Companion Quarterly Vol 29 No3 September 2018

COMPANION QUARTERLY – Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA

Companion Quarterly

OFFICIAL NEWSLETTER OF THE COMPANION ANIMAL VETERINARIANS BRANCH OF THE NZVA Volume 29, No. 3 | September 2018

VOLUME 29 NO 3 September 2018

Electric training collars: torture or training?

Initial management of GDV: what you need to know

Time to rethink tramadol for dogs with osteoarthritis?

Congenital spinal malformation in a young dog

Report: Highlights from Vet Ophthalmology course Part II

Volume 29 | No. 3 | September 2018 ISSN No. 2463-753X EXECUTIVE COMMITTEE 2018 cav@vets.org.nz

CONTENTS

President

John Munday

Companion Quarterly

Operations Manager Rochelle Ferguson

Treasurer

Simon Clark

Committee Members Simon Clark Nina Field Toni Anns Natalie Lloyd Alison Pickering Becky Murphy Paula Short

EDITORAL COMMITTEE Sarah Fowler (Editor) Bart Karalus Ian Millward Juliet Matthews Aurore Scordino Shanaka Sarathchandra

Address for submitting copy/ correspondence

Sarah Fowler 66 Callum Brae Drive, Rototuna, Hamilton 3210 T (H) 07 845 7455 | M 027 358 4674 E sarah.fowler@gmail.com

2 Editorial 4 CAV activities and meeting highlights

8 CAV Noticeboard 10 Mailbox 12 News in brief 18 What is your diagnosis?

Sarah Lee

20 Clinical update: time to rethink the use of tramadol for dogs with osteoarthritis?

Andrew Worth

Advertising Manager

Christine Moloney 25 Manchester St, Feilding T 06 323 6161 | F 06 323 6179 E Christine.moloney@tvg.co.nz

NZVA website www.nzva.org.nz

26 Electric training collars: torture or training?

E.L. Flint

30 Initial management of canine

gastric dilatation and volvulus: what you need to know Philip Hyndman

CAV website www.cas.nzva.org.nz Copyright

The whole of the content of the Companion Quarterly is copyright, The Companion Animal Veterinarians Branch of the NZVA (CAV) and The New Zealand Veterinary Association (NZVA) Inc.

36 Case report: unusual congenital spinal malformation causing neurologic dysfunction in a young dog Miriam Bates, Richard Jerram, Benjamin Wernham

Cover photograph

Leo surveys his domain. Photo courtesy of Mark Richardson.

Newsletter design and setting

44 Conference Report: highlights from the course in Veterinary Ophthalmology II at the European School for Advanced Veterinary Studies: Part II Jos van Hees

Penny May T 021-255-1140 E penfriend1163@gmail.com

Disclaimer The Companion Quarterly is a non peer reviewed publication. It is published by the Companion Animal Veterinarians Branch of the NZVA (CAV), a branch of the New Zealand Veterinary Association Incorporated (NZVA). The views expressed in the articles and letters do not necessarily represent those of the editorial committee of the Companion Quarterly, the CAV executive, the NZVA, and neither CAV nor the editor endorses any products or services advertised. CAV is not the source of the information reproduced in this publication and has not independently verified the truth of the information. It does not accept legal responsibility for the truth or accuracy of the information contained herein. Neither CAV nor the editor accepts any liability whatsoever for the contents of this publication or for any consequences that may result from the use of any information contained herein or advice given herein. The provision is intended to exclude CAV, NZVA, the editor and the staff from all liability whatsoever, including liability for negligence in the publication or reproduction of the materials set out herein.

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Conference Report: Veterinary Behaviour Chapter programme of ANZCVS Science Week Dr Elsa Flint

49 NZVJ Update 50 What is your diagnosis? The answers

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NZVA Conference 2018: All Creatures Great and Small

Vets in Stress Programme

57 Massey News 58 Companion Animal Health

24 Hour Freephone Confidential Counselling Service

Foundation update

59 CPD Record 60 Authors' Guidelines

0508 664 981 Helps you solve personal and work problems, including: Relationship problems Drug and alcohol issues Work issues Change Stress Grief

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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EDITORIAL

Conferences and collegiality During the last couple of months I have been fortunate enough to have attended both the New Zealand Veterinary Association meeting in Hamilton and the Australia and New Zealand College of Veterinary Scientists ‘Science Week’ meeting in Gold Coast.

As somebody who is interested in research, I always enjoy hearing about the latest research that is being performed within the veterinary fields.

However, it always strikes me that the most memorable and rewarding thing about attending such meetings is the ability to meet with people, renewing old friendships and meeting new people.

Although I work at a large organization, this ability to meet with fellow veterinarians and discuss their triumphs and tribulations is very valuable to me as it reminds me that we are all members of a wider veterinary community.

During both meetings there was a big emphasis on burnout in the profession and the possibility that people in the veterinary profession may enjoy their jobs less than people that work in other fields. Wellbeing is a current emphasis of CAV and the executive committee recently decided to find out whether companion animal vets were unhappy in their jobs compared to other professions by initiating an on-line happiness survey of companion animal veterinarians.

Once the results have been collated and analysed it is planned that the results of this survey will be discussed in a future Companion Quarterly.

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An interesting development at Massey that was discussed at the NZVA conference, is the new selection process for students hoping to get into the veterinary course. In the new selection process, non-academic criteria have been included to try to train more students who have not only the academic skill, but also the personal attributes that will enhance their success in the veterinary industry. This is the second year that the new selection criteria have been used so that it will be a few years before the benefit of the new criteria can be determined. Of course, it has to be recognised that veterinarians fill many roles other than clinical practice and currently most people in all walks of life will expect to have at least one career change during their working lives. Therefore it is important that the selection process has enough scope to enable people with different strengths to enter the course.

The plenary session of the ANZCVS meeting focussed on techniques that could be useful for people in any profession to deal with stressful circumstances more easily, and ways to feel happier and more fulfilled. The speaker offered many techniques that have been used to help people in other medical fields such as doctors and dentists. However, it was interesting that a good determiner of overall happiness is the number of friends and colleagues that people interact with and the feeling a person has of ‘belonging’ in their profession. As I was sitting in the

conference listening to this, it seems to me the benefit of the conference has come a complete circle. Not only am I learning about wellness techniques, but I am maintaining old friendships with classmates and meeting new members of my profession. By talking to colleagues who have all trained as veterinarians, it was great to discuss how their careers have progressed and what roles within veterinary profession that had. As I talked to fellow veterinarians it filled me with a strong sense of pride about how far we have all come and how we have all contributed to make our profession better.

As I left the conference I couldn’t help but be reminded how enjoyable such meetings are. I certainly recommend people attend their branch and national meetings as much as they can – both for the education value, but also to remind yourself that we are all part of a valued, trusted, forward-thinking and vibrant profession.

John S. Munday CAV President l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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WORKING TO PROMOTE AND SUPPORT COMPANION ANIMAL PRACTICE IN NEW ZEALAND

CAV activities and meeting highlights

Dangerous dog education

CAV have been invited by the Department of Internal Affairs to sit on a Dog Control and Safety Working Group comprised of selected group of stakeholders. This is an opportunity for CAV to put forward the solutions outlined in the NZVA dangerous dog position description directly to the Associate Minister of Local Government, Meka Whaitiri. It is pleasing to see the Minister choosing not to progress the breed specific legislation previously drafted by Louise Upston and instead undertaking consultation with stakeholders with a view to developing educative measures and enforcement best practices to address this complex problem.

Rabbit calicivirus RHDV2

Following advice from MPI that RHDV2 had been discovered in New Zealand, CAV have sent out member communications to all NZVA members and set up a discussion forum to keep members abreast of developments. We also provided education to the public through the NZVA Facebook page and a Radio New Zealand interview.

Greyhound Racing New Zealand (GRNZ) welfare committee work

The updated Greyhound Health and Welfare standards will now require that all greyhounds registered to race and breed must have up-to-date vaccinations against infectious canine cough as well as canine parvovirus, canine adenovirus and distemper.

Trainers will have to supply proof of each dog’s vaccination status to Greyhound Racing New Zealand each year in order to be able to nominate their dogs to race.

CAV website

To improve the member experience and make information easier to find, CAV

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have moved the member information from the group pages on the NZVA website to a separate CAV website. This also includes a section for the public that will have policies on general pet ownership topics available in a user friendly format. To support our website (www.nzva.org.nz/cav), CAV have also established member-only closed Facebook group. Do check them out and keep up-to-date with companion animal topics in New Zealand. See the August e-CAV for links and information on how to access.

Brachycephalic issues

The Auckland branch of the NZVA hosted a meeting in July with a panel discussion of veterinarians and breeders to air the issues associated with brachycephaly. CAV arranged to have this meeting filmed so that all members could benefit from hearing the discussion.

To further inform members around these issues, we have also made a copy of the lecture that Prof. Peter Sandøe, a bioethicist from the University of Copenhagen, gave at Massey in July called “What is wrong with my bulldog”.

Both of these can be viewed via links in the August e-CAV.

Feral cat management

CAV made a submission to the Environmental Protection Authority against a proposal put forward by the manufacturers of PredaStop (a poison used to target feral cats). The proposal was that the notification zone of households close to a poison drop site should be reduced from 3 km to 500 m.

CAV’s opposition is based on:

• Published research recommends an

exclusion zone of at least 2.4 km be

used.

• PredaStop is licensed for use in feral

cats. Feral cats are not generally found close to human habitation. If used in accordance with its registered

purpose, there should be minimal costs associated with 3 kilometre notification requirements.

• Owned cats are valued family members

and best practice methods of pest control should be employed to protect their welfare.

• Ensuring risks are mitigated for non-target animals is paramount in ensuring communities support environmental protection

Animal welfare advocacy hui

This hui was called by the Animal Welfare Minister, Meka Whiteri and attended by 65 delegates from a wide range of animal welfare groups. CAV presented on four areas of animal welfare:

• Welfare issues associated with selected breeding

• Concerns with breed specific

legislation being used to manage the dangerous dog problem • The need for a nationwide legal framework to manage cats • Concerns regarding the use of electronic behaviour modifying collars in dogs

Based on conversations from this hui, MPI have released a “Framework for action on animal welfare in New Zealand”. This document sets out four areas in which the government plans to focus on to improve animal welfare. It includes developing an independent voice for animal welfare and will explore options that include appointing a commissioner for animals. You can download the framework here: http://www.mpi.govt. nz/dmsdocument/29603/send.

Australian Small Animal Veterinarians branch

During conference, CAV hosted Dr Michael O’Donoghue from the ASAV branch. This was an opportunity to compare notes on activities. Topics that are occupying ASAV at this time are development of the an Advanced Practitioner Certificate scheme and

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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NZVA Conference and CAV Service Award

safety concerns with petfood after an association between feeding Petcare Advance Dermocare dogfood and an unusual increase in the incidence of megaesophagus cases was found.

Companion Animal Health Foundation

CAV are proud to support the work done by the Foundation in promoting companion animal health and welfare through research grants. A donation of $10,000 for 2018 was approved.

NZ Companion Animal Council (NZCAC)

The NZCAC will hold their biannual conference in Auckland on September 17–18. Paula Short will be representing CAV at this event.

This year’s conference was a great success with three days packed full of continuing professional development.

The Friday workshop on dentistry was also fully subscribed and feedback has been very positive. The CAV dinner was a great opportunity to catch up with everyone and recognise Dr Cath Watson’s work for CAV as she was presented with the 2018 CAV Service Award.

Executive committee member updates We received four nominations and had four vacant committee seats so no election was needed. Aimee Brooker and John Munday will both serve a second term on the committee and we welcome two new members Alison Pickering and Becky Murphy. l

Our thanks go to Dr Richard Jerram and the rest of the CPD advisory team for their work in pulling another fabulous conference together. We are all looking forward to next May in Wellington.

Bacterial bits and pieces A new family of antibiotics

DNA extracted from soil samples and screened for genetic sequences involved in the production of various antibiotics have yielded a new family of antibiotics named by investigators as "malacidins". The antibiotic killed MRSA in infected rats, but it may be some time before it gets to be approved for clinical use.

It’s doubtful that such an antibiotic would become available for veterinary use.

a novel retenoid (teenagers with scarring acne know about these) kills persisters. Further, it is thought that the use of this retenoid may reduce the length of antimicrobial treatment in this type of patient. Experimentally it killed MRSA by distorting the lipid bilayer of the cell membrane. We wait and hope!

References available on request

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No plans to protect new antibiotics from resistance development

A survey of companies and researchers involved in the development of new antibiotics found that none had plans to protect their prospective antibiotic against the rapid rise of resistance. Given the cost versus volume sold equation it seems unlikely that new antibiotics will provide more than transitory relief from antibiotic resistant bacteria.

Bacterial persisters are thought to be a significant cause of chronic or relapsing bacterial infections. "Persisters" resist antimicrobial treatment by entering a dormant state in which they become metabolically inactive. So hope is on the horizon for those recurrent pyoderma dogs with the discovery that

Photo courtesy of pixabay.com

Contact: Allan Bell, Dermvetonline, dermvet.bell@xtra.co.nz

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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The CAV Noticeboard Hill’s Pet Nutrition/CAV Educating the Educators Scholarship This scholarship provides assistance for veterinary educators to attend advanced level continuing education events outside New Zealand, in exchange for articles, reports and presentations on their area of interest.

Through this partnership, we recognise the importance in supporting our leading veterinarians’ participation in international conferences to ensure they remain up to date, and disseminate this knowledge to the wider CAV membership.

This scholarship is open to both CAV members and non-members. Successful applicants are

usually specialists in their field but we also support those who have developed advanced skills in a specialist area.

If you would like to partner with us to improve the knowledge of NZ veterinarians, then see our website, or contact cav@vets.org.nz for application forms and a list of the terms and conditions.

We are very grateful to Hill’s Pet Nutrition as the principle sponsor along with support we receive from the School of Veterinary Science at Massey University and VetLearn.

CAV/CAHF Project Grant 2018 The Companion Animal Health Foundation is a charitable trust that acts as the research funding arm for CAV. Funding applications are invited in March and September for research projects that will enhance companion animal health and welfare.

See the CAHF website (www.healthypets.org.nz) to find out how we are supporting projects on elbow dysplasia, bone marrow sampling techniques and FIV

WINNER

Article of the Issue

Danielle Aberdein

prevalence. Any queries on how to make an application or donate contact Rochelle Ferguson (CAV Operations Manager) on cav@vets.org.nz

G SCH RAN OL TS & AR SH Ava IPS ilab CAV le to me mb ers

“Feline autoimmune lymphoproliferative syndrome (FALPS): a fatal inherited disease of British Shorthair cats" June 2018 | Volume 29 (2) | Pages 20–22

EYEVET Services Limited

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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MAILBOX

Dear Editor .....

I WOULD LIKE TO REPLY to Prof. Munday’s excellent editorial on critical thinking published in the June issue of Companion Quarterly. As a general practitioner, and more recently an 'industry vet' with an interest in epidemiology, this has been a subject that I keep returning to. It would be good to see broader application of the principles of evidence-based veterinary medicine (EBVM) across the profession; to both inform clinicians in their decision making, and allow them to critically assess marketing and academic literature. The question I am struggling to answer is how best to work towards this goal. A CPD course? An EBVM chapter within NZVA? Promotion of a 'knowledge network' such as that initiated by the Royal College of Veterinary Surgeons (RCVS) in the UK? I'm keen to hear what you think!

Contrary to the opinions of some, I do not believe that the promotion and use of EBVM needs to exclude the concurrent application of clinical experience and good judgment. I'm keen to hear from CAV readers who share an interest in this topic and have ideas on how to improve access to and understanding of EBVM in NZ.

In the meantime I'd like to share some resources I have found which your readers may find helpful:

I HAVE JUST BEEN looking through the June 2018 issue of Companion Quarterly and found the “What is your diagnosis” article on lead poisoning. On page 45, it states that DMSA (succimer) is not able to be sourced through human pharmacies in New Zealand. A few years ago I submitted a case report on lead toxicity and included supply information for succimer. (Krupitza T. Challenges of treating lead poisoning.

Vetscript, 25(6), 18–20, 2012). I emailed the pharmacy where we got it last time and they informed me that it is available for veterinarians to order for their patients using the prescription form available on the company’s website. Here is their contact information:

This link contains a brief tutorial which is a good introduction to the subject: http://www.ebvmlearning.org/ The RCVS has a decent portal with a good overview on what EBVM is, and a more detailed 'toolkit' is available linked from this page: https://knowledge.rcvs.org.uk/evidence-based-veterinarymedicine/ The following link has some interesting evidence-based summaries aiming to answer particular clinical questions.

Admittedly the range of topics is small, but it’s a start. Perhaps interested parties in NZ could contribute to further BETs? http://bestbetsforvets.org/ This link has three podcasts available for those who prefer to listen www.ebvma.org

Best regards, Keara Brownlie, BVSc Companion Animal Veterinary Advisor – Zoetis NZ keara.brownlie@zoetis.com

Pharmaceutical Compounding NZ Ltd, Ph: +64 9 4421727 ext 779 Fax: +64 9 4425851 Web: www.pharmaceutical.co.nz Tania Krupitza l

Did you know?...........

You can access useful articles from the New Zealand Veterinary Journal, grouped by subject from the NZVA Resource page?

Go to http://www.nzva.org.nz/?page=resourcecentre, then click on ‘Our Publications’ and select ‘Browse selected papers in the article collections’ under New Zealand Veterinary Journal. There you’ll find a series of collections covering a variety of topics of particular interest to veterinary clinicians including Companion Animals.

Each topic contains review articles, scientific articles and clinical communications that have been published in the NZVJ, mostly since 2010. Just select a topic and you will find the title of the articles with a direct link for downloading the paper from SciQuest.

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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NEWS IN BRIEF

Two new members join the CAV Executive Committee In this issue we would like to introduce two new members of the CAV Executive Committee. Welcome aboard to Alison Pickering and Becky Murphy.

Becky Murphy

Photo courtesy of Becky Murphy

I spent my childhood in sunny Nelson where I regularly participated in obedience, agility and conformation showing with my parents’ dogs. My first ‘show dog’ was a loopy Dobermann, Rusty, who didn’t do too badly and hooked me to the game. After Rusty came Holly, my beagle. She was superb and was my real introduction to the ‘dog world’ with her winnings taking us around the country.

I left Nelson and did a BSc at the University of Canterbury, finding myself subsequently employed in a human medical laboratory in the microbiology department. A few years down the track my husband and I relocated to Palmerston North where he works as a consulting engineer. With Massey being just around the corner, and the

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laboratory work not exciting me too much anymore, I managed to end up doing a BVSc. Our first daughter was born not long after I graduated, and I spent the years the followed working ever increasing hours as a companion animal veterinarian in a mixed practice in the Rangitikei. Our second daughter was born 4 years ago, which prompted a lifestyle change to try and suit the family a bit more. Since then I have started my own business, which is limited to genetic health testing and canine reproduction.

The same week the business started, the (then) NZ Kennel Club (now Dogs NZ) advertised for a canine health and welfare officer. I ticked all the boxes and decided to apply. Two and a half years later I am still with Dogs NZ and managing my business and family and could not be happier.

It’s great to be part of CAV. I hope to be able to add value to all facets but especially those related to the responsible production of our pets. It’s the collaborative approach between breeder and veterinarian which will have the greatest impact and I will keep chipping away at it!

I have worked as a community practice veterinarian at the Massey Veterinary Teaching Hospital. Teaching vet and vet tech students while working alongside referral and specialist veterinarians provided me with the opportunity to develop my medical and diagnostic skills.

While at Massey I completed my Masters degree in the epidemiology of canine leptospirosis in New Zealand.

I have worked with Pacific Island clinics in Rarotonga, Vanuatu and Samoa, a future career goal is to combine my passion for working with charity clinics and my interest in public health.

As a CAV committee member, I am looking forward to using my experience to support and promote the interests companion animals in New Zealand.

Given the highs, lows and challenges of the profession I want to encourage CAV members to continue to communicate, support and look out for each other, participate in the CAV community, communications and the CAV Facebook page. “The whole is greater than the sum of all its parts”(Aristotle).

Alison Pickering Hello! I am a companion animal veterinarian based in the beautiful Bay of Plenty. My professional areas of interest include dermatology, diagnostic imaging and public health, and I also enjoy working up complex medical cases. I especially enjoy working with my feline patients, and would love to see practices moving towards being more cat friendly!

Photo courtesy of Alison Pickering

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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NEWS IN BRIEF

2018 CAV Service Award We are pleased to announce that the CAV Service Award for 2018 has been awarded to Cath Watson. The Award was presented to Dr. Watson at the CAV dinner held during the 2018 NZVA Conference in Hamilton in June.

Cath graduated with distinction from Massey University in 1999. Initially intending to follow a career in dairy practice. The companion animal call-up came around 5 years later, following a 2-year stint in an Invercargill mixed practice, and a 3-year working overseas holiday.

Settling back into Invercargill and marrying a classmate, Cath made the transition to working as a companion animal practitioner, and developed a special interest in imaging. In 2008, Cath became a director of the seven-vet mixed practice, Waikiwi Veterinarians and joined the CAV committee.

When Cath began her work on the CAV executive committee, a bid to host the WSAVA 2013 conference had just been made.

The bid was accepted and the committee put in a significant amount of work over the next 5 years to ensure its success.

Cath was nominated as CAV President 1 year out from the WSAVA conference in February 2012, and led the committee through this significant event in February 2013, continuing on as President until 2015. Resigning from the CAV exec in 2016, Cath has served a total of 8½ years for CAV. Committee work requires consideration of many view points and an appreciation that more than one way exists to solve a problem. Cath understands this, and has demonstrated a steady hand and a considered approach in her CAV leadership.

Her ability to see the bigger picture, contributed to the success of the NZVA realignment project that sought to harmonise the work of the NZVA special interest branches and ultimately strengthen the association.

Cath has been a fabulous representative for CAV, developing relationships with stakeholders that led to better understanding, as well as progress on animal and veterinary issues. Cath was a key player in the work that was done to support the ban on tail docking, which will be enacted on 1 October this year. Significant advances were made by CAV with the dangerous dog working group, of which Cath was a member. This group developed a comprehensive NZVA position on managing dangerous dogs, which is the basis for our engagement with media and other stakeholders today.

With her wildlife conservation involvement, Cath’s knowledge supported CAV’s involvement with other interested parties leading to the development of the cat management strategy.

Continuing education is at the core of CAV work and Cath lead the grants subcommittee, providing a thoughtful fair division of resources to provide maximum benefit to members. Cath has also been active in dog breeding issues, contributing a companion animal viewpoint to NAWAC on selective breeding and even fronting up to a meeting with the Southern bulldog breeders for a chat.

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Photo courtesy of Cath Watson

Despite retiring from the committee in 2016, Cath continues as the CAV representative to the Dogs NZ health and welfare committee. She is a chair of the CAV research arm, The Companion Animal Health Foundation and a current NZVA Board Member.

CAV are very grateful to have a member who has been prepared to use her skills and experience to give back to the profession, although when congratulating her on this when she retired from the committee late last year, she was quick to say that she gained more from being involved with CAV than she ever gave.

Anyone who knows Cath will also be aware of her deep love of the great outdoors and physical activity. Cath has had the good sense to balance her professional achievements with personal pursuits. Her Facebook holiday photos include snaps of her kayaking rivers, mountain biking around the South Island and skiing in the Norwegian mountains. Cath can also claim membership of the exclusive Coast to Coast competitors club, for those who have completed at least five races.

It is with great pleasure that we present our thoroughly deserved 2018 CAV Service Award to Dr Cath Watson. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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What is your diagnosis?

THE QUESTIONS… SARAH LEE BVSc MANZCVSc (Path), Small Animal Clinician

Case history:

A 20 kg 3-year-old male neutered Welsh Springer Spaniel named Paddy was presented to the veterinary clinic with a history of intermittent vomiting and diarrhoea, inappetence, polydipsia, vague depression and lameness. Over the previous month his owners had noticed he had become lethargic and seemed reluctant to run and jump around on the farm like he used to.

On physical examination, Paddy was noted to be in poor body condition (2.5/5), and had moist pododermatitis of all four feet, but particularly the fore feet.

Pre-scapular lymph nodes were enlarged and he had a temperature of 39.5°C. Repeatable signs of pain on palpation of the cranial abdomen, and discomfort on palpation of the kidney/sublumbar region were detected. His anal glands were full but no masses were palpated.

No other abnormalities were detected on physical exam. Paddy urinated freely on abdominal palpation and a free catch sample was obtained. A blood sample was collected by jugular venipuncture and analysed on in-house haematology (IDEXX Procyte) and serum biochemistry (IDEXX Catalyst One) analysers (Table 1).

the pancreas was patchily hypoechoic with an irregular surface. Adjacent abdominal lymph nodes were enlarged (up to 4.3 cm long) with hypoechoic areas in the cortical zones. The spleen appeared moderately enlarged and had a generalised mottled appearance.

Ultrasound-guided FNA were taken of the abdominal lymph nodes, as well as prescapular lymph nodes for cytological review.

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Questions

1. What is Paddy’s problem list?

Table 1. Serum biochemistry results at initial presentation for a 3-year-old male Welsh Springer Spaniel presenting with gastrointestinal signs, polydipsia, lameness and pyrexia.

Analyte (units)

Reference interval

Test 1a

Glucose (mmol/L)

4.11–7.95

5.77

Creatinine (μmol/L)

44–159

96

Urea (mmol/L)

2.5–9.6

10.2

Phosphate (mmol/L)

0.81–2.20

1.42

Urea/Crea

26

Calcium (mmol/L)

1.98–3.00

3.66

Total Protein (g/L)

52–82

68

Albumin (g/L)

23–40

26

Globulin (g/L)

25–45

Alb/Glob ratio 10–125

50

Alkaline phosphatase (U/L)

12–212

10

Gamma glutamyltransferase (U/L)

0–11

10

Bilirubin (μmol/L)

0–15

8

2.84–8.26

2.96

Amylase (U/L)

500–1500

>2,500

Lipase (U/L)

200–1800

>6,000

Sodium (mmol/L)

144–160

150

Potassium (mmol/L)

3.5–5.8

3.9

109–122

106

Na/K ratio Chloride (mmol/L)

a

42 0.6

Alanine aminotransferase (U/L)

Cholesterol (mmol/L)

Haematology was unremarkable Urine specific gravity was 1.005 with 1+ blood, pH6 on dipstick. As expected in dilute urine, the urine sediment was unremarkable. Testing for canine pancreas-specific lipase (SNAP cPL test; IDEXX) was abnormal.

Screening abdominal radiographs were unremarkable. However, abdominal ultrasound showed that the left lobe of

2. What are your differential diagnoses?

3. How would you confirm your diagnosis?

4. What treatment options are available?

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Results in red are greater than the reference range and those in blue are less than the reference range.

Answers on page 50

Contact: Cambridge Veterinary Services, 41 Empire Street, Cambridge

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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CLINICAL UPDATE

Time to rethink the use of tramadol for dogs with osteoarthritis?

Below is an abstract reprinted from the Journal of the American Veterinary Medical Association which is relevant to small animal practitioners. The use of tramadol is widespread in New Zealand but needs to be re-evaluated in the light of this properly conducted, placebo-controlled cross-over study. A thought provoking comment and the authors response are also shown below.

Abstract

JAVMA 252 (4), 427–32, 2018 https://avmajournals.avma.org/doi/ abs/10.2460/javma.252.4.427

Lack of effectiveness of tramadol hydrochloride for the treatment of pain and joint dysfunction in dogs with chronic osteoarthritis Budsberg SC, Torres BT, Kleine SA, Sandberg GS and Berjeski AK

Objective: To investigate the effectiveness of tramadol for treatment of osteoarthritis in dogs.

Design: Randomized, blinded, placebocontrolled crossover study.

Animals: 40 dogs with clinical osteoarthritis of the elbow or stifle joint.

Procedures: Dogs orally received 3 times/d (morning, midday, and night) for a 10-day period each of 3 identically appearing treatments (placebo; carprofen at 2.2 mg/kg [1 mg/lb], q 12 h [morning and night], with placebo at midday; or tramadol hydrochloride at 5 mg/kg [2.3 mg/lb], q 8 h) in random order, with treatment sessions separated by a minimum 7-day washout period.

Vertical ground reaction forces (vertical impulse [VI] and peak vertical force [PVF]) were measured and Canine Brief

Contact: Andrew Worth, A.J.Worth@massey. ac.nz?

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Photo source: pixabay.com

Pain Inventory (CBPI) scores assigned prior to (baseline) and at the end of each treatment period. Repeated-measures ANOVA was performed to compare VI and PVF data among and within treatments, and the χ2 test was used to compare proportions of dogs with a CBPI-defined positive response to treatment.

Results: 35 dogs completed the study.

No significant changes from baseline in VI and PVF were identified for placebo and tramadol treatments; however, these values increased significantly

with carprofen treatment. Changes from baseline in VI and PVF values were significantly greater with carprofen versus placebo or tramadol treatment. A significant improvement from baseline in CBPI scores was identified with carprofen treatment but not placebo or tramadol treatment.

Conclusions and clinical relevance: 10 days of treatment with tramadol as administered (5 mg/kg, PO, q 8 h) provided no clinical benefit for dogs with osteoarthritis of the elbow or stifle joint.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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Letters to the editor

JAVMA, 252 (10), 1198–1199, 2018 https://doi.org/10.2460/javma.252.10.1198

Tramadol for treatment of pain in dogs

I was interested to read the recent report1 on the lack of effectiveness of tramadol in treating pain in dogs with chronic osteoarthritis and thank the authors for emphasizing the need for science-based treatments in veterinary medicine. I hope further appropriately controlled evaluations of therapeutic modalities, both new and tried-and-true, continue to see publication. I must admit to being a little dismayed by the authors’ results, as I have used tramadol for years to manage acute (e.g., postoperative) and chronic pain in dogs on the recommendation of respected and trusted colleagues, board-certified specialists, and continuing education speakers. As anyone experienced in pain management can attest, multimodal treatments are generally preferable, and I hope future studies will look into the value, or lack thereof, of using medications such as tramadol in addition to, rather than instead of, NSAIDs and other analgesics.

Clinical experience and judgement are essential in the practice of veterinary medicine, but all knowledge is contingent on new scientific evidence. I appreciate that well-done studies can be costly and time-consuming but hope that investigators will continue to provide this kind of science-based information and

that my colleagues will reflect on our oath to use our “scientific knowledge and skills for the benefit of society through the protection of animal health and welfare.”2 Edward L. (Bear) Thompson, DVM Budsberg SC, Torres BT, Kleine SA, et al. Lack of effectiveness of tramadol hydrochloride for the treatment of pain and joint dysfunction in dogs with chronic osteoarthritis. J Am Vet Med Assoc 2018;252:427–432. [Google Scholar] AVMA. Veterinarian's Oath. Available at: www.avma. org/KB/Policies/Pages/veterinarians-oath.aspx.

Accessed Mar 2, 2018. [Google Scholar]

The authors respond

The authors thank Dr. Thompson for his thoughtful letter regarding our study showing a complete lack of effectiveness of tramadol in dogs with pain and dysfunction due to chronic osteoarthritis.

Dr. Thompson brings up 2 points that we would like to discuss.

The first point is Dr. Thompson's comment that he used tramadol on the recommendation of respected and trusted colleagues, board-certified specialists, and continuing education speakers.

Many clinicians use the exact same sources to help guide patient treatment.

However, one of the tenets of evidencebased medicine is that “expert opinion” is the weakest form of evidence when making clinical decisions about patient care. Unfortunately, drugs like tramadol have been recommended by all of the aforementioned individuals without clinical trials to support their use. It is incumbent on everyone who provides these types of treatment recommendations to know

and understand the supporting data— or lack thereof—before disseminating them. Many clinicians, if they critically looked at the information used in the daily treatment of patients, would likely be shocked to find just how little clinical data are truly available to support current recommendations.

The second point that Dr. Thompson brings up is the need for more clinical trials.

No truer words have ever been spoken.

Yes, these trials take time, dedicated investigators, and a considerable amount of money. To that end, we would like to acknowledge the support that our project received from the Morris Animal Foundation, which provided nearly 75% of the funds to make this study happen.

Without the Morris Animal Foundation's support, tramadol would still be seen as a viable treatment by many clinicians for the foreseeable future. Dr. Thompson hopes that more studies will be done, but the authors know that for this to happen, more money must be made available to clinical investigators. Our profession can be an important contributor to that end, and the authors hope that our study encourages more donations be made to entities that support clinical research, like the Morris Animal Foundation. Quality research requires adequate funding, and often the monetary costs can be substantial. It is important that veterinarians be part of the solution.

Steven C. Budsberg, DVM, MS Bryan T. Torres, DVM, PhD

Bees under threat After being banned and unbanned in Europe, some of the neonicotinic insecticides have been rebanned from use as horticultural sprays outside of greenhouses use. These compounds have been deemed to be significant in the reduction of insect populations generally and bees especially.

Included in the banned range is imidacloprid, a drug with veterinary use for flea control. Collars and "spot-ons" may not seem to pose a significant risk to bees at first sight, but imidacloprid is absorbed by plants root systems and foliage.

Imidacloprid originating from companion animal use may be an unquantified risk to bees especially in cities.

References available on request l Contact: Allan Bell, Dermvetonline, dermvet.bell@xtra.co.nz Photo courtesty of pixabay.com

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INDUSTRY NEWS

Virbac technical update – what’s new in shampoo?

In 2017 Virbac updated the formulation of some of our shampoos to include a range of innovative and unique technologies that we refer to collectively as Skin Innovative Science™ or SIS™.

The two components of SIS™ are Glycotechnology™ and Defensin Technology™.

Glycotechnology™ involves the addition of various sugars that have beneficial effects by both binding to pathogenic organisms’ attachment ligands, which reduces their ability to attach to keratinocytes and set up infection, and by also down regulating inflammatory responses to reduce pruritis and consequent self-trauma. Defensin Technology™ refers to the inclusion of extracts from the plants Boldo and Meadowsweet. These plant extracts increase the expression of components of the innate immune system called anti-microbial peptides, or AMPs. AMPs include β-defensins and cathelicidin.

We refer to β-defensins and cathelicidin together as “defensins” for simplicity.

The goal of Defensin Technology™ is to produce benefits such as up-regulated innate immune defences, while not stimulating the detrimental effects of inflammation.

study examined skin cultures collected from both healthy and atopic Beagle dogs. The experiment observed the expression of mRNA associated with four products; β-defensin, cathelicidin, interleukin-8 (IL-8) and tumour necrosis factor-α (TNFα). IL-8 and TNFα gene expression were observed as metrics of the detrimental effects of inflammation. This study demonstrated no pro-inflammatory effects of either extract or combination of the extracts, while increasing the secretion of the beneficial β-defensin and cathelicidin. The effect was observed in both atopic and healthy keratinocytes, despite the atopic keratinocytes having a higher expression of β-defensin and cathelicidin than healthy skin prior to treatment.

The purpose of increasing the secretion of these defensins is to aid in the management of secondary bacterial infections of the skin.

Atopic dogs are especially prone to these secondary infections, and the authors of this study emphasised the importance of advances such as SIS™ to help reduce the need for antibiotics in the treatment of such cases. They also emphasised that AMPs are still effective against bacteria even if the organisms have developed antimicrobial resistance.

By using Virbac shampoos with SIS™ included, atopic dogs will need shorter and less frequent courses of antibiotics.

A recently published paper by Santoro et al.i has investigated the effects of these plant extracts further. This i Santoro, D., Ahrens, K., Vesny, R., Navarro, C., Gatto, H., & Marsella, R. (2017). Evaluation of the in vitro effect of Boldo and Meadowsweet plant extracts on the expression of antimicrobial peptides and inflammatory markers in canine keratinocytes. Research in veterinary science, 115, 255–262.

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FEATURE ARTICLE

Electric training collars: torture or training?

This article was written as part of the requirements for receiving the Hill's Pet Nutrition/CAV Educating the Educators Grant

E.L. FLINT, MSc, BVSc, MANZCVS, PhD

Abstract

In recent years there has been an increasing trend towards the use of electric training collars for controlling unwanted barking, for stopping unwanted behaviours, and even for general training. This is a welfare concern. Studies show that there is no training advantage in using these devices and that the detrimental effects are many. These include redirected aggression (onto humans or other dogs), trauma resulting in learned helplessness, and ongoing detrimental effects on general health resulting from chronic stress. It is important that veterinarians and veterinary clinic staff understand how detrimental these devices can be, and are able to advise clients accordingly.

Introduction

As people continue to become timepoor and society less tolerant, there is a tendency to look for quick-fix techniques in dog training and management.

Unfortunately, remote operated electric collars are marketed as just that for anything from running away, to aggression toward other dogs. Some trainers advocate their use on puppies that are exuberantly rushing to greet people when out walking. This can and does result in traumatised animals that no longer trust people and can become aggressive towards strangers.

Such collars are also used in an attempt to stop dogs from chasing stock and in kiwi aversion training. Electric collars are sometimes used to stop dogs barking in situations where dogs are disturbing neighbours. These collars are often advocated by dog control officers dealing with barking complaints after Contact: elsaflint1@gmail.com, ph. 027-2649777 26

little or no investigation as to the reason for the barking. Another popular use is in boundary control. Hidden fences that trigger a shock when the dog moves within a certain range of the boundary are popular with people who can’t or don’t wish to fence their property.

Electric collars used in any of the above situations can potentially result in unwanted side effects and unnecessary trauma.

Remote training collars

Some trainers attempt to use these to “fix” inter-dog aggression which often escalates the behaviour as the dog makes an association with the presence of another dog and pain, or results in a dog that avoids others at all costs or panics and becomes extremely aggressive at the sight of another dog.

The use of these collars to teach dogs to return on command is flawed. Dogs are often aware that the handler is inflicting this punishment so why would they return? Many dogs are so traumatised that they scream and lie on the ground shaking not knowing how to escape the pain. When the collar is put on in the future the dog shuts down and does very little (learned helplessness). Even if their reaction is not so extreme, dogs trained with electric collars may show ongoing signs of stress during training and in the presence of their handlers.

A study by Schilder and Van der Borg (2004) observed 32 dogs trained to the same level, where half of the dogs were trained using shock collars and the other half were not. The researchers did not do any direct experimentation on the dogs but recorded their behaviour during standard training sessions.

Behaviours associated with pain, fear and submission (lowered tail and ears, crouched posture, yelping, snapping, licking lips nervously) were observed immediately after administration of

electric shocks, indicating that the collar was painful, but no physical damage was detected. There was also a small but consistent difference in the longer-term behaviour of dogs trained using the shock collar. They tended to express fear related behaviour such as walking with a crouched posture with lowered ears and licking their lips after the training sessions when in the presence of their trainer, even outside of the training grounds. The authors conclude that, although training can be achieved by using shock collars, the dogs associate a painful shock with training (and the trainer) which leads to constant fear and a long-term negative effect on the welfare of working dogs. This result further adds to the concerns that negative reinforcement and punishment training is detrimental to the welfare of animals (Mills et al. 2014). Cooper et al.

(2014) show that there is no training advantage in the use of punishment as opposed to positive reinforcement.

Electronic containment systems

While some owners seem to think these systems work well for their dogs, they can also lead to chronic stress as the dog has to be on the alert when outside, being careful not to inadvertently enter the trigger zone. Polsky (2000) describes five cases of human directed aggression related to the use of containment systems. In these cases, the dogs received a shock and redirected onto a human. Bites were severe and uninhibited. I have seen dogs so traumatised by these systems that they refused to go outside when wearing the collar. I have also had reports from owners of their dogs running across the boundary ignoring the shock when highly aroused chasing a cat or a bird, and then being unable to return home afterwards when no longer in a high enough state of arousal to ignore the pain of the shock.

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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Escaping is one of the behaviours associated with separation distress.

Dogs attempt to locate their owners and will scale fences and jump through glass windows to do so in extreme cases. These dogs are also likely to cross invisible fence lines and find it impossible to return. Even if they don’t cross they are likely to try, and get repeatedly shocked when already highly anxious.

Learning theory and electric collars Positive training

Really these systems should not be necessary. If it is impossible to fully fence a property it is surely possible to build a large compound/courtyard with indoor access in which to accommodate the dog.

Teaching or shaping a behaviour is based on rewarding the desired behaviour, or in early stages, an approximation of that behaviour. It is important that an animal understands what is expected and looks forward to the result of compliance.

Unwanted behaviour is extinguished by lack of reinforcement or redirected into another pattern of behaviour that is acceptable and is rewarded. This is the method of training advocated by behavioural scientists and is proven to be effective over time.

Anti bark collars

Punishment

Electric anti-bark collars are often recommended by dog control officers as a solution for unwanted barking with no attempt made to investigate why the dog is barking. This results in dogs that are suffering separation distress becoming even more anxious as they are punished for expressing their distress, and in dogs being punished for alerting to potential intruders or threats (normal behaviour). It is concerning that this sort of abuse is sanctioned by those in positions of authority. Dogs do not bark for no reason. If a dog is barking excessively the situation should be properly investigated with the help of someone suitably qualified.

Punishment is not advocated in modern training although there may be some circumstances where an aversive stimulus is required to interrupt a behaviour. The animal is then redirected onto another behaviour that is positively reinforced. To use punishment effectively, the aversive stimulus must occur within seconds of the unwanted behaviour occurring, there must be no doubt as to which behaviour caused the aversive stimulus, and there must be an alternative behaviour positively reinforced.

Electric training collars do not achieve this effectively and cannot be considered an appropriate method of behaviour

modification (Overall 2007). For example, a dog that is running on the beach and bounces up to dog or a person is performing several actions.

It is running, it might be barking, it is probably wagging its tail. Suddenly it gets hurt. Which behaviour is being punished? What should the dog then do? If it stops in its tracks, where is the reward for stopping and what alternative behaviour is given to teach the dog how to approach and interact with a person?

The dog might learn that if it experiences a shock, stopping in its tracks will avoid further pain, but what has that taught the dog about how to interact with people?

The dog might eventually associate people with pain, and so avoid them out of fear in future – is that what we want and is it necessary to inflict pain to achieve this?

The dog might associate people with pain, and become aggressive towards them, so a greater problem has been created.

The dog may become fearful of doing anything on the beach because sometimes pain is inflicted and it doesn’t understand why.

The dog may associate the owner holding the remote with the pain, resulting in a breakdown of the

Source: pixabay.com

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relationship, and in some cases aggression toward the owner.

Dogs that are aggressive or overexcited when they see other dogs and are then subjected to a shock often become more aggressive associating dogs with pain. They may become so frenzied that they redirect onto their owners.

Conclusion

It is apparent that while punishment in the form of electric collars might achieve compliance in some animals, the ethics of using them is questionable. It has been shown that using electric collars in training causes stress which can be detrimental to the general health of the animal subjected to it. Electric collar use has been associated with aggression towards owners and subsequent injury.

Studies have shown that there is no training advantage in using punishment and that the potential for unwanted side effects when using electric collars is significant. As veterinarians our concern should be primarily for the welfare of the animals in our care and it is up to us to educate owners who do not understand the pitfalls of using these techniques.

Case example

Sasha, a 2-year-old German Shepherd bitch was presented as uncontrollable when out on-lead near other dogs.

Sasha had been subjected to electric collar training because she became excited and pulled towards and barked at other dogs when on-lead. She had started this after being attacked twice by

off-lead dogs when out walking. After the training she had become extremely aggressive at the sight of another dog even at a distance. Her owner had resorted to walking her late at night and running away with her if another dog should appear. Sasha was able to go to a day care that she had attended since puppy hood and interact freely off lead with other dogs. At home Sasha was cuddly playful and affectionate.

During consultation she was hypervigilant while walking and constantly lip-licked and yawned. A barking dog two streets away sent her into a frenzy, causing her to spin on the lead, froth at the mouth and scream.

Diagnosis

• Severe fear-based dog-directed reactivity • PTSD

Treatment

• Fluoxetine 1 mg/kg once daily • Halti head collar and training lead • Desensitisation sessions Sasha responded to the above regimen and was able to cope with the sight of test dogs approaching and walking in close proximity at my training area and in a large public on lead only park.

However she still could not cope with dogs in her local streets, becoming extremely agitated as they approached.

The addition of trazodone (2–3, 50-mg capsules, 2 hours before walking) helped her to remain calmer when other dogs

appeared. If one appeared suddenly, triggering a reaction, she settled quickly.

She needed repeated positive exposures to other on-lead non-reactive dogs while on anti-anxiety medication to help her learn a new behaviour when presented with the trigger of other dogs in a street situation.

References

Blackwell EJ, Bolster C, Richards G, Loftus BA, Casey RA. The use of electronic collars for training domestic dogs: estimated prevalence, reasons and risk factors for use, and owner perceived success as compared to other training methods. BMC Veterinary Research 8, 93, 2012 Cooper JJ, Cracknell N, Hardiman J, Wright H, Mills D. The welfare consequences and efficacy of training pet dogs with remote electronic training collars in comparison to reward-based training. PloS one 9, e102722, 2014 Mills D, Karagiannis C, Zulch H. Stressits effects on health and behaviour a guide for practitioners. Veterinary Clinics of North America: Small Animal Practice 44, 525–41, 2014 Overall KL. Why electric shock is not behaviour modification. Journal of Veterinary Behavior: Clinical Applications and Research 2, 1–4, 2007 Polsky R. Can aggression in dogs be elicited through the use of electronic containment systems? Journal of Applied Animal Welfare Science 3, 345–57, 2000 Schilder MDH, van der Borg JAM. Training dogs with the help of the shock collar: short and long term behavioural effects. Applied Animal Behaviour Science 85, 319–34, 2004 Ziv G. The effects of using aversive training methods in dogs – A review. Journal of Veterinary Behaviour 19, 50–60, 2017 l

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FEATURE ARTICLE

Initial management of canine gastric dilatation and volvulus: what you need to know PHILIP HYNDMAN, BVSc,

Surgery Intern at The Veterinary Emergency Clinic and Referral Centre (Toronto, Canada)

Gastric dilatation and volvulus (GDV) is an acute and progressive syndrome, characterised by displacement and rapid gaseous distension of the stomach with polysystemic and life-threatening consequences. Despite extensive investigation, the definitive etiology and pathogenesis of this syndrome are still poorly understood. The occurrence of GDV is nevertheless considered to be the end stage of a multifactorial subclinical disease process. Developing an understanding of this disease and its appropriate preoperative management will optimise patient survival while enabling appropriate client communication and decision making.

Understanding the consequences of gastric dilatation and volvulus: why is GDV so life threatening?

Following gastric dilatation, the stomach can rotate on its axis such that the pylorus moves ventral to the gastic body progressively displacing toward the left abdominal wall. With displacement of the pylorus and proximal duodenum the oesophagus becomes progressively compressed preventing effective eructation. Aerophagia, and then bacterial fermentation progressively raises the gastric intraluminal pressure which increases compression of local structures.

This has many important consequences for the patient. Restricted respiratory excursion, reduced pulmonary perfusion, ventilation-perfusion mismatch, and aspiration pneumonia all reduce the capacity of the respiratory system. Direct compression and stretching of the gastric wall, in conjunction with thrombosis and avulsion of short gastric arteries in the face of systemic hypotension, contribute to gastric necrosis which typically affects Contact: Philhyndman88@gmail.com 30

the fundus. In severe cases, this can result in gastric rupture and septic peritonitis.

The spleen, dragged with the displaced stomach, can avulse, torse, and become congested contributing to distributive shock while acting as a significant source of ischemic reperfusion injury. Cardiovascular dysfunction and arrhythmias, attributed to caudal vena cava, splenic, and portal vessel compression, distributive splanchnic pooling, portal hypertension, global hypotension, mixed acid-base abnormalities, bacterial translocation, and ischemic reperfusion injury, contribute to early morbidity and mortality. Even with rapid and appropriate treatment, these patients are at risk of rapid deterioration with endotoxic shock, disseminated intravascular coagulation (DIC), systemic inflammatory response syndrome, multiple organ dysfunction, and acute kidney injury all being possible. With time, the consequences of shock accumulate, resulting in a progressively less favorable prognosis for the patient.

Risk factors

Although the exact etiology of GDV is unknown, a number of retrospective studies have identified risk factors for its development in dogs. These include; increasing age and weight, poor body condition, and being male or deepchested. Patients with a first-degree relative affected by GDV are considered at higher risk. Further, purebreds have an increased risk of GDV compared to mixed breeds with Great Danes, German Shepherds, and Standard Poodles among the breeds considered to be predisposed.

Dietary risk factors include rapid eating, eating one meal daily, having a raised feeding bowl, aerophagia, high water consumption, exercise after eating, and consumption of processed foods containing grain and soy. Interestingly, having a fearful or anxious temperament is associated with an increased risk for GDV, while a happy temperament appears to be protective. These known risk factors should be considered when evaluating the patient’s history.

Preoperative management

The GDV patient demands a swift diagnosis followed by efficient intervention and stabilisation to optimise patient outcome and limit morbidity and mortality. During the initial physical examination and history taking, the clinician must be mindful to not overlook comorbidities and other individual patient factors. After diagnosis, gastric pressure should be relieved and stabilisation efforts instituted rapidly. The aim of client communication is to ensure clients have appropriate expectations for patient outcome, potential complications, and financial commitment. The following text accompanies a suggested guideline (see figure) for initial management of the GDV patient.

Clinical evaluation

A patient presenting with acute onset of non-productive retching, hypersalivation, abdominal distension, depression, weakness, collapse, and/or restlessness should prompt immediate examination and suspicion of GDV. Clinical examination may reveal abdominal tympany, tachycardia, mucosal pallor, tachypnea, dyspnea, hypothermia, variable degrees of shock, and a dull, stuporous, or comatose state. Presentation of the GDV patient may range from bright, alert and responsive patients with acute onset of non-productive retching, to dull patients with decompensating shock. A focus on reaching a diagnosis can be prioritised in the former, while aggressive stabilisation is required for the later. Assessment of the degree of shock through measurement of vital parameters and blood pressure, and quick assessment tests will determine the need for immediate supportive therapy.

Reaching a diagnosis

A high level of suspicion for GDV is often reached from patient signalment, history, and clinical examination. In cases in which GDV is strongly suspected, basic stabilisation can, and should, be initiated without the need for a definitive diagnosis.

Radiography Radiographic imaging is invaluable, not only for confirming the diagnosis but also in the evaluation of gastric wall

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integrity and co-morbidities. Where patient stability permits, a right lateral abdominal radiograph will reveal a large ventral compartment (the fundus) and a smaller gas-filled dorsal pylorus with a band of tissue separating the two. This view will enable the differentiation of GDV from gastric dilatation without volvulus, food engorgement, abdominal effusion, mesenteric volvulus, and abdominal mass effects. Loss of serosal detail may indicate hemorrhage from avulsed splenic vessels while increased contrast can indicate pneumoperitoneum associated with gastric rupture and a poor prognosis. Radiographic evidence of gastric pneumatosis (gas within the gastric wall), visualised as a linear to curvilinear radiolucency, parallel to the gastric wall in the regions of the body and fundus, occurs in about 9% of the GDV patients. This radiographic finding is relatively specific (92.7%) but poorly sensitive, for gastric necrosis. Similarly pneumoperitoneum also has a high specificity (90%) but low sensitivity for predicting gastric necrosis.

The significance of pneumatosis and pneumoperitoneum must be interpreted in light of gastric decompression procedures if performed prior to imaging.

Thoracic radiographs should be considered to evaluate for aspiration pneumonia, evidence of neoplastic processes, and other thoracic co-morbidities. As GDV patients are typically older, large and giant breed dogs, identification of further complicating disease may significantly alter the client’s decision to proceed with surgery.

In a review of pre-operative thoracic radiographs of 101 GDV patients, the most common abnormalities identified included a small vena cava (40%) and microcardia (34%) likely reflecting hypovolemic shock, esophageal dilation (39%), and aspiration pneumonia (14%). Dogs without radiographic evidence of cardiomegaly had a 10.2 greater odds of surviving to discharge. The cause of this was not determined, however, the authors of this study hypothesise this finding may be the consequence of GDV and its treatment on subclinical cardiac disease.

Blood testing Analysis of serum biochemistry and haematological parameters may be helpful, not in diagnosis, but rather in guiding stabilisation efforts. Commonly identified abnormalities include thrombocytopenia, leukocytosis or leukopenia, hemoconcentration, prolonged coagulation profiles, mixed acid-base disorders with a high anion gap, increased ALP, hyperbilirubinemia, and hypokalemia.

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Measurement of lactate concentration in serum has been investigated recently as a useful indicator of gastric necrosis, prognosis, and appropriate aggressiveness of stabilisation therapy. Lactate concentrations should be assessed at initial presentation and then periodically through stabilisation where available. Patients with relatively higher lactate levels that do not respond to intervention typically experience longer hospitalisation times, and a higher risk of gastric necrosis and mortality. These studies showed that increased survival was correlated with a lower initial lactate concentration, a final lactate concentration after stabilisation <6.4 mmol/L, an absolute change in lactate concentration of >4 mmol/L, and a percentage change in lactate concentration >42.5%. However, focus should not be directed toward achieving specific numbers, but rather toward using lactate as a useful guide for assessing the appropriateness of resuscitation efforts.

Note that the magnitude of increase in lactate concentration typically reflects the severity of lactate production and not its reversibility.

Following initial examination: stabilisation, treatment, and additional diagnostic considerations

Appropriate management of the GDV patient encompasses rapid diagnosis, aggressive stabilisation and treatment of shock, gastric decompression, prompt surgical correction, gastropexy to prevent recurrence, and intensive postoperative care.

Efforts during the pre-operative period center on decompression of the distended stomach and aggressive fluid therapy to restore intravascular volume and reestablish perfusion and oxygen delivery to hypoxic tissues. Resolution of shock in a timely fashion is critical, as the consequences of gastric distension and cardiovascular dysfunction will accumulate with time.

Fluid therapy Administration of crystalloid fluids via one or two large-bore catheters in the jugular or cephalic veins is recommended in the early stabilisation period. Practically, 20 mL/kg should be administered as a bolus over 15 minutes. Administering separate boluses enables the clinician to pause to assess the response to treatment prior to administering further fluid therapy.

Repeated patient evaluation, assessment of resuscitation end targets, intervention, and re-evaluation is essential during the perioperative period. The hindlimbs should not be used for venous access due to compression of the caudal vena cava which can result in poor cardiac

return from the caudal half of the body.

Crystalloid fluid therapy is typically sufficient for resuscitation, however, the use of synthetic colloids and/or hypertonic saline can be considered for the debilitated or poorly responsive GDV patient.

GDV patients experience complex acid-base and electrolyte alterations contributing to an overriding acidosis.

Following initial stabilisation, treatment of specific acid-base and electrolyte abnormalities (e.g. potassium and bicarbonate therapy), should be based on current blood gas analysis. Where this is not available, correction of commonly encountered electrolyte imbalances can be initiated. Hypokalemia commonly occurs in the GDV patient due to administration of large volumes of low-potassium fluids, in conjunction with potassium loss via vomiting, gastric lavage, gastric sequestion, and intracellular shifting. Supplementation of potassium in isotonic crystalloid fluids at 0.1â&#x20AC;&#x201C;0.5 mEq/ kg/hour is commonly needed following stabilisation (no more than 0.5 mEq/kg/ hour). Serum potassium concentrations should be assessed to guide appropriate therapy. Hyperchloremic metabolic alkalosis also commonly occurs, as a result of transcellular shifting and activation of the renin-angiotensin-aldosterone system, however, specific treatment, beyond standard I/V fluid therapy, is not usually required.

There is no consensus on the ideal products and protocols to achieve fluid resuscitation in all GDV patients. Decisions should be made on a case-by-case basis using resuscitation endpoints for shock, PCV, total solids, and lactate to guide fluid therapy.

Gastric decompression Gastric decompression is indicated in almost every case, as relieving intragastric and intra-abdominal pressure improves cardiovascular and respiratory function. This can be achieved via orogastric intubation and/or percutaneous trocarisation which are reported to have success rates of 75.5% and 86% respectfully with no statistical difference between success of the two methods. This study also found no evidence of gastric perforation or aspiration pneumonia, and splenic laceration occured in only 1/85 dogs. It is important to consider that repeat decompression may be required in cases of prolonged stabilisation and that the two techniques can often be complementary.

Ideally, decompression is performed following confirmation of diagnosis, adequate stabilisation, and provision of sedation and pain relief where applicable.

Diazepam administered I/V at 0.2â&#x20AC;&#x201C;0.25 mg/

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Figure 1. Suggested approach and guidelines for the presenting gastric dilation and volvulus patient.

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kg typically provides sufficient sedation to perform these procedures.

• Orogastric: PVC tubes are available

commercially in a variety of sizes.

Ideally, the selected tube should be small enough to pass easily, while large enough to optimise the removal of gas, fluid, and ingesta. Measure the tube from the nares to the caudal edge of the last rib. Mark this length with tape on the orogastric tube. Use a guard (roll of vetwrap or tape) to guide the lubricated orogastric tube through the oral cavity, over the back of the tongue and down the oesophagus. Insufflate the tube to aid passage. Do not push or force the tube. Once the appropriate location of the tip of the tube is suspected, place the other end of the tube into a bucket of water. If gastric distension is predominantly due to gas then bubbles should be produced. Commonly, gas will be accompanied by food or liquid. Use gravity, with the tube below the level of the stomach to promote siphoning. When removing the tube, kink it to limit backflow. The oral cavity and pharynx should be assessed for regurgitation after this procedure and the oesophagus suctioned if indicated.

• Percutaneous trocharisation: using

tympany and palpation for localisation, clip and surgically prepare a 6 x 6 cm site in either the left or right paralumbar fossa. Insert a 14 or 16 gauge, over-theneedle catheter perpendicularly through the skin, abdominal musculature, and stomach wall. Remove (or alternatively leave) the stylet, and attach an extension set, with the other end submerged in water to observe gas passing (represented by bubbling). Once confirmed, an active suction unit can be attached to speed this process.

• If the case is to be referred? Following initial decompression, depending on your location relative to a referral facility, further decompression is highly likely to be beneficial and will often be required.

Under the same sedation, a nasogastric tube can be placed to enable continued decompression during transport and prior to surgery.

Lidocaine in the treatment of the GDV patient.

Cardiac arrhythmias are detected in up to 45% of GDV patients and are associated with a higher rate of splenectomy or partial gastrectomy, and significant increases in overall mortality.

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Current recommendations are to treat cardiac arrhythmias when clinical effects are identified, namely weakness, syncope, and tachycardia >150 bpm.

Therapy consists of lidocaine 1–2 mg/ kg administered slowly over 1–2 minutes.

The onset of action is approximately 1–2 minutes and the duration of action is 15–20 minutes. Following treatment, the clinician should assess for a positive response seen as reduced ventricular rate, associated with improved perfusion, or conversion to a sinus rhythm. If necessary, the dose may be repeated up to four times. Alternatively, if the initial dose is effective, a constant rate infusion at 25–75 µg/kg/minute for 24 hours may be considered. Side effects can include nausea, seizures, vomiting, and lidocaine toxicity. It is important that underlying and contributing acid-base, electrolyte and hemostatic disturbances are addressed in conjunction with this treatment as the arrhythmia may be providing cardiac output in a debilitated patient.

A further consideration exists for lidocaine as part of the anesthetic protocol.

Administered at induction and then continued as a constant rate infusion, lidocaine provides analgesia with MACsparing effects and cardioprotective and gastroprotective properties.

Prognosis

GDV has historically been associated with a high mortality rate, however, more recent reports give a more optimistic outlook with mortality rates of approximately 10%.

Throughout the literature, gastric necrosis, identified in up to 10–37% of cases, is recognised as an important prognostic indicator, with affected cases 11 times more likely to die. Other factors associated with death included clinical signs for over 5–6 hours prior to presentation, hypotension, hypothermia, hypovolemic shock, high serum lactate, splenectomy, gastrectomy, severe electrolyte disturbances, peritonitis, sepsis, DIC, acute kidney injury and both pre and postoperative cardiac arrhythmias. Patients presenting in a depressed or comatose state are 3 and 36 times more likely to die than alert cases. An interesting factor associated with a decrease in mortality rate was increased time from presentation to surgery. This is proposed to be the effect of more thorough stabilisation rather than the observation of more stable cases not being rushed into surgery.

Summary

Gastric dilatation and volvulus is an acute life-threatening condition that affects multiple organ systems. A tentative diagnosis for GDV can often be reached when appropriate risk factors, presenting clinical signs, and clinical examination findings are identified. A right lateral abdominal radiograph can provide valuable information confirming the diagnosis and assessing for comorbidities.

A multifaceted and aggressive stabilisation approach in the resuscitation period will optimise patient stability prior to general anesthesia and surgical correction.

Useful reading

Bruchim Y, Itay S, Shira B-H, Kelmer E, Sigal Y, Itamar A, Gilad S. Evaluation of lidocaine treatment on frequency of cardiac arrhythmias, acute kidney injury, and hospitalisation time in dogs with gastric dilatation volvulus. Journal of Veterinary Emergency and Critical Care 22, 4, 419–27, 2012 Glickman LT, Glickman NW, Schellenberg DB, Raghavan M, Lee T. Non-dietary risk factors for gastric dilatation-volvulus in large and giant breed dogs. Journal of the American Veterinary Medical Association 217, 10, 1492–9, 2000 Goodrich ZJ, Powell LL, Hulting KJ. Assessment of two methods of gastric decompression for the initial management of gastric dilatationvolvulus. Journal of Small Animal Practice 54, 75–9, 2013 Green JL, Cimino Brown D, Agnello KA. Preoperative thoracic radiographic findings in dogs presenting for gastric dilatation-volvulus (2000–2010): 101 cases. Journal of Veterinary Emergency and Critical Care 22, 5, 595–600, 2012 Kyes J, Johnson JA. Hypertonic saline solutions in shock resuscitation. Vetlearn Compendium: Continuing Education for Veterinarians 1–9, 2011 Mazzaferro EM. Gastric dilation volvulus.

In: Monnet E (ed). Small Animal Soft Tissue Surgery. Pp 341–59. John Wiley & Sons Inc, NJ, USA, 2013 Mooney E, Raw C, Hughes D. Plasma lactate concentration as a prognostic biomarker in dogs with gastric dilation and volvulus. Topics in Companion Animal Medicine 29, 71–6, 2014 Sharp CR, Rozanski EA. Cardiovascular and systemic effects of gastric dilatation and volvulus in dogs. Topics in Companion Animal Medicine 29, 67–70, 2014 Tivers M, Brockman D. Gastric dilation-volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation. In Practice 31, 66–9, 2009 Tivers MS, Adamantos S. Gastric dilatation and volvulus. In: Aronson LR (ed). Small Animal Surgical Emergencies, pp. 49–62. John Wiley & Sons, Ltd, Chichester, UK, 2015 l

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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CASE REPORT

Unusual congenital spinal malformation causing neurologic dysfunction in a young dog MIRIAM BATES, BVSc (dist.),

VSA Zoetis Intern

RICHARD JERRAM, BVSc, DACVS, Registered Specialist in Small Animal Surgery; BENJAMIN WERNHAM, BVSc, MVSc, MVS, FANZCVS (Radiology), Specialist Veterinary Radiologist

Summary

A 20-month-old, male neutered, Golden Retriever dog was evaluated for acute onset of hindlimb paresis. Physical examination resulted in neurolocalisation of the lesion to between the fourth lumbar (L4) and third sacral (S3) spinal cord segments. A soft tissue mass was identified using computed tomography (CT). The mass was intimately associated with the first lumbar vertebra (L1), which was severely malformed and causing profound stenosis of the spinal canal. Following excision of the mass and surgical decompression of the spinal cord, the dog made an excellent neurological recovery. Histopathology indicated the mass was a vascular hamartoma invading the neighbouring lumbar vertebrae and stimulating bony proliferation. Vascular hamartomas are a rare presentation, but should be considered as a differential diagnosis where clinical and imaging findings are consistent with the presence of a vascular mass in a young animal. This report provides a basis for the discussion of congenital spinal malformations, and circumstances causing aberrant neurolocalisation of spinal lesions.

Contact: Veterinary Specialists Auckland, New Zealand, miriam.bates@vsnz.co.nz

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Photo courtesy of Miriam Bates

Case history

A 20-month-old, male neutered, Golden Retriever dog presented for evaluation of acute onset hindlimb paresis after suffering a fall during play a week prior.

The dog had also been urinating and defaecating inappropriately indoors, and the owners reported he had difficulty rising.

The dog had been examined 8 months earlier for evaluation of an unusual hindlimb gait which was noted by the dogâ&#x20AC;&#x2122;s breeder during showing. The dog had fallen from the car several weeks prior to that examination, and it was suspected that this had precipitated the lameness. The dog had been treated with 2 mg/kg carprofen (Rimadyl; Zoetis NZ) given, orally twice a day for 5 days, and ongoing physiotherapy and hydrotherapy. The dog was judged to

have made a satisfactory recovery from this event and further diagnostic testing was not pursued.

Clinical presentation

On examination, the dog was bright, alert, and responsive. Assessment of temperature, respiration, and heart rate were normal. Thoracic auscultation was unremarkable and abdominal palpation was normal. Lymph nodes were not palpably enlarged.

The dog ambulated with marked hindlimb ataxia and paresis, was reluctant to turn tight circles, and collapsed when walked backwards. He demonstrated some difficulty rising but was able to do so unassisted.

On neurologic examination, placing responses were slow to absent in both hindlimbs, and were subjectively slower

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on the left compared to the right hindlimb. Myotatic reflexes were hyporeflexive in both hindlimbs. Withdrawal responses in the hindlimbs were present but reduced compared to the forelimbs. Thoracic limb, cranial nerve, and anal reflexes were normal. There was some discomfort on palpation of the lumbosacral spine and medial palpation of the ventral iliac region. No other neurologic nor orthopaedic abnormalities were detected.

a

Diagnostic evaluation

Based on the initial presentation of hindlimb paresis and apparent urinary incontinence, a myelopathy affecting the spinal segments between L4 and S3 was suspected. Imaging using CT (Siemens Somatom Emotion 6; Siemens Healthineers, Erlangen, Germany) was performed under sedation with I/V 0.02 mg/kg medetomidine (Domitor; Zoetis NZ) and 0.1 mg/kg butorphanol (Ilium Butorgesic; Ethical Agents Ltd) with the dog positioned in dorsal recumbency. A full scan of the entire spine was performed before and after I/V administration of contrast medium (600 mg/ kg Omnipaque; GE Healthcare). Sedation was reversed with I/M 0.1 mg/kg atipamezole (Antisedan; Zoetis NZ) after which the dog recovered well and was discharged from the hospital.

The CT revealed a soft tissue mass associated with the left lumbar multifidus and iliocostalis muscles adjacent to the L1 vertebra (Figure 1). The mass had an irregular margin and was markedly and homogeneously contrast-enhancing. There was moderate, diffuse enlargement of the left lumbar artery originating at the abdominal aorta and converging with the mass. The L1 vertebra was severely malformed, with marked asymmetric thickening of the left side of the lamina and pedicle, and malformation of the spinous process and left cranial articular process. There was subtle periosteal reaction associated with the right side of the spinal canal. The spinal canal was severely stenotic, resulting in marked spinal cord compression over the length of the L1 vertebra (Figure 2).

There was evidence of severe spinal cord atrophy from the caudal third of the T13 vertebral body to the cranial third of the L2 vertebral body. There was moderate stenosis of the L1â&#x20AC;&#x201C;L2 intervertebral foramen.

An incidental finding of otitis externa of the left ear was identified by CT. Cytology of swabs from the ear canal demonstrated overgrowth of yeast suspected to be Malassezia pachydermatis. No bacteria were identified.

In an attempt to provide a more precise diagnosis, an ultrasound-guided tissue biopsy of the mass lesion under general anaesthesia was recommended. Three days later, the dog returned to the hospital and another I/V catheter was placed. The dog was premedicated S/C with 0.8 mg/kg morphine (DBL Morphine Sulphate Injection; Hospira) and 0.022 mg/kg atropine (Phoenix Atropine; Phoenix Pharm Distributors Ltd), and induced with 0.25 mg/kg diazepam (Ilium Diazepam; Ethical Agents) followed by 4 mg/kg of propofol (Fresofol; Fresenius Kabi) given I/V to effect. General anaesthesia was maintained using isoflurane in oxygen. Hartmannâ&#x20AC;&#x2122;s solution was administered at 10 mL/kg, I/V throughout the procedure.

Thirteen core biopsies were taken of the mass using a 14-gauge Tru-Cut biopsy needle under ultrasound guidance.

These were used to prepare impression smears of the tissue which were submitted along with the biopsies to Gribbles

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b

Figure 1. Pre-contrast transverse CT image at the level of L1 before (a) and after (b) administration of radio-opaque contrast medium, viewed in a soft tissue window. The soft tissue mass (arrows) is apparent immediately adjacent to the left aspect of L1, intimately associated with the left lumbar multifidus muscles. There is marked contrast enhancement of the mass which reflects its highly vascular nature.

Veterinary Laboratory, for cytology and histopathology.

The dog was discharged with 0.5 mg/kg prednisone (Apoprednisone; Apotex NZ Ltd) to be given orally, once daily.

This was prescribed for its potent anti-inflammatory effects, to help relieve spinal compression due to suspected local inflammation.

The cytology of the impression smears revealed free lipid and blood. The histopathology findings demonstrated mature connective tissue, adipose tissue, and muscle tissue with mild inflammation of uncertain significance.

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a

lipoma. However, given the extent of disease and spinal cord compression, as well as the absence of a fat-attenuating mass on CT imaging, it was assumed that the histopathology was not representative of the lesion. Other differential diagnoses included an infectious/inflammatory process such as osteomyelitis, or a developmental malformation secondary to an early traumatic event.

Treatment

One week following initial presentation, the dog was admitted for surgical excision of the mass. The osseous component of the mass was causing significant impingement of the spinal cord and the aim of surgery was decompression of the spinal cord and stabilisation of the spine.

Surgical report

b

Figure 2. Pre-contrast CT image viewed in a bone window. (a) A transverse view at the level of L1. There is severe thickening of the lamina and left side of the pedicle and vertebral body of the L1 vertebrae, resulting in severe stenosis of the vertebral canal. Note the diffuse, punctate lucencies within the cancellous bone of the thickened region of the vertebra and the malformed spinous process. (b) Sagittal reformat of the thoracolumbar spine. There is severe thickening of the left lamina and pedicle of L1 causing profound spinal canal stenosis, impinging on the dorsal spinal cord.

Differential diagnoses

Given the clinical presentation and imaging findings, a neoplastic process affecting the first lumbar vertebra and surrounding tissues was suspected. Primary consideration was given to soft tissue neoplasms (e.g. rhabdomyosarcoma, fibrosarcoma, lymphoma) with infiltration of the vertebra, rather than a primarily osseous process. The cytology and histopathology results supported a diagnosis of an infiltrative

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General anaesthesia was as previously described. Cefazolin (AFT Pharmaceuticals) was administered I/V at 22 mg/kg 15 minutes prior to the opening incision, and every 90 minutes thereafter. The dog was positioned in ventral recumbency. A dorsal approach was made to the first lumbar vertebra. The left multifidus lumborum muscle was elevated and resected such that normal muscle remained between the mass and the site of excision. During dissection there was brisk and substantial haemorrhage from an aberrant blood vessel confluent with the mass, and approximately 1.5 L of blood was lost. Subsequent to this haemorrhage, the dogâ&#x20AC;&#x2122;s packed cell volume (PCV) was 40% (reference range: 37â&#x20AC;&#x201C;55%) reflecting the peracute nature of the blood loss. Based on the clinical evidence of substantial haemorrhage an emergency blood transfusion was instituted without blood typing or cross-matching. Following transfusion of 400 mL of packed red blood cells, the PCV was 40%, with total protein of 48 g/L (reference range: 54â&#x20AC;&#x201C;71 g/L). NaCl (0.9%) was administered at 2 mL/kg/hour throughout the transfusion.

Complete control of haemorrhage required elevation and removal of the soft tissue component of the mass from the dorsal aspect of the L1 vertebra, improving visualisation of the blood vessel. Haemostasis was achieved using manual tamponade, electrocautery, and stainless steel haemostatic clips (Ligaclips). Grossly, the soft tissue component of the mass appeared to be composed of a cavernous structure with walls resembling a blood vessel. A dorsolateral laminectomy was performed, removing the dorsal and left lateral lamina of the L1 vertebra. The cancellous bone of the body of the L1 vertebra was grossly abnormal. It was thickened and had a porous, honeycomb appearance. The spinal cord was significantly thinner along the length of the L1 vertebra compared to the grossly normal spinal cord at either end of the operative site. Complete dorsal decompression of the spinal cord was achieved (Figure 3). The musculature of the right side of the lumbar spine was elevated to facilitate the placement of a seven-hole 3.5 mm String-of-Pearls locking plate with screws placed in the pedicles of the T13, L1, and L2 vertebrae.

Satisfactory postoperative stability of the spine was achieved. A fat graft was placed over the surgical site. The dorsal fascia was closed in a simple continuous pattern using 0 polydiaxanone (PDS II; Ethicon) suture material. The subcutaneous tissues were closed in three layers in a simple continuous pattern using 2/0 and 3/0 polyglecapone 25 (Monocryl; Ethicon) suture material.

The skin was closed in a Ford interlocking pattern using 3/0 nylon (Ethilon, Ethicon) suture material.

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a

Figure 3. Intra-operative photograph of the surgical site following dorsolateral laminectomy of L1. The spinous processes of T13 and L1 have been labelled. The left and right sides of the site have been labelled as ‘L’ and ‘R’, respectively. Extensive resection of the soft tissue to the left of the lumbar spine is evident. An area of spinal cord atrophy (black arrows) is visible, but the full extent of atrophy is not demonstrated due to the angle of the photograph. The stump of the blood vessel responsible for the major episode of intraoperative blood loss is visible (white arrows).

Post-operative management

b

A postoperative non-contrast CT scan was performed which showed satisfactory decompression and stabilisation of the spine, and accurate placement of implants (Figure 4).

The dog was transferred to the after-hours emergency team for intensive overnight monitoring and management. A Foley indwelling urinary catheter attached to a closed collection system was placed following surgery. The soft tissue mass and sample of vertebral laminae were submitted to Gribbles Veterinary Laboratory for histopathological evaluation.

Postoperative analgesia was provided with a continuous rate intravenous infusion of 0.0024 mg/kg/hour fentanyl (Mercury Pharma), 1.5 mg/kg/hour lignocaine (Lopaine; Ethical Agents), and 0.60 mg/kg/hour ketamine (Phoenix Ketamine; Phoenix Pharm) (FLK). On recovery, the dog exhibited some dysphoria and was administered I/V medtomidine at 1 µg/kg, to minimise the risk of self-trauma. The dog also received I/V Hartmann’s solution at 2.5 mL/kg/hour, I/V cefazolin at 22 mg/kg, I/V, every 8 hours, and 0.3 mg/kg ondansetron (Claris) administered slowly I/V twice daily. The surgical site was treated with cold therapy (ice) every 3 hours.

The following day, the dog was transitioned from the FLK infusion to I/V methadone (Phebra) at 0.2 mg/kg, every 4–6 hours for 24 hours, and then to I/V buprenorphine at 0.02 mg/ kg, every 6–8 hours until discharge. The dog was discharged 5 days after surgery with instructions for 6 weeks of strict crate rest with short leash walks for toileting only. The dog was prescribed with 25 mg/kg gabapentin (Nupentin 300; Mylan NZ Ltd), given orally twice daily; 0.5 mg/kg prednisone (ApoPrednisone; Apotex NZ Ltd), given orally once daily; and 6.25 mg amoxicillin/clavulanic acid (Clavubactin; Knight Benedikt), given orally twice daily. The dog was also prescribed trazodone (Compounded by Optimus Healthcare Ltd) for behavioural modification during the rest period. This was given orally, twice daily, initially at a dose of 7 mg/kg for 3 weeks, tapering to 4 mg/kg for 3 weeks, and then 3 mg/kg for 3 weeks. The

Figure 4. Post-operative CT image viewed in a bone window. (a) A transverse view at the level of L1, demonstrating the extent of surgical resection. The mass has been excised, and the left dorsolateral aspect of the L1 vertebra removed. The orthopaedic implants (*) are causing beam hardening artefact. Free gas is present throughout the surgical site (arrows). (b) Post-operative sagittal reformat of the thoracolumbar spine, demonstrating complete decompression of the dorsal aspect of the spinal cord. Free gas is present throughout the surgical site (arrows).

dog received a physiotherapy session with a recognised veterinary physiotherapist at discharge and received ongoing physiotherapy care during the recovery period.

Outcome and follow-up

Histopathological analysis of the mass provided a definitive diagnosis of vascular hamartoma. The mass was determined to have been resected with clean surgical margins. The histopathology report described that within the soft tissue

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component of the mass there was irregular proliferation of variably-sized blood vessels. In some areas there was proliferation of pericytes. The vascular channels were interspersed between areas of normal adipocytes, fibrous connective tissue, and skeletal muscle.

These blood vessels appeared to extend between the vertebral compact bone into the bone marrow.

Neurological assessment following surgery demonstrated the dog had normal pain sensation in both hind limbs. Within 24 hours of surgery the dog was using his hindlimbs to move in his cage, and by 48 hours postoperatively the dog was able to walk with some assistance from a sling. At this stage, he was also attempting to posture to urinate, so the urinary catheter was removed, and he was able to urinate normally.

Six weeks postoperatively, the dog had some mild hindlimb paresis but was ambulating well with no significant gait abnormalities. There was no pain over the surgical site. A CT scan of the spine showed no evidence of regrowth of the mass, and no evidence of significant movement of the surgical implants. The spinal cord was still sufficiently decompressed. Four months postoperatively, the owner reports that the dog has resumed the same level of activity which he had prior to surgery.

Discussion

Hamartomas are non-neoplastic, proliferative masses composed of tissue that is native to the area in which they occur (Zaki 1979; Misdorp 2002).

Vascular hamartomas are composed of variably-sized vascular structures lined by mature endothelial cells, and can occur in many locations in the body.

The presence of normal tissue between the vascular channels distinguishes this mass from a neoplastic proliferation of blood vessels such as a haemangioma (Smith and Van Winkle 2001). These masses exert a clinical effect through compression of neighbouring structures, and their tendency for haemorrhage and thrombosis (Borel et al. 2014). These masses are rare in dogs, but may be more common in cats. A case series of vertebral angiomatosis affecting the thoracic vertebrae in cats has been described (Westworth and Sturges 2010)

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Hamartomas are considered to be congenital malformations. They are present at birth, grow with the animal, and cease to grow once the animal reaches skeletal maturity (Borel et al.

2014). A study of cerebral vascular hamartomas in five dogs by Smith and Van Winkle (2001) found that vascular hamartomas are accompanied by local capillary proliferation. The authors identified that pericytes (mesenchymal cells which facilitate and direct angiogenesis) were found in all hamartomas in the study. Therefore, it is possible that paracrine signalling from these cells stimulates angiogenesis peripheral to the mass. Angiogenesis peripheral to the mass may account for the progressive neurological dysfunction seen in the few reported cases of spinal vascular hamartomas, despite being composed of well-differentiated tissue which should not continue to grow in the mature animal (Parkes et al. 2009; Yasuno et al. 2011; Taylor-Brown et al.

2018).

Congenital spinal malformations do not always cause clinically significant neurological dysfunction. For example, congenital stenosis of the spinal canal of the thoracic vertebrae impinging on the spinal cord has been reported in clinically normal Doberman Pinschers (Westworth and Sturges 2010). However, these malformations can predispose the animal to developing myelopathy following an event causing secondary stenosis of the spinal canal, such as intervertebral disc extrusion (Westworth and Sturges 2010).

When a lesion is identified on imaging studies, it is important to correlate the clinical significance of this lesion with the presentation and clinical neurolocalisation of the animal. In this case, the lesion was present at the L1 vertebra, but physical examination localised the lesion to the spinal segments between L4–S3.

This phenomenon is reported in the literature. Degenerative myelopathy occurs within the T3–L3 region of the spinal cord but may neurolocalise to the L4–S3 region when the patellar reflex is lost (Sharp and Wheeler 2005).

A mild neuropathy of the dorsal nerve roots in the lumbosacral region of the spine, commonly seen on post-mortem examination of older dogs, has been

hypothesised to result in this event (de Lahunta and Glass 2009). However, this is less likely in a young animal.

Alternatively, the expansile lesion of the lumbar vertebrae could have caused chronic, compressive damage to the spinal cord resulting in axonal atrophy (Zachary 2009). This spinal axonopathy occurs distal to the site of injury, so in this instance would be expected to cause lesions in the dorsal gray matter column of the L4–S3 spinal cord segments (de Lahunta and Glass 2009). Chronic spinal cord compression also results in necrosis of glial cells, which function to remove glutamate from the cerebrospinal fluid.

Glutamate exerts an excitotoxic effect on neurons and accumulation of this neurotransmitter may lead to depression of the patellar reflex (Abdelhakiem et al.

2015).

While it is possible to identify spinal malformations radiographically, this imaging modality is poorly sensitive compared to advanced imaging such as magnetic resonance imaging (MRI) and CT, which are also better at identifying the extent of spinal cord involvement (Westworth and Sturges 2010). This is exemplified in this case, where excellent quality radiographs of both elbow joints, the spine, coxofemoral joints, pelvis, and stifle joints were available for interpretation in 2017 following the first episode of neurological dysfunction.

No radiographic abnormalities were detected at the time. However, once the extent of the lesion was identified on CT in 2018, these radiographs were revisited.

In hindsight, the lesion affecting the L1 vertebra was subtle, but apparent, on the periphery of the spinal views. Mackillop (2011) described the characteristic findings on MRI associated with vascular hamartomas. Unfortunately, they are difficult to distinguish from a haematoma or haemorrhagic neoplasm such as haemangioma.

The prognosis following complete surgical resection of a vascular hamartoma affecting the vertebra is good. The mass is not neoplastic and unlikely to regrow if completely excised (Middleton et al. 1999; Parkes et al. 2009; Yasuno et al. 2011; Taylor-Brown et al.

2018). However, there are significant intraoperative risks relating to the proximity of the mass to the spinal cord, and the propensity of the mass

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for haemorrhage. Parkes et al. (2009) described life-threatening haemorrhage in a 15-month-old DSH cat from which a vascular hamartoma of the cervical spine was excised. The haemorrhage originated from the mass itself. A similar complication was faced by the authors of this case report, and an emergency transfusion of packed red blood cells was administered intraoperatively. Therefore, if a vascular hamartoma is a possible differential diagnosis based on imaging findings, dissection should proceed with care. Furthermore, it may be prudent to perform the surgery only in facilities where there is access to transfusion and haemostasis equipment.

Conclusion

Vascular malformations affecting the spine are a rare presentation, but should be considered in a young animal with clinical findings consistent with a soft tissue mass (Westworth and Sturges 2010). Hamartomas are a congenital malformation, but they may not manifest until later in the animal’s life.

Clinical signs relate to compression of surrounding structures, haemorrhage, and thrombosis. Therefore, signs are non-specific and advanced imaging may be necessary to elucidate the presence

of the mass. In this case, the dog made an excellent clinical recovery following complete excision of the mass. Given the character of the mass, regrowth is not expected. Previous literature demonstrates good long-term outcomes in animals where complete excision was achieved (Taylor-Brown et al. 2018).

Acknowledgements

Special thanks to pathologists Dr. Michael Hardcastle, Dr. Cathy Harvey, and Dr. Lisa Hulme-Moir as well as Dr Damian Chase for surgical assistance.

References

Abdelhakiem M, Asai Y, Kamishina H, Katayama M, Uzuka Y. The accuracy of the patellar reflex for localisation of the site of a single level thoracolumbar disc herniation in dogs. Turkish Journal of Veterinary and Animal Sciences 39, 589–93, 2015 Borel N, Grest P, Junge H, Eser MW. Vascular hamartoma in the central nervous system of a foal. Journal of Veterinary Diagnostic Investigation 26, 805–9, 2014 De Lahunta A, Glass E. Veterinary Neuroanatomy and Clinical Neurology (3rd Edtn.). Elsevier, St. Louis, MO, USA, 2009 MacKillop E. Magnetic resonance imaging of intracranial malformations in dogs and cats. Veterinary Radiology and Ultrasound 52, 542–51, 2011

Misdorp W. Congenital tumours and tumour-like lesions in domestic animals.

1. Cattle: a review. Veterinary Quarterly 24, 1–11, 2002 Parkes JD, Kline KL, Riedesel EA, Haynes JS. A vascular hamartoma arising from the cervical spine of a cat.

Journal of Feline Medicine and Surgery 11, 724–7, 2009 Sharp NJH, Wheeler SJ. Small Animal Spinal Disorders: Diagnosis and Surgery (2nd Edtn.). Elsevier, Philadelphia, PA, USA, 2005 Taylor-Brown FE, Lamb CR, Martineau H, Muir C, Beltran E. Imaging diagnosis – Imaging and histopathologic characteristics of a vertebral hamartoma in a cat. Veterinary Radiology and Ultrasound 59, 12–6, 2018 Westworth DR, Sturges BK. Congenital spinal malformations in small animals.

The Veterinary Clinics of North America: Small Animal Practice 40, 951–81, 2010 Yasuno K, Kobayashi R, Ohmuro T, Kamiie J, Sahara H, Shirota K. Caudal vascular hamartoma accompanied by aberrant arteriovenous structures in a dog. Journal of Veterinary Diagnostic Investigation 23, 1051–5, 2011 Zachary JF. Pathologic Basis of Veterinary Disease (6th Edtn.). Elsevier, St Louis, MO, USA, 2012 Zaki FA. Vascular malformation (cavernous angioma) of the spinal cord in a dog.

Journal of Small Animal Practice 20, 417–22, 1979 l

Cattle tick vector for emerging disease Haemaphysalis longicornis was long regarded as benign in New Zealand relative to other tick species and the organisms they carry. The events of the last few years have changed that perception. Theileriosis has become a significant problem in dairy cattle in the northern North Island. Now “our” tick has been found to transmit a potentially fatal virus to people in east Asia. The virus from the genus Phlebovirus causes severe fever with thrombocytopenia, leucocytopenia and gastrointestinal problems in people. First reports were from China in 2010. Imaginatively it is called the SFTS (severe fever with thrombocytopaenia) syndrome! China (2,600 affected in 2016), Korea (270 in 2017) and Japan seem worst affected with increasing numbers of cases over the last 8 years. Tick bites are the main source of infection but person-to-person infection via blood is confirmed. Domestic animals seem to seroconvert without recorded symptoms. There is a significant, though

Contact: Allan Bell, Dermvetonline, dermvet.bell@xtra.co.nz

reducing, death rate in humans (3–20%). While companion animals do not seem at risk there are two worrying reports from Japan; one woman apparently infected from a cat bite and a man infected by his dog. I have been unable to find a record of a local case. Once again, we are dependent on effective biosecurity..

References available on request l

Photo courtesty of pixabay.com

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CONFERENCE REPORT

Highlights from the course in Veterinary Ophthalmology II at the European School for Advanced Veterinary Studies (ESAVS): Part II Toulouse, France, 26–30 June 2017 This article was written as part of the requirements for receiving the Hill’s Pet Nutrition/CAV Educating the Educators Grant

JOS VAN HEES, BVSc

(Hons), MANZCVS, Special interest veterinary practitioner in ophthalmology.

I was fortunate to be awarded a Hill’s Pet Nutrition/CAV Educating the Educators Scholarship to assist in attending the ESAVS Ophthalmology II course in Toulouse, France. This week-long course, held at the National Veterinary School of Toulouse focused on ophthalmology surgery with over 50% of the time spent in wet labs practising eyelid, corneal and lens surgery and the remainder of the time spent in lectures.

The following is Part II of a selection of topics relevant to small animal veterinarians that were covered in the course lectures. Part I was published in the June issue of Companion Quarterly and covered diseases of the globe, and surgery of the globe and lens.

Skin diseases of eyelids

From a lecture by Dr Marie-Christine Cadiergues (National Vet School Toulouse, France) A series of clinical cases were presented.

The eyelid skin is part of the integument Contact: Queenstown Eye Vet Ltd, PO Box 2900, Wakatipu, 9349, NZ 027-417-2932

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and may be affected on its own or as part of generalised skin disease.

Differential diagnoses

• Parasites: scabies, demodecosis,

fleas including the rabbit flea which attaches around the eyes.

• Bacterial Infection: pyoderma – superficial and deep, mucocutaneous pyoderma • Yeast Infection: Malassezia • Fungal Infection: dermatophytes • Allergy: fleas, food, environmental • Immune mediated: superficial pemphigus, cutaneous lupus, juvenile cellulitis or puppy strangles.

• Inherited: ischaemic dermatopathy of Jack Russell terriers – nonpruritic areas of alopecia affecting the extremities and eyelids.

The approach to diagnosis of eyelid skin disease is similar to that of generalised skin disease. The pattern of distribution of skin affected is helpful. The presence of chronic pruritus suggests parasites, infection or allergy may be involved.

Diagnostic tests

• Cytology: impression smears.

• Skin scrapings for parasites. To

detect scabies, a large area should be superficially scraped to increase

•

• • • •

•

• •

the chance of finding the mites. A negative scrape for scabies does not rule it out. Deeper scrapes are useful for Demodex.

Trichoscopy: hairs are plucked and examined under the microscope – useful to detect demodex. Demodex targets follicles and does not affect hairless areas e.g. planum nasale.

Tape strips to detect Malassezia Woods lamp examination; some dermatophytes fluoresce.

Fungal culture for dermatophytes Skin biopsies and histopathology of pustules and crusts. Skin preparation should be carefully clipped with scissors. Do not scrub the skin as this will remove the stratum corneum.

Response to ectoparasite treatment: selamectin applied topically once monthly. It is systemic so not removed by regular shampooing. Selamectin is affective against scabies.

Response to antibiotic therapy (4 weeks): allergy may be considered once infection and parasites have been ruled out.

Dietary trial for food allergy: hydrolysed diet fed exclusively for 6–8 weeks.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Fontana: melanin Perl: iron, u Von Kossa: calcium, u Gram and Ziehl Nielson: bacteria u Immunostaining: uses specific antibodies for tumour phenotyping, proliferation index u u

Neoplasia of the orbit, adnexa and eyelids From a lecture by Professor RaymondLetron (National Vet School Toulouse, France).

A malignant neoplasm differs from a benign one in being invasive, in having the ability to metastasize, and in showing anaplasia.

General management of ocular neoplasia involves: Photo credit: pixabay.com

• Response to corticosteroids:

prednisone 0.5 mg/kg every 48 hours for 3–4 weeks given at the beginning of a dietary trial and upgraded parasite control will alleviate pruritus. If pruritus relapses once prednisone is stopped then atopy is likely. Atopy is diagnosed by exclusion.

Treatment will depend on the cause:

• Juvenile pyoderma: systemic

•

•

•

•

glucocorticoids e.g. prednisone 0.5–1 mg/kg once daily then taper and continue for 2 weeks after lesions resolve (+/- antibiotics).

Pemphigus: prednisone 1 mg/kg (3–5 weeks), then taper dose and maintain on minimum dose possible. Topical ciclosporin or tacrolimus is useful if poorly responsive to steroids.

Malassezia: topical clotrimazole for 3 weeks, or antifungal shampoo (e.g.

Malaseb) and treat any underlying cause for skin damage causing yeast overgrowth.

Atopy: combine skin care (shampoos and emollients), immunomodulatory therapy (Apoquel daily, low dose prednisone or ciclosporin twice weekly adapted to patient and owner), specific immunotherapy, control ectoparasites and aggravating factors.

Food allergy: hypoallergenic diet.

Ocular pathology

From a lecture by Professor RaymondLetron (National Vet School Toulouse, France)

Optimisation of ocular specimens for histopathology

• Provide a good quality sample – avoid crushing the biopsy

• Immediately immerse specimen in • • • • • •

fixative (10% formalin) The eyeball should not be opened but injected with fixative Provide guide marks for orientation of the specimen with suture or indelible ink Send fine needle aspirates (FNA) separately Provide a case history Give a precise description of lesions on the histopathology form State your diagnostic hypothesis and any questions

Staining

• Basic stain: haematoxylin and eosin • Special stains: Trichrome: connective tissue, PAS: mucin, basal membrane, and mycotic agents, u Luxol fast blue: optic nerve u u

• History, complete clinical and

ophthalmic examination and TNM staging (see below) • Histopathologic diagnosis (tumour type) • Treatment: surgery, chemotherapy and radiotherapy

TNM staging

• T Primary tumour: size and local

extension. Requires a complete ophthalmic exam with fundic examination, intraocular pressure (IOP) measurement, ocular and orbital ultrasound, skull radiographs....

Intraocular tumours with scleral infiltration have a guarded prognosis.

• N Lymph node involvement: palpation, FNA, biopsy of parotid and submandibular lymph nodes • M extent of distant metastases/ systemic involvement: imaging techniques….

Histopathology

• Tumour type: benign or malignant • Malignant tumours maybe locally

invasive (squamous cell carcinoma (SCC), fibrosarcoma and some other sarcomas) while metastatic spread occurs with lymphoma, melanoma, mast cell tumour and some sarcomas.

• Extent of ocular involvement/margins • Prognosis and follow up recommendations

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Therapeutic choice

• Treatment is mostly surgical: local

excision, evisceration, enucleation or exenteration • Chemotherapy: useful for mast cell tumour, malignant melanoma, lymphoma, fibrosarcoma, hemangiosarcoma.

• Radiation therapy: if available.

Useful for eyelid mast cell tumours, lymphoma, recurrent sarcomas, SCC • Prognosis depends on location, tumour type and extension of disease.

Eyelid tumours:

• Epidemiology: common • In the dog, eyelid tumours are •

• • • • •

usually benign: sebaceous adenoma, melanocytoma, papilloma In the cat, eyelid tumours are more often malignant: sarcomas and squamous cell carcinoma (SCC make up 2/3 of feline eyelid tumours, and are associated with UV exposure).

Other types: hemangioma/sarcoma, histiocytic sarcoma, mast cell tumours, apocrine hidrocystomas (cats).

Clinical signs: irritation Diagnosis: cytology, excisional biopsy Treatment: excision, +/- lid reconstruction Prognosis: dogs – good; cats – depends on adequate surgical margins and extension.

Orbital and optic nerve tumours

• Epidemiology: uncommon, often

malignant and occur in adult/aged animals.

• Tumour type: u Primary tumours (more often in dogs): meningioma, adenomas and adenosarcomas of lacrimal gland, third eyelid gland and zygomatic salivary glands. Also see SCC (cats), sarcomas (liposarcomas and rhabdomyosarcomas). u Secondary tumours (more common in cats): lymphoma, nasal adenocarcinomas and invasive adjacent tumours.

• Clinical signs: due to a space occupying lesion in the orbit (exophthalmos, exposure keratitis, strabismus, globe resistance to retropulsion).

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• Diagnosis: often late! Cytology, biopsy, search for metastasis.

• Treatment: if no metastasis then exenteration +/- chemo/radiotherapy (limited availability).

• Prognosis: poor

Conjunctival, corneal and scleral tumours

• Uncommon in the cat and dog and

mostly benign (conservative surgery with exceptions) • Diagnosis: cytology, biopsy, excision with histopathology • Treatment: surgical excision, chemotherapy • Prognosis: variable, good in general if adequate surgical margins Conjunctival tumours • Limbal (epibulbar) melanoma: circumscribed, slow growing, heavily pigmented, usually temporal, subconjunctival nodule arising from the corneoscleral junction melanocytes. Usually benign; metastasis not reported. Differential diagnosis is uveal melanoma with trans-scleral extension. Treatment is regular observation for intra-ocular extension, conservative surgery, or cryotherapy or enucleation if there are complications and invasion. (This is radically different from intraocular melanoma.)

• Hemangioma, hemangiosarcoma.

Both canine and feline conjunctival tumours of vascular endothelial origin have a strong site predilection for nonpigmented epithelium of the leading edge of nictitating membrane and temporal bulbar conjunctiva suggesting UV light is a significant risk factor. Early surgical therapy is recommended and may be curative, however recurrence is possible and more likely with hemangiosarcoma (50%).

• Mast cell tumour: in a study of 32 cases of conjunctival mast cell tumours of varying grades that were surgically excised in dogs, no dogs were identified that died of mast cell-related disease.

• Lymphoma is the most common secondary conjunctival tumour.

• Histiocytosis

• Conjunctival melanoma: highly

aggressive (infiltration and metastasis).

In dogs, there is a predilection for the bulbar surface of the nictitating membrane, and frequent recurrence but uncommon metastasis. In cats, conjunctival melanoma is most frequently found on the bulbar conjunctiva. Cats have a poorer longterm prognosis with recurrence and metastasis, than the same neoplasm in dogs.

• Squamous cell carcinoma and papilloma • Nictitating membrane tumours are rare in dogs and are of various histological types (papilloma, SCC, adenoma and adenocarcinoma, melanoma, mast cell tumour, lymphoma and hemangioma/ sarcoma).

• Nictitating membrane gland adenoma and adenocarcinoma are locally infiltrative and resection of the entire third eyelid is required for cure. Only very neglected cases will metastasise.

Corneal tumours • These are extremely rare • Corneal squamous cell carcinoma and hemangiosarcoma have both been reported in the dog. Chronic corneal irritation, UV exposure and keratitis are suspected contributing factors.

• Treatment is surgical removal by superficial keratectomy followed by treatment for keratitis and application of 0.1% hyaluronate sodium ophthalmic solution to reduce chronic irritation.

Intraocular tumours

• Intraocular tumours are noticed

by owners because of change in appearance of the eye – they cause hyphaema, pupil changes and distortion, buphthalmos.

• Both benign and malignant intraocular tumours cause secondary disease in the eye i.e. keratitis, uveitis, glaucoma, retinal detachment.

• Intraocular melanomas: most common intraocular tumour in dogs and cats. Affects the anterior uvea. They frequently metastasizes in cats but most are benign in dogs and rarely metastasize. These melanomas maybe nodular or diffuse lesions and may or may not be pigmented.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Glaucoma is caused by infiltration of the iridocorneal angle by tumour cells.

Even with benign melanoma, globe destruction and blindness occur with time.

• Feline uveal melanomas: are often malignant with haematogenous metastasis to lung and liver and associated mortality. They present as a nodular or diffuse increase in pigmentation of the anterior surface of the iris with or without glaucoma. u Diagnosis is based on clinical signs. Needle paracentesis of the aqueous humour for cytology is not reliable. Iris biopsy often causes haemorrhage and complications. Ultrasound is useful for assessing the thickness of the iris. Topical Mydriacyl can be used to see how the pupil dilates. If dyscoria occurs, this suggests infiltration of the iris rather than just surface pigmentation. Most cats with metastasis have extension of the neoplasm beyond the iris and/or

neoplastic cells within the venous plexus at histology. u Treatment: isolated benign non-evolutive lesion (naevus): regular observation and iridectomy. If the eye is blind, painful, glaucomatous, shows dyscoria, has uveitis, or infiltration into the iridocorneal angle then enucleation is advisable. u Prognosis is guarded; feline melanoma is an aggressive tumour with a high metastasis rate.

• Ciliary body epithelial tumours • Feline post traumatic ocular sarcoma: uncommon, occurs in older animals.

There may be a history of prior trauma, chronic uveitis, disrupted lens capsule.

Tumour types seen are fibrosarcomas, osteosarcomas and anaplastic sarcomas. These rapidly grow in the iris, sclera and retina, progressing along the optic nerve to the brain, with haematogenous and lymphatic metastasis.

Treatment: exenteration and prognosis is poor. Prophylactic enucleation should be considered for atrophic or blind globes following trauma in cats.

• Secondary (metastatic) tumours: any malignant tumour can spread to the eye. The anterior uvea in the dog and choroid in the cat are preferential metastatic sites. u

Conclusions – ocular neoplasia

• Suspicion of intraocular tumour: with uveitis, hyphema and glaucoma.

• Prognosis: depends on location and

type • Malignancy: increases from the front to the back of the eye. Malignancy of eyelid and epibulbar tumours < intraocular tumours < retrobulbar tumours. Malignancy in cats > dogs.

• Metastasis: uncommon, even for malignant ocular tumours (with exceptions e.g. feline uveal melanomas and post traumatic ocular sarcomas) • Therapy: surgical, if early and adequate margins is often curative. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

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CONFERENCE REPORT

Veterinary Behaviour Chapter programme of ANZCVS Science Week Gold Coast, Australia, July 2017 This article was written as part of the requirements for receiving the Hill’s Pet Nutrition/CAV Educating the Educators Scholarship

Dr ELSA FLINT, MSc, BVSc,

up in treating behaviour problems. I presented a talk about handling fearful animals in practice.

The behaviour component of Science week in 2017 had topical themes of fear free practice and appropriate and compassionate animal handling. The keynote speaker was Dr Paul McGreevy from Sydney University who spoke about dogmanship and the three As; affective state, arousal and attachment, that influence animal behaviour and trainability. Paul also spoke about his equine research on the negative impact on horse welfare of whips and tongue ties, bits and severe nose bands.

Dr Chalette Brown spoke about managing the interactions of babies and pets. This is something that comes up regularly in practice and it is useful to have a conversation with pregnant owners about their plans for integrating pets and babies. A client handout is a great idea.

MANCVS, PhD

Behavioural medications

Dr Kersti Seksel outlined the use of medication to relieve anxiety, before surgery. Recommended drugs included benzodiazepines, trazodone, and gabapentin. Dr Thiery Beths discussed the relevance of short and long term antianxiety medications to anaesthesia protocols and other peri-operative medications. His take home message was that while animals on antianxiety medication do not need to stop taking these before having anaesthesia, drug interactions are possible and practitioners should be aware of these.

Dr Jacqui Ley reviewed common medications used in behavioural therapy and Dr Andrew O’Shea spoke about the importance of monitoring and follow Contact: elsaflint1@gmail.com, ph. 027-264-9777

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Animal training

Dr Karen Dawes spoke about the impact of rearing and training practices on wastage in greyhounds and the difficulties in rehoming some of these dogs. Karen is very active in improving greyhound welfare. She identified the main problems as separation anxiety and predatory aggression (especially in those trained using live prey, a practice that is now banned in Australia and to my knowledge has never happened here).

Dr Jen Nesbitt-Hawes gave an overview of reactive dog classes and pointed out that there is little benefit in working with a group of dog reactive dogs together which is something that unfortunately seems to happen in some training classes. Take care to refer to knowledgeable trainers. Dr Cam Day discussed his approach to training dogs to be calm as part of his approach to behavioural therapy.

Dr Gaille Perry talked about the Delta dog training course which is something New Zealand trainers can enrol for and attend in Australia. It is a comprehensive

course with a practical component and means the public have some idea that a trainer has a solid knowledge base and hasn’t just put up a sign. It would be great if we had Delta-trained trainers here.

There was a panel discussion including a Skype attendance by Steve Dale about the benefits of Kitten Kindies. Essentially these are designed to teach owners about cat behaviour and how to better manage their cats’ behavioural as well as physical needs. We don’t see many of these held in New Zealand. It may be something that more practices should consider as a practice builder.

Behaviour in the context of animal care facilities

There was an update on current research in behaviour assessments in shelter situations and the difficulties of extrapolating results to real life situations.

This is something that definitely needs to be addressed in New Zealand.

Dr Nela Graham spoke of her experiences working with a dog daycare centre to improve facilities and management. I think this is something that could be considered in New Zealand. Some form of accreditation for day care centres would be useful.

Other tidbits

Dr Kersti Seksel talked about her research on the behavioural knowledge of vet students and so far, her research shows that their knowledge is seriously limited. It seems that this component of veterinary medicine tends to be

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

underemphasised in most veterinary schools.

There were speakers on handling exotic species including birds and reptiles and a presentation from Dr Katrina Gregory, a veterinarian who travels world-wide teaching zookeepers how to train animals to present themselves for medication and blood sampling.

She also works very successfully with

aquatic animals. Her presentation made me think about how much more prepared our domestic animals could be for certain procedures if we could motivate owners to train them from a young age. Perhaps this would be a good extension to puppy school classes.

There is definitely scope for training animals who are diabetic for example to be comfortable with repeated blood

sampling. There is also application to large animal practice. Overall it was a useful and interesting programme which hopefully had something of interest to offer vets in various branches of veterinary practice. I am grateful to have received the Hill's Pet Nutrition/ CAV Educating the Educators scholarship which helped to fund my attendance. l

NZVJ Update

The September issue of the New Zealand Veterinary Journal has a focus on infectious diseases of companion animals. This feature series was generously supported by the Companion Animal Veterinarians Branch and Virbac New Zealand. The first review by Els Acke, is an update on campylobacteriosis in dogs and cats, including risk factors for infection with Campylobacter spp., clinical signs, diagnosis and treatment recommendations. Those with an interest in the history of medicine will be fascinated by Richard Squiresâ&#x20AC;&#x2122; review of bacteriophage therapy for management of bacterial infections in veterinary practice. Bacteriophages are viruses that infect and kill bacteria and

they have been used for the treatment of bacterial infections in humans and animals since the 1920s. Interest in bacteriophage therapy declined after the development of antibiotics in the 1940s. However there has been a recent upsurge in interest, especially in the last decade, in the clinical use of bacteriophages for the treatment of bacterial infections, particular those caused by multidrug resistant organisms.

Also in this issue, Harriet Sowman and colleagues from the School of Veterinary Science at Massey University, present the results of a NZ survey of pathogens known to cause respiratory disease in dogs. They found evidence of infection with canine respiratory coronavirus and Mycoplasma cynos in dogs that were showing signs of respiratory disease consistent with infectious canine tracheobronchitis (aka kennel cough), but also in those that were healthy. However among diseased dogs, 74% were negative for all nine pathogens tested, showing that further studies are needed to determine if other novel respiratory pathogens are involved in the development of infectious canine tracheobronchitis.

To accompany this special issue the NZVJ team have also collected articles on infectious diseases of companion animals

that have been previously published in the NZVJ into a virtual special issue, which can be accessed on the NZVJ website at https://www.tandfonline.com/action/ journalInformation?show=specialIssues &journalCode=tnzv20. The virtual issue contains articles on a broad range of topics such as the first report of multi-drug resistant Staphylococcus pseudintermedius in a dog in New Zealand, risk factors for cats testing positive for feline leukaemia virus or feline immunodeficiency virus, as well as reviews from the World Small Animal Congress held in 2013 and some historical papers from the 1970s and 1980s.

The September issue also includes articles on a range of other topics; from the development of an equation to predict fat free mass in lean working farm dogs to a report of evidence for Bartonella spp infection in rats from Tongariro National Park.

Members of the NZVA can access any articles published in the NZVJ by logging in to SciQuest (www.sciquest.org.nz).

SARAH FOWLER BSc, BVSc, MSc, PhD, Editor, Companion Quarterly and Scientific Editor, NZVJ l

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What is your diagnosis?

THE ANSWERSâ&#x20AC;Ś 1. Problem list:

For simplification, the clinical problems have been grouped into general body systems.

1) Intermittent anorexia, vomiting and diarrhoea. Pyrexia with cranial abdominal pain and elevated amylase, lipase and abnormal cPL. 2) Enlarged abdominal lymph nodes with irregular pancreas and spleen on ultrasound 3) Hypercalcaemia, polydipsia and hyposthenuria 4) Pododermatitis and lameness with enlarged prescapular lymph nodes

2. Differential diagnoses would include:

1) With the clinical GIT symptoms, the most likely differentials include: acute pancreatitis, pancreatic neoplasia, intestinal foreign body, liver disease 2) Lymphadenopathy: reactive hyperplasia secondary to pancreatitis and pododermatitis, lymphadenitis, immune mediated disease, lymphoma/neoplasia or metastatic disease.

3) Hypercalcaemia: spurious, lipaemia, haemolysis, malignancy, hyperparathyroidism, vitamin D toxicosis, hyperproteinaemia, Addisonâ&#x20AC;&#x2122;s disease, osteolytic disease, nutritional causes and idiopathic.

There are many causes of polyuria/ polydipsia and hyposthenuria, however since hypercalcemia is known to cause these effects, it was presumed that they were sequential to hypercalcemia in this case.

4) Pododermatitis: infectious/parasitic agents, immunologic conditions, contact irritants/allergens, trauma, or less likely metabolic disorders, neoplasia, genetic/inherited diseases

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3. Confirm diagnoses by:

Pancreatitis. There is currently no single specific test for pancreatitis, and diagnosis is based on a combination of compatible clinical, clinicopathological and imaging findings (Armstrong 2014). The combination of clinical signs (vomiting and abdominal pain) and clinicopathologic and imaging findings in this case supported a high clinical suspicion of acute pancreatitis.

Screening abdominal radiographs were not consistent with a gastrointestinal foreign body. Ultrasound-guided FNA (and cytological evaluation) of the pancreas may have added some further support to the diagnosis (Sharkey 2013).

Ruling out of other diseases (such as intestinal foreign body or liver disease) with thorough examination, radiographs, serum biochemistry, ultrasound and contrast studies is important. Biopsy of the pancreas is rarely indicated due to the anaesthetic risk in these patients as well as difficulty in interpreting the significance of lymphocytic inflammation. Multiple biopsies are often required (Armstrong 2014).

Lymphadenopathy. Cytological evaluation of FNA of multiple lymph nodes would be the first step in establishing the cause for lymphadenopathy. Screening radiographs of the thorax and abdomen, routine serum biochemistry and haematology, or abdominal ultrasonography to evaluate the presence of organomegaly or mediastinal masses with collection of further samples for cytology can add support to a diagnosis. A lymph node biopsy (with evaluation of the architecture of the node) can be helpful in ambiguous cases, along with immunohistochemistry or clonality studies such as PARR (PCR for antigen receptor gene rearrangements).

Hypercalcaemia. The concentration of total Ca in serum represents the sum of protein-bound calcium (approx. 50% of

total Ca), complexed calcium (approx.

10% of total Ca) and ionised calcium (approx. 40% of total Ca). While total serum calcium often parallels ionised calcium, it can be influenced by protein (albumin) levels and measurement can be affected by lipaemia (Duncan and Prasse 2003) and haemolysis (Bergman 2012). Because ionised Ca is the most tightly regulated fraction and is biologically active (and hence causing the clinical effects), measurement of the ionised Ca concentration provides greater specificity and sensitivity in determining hypercalcaemia. Repeat testing of serum calcium concentrations and confirmation of hypercalcaemia in the ionised fraction would support the diagnosis of a true hypercalcaemia (Jarrett 2006).

Pododermatitis. Skin scrapings would assist in identifying any infectious agents involved in the inflamed skin. Evaluation of the housing environment, exercise regime, hygiene, flooring materials may help to identify any traumatic or irritant factors. Culture and sensitivity and skin biopsies could also be useful if the feet were non responsive to empirical therapy.

4. Treatment and outcome:

Six direct smears of multiple lymph nodes (three abdominal and three prescapular) were examined by a Registered Specialist Veterinary Clinical Pathologist, and peerreviewed. All six slides were similar and contained a heterogeneous lymphoid cell population, considered consistent with reactive lymphoid hyperplasia. This generally occurs due to antigenic stimulation associated with inflammatory, immune-mediated, infectious or even neoplastic processes in the area drained by the lymph nodes.

At this stage, the lymphadenopathy was considered to be associated with the likely pancreatitis, and moist pododermatitis.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

As Paddy’s malaise was intermittent and chronic, he was still eating and drinking and was well hydrated, he was treated as an outpatient. His feet were clipped and cleaned with diluted chlorhexidine solution, and he was prescribed maropitant (Cerenia; Zoetis New Zealand) at 2 mg/kg PO once daily for 4 days, amoxicillin/clavulanic acid (Juroclav; Jurox New Zealand) at 12.5 mg/kg twice daily for 10 days, carprofen (Rimadyl; Zoetis New Zealand) 1.8 mg/kg twice daily for 7 days, and Royal Canin Canine Intestinal Low Fat canned food.

Table 2. Serum biochemistry results for 3-year-old male Welsh Springer Spaniel presenting with gastrointestinal signs, polydipsia, lameness and pyrexia, measured 4 (Test 2) and 8 (Test 3) days after initial presentation.

Analyte (units)

To measure ionised Ca a fasting serum sample was collected. As per recommended sample requirements the collection tube was filled to near capacity and the remaining air removed. The sample was submitted chilled to the closest approved referral veterinary laboratory for immediate testing of serum ionised calcium. The concentration of ionised Ca in serum was normal at 1.37 mmol/L (reference range 1.25–1.45mmol/L).

Paddy was placed on I/V fluids (PlasmaLyte 148 in water) at twice maintenance rates (80 mL/hour), and maropitant and amoxicillin/clavulanic acid S/C were continued. Mirtazepine (0.75 mg/kg Apo-mirtazepine; Apotex NZ Ltd) was administered orally after 12 hours. Paddy started eating well, and was significantly brighter and more active, chewing the I/V line and bouncing in his kennel.

Within 24 hours, Paddy’s temperature

Test 2a

Test 3a 5.90

Glucose (mmol/L)

4.11–7.95

5.16

Creatinine (μmol/L)

44–159

152

171

Urea (mmol/L)

2.5–9.6

14.0

18.4

23

27

Urea/Crea Phosphate (mmol/L)

0.81–2.20

1.82

2.49

Calcium (mmol/L)

1.98–3.00

>4.00

3.92

Total Protein (g/L)

52–82

65

72

Albumin (g/L)

23–40

25

27

Globulin (g/L)

25–45

40

45

Alb/Glob ratio

Three days later, Paddy was re-admitted into the hospital after suddenly becoming depressed and not eating for 12 hours. His temperature was 39.5°C and he had lost 1.4 kg body weight.

There was mild cranial abdominal pain remaining. The pododermatitis appeared to be improving.

Haematology, serum biochemistry and urinalysis were repeated (Table 2, test 2) revealing that Paddy’s USG was now 1.013 with pH5, protein 1+ and RBC 4+.

The most significant findings in these tests were persistent hypercalcaemia, even further elevated urea and the apparent resolution of the elevated lipase and amylase. It was also noted that creatinine levels, while still within the reference range, had increased since the last serum analysis. The urine was now close to isosthenuric, and there was still no evidence of inflammation (or stress) in the CBC results.

Reference interval

0.6

0.6

Alanine aminotransferase (U/L)

10–125

32

29

Alkaline phosphatase (U/L)

12–212

43

52

Gamma glutamyltransferase (U/L)

0–11

12

13

Bilirubin (μmol/L)

0–15

6

8

Cholesterol (mmol/L)

2.84–8.26

2.74

3.18

Amylase (U/L)

500–1500

886

671

Lipase (U/L)

200–1800

801

854

Sodium (mmol/L)

144–160

147

155

Potassium (mmol/L)

3.5–5.8

3.9

4.3

37

36

109–122

104

110

Na/K ratio Chloride (mmol/L)

a

Results in red are greater than the reference range and those in blue are less than the reference range.

was 38.5°C, he was eating and drinking normally and was discharged 48 hours later. Carprofen was ceased at this point.

However, 24 hours later Paddy was admitted yet again to the veterinary hospital, very depressed, lethargic and anorectic. His temperature was 38.4°C, and he appeared painful to touch.

Serum biochemistry and haematology was again repeated on the in-house analyser (Table 2, test 3) and a urine sample collected for urinalysis.

Paddy’s USG was 1.010, pH5, with no evidence of haematuria or proteinuria.

There was now azotemia, evidence of hyperphosphatemia and isosthenuria.

The hypercalcaemia persisted. There was still no evidence of stress nor inflammation in the CBC. To rule out atypical Addison’s disease as a cause for the hypercalcaemia and lack of changes in the CBC (and no evidence of concurrent electrolyte disturbances), a serum sample was sent to closest approved referral veterinary laboratory for measurement of baseline cortisol concentrations. Paddy’s resting cortisol level was 281 nmol/L. Since this is >55nmol/L, atypical Addison’s disease (hypoadrenocoticism) was very unlikely.

As Paddy’s response to supportive fluids, and medications including additional buprenorphine (0.027 mg/ kg I/M Bupredyne; Jurox NZ Ltd) and dexamethasone (0.17 mg/kg I/V Dexadreson; MSD Animal Health) was minimal, referral to a specialist was offered but his owners declined. The owners elected euthanasia and Paddy was sent for necropsy at Massey University School of Veterinary Sciences.

The gross and histological findings confirmed the presence of: i) Multicentric lymphoma affecting multiple lymph nodes, including sub-lumbar and mesenteric nodes, spleen and possibly liver (neoplastic cells were small cell). ii) Mild interstitial lymphoplasmacytic nephritis with renal tubular necrosis and mineralisation iii) Moderate multifocal lymphocytic subacute hepatitis iv) Mild multifocal lymphocytic subacute pancreatitis

Discussion

This case is interesting from pathophysiology perspective but it also highlights the importance

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of accurately interpreting unexpected, or even normal results in the clinical setting. It is very likely that, in this case, lymphoma was the cause of the elevated concentration of total Ca. When hypercalcemia is identified in conjunction with normal to low serum phosphorus concentrations, the main differentials are hypercalcaemia of malignancy and primary hyperparathyroidism (Dann and Hill 2009).

Hypercalcaemia of malignancy is the most common cause of hypercalcaemia in dogs – neoplasia is diagnosed in approximately two thirds of dogs with hypercalcaemia (Bergman 2012). Lymphoma is the most common cause, followed by multiple myeloma and apocrine adenocarcinoma of the anal sac. Other less common malignancies such as some mammary, nasal, thyroid, pancreatic, pulmonary and squamous cell carcinomas can also be the cause (Elliot 2001, Neiger 2005).

Hypercalcaemia occurs in 10–35% of dogs with lymphoma (Bergman 2012), and more than 90% of dogs with lymphoma and hypercalcemia have enlarged lymph nodes (Duncan and Prasse 2003).

The neoplastic mechanisms which produce hypercalcaemia are multiple and vary with the type of tumour. Most commonly, neoplastic cells produce parathyroid-related peptide (PTHrp) which mimics the biological actions of parathyroid hormone (Neiger 2005). It promotes calcium mobilisation from bone, increases renal tubular calcium retention and increases production of active vitamin D, which in turn increases intestinal absorption of calcium. Less frequently, local bone resorption caused by metastases in the bone marrow contributes to hypercalcaemia (Jarrett 2006).

The elevated calcium concentration has direct effects on kidney function, sometimes causing acute renal failure even without mineralisation (Wismer 2017). Hypercalcaemia first reduces responsiveness to antidiuretic hormone in the distal tubules (causing inability to concentrate urine), then decreases renal blood flow and glomerular filtration rate due to vasoconstriction. Ca deposition in the renal parenchyma compounds prerenal and renal azotemia and the renal epithelium degenerates and becomes necrotic (Bergman 2012). Further deposition of mineral in soft tissues, along with pathologic bone fractures can also occur. Initially there is hypophosphatemia but as the disease becomes more severe or chronic, the serum phosphorus concentration will often increase with the development of nephrocalcinosis and renal failure (Duncan and Prasse 2003).

Ideally, measurements of parathyroid hormone and PTH-rp would help to distinguish hypercalcaemia of malignancy from hyperparathyroidism, however these tests are currently unavailable in New Zealand, and costly to send to the USA. Interestingly, ultrasound of the parathyroid glands is reported to have a sensitivity of 90% in the detection of hyperparathyroidism secondary to neoplasia or hyperplasia (Dann and Hill 2009). The initial set of blood results in this case identified hypercalcaemia and with normal phosphate concentration (suggesting either malignancy or hyperparathyroidism) however ultrasound of the parathyroid glands was not performed. The final set of blood results identified increasing concentration of phosphorus in serum (in conjunction with the presence of isosthenuria and azotemia), most likely as a result of the developing nephrocalcinosis and renal failure.

As calcium ions are involved in many intra- and extracellular functions, the clinical signs of hypercalcaemia can often be 52

Paddy.

Photo courtesy of Stephanie Crofskey

mild and non-specific. Clinical signs often relate to the renal, gastrointestinal and neuromuscular systems, however the most commonly reported clinical signs of hypercalcaemia in the dog are polyuria, polydipsia, and anorexia. Weakness, bradycardia, calcium phosphate urolithaiasis, coma, seizures, renal failure, soft tissue mineralisation, bone resorption and fibrous osteodystrophy can be sequelae of prolonged hypercalcaemia (Dann and Hill 2009).

One of the confounding factors in this case, was that the concentration of ionised Ca was within the reference range, despite an elevated total Ca in serum. While initially such a result may create doubt with respect to whether the hypercalcaemia is ‘genuine', it is important to understand why and when this may occur. Ionised Ca concentration is affected by acid-base status; alkalosis decreases ionised Ca, while acidosis increases it (Duncan and Prasse 2003). In addition, sample haemolysis, lipaemia, pH, time delay and sample temperature can all affect measured concentrations of ionised Ca, so the accuracy of this test is inherently at risk of metabolic influences and artefactual errors. The sample submitted for measurement of ionised Ca did not appear grossly haemolysed and all practical precautions were taken to attempt to reduce artefactual error caused by sample handling. Sample pH, HCO3 and TCO2 were not assessed and thus it is possible Paddy was alkalotic potentially due to loss of chloride ions through vomiting (with a paradoxical aciduria).

When hypercalcaemia is secondary to renal failure, the ionised Ca can be low-normal whereas when renal dysfunction is secondary to hypercalcaemia, both total and ionised Ca concentrations can be increased (Dann and Hill 2009). These findings would suggest that renal failure was the driver of the hypercalcaemia in Paddy’s case. At the time of sampling, ionised Ca, the serum creatinine concentration was increasing and USG was 1.013 supporting this hypothesis. However, the results of the earlier serum biochemistry and urinalysis showed normal creatinine concentration with hyposthenuric urine, and a significant (and as it transpired, persistent) hypercalcaemia, it is more likely that the hypercalcaemia was the cause of

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

the developing renal compromise.

In addition, hypercalcaemia is not a common complication of renal disease in dogs. While the ionised calcium level was within the reference range, interpreting all of the other clinical signs and diagnostic tests suggested that the hypercalcaemia was indeed real.

The other confounding factor in this case was the cytology of FNA from the abdominal and prescapular lymph nodes which did not identify lymphoma. The findings suggested reactive lymphoid hyperplasia. As mentioned earlier, this can be a feature of an inflammatory, immune-mediated, infectious or even neoplastic process draining to the lymph nodes. It would be reasonable to assume the reactive lymph nodes were a result of the likely pancreatitis and pododermatitis. In one study the overall diagnostic accuracy (meaning the agreement between cytological and histological diagnoses) of cytology of lymph node aspirates is 74.1%.

Furthermore mesenteric and other intraabdominal lymph nodes were more likely to give false-negative cytology results (cytology not diagnostic for neoplasia) compared with other lymph nodes (Ku 2016). Several mechanisms could account for the diagnosis of reactive lymphoid hyperplasia in the abdominal and prescapular nodes.

The nodes sampled may not yet been affected by lymphoma, sampling of the nodes for cytology may have occurred earlier in the process of infiltration than that seen at necropsy or the sample needle may have sampled a nonaffected section of a partially affected node.

An additional confounding factor was that the lymphoma in this case was comprised histologically of small (lymphocytic) cells. It is often reported that small cell lymphomas or indolent lymphoma can be challenging to diagnose cytologically as the neoplastic cells have similar morphology to the small mature lymphocytes that predominate in a normal or reactive lymph node. Histopathological evidence of disrupted nodal architecture is often required to make a diagnosis (Pohlman 2013).

In this case, redirecting the needle several times during aspiration and evaluating aspirates from multiple lymph nodes and abdominal organs (spleen and liver) may have improved

the sensitivity of cytological evaluation.

Biopsy of an abdominal lymph node (or even exploratory laparotomy) and immunohistochemistry may also have been helpful.

While the clinical suspicion of pancreatitis in this case was based on numerous compatible clinical, clinicopathological and imaging findings, there is a possibility that the initial hyperamylasemia and hyperlipasemia, and even the elevated cPLi in this case, were a result of multiple concurrent processes; namely mild multifocal lymphocytic subacute pancreatitis, moderate multifocal lymphocytic subacute hepatitis, reduced renal clearance by compromised kidneys and possibly some low grade intestinal disease. A paraneoplastic cause cannot be ruled out either. The cause of the return of these enzymes to the reference intervals within 4 days cannot be easily explained however.

The role of calcium and pancreatitis in this case is not clear. There are numerous potential aetiologies that can cause, or are associated with, acute pancreatitis in dogs such as dietary factors, hyperlipoproteinaemia, drugs and toxins, breed, overweight body condition, small breed size, prior gastrointestinal diseases, diabetes mellitus, hyperadrenocorticism, trauma to the pancreas or its ducts and even hypercalcaemia. However, despite the experimental association between premature trypsin activation (a physiologic initiator of acute pancreatitis) and hypercalcaemia, diseases (such as lymphoma) that cause hypercalcaemia do not have a reported association with pancreatitis in dogs (Armstrong 2014).

This case emphasises the importance of considering unexpected causes of both positive and negative diagnostic findings, and to become familiar with the limitations of the tests performed.

Accurate interpretation of normal results is as important as abnormal results. In this case, despite a ‘normal’ ionised calcium, a cytological interpretation lymphoid hyperplasia, pododermatitis and a suspected pancreatitis, the primary (and life threatening) problem was hypercalcaemia arising from multicentric lymphoma. Repeat testing of blood samples and cytology of lymph nodes, or proceeding with biopsy of abdominal nodes or exploratory laparotomy may have enhanced the efficiency of the diagnosis.

Acknowledgements

I would like to acknowledge the following people for their advice, knowledge and support: dawn Seddon at Gribbles Veterinary Pathology, Jon Meyer at IDEXX Laboratories, the Crofskey family and the wonderful staff at Cambridge Veterinary Services.

References

Armstrong J. Canine pancreatitis: diagnosis. Proceedings of the Companion Animal Society of the NZVA Annual Conference. Pp 2.19.1–2.19.4, 2014 Bergman P. Paraneoplastic Hypercalcaemia. Topics in Companion Animal Medicine 27, 156–8, 2012 Dann H, Hill K. Canine hypercalcaemia: a case study. Companion Animal Society Newsletter of the New Zealand Veterinary Association, 20(3), 28–32, 2009 Duncan and Prasse’s Veterinary Laboratory Medicine Clinical Pathology 4th Edtn.

Iowa State Press Blackwell Publishing Professional, Ames IA, USA, 2003 Elliot J, Dobson JM, Dunn JK et al.

Hypercalcaemia in the dog – a study of 40 cases. Journal of Small Animal Practice, 32, 564–71, 1991 Hughes KH. Molecular diagnostics for canine and feline lymphoproliferative disease. Veterinary Cancer Society Conference 2017 Jarrett R. An investigation of hypercalcaemia and cytopenia in a dog.

Companion Animal Society Newsletter of the New Zealand Veterinary Association, 17(1), 32–5, 2006 Ku C-K, Kass PH, Christopher MM. Cytologic-histologic concordance in the diagnosis of neoplasia in canine and feline lymph nodes: a retrospective study of 367 cases. Veterinary and Comparative Oncology 15, 4, 1206–17, 2016 Messinger JS, Windham WR, Ward CR. Ionized hypercalcaemia in dogs: a retrospective study of 109 cases (1998–2003). Veterinary Internal Medicine 23, 514–9, 2009 Neiger R. Hypercalcaemia – cause and therapy. Proceedings of the 50th Congresso Nazionale Multisala SCIVAC, Rimini, Italia, 2005 Paran E, Hugonnard M. Agreement of feline and canine pancreas-specific lipase with pancreatic ultrasonographic findings in 62 cats and 54 dogs with suspicion of pancreatitis: a retrospective study (2007–2013). 26th ECVIM-CA Congress, 2016 Pohlman L. Evaluation of lymph node sspirates. Western Veterinary Conference, 2013 Sharkey L. Pancreatic cytology: an update.

ACVIM Conference Proceedings 2013 Twedt D. Acute pancreatitis in the dog.

Atlantic Coast Veterinary Conference 2017 Wismer T. Nephrotoxicants in dogs and cats. International Veterinary Emergency and Critical Care Symposium 2017 l

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NZVA Conference 2018: All Creatures Great and Small Claudelands Events Centre, Hamilton 19â&#x20AC;&#x201C;22 June 2018

It was great to see our Companion Quarterly sponsors out in force at the 2018 NZVA Conference. We are grateful for their ongoing support.

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NZVA Conference 2018: All Creatures Great and Small Claudelands Events Centre, Hamilton 19â&#x20AC;&#x201C;22 June 2018

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NZVA Conference 2018: All Creatures Great and Small Claudelands Events Centre, Hamilton 19â&#x20AC;&#x201C;22 June 2018

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

Massey News People

Arnon Gal is leaving Massey for the University of Illinois. Arnon has been an active researcher, clinician and teacher with a passion for endocrinology, and will be missed. An internist position is being advertised and the medicine service will continue in the hands of Associate Professor Craig Ruaux, ably assisted by Matt Kopke our current internal medicine resident-in-training.

Matt completed his BVSc degree and a rotating internship at the University of Pretoria Onderstepoort, Faculty of Veterinary Science. He then obtained a BVSc (Honours) degree with the focus on small animal internal medicine and diagnostic imaging, while at the same time completing a small animal internal medicine internship. After a year in a specialist practice in Johannesburg, South Africa, he moved to New Zealand last year.

Suzanne Busser, who has just completed an internship at the MUVTH is now working alongside Valerie Poirier in the Oncology service. Valerie will be spending part of 2018 back in Canada working on her PhD in radiation oncology.

Our new first year resident in small animal surgery, Sacha Devereux is from Ireland and studied veterinary medicine at University College Dublin. She has completed a rotating internship at the University of Saskatchewan followed by a surgical Internship at Cornell University.

The MUVTH’s new rotating interns for 2018 are: Jos Bongers, a graduate from Utrecht in the Netherlands; Ethel Koh, a Massey grad originally from Singapore; Emily Short, a Massey grad who has worked in the Bay of Plenty; Helen Mather, another recent Kiwi grad who has worked in mixed practice in Awapuni; Tamara Elsmore, also a Massey grad, and Kylee Goggin, a graduate of James Cook University.

Imaging

Mark Owen and his company, NZRadVet, continue to provide support to the Imaging group at the Teaching Hospital (Ron Green and Paul Wightman). In a collaboration with the Teaching Hospital, NZRadVet has also employed an imaging resident; Sarah Pemberton. Sarah is a Massey graduate, who completed her ANZCVS Membership qualifications in radiology whilst in general practice. She then headed to the USA beginning an imaging residency at Purdue University.

Sarah and her husband have recently returned to NZ for the birth of their first child. After completing maternity leave, Sarah has now resumed her European training programme under Mark’s supervision utilising the busy and varied caseload within the VTH.

Upcoming events on the CPD calendar – save the dates

• Massey University Working Dog Centre Research Colloquium October 16th 2018

- Featuring researchers from the WDC presenting on a wide range of topics of interest to veterinarians and those involved with farm and service dogs.

- Special guest, Dr Cindy Otto, associate professor at the University of Pennsylvania. Dr Otto is boardcertified in both emergency and critical care and sports medicine.

Her work monitoring the health and behaviour of Urban Search and Rescue dogs used at the World Trade Center following the 9/11 disaster, inspired her to establish the Penn Vet Working Dog Center in 2007. The Penn Vet WDC serves as a national research/ development centre for detection dogs. She will speak on olfaction.

• Massey University Small Animal Hospital Patron’s Day December 7th (TBC)

- Our annual day of CPD for our patrons will once again occur at the end of the year. Free to all those practices that refer cases and open to all other veterinarians for a small fee, this is our chance to give something back and introduce new staff as well as network with our colleagues. I hope to see you there. l

Would you like to see your pet on the cover of Companion Quarterly?

We now have a new cover photo for each issue of Companion Quarterly. This means we are always on the lookout for suitable photos. Photos selected for the cover must be landscape orientation (or able to be cropped to this), crisp and well focused, and of high resolution (at least 300 DPI). They must also be well composed and interesting.

Please send any suitable images to the Editor (sarah.fowler@ gmail.com). If however you have a favourite snap of your fur-family that’s not quite up to cover standards, please send that in too: photos that are not selected for the cover may be printed on the back inside cover.

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Companion Animal Health Foundation update Promoting animal health and welfare to benefit companion animals in New Zealand CATH WATSON, CAHF Chair There are some exciting times ahead for CAHF as we look to brainstorm ideas for the future in late August. By the time you read this we will have a plan for the future and it may just involve you…

CAHF is YOUR charity. It aims to fund projects that improve the health and welfare of companion animals in New Zealand, so that means it directly benefits you and your patients. It was established by CAV 20 years ago, and became a charitable trust 12 years ago.

It exists because of you, and to thrive in the future, it needs your support.

On that note, it has been wonderful to see a number of practices starting to take up the challenge of raising $500 for CAHF – has yours? By joining our $500 Project, we are asking practices to pledge to raise $500 by whatever means they can; external fundraising events, organizing your own internal fundraiser for your practice, or simply by making an individual donation. Please visit our updated website http://www.cahf.org. nz/help/donate for details. Donations can also be made on our Give-A-Little page: https://givealittle.co.nz/org/ healthypets There are some interesting projects underway at the moment, with the addition of a pilot study by clinical practitioner Heidi Ward-McGrath following our March funding round. Her project will assess the effectiveness of the product totarol in treating superficial dermatitis in dogs and has been supported by a number of experienced mentors. Applications for the next

Photo credit: Orla Fitzpatrick

funding round close on 30th September, so if you have a project you think meet the criteria, visit http://cahf.org.nz for details and an application form. Perhaps your MVM research project is suitable?

Finally, we sadly say goodbye to one of our trustees, Jodi Salinsky. Jodi has been at trustee for at least 11 years, and during this time as been a strong advocate for companion animal research through CAHF, overseeing the approval of a

number of successful applications to the benefit of companion animal practice in NZ. Kate Hill has also decided to step down as a trustee, but will continue as an assessor of grant applications. It’s great to be able to retain her expertise in this role, especially as she has also been a successful applicant in the past. Thank you to both Jodi and Kate for the time they have contributed to CAHF over many years. l

Contact: www.cahf.org.nz

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

CPD RECORD

Read articles from Companion Quarterly 29(3) September 2018

Date of Activity: …………………………

Activity description Read articles in the September 2018 issue of Companion Quarterly (tick those that apply) o o o o

What is Your Diagnosis (Sarah Lee) Time to rethink the use of tramadol for dogs with osteoarthritis? (Andrew Worth and others) Electric training collars: torture or training? (Elsa Flint) Unusual congenital spinal malformation causing neurologic dysfunction in a young dog (Miriam Bates et al.) o Initial management of canine gastric dilatation and volvulus: what you need to know (Philip Hyndman) o Highlights from the course in Veterinary Ophthalmology II at the European School for Advanced Veterinary Studies (ESAVS): Part II (Jos van Hees) o Veterinary Behaviour Chapter programme of ANZCVS Science Week (Elsa Flint) o ………………………………………………………………………………………………………… o ………………………………………………………………………………………………………… o …………………………………………………………………………………………………………

Activity type: Category: Self-directed activity Self-Directed Activity Type: Updating knowledge or preparatory reading/research Hours claimed: VCNZ Points (0.5 per hour reading): Reflective record: Actual learning outcomes and the impact on your practice What did you teach or learn from this activity? ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................

How do you think this will impact on your practice? ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................

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Instructions for Authors submitting articles to the Companion Quarterly SARAH FOWLER (Editor), for

the Companion Quarterly Editorial Committee

The Companion Quarterly is published quarterly in the first week of March, June, September and December of each year. The printing costs are covered by the advertisements. There is therefore a limit of about 55–60 pages to the size of each issue. There is a balance between political issues, articles for continuing education and other news.

Authors are expected to submit their articles and conference in a final form suitable for publication. If practitioners wish assistance with writing, please contact the editor. Also look at previous issues to see the layout.

Articles

The article should have a title. Following the title the names of the authors, their degrees, titles, contact details should be present.

Submit articles preferably by email, or disk if this is not possible.

Submit articles in adequate time for reading and alterations before publication.

Contributions must be original. Articles or extracts from articles may be completely copied only if there is permission from the original authors and source of publication. It is the responsibility of the author(s) rather than the editorial committee to obtain this permission.

The author(s) should disclose if they have published the same article or a very similar article elsewhere.

Articles that are clearly editorials/advertising will be labelled as such at the discretion of the editorial committee. These include articles/editorials that are repeated from other publications such as VetScript and that contain obvious product placement comments.

Proof reading

The authors should proof read their article looking for mistakes, spelling errors, omitted details. While the editorial committee reads through the articles, the articles should be presented error-free.

Articles and conference reports from recipients of grants and scholarships It is the responsibility of recipients of any grants and scholarships to supply any conference reports and articles written as part of the requirements in the final form suitable for publication.

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References

A list of references should be supplied if appropriate. Follow the guidelines for the New Zealand Veterinary Journal for method of reporting of references.

The number of references should be kept to a reasonable number relative to the length of article. Keep numbers of references to a minimum when discussing a single point, i.e. do not be repetitive with numerous references when a few will do. The editorial committee will omit references if the list is judged to be excessively long.

Figures

Good quality illustrations that clearly illustrate the necessary points should be submitted with the article.

Submit any photos or graphics in their original forms (i.e. JPG, PDF, TIF files) as they lose their clarity when extracting them from Word or Publisher documents.

If positions of figures are not obvious from the text, send a hard copy or some other form of instruction as to where they should be placed.

Figures should be clearly numbered labelled as to top and bottom where necessary.

Features on the figures should be clearly labelled by the author(s).

The figure captions should be concise and accurate, and supplied with the text on a separate page at the end of the article.

Diagrams/figures can be copied from textbooks only if there is permission from the original author and the source is clearly acknowledged. It is the responsibility of the author(s) to obtain this permission before submitting the article to the Quarterly editorial committee.

Timing of article submission and publication

Articles will be published as soon as possible after submission. The newsletter goes out in the first week of March, June, September and December. Articles therefore need to be submitted at least one month before (i.e. by the end of January, April, July and October) but preferably earlier to allow one month for the collation, printing, binding and posting of the Quarterly.

Depending on when the articles are received, the size of that particular issue and the need for refereeing, at the editor’s discretion articles may be held over for a later issue.

Refereeing

Articles may be sent to appropriate people in that field of expertise for refereeing/proof reading if the editorial committee deems this

is necessary. This is to ensure accuracy within the text to protect readers, the authors CAV and the clients and the patients of veterinary practitioners.

SciQuest and the NZVA website

Selected scientific articles will be placed on the SciQuest website for access by NZVA. There will be a delay of a year to ensure that practitioners still see a benefit in becoming CAV members.

The entire newsletter is now being placed on the CAV website but the most recent issues (i.e. those within a year of publication) are available only to CAV members.

Article of the issue and student article

Prizes are sponsored for the best case report and general article in each quarterly issue.

The best overall article in each category for the year is then decided in May and the overall prize awarded at the Annual dinner in June. The members of the editorial committee will judge the articles on their clarity, conciseness, and usefulness to practitioners.

Articles that are submitted to the Quarterly as part of an obligation due to the author(s) receiving Educating the Educator or Study/ Research Grants from CAV are not eligible for the article of the issue prizes. Articles submitted by the editor and the members of the editorial committee are also not eligible for the prizes.

There is a separate undergraduate student article competition.

Planning a case report?

Some hints as to how do so!

When writing an article take time to look at how articles in other journals are arranged. While articles for the Quarterly are not as detailed as the NZVJ the information needs to be arranged in a logical manner to make it easy for the reader to follow. Therefore follow some logical headings as detailed below. Not all of these headings will need to be used in all articles and some may be combined depending on the type of case and amount and type of information available.

• Introduction • History • Clinical signs • Materials and methods • Results (of investigations e.g. laboratory results, radiography).

• Discussion • Conclusion • Acknowledgments • References. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 3 | September 2018

COMPANION QUARTERLY â&#x20AC;&#x201C; Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA

Companion Quarterly

OFFICIAL NEWSLETTER OF THE COMPANION ANIMAL VETERINARIANS BRANCH OF THE NZVA Volume 29, No. 3 | September 2018

VOLUME 29 NO 3 September 2018

Electric training collars: torture or training?

Initial management of GDV: what you need to know

Time to rethink tramadol for dogs with osteoarthritis?

Congenital spinal malformation in a young dog

Report: Highlights from Vet Ophthalmology course Part II