3rd MyVet Hospital Group Symposium - Inanda Vetsinandavets.com/wp-content/uploads/2020/02/MyVet 3rd Annual Sym… · which time he completed the fast-track MBA certificate and diploma

VETERINARY SYMPOSIUM 2020

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3rd MyVet Hospital Group

Symposium

Makaranga Lodge

09 February 2020 Editors: Dr Anthony Zambelli & Ms Amanda Shaw

Master of Ceremonies: Dr Kenneth Joubert


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Dear Colleagues, Welcome to our third annual veterinary symposium. My team of dedicated staff, led by Ms Amanda Shaw, has assembled a useful, coherent and I am sure you will find, enjoyable series of “upskills” for all attendees. Every year we analyse the feedback you give us, to select topics that you want to learn about. There’s obviously more than we can cover in one day, so the choices are very difficult. This year we have chosen to focus on the head, neck, skin and endocrinology – both medical and surgical. Dr Kenneth Joubert will be our MC this year, guiding us through the topics of the day, and welcoming a new speaker – Dr Sara Boyd, a specialist surgeon with over two decades of experience – who has joined our group. We remain, as ever, dedicated as a group, and with our visiting consultants, to assisting your practice to extend your service and veterinary capabilities. Any practice in KZN should be able offer its clients and patients some hope, help or treatment, that is already available to humans – even without hiring new staff or investing in expensive equipment. We are here to be an extension of your practice, and we strive to constantly improve our service offering to you, and with you. The veterinary healthcare industry in SA is under enormous stress at the moment, as well as having increasingly demanding clients presenting us with a progressively first-world (aging) pet population with more chronic illnesses, as well as some local combinations such as infectious diseases and skin cancer. We must rise to these challenges using the skills and tools available to us. Our corporate sponsors make this sort of learning opportunity possible, provide aftercare and tech support, and the products we use, to achieve our goals – they make us more versatile, flexible and responsive to our pets’ needs. Please thank the representatives of Royal Canin, Virbac, Zoetis and IDEXX when you see them, and interact with their staff on the day, to understand how vets and our support industries can work together. I particularly want to thank Ms Shaw for months of planning and effort, without which this would not be possible; Dr Joubert for chairing the sessions; Drs Greenberg, Pimosenco, Ruiz and Boyd, for their time spent on developing lectures and notes; my staff for assisting on the day; Makaranga Lodge for hosting us yet again; and all of you for supporting us, working with us, telling us what you need, and helping us grow from a small practice of 6, to a group of over 50 staff. We look forward to many years collaboration for the betterment of all our mutual clients, our profession and the pet healthcare industry. Welcome, with sincere thanks Anthony Zambelli Director, MyVet Hospital Group Inanda Veterinary Specialist Centre


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Agenda 09.00 - 9.30am - Arrival and Registration

“Practical Tips and Techniques for Surgery of the Head: Ear, Nose and Throat” – pg 9

Dr Sara Boyd

“Oral Tumours: From diagnosis to Treatment. What to Expect.” – pg 17

Dr Jose Ruiz

~Tea~

“Secrets to Success in Dermatology”– pg 33

Dr Anthony Zambelli

“Case Based Approach to Endocrine Conditions” – pg 51

Dr Arina Pimosenco

Royal Canin’s Gastrointestinal Range: What to Use and When

Dr Michelle Harman

~Lunch~

“Canine Behaviour Disorders Influenced by Owners & Environment” – pg 63

Dr Melvyn Greenberg

“How Do We Become the Best Vet/Vet Nurse We Can be?” – pg 67

Dr Kenneth Joubert

16.05pm – Closing


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Speakers

Dr. Sara Boyd BVsc MMedVet (Surgery)

Sara was born and grew up in Johannesburg, South Africa. She graduated in 1997 from Onderstepoort Veterinary Faculty with a BVSc. After working in the UK for 2 years, she returned to Onderstepoort as a surgical resident and later, a senior lecturer. She completed her MMVedVet degree in April 2004. She has been an owner and partner in Johannesburg Specialist Veterinary Centre for the past 20 years, prior to going on her own as a consulting Specialist Small Animal Surgeon. Sara is involved in presenting CPD courses both in South Africa and abroad. Her special interests lie in the field of soft tissue and neurosurgery. She remains proficient in the field of Orthopaedics and is one of the few South African surgeons regularly performing TPLO and Canine Cementless Total Hip Replacement. She is married to Mark Boyd and has 3 children.

Dr. José Carlos Almansa Ruiz DVM (Hons) MSc (Vet), Resident, Veterinary Dentistry Member of the Royal College of Veterinary Surgeons

José is originally from Spain. He qualified from the Universidad Complutense de Madrid in 2008. Thereafter he completed his honours degree in dentistry and maxillofacial surgery while working in a busy afterhours hospital in Madrid. In 2009, he relocated to Pretoria where he undertook an internship in dentistry and maxillofacial surgery under Prof. Gerhard Steenkamp for 18 months, while concurrently undertaking an MSc degree. In 2011, he relocated to the UK where he worked in the greater London area working as a general practitioner

and getting referrals in dentistry and maxillofacial surgery from Kent and Surrey areas. In 2012, he started his European Diploma in Veterinary dentistry through the alternative pathway under the supervision of Dr. Lisa Milella, for which he is hoping to submit his credentials in this year. In 2014 he completed the AOVET Course-Masters in Operative Treatment of Craniomaxillofacial Trauma and Reconstruction. In 2015, he moved back to South Africa, this time to Cape Town, where he joined Tygerberg Animal Hospital as a veterinarian with a special interest in Dentistry and Maxillofacial surgery. At the beginning of 2017 he moved back to Pretoria where he joined VetDentSA. He is a consultant for Inanda Veterinary Hospital in Durban and Tygerberg Animal Hospital in Cape Town. José has a special interest in Wildlife Dentistry and Maxillofacial surgery where he is an active researcher. He has presented in national and international congresses.


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Dr. Kenneth Joubert BVSc MMed Vet (Anaes)

Kenneth graduated with a BVSc from The University of Pretoria in 1995. After graduating he joined small animal practice in Johannesburg for 2 years before returning to the University of Pretoria. In 2000 he obtained a MMedVet (Anaes) and held the position of senior lecturer in anaesthesiology at the university. In 2004 he left the university to re-join private practice before starting his own referral practice in anaesthesiology, pain management and critical care. Kenneth has published 37 scientific publications, delivered 80 scientific presentations, delivered 142 continuing education talks, done 14 multimedia presentations, published 39 non-scientific articles, presented 7 course, written one book chapter and attended 66 congress of continuing education. Kenneth currently holds an extra-ordinary lecturing post in

Pharmacology in the department of Paraclinical Sciences at the University of Pretoria and runs a private practice dedicated to anaesthesia, analgesia and intensive care. He has regularly examined students in pharmacology, anaesthesiology and clinical studies. Kenneth has and is currently involved in the supervision of 4 students. Kenneth has a keen interest in total intravenous anaesthesia, intensive care, ventilation and cardiology. His research interests included non-steroidal anti-inflammatory agents, anaesthetic depth monitoring and total intra-venous anaesthesia. Kenneth chaired the Faculty Ethics Committee (Animal Use and Care Committee) until it was dissolved to form a University based Animal Use and Care Committee. I was then a member of the Senate committee for Research Ethics and Integrity and the Animal Use and Care Committee of the University of Pretoria. Kenneth currently serves on the AUCC (RECA) Nelson Mandela Metropolitan University and the Ethical Review Group of the AVA. He is also a member of the Education Committee and the Standard Committee of the South African Veterinary Council. In 2019 he joined Inanda Veterinary Hospital.

Dr. Arina Pimosenco DVM cum laude BVSc(Hons)

Arina qualified as a veterinary surgeon cum laude in 2007 in Eastern Europe. She has worked in Johannesburg suburbs mostly with small animals from 2009 to 2016. She also completed her Honours Degree in Veterinary Medicine, Clinical Pathology and Radiology in 2014 from Onderstepoort. Arina likes challenging diagnostics and endless opportunities of veterinary medicine to help our furry family members. She joined Inanda Veterinary team in May 2016 and has been privileged to work for Veterinary Medicine Specialist Dr Anthony Zambelli, where she continues professional development in the veterinary field of choice. Arina is currently doing Advanced Practitioner course in Small Animal Medicine with European School of Veterinary Postgraduate Studies (ESVPS) and Harper Adams University in UK.


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Dr. Melvyn Greenberg BVSc

Melvyn Qualified with B.V.Sc. at Onderstepoort in1973, receiving the Pfizer Clinics Prize in final year. He has been a Small animal private practitioner since January 1974 with a special interest in animal behaviour from the outset. He received the Boswell Award from the SAVA in 1995 and the Rick Massey Trophy from the Witwatersrand Branch of the SAVA in 1999 for outstanding service to the veterinary profession, and he co-founded the Animal Behaviour Consultants Group in 1994 due to the plethora of behaviour disorders amongst pets, hoping that all qualifying consultants “talk the same language”. He also hosted a Pet Care line, initially as Capitol Vet on Capitol Radio, then as Dr Platzhund on Radio 702 (and later Cape talk) over a period of 22 years – borne, initially, out of the need to advise the public on how to prevent dogs from biting people. He was the first veterinarian to conduct puppy socialisation classes at the veterinary practice level, and then helped promote it nationwide. He is the author of Dr Platzhund’s Pet Pointers, published in 1998 containing close to two dozen common pet-related problems but has also written thousands of articles in hundreds of local and national printed media, on behaviour issues, over 33 years He has been an invited guest on animal related issues on many television programmes throughout the country which included a personal 13 -episode series The Creature Feature. He was an expert witness in 18 serious court cases involving canine aggression causing human injury, mutilation or death, and was initially a resident advisor to Mutual & Federal and then to the legal fraternity at large.

Dr. Anthony Zambelli BSc(Hons) BVSc DiplSnrMgmt MMedVet(Med) (cum laude)

Anthony qualified as a vet in 1998, concurrently completing the intercalated honours degree in Zoology from Wits in 1995. After 5 years in private practice in the UK, during which time he completed the fast-track MBA certificate and diploma courses in senior management through the Open University, he returned to SA to undertake specialist training and a lectureship at OP. He completed his MMedVet(Med) in 2006, graduating cum laude in 2008. He started in private practice in 2006, before branching out to start up Inanda Vets in 2011. With Dan Ohad and Remo Lobetti he completed a long term study in Boerboel Cardiomyopathy, as well as a study on hypertriglyceridaemia in Miniature Schnauzers. He is currently a student of UNISA, in his 4th

year of a degree in Chemistry and Archaeology.


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(notes)


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Practical Tips and Techniques for

Surgery of the Head: Ear, Nose and

Throat Dr Sara Boyd BVSc MMed Vet (Surgery)

INTRODUCTION Surgery of the “head” is a very wide based topic, however it encompasses commonly

presenting conditions, many of which can be adequately addressed in a general

practice type set-up. The aim of this talk is to try and provide some practical treatment

tips for these cases; it will cover the principles of surgical ear techniques that are

available, surgery of the external nasal passages and surgery of the oral cavity and

soft tissues of throat. Oral tumours and their treatment does not fall within the scope

of this talk and is addressed as a separate topic in this symposium.

Ear

A large number of conditions that affect the ear do not require surgical intervention;

however, surgery may be required in the presence of severe recurrent ear disease

that is refractory to medical treatment, if condition involves neoplasia or if owner

compliance is lacking. End stage ear canals often require surgical intervention and

three surgical procedures have been well described in the definitive treatment of Otitis

Externa (OE) in both dogs and cats. The aim of all of them is similar: to remove the

source of the infection and to improve ventilation and drainage of the ear canal.

Surgical anatomy: The

external ear canal is a

cartilage tube that

extends from the

external auditory

meatus on the skull to

the external pinnae. It

consists of a short

vertical canal and a

slightly longer horizontal

canal which ends at the

tympanic membrane. It

is lined by epithelium

that is continuous with

the skin and therefore FIGURE 1. SCHEMATIC DIAGRAM OF THE SKULL ANATOMY AND

TYMPANIC BULLA OF THE DOG

https://www.vin.com/apputil/content/defaultadv1.aspx?pId=11268&meta=generic&catId=32737&id=3866520&ind=252&objTypeID=17


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prone to the same conditions and allergies that the skin suffers from. The tympanic

bulla or middle ear lies on the medial aspect of the ear drum and contains the auditory

ossicles. It also has the sympathetic nerve running through it and the hypoglossal

nerve and external carotid artery running directly ventral to it. The facial nerve runs

just caudal and ventral to the external auditory meatus and is very prone to injury

during surgery, especially with chronic ear disease. The last structure that may be

damaged during surgery is the Retroglenoid vein which lies rostral to the tympanic

bulla. This causes significant haemorrhage at the time of surgery but has no long term

ill-effects. In cats the tympanic bulla has two distinct compartments, a larger ventro-

medial one and a smaller dorso-lateral one. The medial portion of the ear canal is the

inner ear which lies in the petrous part of the temporal bone. When this is affected

more serious clinical and vestibular neurological signs may be present.

The most commonly executed surgical procedures for the treatment of chronic Otitis

Externa and media include: a lateral ear canal ablation, vertical ear canal ablation,

ventral bulla osteotomy (VBO) and lastly a total ear canal ablation (TECA) together

with a lateral bulla osteotomy (LBO). This is fondly known as a TECABO!

Lateral Ear Canal Resection: This is the resection of the lateral wall of the vertical ear

canal in order to facilitate air flow and drainage and allow better access to the rest of

the ear canal for topical treatment applications. The modified version where a cartilage

drainage plate is created to prevent hair growth around the opening is known as the

Zepp’s procedure. The procedure, although popular is rarely successful as it often fails

to remove the underlying cause. One exception to this is in the presence of an isolated

lesion on the lateral wall of the vertical canal.

Vertical Ear Canal Ablation: This is similar to the above procedure but requires

dissection and resection of the entire vertical canal. Again, its indications are limited

to those conditions that only affect the vertical canal. It does create a much better

cosmetic appearance than that of a lateral wall resection.

Ventral Bulla Osteotomy: This procedure is designed to provide drainage at the most

ventral portion of the tympanic bulla. The indications are for primary conditions of the

middle ear where an intact ear drum and a normal external ear canal exist and for

failed TECA procedures. It requires technically difficult dissection, especially in the

dog. In cats is the procedure of choice for removing inflammatory polyps and the entire

lining of the tympanic bulla.

Total Ear Canal Ablation and Lateral Bulla Osteotomy: This is a salvage procedure,

but is by far the most effective surgical treatment for end-stage ear canal disease. End

stage ear canals have the following characteristics: hyperplasia of the epithelium,

hypertrophy of the glands, collapse and/or stenosis of the horizontal part of the ear

canal, calcification of the peri-auricular soft tissue. Many of these cases also have a

ruptured tympanic membrane and concurrent otitis media. By removing the entire

lining of both the external ear canal and the tympanic bulla, TECA/LBO provides a

definitive cure for these animals. It is however a complicated procedure with serious


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potential complications if it is performed by someone who is not totally familiar with the

anatomy of this area. Described complications of this surgical procedure include:

fascial nerve palsy, vestibular syndrome, Horner’s syndrome (in cats), chronic

recurrent draining sinus tracts and poor carriage of the external pinnae.

Nose

Many of the nasal and oral issues mentioned above: fall under the category of Upper

Airway Obstruction Syndrome (UAOS) or Brachycephalic Airway Syndrome (BAS)

and refers to a combination of problems causing partial or complete obstruction to the

upper airway. Breeds commonly affected include: English and French Bulldogs,

Boxers, Boston Terriers, Pug and Staffordshire Bull Terriers. These breeds all have

the typically compressed face characterised by an inherited developmental defect

where facial bones grow to normal width, but reduced length. The soft tissues of the

head are not proportionately reduced and are often even redundant. The components

of BAS include: stenotic nares, elongated soft palate, everted laryngeal saccules and

tracheal hypoplasia.

Stenotic nares are visually apparent and easy to diagnose. Observing the external

openings during inspiration, we can clearly see whether there is paradoxical closure

as the animal inspires. Sneezing, inspiratory stridors or mucopurulent discharges are

further clues to stenotic nares. Other causes of nasal obstruction include traumatic,

neoplastic, foreign body inhalation or infectious causes of nasal disease.

Stenotic nares are found frequently in Brachycephalic breeds. Although a minor

component of the syndrome, having insufficient external passage for air causes

animals to open-mouth breathe and increases respiratory flow rates through the rest

of the airway. The surgical repair is not technically demanding, it consists of performing

bilateral wedge naroplasties. It is important that these wedges are sufficiently deep to

open the nares at least 7-10mm into the nasal passages. Fine absorbable suture

material is used to close the defects and haemorrhage is usually easily controlled.

Mouth and Lip Surgery

Many simple reconstructive techniques are available to repair (sometimes substantial)

defects to the nasal and lip region. Resection of tumours is another prime indication

for these types of procedures. Techniques used may be as simple as accurate

anatomical reconstruction or as complicated as lip to lid transposition flaps. During the

presentation, a variety of clinical cases will be used to demonstrate the techniques. At

all times it must be remembered that the lips and mouth are a highly mobile structures

and adequate tension relieving techniques are essential to their success. On the

upside: these oral cavity of blessed with a prolific blood supply, so healing is fast and

patient morbidity low.


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Throat

Staphylectomy is the resection of an elongated soft palate. This is performed via an

oral approach and aims to remove excessive tissue so that the obstruction to the

dorsal glottis is removed. The excessive tissue is clamped and sharply resected. A

monofilament absorbable suture material in a continuous pattern is used to close the

defect. Intraoperative haemorrhage and oedema, as well as the post-operative risks

of dog developing obstruction from the surgery are further causes for concern. More

advanced techniques for resection using laser excision has been performed

successfully, however the equipment needed is expensive and not readily available.

Further upper airway obstruction can be caused by eversion of the laryngeal ventricles

into the opening of the glottis. These ventricles are mucosal diverticulae that are

situated rostal and lateral to the vocal folds. When excessive negative pressure is

experienced within the upper airway, these ventricles tend to evert towards the midline

and become extremely oedematous. They then block the lower half of the airway at

the level of the laryngeal glottis. Many affected animals have a combination of the

above conditions which can lead to a decrease in glottis aperture of as much as 80 to

90%. Surgical correction is straight forward resection of the distal saccules, which is

only hindered by difficulty with visualisation due to caudal position and presence of an

ET tube.

Stabilising the patient in respiratory distress

The classic signs of acute respiratory distress include open mouth, laboured breathing,

cyanosis, abducted forelimbs, restlessness and even collapse. Animals exhibiting

these signs should be handled with care so as not to compromise them any further.

Removing them from their distressed owners and taking them to a cool, quiet

environment where oxygen supplementation can be administered, is the first important

step. Supplementary oxygen can be started immediately. Concurrent hyperthermia is

common and cooling techniques including icepacks in the axilla, inguinal area or on

the extremities or surrounding the IV line should be employed. Wetting the animal and

directing an electric fan on them, may also help to bring the body temperature back to

normal. Before physical examination is possible, the dog may require a sedative like

Buprenorphine and possibly even treatment with a short acting, IV corticosteroid. They

should be allowed to remain unrestrained and, in the position that they find most

comfortable.

In more severe cases, where laryngeal oedema has developed, the veterinarian may

have to consider endotracheal intubation or even an emergency tracheostomy. IV fluid

administration is not usually necessary in the immediate stabilisation and care should

be taken, if administered, not to overhydrate the already compromised lungs.

Establishing the cause of the respiratory distress

By assessing the abnormal respiratory sounds at various levels, we can gain clues as

to the underlying origin of the obstruction. It is important to note at his point that


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animals should never make a noise when breathing. Even young animals which

present with noisy breathing, must have some form of obstruction. This should be

recognised by veterinarians and corrected as early as possible.

Gentle pressure over the laryngeal area often exacerbates respiratory compromise at

the level of the larynx. Auscultation is useful for localizing the obstruction to this region.

A characteristic inspiratory stertor, is a common finding in laryngeal obstruction cases.

Once the problem has been isolated to the larynx, survey radiographs of the laryngeal

region are useful and should accompany the standard views of the thoracic cavity.

Routinely, radiographs are followed by a full visual examination of the laryngeal region

with the animal lightly anaesthetised. This helps differentiate laryngeal paralysis from

laryngeal collapse, elongated soft palate or everted laryngeal ventricles.

Visual examination of the upper airway

These patients are considered anaesthetic risks and every precaution should be taken

to make sure that they survive the initial diagnostic procedures. Laryngeal function can

be inhibited by certain drugs and these should be avoided if an accurate assessment

of laryngeal function is to be made. Preoxygenation of affected dogs for 3-5 minutes

with 100% oxygen prior to induction can significantly decrease risks. Propofol is

generally used as the author’s induction agent of choice, as it has the advantage of

having a very short half-life. The animal should only be anaesthetised to the level

where the tongue can be retracted, but the swallowing mechanism is not affected.

Tongue should not be pulled too forcefully, as this can give a false under-estimation

of the length of the soft palate. Endotracheal tubes and oxygen supplementation are

always on hand and in case blood oxygen saturation levels cannot be maintained.

An accurate light source and a long tongue depressor or laryngoscope is required in

order to assess the length of the soft palate in relation to the tip of the epiglottis. The

normal guideline is that a 1-3 mm overlap is acceptable. In the case of an elongated

soft palate, there may be as much as a 12-20mm overlap. In English Bulldogs, this

redundant soft palate tissue may also be exceedingly thick.

The soft palate should then be elevated to visualise the entrance to the glottis. This

allows the relationship between the corniculate and cuneiform processes of the

arytenoid cartilages to be assessed. Any contact or overlap between them, may

indicate a degree of concurrent laryngeal collapse.

During inspiration, it is important to establish whether the vocal cords are abducting

appropriately. In the case of laryngeal paralysis, the vocal folds cannot be adequately

abducted and so they obstruct the laryngeal glottis. This exacerbates the negative

pressure within the airway and leads to a vicious cycle of respiratory obstruction and

eventually upper airway collapse. A useful aid in confirming whether paralysis is

present or not, is to inject the animal with Doxapram (Dopram) at a dose of 0.5-2 mg/kg

IV whilst observing the vocal folds for movement. The increased respiratory effort that

occurs when Dopram is given, makes it easier to see whether there is adequate

abduction and exacerbates paradoxical movement.


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If all of the above structures appear within normal limits and no obvious cause for the

respiratory obstruction can be identified, then endoscopy of the trachea and bronchi

is indicated.

CONCLUSION Surgery of the head is one of the few places where simple techniques and

unsophisticated equipment can be used in first opinion practices to significantly

improve outcomes. The golden rules are that surgeons make a correct diagnosis,

understand the aim of the technique and follow sound surgical principles in the

correction of the initial condition.

REFERENCES 1. Fossum TW. Surgery of the upper respiratory system. In: Fossum TW. Small

Animal Surgery (4th). Missouri: Elsevier Mosby:2013: 906-957.

2. Fasanella FJ, Shivley JM, Wardlaw JL et al. Brachycephalic airway obstructive

syndrome in dogs: 90 cases (1991-2008). J Am Vet Med Assoc 2010;237:1048.

3. Hedlund CS. Surgical management of brachycephalic syndrome. In: Bojrab MJ.

Current Techniques in Small Animal Surgery (4th): Pennsylvania: Williams and

Wilkens: 1998: 357-376.

4. Poncet CM, Dupre GP, Freiche VG, et al. Long term results of upper respiratory

syndrome: surgery and gastrointestinal tract medical therapy in 51

brachycephalic dogs. J Small Anim Pract 2006;47:137.

5. Riecks TW, Birchard SJ, Stephens JA. Surgical correction of brachycephalic

syndrome in dogs: 62 cases (1991-2004). J Am Vet Med Assoc 2007;230:1324.

6. Torrez CV, Hunt GB. Results of surgical correction of abnormalities associated

with brachycephalic airway obstruction syndrome in dogs in Australia, J Small

Anim Pract 2006:47: 150.


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(notes)


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Oral Tumours: From Diagnosis to

Treatment. What to Expect. Dr. José C. Almansa Ruiz DVM (Hons) MSc (Vet)

EVDC Resident, Board Ready

Malignant Oral tumours represent 6-7% of all the tumours diagnosed in canine

patients; the incidence is lower in cats. Oral neoplasms should be differentiated from

inflammatory processes, infection, and developmental or congenital lesions. A variety

of odontogenic and non-odontogenic tumours occur in the oral cavity. These

neoplasms may appear as ulcerated, non-healing lesions or a more conventional

mass-like structure. The pet owner more readily notices lesions when they occur in

the rostral aspects of the maxilla or mandible. Encouraging clients to brush their pets

teeth will also help for them to “keep an eye” in their pets oral health. Unfortunately,

pet owners only generally notice these neoplasms when they are in an advance stage

of development. Hence, the important to act quickly when is first presented to the

general practitioner.

Staging the oral neoplasia: On the initial presentation, a conscious examination of the mass is performed if the

patient allows it, although an examination under general anaesthesia is still required

as part of the clinical staging of the tumour. Part of this initial assessment of the patient

must always include a CBC, biochemistry panel and in older patients a urine analysis.

The TNM system is used to stage these lesions (See addendum). During the clinical

assessment of the lesion, features like ulceration, mobility, size, location, consistency,

are important for the pathologist to give us a more accurate diagnosis. Part of the

staging involves evaluation the regional lymph nodes bilaterally. The mandibular

lymph nodes are the only regional lymph nodes superficial enough to be palpated,

during this process size and mobility must be recorded. Enlargement of the lymph

node does not necessarily mean local metastasis, but also could be a reactive lymph

node. The absence of mobility may be an indicator of the invasion of the lymph node

capsule by the tumour. A study performed by Williams et al (2003) reported on 100

cancer patients undergoing clinical examination of the lymph nodes and

lymphadenectomies, reported that 70% of cases with Lymphadenomegaly had

metastatic disease and 40% of cases without lymphadenomegaly had metastatic

disease (Williams / Packer 2003).


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Lymph nodes can also be evaluated using contrast-enhanced CT imaging, one study

looked at the diagnostic accuracy of CT for determining metastatic mandibular and

medial retropharyngeal lymph nodes in dogs with either nasal or oral cancers reporting

a sensitivity of 12.5 and 10.5%, and the specificity was 91.1 and 96.7%, for mandibular

and medial retropharyngeal lymph nodes, respectively. Due to the low sensitivity,

contrast-enhanced CT imaging is not a reliable tool to predict lymphnode metastasis.

Guided ultrasound fine needle aspiration permits sampling of the mandibular,

retropharyngeal and parotid lymphocentres; the withdraw of this practice is the

possibility of missing microscopic metastatic disease if no gross lesions are present in

the sampled lymph nodes. More recent studies have confirmed the lesser reliability of

FNA assessing metastasis, with one study reporting 77.2% accuracy in dogs and cats

and another reporting an incidence of 72.8% and 85.9% diagnostic samples in dogs

and cats, respectively (Ku/Kass 2017 and Amore-Fuster/Cripps 2015). Furthermore,

things get a little bit complicated when evaluating metastatic disease in melanocytic

tumours due to the difficulty to differentiate melanocytophages from melanocytes in

the regional lymphnodes.

Billateral lymphadenectomy of the medial retropharyngeal and mandibular

lymphocentrums reported an incidence of metastatic disease in 48 canine patients

suffering from oral melanoma and oral squamous cell carcinoma of 33% in at least

once lymphocentrum (Grimes/Mestrinho 2019). Odenweller et al evaluated metastatic

disease in 98 dogs and 10 cats presented with oral and maxillofacial neoplasms;

unilateral excisional biopsies were performed, including the parotid lymphocentrum,

reporting an overall metastatic rate of 14%. Of the cases with metastatic disease,

26.7% did not involve the mandibular lymphocentrum. Hence, the importance of not

to rely only on the palpation, aspiration or biopsy of the mandibular lymphocentrum.

To date no clinical studies have reported a correlation between performing unilateral

or bilateral lymphadenectomies and the survival times. It is the author’s opinion that a

more aggressive treatment can be instated based on a more accurate staging.

Imaging can be used to assess the extent of local disease and response to treatment,

identify lymph nodes that may have metastatic disease, screen distant organs for

possible metastasis, and allow image-guided sampling of suspected neoplastic

lesions. Choosing the best imaging technique for a patient depends on several factors

including where and what is being imaged, what information is needed, and also

sometimes cost of the imaging procedure to decide on a best course of action for an

individual patient. Computed tomography is routinely used in maxillofacial surgery to

evaluate the invasion of bone and extension into adjacent structures; it also helps

determine if a tumour is resectable and helps the surgeon to map the osteotomy sites.

These reconstructions are also a great education tool for clients, this way they can

“see” what has been planned surgically for their pet and they feel more confident about

the procedure. If the mass is not resectable, and radiation therapy is indicated, i.e

nasal adenocarcinomas, the CT is extremely important to plan it. The CT scan /

radiographs of the thorax should be done using positive pressure ventilation. CT has

been found to be significantly more sensitive than thoracic radiographs for detecting


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soft tissue nodules. Only 9% of CT-detected pulmonary nodules are identified on

thoracic radiographs The lower size threshold is approximately 1 mm to detect

pulmonary nodules on CT images and 7–9 mm to reliably detect nodules on

radiographs.

Some authors recommend abdominal ultrasound as part of the initial work up; the

reasoning behind it is that in 3% of oncology patients additional synchronous tumours

may be present (Rebhun JAAHA 2010 / Bigio Vet Comp Oncol 2017/ Magestro Vet

Comp Oncol. 2017).

Obtaining a good biopsy sample is extremely important for the surgical and medical

planning of the patient. The mainstay of planning the biopsy sites relies on diagnostic

imaging, being the gold standard advanced CT imaging (CT or MRI). A good biopsy

must have a representative sample of the most severe, showing more changes area/s

of the lesion. To achieve this, the clinician must select the best biopsy technique, the

correct sample site and submit the sample correctly. The biopsy sample should always

represent the worst part of the mass; this may mean collection of more than one

sample. Biopsying healthy tissue next to the lesion for comparison as in skin biopsies

is contraindicated. The biopsy tract should not transect a healthy tissue plane as

during this procedure neoplastic cells may seed along this tract. It is also advisable to

obtain microbiological samples in case the changes seen were related to infection and

not to neoplasia.

There are two types of biopsy, closed or open, the gold standard in oral and

maxillofacial oncology is open biopsies. The decision to perform an excisional biopsy

is a complex one. This type of biopsy should be reserved to small pedunculated

masses, that their removal would not affect the treatment plan. Incisional biopsies

using a 4-6 mm punch biopsies at a minimum depth of 2 mm are recommended to

biopsy a soft tissue mass. Once the punch is at the desire depth the punch is tilted in

order to “scoop” the sample. These samples should be placed on a clear paper for

1min with the connective tissue facing down on the paper to prevent the sample from

curling during fixation and to help orientate the sample. The sample will then be

transfer to a container with a volume of fixative 20 times more than the size of the

sample to prevent degeneration of the sample. It is the opinion of the author to include

bone when possible into the sample to help the pathologist get a more accurate

diagnosis. Sometimes the mass to biopsy has a mineralized consistency, in those

occasions the use of a chisel and mallet or a michele trephine is indicated to collect a

representative sample.

Epidemiology of common oral neoplasms:

DOGS Oral tumours in dogs represent approximately 5.4 % of all canine tumours. The

distribution in South Africa based on a study performed between 2000-2008 reported

Osteosarcoma to be the most commonly diagnosed malignant oral neoplasia, followed

by malignant melanoma and squamous cell carcinoma. The incidence of


20

osteosarcoma in the literature is much less, with melanomas, fibrosarcomas and

squamous cell carcinomas being the three most common malignant tumours in the

oral cavity of dogs.

There are several reported risk factors associated to some of these neoplasms. Dogs

living in urban industrialised regions are more predisposed to develop tonsillar SCC

as opposed to rural environments; this may be due to increased exposure to

environmental carcinogens. Canine oral papillomavirus is known to be involved in the

development of oral papillomas in dogs. Furthermore, it is thought that there can be

progression of viral papillomas to carcinomas in dogs. Lastly, oral osteosarcomas

have been reported to develop secondary to exposure to ionizing radiation, a known

carcinogen.

CATS The proportion of oral tumours is slightly higher with 7.4% - 10.6% of all feline

neoplasms. The most common neoplasia is SCC, comprising 68 - 98% of all oral

malignant tumours. There are several reported risk factors associated with this

neoplasia:

• Flea collars had five times increased risk of developing oral SCC

• Canned food diet (3.6 times increased risk),

• Canned tuna fish diet (> 4-fold increase),

• Exposure to household environmental tobacco smoke (2x increase, not

significant). Bertone JVIM 2003

• Relationship between oral SCC and exposure to household environmental

tobacco smoke, and furthermore implicated p53 as a potential site for

carcinogen-related mutation, with cats exposed to smoke 4.5 times more likely

to overexpress p53 based on evaluation of tumour biopsy samples, and those

exposed for 5 years or longer were 7 times more likely to overexpress p53

(Snyder Vet Path 2004).

CANINE ACANTHOMATOUS AMELOBLASTOMA (CAA)

CAA is a subtype of ameloblastoma that is very specific of dogs. Although considered

a benign lesion that does not metastasize, it has tropism for bone, medular, cortical or

alveolar bone, causing osteolysis and mobility of teeth. The term acanthomatous

means “thorn like”, referring to an internal sheet of interlocking polygonal epithelial

cells reminiscent of the epithelial cells of the stratum spinosum of the skin or oral

mucosa. This feature is unique to CAA.

En-bloc resection is the gold standard of treatment, and is generally curative. It

manifests grossly as a gray to pink, irregular, exophytic, verrucous mucosal mass that

arises immediately adjacent to teeth. It is indistinguishable from peripheral

odontogenic fibroma (POF) / fibromatous epulis of periodontal ligament origin

(FEPLO), squamous cell carcinoma, pyogenic granuloma and gingival hyperplasia;

hence when dealing with a patient with gingival enlargement, it is extremely important

to send for histopathology all the excised tissue. Approximately 50% of CAA occur in


21

the rostral mandible, but they can be found anywhere in the jaws. Golden retrievers

are over represented in the biggest study to date in CAA (Goldschmitdt et al JVD

2017). The treatment options are en-bloc resection with 1 cm margins, intra-lesional

bleomycin injections and radiation therapy. The author discourages radiating these

lesions due to the possibility of transforming them into SCC.

SCC DOG

It is the 2nd most common oral tumour in dogs 24.5%. Can be found in different sites

of of the oral cavity, involving the gingiva, tonsil, oral mucosa, lip and palate. There

are two different types with very different prognosis: non-tonsillar and tonsillar

categories. At histological level in dogs, OSCC can be divided into histologic subtypes

that are in many but not all aspects similar to OSCC in humans. These subtypes

include well-, moderately, and poorly differentiated conventional SCCs as well as more

rare subtypes such as papillary and basaloid SCCs and adenosquamous and spindle

cell carcinomas. They generally show a “moth eaten” appearance on intra-oral

radiographs. The 1-year survival rate ranges from 84% to 91% and the metastatic rate

ranges from 3% to 36% in dogs following surgical resection of OSCCs. The prognosis

for dogs with OSCC is generally excellent following radical surgical excision of the

tumour via mandibulectomy, maxillectomy, or glossectomy.

Mandibular/maxillary SCC: The prognosis reported when aggressive surgical resection (at least 1cm – (2cm

better!)) is excellent. These margins must always be evaluated based upon pre-op CT

imaging (remains the standard of care – with adjunctive therapy in specific cases). In

non-tonsillar OSCC, fewer than 15% of dogs have detectable nodal metastases and

fewer than 5% of dogs have radiographic evidence of pulmonary metastasis at the

time of diagnosis.

The outcomes reported following mandibulectomy or maxillectomy for SCC included

MSTs of 3.5 to 19.2 months, a disease-free interval of 26 months, and 1-year survival

rates of 57% to 91% (Kosovsky Vet Surg 1991, Schwarz JAAHA 1991, White JSAP

1991, Wallace Vet Surg 1992). However, more recent results for SCC treatment

outcomes have been reported and include more optimistic rates, such as a 1-year

survival rate of 93.5% for 21 dogs that had undergone curative-intent surgery and an

MST of 365 days for dogs > 10 years old (Fulton, J Am Vet Med Assoc 2013). The 1-

year survival rate for all dogs that were surgically treated was 93.5%; the 1-year

survival rate was 100% for dogs <2 years old and 75% for dogs that were 2 to10 years

old. However, age was not associated with survival time for dogs with OSCC that were

treated with curative-intent surgery (Fulton, J Am Vet Med Assoc 2013). This same

article reported an increased risk of death when increasing tumor associated

inflammation (TAI), perineural invasion (PNI) and lymphovascular invasion (LVI) were

noticed on histopathological evaluation.


22

Radiation therapy alone has a median survival time of 16-36 months. It is better for

smaller lesions – showing longer survival times. (Burk 1996). One year survival in 70%

of patients and 30% of recurrence rate. Radiation therapy used post-op after

incomplete surgical excision of oral SCC had longer median survival time (2051 days)

compared to those with incomplete excision and no radiotherapy (181 days). (Riggs,

J Am Vet Med Assoc 2018). Radiation therapy has been considered as an adjunctive

therapy to reduce tumour size prior to surgery (Mestrinho, Aust Vet J 2012). Maxillary

SCC in 1 dog non-resectable at presentation. Radiotherapy and chemotherapy

(carboplatin and doxorubicin) decreased tumour size to allow for surgical resection –

free from local disease for 421 days. The use of piroxicam has reported the following

results:

• Piroxicam alone (0.3mg/kg PO SID) (Schmidt, J Am Vet Med Assoc 2001) –

Response rate 17.6%. MST 180d.

• Piroxicam and cisplatin (Boria, J Am Vet Med Assoc 2004) 5/ dogs responding

to tx –However renal toxicity in 41%! So limited clinical usefulness.

• Piroxicam and carboplatin (de Vos, Vet Comp Oncol 2005) – 7 dogs with T3

oral SCC (tumour >4cm) had complete response in 57% with median follow-up

time of 534 days.

There is a novel treatment published in the literature: Intralesional bleomycin and feline

IL-12 DNA combined with translesional electroporation (Reed, Cancer Gene Ther

2010) - 2 dogs with mandibular/maxillary SCC. Both had complete response and

tumour free 3 and 5 years later. The second report of this treatment with a slight

variation (electroporation and IV bleomycin) in a bigger population (11 dogs) reported

complete remission in 8 dogs and partial remission in 2. The recurrence rate was

27.3%. All dogs with tumours less than 1-2cm had complete remission without

recurrence. (Simcic, Vet Comp Oncol 2019).

Lingual/sublingual SCC: With a metastatic rate of 37.5% (Carpenter JAAHA 1993), it is the second most

common lingual tumour in dogs after MM (Dennis, J Am Vet Med Assoc 2006).

Females are more at risk in all breeds, with poodles, labs and samoyeds

overrepresented. The typical presentation is bilateral symmetrical involvement

(61.9%), infiltrating the full thickness of the tongue (52.4%) and involving the rostral

two-thirds (85.7%). A very good functional outcome has been reported associated with

radical glossectomy in 5 dogs – Subtotal (50% resection) or total glossectomy (100%

resection) (Dvorak, J Am Anim Hosp Assoc 2004). Hypersalivation is the most

common reported complaint following aggressive resection.

Tonsillar SCC: It has a high rate of metastasis, with 98% metastasizing to the regional lymph nodes

(via lymphatics) and 63% to more distant anatomic sites (presumably

hematogenously). The high rate of metastasis is related to a rich blood supply and


23

lymphatics draining to ipsilateral and contralateral lymphocentres. There are ten times

more common in urban vs rural areas with a median age of 10 years. They range from

microscopic primary tumours with advanced metastatic disease to bulky exophytic

tumours.

Surgical resection followed by radiotherapy (9 Gy once a week for 4 weeks) and

carboplatin treatment (300mg/m2) in 5 dogs reported a median survival time of 211

days, with 2 dogs been alive and disease free at 826 and 1628 (Murphy, JSAP 2006).

In a multi-centre study of 44 dogs treated with surgery, radiotherapy and/or

chemotherapy reported an overall median survival time of 179 days (Mas, JSAP

2011). They concluded that no matter what treatment modality was used the survival

time was short, although there were a small number of long-term survivors.

Papillary SCC: It is a lesser aggressive variant reported in young dogs, but also can be seen in adult

dogs (Nemec, J Comp Pathol 2014). It is a distinct histopathological sub-type of SCC.

A Retrospective study of 12 dogs – median age 9 years. They presented as a

verrucous pink mass arising from the gingiva of rostral maxilla or mandible. May be

associated with papillomavirus? – Although no strong evidence. They are locally

aggressive with underlying bone lysis. Respond well to aggressive local surgery and

radiotherapy. No reports of metastasis. Often curative.

SCC CATS

SCC represents 61-64% of all oral tumours in cats. Cats with advanced OSCC

presented with metastasis of the mandibular lymphnodes or lung metastasis did not

have a shorter MST (Soltero-Rivera JFMS 2014). FOSCC exhibit overexpression of

COX-1 and COX-2. A study performed in the UK on feline patients treated by their

general practitioners reported an overall median survival time was 44 days (Hayes

JSAP 2007).

Mandibular/maxillary The maxilla and mandible can equally be affected. Most cats are referred for a non-

healing surgical site or “abscess”. There is generally bone enlargement with facial

asymmetry, ulceration and difficulty eating. 73.1% had marked osteolysis on

radiographs. Cats with oral SCC are typically diagnosed late and the response to

therapy is poor. Cats with mandibular swellings in 50% of cases will have a tumour.

Sometimes there is no difference on rads between tumour and osteomyelitis.

(Kapatkin JAAHA 1991). The MST of any treatment method is 60 days (Gendler

JAVMA 2010 and Postorino JAHA 1993). When performing a mandibulectomy

combined with radiation or chemo in SCC affecting the mandible, there is a 1 yr

survival rate of 51%, 2 yr survival rate of 34%. (Northrup JAAHA 2006). If radiation

therapy is used on its own the MST is only 36-97 days (Bregazzi 2001 Vet radio

ultrasound).


24

Lingual/Sublingual and Tonsillar Lingual SCC is locally very aggressive and difficult to treat. There are two growth

patterns recognised, a destructive or an irregular proliferative pattern.

Fidel et al reported a combined protocol using chemotherapy and radiation therapy

comprising 14 fractions of 3.5 Gy given within a 9-day period with the addition of

carboplatin given at 90–100 mg/m2 on day 1 and day 4.5. Treatments were twice daily

with a 6-hour delay between treatments. Cats with tumours of tonsil origin or cheek

responded best to therapy and were long-term survivors with a mean survival of 724

days and the median had not been reached because of continued survival of 4 cats

(Fidel JVIM 2011).

Oral Malignant Melanoma (OMM) DOGS

It is the most common malignant neoplasia in the oral cavity of dogs. The term

melanoma is a misnomer, as this lesion is a sarcoma; a synonym will be

melanosarcoma. Occurs most frequently in aged patients over 11 years of age. Breeds

with highly pigmented oral mucosa (Chow-Chow and Scottish Terrier) seem to be

over-represented. The gross appearance of oral melanoma varies from coal black,

patchy black and white, pink/red (tumour associated granulation tissue), purple, or

white (amelanotic). Melanomas readily invade soft tissues and bone and may be

associated with extensive local tissue destruction. Disruption of the dental arcade or

pathologic fractures can occur if the melanoma invades the jaw. Mostly gingival but

can be labial mucosa, palate, buccal mucosa and tongue.

Can metastasise to brain, meninges, pituitary gland, striated muscle, pleura,

pericardium, heart, prostate, pancreas, adrenal glands, liver, kidney, spleen, ileum,

omentum, mediastinal lymph nodes, thyroid, prostate, salivary gland, stomach, testis

and eyes, tonsils.

HISTOLOGY

There are three main categories based on microscopic features of the predominant

cell type including polygonal (epithelioid), spindle and mixed (epithelioid and spindle)

cells. Different studies disagree re distribution of types.

Dx: A variety of useful antibodies for IHC assays are now available for the diagnosis

of canine oral melanoma: S100, Melan A, PNL2 and tyrosinase-related proteins 1 and

2. S100 may be the most sensitive, but it is the least specific of this antibody stains.

TREATMENT OPTIONS:

Curative Intent Surgery Cornerstone combined with vaccine/chemotherapy or radiation therapy. The case

series published by Tuohy et al (JAVMA 2014) analysing 70 patients undergoing

curative intent surgery described a median progression-free interval and ST of 508

and 723 days, respectively. Thirty-two (45.7%) dogs had disease progression.

Significant associations with PFI or ST were found for administration of adjuvant


25

therapy, presence of metastatic disease at the time of diagnosis, higher tumor stage

(III or IV), and increased tumor size (> 3 cm). Co-adjuvant treatment was associated

with a 130% increased hazard of disease progression; the presence of metastasis at

the time of diagnosis was associated with a 281% increased hazard of death. A second

paper (Boston JAVMA 2014) evaluating the efficacy of systemic therapies after

surgical excision of oral melanomas indicated that surgical treatment of oral malignant

melanoma in dogs can result in an MST of 346 days, with long-term survival in 29%

of cases. Dogs that were treated with surgery alone had an MST of 352 days, and we

were not able to detect a survival advantage with any form of postoperative adjuvant

therapy. Interestingly this paper reported no difference on MST between marginal

resections and wide or radical resections.

Xenogeneic DNA vaccination Vaccine (Oncept in the UK) contains plasmid DNA-targeting tyrosinase, a glycoprotein

essential for melanin synthesis and demonstrated to be overexpressed in melanomas

(Bergman & Wolchok 2008), conflicting results so far but is potentially therapeutic in

stage II/III locoregionally controlled disease.

Results of Grosenbaug (2011) documented a statistically significant improvement in

survival for vaccinates (more than 1075 days) compared to historic controls. Verganti

(2017) reported only a disease free interval of 477 days in vaccinated dogs vs 491 for

non-vaccinates and a MST of 455 days. In Ottnod’s (2013) study, disease free interval

for vaccinates was 171d, and for non vaccinates it was 258 days.

In the Verganti (2017) study, effects of vaccine were seen early on (in loading period)

but 50% of patients with stages I to III disease died due to local recurrence (with or

without regional lymph node involvement; 17·9%) or due to metastatic disease

(29·6%) to the lymph nodes, lungs, liver, brain, tonsil and skin which means melanoma

vaccine may not be effective in all the patients treated or works only for a limited time.

Patients with macroscopic disease had a 44·4% response rate to the vaccine and the

MST for dogs with stage IV disease was 178 days.

a) Carboplatin: Response rate 28%

b) Cisplatin and piroxicam: response rate 18% both drugs nephrotoxic!

c) Palliative radiation: MST 7.9 months (prognosis not dependent on stage- they

all respond the same)

d) Definitive-intent radiation therapy (Proulx 2003) MST 7 months

e) Hypofractionated radiation + low-dose cisplatin or carboplatin as a radiation

sensitizer- mst 363 days.

FIBROSARCOMA DOG

It is one of the three most common tumours reported in the oral cavity of dogs. It is

locally aggressive with a low rate of metastasis (<25%). Golden retriever breeds are

overrepresented. Schwartz et al. reported a 31% rate of recurrence for mandibular

FSA after mandibulectomy and a 57% rate of recurrence for maxillary FSA after

resection.


26

Frazier et al. Vet and Comp. Oncology 2011:

A total of 29 dogs were included in this study. The overall survival time (from surgery

to tumour related death) reported here was 24.8 months. Seven dogs (24.1%)

developed metastasis: three to regional (mandibular) lymph node only, three to lung

only and one to both regional lymph node and lung. The median survival time of the

seven dogs that developed metastasis was 391 days. Golden Retriever or Golden

Retriever mixed breed dogs were more likely to experience local recurrence than other

breeds (P = 0.03).

The median survival time (MST) of all dogs was 743 days (95% CI 569–1598 days).

The 1-and 2-year survival times were 87.7% (95% CI66.5–95.9) and 57.8% (95% CI

31.6–77), respectively. The median survival times of dogs treated with surgery alone

or with surgery and radiation therapy were not statistically different (1024 days and

576 days, respectively; P = 0.40). The MST for dogs with complete excision was not

statistically different from those with incomplete excision (1598 days versus 576 days,

respectively; P = 0.09);

Gardner et al VCO 2015. 65 Dogs receiving different therapies:

Approach Median survival

time (d)

Notes

Conservative surgery 301

Aggressive surgery (removal of bone), 526 some of these had radiation

Palliative intent radiation therapy – 24-

30gy

204

Definitive radiation therapy (no sx) – 54-

60Gy

825 these were all T3

Chemotherapy (Doxorubicin or

Lomustine)

Use of chemo didn’t stat sig affect MST

No Tx 205

RADIATION AND SURGERY 505

RADIATION (CURATIVE INTENT) AND

SURGERY

575 not stat sig vs palliative and

surgery

Soft tissue sarcomas have been historically considered resistant to radiation therapy,

requiring doses above 50 Gy to markedly affect the neoplastic tissue. Although

radiation therapy can be used to treat macroscopic disease, it is most efficacious when

employed against microscopic disease.


27

Hi-lo fibrosarcomas: Median age 8yo and 52% were golden retrievers (Ciekot et al JAVMA 1994).

Histopath: fibroblasts with abundant collagenous tissue. Recognised as ‘Low grade’

due to

• low numbers of fibrocytes,

• low mitotic index (0-1 mitotic figues per HPF),

• minimal cellular anaplasia,

• minimal pleomorphism,

• abundant collagenous matrix.

• Poor demarkation from surrounding tissue

Innocuous histo appearance but these are invasive: invade ST and bone and met to

local LN. 72.7% of dogs evaluated found to have underlying bone lysis

‘Fibrosarcoma’ doesn’t distinguish between low grade and high grade.

OSTEOSARCOMA DOG It is the most common bone tumor in dogs. Osteosarcomas are divided into

appendicular and axial, with 49% of axial osteosarcomas occurring in the mandible or

maxilla. Osteosarcomas of the maxillofacial region most often arise from the bone

medullary region. Although can also be juxtacortical OSA (Periosteal and parosteal

OSA) (Murphy Veterinary Oral and Maxillofacial Pathology 2019). The mean age at

diagnosis of canine oral and maxillofacial osteosarcoma is 9–10 years. Seventy three

per cent of dogs with maxillary osteosarcoma, and 100% of mandibular osteosarcoma

have been reported to weigh more than 20 kg. Mixed-breed dogs, German shepherds,

golden retrievers and Labrador retrievers were most commonly presented. Factors

such as ionizing radiation, genetics, bone tumour viruses, chemicals, chronic irritation

due to fractures repaired by metallic implants, bone infarcts, skeletal diseases or

disorders as well as body size and sex are believed to be involved in pathogenesis.

While osteosarcoma in general is known to be a disease with rapid local progression

and mortality due to early lung metastasis, comparatively, oral and maxillofacial

osteosarcoma have been found to progress slower and show lower tendency to

metastasize than other axial subtypes. As with osteosarcomas at other locations,

clinical signs are caused by the expansive mass and tissue destruction.

There are six histologic subtypes of OSA – osteoblastic (osteoblasts predominate),

fibroblastic (fibroblast-like spindle cells arranged in patterns reminiscent of

fibrosarcoma), chondroblastic (extensive regions of chondroblastic differentiation with

chondroid matrix deposition), giant cell (large numbers of intermixed multinucleate

cells), telangiectatic (endothelium like sarcoma cells form blood-filled cavities and

sinuses reminiscent of hemangiosarcoma), and poorly differentiated OSA (neoplastic

cells are anaplastic). Osteoblastic OSA is further subdivided into productive (abundant

tumor associated osteoid matrix (TAOM)) or nonproductive (minimal TAOM) (Murphy

Veterinary Oral and Maxillofacial Pathology 2019).


28

It has been reported that half of dogs treated surgically for mandibular osteosarcoma

had recurrence, while 90% of dogs treated surgically with or without adjunctive

therapies for maxillary osteosarcoma had local recurrence. Of dogs with axial

osteosarcoma, 11–13% had metastasis at presentation and 35–46% developed

metastasis after diagnosis (Heyman Vet Surg 1992). Haematogenous metastasis

(most frequently to pulmonary tissue) is the most common route of spread, whereas

lymphatic involvement is rare (Withrow Clin Orthop and Related Research 1991). A

case series of 51 dogs with osteosarcoma treated by partial mandibulectomy alone

(32 dogs), partial mandibulectomy and chemotherapy (10 dogs), partial

mandibulectomy and radiation therapy (3 dogs), or radionucleotide as sole treatment

(2 dogs) found that the group treated with surgery alone achieved a 1-year-survival

rate of 71%, compared with the entire group’s 1-year-survival rate of 60 % (Straw

JAVMA 1996). The benefit on the use of adjuvant chemotherapy or radiation therapy

is unclear in the literature.

MULTILOBULAR OSTEOCHONDROSARCOMA Uncommon tumour in dogs, rare in cats, and typically involves the flat bones of the

cranium. Study of 39 dogs with MLO: maxilla (11), mandible (14), calvarium (14), and

1 each at various other sites. MLO has a stippled appearance on radiographs due to

the multilobular arrangement of osseous, cartilaginous tissue or both surrounded by

mesenchymal stroma; and a “pop corn” appearance on CT imaging. Studies: 25 dogs

had sx, 9dogs had sx + adjunctive tx. Of the dogs treated, 47% had local tumour

recurrence, and 56% had documented metastasis

EXTRAMEDULLARY PLASMACYTOMAS In a retrospective study of EMP’s Treatment included none (3), surgery with local

recurrence (7) with a median time to recurrence of 50 days (range 23–690 days), and

a few had chemotherapy and/or radiation therapy. At the time of the study, 5 were

alive and 11 had died with a median survival of 474 days (range 37–2906 days).

The primary mode of therapy is surgical excision and the majority of dogs have long-

term local control. Plasmacytomas are considered to be radiation-sensitive; however,

data are lacking on the efficacy of radiation therapy in canine oral plasmacytomas


29

Addendum Owen, LN. TNM classification of tumours in domestic animals. Geneva: World Health

Organisation, 1980.


30


31


32

(notes)


33

Secrets to Success In Dermatology Dr Anthony Zambelli

BSc(Hons) BVSc DiplSnrMgmt MMedVet(Med) (cum laude)

Introduction – the journey of dermatological success and

failure In the Aeneid of Virgil, Aeneas journeys from his once-great, but ruined city of Troy

with his son by his side, and his old father on his back. Over many trials and

tribulations, he survives the sirens, luring him to destruction, overcomes the great

cyclops with cunning and a plan, and eventually founds what was to become the

Roman state – the world’s most enduring empire.

What has this to do with dermatology? Well, a whole lot.

As third year veterinary students, we are taught dermatology by some great people,

whose experience and understanding of the nuances – and simplicity – of dermatology

– outstrips our own. I know this experience. The night before my first dermatology

lecture, I prepared until 3 am. I admit that by the time I crawled into bed, I was

confused. All the conditions seemed the same. The German Shepherd appeared

everywhere. Itching and lesions were not as clear as I thought.

Fast forward to private practice. That first year was disastrous. I couldn’t distinguish

any patterns, patients came back, and my first couple of mentors’ advices was – well

just give some preds and it will go away. I was learning the drugs, it seemed all over

again, and I had as many successes as failures. Certainly, no one was rushing back

to see me – any more than they thought any of us knew what we were doing. Then I

moved practices. My new employers advised workups. Diligently adhering to this, I

booked in workup after workup. This meant my patients were worked up not in 15

minutes in the consult room, by pattern recognition1; but in the hospital, where I had

time to read up, work through DD lists and repeat a scrape, or allow the Wood’s lamp

to properly heal up. This was becoming evidence-based medicine2. I even remember

the moment it all clicked. A JRT with pruritis and just some redness. I had booked it

in, taken a complete history, and done scrapes, plucks, tape strips – all negative. I

also had brought my textbook with and worked – for the umpteenth time – through the

chapter on pruritis in dogs. Then it all clicked. I changed my approach and managed

what I knew was there – in this case, atopy – by exclusion of other causes. Suddenly

1 Pattern recognition as a means of diagnosis and treatment requires that the vet has seen every

manifestation of every disease, and has PERFECT recall

2 Collecting evidence to support or rule out a suspected diagnosis – treating – and then reassessing

the results and adjusting interventions accordingly.


34

patients started coming right. I developed a reputation for success – durable, simple

and also, because I spent time explaining my plans to clients – understandable.

So rather than teaching dermatology all over again, in this lecture, I will share some of

my observations, techniques and pearls. But as an individual vet, or a practice, my

first piece of advice for success is:

Tip #1 – Book skin cases in for investigation, don’t manage as outpatients

During the lecture I will show how booking in gives you time, space and the opportunity

for collaboration with colleagues to get more and better information. If nothing else, it

fills a cage – that you charge for – and allows unhurried, multiple skin scrapes, photos

etc.

You should master the techniques of:

• Skin scrapes (the tape technique may also be touched on).

o Shar Pei have very deep follicles so skin biopsy is often better if looking

for Demodex

o You need a minimum of 4 – 6 scrapes to be happy. 1 Demodex is not

diagnostic, but 1 Sarcoptes is.

o Painful – so sedate – which means a presedative clinical check

• Hair plucks

o Place the plucks onto a slide with a drop or two of KOH and let sit on the

microscope (sadly, new LED microscope lights don’t make much heat –

use a lighter) and then a drop of lactophenol cotton blue if dermatophytes

are suspected3

• Wood’s Lamp

o They need warming

o They only pick up a minority of cases

o Cats (esp Persians and kittens) and Yorkies are particularly prone to this

• Tape strip

o The scotch tape with serrated edges is the best for this, and only use the

blue stain

o Malassezia >4/HPF is very significant

o Bacteria adhered to corneocytes can be normal, but not when

associated with neutrophils

• Biopsy

o Biopsy parallel to the hair shaft, not perpendicular to the skin

• History

o Firstly, don’t neglect the normal medical history and examination

o Secondly, do a distribution map

o Thirdly, get a full history

3 LCB is toxic so don’t inhale or get on your skin


35

▪ This means dermatology initial consults can be long, and a

surcharge (for time) is appropriate – we book a double

appointment for skin consults

• Fleas

o Always check for fleas although with the advent of modern flea meds,

this is less common – but not impossible. Also, check clients’ compliance

with treatment (eg Bravecto every 6 months is NOT compliant with

manufacturer instructions!)

Tip #2 – Dermatology is both Nuance and simplicity

Of all the areas of internal medicine, dermatology is the easiest to be a success in.

Why?

#1 the entire organ is readily available and visible to you – easier to see patterns,

pathology, response to treatment (or otherwise)

#2 there are very few tests required/applicable or available for dermatology. Let’s list

them, in frequency of use (approximate):

• Flea comb

• Tape strip

• Skin scrape

• Hair pluck

• Wood’s lamp

• Cytology

• Histopathology (sometimes Ziehl-Nielsen or PAS stains, or

immunohistochemistry for some tumours like c-kit for MCT; CD3/79a for

lymphomas; S100 or desmin for PMNST etc)

• Culture (usually aerobic and fungal is sufficient)

• ACTH stimulation / LDDST testing and abdominal US for Cushing’s Syndrome

• T4 and cTSH testing for hypothyroidism

• HESKA blood allergy test

• Chemistry eg ALP, ALT, Alb, NH3/Bile acids for hepatocutaneous syndrome

• Occasionally imaging for paraneoplastic exfoliate dermatitis in feline thymoma

or while staging tumours – now we are onto rare circumstances

So with these few laboratory tests (some in house), and not much more, it should be

easy to make a diagnosis, right? Not so fast I hear you say.

I would argue that a good physical examination, a thorough history – especially of what

has been done and worked before, can give you a good idea of what the likely

diagnosis is – NOT necessarily as a justification for using the same dose of cortisone

or to validate a change of the same antibiotic without a diagnosis.


36

Remember – with a diagnosis your treatment will work more rapidly, completely and

durably – your aim. Simply chucking treatments at a patient in rapid, frenzied and ever

more desperate and despondent fashion is NOT going to get you durable results –

and the client will go elsewhere.

So where lies the difficulty? Primarily in the lack of systematic use of appropriate tests

– particularly the history and physical examination. I cannot emphasise this point

enough. You need to ask the questions, and record the answers, to get the correct

idea of what efforts are wasted, and which might be fruitful. Always adopt a careful,

logical approach, explaining each step to the client as you go – to recruit them into a

possible 2- or 3-step investigation (if you are getting to visit 3, or relapse 3, that’s your

indication to refer the patient – before they do it themselves).

ABSOLUTE (=PATTERN) Recognition of clinical signs is unreliable. It depends on

you, the clinician, having seen every manifestation of every disease, and having

perfect recall – an impossibility. Another reason is that many conditions can appear

very similar, and this is only exacerbated by delays in, or prior therapy (especially

glucocorticoids). Lastly, conditions may superimpose on the PRESENTING picture.

To unravel these, you must be systematic:

1) Take a history – back to puppyhood if necessary

2) Do a complete physical examination (this is not a “dermatology” problem, but a

health issue)

3) Make a list of likely, less likely and unlike differential diagnoses

4) Book the patient into your hospital and do the initial diagnostic tests. If a

slide/scrape/pluck etc is not up to scratch, do it again until you are satisfied.

Use chemical restraint if need be

5) Having narrowed your DDx, do a definitive test. For example, a bacterial

pyoderma responds well (maybe not always completely) to an empirical

antibiotic (purbac, Rilexine and clindamycin being the appropriate empirical

choices) AND/OR Pyoderm shampoo; an adverse food reaction to a dietary

trial; hypothyroidism can usually be diagnosed with a T4 and cTSH; and so

forth. Now you have a diagnosis – but remember, there could be 2, or 3 – or

even 5!

History is the single most useful procedure in making a diagnosis. 70% of diagnoses

are arrived at successfully with a thorough history; another 25% by routine tests; and

only 5% (or fewer) need a specialist – but it’s critical to establish which those 5% are.

Frequently, you will not make a specific diagnosis at the initial consult – and it’s

important to communicate this to owners from the outset, since many arrive with an

unjustified expectation of “instant diagnosis and cure”. But if you start at the beginning,

don’t skip any steps, and they follow your instructions diligently, you will always arrive

at an answer.


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So what are some key pieces of infestation in taking the history for a pruritic animal

(there are other patterns and therefore starting points/history for dermatology, but let’s

face it – pruritis is #1)

• Age, sex and breed

• Age of onset of pruritis, and its seasonality

• Site and nature of lesions – if any

• Severity and any prior response to glucocorticoids

• Evidence of transmission

• Presence of fleas

• Diet (note – I put this last)

#3 – Duration and onset tell you a lot

A non-cretinous, hairless puppy with bad itching does not warrant a T4/TSH test – but

the same obese, slow, bradycardic, yeast-smelling Labrador of 9 years of age, does.

A dog that began itching at 6 months of age, is now 3 and has lichenification, malodour,

alopecia and hyperpigmentation on the paws, ventrum, perianally and a history of

responding to corticosteroids – probably has atopy, with secondary infections – not a

dietary sensitivity. A cat with crusted edges to the ears, now spreading to the

periauricular area and face may have mites, but could also have an autoimmune

condition such as pemphigus, dermatophytosis, or even mycobacterium. A dog with

recurrent pododermatitis might have “an allergy” – but which one, and how does the

treatment of a dietary, atopic sensu stricto, and contact allergic dermatitis differ?

Age of onset is one of the most useful tools is narrowing diagnoses down. It doesn’t

eliminate it – any dog of any age can become atopic, or develop an adverse food

reaction – but merely moves diagnoses up and down the list.

Tip #4 – learn the patterns to ask the right questions

This just requires practice and a little learning. For example, the criteria laid out by

Favrot(Bizikova et al., 2015):

Age at onset under 3 years of age Dog living mostly indoors Glucocorticoid-responsive pruritus Chronic or recurrent yeast infections Affected front feet Affected ear pinnae Nonaffected ear margins Nonaffected dorsolumbar area Sensitivity for five criteria, 85.4%; specificity for five criteria, 79.1% Sensitivity for six criteria, 58.2%; specificity for six criteria, 88.5%

Is interesting and useful. Ear margins affected? Unlikely to be atopy. Young dog? More

likely? Multiple criteria? More likely. Labrador, Shar pei or French bulldog – earlier age

of onset (4 – 6months even)


38

The use of these criteria lies in their ability to REFINE and clearly delineate your

potential workups or treatments.

Tip #5 – Schedule Revisits

If you don’t think it’s important for completion of a medication or resolution of a medical

problem that the owner presented their to pet you for, they won’t think its important

either. So even if you diagnose fleas, give some ectoparasiticide, schedule a support

staffer to call the client in a reasonable period – say 2-4 days in this instance – to follow

up. A failure (real or perceived) of treatment efficacy – revisit. Re-examine the patient,

note changes, assess results, counsel the client on what it means. I find a good

narrative is to sketch out these potential steps at Visit #1, so if they must come to visit

#2 and you want to embark on a treatment change or diagnostic test, you say “well,

as WE agreed, if Fido was still itchy after the Spot on we used, we would admit him

for a more detailed skin workup to get to the bottom of what looks like a couple of

overlapping conditions”. You lay the ground for your next step (even if, as it might turn

out, that is not necessary), at your first visit, and tell them the way forward. Engage

the client into the workup and management, support them and follow up on their

efficacy.

Tip #6 - Food myths

The real prevalence of PROVEN canine adverse food reactions in specialist

dermatology practice – a mere subset of dermatology conditions (GP & SP) is 7 –

12%. Assuming only 10-20% of consultations are for skin complaints, this means true

AFR are only <1% of your total skin complaints. Don’t get me wrong – dogs and cats

can respond to a dietary change for several reasons UNRELATED TO ALLERGY

(immunology). Think about it – more than ½ your patients are on supermarket or home

food, which may be suboptimal, in the instance of a health challenge posed by skin

conditions and infection. Hair and skin (and most immune-driven processes like the

defence against parasites and infection) are driven by protein- and fat-intensive

processes (arachidonic acid, repair, etc). Most “skin” diets – novel protein, hydrolysed,

skin support – are distinguished from other diets by 2 main features:

• Higher quality, readily absorbable (biologically available) proteins; and

• High levels of anti-inflammatory fats and sometime plant extracts

So just changing a diet and seeing a response – particularly in mild-moderate cases

– does NOT equate to a “dietary allergy”, but rather to a “dietary modification

responsive dermatosis”. To diagnose a true AFR, you MUST fulfil certain conditions:

• Eliminate other conditions including atopy (can be controlled in <2-4 weeks with

appropriate meds, so easier to do than AFR); and

• A proper dietary trial with a hydrolysed protein (not novel protein – that comes

later) done over 2 x 8 weeks with a 1-2 week challenge trial in between, and

the use of an objective scoring system plus photos.


39

Tip #6A - How to do a proper dietary trial • Choose a hydrolysed protein diet

o Royal Canin Anallergenic is the most effective one available (Bizikova

and Olivry, 2016)

o Royal Canin Hypoallergenic or HA Moderate Calorie (I find many

applications for the latter, given the high coincidence of obesity or other

conditions such as diabetes, pancreatitis etc in some dogs)

o Hill’s Prescription Diet Z/D

• Do a baseline CADLI score (Plant et al., 2012)

o CADLI scoring takes 90 seconds versus 12.5 minutes for the research-

oriented CADESI-04 scoring (for dogs)

o For Cats, you can use FEDESI scores although it seems less accurate

and is best used to chart / prove IMPROVEMENTS in pruritis, rather than

comparisons with other patients/scores.

o o Score each area from 0 – 5 for the ACUTE (left column) and CHRONIC

(right column) changes. Add the scores (max 10 for a region, x 5 regions

= score /50).

o Get patient back in 4 weeks and 8 weeks for photos and rescore


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o If reduced by >50% by week 8, do a challenge trial with the original diet.

As soon as the patient starts itching again, or by week 2 (whichever

comes first), you get them in, photos and score again, and back onto the

hydrolysed diet

o Checkup, photos and score at week 4 and 8.

o You should get a set of results like these I got from 5 patients:

o o (Bizikova et al., 2015, Noli and Cena, 2015, Plant et al., 2012)

o If the patient is stable on the diet, I’d just leave it on that. If that doesn’t

do it – refer these kinds of multifactorial patients. If stable for a while (2-

6 months) and the diet is too expensive, try switching to a novel protein

diet.

▪ RC Sensitivity Control

▪ Hill’s Prescription Diet d/d

▪ Acana Singles

• If you are dealing with a diet with mild skin disease, or that responded to

management for ectoparasites, atopy, autoimmune skin conditions, endocrine

dermatopathy, then rather use a diet to support and manage skin conditions

such as:

o RC Skin Support

o RC Skin Care

o Hill’s Derm Defence

• I do think it’s fair to mention that starting a dietary trial with 0.5mg/kg/day of

prednisolone for a week is not only humane and acceptable, but has been

shown to allow for a quicker dietary trial with better compliance.


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Tip #7 - Ears – clean vs medicate

My mantra on this: ears are overmedicated and under cleaned The most frightening culture results we see in our referral practice come from otitis

externa-media. The chief problems, and what you should not do, to avoid this, is:

• Not doing ear smears and treating according to cytology

o Cocci – narrower spectrum antibiotics, no antifungals, probably respond

best to managing with aggressive cleaning using Epi-Otic and treating

the underlying condition (fleas, atopy, AFR)

o Rods – definitely culture (aerobic) – aggressive cleaning, and always

visualise the eardrum as aminoglycosides are oto- and vestibulotoxic

sometimes even with an intact tympanum

o Malassezia – same as for cocci, although antifungals are useful for very

heavy or stubborn infections; rarely if ever require systemic antifungals

▪ Ketoconazole – frequent GIT side effects, depressed adrenal

function

▪ Itraconazole – expensive, hepatotoxic to cats

▪ Nystatin – bitter, narrow spectrum, frequent dosing (q6h) required

▪ Terbinafine – may be useful, but in combination with other drugs

• The general rule is that any recurrent, stubborn or unusual

yeast or fungus should be referred as the management

can be complex and use drug you may be unfamiliar

with(Pedrosa et al., 2019, Schlemmer et al., 2019)

• Not visualising the eardrum – to do this properly, in a painful ear, in the consult

room, is an act of extreme hubris. Syringing ears under sedation is humane and

more effective but to do it properly requires the proper equipment – control the

pressure of the water, and always, always visualise the patient’s ear canal at

all times. When I moved to an expensive video-otoscopic system, I was

gobsmacked. What had I been thinking I was seeing all these 20 years as a

vet? Because suddenly I was able to visualise, manipulate, sample and – if

nothing else – safely clean the canal so that the patient was started on home

therapy with “a clean slate”. It was astounding!


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• Compare these 2 images from the same patient – the left through a standard

otoscope, the right from my video otoscope:

A key component of understanding the management of ears is that they are like grill

pans. You cook on a grill pan, you get sticky sauce adhered to the surface. All the

medication in the world will not clear up the grease – especially in an old, scarred pan

(ie atopic ear) – until you physically clean the surface material OFF, to allow the

cleaning (ie medicated) liquid to act on the epidermis. So rather clean 4x daily if you

must, before even considering a medication. If you are reaching for silver

sulphadiazine, acidified ear cleaners, chloramphenicol oral capsules, vancomycin –

whatever – these cases have a more serious underlying problem and must be referred

to work up an otitis media or manage exactly the kind of bacteria you DON’T want in

your hospital or on your hands. If you cannot see the eardrum, don’t put an ototoxic

agent. Recruit our staff, with our equipment and expertise, to help clear the stage so

you can then proceed with a curative effort, rather than just kicking the can down the

road.

When dispensing medication, or ear cleaners, TEACH clients how to use medication

on one ear, and then check their technique in your consult room. If they struggle,

encourage them to seek help from a nurse/vet ASAP – it’s all about training. 3/5 clients

tell me the vet has never taken this simple step with them. It is a worthwhile investment

of your time. I even go so far as to show them how to open medication bottles –

someone recently complained the Epiotic was hurting his dog and was wasteful – he

completely removed the white screw cap, leaving the blue plastic core!

Lastly, in this aspect, I will emphasise that for chronic otitis without infection, there is

a lot of value in teaching clients to embark on regular ear cleaning. Clean, healthy ears

do not require this – we are talking about diseased ears. Get them to taper down from

2/day (during treatment) to 1/day then M/W/F then at least 1-2/week, for life.

Encourage them by emphasising that the Epi Otic is an OTC, and they don’t need a

consult. But here is the most important thing you must tell them:


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• Sniff and visually check your dog’s ear every day. If its red, itchy, smelly or

discharging, increase cleaning to 2-4x/day

o If you haven’t seen an improvement by morning 3, you must bring your

pet in for a thorough otoscopy and possibly medicated drops;

o If you are seeing an improvement, then continue 2/day for the remainder

of a week, then 1/day for a week, then back to your maintenance

schedule

o This way, you avoid unnecessary medication, serve as my surveillance

team, minimise costs, but don’t miss those instances when your dog

really should see me

Tip #7A – some useful (new) tools for otitis • Always advise clients to medicate only 20 minutes after an ear cleaning

• Flixonase (fluticasone) Nasules – used 1-2/day for 7 – 14 days, at night, 20

minutes after ear cleaning, can reduce inflammation and keep atopic ears

happy, with no steroid absorption

• For very painful ears, consider a single injection of Kortico at a dose of

0.1ml/10kg body weight, possibly with other analgesia such as paracetamol

and/or an opioid, and then scope 1-2 days later, after some ear cleaning at

home

• For a narrowed canal, consider a contrast canalogram – very useful and

objective measure. Do a DV image before and after contrast in both ears

(remember your markers). Use a linen saver over the X ray table/plate to avoid

spillage (Eom et al., 2000).

Tip #8 - Shampooing

This is my take on shampoos (topical therapy):

• Vets don’t use them enough for infection control, and rely too quickly on oral

antibiotics

• Vets overstock unnecessarily on variations of shampoos, rather than becoming

very comfortable and knowledgeable about a few topical products

• Vets formulate too often when existing products will meet their needs; why do

some ask for 2% CHX, 3% or 5%? Do any of us understand the reason for such

concentration differences? Rather just use a professionally developed product

than ask a formulator to make up some hodge-podge.

• Vets don’t tell clients to shampoo frequently enough, or avail their own staff to

clients to expedite this and ensure success

• Vets are not transitioning from 1 product to another when the situation improves

o For example, when managing an atopic dog with secondary bacteria, I

use Pyoderm (Virbac) q2d x 14d, then have a revisit – if improved, we

drop to 2/week x 2 weeks, then based on continued improvement

(email/phone contact may be enough), 1/week, then when there is no

infection, I will transition them onto Allermyl 1/week for life.


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o For Furunculosis, Demodecosis and proven Sebaceous Adenitis or

Seborrhoea, I will use Benzoyl Peroxide (Demodex) or Sebolytic (Virbac

– other 3 diagnoses). Apply these at the same intervals as in the

previous paragraph, for 10+ minutes. If there is significant infection as

well, the Pyoderm should FOLLOW these “degreasers” and keratolytics,

not precede them.

o Advise the use of sponges to apply medication, which should be

discarded after 1-2 weeks

o Advise the use of kitchen gloves used for only this purpose

I have a set of instructions I give clients on how and what to do – available if you would

like.

I also encourage people who may struggle (the client may have limited time, or back

pain, or whatever) – just drop the dog off with the shampoo and we will do it for them.

ALL YOU SHOULD CARE ABOUT IS RESULTS. Do what you must to achieve them.

Tip #9 - Adjuvants and success

Once you have the fundamentals of a patient’s condition under control, then, and only

then, start trying for 100% control, and here is where adjuvant therapies can help.

What I mean by this is that we chuck an enormous amount of medication and

supplements and diets and whatnot at clients, overwhelming them, creating a “pill

burden” on client and patient, and a big bill. Any failure of compliance or medical

efficacy – we are to blame, and they go elsewhere.

Sometimes you must win a war in stages. Sun Tzu said "Opportunities multiply as they

are seized." He realised that momentum was very important to warfare – and in

medicine. Win a couple of easy battles – flea control, infection control, improved

patient comfort, reduce pruritis by 70-80% - and then encourage the client by

complimenting their successes and then say “ok, we are 80% better – let’s see if we

can make Fido 100% itch free and not smelly. Now we can talk about improving his

skin health with a proper skin support diet, and a skin barrier rinse like Allermyl, since

we no longer have a big uphill battle. The key is to keep the skin healthy, so we don’t

get these flareups. Well done for getting him to this point! Let’s keep up the

momentum!”

Some products we use as adjuvants are:

• Ω3 fatty acid supplements like Dermofocus

• Allermyl and Allercalm shampoos

• Pyospot spot ons

• Redonyl capsules

• Older, sedating antihistamines like chlorpheniramine – used as a chronic not

single-use medication

• Skin support diets


45

• Cothivet to stop lick of acral granulomas that are almost but completely

controlled

• Cortavance spray for managing contact spots, thereby preventing more

widespread flare ups

• Epiotic used as “maintenance” therapy for ears as part of a surveillance

program

• Tushy Wipes to keep the perianal area clean and comfortable

Tip #10 - When (and how and why) to biopsy

Biopsy when there are lesions. Pustules in a setting likely to be atopy are not

warranted, unless the infection is widespread, recurrent, resistant to empirical therapy

(2-3 weeks of rilexine/clindamycin/purbac), or near the face, ear margins or

mucocutaneous junctions (these may be autoimmune). Crusting, ulcerated,

seborrheic and depigmenting lesions, as well as nodules – these should be biopsied.

Pathologists appreciate a few things – and an appreciative pathologist will give you

useful answers:

1) A history – maybe some photos emailed to them as support

2) A few DDx – what are your 2-3 most favoured suspicions?

3) 2+ samples taken parallel to the hair shaft, not perpendicular to the skin.

4) Carefully cared-for samples, not crushed or floating in formalin

5) Cultures are helpful – generally, aerobic +/- fungal (=dermatophyte) is all that’s

need, but indicate prior antibiotic therapy – I will wait 2 days off abcs before

doing this

6) Culture swabs should always be accompanied by your own inhouse cytology

evaluation to help you learn from what you saw

Future directions

So where is dermatology heading?

Certainly, the advent of the newer chewable, long acting agents like Symparica,

Bravecto, Nexgard and such; and effective long-term measures such as Seresto

collars, have all but eliminated flea-associated dermatitis in my practice. But clients

still need reminders to keep them scheduled properly.

This has shifted the demographics towards atopic skin conditions. When mild, we

manage them with low-intensity yet effective measures like diets, Cortavance and

topical therapy. When more severe or chronic, Atopica has been a mainstay of our

practice, but Apoquel has shifted the paradigm significantly. Nonetheless, these

products require a diagnostic workup before use to ensure there aren’t false

expectations created.

There is a profusion of diets – vastly over- and misused in my opinion. Diet is a

valuable and effective tool for the management of so many medical conditions – not


46

just dermatological ones – but must be used with discretion, as part of an iterative

plan, and for specific reasons.

Immunotherapy (ASIT vaccines) are useful, but perhaps less so than once imagined,

and should be used with the input of a botanist and a specialist for ideal outcomes –

which are modest at best, and slow (and expensive) to realise. Food allergy tests are

invalid and downright fraudulent in pets, in my opinion, and doing allergy tests with a

lab unable to then produce a desensitising vaccine just creates client anger. Going

forward, should Cytopoint make it to our shores, this represents a different angle on

immunotherapy for atopy, but is still many years away – if we don’t support Apoquel

and use it properly, then we won’t get Cytopoint – remember what happened to

Ypozane, the Nobivac biliary vaccine and Cardiguard?

The future holds some exciting prospects for understanding the immunology of many

conditions, and profiling patients according to these genetics, for more focussed

therapy, with fewer side effects. We must be on guard that we don’t think that we have

“defeated” ectoparasites, and always, always, seek to manage antibiotics sensibly and

with an eye to our own future.

References BIZIKOVA, P. & OLIVRY, T. 2016. A randomized, double-blinded crossover trial testing the benefit of two hydrolysed poultry-based commercial diets for dogs with spontaneous pruritic chicken allergy. Vet Dermatol, 27, 289-e70.

BIZIKOVA, P., SANTORO, D., MARSELLA, R., NUTTALL, T., EISENSCHENK, M. N. & PUCHEU-HASTON, C. M. 2015. Review: Clinical and histological manifestations of canine atopic dermatitis. Vet Dermatol, 26, 79-e24.

EOM, K., LEE, H. C. & YOON, J. H. 2000. CANALOGRAPHIC EVALUATION OF THE EXTERNAL EAR CANAL IN DOGS. Veterinary Radiology & Ultrasound, 41, 231-234.

NOLI, C. & CENA, T. 2015. Comparison of FEDESI and SCORFAD scoring systems for the evaluation of skin lesions in allergic cats. Vet Dermatol, 26, 481-3, e112-3.

PEDROSA, A. F., LISBOA, C., FARIA-RAMOS, I., SILVA, R., RICARDO, E., TEIXEIRA-SANTOS, R., MIRANDA, I. & RODRIGUES, A. G. 2019. Epidemiology and susceptibility profile to classic antifungals and over-the-counter products of Malassezia clinical isolates from a Portuguese University Hospital: a prospective study. J Med Microbiol, 68, 778-784.

PLANT, J. D., GORTEL, K., KOVALIK, M., POLISSAR, N. L. & NERADILEK, M. B. 2012. Development and validation of the Canine Atopic Dermatitis Lesion Index, a scale for the rapid scoring of lesion severity in canine atopic dermatitis. Vet Dermatol, 23, 515-e103.

SCHLEMMER, K. B., DE JESUS, F. P. K., LORETO, E. S., FARIAS, J. B., ALVES, S. H., FERREIRO, L. & SANTURIO, J. M. 2019. In vitro combination of antifungal agents against Malassezia pachydermatis. Med Mycol, 57, 324-327.


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(notes)


51

Case Based Approach to Endocrine

Conditions Dr Arina Pimosenco DVM cum laude BVSc(Hons)

Introduction Endocrinal diseases in veterinary practice are often presented not only as challenging

to diagnose but to recognize and manage their potential complications. The topic of

this presentation is focused on some of the cases we see in referral hospital and can

be certainly encountered in general veterinary practice.

Case 1. “Gracie”

Gracie was a 11 years female spayed German Shepherd Dog Cross, when she was

presented for the sudden onset of cluster seizures. Biochemistry panel sent to the

external laboratory and provided with the clinical history did not include glucose

measurement.

What did we do? We measured blood glucose and serum ammonia. Ammonia was low normal. The

blood glucose has been constantly low ranging from 0.7-1.3 mmol/L at all times,

despite regular frequent feeding. Intravenous dextrose boluses (0.1-0.2 ml/10 kg)

resulted in short effect only.

The most common differential diagnoses for persistent hypoglycaemia were ruled out

as follows:

o Xylitol toxicity, Insulin overdose were excluded based on history;

o Liver failure based on normal ammonia/bile acids;

o Addison’s disease based on adequate response to ACTH stimulation test

(cortisol levels 118/319 nmol/L)

o Sepsis based on examination, imaging and clinical pathology;

o Extra pancreatic neoplasia based on imaging.

After exclusion of these aetiologies, Beta-cell pancreatic tumour (insulinoma) was

suspected. Unfortunately, insulin/glucose assay could not be performed due to

external laboratory issues. Insulin/glucose ratio greater than 4.2 is considered

diagnostic for insulinoma.

Abdominal ultrasonography revealed a spherical hypoechoic nodule measured 1,1 x

1,1 cm in the left pancreatic lobe.

Initial management involved dexamethasone administration as an insulin antagonist

and correction of hypoglycaemia. Surgical intervention revealed a discrete solitary

nodule correlating with ultrasonography findings and no visual evidence of metastatic


52

disease. Histopathology confirmed insulinoma with clear surgical margins. Gracie has

made an uneventful and rapid recovery after surgery and her owners have been given

an oncology surveillance program.

In the events when widespread metastasis exists or persistent hypoglycaemia recur

soon after surgery, medical management should be considered. It involves following

options: prednisolone 0.5-1.0 mg/kg daily in divided doses, diazoxide, acetazolamide

(not readily available) and

Streptozocin (a toxic, expensive and difficult drug to obtain and manage). Relapsed

metastasis can be destroyed with microwave ablation (refer to IVSC for options).

Take Home Message:

➢ -Not all “neuro” symptoms are neuro – some are endocrine;

➢ -Always check blood glucose in weak, hypotensive, pale or seizuring patients;

➢ -Insulinoma without extensive extra pancreatic metastasis can be treated

successfully by surgical or a combination of surgical and medical management

with median survival time after surgery of 14 months. (Polton, et al., 2007)

Case 2. “Nicky Pooh” Nicky Pooh was a 10 years old female spayed Jack Russel Terrier when she was

referred to us for collapsed trachea and suspected hyperadrenocorticism (HAC).

Clinical examination revealed overweight, pot-bellied and constantly panting, pot-

bellied patient with polyuria, polydipsia (>100 ml/kg/day) and polyphagia. Clinical

pathology showed glucose of 10.81, ALT 265, ALP 951, GGT 103. Urinalysis results

were as follows: S.G. 1.012, Protein 2+, cocci, rest normal and negative. Haematology

showed stress leukogram only.

She is not a typical breed for genetic predisposition of collapsed trachea and her main

respiratory symptom was constant panting. Thoracic radiographs were unremarkable

with and seemingly narrowed trachea caused by superimposition of the longus colli

muscles and oesophagus, therefore being an artefact for collapsed trachea.

What would you do as the next diagnostic step?

We would exclude or confirm following:

o Hyperadrenocorticism (HAC) by firstly, abdominal ultrasonography (US), and

secondly, followed by specific tests, like ACTH stim test for suspected pituitary-

dependent HAC (PDHAC) and LDDST for suspected adrenal-dependant HAC

(ADHAC);

NB: LDDST is a very sensitive test, but rather considered a screening test due to many

false positives. We prefer to screen with the ACTH stim test + abdominal US


53

o Hypothyroidism by TT4 followed by TSH test;

o Diabetes Mellitus (DM) by checking blood and urine glucose, and possibly serum

fructosamine level.

If post ACTH stim cortisol level is in grey area of 400-550 nmol/L, consider following:

o A 4-fold increased from basal, in a patient with supporting history, clinical and

ultrasound findings, can also be considered a confirmation of PDHAC

o Re-check ACTH stim test in 4-6 weeks;

o Is it atypical PDHAC, adrenal mass, ectopic ACTH tumour, other diagnosis?

o 17 alpha-OH progesterone assay (pre and post ACTH) – another

adrenocortical hormone.

HDDS test (High Dose Dexamethasone Suppression) and Endogenous ACTH assay

can be used to distinguish between ADHAC (resulting in low ACTH) and PDHAC (high

ACTH).

Nicky Pooh’s diagnosis as PDHAC was confirmed via combination of abdominal US

and ACTH stim test. Her adrenals were bilaterally enlarged and measured 7 and 7,7

mm (Bento et al., 2016, Benchekroun et al., 2010).

So what about panting? Cushing’s disease can be responsible for the diaphragmatic

weakness due to metabolic protein catabolism and intercostal muscular wasting –

although this sarcopaenia is not considered to be clinically dangerous. Treatment was

challenging for this patient and she was tried on different doses of trilostane for 4-5

months with poor post-ACTH cortisol responses and ongoing clinical signs of

Cushing’s disease, including various complications:

o urinary tract infection, treated with the appropriate antibiotics according to the

culture and sensitivity;

o an episode of acute pancreatitis, managed medically;

o end-stage gall bladder mucocele, which has been surgically removed;

o deep venous thrombosis affecting her right forelimb, treated successfully with

anticoagulation.

It was evident trilostane was not controlling HAC and her treatment was switched to

mitotane (Lysodren®) which was very effective in her case. This drug is a bit trickier

to manage, however, and has recently become very expensive; it requires a Section

21 licence and is toxic with chronic exposure so the client must sign consents. This is

worth of referral for management.

Subsequently, she was also diagnosed with hypothyroidism and prescribed Leventa®,

which improved her quality of life even further.

Take Home Message:

➢ Cushing’s disease is a “jigsaw puzzle” of different clinical signs, especially in a

small dog;

➢ Ideally imaging is best to be done before specific tests for HAC chosen;


54

➢ Confirm suspected PDHAC with ACTH stim test;

➢ No test is 100% accurate

➢ Watch for complications:

o UTI & other infections

o Poor wound healing

o Thrombosis

o Gall Bladder Mucocele

o Diabetes and pancreatitis

o Hypertension, resulting in: CHF, Glomerulonephritis, Intraocular

haemorrhage, retinal detachment

➢ There could be two or more endocrinopathies in one patient. These are

referral level patients.

Case 3. “Itsy-Bitsy” Itsy-Bitsy was 11 years old spayed female Abyssinian cat, referred for further

investigation of her chronic kidney disease and general anaesthetic safety discussion

for elective procedure (dental and eyelid mass removal) in February 2016. She was

classified as having IRIS Stage II, proteinuric, hypertensive (160/80) CKD. Her

hypertension and proteinuria have resolved on amlodipine (starting dosage 0.625 mg

per cat OID) in a month time.

In March 2018 she presented with acute onset of rhinitis, suspected to be due to

Herpes Virus.

In April 2018 owner suspected Itsy-Bitsy developed DM, as she had developed PU/PD

and PP. Blood glucose was 32.6, urine S.G. 1.035 and glucose in urine 4+. She was

admitted for inpatient stabilisation and glucose curves. She also developed a urinary

tract infection as DM/CKD complication, so marbofloxacin was prescribed pending

culture and sensitivity results.

Her urine culture results came back as a very resistant Enterococcus faecalis isolate,

and an extended antibiogram showed sensitivity to ceftazidime which was

subsequently used q24h IM 20-50mg/kg for five days. Urine culture was repeated and

the infection was successfully cleared. Her insulin dose was increased to 5 IU q12h at

this stage and this dose brought her blood glucose down to 3.5-9.4 mmol/L.

Ceftazidime is renally excreted so careful management of dosimetry and renal

monitoring were required.

In the beginning of May 2018 she was admitted for a medical boarding, and after her

evening 5 IU of Lantus dosage she became depressed and lethargic with following

findings: T- 37.6, P 217, blood glucose 4.3-7.3 (glucose curve range), blood pressure

of 139/82, urea 15.7, Na 168, Total bilirubin 18. She appeared blind, uncoordinated,

anxious. Fundus examination did not reveal any abnormalities.


55

So what happened?

The cat had a resolution of the DM which coincided with hospitalisation. As a result, it

had a RELATIVE INSULIN OVERDOSE. The latter caused acute onset of

hypoglycaemic encephalopathy.

How did we manage it?

Management involved insulin therapy discontinuation, mannitol, vitamins B1 and B12

administration, Karsivan®, frequent feeding, IV fluids, glucose monitoring and

supportive care.

Itsy’s progress was steady with regards to blood glucose and recovery from

hypoglycaemic encephalopathy. She was mostly normoglycaemic with a few

intermittent moderate blood glucose elevations every 2-3 days for the next three

weeks. Insulin dose and needs of administration were carefully adjusted with home

glucose monitoring. One month after this initial episode of hypoglycaemia she was

doing well, had return of mobility and vision, her fructosamine level was 196 (N 191-

349) and a glucose curve confirmed there was no insulin required.

Analysis of the preceding events happened with this cat revolves further questions:

o Did she have insulin resistance complicated by UTI/URTI?

o It resolved partially due to intermittent activity/reserves in pancreatic

Beta-cells?

Take Home Message:

➢ CERTAIN cats get temporary diabetic states, SOME go on to “stutter” into full

DM, others don’t

➢ Watch diabetics for life

➢ Use fructosamine for monitoring, especially in cats

➢ Look for insulin resistance and diabetic honeymoons

Case 4. “Bacardi” Bacardi was a 12 years old spayed female domestic short hair cat with poor BCS 1.5/5.

She was diagnosed as hyperthyroid more than 1-year prior the presentation. She had

been managed medically by carbimazole 3X 5 mg OID, as surgery seemed “too

dangerous”. The reason for referral was suspected cerebrovascular insult/transient

ischemic accident (CVA/TIA)

Clinical examination revealed underweight, tachycardic (HR 203) and a “difficult to

handle” cat with palpable goitre.

So why did she have a suspected CVA/TIA?


56

What are complications of hyperthyroidism?

Bacardi appeared to have hypertension (BP 163/97). Hypertension can cause cardiac

and renal disease, as well as end target organ damage (heart, kidneys, brain, eyes).

Bacardi’s kidney function tests were within normal limits: Urea, creatinine, SDMA were

normal with urine protein to creatinine ratio (UPC) <0.2. However, she had

hypertrophic cardiomyopathy (HCM) with left atrial enlargement.

We began with management of the HCM, hypertension and prevention of FATE (feline

aortic thromboembolism) with amlodipine, diltiazem and clopidogrel (Plavix). It has

been reported that, clopidogrel is more effective as antiplatelet aggregation agent and

much safer for cats compared to aspirin (Hogan et al., 2004). We find this drug easier

to manage. The original (Plavix) is used for oral dosing as it quarters more easily and

evenly; the generics (Mispro) can be used if being ground into a powder for

compounding. V-tech also offer clopidogrel-containing carnivore pastes – discuss the

exact formulation with us after diagnosis.

Medical management of hyperthyroidism was adjusted (2.5-5mg q 8-12h). using

carbimazole with more regular dosing

Surgical intervention performed in 3 weeks’ time. It involved bilateral thyroidectomy

(intracapsular) with ex vivo dissection of the parathyroid glands and re-implantation in

a sternothyroideus pouch, which was performed successfully with stable anaesthesia.

Blood pressure and TT4 levels started to stabilise soon after surgery.

NB: Watch out for the following complications:

o Hypocalcaemia in cases of bilateral thyroidectomy (20% chance);

o Hypothyroidism (33% in a recent study) with subsequent worsening of

azotaemia especially if a cat was azotaemic before definitive therapy

(bilateral thyroidectomy /radioiodine therapy) due to reduced glomerular

filtration rate;

o -Hypertension and medical management of TT4 level needs to be

stabilised as well as possible before definitive procedure (usually takes

3-4 weeks);

o Recurrent hyperthyroidism in surgical cases due to recurrent

adenoma/carcinoma (22% in a recent study) or ectopic thyroid tissue (1

in 200 thyroidectomies). (Covey, et al., 2019)

Bacardi developed a transient hypocalcaemia which was successfully managed with

IV calcium gluconate infusions and vitamin D3 oral supplement.

Shortly after surgery her body weight and quality of life improved significantly.


57

Take Home Message:

➢ Stabilise hypothyroidism and its secondary diseases by medical management

within 3-4 weeks and refer for definite treatment options, like thyroidectomy

(radioiodine is not available yet)

➢ Y/D diet is not as effective as we would like it to be in all patients and depends

heavily on client and patient compliance. When cats are extremely sarcopaenic,

some authorities consider it’s protein levels to be too low to regain musculature.

➢ Monitor TT4 and BP regularly

Case 5. “Max” Max was an 8 years neutered male dog with BCS 3.5/5, presented with following:

panting a lot, lower lips sagging, drooling, no pupillary light response, poor palpebral

response. Owner’s main complaint was that the dog’s food kept falling out of his mouth

and he had unusual lethargy. Everything else was within normal limits on physical

examination.

What would be your next step?

Neuro examination revealed following abnormalities:

Partial Bilateral Oculomotor (III), Trigeminal (V) AND Facial (VII) paralysis

Biochemistry abnormalities were as follows:

ALT 577 ALP 554 GGT 43 CRP 4.0

What else would you do?

TT4 was very low 8 nmol/L, and cTSH was 1.16 ng/ml. It was diagnostic for

hypothyroidism.

Leventa® and an eye lubricant were prescribed and the owner was advised to return

in 3 weeks for a check-up and repeat TT4 level.

Clinical response to hormonal replacement therapy was noted by the owner within 14

days. Max had his follow-up only in 4 weeks’ time and by the his TT4 level was 16. As

our aim is middle range – 25, we’ve increased the dose of Leventa slightly. Clinically,

Max improved a lot, was able to eat his pellets without dropping them, he became

active and happy, his neuro deficits improved with the right side of his face by 99%

and the left by 70%.

Hypothyroidism has been associated with variety of neurological disorders. The

mechanism responsible for neurological abnormalities is not completely understood.

One of the proposed theories of underlying pathogenesis is hypothyroid dogs are

prone to hyperlipidaemia, hypercholesterolemia, leading to atherosclerosis,


58

thromboembolic events, and subsequently resulting in poor blood supply to nervous

tissue.

NB: Many factors and medications can affect TT4 level, like corticosteroids,

phenobarbitone, sulphonamides, non-thyroid illness, anaesthesia, anti T4/T3

antibodies, etc.

Take Home Message:

➢ Learn all the manifestations of hypothyroidism

➢ Rather DO NOT treat without absolute confirmation

➢ TT4 AND TSH for diagnosis

➢ Understand the conditions and drugs that affect T4 measurements

Case 6. “Cola” Cola was a 10 years old spayed female Labrador Retriever cross dog, presented for

severe PU/PD with urinary “overflow” and decreased appetite. Physical examination

was unremarkable, except slightly dull coat.

What are the most common to the least common differential diagnosis for

primary PU/secondary PD?

o Diabetes Mellitus

o Chronic renal failure

o Liver disease

o HAC

o Hypercalcemia

o Drug induced (steroids, furosemide)

o Neoplasia

o Hypoadrenocorticism

o Hypokalaemia

o Endotoxaemia (pyometra)

o Central/nephrogenic diabetes insipidus

o Hyperthyroidism

o Fanconi’s syndrome

o Primary renal glucosuria

o Phaeochromocytoma

o Post-ureteral obstruction diuresis

o Polyuric acute renal failure

Urine analysis revealed S.G. of 1.007. Biochemistry abnormalities were as follows:

ALKP 474, Total Ca 3.20. The cause of PU/PD was narrowed down to hypercalcemia.

What would you do next?


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What are the most common pathological processes causing hypercalcaemia

in dogs? Hypercalcemia of malignancy (mainly lymphosarcoma, anal sac adenocarcinoma,

multiple myeloma), hypoadrenocorticism, primary hyperparathyroidism, chronic renal

failure, granulomatous diseases (fungal, chronic panniculitis), non-malignant skeletal

lesions, hypervitaminosis D.

So, the search started. As mentioned before, clinical examination including peripheral

lymph nodes, abdominal palpation and rectal examination were unremarkable.

Thoracic radiography did not reveal any abnormalities. Abdominal ultrasonography

revealed left liver lobes a little more hyperechoic and granular parenchyma, with

multiple small (5mm or smaller) isoechoic, poorly marginated, irregular areas.

Parathyroid ultrasonography showed the right cranial parathyroid gland was markedly

larger (4.8 mm) in long axis, compared to other parathyroid glands.

Primary hyperparathyroidism caused by parathyroid gland adenoma was highly

suspected. Evaluation of ionized serum calcium, PTH (parathyroid hormone) and

PTHrP (parathyroid hormone-related protein) would be very useful to confirm our

diagnosis but it is not available in local veterinary laboratories.

In doubtful cases, ultrasound-guided alcohol ablation (Guttin et al., 2015) of the

parathyroid nodule/mass can by performed with subsequent temporary decrease in

total calcium level. This is a cheap and useful diagnostic test but takes a lot of skill to

avoid the local structures and ablate a 2mm nodule!

Medical management involved IV sodium chloride 0.9% and injectable furosemide to

promote calcium excretion in urine. Total calcium remained high, but Cola’s appetite

has been improved and clinically she remained stable. Right cranial gland

parathyroidectomy was successfully performed and trucut liver biopsy was done

shortly. Total calcium was checked again next day after surgery and it was decreased

to 2.69. Cola was discharged in 2 days after surgery with total Ca level of 2.48 and

reduced signs of PU/PD. She was prescribed oral supplement low doses of Vitamin

D3.

NB: Due to one overactive parathyroid gland other three become atrophied and

inadequate production of PTH, patients after parathyroidectomy must be monitored

for hypocalcaemia daily and can be supplemented with oral vitamin D3 preventatively

for a few weeks after surgery and monitor Calcium level after weaning off vitamin D.

Histopathology revealed parathyroid adenoma with degenerative hepatopathy. The

latter could be a consequence of endocrine imbalances induced by the parathyroid

adenoma.

Cola made full recovery, was free from PU/PD signs, and we managed to avoid post-

operative hypocalcaemia.


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Take Home Message:

➢ Primary hyperparathyroidism is seen more often than previously thought

➢ It is curative disease with good life-expectancy provided kidney functions

are not affected

➢ When renal, cardiac function is affected by chronic hypercalcaemia,

prognosis is not as great

Conclusion Endocrine cases can be manifested in various ways with cardiovascular, neurological

and metabolic clinical picture. They can cause many severe and fatal complications if

not recognized and managed early in the pathological process. We possess many

diagnostic tools to diagnose endocrine diseases, as well as we do not have many

hormonal assays easily available in South Africa, which makes this matter even more

challenging.

References BENCHEKROUN, G., DE FORNEL-THIBAUD, P., RODRIGUEZ PINEIRO, M. I., RAULT, D., BESSO, J., COHEN, A., HERNANDEZ, J., STAMBOULI, F., GOMES, E., GARNIER, F., BEGON, D., MAUREY-GUENEC, C. & ROSENBERG, D. 2010. Ultrasonography criteria for differentiating ACTH dependency from ACTH independency in 47 dogs with hyperadrenocorticism and equivocal adrenal asymmetry. J Vet Intern Med, 24, 1077-85.

BENTO, P. L., CENTER, S. A., RANDOLPH, J. F., YEAGER, A. E. & BICALHO, R. C. 2016. Associations between sex, body weight, age, and ultrasonographically determined adrenal gland thickness in dogs with non–adrenal gland illness. Journal of the American Veterinary Medical Association, 248, 652-660.

GUTTIN, T., KNOX, V. W. & DIROFF, J. S. 2015. Outcomes for dogs with primary hyperparathyroidism following treatment with percutaneous ultrasound-guided ethanol ablation of presumed functional parathyroid nodules: 27 cases (2008–2011). Journal of the American Veterinary Medical Association, 247, 771-777.

HOGAN, D. F., ANDREWS, D. A., GREEN, H. W., 3RD, TALBOT, K. K., WARD, M. P. & CALLOWAY, B. M. 2004. Antiplatelet effects and pharmacodynamics of clopidogrel in cats. Journal of the American Veterinary Medical Association, 2004, 1406-1411.


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63

Canine Behaviour Disorders Influenced

by Owners & Environment Dr Melvyn Greenberg

BVSc

If you treat your dog like a human, your dog is going to treat you like a dog!

Since the 1930s humankind has moved from small-holdings, semi-rural and rural

areas to high-density dwellings - Human lifestyle alteration has been profound where

women have become more career-oriented and relationship leaders – the patriarch

has weakened to the level that dogs are manipulating children, children are permitted

to dictate to their parents and submissive new age leadership sees adults negotiating

with their offspring on matters that are of no concern to them such as ideal pet

selection – the pup will seek the weakest member of the family, hone in and become

selected as the most loving “because it chose me”….the entire family structure has

done a somersault – children are sent to creches, grandparents and great-

grandparents are condemned to retirement villages and old age homes – families have

become more isolated from the community – people have become more insecure,

depressed, isolated, anxious, tired, lazy and lonely using pets as substitute

relationships, pouring their emotions on to dogs who just want to be dogs – the dogs

are mostly home alone diurnally while nocturnally they are overindulged, thus creating

serious anxiety issues for dogs in dysfunctional families

Walled-in properties – Architects and interior designers, while they offer no

consideration for the practical comfort of pets – slippery floors, stairs, low furniture,

minimal garden space, and especially four walls……….there is no visual stimulation –

no association foA all their senses – space is irrelevant in a prison environment – dogs

do not live with appreciation for being rescued, having good food and a lovely home –

aesthetics are meaningless – they want to explore, smell, “read the newspapers” and

smell “WhatsApp” another dog’s perineum

If people are becoming recognisably bipolar, obsessive compulsive, nervous, anxious,

aggressive, frustrated, indecisive, dysfunctional, inconsistent, manic and phobic, how

does a dog survive this onslaught of emotion and attitude??!

People have lost contact with reality after having coexisted 30,000 years with a canine

– TV and cinema are regarded as gospel in the communication concepts with animals?

– humans have become less skilful, highly submissive and far less instinctive with

animals. People do not know how to develop well-balanced relationships anymore.

This negative downward trend has reached a level where the average lifespan of a


64

dog in the USA has dropped to a frighteningly low level, more dogs are euthanased in

the USA annually due to behaviour problems than medical and surgical conditions

combined – and more than the total population of dogs in South Africa – we have to

be introspective and enquiring: Man is no longer dog’s best friend!!!

Misinformation in pre-graduate veterinary education, charlatan behaviourists, bogus

“animal whisperers”, displaced animal rightists and “bunny huggers” have been

promoting the misconception that a hierarchy no longer exists, pack systems are a

thing of past and there is no such role as an alpha male and alpha female……after

millions of years….to the detriment of many dogs. This alone is one of the most

serious crimes of human-animal interaction – these teachings are unscientific,

unethical, unnatural, senseless and potentially dangerous

Anthropomorphism – familial (Dogs have no concept of being related) concepts,

“emotions” of guilt, jealousy, know they have done wrong – my dog loves me…

Potential dog owners never seek the advice from experts on the method of selecting

an ideal puppy from a litter – never 2 pups from same litter – never 2 pups of the same

sex – never 2 pups at the same time……how to select the individual is also

important…..

Selecting a suitable breed for claustrophobic environments:

• Bichon Frise

• Chihuahua

• Chow Chow

• Collie – Bearded, Rough

• Corgi

• Bulldog – English, French

• Poodle – Toy, Miniature, Maltese

• Greyhound

• Griffon

• Italian greyhound/Seguglio/ Whippet

• Japanese Chin

• Spaniels: Cavalier King Charles, King Charles, American Cocker, English Cocker, Clumber

• Lhasa Apso

• Miniature Pinscher

• Miniature Schnauzer

• Papillon

• Pekingese

• Pomeranian

• Pug

• Schipperke

• Shar Pei

• Shetland Sheepdog

• Shi Tzu

• Terriers: Boston, Scottish, West Highland White, Cairn, Yorkshire


65

Why people select certain dogs….

Puppy socialisation 8 weeks to 5 months – essential foundation

Basic obedience training 6 -18 months – if the owner is not trained, the dog can only

be dysfunctional, uneducated and disadvantaged

Advanced obedience training – an option for certain breeds and devoted owners

Ongoing education…..

Domestic blunders = harnesses, jackets, dogs indoors, walking a dog, pulling on a

leash, walking through a doorway, patting and shooshing, collars are costume

jewellery, eye contact

Pack leadership is not dictatorship - New Age = No Leadership

Immediate response to dog’s demands and: Free love – negotiating from a submissive

angle

People talk too much to their animals who are not born with a vocabulary – screech

on greeting – squeal in high-pitched voices to show “affection” for the neoteny – Eye

contact – a dog’s name is merely a familiar command

Meaningful interaction – no democracy in nature – gregarious animals live in a

hierarchy system which they understand – what do dogs need as opposed to what

owners want??!!

Pet owners need to learn to do nothing with their dogs – meditate, relax, show calming

signals – use body language and vocalisation only when necessary

All behaviour disorders are exaggerated instinctive normal behaviour patterns so that

dogs can cope with stress situations. Canine behaviour disorders = 33 common types

Punishment – aversive or diversive, are the only means – owners cannot be

responsible for direct reprimands – causes confusing signals if an owner “loves” and

“”punishes”.

Solving behaviour problems in practice with 10 easy tips.


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67

How Do We Become The Best Vet / Vet

Nurse We Can Be? Dr Kenneth Joubert BVSc, MMedVet (Anaes)

Veterinary Anaesthesia, Analgesia & Critical Care services

[email protected]

“The greater the ignorance the greater the dogmatism” – Sir William Osler said. It

is important for us to question everything we see, hear and do to make sure it is in the

best interests of our patients. To find the best pathway to follow for each individual

patient we see. The information at hand is often based on how a population responds

and not an individual so adjustments needs to me made. How do we do this?

The most dangerous phrase in the English language is “we’ve always done it this

way”. Change and adaption is important. Don’t just blindly follow a practice. Think

about it and how it relates to our patients. So how do we go about getting information

and changing practice for the best? Increasing our knowledge is important. We can

read textbooks and articles and go to conferences and follow trends on the internet

and social media. Textbooks are often 5 years behind the current scientific

advancements while journal articles are about two years behind. Conferences are

more up to date while social media is in the moment. Some of us adopt these practices

early while others wait forever. When should we change practice and based on what

evidence? Not all of the new developments will stand the test of time and many will be

shown to be wrong however if we miss an important one this can dramatically impact

the quality of life of our patients. We often only know the value of new science about

10 years after the breakthrough is made through repetition of scientific work.

The Dunning-Kruger effect teaches us that after learning a new skill we often over rate

our abilities and feel more confident than experienced people. Over time we learn what

we really need to know and how little we actually know. This helps us grow. Safe,

competent experts often realise what they don’t know and have worked out many of

the issues which can go wrong. This takes time. Some people will master a skill but

never perfect it while others will keep pushing themselves to new horizons.

Stress is required to develop. Our response to stress is known as the fight or flight

response. These two are quite obvious but the most common response is neither of

these. It is freeze. In times of severe stress most people will freeze – do nothing. Our

response to freezing can be changed through training, understanding and experience.

In times of severe stress we often revert to our lowest level of training. Small amounts

of stress help stimulate learning and development while no stress in actual fact makes

us complacent. As our heart rate rises we also lose fine motor co-ordination and

cognitive processes. The only way to avoid this is through training.

mailto:[email protected]


68

To function in a team we need to perfect closed loop communication. Giving clear,

precise and directed information has been perfected in the aviation industry to improve

safety. We need to master the art of closed loop communication and the concepts of

a shared understanding that we can all work together and achieve the most important

goals for ourselves and our patients.

“So no degree of commitment to belief makes them knowledge. Indeed, the hallmark

of scientific behaviour is certain scepticism even towards one’s most cherished

theories. Blind commitment to a theory is not an intellectual virtue: it is an intellectual

crime”.

To answer what we should do in our practice in relation to ever burdening increase in

scientific knowledge we should apply the principles of basic research. The scientific

methodology was described in ancient Greece and hold true today. Develop an idea,

make observations and develop questions, test these questions by gathering data and

then refining, expanding or rejecting them. This loop needs to keep turning for growth

to happen. We often do not practice science but base our decision on our last

experience using anecdotes not science to determine our practices. Always be aware

of bad science and look for it.

When events do not go to plan, we can lose control of our environment. Often we find

someone to blame. We should assess what went wrong, why the system failed and

how we improve the system to make it function better. The airline industry has

perfected this and we can learn a lot from how they manage a disaster investigation.

We learn and master skills through repetition. After performing a task once we will lose

more than 80% of that ability in a very short space of time. Repeated regular repetition

is required to retain knowledge. Listen to static types of learning including lectures and

reading - do not lead to a great retention of knowledge. Knowledge is best retained

through practice, discussion in groups and teaching of others. Knowledge alone does

not allow us to become an expert or master a skill. It will help start the road to mastering

a skill but more is needed. This comes from deliberate practice. Deliberate practice

was studied initially in musicians. It is about breaking the skills and knowledge down

into little segments and then slowly reassembling the segments until the final piece is

performed. It can take 10 000 hours to master a skill. Practice should lead you to the

point where you can no longer fail. Coaching is an important aspect of developing

skills. This is standard practice for musicians and sports people but has been lost to

many other professions. Most top performers have multiple coaches. Deliberate

practice and feedback will make you an expert.

Working as a team will enhance your abilities. Practice as a team. Practicing while

playing matches is not the way high performance teams do it. Practice need to happen

before the skill is required.


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When things don’t go to plan - debrief afterwards to find a way to move forward and

correct the issues that arose so that they are no longer a problem.

Look after your team. “Safer care for patients is only possible if we care for those who

care for our patients”. Look after yourself as well. Be aware of compassion fatigue and

post-traumatic stress dis-order. Seek help if you see it in yourself or others.


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(notes)


71

Readers and attendees are advised to check product information and verify dosages

and indications, methods and durations of administration, and contraindications. It is

the responsibility of the treating veterinarian, to determine dosages and the best

treatment for any patient. Neither the publisher nor the editors assume any

responsibility for any injury and/or damage to animals or property.

© 2020 - Tables in these proceedings may be copied for personal use

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