Looking for Success in Dermatology Consultations

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LOOKING FOR SUCCESS

IN DERMATOLOGY Consultations Looking for SUCCESS in Dermatology Consultations

Diagnostic protocol for skin disorders Dr. Carmen Lorente Méndez

Looking for Success in Dermatology Consultations Diagnostic protocol for skin disorders This practical text on small animal dermatology provides the knowledge necessary to successfully diagnose and treat the most common skin diseases, which can account for up to 90% of veterinary consultations. This information is presented together with numerous images as well as a large number of diagnostic algorithms, which add to the practical value of the book.

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TARGET AUDIENCE:

✱ Small animal vets.

Dermatology ✱ Veterinary students FORMAT: 22 × 28 cm NUMBER OF PAGES: 160 NUMBER OF IMAGES: 350 BINDING: hardcover ISBN: 978-84-18020-54-4 PUBLISHING DATE: June 2020

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Author CARMEN LORENTE MÉNDEZ Carmen earned her degree and PhD in veterinary medicine at the Complutense University of Madrid (1988 and 2005). She is recognised by the European Board of Veterinary Specialisation (EBVS) as a European Specialist in Veterinary Dermatology. Dr Lorente is also a Founding Diplomate in Dermatology of the European College of Veterinary Dermatology (ECVD). She currently reconciles her clinical work and duties as the director of Adervet with her position as an international consultant in dermatology at Laboklin.

KEY FEATURES:

➜ Very helpful decision-making tool for day-to-day dermatology consultations. ➜ Clear, well-structured content provides easily referenced information. ➜ Includes diagnostic algorithms and multiple images to illustrate the processes, as well as practical treatment guidelines. ➜ Easy to read and intended for use in clinical practice.

Presentation of the book The skin is the body’s largest organ and practically the most visible, consequently skin diseases are very patent and can cause owners a lot of concern. They can also affect the patient’s quality of life or could be a reflection of potentially life-threatening processes. The observable clinical manifestations are often due to very diverse aetiologies, so a methodical approach, including a thorough differential diagnosis, is therefore essential to gradually rule out potential causes using the most suitable tests and analyses.

In this manual, Carmen Lorente, a renowned specialist in veterinary dermatology, guides us along the right path to achieve successful dermatology consultations. To this end, she presents a work with great clinical application that is perfectly organised and full of highly visual content thanks to a plethora of images, algorithms, information boxes, tables, and diagrams. The end result is a clear explanation of the diagnosis and treatment of the most common skin diseases to affect cats and dogs, which allows readers to get the most from its content.

Looking for Success in Dermatology Consultations: Diagnostic protocol for skin disorders

The author Carmen Lorente Méndez Carmen Lorente Méndez was awarded her degree (1988) and PhD (2005) in veterinary medicine by the Complutense University of Madrid. She is a European Specialist in Veterinary Dermatology (EBVS®) and a diplomate in dermatology of the European College of Veterinary Dermatology (ECVD).

She is a full member of the European Society of Veterinary Dermatology (ESVD), a member of the International Society of Veterinary Dermatopathology (ISVD), the European College of Veterinary Dermatology (ECVD), the Madrid Association of Companion Animal Veterinary Medicine (AMVAC), and the Spanish Association of Small Animal Specialists (AVEPA). She is a member of the Scientific Committee of AMVAC and of AVEPA’s specialist dermatology group GEDA).

She has spoken at numerous conferences, courses, seminars, and workshops, and has authored many articles in national and international publications.

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She began her professional career by founding the Cercedilla veterinary clinic in 1989, where she worked until 2002. In 2000 she moved to Valencia to work as an associate professor at the Faculty of Veterinary Medicine of the CEU Cardenal Herrera University and the head of the dermatology service of the Veterinary Teaching Hospital of the CEU Cardenal Herrera University. In 2007 she returned to Madrid and founded the Adervet veterinary dermatology centre, which she continues to manage. From 2007 to 2009, she combined her work in Adervet with her position as head of internal medicine and dermatology at the Veterinary Teaching Hospital of Alfonso X el Sabio University. She has worked as a consultant for multiple pharmaceutical laboratories and as a dermatopathologist in several laboratories. She currently combines her clinical practice and her directorship of Adervet with her work as an international dermatology consultant at Laboklin.

Table of contents 1. Introduction Dermatology consultation Seeking quality: the theory of simplicity and excellence Theory of excellence The theory of simplicity

2. The search for relevant information Anamnesis: the patient’s voice Anamnesis script

Dermatological examination: collecting objective information Introduction Lesion type

3. Joining the pieces to solve the diagnostic puzzle Diagnostic algorithm: differential diagnoses accordingto the dermatological pattern The difficulty and importance of defining the dermatological pattern Diagnostic algorithm for the pruritic pattern in dogs Diagnostic algorithm for the alopecic pattern in dogs Diagnostic algorithm for the pustular pattern in dogs Diagnostic algorithm for keratoseborrhoeic disorders in dogs Diagnostic algorithm for the erosive–ulcerative pattern in dogs Diagnostic algorithm for the nodular pattern in dogs Diagnostic algorithm for pigmentary alterations

4. A practical guide to dermatological treatments Treatment in dermatology Topical treatment Treatment of ectoparasitic conditions Treatment of pruritus Antibiotic therapy in dermatology

Recommended reading

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LOOKING FOR SUCCESS

IN DERMATOLOGY Consultations Diagnostic protocol for skin disorders Dr. Carmen Lorente Méndez

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DIAGNOSTIC ALGORITHM FOR THE ALOPECIC PATTERN IN DOGS Algorithm for the diagnosis of alopecia Patient with alopecia

Is there primary pruritus?

No

Yes

Follow the diagnostic algorithm for the pruritic pattern (p. 58)

Evaluate the presence of bacterial folliculitis, demodicosis, or dermatophytosis

Diagnostic tests

No

Diagnosis

Yes

Establish the appropriate treatment

Determine the type of alopecia

Focal or multifocal alopecia

Symmetrical or diffuse alopecia

Patchy-to-diffuse alopecia Pyoderma

Noninflammatory alopecia: ■ Alopecia areata ■ Vaccine or post-injection panniculitis ■ Postclipping alopecia ■ Cicatricial alopecia ■ Traction alopecia ■ Immune-mediated mural folliculitis

Alopecia associated with other lesions (erosive–ulcerative pattern): ■ Ischaemic dermatopathies ■ Leishmaniasis ■ Drug reaction

Endocrine diseases: ■ Hypothyroidism ■ Hyperadrenocorticism ■ Sex hormone abnormalities

■ ■ ■ ■ ■ ■ ■ ■

Alopecia X Cyclic flank alopecia Congenital alopecia or hypotrichosis Telogen effluvium Anagen defluxion Pattern baldness Follicular dysplasia Neoplasia

Associated with hair colour: ■ Colourdilution alopecia ■ Black hair follicular dysplasia

Associated with other lesions (keratoseborrhoeic disorders): ■ Sebaceous adenitis ■ Leishmaniasis ■ Epitheliotropic lymphoma

JOINING THE PIECES TO SOLVE THE DIAGNOSTIC PUZZLE DIAGNOSTIC ALGORITHM FOR THE ALOPECIC PATTERN IN DOGS

The description of the lesion and its distribution, and whether or not it is associated with inflammation, helps to better define the dermatological pattern and consequently determine the differential diagnoses compatible with the condition (e.g. generalised multifocal alopecic dermatitis, circumscribed complete alopecia (6 mm) on the back of the head, noninflammatory symmetrical flank alopecia).

While the aetiology of the diseases that involve alopecia is highly varied, the following general forms can be distinguished: 1. Traumatic alopecia, caused by scratching (pruritic pattern) 2. Alopecia associated with inflammation of the hair follicle or folliculitis 3. Alopecia associated with arrest of the follicular cycle 4. Alopecia due to congenital or acquired genetic defects

STEP 2. EVALUATE THE POSSIBLE PRESENCE OF PYODERMA, DEMODICOSIS, AND DERMATOPHYTOSIS Regardless of the type of alopecia, the following should always be included in the differential diagnosis: ■ Bacterial folliculitis (pyoderma) (Figs. 2.1–2.6) ■ Demodicosis (Figs. 3.1–3.8) ■ Dermatophytosis (Figs. 4.1–4.5) Although all are indicative of inflammatory conditions, the clinical picture can vary greatly, ranging from mild folliculitis to severe folliculitis–furunculosis. It is therefore necessary to perform the relevant tests to confirm or rule out each condition.

STEP 1. DETERMINE IF THE ALOPECIA IS OF TRAUMATIC ORIGIN Scratching is a very common cause of alopecia. This type of alopecia should be ascribed to the pruritic pattern, not the alopecic pattern.

When dealing with patients with alopecia we must first determine whether there is primary pruritus.

■ If the answer is yes: follow the algorithm for the pruritic pattern (p. 58). We must establish whether the alopecia is truly due to trauma secondary to pruritus, or whether the pruritus is secondary to the condition that has caused the alopecia.

The anamnesis and the results of the examination can help determine which of the two conditions is primary. The presence of hair shaft fractures on trichography also supports this assumption (Fig. 1).

■ If the answer is no: follow the algorithm for the alopecic pattern.

!

Primary pruritus → continue with the algorithm corresponding to the pruritic pattern.

Primary alopecia → continue with the algorithm corresponding to the alopecic pattern.

It is not always easy to determine which came first, the pruritus or the alopecia. In case of doubt, take both patterns into consideration.

FIGURE 1. Traumatic alopecia of the pinnae, face, and limbs.

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2.1

2.2

2.3

2.4

2.5

2.6 FIGURE 2.1. Diffuse alopecic dermatitis on the back of the trunk in a patient with bacterial folliculitis.

FIGURE 2.2. Alopecic multifocal dermatitis associated with scaling in a patient with pyoderma.

FIGURE 2.3. Diffuse alopecia in a patient with bacterial folliculitis.

FIGURE 2.4. Diffuse partial alopecia on the thigh of a patient with bacterial folliculitis.

FIGURE 2.5. Crusting multifocal alopecia in a Yorkshire Terrier with pyoderma.

FIGURE 2.6. Moth-eaten alopecia associated with bacterial folliculitis

BACTERIAL FOLLICULITIS Bacterial folliculitis is the infection of the hair follicle by bacteria and is probably the most common form of canine pyoderma.

The most characteristic lesion is alopecia, which is more evident in short-haired animals. In long-haired animals it is more common to observe crusting or scaling lesions that cause matting of the hair and subsequent hair loss. Alopecia is often accompanied by pruritus.

The pattern and distribution of alopecia lesions can vary.

Moreover, these lesions can closely resemble alopecia associated with dermatophytosis or demodicosis. These three conditions should therefore be included in the differential diagnosis of

alopecia. Diagnosis can be complicated in the absence of pustular lesions. If these lesions are present, cytology can reveal the presence of cocci inside neutrophils, confirming diagnosis of the infection. In these cases diagnosis is based on the clinical presentation, ruling out demodicosis and dermatophytosis, and the patient’s response to antibiotic treatment. Biopsy can confirm the diagnosis, but is not the test of choice.

Pyoderma is generally secondary to another disease. It is therefore necessary to investigate and control possible underlying diseases (the most common of which are atopic dermatitis and endocrine disease) in order to prevent relapse. In shorthaired animals bacterial folliculitis can occur spontaneously.

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CANINE DEMODICOSIS Canine demodicosis is a common and noncontagious parasitic dermatosis caused by Demodex canis, a mite with an elongated abdomen and short legs. This parasite is part of the normal

fauna of the skin of dogs and its biological cycle occurs completely in the skin, where it lives in the hair follicles and sebaceous glands and feeds on cell debris. Animals acquire the

3.1

3.2

3.3

3.4

3.5

3.7

3.6

FIGURE 3.1. Foci of alopecia in a Pug with juvenile demodicosis.

FIGURE 3.2. Diffuse partial alopecia in a Dalmatian with generalised juvenile demodicosis. Alopecia with erythema in young dogs is highly indicative of demodicosis.

FIGURE 3.3. Localised complete alopecia in a patient with demodicosis.

Note the condition of the follicles, the micronodular appearance of the skin, and the presence of comedones.

FIGURE 3.4. Generalised complete alopecia in a patient with generalised juvenile demodicosis.

3.8

FIGURE 3.5. Large foci of multifocal alopecia in a patient with demodicosis.

FIGURE 3.6. Perioral alopecic dermatitis with hyperpigmentation, acanthosis, and scaling in a dog with adult demodicosis.

FIGURE 3.7. Multifocal alopecia in an American Pit Bull Terrier with demodicosis.

FIGURE 3.8. Diffuse alopecia with hyperpigmentation in a patient with demodicosis.

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parasite during the first 2–3 days of life through intimate contact with the mother (e.g. during suckling).

Demodicosis is a multifactorial disorder involving genetic, immune, bacterial, and parasitic factors.

Clinically, demodicosis is an alopecic disease. While pruritus is not observed initially, progression results in hair follicle destruction and bacterial complications, giving rise to pruritus and keratoseborrhoeic disorders.

Two main clinical presentations are described: ■ Localised canine demodicosis: defined as the presence of less than 5 alopecic lesions. This form is considered a mild disease and treatment is not advised (self-resolving in 90 % of cases). In the 10 % of cases in which localised demodicosis becomes generalised, treatment is essential.

■ Generalised canine demodicosis: defined as the presence of five or more circular alopecic lesions, lesions affecting an entire body region, pododermatitis, or secondary pyoderma.

It is a serious and sometimes frustrating disease. This condition is sometimes referred to as “red mange”, owing to the appearance early in the disease of alopecia and erythema.

Many patients with demodicosis present with intense scaling followed by the formation of scaling plaques and crusts.

Bacterial complication is also common. Lesions can initially appear on the face, in particular the periocular and perioral region, subsequently spreading to the trunk and limbs. In patients with involvement of the paws of the forelimbs and/or hindlimbs lesion resolution may require treatment for several months.

Juvenile demodicosis, which affects puppies (3–18 months of age), involves genetic factors and an immature immune system.

If demodicosis first appears in animals aged 4 years or more it is referred to as adult demodicosis. In these cases it can be secondary to a debilitating disease or immunosuppression (e.g. hyperadrenocorticism, hypothyroidism, cancer, corticotherapy, chemotherapy).

DERMATOPHYTOSIS Dermatophytosis is the infection of the hair by dermatophytes, keratophilic fungi that consume keratin. The most frequently isolated species are Microsporum canis, Microsporum gypseum, and Trichophyton mentagrophytes. It is a contagious disease, affecting other animals and humans (zoonosis). Transmission occurs directly or through contact with items contaminated with fungal spores.

The characteristic lesion is an area of circumscribed alopecia that spreads centrifugally. Erythema and scaly crusts may accompany the alopecia, which can be focal, multifocal, or generalised.

Cats are more prone to dermatophyte infections, although certain dog breeds (e.g. Yorkshire Terrier) are predisposed to this disease. These infections more commonly affect young, older, and immunocompromised animals.

Dermatophytosis is probably an overdiagnosed disease. It is very important to establish a definitive diagnosis before instituting treatment, since the drugs used can have side effects and long treatments (>1 month) are usually required.

Tests to evaluate the presence of pyoderma, demodicosis, or dermatophytosis Wood’s lamp to detect fluorescence associated with dermatophyte infection.

Trichography, which is used to: ■

Evaluate the presence of follicular casts or scaling around the hair.

■

Evaluate the presence of Demodex.

■

Evaluate the presence of unstructured hair shafts harbouring fungal elements.

Superficial skin scraping: to identify Demodex (trichography is preferable).

Cytology: to identify inflammatory cells and infectious agents in patients that present other lesions such as pustules, crusts, or epidermal collarettes.

Dermatophyte culture: if dermatophytosis is suspected.

Biopsy: biopsy is not the test of choice for the diagnosis of these conditions, which can be diagnosed using an appropriate clinical approach and the aforementioned tests.

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4.1

4.3

4.2

4.4 4.5 FIGURE 4.1. Focal alopecia and erythema in a patient with dermatophytosis.

FIGURE 4.2. Multifocal alopecia in a patient with dermatophytosis. Well-circumscribed foci of alopecia and scaling can be observed.

FIGURE 4.3. Focal inflammatory alopecia caused by dermatophytes. The skin has a granular appearance associated with folliculitis and abundant scaling.

FIGURE 4.4. Multifocal alopecia in a patient with dermatophytosis (early-stage lesions).

FIGURE 4.5. Scaling–crusting alopecia in a Yorkshire Terrier with dermatophytosis.

STEP 3. EVALUATE OTHER DIFFERENTIAL DIAGNOSES Depending on the characteristics of the alopecia, several other diseases must be considered.

Differential diagnoses according to the features of the alopecia ■

Focal or multifocal alopecia ■

■

■

Noninflammatory alopecia:

Symmetrical or diffuse alopecia ■

Endocrine diseases: hypothyroidism, hyperadrenocorticism, sex hormone abnormalities

■

Alopecia areata

■

Vaccine or post-injection panniculitis

■

Postclipping alopecia

■

Alopecia X

■

Cicatricial alopecia

■

Cyclic alopecia

■

Traction alopecia

■

Congenital alopecia or hypotrichosis

■

Immune-mediated mural folliculitis

■

Pattern baldness

Alopecia associated with other lesions:

■

Telogen effluvium

■

Ischaemic dermatopathies

■

Anagen defluxion

■

Leishmaniasis

■

Follicular dysplasias

■

Drug reaction

■

Patchy-to-diffuse alopecia ■

Colour-dilution alopecia

■

Black hair follicular dysplasia

■

Sebaceous adenitis

■

Leishmaniasis

■

Epitheliotropic lymphoma

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FOCAL OR MULTIFOCAL ALOPECIA or multifocal alopecia ➜ Focal Noninflammatory alopecia:

■

Symmetrical or diffuse alopecia

■

Endocrine diseases: hypothyroidism, hyperadrenocorticism, sex hormone abnormalities

■ ■ ■ ■ ■ ■ ■

Alopecia X

■

■

!

■

Alopecia areata

■

Vaccine or post-injection panniculitis

■

Postclipping alopecia

■

Cicatricial alopecia

■

Traction alopecia

■

Immune-mediated mural folliculitis

Alopecia associated with other lesions: ■

Ischaemic dermatopathies

■

Leishmaniasis

■

Drug reaction

■

Cyclic alopecia Congenital alopecia or hypotrichosis Pattern baldness Telogen effluvium Anagen defluxion Follicular dysplasias

Patchy-to-diffuse alopecia

■ ■ ■ ■ ■

Colour-dilution alopecia Black hair follicular dysplasia Sebaceous adenitis Leishmaniasis Epitheliotropic lymphoma

This is the most typical clinical presentation of bacterial folliculitis, demodicosis, and dermatophytosis.

FIGURE 5. Postclipping alopecia in an English Bulldog. Although typical of Nordic breeds, other breeds can also be affected. Some strands of hair have grown in the affected area.

Noninflammatory alopecia In patients with noninflammatory alopecia the differential diagnosis should include the following: ■ Alopecia areata: while the aetiology is poorly understood, a significant immunological component is suspected. Destruction of follicular bulbs gives rise to focal, regional, multifocal, or (in rare cases) generalised noninflammatory alopecia.

The prognosis, in terms of recovery of the hair, is uncertain; while hair can regrow this can take from months to years.

When the hair does grow back the colour may have changed to white, although this has no implications for the animal’s health. Diagnosis requires biopsy.

■ Vaccine or post-injection panniculitis–vasculitis: circumscribed alopecia associated with the site of inoculation of a vaccine (typically the rabies vaccine) or an injectable agent.

This condition is characterised by inflammation of the adipose panniculus. Although no other lesions may be evident, associated lesions include nodules, ulceration, and oily secretion. Diagnosis is established based on the patient’s clinical history and the results of the dermatological examination, having first ruled out other diseases. Confirmation of the diagnosis requires biopsy.

■

■

■

■

Postclipping alopecia: this is a localised form of alopecia caused by shaving or clipping of the hair in a specific area.

Nordic breeds are predisposed owing to the peculiar characteristics of their follicular cycle. Hair may take several months to regrow in shaved areas. This is an aesthetic defect and does not affect the health of the animal. Diagnosis is established based on the patient’s clinical history and the results of the dermatological examination, having first ruled out other diseases (Fig. 5).

Cicatricial alopecia: alopecia associated with trauma or recovery from severe, deep inflammation. This form of alopecia can be diagnosed based on the animal’s clinical history and the results of the dermatological examination (Figs. 6.1 and 6.2).

Traction alopecia: circumscribed alopecia caused by ischaemia due to the use of hair ties or ornamental hair styles. This form of alopecia usually results in a permanent aesthetic defect. It can be diagnosed based on the animal’s clinical history and the results of the dermatological examination.

Immune-mediated mural folliculitis: granulomatous mural folliculitis, eosinophilic mural folliculitis, and mucinous mural folliculitis. These are rare conditions that are clinically characterised by alopecia, which is usually noninflammatory. Diagnosis requires biopsy.

JOINING THE PIECES TO SOLVE THE DIAGNOSTIC PUZZLE DIAGNOSTIC ALGORITHM FOR THE ALOPECIC PATTERN IN DOGS

FIGURE 6.1. Cicatricial alopecia. The existing scar on the skin is evident. The patient’s medical history indicates previous trauma.

FIGURE 6.2. Cicatricial alopecia of the face caused by severe pre-existing lesions.

This type of alopecia usually persists after severe juvenile cellulitis lesions or ischaemic dermatopathies.

FIGURE 7. Cicatricial alopecia with crusts in a patient with ischaemic dermatopathy.

Ulcerative and crusted lesions are observed in the acute phase.

Alopecia associated with other lesions These usually correspond to the erosive-ulcerative dermatological pattern (p. 106): ■ Ischaemic dermatopathies (Fig. 7) ■ Leishmaniasis ■ Drug reaction

SYMMETRICAL OR DIFFUSE ALOPECIA ■

Focal or multifocal alopecia

■

■

Noninflammatory alopecia:

■ ■

Alopecia areata

■ ■ ■ ■

Postclipping alopecia

or diffuse ➜Symmetrical alopecia

Vaccine or post-injection panniculitis

■

Endocrine diseases: hypothyroidism, hyperadrenocorticism, sex hormone abnormalities

■

Alopecia X

■

Cyclic alopecia

■

Congenital alopecia or hypotrichosis

■

Pattern baldness

■

Telogen effluvium

■

Anagen defluxion

■

Follicular dysplasias

Cicatricial alopecia Traction alopecia Immune-mediated mural folliculitis

Alopecia associated with other lesions:

■ ■ ■

Ischaemic dermatopathies Leishmaniasis Drug reaction

■

Patchy-to-diffuse alopecia

■ ■ ■ ■ ■

Colour-dilution alopecia Black hair follicular dysplasia Sebaceous adenitis Leishmaniasis Epitheliotropic lymphoma

The diagnostic protocol is based on the following tests: ■ General blood test and endocrine functionality tests (according to the differential diagnosis) ■ Abdominal ultrasound

Endocrinopathies In the context of endocrinopathies, alopecia involves follicular arrest, which is significantly influenced by certain hormones.

Alopecia manifests when new hair fails to regrow after hair loss during the telogen phase. Alopecia is progressive and tends to mainly affect the trunk. The limbs and head are not usually affected. Hair is initially lost in areas exposed to greater trauma or friction, such as the neck or the caudal third. Hyperpigmentation of the skin and recurrent pyoderma are common. Skin changes may be the first evident sign, but are typically accompanied by other general clinical signs characteristic of the specific disease.

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Hypothyroidism Hypothyroidism is the most frequent endocrine disease of dogs and usually presents with cutaneous manifestations, even before the appearance of other systemic signs. Lesions include poor quality hair and progressive bilateral alopecia that usually initially affects areas exposed to greater friction, such as the neck, pressure points, and the flanks (Fig. 8.1). Hyperpigmentation, acanthosis, and hyperkeratosis of alopecic areas are

common, as are comedones and seborrhoea. Hair loss from the tail (“rat tail”) and the nasal bridge is also described (Figs. 8.2 and 8.3). In many cases secondary infections develop, while in others pyoderma may be the only evident clinical sign. Secondary infections are related to functional impairment of the skin barrier and the immune system. Glycosaminoglycans accumulate in the dermis, in some cases leading to myxoedema, which manifests clinically as a “sad” facial expression.

Clinical signs of hypothyroidism Because thyroid hormones have a marked influence on all systems, hypothyroidism gives rise to a wide variety of clinical signs.

General clinical signs

Lethargy, mental depression, weight gain, intolerance to exercise and cold, hypothermia. Myxoedema coma.

Dermatological presentation

Alopecia, hyperpigmentation, seborrhoea, comedones, recurrent pyoderma. Alopecia of the tail (“rat tail”) or nasal bridge. Patients with advanced hypothyroidism may have a “sad” facial expression, caused by myxoedema.

Neurological signs

Weakness, ataxia, abnormal gait and reflexes, cerebral dysfunction, decreased spinal reflexes, cranial nerve dysfunction.

Cardiovascular signs

Tests for the diagnosis of hypothyroidism Although very frequent, hypothyroidism is overdiagnosed. The clinical signs are very nonspecific and are shared with many other diseases.

The presence of low levels of thyroid hormones (thyroxine or T4) is very common in sick animals, and can lead to diagnostic errors. T4 and TSH (thyrotropin) levels should always be evaluated to establish a correct diagnosis, and even then a definitive diagnosis may not be established.

Between 10 % and 20 % of animals with T4 values <12 nmol/l (1 μg/dl) are not hypothyroid.

Assumptions that can be made based on the results (see algorithm for the diagnosis of hypothyroidism): ■

If total T4 (TT4) and TSH are in the reference range: the animal is euthyroid.

■

If TT4 levels are low and TSH levels are normal: the patient does not have a thyroid disease, but has so-called euthyroid sick syndrome.

■

If TT4 levels are low and TSH levels are high and no recent treatment has been administered: the animal is hypothyroid.

■

If TT4 levels are normal and TSH levels are high: the animal may be recovering from a nonthyroid disease or drug treatment.

■

In general, if TSH levels are >0.6 ng/ml, hypothyroidism can be confirmed. Values >0.5 ng/ml are highly indicative of hypothyroidism.

Bradycardia.

Reproductive signs

Irregular oestrous cycles, silent heat, spontaneous abortion, galactorrhea.

Ocular signs

Blepharoptosis, keratoconjunctivitis sicca, corneal lipidosis, retinal detachment, uveitis, glaucoma.

Gastrointestinal signs

Constipation, diarrhoea.

Muscle signs

Myopathy, megaoesophagus, laryngeal paralysis.

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Algorithm for the diagnosis of hypothyroidism

Suspicion of hypothyroidism based on medical history and clinical signs observed

Haematology and serum biochemistry to rule out other compatible systemic diseases In patients with hypothyroidism hypercholesterolaemia, anaemia, and increases in liver enzymes can be observed

T4 and TSH measurement

T4 <12 nmol/l 80–90 % hypothyroidism

TSH <0.5 ng/ml

TSH >0.5 ng/ml

Hypothyroid patient

T4= 12–18 nmol/l

TSH <0.5 ng/ml

TSH >0.6 ng/ml Hypothyroidism

T4 >19 nmol/l

TSH <0.5 ng/ml

Hypothyroid patient

Euthyroid sick syndrome

Euthyroid sick syndrome

Recent medication

Recent medication

Hypothyroidism in the initial phase?

Hypothyroidism unlikely *

TSH >0.5 ng/ml

Recovery from a nonthyroid disease or drug treatment

Search for another cause

* If the results indicate that hypothyroidism is unlikely but no other causes are found and suspicion persists, the analysis should be repeated 3 months later.

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FIGURE 8.1. Symmetrical or generalised alopecia of the trunk.

FIGURE 8.2. Alopecia of the nasal bridge. This may appear in patients with hypothyroidism.

Note the dry, dull appearance of the haircoat.

FIGURE 8.3. Symmetrical alopecia and sparse, dull, easily plucked hair. This presentation is typical of endocrine diseases.

Hyperadrenocorticism The dermatological changes observed in patients with hyperadrenocorticism are a consequence of high levels of glucocorticoids, which inhibit fibroblast proliferation and collagen production and cause alterations in cornification, arrest of the follicular cycle, and atrophy of skin appendages. Cutaneous manifestations include cutaneous atrophy with alopecia, thin skin, susceptibility to capillary bleeding, impaired or delayed healing, and predisposition to secondary infections due to

FIGURE 9.1. Calcinosis cutis is a characteristic lesion of hyperadrenocorticism, especially iatrogenic forms.

immunosuppression. Comedones are very common, and the skin appears thin, like cigarette paper, making the blood vessels easily visible. The skin may also be dry and itchy. Calcinosis cutis, although infrequent, is highly characteristic of hyperadrenocorticism (Figs. 9.1 and 9.2).

Hyperadrenocorticism can be spontaneous, caused by micro- or macroadenomas of the pituitary gland or adrenal gland tumours, or iatrogenic (Fig. 9.3).

FIGURE 9.2. Alopecia and calcinosis cutis lesions in a patient with hyperadrenocorticism.

FIGURE 9.3. Noninflammatory alopecia associated with the use of topical glucocorticoids.

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