Clinical Approach to Scaling Dermatitis. OUTLINE

• What is scale? • Huge differential list. A cause-based clinical approach • Symptomatic therapy • Examples: – Golden retriever ichthyoisis – Idiopathic nasal hyperkeratosis

Dr. Rob Hilton BVSc (Hons) MACVSc (Canine Medicine) Cert.VD MRCVS – Hepatocutaneous syndrome – Sebaceous adenitis

Crust and scale are NOT the same. Crust What is scale ? = dried exudate with blood and/or leucocytes • Dry Scale = seborrhea sicca = accumulations of mature epidermal keratatinocytes (corneocytes) = orthokeratosis and/or immature epidermal keratinocytes (parakeratosis) +/- • Hair follicle keratinocytes (principally external and internal root sheaths) +/- • Excess sebaceous secretions (seborrhea oleosa)

1 Dry Scale (Seborrhea sicca) Seborrhea oleosa

Demodicosis •Congenital & nevi Hypothyroidism •Malassezia •Bacterial overgrowth syndrome •Male feminization syndrome

Alopecia and dry scale on the flank Follicular Casts secondary to exposure from endocrine alopecia.

•Dry Scale adhering to hair shafts •Severe follicular pathology

2 Comedones Follicular Casts and dry scale

•Commonly associated with Cushing’s disease or . •Indicate severe follicular disease •Keratin/sebum plugs in hair follicles.

A cause-based approach to (1) Excessive production of the stratum scaling disorders corneum The list of differentials is very long. • Congenital defects ( Primary seborrhea, Nevi) • Reaction to physical agents (UV radiation , irritant chemicals, trauma.) 1. Excessive production of the stratum • Infection (bacteria and dermatophytes and yeast) corneum • Ectoparasites (Fleas, Sarcoptes , Demodex , Cheyletiella ) • Reactions to disease within the epidermis or dermo-epidermal 2. Ineffective exfoliation of the stratum junction - Pyoderma , immune-mediated disease, lymphona corneum. • Metabolic causes - Zinc responsive dermatitis, hypothyroidism, hepato-cutaneous syndrome, vitamin A responsive dermatosis, 3. Defects of epidermal hydro-lipid film feline thymoma, poor diet • Idiopathic keratinization defects (e.g. ear margin dermatosis, naso/digital hyperkeratosis, feline acne)

3 (2) Insufficient or defective destruction and exfoliation of the stratum corneum Idiopathic keratosis/Nevi

• Congenital • Lack of grooming in sick cats (3)Protective surface lipid film defects

•Defects of production •Lack of essential fatty acids (from poor quality diets or improper storage and oxidation). •Destruction of the sebaceous glands (sebaceous adenitis, Leishmania) Idiopathic keratosis Epidermal dysplasia •Hypothyroidism •Excessive shampoos that remove surface lipids

Scaling with collarettes and crusts. Scale as a reaction to pyoderma DDX Pyoderma or Pemphigus Foliaceus

• Especially Nordic breeds • DDX includes – Zinc responsive dermatosis – Malassezia – Sebaceous adenitis – Pemphigus

4 Scaling dermatitis due to disease at Scaling form of pemphigus dermo-epidermal junction foliaceus. Lesions not limited to head so <> P. erythematosus

Lupoid dermatosis of German Short-haired Pointers

Don’t forget: Sarcoptes, Dermatophytosis trichogram: Demodex and Dermatophytes “rotten log appearance”

5 Full history, clinical and dermatological Symptomatic management of examination scale

•Superficial skin scrapings, deep skin scrapings Parasites •Sticky tape cytology identified : • Shampoo therapy •Trichogram and fungal Treat culture • Hydration of skin

•Ectoparasite elimination Response: • Systemic therapy trial Search for •Antimicrobial response underlying cause trial • Control of secondary infection

If not complete resolution, skin biopsy and metabolic function tests.

Symptomatic management of Sulfur and Salicylic acid scale General properties of • Keratolytic & keratoplastic shampoos • Detergent (Dissolve lipids/sebum) • Synergistic actions at 2% • Keratolytic (Break cohesion concentration between the corneocytes ) • Moderate antimicrobial • Keratoplastic (“Normalize” the turnover of the epidermis and the action process of keratinization due to their effects on the basal epidermal cells.) • Generally tolerated by • Antibacterial and anti-Malassezia cats • Moisturizing • Not aggressively drying

6 Selenium sulfide 1% Benzyl Peroxide • Keratolytic and keratoplastic with degreasing action • Disinfectant, astringent and • Also causes excess drying . Needs to be keratolytic properties. combined with hydration of skin • Reputed capacity to flush debris • Useful for initial therapy of heavy or greasy from hair follicles . scale or in cases refractory to less aggressive • Good degreasing action • Causes excessive drying of the therapy . skin . Hydrating conditioner is required after each bath. • Dark coated dogs tend to bleach or Coal Tar products. discolour . •Very aggressive keratolytic and keratoplastic • Do not use in cats . Toxic if ingested. •Variable contents of tar components • Generally used short term •No longer registered for Veterinary use

Hydration of the Skin Hydration of the Skin

• Hygroscopic agents • Emollients (humectants) • High molecular weight • Decrease epidermal molecules that hydrate the water loss. epidermis osmotically via dermal vasculature. • E.G. paraffin oil • Urea, glycerin, lactic acid and propylene glycol. • Used as a post-bath • Propylene glycol has conditioner after the antiseptic, lipid solvent and skin has been keratolytic properties. hydrated. • 25-33% propylene glycol in water for hydration or 45-70% as a keratolytic

7 Systemic therapy - Retinoids Other systemic agents

• Act directly on nuclear receptors • Vitamin A (600-800 IU/kg daily) is less potent than • “Normalize” keratinocyte and differentiation. synthetic retinoids, acting on cytoplasmic receptors and • Benefits are not evident until 2-3 months of therapy. then on the nucleus via transport molecules. • Dose can be tapered down for maintenance. • Vitamin D3 (calcitriol 10ngm/kg daily) has off label • Potential side effects of retinoid therapy include retinoid-like action but has the potential of causing keratoconjunctivitis sicca, liver damage and alterations in severe disturbances in calcium/phosphorous lipid metabolism. metabolism. Monitoring is required. • Highly teratogenic, and should not be used in breeding • Fatty acid supplements improve dry scale. Linoleic acid , animals. Effects may extend for years after as found in sunflower or safflower oil, decreases scale administration has ceased. Clients need to be informed and improve coat quality. No specific dose rates have of the teratogenic potential of these agents and should wear gloves during administration. been clinically trialed, but doses of 1ml /2-4 kg are indicative. Excessive use can result in diarrhea. • Expensive, cost may limit their use. Acitretin 1mg/kg Omega3/6 fatty acid supplements (1ml/4kg daily) have an anti-inflammatory effect.

Golden Retriever Ichthyosis Golden Retriever Ichthyosis Clinical signs • Inherited . Autosomal recessive or • May present from 12 weeks – 4 years of incomplete dominance age. • Recognized clinically but only recently • Flakes of dry scale from small to 1cm 3 +/- characterized focal areas of flakey seborrhea oleosa. • Primary keratinization defect with electron- microscopic membrane lesions in strata • Scale accumulation in ears +/- otitis granulosum and corneum and retention of externa desmosomes between mature • Not pruritic unless secondary bacterial or keratinocytes. yeast infection present.

8 Golden Retriever Ichthyosis Golden Retriever Ichthyosis Typical scale Focal greasy scale

Golden Retriever Ichthyosis Golden Retriever Ichthyosis Management

• Differential diagnosis • Shampoo therapy . Selenium sulfide – Allergic dermatitis (pruritic/inflammatory) initially (if severe) -> maintenance with – Demodicosis and other skin parasites – Primary or secondary pyoderma /Malassezia sulfur/salicylic acid shampoo weekly . infection • Vitamin A – Hypothyroidism • Definitive diagnosis is histological after • Linoleic acid supplementation secondary infection has been resolved. • Control of secondary infections

9 Hereditary nasal parakeratosis of Idiopathic Nasal Hyperkeratosis Labrador retrievers and crosses • Hereditary nasal parakeratosis of • Autosomal recessive Labrador retrievers and crosses. • Lesions usually appear before 12 months of age. • Adherent accumulations of dry scale. In more severe • Nasal Hyperkeratosis Associated with cases, fissures and erosions Xeromycteria "Parasympathetic nose” develop. • Secodary infection and inflamation may lead to depigmentation of the • Senile idiopathic naso/digital remaining nasal planum. • Not exacerbated by UV light hyperkeratosis. exposure. • Sometimes clinically seen in other breeds

Inherited nasal hyperkeratosis Nasal Hyperkeratosis Associated with Xeromycteria ("Parasympathetic" nose)

• The lateral nasal gland of the dog is responsible for the moisture of the nasal mucosa. Duct opens 2cm from nares and moisture translocates over the surface of the planum. • Parasympathetic innervation (together with lacrimal glands) with the facial nerve. • May be injured in otitis media • Lesions may be unilateral or bilateral. • Resolution of otitis media (if present) may result in Photos courtesy of Dr Judith Nimmo spontaneous improvement .

10 Senile idiopathic naso/digital Nasal Hyperkeratosis, diagnosis hyperkeratosis • Immune mediated disease • Older dogs • Mucocutaneous pyoderma • Increased horny tissue on the • Solar dermatitis nose and/or footpads • Hepatocutaneous syndrome accompanied in some cases by • Zinc responsive dermatosis fissures and secondary • Neoplasia infection. • Post distemper hyperkeratosis • Projections of firm, feathered, and cracked horny tissue. In some cases only the margins of the nose or footpads are affected while in others, the entire nose or footpad area can be affected.

Idiopathic nasal hyperkeratosis, Nasal Hyperkeratosis, approach Therapy Full history, clinical and dermatological • Needs to be tailored to individual. examination => clinical • Water soaks and sorbolene or petroleum jelly assessment • 50-60% propylene glycol • Topical and systemic antibiotics for secondary Treatment of infection secondary infection for 3 weeks • Systemic fatty acid therapy • Vitamin A? • Topical corticosteroids?? If not complete resolution, biopsy and metabolic function tests.

11 Hepatocutaneous syndrome (superficial epidermal necrolysis, necrolytic migratory Hepatocutaneous Syndrome erythema) • Degeneration and hyperplasia of keratinocytes Necrotizing dermatitis + hyperkeratosis associated with: – Chronic liver disease • Footpad hyperkeratosis +/- fissures – Diabetes mellitus – Pancreatic glucagonoma. Less common in dogs vs • Erythema and erosion with hyperkeratosis humans – Mucocutaneous junctions (lips, nasal planum • Aetiopathogenisis unclear (defective protein and genitalia) and/or zinc metabolism?) • Older dogs . – Friction points (elbows, hocks and distal • Skin signs may present before signs of liver extremities) disease

Hepatocutaneous syndrome Hepatocutaneous syndrome

12 Hepatocutaneous syndrome Hepatocutaneous syndrome Laboratory findings + infection Variable • Elevated liver enzymes • Decreased albumen • Elevated post-prandial serum bile acids • Hyperglycemia • Non-regenerative anemia. • Ultrasound may reveal changes to the hepatic parenchyma that are more severe than suggested by biochemistry.

Biochemistry values in hepato- Hepatocutaneous syndrome cutaneous syndrome • DDX includes: – Zinc responsive dermatitis – Immune mediated disease – Mucocutaneous pyoderma – Naso-digital hyperkeratosis

• Definitive diagnosis: – Histopathology (without secondary infection) – Demonstration of underlying cause

13 Hepatocutaneous syndrome Sebaceous Adenitis

• Prognosis is often poor unless underlying • Inflammation and disease can be corrected. destruction of the • Suggested therapies sebaceous glands – Amino acid supplements (e.g. eggs, infusions??)

– Zinc supplements (ZnSO 4 10mg/kg) – Moisturizing hyperkeratosis areas • Probably immune – Essential fatty acids mediated (cell • Treatment of secondary bacterial and yeast mediated) with an infections inherited • Corticosteroids???? predisposition

Sebaceous glands Clinical signs Clinical aspects • Presents in early to middle age • Predisposed breeds : Akita, Standard , Springer • Holocrine glands : Spaniel, Nordic breeds, Samoyed, Hovawart, Visla but slough into central any other breed can be affected duct • Maintains pliability of Long-haired Breeds Short-haired Breeds skin and hair by •Accumulations of adherent lubrication and •Circular or fingerprint-like scale and follicular casts. areas of alopecia, often retaining moisture •Inflammatory alopecia beginning on head that • Production of •Pruritus associated with coalesce. antimicrobial lipids for secondary infection •Very fine scale and +/- very • begins on head. the surface hydro-lipid fine follicular casts Other breeds more multifocal film •Cerumenous otitis

14 Advanced stage of sebaceous adenitis in an Early stage of sebaceous adenitis in an Akita. Akita. Tightly adhering scale, follicular casts, Tightly adhering scale and secondary infection otitis and secondary infection

Appearance of sebaceous adenitis in short- Sebaceous adenitis 3yo Maltese haired breeds.

15 Diagnosis Treatment of sebaceous adenitis

• Zinc responsive dermatosis (Nordic breeds) Objectives • Pyoderma/ (especially Nordic breeds) • Restore the hydration and barrier function • Demodicosis and other skin parasites of the skin • Allergic dermatitis • Dermatophytosis • Arrest destruction of sebaceous glands • All other listed causes of scale and permit regeneration • Removal of scale Definitive diagnosis is based • Treat and prevent secondary bacterial and on skin biopsy and yeast infection histopathology

Topical therapy protocol Linek M: Veterinary Focus / / Vol 18 No 1 / / 2008 Systemic therapy

Step 1: - Lathering the dog with a Step 3: - Removal of the oil by combined product of sulfur and Cyclosporine. salicylic acid. a final lathering with a mild • Leaving the shampoo on for a cleansing and antimicrobial • 5mg/kg SID. Multiple reports of minimum of 10 minutes shampoo • Gentle brush-massage during Step 4: - Final application of a efficiency provided not all of sebaceous this time which helps to remove conditioner or a mixture of a significant amount of scales propylene glycol and water gland structures totally destroyed. • Thorough rinse-off and towel dry (final concentration of 50-70% Step 2: - Oil soak with any light propylene glycol), which acts mineral oil containing bath oil (generic baby oil). as a humectant. This mixture • Systemic drug of choice but off label • This is rubbed in the hair coat can be additionally applied in and allowed to soak for two the times between the more hours. labour intensive oil soaks.

16 Cyclosporine mechanisms Ketoconazole and cyclosporine • The metabolism and excretion is an active process . Pumping of the drug through the cell membrane via microsomal cytochrome P-450 . Ketoconazole actively competes for cytochrome P-450, increasing blood levels of cyclosporine. • The effect of ketoconazole on cyclosporine blood levels is dose dependent. Ketoconazole at 4.7mg/kg SID has been shown to reduce cyclosporine dose rates needed for steady blood levels by average of 38% while doses of 13.6mg/kg SID reduced cyclosporine doses by 75%. • There is considerable individual variation. . • Clear clinical protocols using ketoconazole and other agents to reduce cost are yet to be defined but many authors recommend the use of ketoconazole at 10mg/kg SID, given concurrently with or just before cyclosporine, 2mg/kg (indicative dose). • The use of ketoconazole in the off-label manner has benefits in reducing Malassezia colonization but patients should be monitored for adverse effects, especially hepatitis.

Other systemic therapies for Thank you sebaceous adenitis Questions and discussion References available on request • Retinoids - $$$ and teratogenicity • Vitamin A • Essential fatty acid therapy – Omega 3/6 - anti-inflammatory – Linoleic acid – restoring barrier • (Pulse?) antimicrobial therapy

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