Correct ResponseCautionHydroxyzine, an antihistamine used for the treatment of allergies, is an antagonist of serotonin (5-hydroxytryptamine [5-HT]) receptors, specifically 5-HT2A. Because it may increase the risk for serotonin syndrome, hydroxyzine should be used with caution in dogs receiving trazodone.2,3

Amitriptyline

Correct ResponseCautionAmitriptyline is a tricyclic antidepressant and therefore should be used with caution in dogs receiving trazodone, as amitriptyline can increase serotonin concentrations, resulting in serotonin syndrome.2,3,5,6

Omeprazole

Correct ResponseSafeOmeprazole is a proton pump inhibitor used for the treatment of GI ulcers. It is safe to use in dogs receiving trazodone.

Tramadol

Correct ResponseCautionTramadol is commonly prescribed for the potential analgesic effects provided by its parent compound and its metabolites as µ-receptor agonists. However, tramadol also inhibits the reuptake of serotonin and norepinephrine.7 Therefore, use of tramadol in dogs receiving trazodone could lead to increased concentrations of serotonin and resultant serotonin syndrome (see Mechanism of Action).3,8

Carprofen

Correct ResponseSafeCarprofen is an NSAID used to treat pain and inflammation. Several case studies reported no complications when trazodone was administered to dogs receiving NSAIDs for postoperative pain.2,5,8

Tylenol #4

Correct ResponseSafeTylenol #4 is acetaminophen with codeine. Acetaminophen has antipyretic and analgesic properties, and codeine is a pure µ-opioid agonist used for pain relief. Opioids may cause histamine release, resulting in hypotension. However, in an otherwise healthy dog, Tylenol #4 should be safe to administer with trazodone.

Ivermectin

Correct ResponseSafeIvermectin is an antiparasitic agent that works on glutamate-gated chloride ion channels. It is also a GABA agonist. Ivermectin should be safe to administer with trazodone in this patient.

Selegiline

Correct Response Do Not UseMonoamine oxidase inhibitors (MAOIs; eg, amitraz, isocarboxazid, phenelzine, selegiline, tranylcypromine) are antidepressants primarily prescribed for humans; they are infrequently used in dogs, but of the MAOIs that are used, selegiline is the most common. The main function of monoamine oxidase is to break down dopamine, norepinephrine, and serotonin. MAOIs work by blocking these enzymes, causing an increase in serotonin concentration and other neurotransmitters in the brain.2,3,7 Although MAOIs are not commonly used in dogs, it is important to know that concurrent use of trazodone and MAOIs is contraindicated because of the resultant increase in serotonin concentration and risk for serotonin syndrome.2,3,7

Gabapentin

Correct ResponseSafeGabapentin is an anticonvulsant agent that is also used to treat neuropathic pain. Although its mechanism of action is not well understood, it is known to involve inhibition of the α2δ-1 subunit of voltage-gated calcium channels. Because gabapentin’s mechanism of action differs from that of trazodone, it is considered safe to use concurrently.2,9

MECHANISM OF ACTION

Trazodone, an antidepressant used to treat anxiety in dogs, antagonizes 5-HT2A receptors2 and inhibits serotonin reuptake.1,10 The drug also antagonizes α1-adrenergic receptors, causing some vasodilatory effects, as well as histamine 1 receptors and T-type calcium channels, which could potentially result in adverse cardiovascular effects.10 The anxiolytic properties of trazodone seem to be related to the receptor site activities, which alter serotonin concentrations.1 The neurotransmitter serotonin is primarily found in the GI tract, platelets, and CNS.3 

Plasma concentrations of trazodone may increase when the drug is administered in combination with drugs that are selective serotonin reuptake inhibitors and tricyclic antidepressants; if concentrations subsequently increase excessively in the CNS, serotonin syndrome may develop.7 Signs of serotonin syndrome include confusion, agitation, hyperthermia, tachycardia, seizures, ataxia, tremors, myoclonus, coma, diarrhea, vomiting, inappetence, and hyper- or hypotension.3,8,11

5-HT = 5-hydroxytryptamine, CYP3A = cytochrome P450 3A, GABA = γ-aminobutyric acid, MAOI = monoamine oxidase inhibitor

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Top 5 Lip Depigmentation Causes in Dogs

Alexander Werner Resnick, VMD, DACVD, Animal Dermatology Center

Dermatology

|Peer Reviewed

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Top 5 Lip Depigmentation Causes in Dogs

Skin pigmentation in mammals is primarily produced by the transfer of eumelanin (ie, black–brown pigment) and pheomelanin (ie, yellow–red pigment) within melanosomes through the dendritic processes of melanocytes to adjacent keratinocytes in the basal cell layer.1 In dogs, the dendritic processes of one melanocyte are associated with 10 to 20 keratinocytes to produce the epidermal melanin unit.2

Because of the cytotoxicity of synthesis intermediates, melanogenesis is confined within melanocytes to the membrane-bound melanosomes.2 Abnormal loss or absence of pigmentation (ie, leukoderma or hypomelanosis, respectively) can be caused by reduced pigment production and/or loss of melanocytes.  

The lip margin in dogs is highly visible and often darkly pigmented. Both the degree and pattern of normal pigmentation differ by breed type and individual dog. Thus, determining whether pigmentation changes suggest a pathologic process must be based on what is normal or abnormal for each dog and on the presence or absence of inflammation and/or pigmentation changes at other locations. In general, acute inflammation often produces depigmentation, whereas chronic inflammation may lead to hyperpigmentation.

Following are the author’s top 5 causes of lip depigmentation in dogs.

1

Mucocutaneous Pyoderma

Mucocutaneous pyoderma is an inflammatory dermatitis that primarily affects the lip margins and perioral skin. Lesions are distinctive and typically consist of swelling of the lips, most notably at the commissures and lip folds, that progresses first to crusting and exudation then to focal erosions and ulcerations (Figure 1).3 Localized depigmentation is a common sequela. Intertrigo (ie, when one skin area comes in contact with other skin areas) causes inflammation as well as accumulation of moisture and debris. Lip fold intertrigo is often associated with development of mucocutaneous pyoderma (Figure 2); infection may also result from chronic excoriation caused by allergic reaction. Significant malodor, frequently mistaken as halitosis, and tenderness of infected tissues may be present.

Mucocutaneous pyoderma affecting the lip margins of a 13-year-old neutered male crossbreed Chihuahua. Adherent crusts can be seen overlying mildly eroded skin on the lower lip margin (arrows) and are most severe around the lip fold (arrowhead).
Mucocutaneous pyoderma affecting the lip margins of a 13-year-old neutered male crossbreed Chihuahua. Adherent crusts can be seen overlying mildly eroded skin on the lower lip margin (arrows) and are most severe around the lip fold (arrowhead).

FIGURE 1 Mucocutaneous pyoderma affecting the lip margins of a 13-year-old neutered male crossbreed Chihuahua. Adherent crusts can be seen overlying mildly eroded skin on the lower lip margin (arrows) and are most severe around the lip fold (arrowhead).

FIGURE 1 Mucocutaneous pyoderma affecting the lip margins of a 13-year-old neutered male crossbreed Chihuahua. Adherent crusts can be seen overlying mildly eroded skin on the lower lip margin (arrows) and are most severe around the lip fold (arrowhead).

Mucocutaneous pyoderma causing erosions at the lip folds, with secondary depigmentation of the lip margins in a 4-year-old spayed Maltese
Mucocutaneous pyoderma causing erosions at the lip folds, with secondary depigmentation of the lip margins in a 4-year-old spayed Maltese

FIGURE 2 Mucocutaneous pyoderma causing erosions at the lip folds, with secondary depigmentation of the lip margins in a 4-year-old spayed Maltese

FIGURE 2 Mucocutaneous pyoderma causing erosions at the lip folds, with secondary depigmentation of the lip margins in a 4-year-old spayed Maltese

Diagnosis is made by excluding other dermatoses associated with depigmentation and by finding large numbers of bacteria in epidermal exudates. Culture and susceptibility testing is indicated in patients that fail to respond to treatment with a first-choice antibiotic.4 Initial treatment includes gentle clipping and cleaning of the lip margins. Application of a topical antiseptic or antibiotic can be sufficient, but oral antibiotic therapy may be required in severe or chronic cases. Recurrence is best prevented through regular cleaning of affected areas and correction of any secondary cause (eg, allergy, damage from excessive chewing).

2

Discoid Lupus Erythematosus

Discoid lupus erythematosus (DLE), more specifically facial-predominant DLE, is a common but usually mild variant of cutaneous lupus erythematosus.5,6 Many factors, including genetic and environmental triggers, are believed to influence the development of autoimmunity in patients with DLE. Lesions often worsen with sun exposure. 

Deposition of autoantibodies and complement at the epidermal basement membrane zone results in lymphocytic lichenoid-interface dermatitis, with keratinocyte apoptosis, loss of melanosomes from melanocytes (ie, pigmentary incontinence), and reduced melanin production.7 Whereas depigmentation occurs secondary to inflammation in other conditions, loss of pigmentation is an initial sign of DLE. In these patients, the nasal planum is the primary location of lesions; however, diffuse-to-patchy lightening of the pigmentation around the lip margins occurs in most cases (Figure 3).

Significant depigmentation with loss of cobblestone-like appearance and crusting of the nasal planum in a 9-year-old neutered male American Eskimo dog with discoid lupus erythematosus. Mottled depigmentation of the adjacent skin is also present (A). Regions of depigmentation (B; arrows) adjacent to normally pigmented skin (arrowhead) are evident on the lip margins.
Significant depigmentation with loss of cobblestone-like appearance and crusting of the nasal planum in a 9-year-old neutered male American Eskimo dog with discoid lupus erythematosus. Mottled depigmentation of the adjacent skin is also present (A). Regions of depigmentation (B; arrows) adjacent to normally pigmented skin (arrowhead) are evident on the lip margins.

FIGURE 3 Significant depigmentation with loss of cobblestone-like appearance and crusting of the nasal planum in a 9-year-old neutered male American Eskimo dog with discoid lupus erythematosus. Mottled depigmentation of the adjacent skin is also present (A). Regions of depigmentation (B; arrows) adjacent to normally pigmented skin (arrowhead) are evident on the lip margins.

Significant depigmentation with loss of cobblestone-like appearance and crusting of the nasal planum in a 9-year-old neutered male American Eskimo dog with discoid lupus erythematosus. Mottled depigmentation of the adjacent skin is also present (A). Regions of depigmentation (B; arrows) adjacent to normally pigmented skin (arrowhead) are evident on the lip margins.
Significant depigmentation with loss of cobblestone-like appearance and crusting of the nasal planum in a 9-year-old neutered male American Eskimo dog with discoid lupus erythematosus. Mottled depigmentation of the adjacent skin is also present (A). Regions of depigmentation (B; arrows) adjacent to normally pigmented skin (arrowhead) are evident on the lip margins.

FIGURE 3 Significant depigmentation with loss of cobblestone-like appearance and crusting of the nasal planum in a 9-year-old neutered male American Eskimo dog with discoid lupus erythematosus. Mottled depigmentation of the adjacent skin is also present (A). Regions of depigmentation (B; arrows) adjacent to normally pigmented skin (arrowhead) are evident on the lip margins.

FIGURE 3 Significant depigmentation with loss of cobblestone-like appearance and crusting of the nasal planum in a 9-year-old neutered male American Eskimo dog with discoid lupus erythematosus. Mottled depigmentation of the adjacent skin is also present (A). Regions of depigmentation (B; arrows) adjacent to normally pigmented skin (arrowhead) are evident on the lip margins.

Diagnosis requires biopsy with histologic confirmation. Treatment primarily consists of sun avoidance and administration of topical corticosteroids or tetracycline-derivative antibiotics (eg, doxycycline [10 mg/kg PO q24h], minocycline [5 mg/kg PO q12h]) combined with niacinamide (250 mg PO q12-24h in dogs weighing <22 lb [10 kg] and 500 mg PO q12-24h in dogs weighing >22 lb [10 kg]).8 Long-term treatment with oral corticosteroids or immunosuppressive therapy is rarely required.

3

Epitheliotropic Lymphoma

Epitheliotropic lymphoma is an uncommon cutaneous neoplasia of older animals. In dogs, this disease is commonly associated with infiltration by CD8+ cells, whereas in humans, disease most often results from infiltration by CD4+ cells.9 Studies have suggested a 12-fold increased risk in patients with chronic atopy.10 The mucocutaneous form is often mistaken for other causes of inflammation around the lip margins and oral cavity; depigmentation is often associated with intense inflammation (Figure 4).

Diffuse depigmentation on the lip margins and nasal planum of a 9-year-old neutered male shih tzu with epitheliotropic lymphoma
Diffuse depigmentation on the lip margins and nasal planum of a 9-year-old neutered male shih tzu with epitheliotropic lymphoma

FIGURE 4 Diffuse depigmentation on the lip margins and nasal planum of a 9-year-old neutered male shih tzu with epitheliotropic lymphoma

FIGURE 4 Diffuse depigmentation on the lip margins and nasal planum of a 9-year-old neutered male shih tzu with epitheliotropic lymphoma

Diagnosis requires biopsy with histologic confirmation. Overall prognosis is poor except when a lesion or lesions are identified early in disease and excised. Referral to a veterinary oncologist or dermatologist for treatment is advised.

4

Vitiligo

Vitiligo is an acquired, possibly immune-mediated, disease associated with melanocyte destruction. There may be a genetic basis for increased melanocyte susceptibility to damage as well as increased risk for developing antimelanocyte antibodies. Vitiligo has an increased incidence in certain breeds (ie, rottweilers, Old English sheepdogs).11,12 Striking depigmented patches can develop on multiple areas of the body (Figures 5 and 6). Lesions are distinctive and are not typically associated with inflammation. Both skin (leukoderma) and hair (leukotrichia) may be affected. Systemic signs are absent.

Vitiligo producing noninflammatory, well demarcated patches of depigmentation on the lip margins of a 3-year-old spayed Airedale terrier. Similar changes affect the nasal planum. Unlike lesions in patients with mucocutaneous pyoderma and discoid lupus erythematosus, inflammation and crusting are not associated with depigmentation.
Vitiligo producing noninflammatory, well demarcated patches of depigmentation on the lip margins of a 3-year-old spayed Airedale terrier. Similar changes affect the nasal planum. Unlike lesions in patients with mucocutaneous pyoderma and discoid lupus erythematosus, inflammation and crusting are not associated with depigmentation.

FIGURE 5 Vitiligo producing noninflammatory, well demarcated patches of depigmentation on the lip margins of a 3-year-old spayed Airedale terrier. Similar changes affect the nasal planum. Unlike lesions in patients with mucocutaneous pyoderma and discoid lupus erythematosus, inflammation and crusting are not associated with depigmentation.

FIGURE 5 Vitiligo producing noninflammatory, well demarcated patches of depigmentation on the lip margins of a 3-year-old spayed Airedale terrier. Similar changes affect the nasal planum. Unlike lesions in patients with mucocutaneous pyoderma and discoid lupus erythematosus, inflammation and crusting are not associated with depigmentation.

Discrete, strikingly depigmented patches of vitiligo and leukotrichia affecting the lip margins, muzzle, and nasal planum of an adult crossbreed German shepherd dog
Discrete, strikingly depigmented patches of vitiligo and leukotrichia affecting the lip margins, muzzle, and nasal planum of an adult crossbreed German shepherd dog

FIGURE 6 Discrete, strikingly depigmented patches of vitiligo and leukotrichia affecting the lip margins, muzzle, and nasal planum of an adult crossbreed German shepherd dog

FIGURE 6 Discrete, strikingly depigmented patches of vitiligo and leukotrichia affecting the lip margins, muzzle, and nasal planum of an adult crossbreed German shepherd dog

Diagnosis requires biopsy with histopathologic examination to exclude inflammatory causes of depigmentation. No effective treatment has been reported, and lesions may spontaneously regain pigmentation.

5

Uveodermatologic Syndrome

Similar to Vogt-Koyanagi-Harada disease in humans, uveodermatologic syndrome (often called Vogt-Koyanagi-Harada–like syndrome) is a multisystem autoimmune disease that affects pigmented tissues of the eye, ear, nervous system, skin, and hair.13,14 The syndrome is seen most often in young adult to middle-aged Akitas, Samoyeds, and Siberian huskies.13 Bilateral acute-onset painful uveitis is typically the first and most severe sign. Skin and hair coat depigmentation are secondary but occasionally can be concurrent. Skin lesions consist of whitening of the face, muzzle, and hair coat, with less frequent generalization. Erythema and erosions are uncommon but can occur (Figure 7).

Severe lesions of erosion and depigmentation in a 1-year-old neutered male Akita with uveodermatologic syndrome. On presentation, uveitis had progressed to permanent blindness.
Severe lesions of erosion and depigmentation in a 1-year-old neutered male Akita with uveodermatologic syndrome. On presentation, uveitis had progressed to permanent blindness.

FIGURE 7 Severe lesions of erosion and depigmentation in a 1-year-old neutered male Akita with uveodermatologic syndrome. On presentation, uveitis had progressed to permanent blindness.

FIGURE 7 Severe lesions of erosion and depigmentation in a 1-year-old neutered male Akita with uveodermatologic syndrome. On presentation, uveitis had progressed to permanent blindness.

Diagnosis is often made by ophthalmologic examination correlating with the cutaneous signs mentioned previously. Biopsy sampling with histopathologic examination is recommended in patients that lack active ocular signs. Aggressive, rapid initiation of immunosuppressive therapy is recommended to prevent formation of posterior synechiae and secondary glaucoma, cataracts, or blindness; prognosis is fair to good for patients appropriately treated.13,15

Conclusion

In patients with pigmentation disorders, the most important determination to make is whether loss of pigmentation developed before, after, or concurrently with inflammation (or absence of inflammation). Mucocutaneous pyoderma and epitheliotropic lymphoma can cause depigmentation secondary to intense inflammation but will rarely cause leukotrichia. In patients with DLE, depigmentation precedes inflammation and does not cause leukotrichia. In those with uveodermatologic syndrome, depigmentation of the skin and hair coat typically follows uveitis and is often associated with minimal inflammation of the skin. Vitiligo is rarely inflammatory. Patients with mucocutaneous pyoderma should respond to appropriate antibacterial therapy; for patients with lip depigmentation that fail to respond to antibacterial therapy, biopsy and histopathologic examination are required to determine the cause and to formulate an appropriate treatment plan.

DLE = discoid lupus erythematosus

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Acute Respiratory Distress in a Brachycephalic Dog

Gretchen Statz, DVM, DACVECC, Antech Diagnostics, Veterinary Emergency and Specialty Care, Indianapolis, Indiana

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Acute Respiratory Distress in a Brachycephalic Dog

THE CASE

Yoyo, a 10-year-old neutered male Boston terrier, is presented to the emergency room for increased respiratory effort of 24 hours’ duration. On presentation, the dog starts coughing and gagging, then develops wheezing that progressively worsens. He had been eating normally before onset of respiratory distress.

Yoyo has always been overweight but otherwise healthy and is not on any medications. The results of a routine physical examination and laboratory work performed 6 months prior are unavailable but were reportedly normal according to the owner. Yoyo has no history of vomiting or regurgitation.

On physical examination, Yoyo is bright and alert. Temperature (101.2°F [38.4°C]) and heart rate (120 bpm) are within normal limits. There is mild serous discharge from the left eye and increased respiratory effort with loud respiratory stridor and soft stertor on inspiration. Respiratory rate is elevated (66 breaths/min), and Yoyo wheezes on exhalation. Heart sounds are muffled bilaterally. His abdomen is pendulous, and BCS is 7/9. 

The owner agrees to CBC, serum chemistry profile, and thoracic radiography. CBC and serum chemistry profile are unremarkable aside from elevated liver values (Table). Airway sampling for cytology and culture was discussed but not pursued, likely because of the patient’s critical condition.

TABLE

Elevated Liver Values

Test Result Reference Range
Alkaline phosphatase 924 U/L (15.4 µkat/L) 0-140 U/L (0-2.3 µkat/L)
Alanine aminotransferase 137 U/L (2.29 µkat/L) 0-120 U/L (0-2.0 µkat/L)
γ-glutamyltransferase 30 U/L (0.50 µkat/L) 0-14 U/L (0-0.23 µkat/L)

 

Thoracic radiographs (Figure) show an alveolar lung pattern in the ventral aspect of the right middle lung lobe that is most consistent with aspiration pneumonia or bronchopneumonia. Hemorrhage, neoplasia, and bronchial obstruction are also on the differential list but are considered less likely. Hepatomegaly is present, as is radiographic evidence of possible palate/pharyngeal region swelling and aerophagia.

Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia.&nbsp;
Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia.&nbsp;

Figure Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia. 

Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia.&nbsp;
Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia.&nbsp;

Figure Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia. 

Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia.&nbsp;
Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia.&nbsp;

Figure Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia. 

Figure Right lateral (A), left lateral (B), and ventrodorsal (C) thoracic radiographs of the patient. Palate/pharyngeal region swelling can be observed (B; arrow), as can an alveolar lung pattern in the ventral aspect of the right middle lung lobe (C; arrow), which is most consistent with aspiration pneumonia or bronchopneumonia. 

Yoyo is admitted to the hospital, placed in an oxygen cage at a fraction of inspired oxygen (FiO2) content of 40%, and treated with ampicillin–sulbactam (22 mg/kg IV q8h), enrofloxacin (10 mg/kg IV q24h), terbutaline (0.01 mg/kg IV q12h1), and nebulization with 0.9% saline. He is placed on IV fluids at 50 mL/hr based on maintenance plus estimated subclinical dehydration, and his respiratory rate and effort are monitored every 2 hours.

What are the next steps?

THE CHOICE IS YOURS …

CASE ROUTE 1

Continue hospitalization with supportive care, oxygen supplementation, and antibiotics for treatment of suspected aspiration pneumonia and to monitor the respiratory rate and effort and oxygen saturation via pulse oximetry.

CASE ROUTE 2

Continue hospitalization with fluids and antibiotics for treatment of suspected aspiration pneumonia and to perform a sedated airway examination and CT scan to further assess the upper airway and lungs.

FiO2 = fraction of inspired oxygen

Disclosure: Dr. Statz is also affiliated with ANTECH Diagnostics.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

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