Companion Quarterly Vol28 No2 June 2017 by Companion Quarterly

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 28, No. 2 | June 2017

VOLUME 28 NO 2 JUNE 2017

A review of femoral head and neck ostectomy

A case of a nasal turbinate cyst in a pug

Go Slow: a foodborne disease of dogs

Juvenile laryngeal paralysis and polyneuropathy in Rottweilers

A week with.....the surgeons at MUVTH

Volume 28 | No. 2 | June 2017 ISSN No. 2463-753X EXECUTIVE COMMITTEE 2017 cas@vets.org.nz

CONTENTS

President

Helen Beattie

Companion Quarterly

Operations Manager Rochelle Ferguson

Treasurer

Aimee Brooker

Committee Members Simon Clark Nina Field John Munday Toni Anns Natalie Lloyd Pauline Calvert Paula Short

EDITORAL COMMITTEE Sarah Fowler (Editor) Bart Karalus Crystal Loh Ian Millward Juliet Matthews Simon Clark Shanaka Sarathchandra

2 Editorial 4 Highlights from CAS Executive Meeting

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

Manabu Kurihara, Ronald Green

Address for submitting copy/ correspondence

14 Go Slow: an emerging food-

Advertising Manager

16 Hypertension in cats – state of

Sarah Fowler 66 Callum Brae Drive, Rototuna, Hamilton 3210 T (H) 07 845 7455 | M 027 358 4674 E sarah.fowler@gmail.com Christine Moloney 25 Manchester St, Feilding T 06 323 6161 | F 06 323 6179 E christine.moloney@totallyvets.co.nz

NZVA website www.nzva.org.nz 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.

Cover photograph

Catherine Bryant's Border Collie, Brock, having fun in the sun. Photograph by Emily Taylor Photography.

Newsletter design and setting 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.

borne disease of dogs Hayley Hunt

the art guidance Boyd R Jones

18 Juvenile Laryngeal Paralysis

and Polyneuropathy (JLPP): an inherited disease of Rottweilers and Black Russian Terriers Sarah Fowler

24 Opioids and gastro-oesophageal reflux, regurgitation and vomiting in the perianaesthetic period. Jeffery Clyne

32 Femoral head and neck

ostectomy: a review of the literature and its efficacy as a treatment for hip dysplasia Michelle Gray

38 Case report: Nasal turbinate

cyst: an unusual cause of stertor in a pug with brachycephalic syndrome Helen Sheard

41 What is your diagnosis? The answers

44 A week with ... the surgeons at Massey University Veterinary Teaching Hospital Helen Sheard

46 WSAVA update: Taking a look at the WSAVA Hereditary Disease Committee

48 CAV Specialist Profile Devon Thompson

50 New Zealand Companion

Vets in Stress Programme 24 Hour Freephone Confidential Counselling Service

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

Animal Health Foundation Update

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

EDITORIAL

Getting our ducks in a row Abbie the cat caused quite a stir recently at SPCA Otago. She's pretty much just your average tabby moggy, unloved by anyone, and delivered to SPCA Otago with the hope that she would find a new forever home. She was pretty shy. But according to the attendant staff, awfully cute. Immediately, my focus turned to her bilaterally, folded pinna. The top half of which were neatly folded forward – odd, but indeed quite cute at the same time. I did a little bit of digging; VIN and an enquiry to the Crazy Cat Lady. Could this be associated with osteochondrodysplasia? Probably, seemed to be the answer, but this was definitely not categorical. Given that predicted poor welfare outcome for Abbie, she was collected up and delivered to my consult, for a gentle goodbye. But it was not to be – those folded ears had gone as crispy as a cornflake, and were quite clearly going to slough off. Abbie cashed in one of her nine lives, has now been desexed and is awaiting an owner who appreciates her rare beauty. Isn't it funny how sometimes in life, many of those proverbial ducks seem to line up all at the same opportune time? Abbie was one of those “ducks”. Opportune, because it was a great opportunity to educate the team at SPCA Otago about the welfare issues faced by Scottish folds, and other specific breeds, and phenotypes. Which was timely, given I had just had a conversation with our marketing manager, and the CEO at SPCA Otago, to ensure that images of welfarecompromised animal are not used to advertise our core business. Of course, we deal with welfare compromise all the time, but let's not use a brachycephalic, airwaycompromised breed for the sake of cuteness. If we do, we risk engagement of our membership with the image, without them understanding the inherent issues they are desiring. The next week the BVA made the fabulous and considered decision to impose restrictions on using welfare-compromised breeds in advertising. This had been a long game – a progression of concern from the coal face veterinarians that they needed and wanted support to address this issue. The AVMA House of Delegates passed a policy, unanimously, and to applause, that supports minimising inherited disorders in the breeding of dogs, cats, and other companion animals.

NAWAC released their view on selective breeding, including strong wording to support CAV and NZVA's submission on banning the breeding of Scottish Folds in New Zealand. This positioning is based on ethical and welfare concerns resulting from the breed’s genetic makeup, and the resultant pre-determined welfare compromise. That's quite a few ducks! It seems that there's a ground swell of movement to get this ball rolling. I'm keen. It is only going to result in better welfare outcomes for a whole bunch of animals in New Zealand. But let's be clear. It's long game – that's the take home message. In no way do I see that poking a stake in the ground, and taking a rigid and superior, uncompromising stand, banning outright, and alienating those with whom we need to work, to be the answer. This journey will be about relationship building, and nurturing, and ensuring that those that are intimately involved with the breeds and types that they love, are assisted to make great choices for the animals. Inside-out approach? Not sure. But I'm clear that the top down approach is not going to win this welfare battle. Communications with breeders, our key stakeholders, and a mass of education at the grass roots is what is required. As an example, I was in discussion with a tertiary education provider (of animal-related qualifications) who had little idea that this was a target on New Zealand’s animal welfare agenda. Then and there they decided they would remove any of these images form their educational material. I suggested that leaving them in and having a conversation about the issues faced by such breeds, and phenotypes, might be a better way to spread the knowledge of the issues these animals face? Let's make it feasible, and desirable to do the right thing, and have a happier, healthy pet population. That's a line of ducks that I'm keen to see float. B. Helen Beattie, CAV President. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

WORKING TO PROMOTE AND SUPPORT COMPANION ANIMAL PRACTICE IN NEW ZEALAND

Highlights from the last CAV Executive Committee meeting (22–23 February 2017) and activities

New committee members

Three new committee members were welcomed to the committee – Simon Clark, Nina Field and Paula Short.

NZ Companion Animal Council

The NZCAC are facilitating a series of forums across the country. These are primarily to support networking of organisations involved with companion animals in each locality. Once established each local group would drive the content with the NZCAC in support. A strategic retreat is planned in May for the purposes of refocusing and reviewing the ongoing strategy.

NZ Companion Animal Foundation A $10,000 donation was approved for the NZCAHF.

Subscription fees

Complimentary CAV membership is available to first year graduates and it was resolved to extend this to second year graduates as well to further support veterinarians in the early stages of their career. With retention of veterinarians in the profession an issue, complimentary membership will also be offered to those on parental leave to support ongoing connection to companion animal practice and provide an avenue for self-directed continuing professional development. There will be no increase in subscription fees for members in 2018.

‘Go Slow’

We alerted the Northland District Health Board following concerns raised by Northland veterinarians about the human health risks from a myopathy seen in local dogs (known as ‘go slow’) following the consumption of wild pork. Research (as yet unpublished) has established a strong correlation between the consumption of wild pork and the onset of clinical signs in dogs. Veterinarians had been given anecdotal reports by farmers and hunters, of people in the region also experiencing myalgia, weakness and fatigue after consuming wild pork. The aetiology of ‘go slow’ in dogs is currently unknown. The signs suggest a toxic aetiology with a plant or fungal toxin considered most likely.

Korean variant of the rabbit haemorrhagic disease virus: RHDV1-K5

The release of this virus was discussed. CAV will keep in touch with MPI/ACVM and the rabbit coordination group in order to communicate information on developments to members. As part of the registration process for approval to import the virus, it is expected that there will be an opportunity for submissions. The CAV position on a submission will be that the risks to domestic rabbits are adequately mitigated before a release is approved.

Allied Veterinary Professional Regulatory Council

Jennifer Hamlin (Chair of the AVPRC) presented an update on the work of establishing the council and the voluntary register. Their goal is to promote professionalism of the allied veterinary professional community by setting and enforcing consistent standards for those who can enter the profession and their continued professional development. The register has grown from 230 in 2016 to 400 in January 2017. A part of achieving consistent standards will be to focus on the regulation of education providers. Education providers currently are not subject to any regulation and last year 400 veterinary nurses graduated with qualifications that ranged widely in their quality.

WSAVA 2017 – Copenhagen

CAV have a complimentary registration to this conference available to a CAV member that wishes to attend. It is available on a first in first served basis, with the only requirement being a conference report being written for the Companion Quarterly. If you are interested contact cav@vets.org.nz.

Educating the Educators

In 2016 grants were made to Angus Fechney (Dentistry), Alastair Coomer (Veterinary Surgery), Andrew Worth (Orthopaedic Surgery), Pru Galloway (Feline Medicine) and Duncan Graham (Dermatology) to support overseas CPD that was then shared with the wider CAV membership.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

Media

CAV contributed to an article on pet obesity in the March issue of the Healthy Food Guide and released a media statement in response to the release of tranche 2 of the government’s dangerous dog action plan.

Greyhounds

The government is conducting an enquiry into greyhound racing. CAV met with Rod Hansen QC to update him on the issues from a veterinary perspective. CAV also continued work as an advisor to greyhound racing’s welfare committee. Work has begun on reviewing their code of welfare. CAV will be contributing advice on breeding management and training methods, along with the importance of early socialisation to improve re-homing prospects for dogs after their racing careers are finished.

Urban animal management Cat management

CAV are representing the NZVA on a Wellington City Council cat reference group to provide support for WCC as they develop their animal policy.

The National Cat Management Strategy Group

Without a government funded secretariat or significant financial contributions from the organisations involved, the next operational steps look more challenging to finance. Opportunities to take the finalised strategy to government and the public, must be sought. Championing specific aspects of the strategy through LGNZ, communities themselves and engaging with specific, relevant forums (e.g. ‘Threatened Species Forum’ being held by DOC) is desirable.

Dangerous dogs

Veterinarians are important stakeholders in this issue, and were given an opportunity to meet with Minister Jacqui Dean (who has replaced Louise Upston as the associate local government minister) to discuss the government’s dangerous dog action plan. Our concerns around breed specific legislation were raised, and we outlined that our preferred approach was to focus on owners and promote the responsibility of dog ownership to all, regardless of the breed of dog they have. The importance that we educate both dog owners and the general public – particularly parents and young children on how to reduce dog aggression was also stated. NZVA/CAV have also been given the opportunity to provide feedback on the draft legislation. l

The NCMSG met and finalised some changes to the strategy document, following feedback from the second round of public consultation. The future of the group and its outputs are limited by funding, and stakeholders are being asked to consider if they can contribute.

WINNER

“Report on the Valentine Charlton Feline Medicine Conference”

Orla Fitzpatrick

June 2017 | Volume 28 (1) | Pages 40–42

Article of the Issue

EYEVET Services Limited

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

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. Applications are usually considered at the end of March and September each year. We have $10,000 per annum to grant and are very keen to have this resource utilised to support and promote companion animal veterinarians. We are very grateful to Hill’s Pet Nutrition as the principle sponsor along with support we receive from the Institute of Veterinary, Animal and Biomedical Sciences and VetLearn.

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

AGM Notice

The AGM of the Companion Animal Veterinarians of the NZVA will be held during the combined conference in Blenheim, 8.30am June 23rd 2017 at the Marlborough Convention Centre.

CAV/CAHF Project Grant 2017 The Companion Animal Health Foundation is a charitable trust that acts as the research funding arm for CAV. Funding applications from CAV members 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 prevalence. Any queries on how to make an application or donate contact Rochelle Ferguson (CAV Operations Manager) on cav@vets.org.nz

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

NEWS IN BRIEF

CAV Executive Committee The CAV Exec. has undergone quite a bit of change recently with 6 new members in the last 18 months. This issue we introduce three of them: Toni Anns: Supporting change and motivating people towards positive growth is how I would like to contribute to the veterinary industry. Over the years I have experienced working full time and part-time in England and New Zealand, not working at all, dabbling in other lines of work, being a stay-at-home Mum, being an only parent, now also a stepparent, and I now currently work fulltime for Zoetis as a veterinary technical adviser. I joined CAV in 2016 because I am privileged in my current role to be able to meet with, and talk to many vets on a daily basis and I can therefore appreciate the many challenges, the different perspectives, the trials and tribulations that happen in our industry today. I aim to be representative of these different opinions. I bring my positivity, my firm belief in health and wellness for people and animals, and my experience in the companion animal industry with the goal of connecting people and encouraging personal and organisational growth. Ultimately, I would love to see elevation in the reputation of this industry, improved collaboration both nationwide and internationally, resulting in an uplift in the personal satisfaction at the end of each vet’s day. Big call, but I like to aim high! Simon Clark: I am the Product Manager and Technical Advisor for Companion Animals and Horses at Virbac New Zealand based in Hamilton. Prior to that, I was a clinical Companion Animal Veterinarian in a variety of clinics. I have completed a rotation CA Internship at Animal Specialty Group in Los Angeles and an MVM majoring in Companion Animals. My wife, Laura, is a CA locum vet and we have three cats with a variety of bizarre illnesses. Natalie Lloyd: I grew up in Wellington and spent most of my spare time in my primary and secondary years of school riding horses in Ohariu Valley, a small rural area 20 mins from Wellington CBD. After a vet paid a visit to my horse who was suffering from an eye injury, I set my

CAV Executive Committee Front row, L to R: Toni Anns, Natalie Lloyd, Paula Short, Aimee Brooke. Back row, L to R: Simon Clark, Rochelle Ferguson, Helen Beattie, Nina Field, John Munday

Photo courtesy of Sue Blaikie

sights on a veterinary degree, graduating from Massey University in 1995. I have worked in companion animal practice in Wellington for most of my career but have also spent time working in the UK as a companion animal vet and in the pet nutrition industry. Until recently I owned, along with my husband David, the Tasman St Vet Centre in Mount Cook Wellington. David and I sold the clinic to National Vet Care at the end of 2016. However, I continue to run the clinic as the

Lead Veterinary Surgeon, ensuring Tasman St Vet Centre still continues practicing to a high standard, but with a little more resource now to call on in times of need. I have a passion for companion animal medicine and have been a member of the NZVA, the Wellington regional branch and the CAV for twenty years. I have joined the CAV executive this year in order to give back a little to an organisation which has supported me throughout my career.

Prize Winners of CAV Continuing Education Grants for 2017

Every year CAV has a draw to select two practitioners, one new member and one continuing member to receive a prize of $500 towards Companion Animal Continuing Education from VetLearn. The winners for 2017 were Ana Hird (new member) and Andrew Whiteside (continuing member). Andrew is a companion animal veterinarian at VetEnt’s Ferrymead clinic in Christchurch. While he is yet to decide how he will spend his prize, Andrew says he will be keeping an eye out for VetLearn’s upcoming hands-on workshops. Ana Hird has recently returned to mixed practice after overseas travel. To help her get back into the swing of things she is interested in putting her prize towards two modules of the VetScholar Veterinary refresher scheme for companion animal practice. l Photograph courtesy of Ana Hird

Photo courtesy of Andrew Whiteside

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

What is your diagnosis? THE QUESTIONS… MANABU KURIHARA, BVSc and RONALD GREEN, DVM, MS, DACVR. Institute of Animal, Veterinary and Biomedical Sciences, Massey University

Case history

A 9-year-old, 3.9-kg entire male Chihuahua was presented for lethargy, reverse sneezing and intermittent regurgitation (2–3 days earlier). On physical examination, the dog was mildly thin (body condition score, 4/9), lethargic, estimated to be 5–8% dehydrated and sneezing but its temperature was normal (38.0°C). On thoracic auscultation, lung sounds were unremarkable but referred upper airway sounds were heard. Mucous membranes were pink. The patient ‘vomited’ white foam once during the physical examination. No other abnormalities were detected on physical examination. A blood sample collected by jugular venipuncture was submitted for complete blood count (CBC) and serum biochemistry. CBC results were within normal limits. Serum biochemistry revealed elevated liver enzymes (ALT 179 mg/ dL, reference range, 20–108 mg/dL; ALP 152 mg/ dL, reference range, 23–107 mg/dL,) and BUN (70 mg/dL; reference range, 15–35 mg/dL). Serum T4 concentration was within normal limits (1.25 μg/dL; reference range, 0.6–2.9 μg/dL). Thoracic radiographs were obtained to investigate the cause of regurgitation and to rule out aspiration pneumonia (Figure 1).

Questions

1. What are your radiographic findings? 2. What is this dog’s problem list? 3. List differentials for the two major problems visible on the radiographs. l Answers revealed on page 41

Contact: mk.vet.animal@gmail.com

Figure 1. Left lateral (A) and ventrodorsal (B) radiographic views of the thorax of a 9-year-old entire male Chihuahua evaluated for lethargy, regurgitation and reverse sneezing.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

CLINICAL UPDATE

Go Slow: an emerging food-borne disease of dogs HAYLEY HUNT BVSc. MVS, IVABS, Massey

University

Go Slow is a myopathy in dogs which usually develops after eating wild pork. Pig dogs are most at risk as they are most likely to have access to wild pork, but all dogs are susceptible.

History, signs and diagnosis

Dogs that are fed or scavenge wild pork while out hunting can show signs within a matter of minutes, while those given wild pig in their kennels (at rest) may not show signs until the next day Affected dogs typically present with lethargy, muscle tremors and collapse, and symptoms worsen with exercise. Some dogs also have vomiting and diarrhoea. In chronic cases, dogs may be normal on physical examination but have a history of tiring easily during hunting or work. Meat, offal and bones from wild pigs have all been linked to cases of Go Slow, and freezing and/or cooking meat does not prevent the disease. Go Slow is more prevalent in Northland than other regions, but cases have been documented throughout the upper North Island, as well as in Gisborne, Wairarapa and Canterbury. In acute cases, serum biochemistry shows a moderate to marked elevation in CK, AST and ALT, indicative of muscle damage. Haematology is usually normal with no inflammatory leukogram. Muscle enzymes may also be elevated in chronic cases with recent exercise, but often normalise during periods of rest.

Treatment and support

Various treatments which support muscle function and repair have been tried with variable success, including B vitamins, vitamin E and selenium. These vitamins and minerals are often given together as a nutritional supplement such as ‘Go Fast’ by Ethical Agents, Exceed from palaMountains, or injectable Metabolase. A high quality diet or prescription liver diet can also aid in recovery, and 1–3 months of rest is usually required. In severe cases, intravenous fluids in the acute stages seem to reduce the severity and duration of clinical signs, and also help to prevent renal damage from myoglobin in dogs that have significant muscle damage. Some dogs with Go Slow make a full recovery, while many improve enough to return to hunting, but struggle on long hunts or hot days. A small proportion of affected dogs never recover despite the best efforts of owners and veterinarians.

Contact: h.hunt@massey.ac.nz, phone 027 3410874

Photo courtesy of the author.

Can people be affected?

In addition to cases in dogs, there are several anecdotal reports of people (generally pig hunters) who believe they have experienced similar symptoms, although there is currently no conclusive evidence that people are affected by Go Slow. The medical profession in Northland has been notified about Go Slow in dogs and the potential public health implications, and hopefully cooperation with human doctors will enable further investigation in this area.

Pathogenesis of Go Slow

The link to wild pork (both fresh and cooked), sudden onset of clinical signs, lack of inflammatory response and geographical distribution of cases support a toxic cause of Go Slow. Tests for commercial pesticides including organophosphates, 1080 and brodifacoum on a small number of pig and dog liver samples have returned negative results, and the mechanisms of these toxins do not fit with the clinical picture of Go Slow. Several types of plants and fungi have been described in association with myopathies in species other than dogs, but in many of these plants the toxic compounds have not yet been characterised, making them difficult to test for. Research is continuing to try and identify the definitive cause of Go Slow. Any practitioners that would like to know more about the disease or have suspected cases are welcome to contact Hayley Hunt at Massey University (phone 027 341084, h.hunt@massey. ac.nz). Special thanks to Jenni Petersen at Norvet Services in Okaihau for her tireless efforts to improve understanding and awareness of Go Slow in dogs. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

CLINICAL UPDATE

Hypertension in cats – state of the art guidance BOYD R. JONES, ONZM, BVSc, FACVSc,

DipECVIM-Ca

Hypertension is a common condition of older cats and can result in severe clinical consequences with damage to the eyes, heart and vasculature, brain and kidneys: so-called target organ damage (TOD). Hypertension can be primary, or more commonly, secondary to other conditions such as chronic kidney disease and hyperthyroidism. The early diagnosis of hypertension is desirable; to prevent or ameliorate TOD before it becomes permanent. However, there are some challenges associated with the diagnosis of hypertension in cats. Obtaining accurate results relies on good, consistent technique using Doppler or high definition oscillometric equipment, and handling the cat carefully to avoid stress. The International Society of Feline Medicine (ISFM) consensus guidelines published in the Journal of Feline Medicine and Surgery (JFMS) have been written by a panel of international experts to provide practitioners with practical information on diagnosing and treating hypertension (Taylor et al. 2017). Importantly, one of the international panel members was Jenny Carter, a practitioner from Auckland. Jenny completed a practice-based study on hypertension in cats as part of her MVM research project. The results of her study were published in the New Zealand Veterinary Journal (Carter et al. 2014). Jenny is to be congratulated for her input into the JFMS consensus paper and her involvement emphasises that research from practice can be a positive and valuable “spin-off” from the Massey MVM programme. The JFMS consensus review features a step-by-step guide to measuring systolic blood pressure, to help practitioners feel confident basing clinical decisions on their results. The panel’s recommendations relate to important areas:

- How to interpret blood pressure measurements - How often to monitor hypertensive patients - Standard protocols to assess systolic blood pressure (BP) - When to treat - Routine therapy and monitoring - Emergency treatment The paper is well illustrated and easy to read. The authors hope the guidelines will encourage more widespread monitoring of BP in cats in veterinary clinics to increase the early identification of this treatable condition, and prevent the severe clinical consequences of untreated hypertension. The authors note that where clinical studies and scientific data were not available, the guidelines represent the opinions of the panel. Readers are recommended to read the full paper which is accessible on line at www.JFMS.com. There is a series of videos at www.youtube.com/icatcare which demonstrate measurement of blood pressure in the cat. The JFMS website/on-line platform has been updated and has new features for electronic access and use. The journal has two components; JFMS and JFMS Open Reports. If you are interested in cats this journal is a must subscribe; email subscriptions@sagepub.co.uk for further details of subscription packages.

References

Carter J, Irving AC, Jones BR. The presence of ocular lesions associated with hypertension in a population of geriatric cats in Auckland, New Zealand. New Zealand Veterinary Journal 62, 21–9, 2014 Taylor SS, Sparkes AH, Briscoe K, Carter J, Cervantes Sala S, Jepson RE, Reynolds BS, Scanson, BA. ISFM Consensus Guidelines on the diagnosis and treatment of hypertension in cats. Journal of Feline Medicine and Surgery 19,288–303, 2017 (DOI:10.117/1098612X17693500)

Professor Jones is an editorial board member of JFMS and was a supervisor for Jenny Carter’s MVM project. l

- Classification of hypertension - Consequences of clinical hypertension Contact: IVABS, Massey University, Palmerston North

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

CLINICAL UPDATE

Juvenile Laryngeal Paralysis and Polyneuropathy (JLPP): an inherited disease of Rottweilers and Black Russian Terriers SARAH FOWLER BSc, BVSc, MSc, PhD. CQ

Editor

What is JLPP?

JLPP is an autosomal recessive inherited disease of Rottweilers and Black Russian Terriers presenting as juvenile onset laryngeal paralysis and polyneuropathy. This has recently been updated to POANV (Polyneuropathy with Ocular Abnormalities and Neuronal Vacuolation) and it has also been described as Neuronal Vacuolation and Spinocerebellar Ataxia/Degeneration (NVSA/D).

Clinical signs

Signs of the disease typically start around 3 months of age and are progressive. It is inevitably terminal and there is no treatment. l Many nerves may be affected but the longest seem to be affected first. So the first signs are usually due to laryngeal paralysis: inspiratory stridor especially during physical exertion/excitement or if hot. There may be a change in the sound of the bark and also dysphagia, regurgitation and aspiration pneumonia l Affected dogs then develop progressive ataxia and paresis/ paralysis, typically of the hindlimbs first, progressing to include the forelimbs.

l Dogs with JLPP may also have ocular abnormalities (micropthalmia, cataracts, miosis) and spongiform encephalopathy. l Dogs are typically euthanized before 1 year of age to prevent suffering.

Differential diagnoses for JLPP

Conditions such as collapsing trachea and infectious canine cough may cause a harsh cough that may sound similar to the stridor caused by laryngeal paralysis, however in both these conditions the noise in expiratory rather than inspiratory. Puppy strangles (juvenile pyoderma) may also cause lymph node enlargement that can obstruct breathing. Degenerative laryngeal paralysis affects older dogs and is not accompanied by generalized paresis/paralysis. There are several progressive neurologic diseases that can occur in young (onset 4 weeks â&#x20AC;&#x201C; 4 years) Rottweilers and which are presumed to be hereditary. JLPP is the only condition

Photograph of the very handsome Austin who does not have JLPP, courtesy of Julie Hansen.

which typically affects the larynx and the limbs. Distemper, though exotic to NZ cause a neuropathy producing signs of weakness, sometimes with pneumonia.

Genetic basis for JLPP

JLPP is inherited as a monogenic autosomal recessive mutation: dogs homozygous for the unfavourable allele will be affected while heterozygotes are unaffected but will carry the unfavourable allele and may pass it to their offspring.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

The genetic defect underlying JLPP has recently been identified. The mutation responsible causes a premature stop codon in the Rab3GAP1 gene leading to a truncated and likely non-functional protein. The Rab3GAP1 protein has a role in axonal transport and synaptic transmission.

What can be done?

Since the mutation responsible for JLPP is known, there is a genetic test available. Unfortunately no veterinary pathology laboratories in NZ currently offer this test and samples must be sent to the UK or US for testing.

Laboklin Laboratory for clinical diagnostics

125 Northenden Rd, Manchester M33 3HF United Kingdom Phone: 0161 282 3066 Fax 0161 973 3434 Email: info@laboklin.co.uk Website: www.laboklin.co.uk Sample requirements: buccal swabs or 0.5–1 ml blood in EDTA Tube Turnaround: 2–3 weeks Price: £48.00 (including VAT)

Orthopedic Foundation for Animals 2300 E Nifong Blvd, Columbia, MO 65201-3806 United States

Phone: (573) 442-0418; Fax: (573)875-5073 Website: www.offa.org Order testkit through the website Price: US$ 65

Recommendations for breeding

The draft recommendations from DOGSNZ/NZ Kennel Club for any autosomal recessive inherited disease states that a mating which has the potential to produce affected puppies should never knowingly be done (carrier to carrier, affected to carrier). However breeding only from clear dogs may negatively impact genetic diversity within a breed, depending on prevalence of the affected allele in that breed. If the prevalence is high then breeding only from clear dogs will increase inbreeding and the likelihood of new inherited disease emerging. If the prevalence is low, as is likely to be the case for JLPP then it is reasonable to only breed from clear dogs so as not to disseminate the affected allele through the population. If a carrier is used in a breeding programme, then the guidelines recommend that the offspring are tested and only those who are clear are kept in the breeding program.

Prevalence of the affected allele and the situation in NZ

Data from Europe suggests a prevalence of 0.5% of Rottweilers as affected (homozygous for the mutant allele) and 19.5% as carriers (heterozygotes). The situation in NZ is unknown at present. As the test has only recently become available, there is little information about the prevalence of the affected allele among Rottweilers in NZ. To date at least 3 carriers have been identified and a single case of a pup that probably died of JLPP 5 years ago (before testing was possible). Rottweiler breeders are taking the lead in promoting knowledge of this fatal disease: Wiki Te Tau, the secretary of the Central Rottweiler Club recently commented "As responsible Rottweiler breeders some have begun the testing process to ensure that this disease is eventually eradicated through only breeding Clear to Clear, Clear to Carrier, but never a Carrier to Carrier. This DNA testing allows NZKC breeders to make informed decisions when breeding, and ensures members do not produce affected puppies. Those members who believe that their dogs do not need to be tested are mistaken. There is no shame in having a carrier in your kennel, the shame would be to deny that this exists within the breed. Knowledge is Power, TEST NOW.” 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.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

FEATURE ARTICLE

Opioids and gastro-oesophageal reflux, regurgitation and vomiting in the perianaesthetic period JEFFREY CLYNE, BSc, BVSc,

MANZCVS (Emergency Medicine and Critical Care). Adelaide Animal Emergency and Referral Centre

Introduction

The effects of opioids on gastrooesophageal reflux (GOR), regurgitation and vomiting are complex and involve multiple interacting factors. Although uncommon, life-threatening consequences, such as aspiration pneumonia and severe oesophageal injury can result, and are usually suspected or diagnosed only after the damage has occurred. Oesophageal exposure to refluxed fluid with a pH of 2.5 even for as little as 20 minutes has been shown to cause strictures in dogs (Pearson et al. 1978). Ovbey et al. (2014) reported an incidence of aspiration pneumonia after anaesthesia of 0.17%, which was significantly associated with administration of hydromorphone and with regurgitation. Oesophagitis is another serious consequence, which can lead to stricture formation where inflammation involves the muscularis. Oesophagitis (Figure 1) can also reduce oesophageal motility and reduce lower oesophageal sphincter tone, making further GOR events more likely (reviewed in Sellon and Willard 2003). When severe oesophageal damage does occur, management can be frustrating and outcomes poor. In one study which included 13 dogs with post-operative oesophageal dysfunction, ten had stricture formation, four had aspiration pneumonia and two were euthanased as a result of their oesophageal dysfunction (Wilson and Wilshaw 2004).

Contact: jeffc@aaerc.com.au

Reflux during anaesthesia involves the release of liquid from the stomach into the oesophagus without this being clinically obvious at the time, while in regurgitation the liquid comes up the oesophagus and emerges externally from the nose or mouth. In dogs, the reported incidence of GOR during anaesthesia is 16.3–55.0% (Wilson et al. 2006) which is much more frequent than for regurgitation where the incidence is around 0.63–5.6% (Wilson et al. 2005; Lamata et al. 2012; De Miguel Garcia et al. 2013). GOR events also usually occur in the initial stages of anaesthesia, while regurgitation events seem to be more evenly spread throughout the anaesthesia (Lamata et al. 2012). The refluxed liquid is usually acidic (pH<4.0), but around 10% of GOR events are alkaline (pH>7.5) due to duodenal fluid (Galatos and Raptopoulos 1995). It is possible that if both acidic and alkaline material are involved, the two components may act synergistically in causing greater damage to the oesophageal mucosa than either would alone (Konturek et al. 1980) which is likely the result of the combination of low pH and bile constituents. In humans with chronic GOR, Oh et al. (2006) reported more severe oesophageal mucosal lesions and decreased lower oesophageal sphincter (LOS) pressures in patients with bile plus acid reflux compared to those with either acid or bile reflux alone. In dogs, pepsin from the stomach is also likely to take part in oesophageal damage (Zacuto et al. 2012). Therefore, while many studies define a GOR event based on oesophageal pH, it may be that a combination of low pH and enzymatic injury causes the most severe and long-term oesophageal damage. Postoperatively, it has been reported that

Figure 1. Endoscopic view of (a) normal canine oesophagus at the level of the lower oesophageal sphincter. There are no signs of inflammation, anatomical lesions or refluxed material. (b) A similar view of the oesophagus of a dog with severe oesophagitis. Photographs courtesy of Dr

Matthew Woodruff.

both regurgitation and vomiting each occur in around 6.6% of dogs (Davies et al. 2015). The oesophagogastric junction is the natural barrier between the stomach and oesophagus, which is made up of the diaphragmatic crura, its associated ligaments, and the LOS. The vast majority of GOR events occur during transient lower oesophageal sphincter relaxations (TLOSR). TLOSR are not

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

associated with swallowing and normally function to allow eructation, but can also allow stomach contents to ascend from the stomach into the oesophagus. Not all TLOSR cause reflux however, and TLOSR with reflux can also occur in healthy individuals without causing problems (Penagini et al. 2002). The phase of respiration also influences GOR occurrence: during expiration, the diaphragmatic crura partially release pressure on the oesophagogastric juction, so responsibility for preventing GOR mainly rests mainly with the LOS, and this is when GOR events tend to occur (reviewed in Holloway 2000).

Effects of opioids on vomiting, GOR and regurgitation

Opioids have emetic and antiemetic effects, which is particularly relevant in the veterinary patient shortly after premedication and during pain management in the post-operative period. The emetic effects of opioids are mediated via stimulation of the chemoreceptor trigger zone, which lies outside of the blood-brain barrier (BBB), while the antiemetic effects are from inhibition of the vomiting centre, which lies within the BBB. Opioids can therefore cause transient vomiting before they are able to cross the BBB, after which their antiemetic effects take hold (Costello and Borison 1977). The risk of vomiting after morphine administration in dogs is dosedependent (Wilson et al. 2005). Opioids are also associated with oesophageal motility dysfunction and an increased risk of aspiration during swallowing in humans (Savilampi et al. 2014). Evidence indicating the effect of opioids on LOS pressure is conflicting and much of the research has been done in people. Paradoxically, most recent human studies support the conclusion that opioids actually increase LOS pressures and thereby probably reduce the risk of GOR in conscious people without underlying gastrointestinal disease (e.g. Penagini and Bianchi 1997). Determining the effects of opioids on GOR incidence is also complicated by the fact that these agents have variable effects on the LOS in the anaesthetised patient and their effects on GOR may be influenced by the duration and type of procedure, patient positioning and the use of other anaesthetic agents that also influence GOR. Strombeck and Harrold (1985) however, reported 26

that in dogs pre-medicated with meperidine, minimum LOS pressures were reduced compared to control dogs. Presumably, these troughs in LOS tone would provide an opportunity for GOR events and oesophageal injury. Significant reductions in LOS pressures were also shown in conscious dogs after administration of oxymorphone and fentanyl-droperidol (Hall et al. 1987). A recent retrospective study involving 5,736 dogs undergoing anaesthesia found an incidence of regurgitation of 1.3% (De Miguel Garcia et al. 2013). Increasing dog size, abdominal surgeries and inclusion of diagnostic procedures during the anaesthesia were found to significantly increase regurgitation risk, but the use of various opioids caused a non-significant reduction in risk compared to medetomidine. Local mechanisms of opioid influence on reflux appear to involve gastric mechanoreceptors and chemoreceptors. In a volume- and pressure-controlled gastric distension experiment in 19 healthy people, Penagini et al. (2004) found that when fundic volumes were kept constant (i.e. not allowed to decrease), morphine’s effect on the LOS was lost. Therefore, morphine was considered to reduce TLOSR indirectly by increasing gastric muscle tone and reducing gastric volume and thereby reducing stimulation of fundic mechanoreceptors. Chemoreceptors in the canine proximal stomach probably also affect TLOSR, since TLOSR were found to be less likely at higher gastric pH (Stakeberg and Lehmann 1999). In addition to their effect on the LOS, opioids have been found to increase acid secretion into the canine stomach (Konturek et al. 1980) and to delay gastric emptying into the human duodenum (reviewed in Wood and Galligan 2004), which may further increase the risk of GOR.

Treatment and prevention of reflux/regurgitation under anaesthesia

The results of Penagini et al. (2004) on the role of fundic pressures in determining opioid-induced GOR suggest that pre-operative fasting of elective patients is sensible and seems to highlight the increased risk in the fed, anaesthetised emergent patient. However, in a study including 240 dogs, Gatalos and Raptopoulos (1995) found that intraoperative GOR events were significantly more frequent in patients

anaesthetised after a more prolonged fast. In fact, there were no reflux episodes in dogs fed a light breakfast 2–4 hours before anaesthesia. This was explained by the increased post-prandial LOS tone that occurs 45–60 minutes after a meal and by the fact that gastric acidity was increased in the dogs that were fasted for longer. A later study showed that gastric pH during anaesthesia in dogs was significantly higher without affecting GOR incidence when a light meal of canned food was given 3 hours before anaesthesia, compared to other food types, and compared to any type of food after a 10-hour fast (Savvas and Raptopoulos 2009). Contrasting results have recently been reported by Viskjer and Sjöström (2017) however, in which GOR was significantly more likely in dogs fasted for a briefer time before anaesthesia. When intraoperative regurgitation does occur, it is important to flush the oesophagus with saline or water and then remove the fluid by suction. In 10 healthy dogs experiencing GOR events under anaesthesia, Wilson (2007) reported that while oesophageal suction alone had little effect on oesophageal pH, lavage with tap water increased the pH above 4.0 in four of the dogs, and subsequent administration of 20 mL of 4.2% sodium bicarbonate into the distal oesophagus was effective in raising the pH above 4.0 in the remainder of the dogs. Importantly, the treatment effect lasted only 1.5 minutes in one dog and 20 minutes in another dog treated only with tap water, but persisted for the duration of the study in all dogs given sodium bicarbonate. Pharmacological treatments can also be considered, the mainstay of which are antacids. Oh et al. (2006) however, cautioned that much of the injury occurs when the pH is between 3.0–5.0, since bile acids tend to precipitate out of solution at a lower pH which limits their participation in mucosal damage. Antacid therapy would therefore be directed at maintaining the pH >6.0 to avoid a weak acid environment, which these authors advise is very difficult to achieve using antacid therapy. With these limitations in mind however, antacids can be used as a preventative measure preoperatively, while intraand post-operatively the objective is to reduce further damage on the oesophageal mucosa from ongoing GOR events. Proton pump inhibitors such as omeprazole are favoured over

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

H2-antagonists due to their greater efficacy. In 47 dogs given methadone in the premedication, Panti et al. (2009) reported an intra-operative GOR incidence of 52% in control animals, and only 18% in patients given 1 mg/kg oral omeprazole at least 4 hours before anaesthesia. The number needed to treat was 2.97, indicating that around one patient would be spared from GOR for every three patients treated with omeprazole. Zacuto et al. (2012) used a pH/impedance probe to test the effects of esomeprazole and an esomeprazole/ cisapride combination on both acid and non-acid reflux events in 61 healthy anaesthetised dogs pre-medicated with hydromorphone. Although esomeprazole alone was associated with significantly longer periods where pH remained above 4.0 compared to the saline control, only the esomeprazole/ cisapride combination was associated with significantly reduced GOR events (i.e. the incidence of GOR events in the esomeprazole and control groups were comparable, but the refluxate was more acidic in the controls). The acid clearance time after an acidic GOR event was also significantly shorter in the esomeprazole compared to the control group (23.2 +/4.3 minutes and 56.6 +/- 66.0 minutes, respectively). H2-antagonists such as ranitidine can also be used in the anaesthetic or post-anaesthetic patient, although Favarato et al. (2012) found no reduction in the incidence of low-pH GOR events compared to control dogs when 2 mg/kg ranitidine was given slow IV. Oesophageal protection in the form of an oral sucralfate slurry is also a sensible adjunct to the postoperative treatment regimen once the animal has regained a swallowing reflex. Maropitant and metoclopramide are two antiemetic agents generally available to veterinarians and their use may also be considered as a preventative or treatment option. In 26 dogs undergoing elective orthopaedic surgery, intravenous maropitant reduced the incidence of vomiting after premedication and before induction from 46% to zero, but did not significantly affect GOR incidence or oesophageal pH during anaesthesia, compared to salineinfused controls (Johnson 2014). This suggests that maropitant given before anaesthesia may mask the outward signs (i.e. vomiting), but will not significantly protect against oesophageal mucosal damage from GOR during 28

anaesthesia. In 90 anaesthetised dogs Wilson et al. (2005) also found no association between vomiting after morphine premedication and GOR during anaesthesia, further emphasising the subclinical nature of GOR during anaesthesia, and supporting the idea that vomiting before induction cannot be used as a predictor of GOR events during surgery. The median interval between anaesthetic induction and the first GOR event was only 10 minutes and the median duration of each GOR event in this group of dogs was 95 minutes. The proportion of dogs experiencing GOR also increased with the duration of anaesthesia. Metoclopramide causes an increase in LOS tone, increased gastric motility and increased pyloric outflow (Plumb 2015). Its clinical effect on GOR during anaesthesia was studied by Wilson et al. (2006) in 52 dogs undergoing orthopaedic procedures. They found that an intravenous bolus of 1 mg/ kg metoclopramide, given after premedication, followed by a constant rate infusion at 1.0 mg/kg/hour reduced the incidence of GOR by 54%, while low bolus doses (0.4 mg/kg) had no effect on GOR. The use of a highdose metoclopramide with or without antacids may therefore be considered in animals with existing oesophagitis or other known upper gastrointestinal problems, and in animals undergoing prolonged anaesthetics. Similar to the studies above, the incidence of vomiting was also not associated with the incidence of GOR in this study. Favarato et al. (2012) used the same high-dose metoclopramide protocol, but found no reduction in GOR incidence in dogs during elective ovariohysterectomy.

Conclusions

Unseen GOR events occur very frequently during anaesthesia, and despite the conflicting evidence on the effect of opioids on the GOR, it would be sensible to assume that opioids contribute to this risk. Pre-existing gastrointestinal disease and those fasted for longer than two to four hours and/ or undergoing prolonged anaesthetics may also be at a higher risk of damaging GOR events. If GOR is suspected during anaesthesia, oesophageal lavage using water or saline (with or without sodium bicarbonate), followed by suctioning is essential. Post-anaesthetic institution of a metoclopramide CRI, antacid

medications and mucosal protectants should also be considered.

References

Costello DJ, Borison HL. Naloxone antagonizes narcotic self-blockade of emesis in the cat. The Journal of Pharmacology and Experimental Therapeutics 203, 222–30, 1977 Davies JA, Fransson BA, Davis AM, Gilbertson AM, Gay JM. Incidence of and risk factors for postoperative regurgitation and vomiting in dogs: 244 cases (2000–2012). Journal of the American Veterinary Medical Association 246, 327–35, 2015 De Miguel Garcia D, Pinchbeck GL, Senior AD. Retrospective study of the risk factors and prevalence of regurgitation in dogs undergoing general anaesthesia. The Open Veterinary Science Journal 7, 6–11, 2013 Favarato ES, Souza MV, Costa PRS, Favarato LSC, Nehme RC, Monteiro BS, Bonfá LP. Evaluation of metoclopramide and ranitidine on the prevention of gastroesophageal reflux episodes in anaesthetized dogs. Research in Veterinary Science 93, 466–7, 2012 Galatos AD, Raptopoulos D. Gastrooesophageal reflux during anaesthesia in the dog: the effect of preoperative fasting and premedication. The Veterinary Record 137, 479–83, 1995 Hall JA, Magne ML, Twedt DC. Effect of diazepam, fentanyl-droperidol, and oxymorphone on gastroesophageal sphincter pressure in healthy dogs. American Journal of Veterinary Research 48, 556–7, 1987 Holloway RH. The anti-reflux barrier and mechanisms of gastro-oesophageal reflux. Balliére’s Clinical Gastroenterology 14, 681–99, 2000. Johnson R. Maropitant prevented vomiting but not gastroesophageal reflux in anesthetized dogs premedicated with acepromazine-hydromorphone. Veterinary Anaesthesia and Analgesia 41, 406–10, 2014 Konturek SJ, Tasler J, Cieszkowski M, Mikoś E, Coy DH, Schally AV. Comparison of methionine-enkephalin and morphine in the stimulation of gastric acid and secretion in the dog. Gastroenterology 78, 294–300, 1980 Lamata C, Loughton V, Jones M, Alibhai H, Armitage-Chan E, Walsh K, Brodbelt D. The risk of passive regurgitation during anaesthesia in a population of referred dogs in the UK. Veterinary Anaesthesia and Analgesia 39, 266–74, 2012 Obvey DH, Wilson DV, Bednarski RM, Hauptman JG, Stanley BL, Radlinsky MG, Larenza MP, Pypendop BH, Rezende ML. Prevalence and risk factors for canine post-anaesthetic aspiration pneumonia (1999–2009): a multicentre study. Veterinary Anaesthesia and Analgesia 41, 127–36, 2014

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

Oh DS, Hagen JA, Fein M, Bremner CG, Dunst CM, DeMeester SR, Lipham J, DeMeester TR. The impact of reflux composition on mucosal injury and esophageal function. Journal of Gastrointestinal Surgery 10, 787–97, 2006 Panti A, Bennett RC, Corletto F, Brearley J, Jeffrey N, Mellanby RJ. The effect of omeprazole on oesophageal pH in dogs during anaesthesia. Journal of Small Animal Practice 50, 540–4, 2009 Pearson H, Darke PGG, Gibbs C, Kelly DF, Orr CM. Reflux oesophagitis and stricture formation after anaesthesia: a review of seven cases in dogs and cats. Journal of Small Animal Practice 19, 507–19, 1978 Penagini R, Carmagnolia S, Cantù P. Review article: gastro-oesophageal reflux disease – pathophysiological issues of clinical relevance. Alimentary Pharmacology and Theraputics 16, 65–71, 2002 Penagini R, Bianchi PA. Effects of morphine on gastroesophageal reflux and transient lower esophageal sphincter relaxation. Gastroenterology 113, 409–14, 1997 Penagini R, Allocca M, Cantù P, Mangano M, Savajardo D, Carmagnola S, Bianchi PA. Relationship between motor function of the proximal stomach

and transient lower oesophageal sphincter relaxation after morphine. Gut 53, 1227–31, 2004 Savilampi J, Ahlstrand R, Magnuson A, Geijer H, Wattwil M. Aspiration induced by remifentanil. Anesthesiology 121, 52–8, 2014 Savvas I, Rallis T, Raptopoulos D. The effect of pre-anaesthetic fasting time and type of food on gastric content volume and acidity in dogs. Veterinary Anaesthesia and Analgesia 36, 539–46, 2009 Sellon RK, Willard MD. Esophagitis and esophageal strictures. The Veterinary Clinics of North America: Small Animal Practice 33, 945–67, 2003 Stakeberg J, Lehmann A. Influence of different intragastric stimuli on triggering of transient lower oesophageal sphincter relaxation in the dog. Neurogastroenterology and Motility 11, 125–32, 1999 Strombeck DR, Harrold D. Effects of atropine, acepromazine, meperidine, and xylazine on gastroesophageal sphincter pressure in the dog. American Journal of Veterinary Research 46, 963–5, 1985 Wilson DV, Wilshaw R. Postanesthetic esophageal dysfunction in 13 dogs. Journal of the American Animal Hospital Association 40, 455–60, 2004

Wilson DV, Evans AT, Miller R. Effects pf preanesthetic administration of morphine on gastroesophageal reflux and regurgitation during anesthesia in dogs. American Journal of Veterinary Research 66, 386–90, 2005 Wilson DV, Evans AT, Mauer WA. Influence of metoclopramide on gastroesophageal reflux in anaesthetized dogs. American Journal of Veterinary Research 67, 26–31, 2006 Wilson DV. The effect of topical treatment on esophageal pH during acid reflux in dogs. Veterinary Anaesthesia and Analgesia 34, 339–43, 2007 Wood JD, Galligan JJ. Function of opioids in the enteric nervous system. Neurogastroenterology and Motility 16, 17–28, 2004 Zacuto AC, Marks SL, Osborn J, Douthitt KL, Hollingshead KL, Hayashi K, Kapatkin AS, Pypendop BH, Belafsky PC. The influence of esomeprazole and cisapride on gastroesophageal reflux during anesthesia in dogs. Journal of Veterinary Internal Medicine 26, 518-25, 2012 l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

FEATURE ARTICLE

Femoral head and neck ostectomy: a review of the literature and its efficacy as a treatment for hip dysplasia MICHELLE GRAY, BVSc, MANZCVS. Locum veterinarian

Introduction

Femoral head and neck ostectomy (FHNO, variously referred to as femoral head and neck excision, femoral head ostectomy/excision, excision/ excisional arthroplasty) is a common surgical solution for intractable hip pain in general veterinary practice. The procedure was first trialed in human medicine over fifty years ago for the treatment of septic joints in tuberculosis patients. Adopted by veterinary surgeons as a salvage procedure for debilitating hip conditions, current indications include irreparable fractures of the femoral head, neck or acetabulum; severe hip dysplasia (HD); aseptic necrosis of the femoral head (Legge-Calve-Perthes disease); and non-reducible or recurrent coxofemoral luxation. Within veterinary literature there exists a large number of articles relating to FHNO, but little strong evidence regarding the value of the procedure. Most publications are retrospective case reports or series, which provide only low quality evidence (grade 3–4) according to the principles of evidence-based medicine. Evaluation of post-surgical outcomes is also limited by the subjectivity of most reports, with the majority of studies relying on (potentially biased) owner and/or veterinarian assessment of outcome, and few including objective data such as kinetic or kinematic measurements (Off and Matis 2010). Variable methodology, including case selection, exclusion criteria, and follow up periods further complicates attempts to evaluate and compare the procedure. Contact: mail.mgray@gmail.com 32

Source: pixabay/com

Surgical outcome

FHNO involves removal of the bony components of the femoral side of the hip joint, resulting in a fibrous joint that cannot be expected to support a completely normal gait; however, despite this, reports on the outcome after FHNO are generally favourable. Retrospective studies have reported success rates of up to 96% in dogs based upon client satisfaction surveys (Off and Matis 2010); even in cases of bilateral surgery (Rawson et al. 2005). Post-operative abnormalities detected by veterinarians include limb shortening due to proximal femoral displacement; muscle atrophy; and periodic lameness or discomfort after excessive exercise (Harasen 2004). Objective force plate analyses have confirmed gait abnormalities including shortened stance time and reduced impulse and propulsive forces of operated legs. Similarly, kinematic evaluations have revealed reduction in the coxofemoral angle consistent with reduced extension of the hip; compensated by an increase in tarsal extension (Off and Matis 2010). Reports of FHNO in cats have also been published, with good efficacy (greater

than 66% with excellent function and no unsatisfactory outcomes) as evaluated by client surveys (Off and Matis 2010; Yap et al. 2015). Liske et al. (2009) have reported dorsal femoral displacement to occur after feline FHNO, however the clinical significance of this has not been established. Failed cases of FHNO have been reported in the literature, resulting in severe and persistent limitations in post-operative function, restricted range of motion, lameness and muscle atrophy (Heo et al. 2015). The reason for FHNO failure has not been confirmed, but is theorised to result from incomplete excision of the femoral neck, or impingement of the sciatic nerve (Fitzpatrick et al. 2011). Revision of the surgery can be attempted, and more recently reports have emerged of conversion of FHNO to total hip replacement (THR). Conversion surgery is however complicated by sclerosis of the femoral canal and the presence of large amounts of fibrous tissue, and frequently requires adaptations from a standard THR (Fitzpatrick et al. 2011). The success rate of FHNO has been associated with a number of factors including:

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

Patient characteristics

Patient weight is a frequently cited factor influencing the outcome of surgery (Schulz and Dejardin 2003), and gait abnormalities are reported to be more evident in larger dogs post-operatively (Off and Matis 2010). Despite this there has been no statistically proven link between patient size and outcome (Harasen 2004) and more recent publications suggest that physical fitness and muscle mass are more important than overall body weight in determining the outcome of surgery (Peycke 2011). Associated with this, the duration of lameness or disability prior to surgery has also been associated with outcome, with the hypothesis that pre-existing muscle atrophy negatively impacts postoperative return to function (Schulz and Dejardin 2003).

Surgical technique

Several adaptations of the standard surgical procedure have been described in case series, however inconsistency in the protocol and time frame for postoperative assessment thwarts any true comparison of efficacy between the different procedures. Variations to the standard craniolateral technique have included dorsal and ventral approaches (Schulz and Dejardin 2003; Piermattei et al. 2006); and the interposition of a range of muscle flaps from the superficial gluteal and biceps femoris muscles between the ostectomised femur and acetabulum (Mann et al. 1993). Subjective results of muscle flap interposition have been variable and kinetic studies have failed to demonstrate an objective improvement in weight bearing (Lewis 1992). These findings, combined with reports of increased post-operative morbidity (a higher incidence of swelling, pyrexia and wound infection) have led to muscle sling techniques falling out of favour (Harasen 2004); however these techniques may be of value if revision surgery is required for failed FHNO. Complete excision of the femoral neck (from just proximal to the lesser trochanter to the medial aspect of the greater trochanter) has been identified as an important determinant of post-operative outcome (Roush 2012). According to a study by Vinayak et al. (2006) this is most accurately evaluated on ventrodorsal radiographic views of the proximal femur with the hind-legs extended and externally rotated. A variety of different tools have 34

been used to create the ostectomy including Gigli wire, osteotomes, and oscillating saws. The use of Gigli wire has been shown to remove less femoral neck and require additional post-osteotomy correction (Bonneau and Breton 1981) and consequently is not currently recommended. A recent cadaver study by O’Donnell et al. (2015) demonstrated that ostectomies performed with an oscillating saw produce less bone fragments, cortical fissures, irregular surfaces and residual neck volume than cuts made with an osteotome, theoretically benefiting patient outcomes; however the in vivo significance remains unproven.

Rehabilitation

The efficacy of FHNO has been reported to be dependent upon post-operative rehabilitation and physiotherapy (Roush 2012). Many authors have advocated passive flexion and extension exercises (Piermattei et al. 2006) and an early return to weight bearing exercise (Roush 2012); however no studies have been performed to evaluate the effect of different rehabilitation regimes on patient outcome. Recovery times for FHNO have been reported to vary from a few days to >8 months in dogs (Harasen 2004) and 1–2 months in cats (Yap et al. 2015).

FHNO and hip dysplasia

Hip dysplasia (HD) is reported to be one of the most common orthopaedic conditions of the dog (Roush 2012); with incidence rates above 45% in some breeds (Schulz and Dejardin 2003) and the potential for true prevalence to be even higher. Management of the condition ranges from conservative measures to surgical interventions including juvenile pelvic symphysiodesis (JPS); triple pelvic osteotomy (TPO); total hip replacement (THR, also referred to as total hip arthroplasty) and FHNO. All of the surgical treatments for HD aim to alleviate pain and maximise function, however they are based upon very different physiologic approaches. JPS and TPO have been advocated as preventative procedures to be performed in the skeletally immature patient; they aim to increase acetabular coverage of the femoral head and thus decrease the occurrence of subluxation, improve force distribution and prevent or delay the development of osteoarthritis (Roush 2012). JPS achieves acetabular ventroversion through premature closure

of the pubic symphysis and alterations in the pelvic growth pattern, while TPO involves multiple ostectomies to physically rotate the acetabulum (Schulz and Dejardin 2003). THR and FHNO are primarily performed as salvage procedures in skeletally mature dogs. THR replaces the abnormal joint with manufactured implants, thus eliminating disease and restoring function; while FHNO targets the the pain associated with bony contact by excising the femoral head and neck and creating a fibrous false joint (Piermattei et al. 2006).

Comparative efficacy of treatments

Direct comparison of the various procedures, and their relative efficacy over conservatively managed patients has seldom been reported despite a multitude of descriptive studies and case series. Conservative therapy alone has been reported to produce a satisfactory outcome in up to 76–86% of dogs with HD (Kapatkin et al. 2002). A review article by Kirkby and Lewis (2012) concluded there is good evidence (grade 2) for the efficacy of weight control in the management of HD, and moderate evidence supporting the benefit of treatment with polysulphated glycosaminoglycans, mesenchymal stem cells and extracorporeal shockwave therapy. Non-steroidal anti-inflammatory therapy is a mainstay of conservative management of HD and long-term therapy has been shown to be both efficacious and safe (Innes et al. 2010). JPS, if performed between 15–20 weeks of age has been shown to result in a significant reduction in the incidence of HD at 2 years (Roush 2012). However it does not eliminate joint laxity or progression of osteoarthritis, especially in puppies with initial severe laxity (House 2011; Roush 2012). In a comparison with TPO there was no significant difference noted in outcome as measured both subjectively and objectively (Manley et al. 2007). No direct comparison with THR or FHNO has been published. Published reports on TPO have demonstrated that over 90% of patients achieve satisfactory limb function post-operatively with consistent clinical improvement as assessed by subjective evaluations (Schulz and Dejardin 2003; Roush 2012). Objective kinetic assessments produce similar results with positive outcomes demonstrated by increases in peak vertical force

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

measurements (Schulz and Dejardin 2003; Roush 2012). As with JPS, the procedure does not completely eliminate laxity or the progression of osteoarthritis, but frequently establishes sufficient stability for a functional outcome (Roush 2012). In Plante et al’s comparison between TPO, FHNO and conservative treatment (1997a, b), results indicated greater efficacy of TPO over FHNO as assessed by owner evaluation, lameness, pain and muscle scoring, goniometric measurements and kinetic evaluations. Both procedures however resulting in better clinical outcomes than conservative treatment alone. THR is perhaps the only surgical intervention for HD with the potential for complete elimination of osteoarthritis and a return to normal limb function post-operatively. Subjective assessments of patient outcome have reported satisfactory outcomes in 95% of cases (Piermattei et al. 2006) and objective force plate analyses have documented a return to normal function within 3–6 months (Roush 2012; Heo et al. 2015). Despite this evidence to suggest that THR results in superior limb function to FHNO, a study in which dogs with bilateral HD had THR of one hip and FHNO of the contralateral side, demonstrated equivalent or greater weight bearing of the FHNO limb (Dueland et al. 1977). No recent direct comparisons are available however, and advances in THR technology are likely to have improved the efficacy of this procedure.

Discussion

Reviewing the published literature on FHNO using the established principles of evidence-based medicine makes it clear that despite a large number of reports there is a paucity of high quality evidence for clinicians to base surgical decisions on, and thus a high likelihood of personal experience and expert opinion overly influencing treatment choices. A lack of randomised, controlled, comparative studies with standardised case criteria and evaluation protocols means that the current literature provides little assistance for those wishing to make evidence-based recommendations about FHNO, and particularly its use in cases of HD. A consequence of the current lack of evidence is wide variation in expert opinions and recommendations as regards FHNO. Proponents argue that the high degree of owner satisfaction

reported with the procedure justify its widespread use (Harasen 2004). Detractors, in contrast, focus on objective evidence of altered limb function and contend that the procedure should be restricted to exceptional circumstances (Off and Matis 2010). In human medicine, patient orientated outcomes are viewed as more important than disease orientated outcomes. Thus the question becomes whether the limb and gait abnormalities observed after FHNO are due to pain, or due to biomechanical alterations of the joint. If the former holds true then kinetic and kinematic evaluations are relevant to treatment decisions. If not, as argued by Piermattei (2006), then they may be a distraction from more relevant patient outcomes. The potential paradox, whereby more accurate objective outcomes may in reality be of less relevant than subjective measures for determining clinical decisions, will remain subject to personal opinion until the nature of any association between gait abnormalities and pain is elucidated. The optimal treatment paradigm for HD still remains to be determined, however based on current literature reports there does appear to be a role for each of JPS, TPO, THR and FHNO provided there is careful patient selection. JPS and TPO, the ‘preventative’ procedures, have their place in the treatment of juvenile animals, although some controversy exists given the lack of knowledge regarding which cases will benefit from surgery versus conservative management (Kapatkin et al. 2002). Once HD results in osteoarthritis, the surgical choice is between FHNO and THR. THR is generally preferred for its ability to restore normal limb function, however it does carry a higher risk of complications (12–13% versus 1–2% for FHNO) which may necessitate repeat surgery (Roush 2012). The evidence supports FHNO as an acceptable alternative in situations where a lack of specialist access or financial constraints preclude THR. Aside from HD, other clinically relevant indications for FHNO include aseptic necrosis of the femoral neck (for which it is historically the treatment of choice); unrepairable fractures of the femoral head, neck or acetabulum; and irreducible or recurrent coxofemoral luxation (Harasen 2004). Client satisfaction rates after FHNO can approach 100%, although completely

normal limb function is rarely reestablished (Off and Matis 2010). A thorough understanding of the patient, treatment and post-operative factors that influence patient outcome will help surgeons to optimise clinical outcome for all of these patients.

Key points 

Many questions remain to be answered regarding FHNO; how relevant gait analysis is to overall patient outcome; what is the most effective rehabilitation program for recovery; and its place in the optimal treatment paradigm for canine HD.  Currently clinical recommendations can only be based upon indirect comparisons of studies and historical data, extrapolation from the limited available evidence and personal experience and opinion. This should be acknowledged in owner discussions.  In any particular patient, treatment recommendations will vary depending upon age, disease severity and owner expectations. Non-clinical factors may dictate treatment choices, however evidence relating to patient outcomes, recovery times and complications is still clinically relevant and aids in managing client expectations.  A number of treatment options exist for hip dysplasia (both conservative and surgical), all of which merit discussion with owners. At this time the evidence base is insufficient to determine the optimal treatment paradigm and further studies are required.  Practical measures to optimise patient outcomes after FHNO include: - Counselling owners pre-operatively about the expected outcome, including the possibility of femoral displacement, gait abnormalities and discomfort after exercise - Using an oscillating orthopaedic saw to perform the ostectomy to minimise bone trauma and optimise femoral neck removal - Evaluating patients with postoperative ventrodorsal radiographs (hind-legs extended and externally rotated) to detect any residual femoral neck - Initiating early weight-bearing activities with daily physiotherapy, along with weight control measures to optimise post-operative recovery

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

References

Bergh MS, Budsberg SC. A systematic review of the literature describing the efficacy of surgical treatments for canine hip dysplasia (1948–2012). Veterinary Surgery 43, 501–6, 2014 Bonneau NH, Breton L. Excision arthroplasty of the femoral head. Canine Practice 8, 13–25, 1981 Dueland R, Bartel DL, Antonson E. Forceplate technique for canine gait analysis of total hip and excision arthroplasty. Journal of the American Animal Hospital Association 13, 547–52, 1977 Fitzpatrick N, Pratola L, Yeadon R, Nikolaou C, Hamilton M, Farrell M. Total hip replacement after failed femoral head and neck excision in two dogs and two cats. Veterinary Surgery 41, 136–42, 2011 Harasen G. The femoral head and neck ostectomy. Canadian Veterinary Journal 45, 163–4, 2004 Heo SY, Seol JW, Lee HB. Total hip replacement in two dogs with unsuccessful femoral head ostectomy. Journal of Veterinary Science 16, 131–4, 2015 House A. Evidence based management of coxofemoral disease. Australian Veterinary Association Proceedings 2011 Viewed on 20/10/2015 at: http://www.vin.com/ doc/?id=6087693. 2011 Innes JF, Clayton J, Lascelles BDX. Review of the safety and efficacy of long term NSAID use in the treatment of canine osteoarthritis. Veterinary Record 166, 226–30, 2010 Kapatkin AS, Mayhew PD, Smith GK. Canine hip dysplasia: evidence-based treatment. Compendium on Continuing Education for the Practicing Veterinarian 28, 590–9, 2002 Kirkby KA, Lewis DD. Canine hip dysplasia: reviewing the evidence for nonsurgical management. Veterinary Surgery 41, 2–9, 2012 Lewis DD. Femoral head and neck excision and the controversy concerning adjunctive soft tissue interposition. Compendium of

Continuing Education for the Veterinary Practitioner 14, 1463–70, 1992 Liske WD, Doyle N, Marcellin-Little DJ, Osborne JA. Total hip replacement in three cats: surgical technique, short term out-come and comparison to femoral head and neck ostectomy. Veterinary and Comparative Orthopaedics and Traumatology 22, 505–10, 2009 Manley PA, Adams WM, Danielson KD, Dueland RT, Linn KA. Long term outcome of juvenile pubic symphiodesis with triple pelvic osteotomy in dogs with hip dysplasia. Journal of the American Veterinary Medical Association 230, 206–10, 2007 Mann FA, Hathcook JT, Wagner-Mann C. Estimation of soft tissue interposition after femoral head and neck excision in dogs using ventrodorsal pelvic radiography. Veterinary Radiology and Ultrasound 34, 230–4, 1993 O’Donnell MD, Warnock JJ, Bobe G, Scholz RP, Wiest JE, Nemanic S. Use of computed tomography to compare two femoral head and neck excision ostectomy techniques as performed by two novice veterinarians. Comparative and Orthopaedics and Traumatology 28, 295–300, 2015 Off W, Matis U. Excision arthroplasty of the hip joint in dogs and cats: clinical, radiographic and gait analysis findings from the Department of Surgery, Veterinary Faculty of the LudwigMaximilians-University of Munich, Germany. Veterinary and Comparative Orthopaedics and Traumatology 23, 297–305, 2010 Peycke LE. Femoral head and neck ostectomy. NAVC Clinician’s Brief 9, 55–9, 2011 Piermattei DL, Flo GL, De Camp CE. Chapter 16: The hip joint. In: Piermattei DL, Flo GL, De Camp CE (Eds) Brinker, Piermattei and Flo’s Handbook of Small Animal Orthopaedics and Fracture Repair. Pp 461–511. Saunders/Elsevier, St Louis, MO, USA, 2006

Plante J, Dupois J, Beauregard G, Bonneau NH, Breton L. Long term results of conservative treatment, excision arthroplasty and triple pelvic osteotomy for the treatment of hip dysplasia in the immature dog: part 1: radiographic and physical results. Veterinary and Comparative Orthopaedics and Traumatology 10, 47–56, 1997a Plante J, Dupois J, Beauregard G, Bonneau NH, Breton L. Long term results of conservative treatment, excision arthroplasty and triple pelvic osteotomy for the treatment of hip dysplasia in the immature dog: part 2: analysis of ground reaction forces. Veterinary and Comparative Orthopaedics and Traumatology 10, 14–9, 1997b Rawson EA, Aronsohn MG, Burk RL. Simultaneous bilateral femoral head and neck ostectomy for the treatment of canine hip dysplasia. Journal of the American Animal Hospital Association 41, 166–70, 2005 Roush JK. Chapter 60: Surgical therapy of canine hip dysplasia. In: Tobias KM, Johnston SA (Eds) Veterinary Surgery Small Animal. Elsevier/Saunders, St Louis, MO, USA, 2012 Schulz KS, Dejardin LM. Chapter 145: Surgical treatment of canine hip dysplasia. In: Slatter D (Ed) Textbook of Small Animal Surgery 3rd Edition. Pp 2029–59. Elsevier Science, Philadelphia, PA, USA, 2003 Vinayak A, Kerwin SC, Ward MP, Bahr A, Peycke LE, Mertens WD. Effects of femur position on radiographic assessment of completeness of femoral head and neck excision in medium to large breed dogs. American Journal of Veterinary Research 67, 64–9, 2006 Yap FW, Dunn AL, Garcia-Fernandez PM, Brown G, Allan RM, Calvo I. Femoral head and neck excision in cats: medium to long-term functional outcome in 18 cats. Journal of Feline Medicine and Surgery 17, 704–10, 2015 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.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

CASE REPORT

Nasal turbinate cyst: an unusual cause of stertor in a pug with brachycephalic syndrome This article was written as part of the requirements for receiving the CAV ‘A Week With…..’ grant

HELEN SHEARD, BVSc

MVM. Companion animal veterinarian at Totally Vets, Feilding

Introduction

Brachycephalic Syndrome describes the result of hereditary anatomic abnormalities (see box) occurring in cats and dogs due to selective breeding for shorter heads and dorso-rotation of the face Pratschke 2014). The shortening of the facial bones is not associated with a concomitant reduction in the soft tissue of the face, leading to issues such as laryngeal obstruction due to an elongated soft palate. Primary abnormalities such as stenotic nares and elongated soft palate contribute to upper airway obstruction by reducing the diameter of the airways. As a result, resistance to airflow increases, producing negative pressure in the upper respiratory tract. This in turn can cause secondary changes such as everted laryngeal saccules and laryngeal oedema, and in severe cases laryngeal collapse (Table 1) (Ginn et al. 2008). Anatomic abnormalities associated with Brachycephalic Syndrome (from Finji and Dupre 2013) Stenotic nares Tortuous nasal cavities Aberrant conchae Elongated soft palate Everted laryngeal saccules Laryngeal collapse Tracheal hypoplasia (English bulldog) Contact: helen.sheard@tvg.co.nz

Table 1. Laryngeal collapse is a progressive condition, divided into three stages of deterioration (Pratschke 2014).

Grade Description Stage 1 Everted laryngeal saccules Stage 2 The above, plus loss of rigidity of arytenoid cartilages and medial displacement of cuneiform processes Stage 3 The above plus collapse of the corniculate processes of the arytenoid cartilage and loss of the dorsal arch of the rima glottis.

Abnormal upper respiratory tract sounds (such as snuffling and stertor) in an affected dog are evidence of some degree of obstructive dyspnea being present. However Packer et al. (2012) found that many owners considered these sounds to be normal for brachycephalic breeds, and not indicative of respiratory distress. Heat tolerance and quality of sleep are also affected by obstructive dyspnea in dogs with Brachycephalic Syndrome. A survey conducted by Roedler et al. (2013) of owners of brachycephalic dogs that had not had corrective surgery, found that 33% were unable to walk for more than ten minutes in summer; that a quarter would suffer sleep apnoea or attempt to fall asleep sitting up, and 11% had choking fits while asleep. Early surgery for affected dogs is usually recommended and commonly includes treatment of both stenotic nares and elongated soft palate. In those dogs affected by Brachycephalic Syndrome,

the soft palate is usually overly thick as well as long, and the surgical technique chosen to correct this should address both issues. Folded flap palatoplasty is currently the surgery of choice. Histological studies have found that the increased thickness is due to increased stroma within the lamina propria, and an increased proportion of salivary tissue when compared to mesaticephalic (medium length skull) dogs. The paired palatinus muscles were also found to be reduced in size, which is likely to result in impaired soft palate function (Crosse et al. 2015). Some of the other abnormalities may require attention, but rarely in the first instance, and there is no treatment for tracheal hypoplasia. As well as obstructive dyspnea, Brachycephalic Syndrome has been associated with digestive disorders, hence a move away from the term Brachycephalic Obstructive Airway Syndrome (Finji and Dupre 2013). A study by Poncet et al. (2005) found that 97% of dogs presenting with respiratory signs attributable to Brachycephalic Syndrome had concurrent clinical signs of gastrointestinal disease such as regurgitation, oesophagitis and vomiting.

Case history

A 4-year-old female spayed pug presented with stertorous breathing and sleep apnoea of several months duration. She had a history of chronic rhinitis and sneezing for 1 year that was

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

being treated with prednisolone and chlorpheniramine (Prednil; Jurox Pty Ltd, NSW Australia) and oesophagitis that was treated with omeprazole (Losec; AstraZeneca Ltd, Auckland, New Zealand). A recent course of doxycycline (Vibravet; Pfizer Animal Health, NSW Australia) had resulted in some improvement in the rhinitis, however clinical signs relapsed once the course had finished. The pug had previously undergone corrective surgery at approximately one year of age to both shorten and thin an elongated soft palate and improve airflow through stenotic nares. At this time she was also found to have stage 1 laryngeal collapse (Table 1). Although CT scans had been offered at previous examinations, the owners had declined given the partial response to medical treatment. However given that full recovery had not been achieved with several months of treatment, they gave permission for the dog to undergo a rhinoscopy procedure and CT scan of the head. Pre-operative bloods revealed moderately elevated ALT (562 IU/L, reference interval 0–75 IU/L) which may have been a result of long-term prednisolone administration, or chronic hypoxia caused by the upper airway obstruction. All other parameters were within normal limits. The following day the dog was anaesthetised and underwent rhinoscopy. The left caudal nasopharynx was observed to be obscured in its entirety by a pink, smooth, rounded mass, from which several biopsies were taken. The CT scan revealed that the mass originated within the left nasal passage and extended caudally to occupy the entire nasal cavity at the level of the nasopharynx (Figure 1). There was no indication that invasion of surrounding bone had occurred. At this point the differential diagnoses included a nasopharyngeal polyp or cyst, neoplasia or tooth root abscess.

Surgical technique

The dog was taken to surgery (Figure 2), which involved a ventral rhinotomy through the hard palate, emerging beneath the mass itself. The mucoperiosteum of the hard palate was elevated laterally to the left alveolar ridge. The mucoperiosteum and soft palate attachments to the caudal edge of the palatine bone were incised. Full

suctioned. The nasal mucosa layer of the hard palate was closed with absorbable suture. A tracheostomy tube was placed in case of airway obstruction as a result of swelling or bleeding post-operatively. Post-operative haemorrhage was minimal and it was noted that there was an immediate improvement in the dog’s stertor. During recovery her chin was propped up on a roll of bandage to avoid any blocking of the tracheostomy tube. The tracheostomy tube was removed 24 hours later and the site left to heal by second intention.

Figure 1. CT image showing (a) transverse section of the head at the level of the caudal nasal passage and (b) a sagittal section through the head. The blue arrow indicates the mass in the left nasal cavity extending caudally to the nasopharynx.

Figure 3. The cyst following removal, shown on a 10 x 10 cm swab.

Histopathology

Figure 2. The dog positioned for surgery in dorsal recumbency.

thickness incision was extended as far caudally as necessary into the soft palate. The edges of the incision were retracted with stay sutures. The left palatine bone was removed with a power driven burr and rongeurs, and was discarded. A smear was collected once there was access to the nasal cavity. The nasal cavity was explored and a 1 cm-diameter cyst-like mass was removed (Figure 3) and submitted for histology and culture. The nasal cavity was then flushed with saline while being actively

Histopathology on biopsies taken during rhinoscopy revealed hyperplastic nasopharyngeal mucosa with areas of dystrophic mineralisation (likely due to inflammation or ischaemia) and hyperplastic glandular tissue (likely due to inflammation; hyperplastic glandular tissue has been found on the soft palate of brachycephalic breeds, but has not been found to extend into the nasopharynx (Crosse et al. 2015). One biopsy section contained turbinate bone and ciliated respiratory epithelium. The pathologist commented that this could be due to caudal extension of turbinates into the nasopharynx. Histology on the mass removed at surgery revealed turbinate tissue, in line with the biopsies taken during rhinoscopy. The mass was assumed to be a congenital turbinate cyst. On follow up several weeks after surgery, the upper respiratory tract issues had resolved and the dog had been successfully weaned off Prednil. Her

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

owners reported that she was brighter, more active and appeared to have a better sense of smell.

Discussion

The histopathology on the mass in this case suggested that nasopharyngeal turbinates were present, however the lesion found at surgery was more suggestive of a turbinate cyst. It may be that the presence of the cyst caused turbinate tissue to extend caudally into the nasopharynx by exerting a mass effect, or that the cyst was present on a section of nasopharyngeal turbinate. Nasopharyngeal turbinates are an abnormality unique to brachycephalic animals and are a result of the shortening of the facial bones without associated shortening of the soft tissue structures. This results in turbinates extending both further caudally and rostrally than in non-brachycephalic breeds. A study of 53 brachycephalic dogs and 10 brachycephalic cats presenting with upper respiratory tract disease identified nasopharyngeal turbinates in 21% and 20% respectively. Interestingly, pugs accounted for 32% of the dogs in the study and 82% of the dogs with nasopharyngeal turbinates. This study postulated that nasopharyngeal turbinates are likely to play a role in upper airway obstruction seen in Brachycephalic Syndrome (Ginn et al. 2008). There is very little in the literature on turbinate cysts. Cysts in the nasopharynx have been described in dogs and may arise as a result of caudal nasal turbinate disease, or due to cystic malformation of the structures adjacent

to the nasopharynx (Hunt and Foster 2009).

Teaching Hospital) as well as Geoff Orbell (New Zealand Veterinary Pathology).

Murgia, et al. (2014) presented a case report on three brachycephalic dogs that had upper airway obstruction due to a mass that was consistent with an intranasal epidermoid cysts. Epidermoid cysts can result from congenital sequestration of epithelial tissue, trauma or a foreign body reaction. They have been reported in a variety of locations including the medial canthus of the eye, in the nasopharynx and within the central nervous system, however Murgia had not found any previous papers describing them in an intranasal location. They therefore concluded that although there were aspects of the masses they found that were consistent with epidermoid cysts, their aetiopathogenesis and origin is still unclear. The exact cause of the mass in our case is, likewise, unclear.

References

In summary, Brachycephalic Syndrome is a complex disease, comprised of both respiratory and gastrointestinal abnormalities. There are many factors that contribute to the upper respiratory obstruction that is the hallmark of this disease: stenotic nares, thickened and overlong soft palate, aberrant conchae and laryngeal collapse. This case report suggests that turbinate cysts should be added to the list of differential diagnoses in a brachycephalic animal that presents with respiratory distress.

Acknowledgements

Many thanks to Dr Aparna Tikekar and Dr Kevin Kang (Massey University Veterinary

Crosse K, Bray J, Orbell G, Preston C. Histological evaluation of the soft palate in dogs affected by brachycephalic obstructive airway syndrome. New Zealand Veterinary Journal, 63, 319–25, 2015 Finji L, Dupre G. Brachycephalic Syndrome: Innovative Surgical Techniques. Retrieved from Clinician's Brief. 2013 Ginn J, Kumar M, McKiernan B, Powers B. Nasopharyngeal turbinates in brachycephalic dogs and cats. Journal of the American Animal Hospital Association, 44, 243–9, 2008 Hunt G, Foster S. Chapter 142: Nasopharyngeal Disorders. In Bonagura J and Twedt D(eds), Kirk's Current Veterinary Therapy (Vol. XIV). Saunders Elsevier, Missouri, USA, 2009 Monnet E. Brachycephalic Airway Syndrome. WSAVA World Congress Proceedings. 2015 Murgia D, Pivetta M, Bowlt K, Volmer C, Holloway A, Dennis R. Intranasal epidermoid cyst causing upper airway obstruction in three brachycephalic dogs. Journal of Small Animal Practice 55 431–5, 2014 Packer R, Hendricks A, Burn C. Do dog owners perceive the clinical signs related to conformational inherited disorders as 'normal' for the breed. A potential constraint to improving canine welfare. Animal Welfare, 21 (S1), 81–93, 2012 Poncet C, Dupre G, Freiche VE. Prevalence of gastrointestinal tract lesions in 73 brachycephalic dogs with upper respiratory syndrome. Journal of Small Animal Practice 46, 273–9, 2005 Pratschke K. Current thinking about Brachycephalic Syndrome: more than just airways. Veterinary Ireland Journal 19, 70–8, 2014 Roedler F, Pohl S, Oechtering G. How does severe brachycephaly affect dogs' lives. Results of a structured preoperative owner questionnaire. The Veterinary Journal, 198, 606–10, 2013 l

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Articles accepted for publication (practitioners): $150 Article accepted for publication (students): $50 (note: in error this was given as $100 in the June 2016 issue of Companion Quarterly) Best article of the issue prize: $100 Best article of the year prize: $400 (sponsored by Eyevet Services) Best student article of the year prize: $400 (sponsored by VetEnt)

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

What is your diagnosis? THE ANSWERSâ&#x20AC;Ś 1 What are your radiographic findings? On the lateral radiographic projection, there is a well-defined, oval-shaped, soft tissue-dense mass measuring approximately 25 x 20 cm in the cranioventral thorax (Figure 2), dorsal to the second sternebra. On the ventrodorsal view, this mass is located on the midline, causing mediastinal widening which bulges more to the left of midline, cranial to the heart. The oesophagus is severely, diffusely dilated with gas, allowing visualization of the dorsal and ventral oesophageal walls, and the longus colli muscles in the lateral view. The tracheal stripe sign can be seen which is an opaque band of soft tissue density that is formed by the summation of the ventral aspect of the oesophageal wall with the dorsal aspect of the tracheal wall. The left caudal wall of the dilated oesophagus is also seen on the ventrodorsal radiographic projection. No pleural effusion and alveolar infiltrates were seen in either view. 2 What is this dogâ&#x20AC;&#x2122;s problem list? The dogâ&#x20AC;&#x2122;s problem list includes regurgitation, lethargy, elevated liver enzymes and BUN, a cranial thoracic mass and diffuse oesophageal dilation. Reverse sneezing, low BCS and upper respiratory tract noise may be explained as secondary to regurgitation, and elevated liver enzymes and BUN could be due to dehydration, however alternative explanations for these clinical signs were not dismissed. 3 List differentials for the two major problems visible on the radiographs. 1) Cranial thoracic mass: a) Mediastinal mass: the most common cranial mediastinal masses in small animals are thymoma and lymphoma. i) Neoplasia: thymoma, lymphoma, histiocytic sarcoma, ectopic thyroid neoplasia and parathyroid tumour ii) Abscess iii) Cyst iv) Granuloma v) Haematoma b) Pulmonary mass: primary neoplasia is the most common cause of pulmonary masses in small animals. i) Neoplasia, primary or secondary ii) Abscess iii) Granuloma iv) Haematoma v) Cyst The radiographic appearance of the mass is consistent with a cranioventral mediastinal mass. The fact that the mass bulges more to the left increases the suspicion for a mass of thymic

Figure 2. The same radiographic images as in Figure 1. On each view, notice the radiopaque walls of the diffusely gas-dilated esophagus (black arrows) that are indicative of megaesophagus. There is also mild ventral displacement of the trachea caused by esophageal distension. The gas-filled esophagus borders the longus colli muscles (asterisk). A well-defined soft tissue mass can be seen in the cranial mediastinum (white arrows).

origin. Less likely is a mass in the cranioventral portion of the cranial segment of the left cranial lung lobe, which sometimes can be seen in that region.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

2) Diffuse oesphageal dilation a) Megaoesphagus i) Congenital ii) Acquired (1) Idiopathic (2) Neuromuscular disease such myasthenia gravis (MG), polymyositis, polyneuropathy, dysautonomia, central CNS disease, botulism or tetanus (3) GIT disease such as oesophagitis, oesophageal obstruction or GDV (4) Endocrine disease such as hypoadrenocorticism or hypothyroidism (5) Toxic causes such as, organophophate or lead toxicity. b) Transient dilation: due to aerophagia or sedation/general anaesthesia Based on the radiographic findings and the patientâ&#x20AC;&#x2122;s history, the generalized oesophageal dilation is most likely due to acquired megaoesophagus. Despite the plethora of differential diagnoses for each of these findings in isolation, the combination of regurgitation with a cranial mediastinal mass and megaesophagus may be explained by a single diagnosis of megaesophagus secondary to MG as an autoimmune paraneoplastic syndrome associated with thymoma.

Treatment and outcome

The dog was treated with symptomatically with subcutaneous fluid therapy (lactated Ringerâ&#x20AC;&#x2122;s solution) and maropitant (Cerenia; Zoetis, Auckland NZ) at 1 mg/kg, S/C. A fine needle aspirate of the mediastinal mass was obtained under ultrasound and submitted to a veterinary pathology laboratory for cytology along with a venous blood sample for an antiacetylcholine receptor antibody titer to test for MG. The client was provided with information concerning management of megaoesophagus and the dog was then discharged from the hospital. Cytology of the FNA of the mediastinal mass showed three cell types (epithelial cells, small lymphocytes, mast cells) were present with no obvious evidence of oncocytes such as lymphoblasts. This is consistent with a diagnosis of thymoma, which are cytologically heterogeneous and composed primarily of a population of small lymphocytes, and occasionally a population of epithelial-like cells and mast cells. The dog was also positive for anti-acetylcholine receptor antibodies with a titre of 16.14 nmol/L (reference range <0.6 nmol/L) confirming a diagnosis of acquired MG. Based on these results, the dog was treated for MG secondary to thymoma. The anticholinesterase inhibitor, pyridostigmine bromide (Mestinon; Bausch & Lomb, Auckland NZ) was prescribed at 1 mg/kg, 12-hourly, by mouth, which was initiated 10 days after discharge. The owner declined any aggressive treatment such as surgical excision, radiotherapy or chemotherapy for the mass. Unfortunately 13 days after initial examination, the dog represented in respiratory arrest. The owner elected euthanasia. While the diagnosis of myasthenia gravis secondary to thymoma was strongly suspected on the basis of history, physical examination, acetylcholine receptor antibody titer, and cytologic and radiographic findings, unfortunately no necropsy

or antemortem biopsy could be performed to confirm this diagnosis.

Discussion

Thymoma is one of the most common causes of cranial mediastinal masses in small animals. Paraneoplastic syndromes such as generalised or focal myasthenia gravis, polymyositis, hypercalcemia, and exfoliative dermatitis have been well characterised in cats and dogs with thymoma. In two studies of canine thymoma, myasthenia gravis was recorded in 30% and 47% of cases. Thoracic radiographs typically show a well-defined soft-tissue mass in the cranial mediastinum. Ventrodorsal (or dorsoventral) projections are more useful than the lateral view in deciding whether a thoracic mass is located in the mediastinum, the lung or elsewhere. However, an etiology for a thoracic mass cannot usually be determined radiographically. Cranioventral mediastinal masses are one of the most commonly encountered mediastinal masses and are often accompanied by pleural effusion. Diagnostic options for determining the nature of a mediastinal mass include an ultrasonographic evaluation which should be considered before more invasive diagnostic techniques are used. Ultrasonographically, cranial mediastinal lymphomas tend to appear as solid masses, whereas thymomas more commonly have a cystic component and mediastinal cysts such as branchial cysts appear as a well circumscribed, thin-walled structures with anechoic fluid. However, cranial mediastinal masses cannot be definitively differentiated based solely on their ultrasonographic appearance. Ultrasoundguided percutaneous sampling of a mediastinal mass via FNA or True-Cut biopsy is a minimally invasive method of obtaining a definitive diagnosis through cytology or histopathology. Since most thymomas are benign, surgical excision is usually curative. Radiotherapy may be effective for thymoma; it can induce remission although complete and long-lasting remission is seldom achieved because radiotherapy eliminates only lymphoid component of thymomas but an epithelial component remains unaffected. Chemotherapy is beneficial in cases in which the thymoma is non-resectable or a major surgical procedure is considered too risky. Combination chemotherapy protocols have been used. However, complete remission is rarely achieved because, as for radiotherapy, only the lymphoid component of the tumour is responsive. Myasthenia gravis is a neuromuscular disorder characterized by muscle weakness that is exacerbated by exercise and alleviated by rest. It occurs in two forms; congenital and acquired. The acquired form of MG is a common immune-mediated disorder in which antibodies are directed against a portion of the nicotinic acetylcholine receptors of the neuromuscular junction. Antibodies bind to the receptors leading to their destruction thus reducing the sensitivity of the postsynaptic membrane to the transmitter acetylcholine and causing muscular weakness. Hyperersalivation and regurgitation are common clinical signs, caused by megaesophagus which is seen in 90% of dogs with acquired myasthenia gravis. MG may also occur in a focal form, in approximately 40% of affected dogs and 14% of affected cats, causing megaesophagus with no detectable appendicular weakness.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

While the cause of MG is typically unknown, it may be caused by antibodies against an epitope expressed on the cells of a thymoma cross-reacting with similar epitopes on the acetylcholine receptor of the neuromuscular junction. Definitive diagnosis of MG is made by demonstrating the presence of a high concentration of antibodies against acetylcholine receptors; although the antibody titer does not correlate directly with the severity of clinical signs. With regard to treatment of MG, administration of anticholinesterase inhibitor drugs and occasionally immunosuppressive drugs may be considered. Anticholinesterase inhibitors interfere with the degradation of acetylcholine and so increase the

amount of acetylcholine available at the neuromuscular junction thus increasing the activity of the remaining acetylcholine receptors. Supportive care may include treatment of aspiration pneumonia with antimicrobials and feeding multiple small meals of a high calorie diet in an upright position to reduce the risk of aspiration. Surgical removal of thymoma should be considered if one is identified since thymectomy may result in a decrease in acetylcholine receptors antibody titer and a dramatic resolution of clinical signs.

References

Aronsohn MG, Schunk KL, Carpenter JL, King NW. Clinical and pathologic features of thymoma in 15 dogs. Journal of the American Veterinary Medical Association 184, 1355–62, 1984

Atwater SW, Powers BE, Park RD, Straw RC, Ogilvie GK, Withrow SJ. Thymoma in dogs: 23 cases (1980–1991). Journal of the American Veterinary Medical Association 205, 1007–13,1994 Gaschen L. The canine and feline esophagus. In: Thrall DE (ed). Textbook of Veterinary Diagnostic Radiology. 6th Edtn. Pp. 500–21. Elsevier Saunders, St Louis, MO, USA, 2013 Reichle JK, Wisner ER. Non-cardiac thoracic ultrasound in 75 feline and canine patients. Veterinary Radiology Ultrasound 41, 154–62, 2000 Thrall DE. The mediastinum. In: Thrall DE (ed). Textbook of Veterinary Diagnostic Radiology. 6th Edtn. Pp. 550–70. Elsevier Saunders, St Louis, MO, USA, 2013 Tidwell AS. Ultrasonography of the thorax (excluding the heart). Veterinary Clinics of North America: Small Animal Practice 28, 993–1015, 1998 Wisner E, Zwingenberger A. Mediastinum and esophagus. In: Atlas of Small Animal CT and MRI. Pp. 408–10, John Wiley & Sons, Iowa, IA, USA, 2015 l

Allan Bell Dermvet-online Consultancy service by a Registered Specialist in Veterinary Dermatology (for veterinarians in the South Island and from Wellington as far north as Lake Taupo) For cases where referral is difficult but help is required. Contact dermvet.bell@xtra.co.nz for cost estimates and protocol

Allan Bell BVSc MACVSc (canine med) FACVSc (dermatology)

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

A WEEK WITH ...

... the surgeons at Massey University Veterinary Teaching Hospital This article was written as part of the requirements of receiving the CAV A Week With….grant HELEN SHEARD BVSc MVM. Companion animal veterinarian at Totally Vets, Feilding The ad for the CAV “A week with…” grant came at just the right time. I was perusing the latest issue of the Companion Quarterly, wondering if I would ever regain my brain function after being on maternity leave. It seemed just the thing to kick off cognition and enthusiasm for practice again! I babbled my way through an application, and was lucky enough to get the chance to spend a week at Massey University’s Veterinary Teaching Hospital with Andrew Worth and the other surgeons. Originally, I was just interested in seeing orthopaedic surgery, but the variety of Massey’s surgical caseload meant that there was always something happening. Some of the more interesting cases (and really there wasn’t anything that could be classed as mundane!) included an adrenalectomy on a foxie with Cushing’s disease, a TPLO, a plethora of stifle and elbow arthroscopies, a tibial tuberosity transposition with trochleoplasty in a young cross breed dog (how I wanted it to be a Tibetan terrier just to carry on the tongue twister!), and a caudal nasopharyngeal mass in a pug removed via a ventral rhinotomy. This last surgery was like removing a gooseberry through a keyhole – a bone window was made in the caudal hard palate ventral to the mass, and it was shelled out from underneath. The pug was only 4 years old and had already undergone surgery a couple of years ago to shorten and thin the caudal soft palate, having been a breed-induced sufferer of obstructive airway disease. When she began suffering from snuffling and stertor that didn’t respond to prednisone and doxycycline, her owners agreed to a CT scan that revealed the nasopharyngeal mass. Post-op must have been the first time in her life that she could breathe properly! In pug-style she celebrated by sleeping for several hours (she had suffered from sleep apnoea as well). The foxie with the adrenal mass also had an impressive surgery. Whole-body CT was used to try to determine whether the mass invaded or impinged on any major structures – in fact it was sitting next to, and had partially wrapped around, the renal artery. The surgery took 3 hours and a trio of surgeons and assistants. The post-op care was far from simple, requiring

The author hanging out with a patient after surgery to remove a barley grass seed. Photo courtesy of Helen Sheard

dexamethasone supplementation and blood pressure monitoring due to persistent high blood pressure. Despite a guarded prognosis before surgery (the surgery carries 50% mortality rate) the foxie was on his way home 3 days later with a very relieved and happy mum. Arthroscopy is being used more and more often at Massey, not only for diagnosing and treating elbow OCD and fragmented medial coronoid processes, but also checking for meniscal damage and debriding the remains of the ruptured cruciate ligament in the stifle prior to TPLO or TTA surgery. With Wildbase on site there was also the occasional incursion of non-mammalian species. A juvenile tuatara with nutritional osteopathy visited to be x-rayed to check healing of a fractured femur. He just sat as still as a rock while he was x-rayed, with no sedation on board. If only it was that easy for every species.

Contact: helen.sheard@tvg.co.nz

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

Student and clinician rounds happened throughout the week, as well as a case presentation by one of the interns or residents. The case presentation I attended was concerning a dog with an unusual soft tissue sarcoma and the immunohistochemical markers used to identify it. The resident and her supervisor discussed the various markers with the same ease as someone chatting about the weather. As well as local veterinarians there were several veterinarians visiting from overseas, and it was a great opportunity to talk with them. Apparently in Japan nearly every clinic has its own CT scanner. I can just see my old boss in Raetihi, coming in covered in deer grease and fizzer calf, wandering out the back to the carport to send a mud-encrusted huntaway through the CT (sorry David)! I guess a lot of the things I saw aren’t things that I can start doing myself in general practice – certainly a CT scanner is not

going to arrive any time soon, and neither is an arthroscope. But that doesn’t really matter – the extra understanding of the disease processes and the surgery involved means I can better help owners who are trying to decide on referral. Going to a busy teaching hospital like Massey, with both veterinary and vet tech students, interns and residents, you might think that one more person to have tailing you would be annoying. Far from it – everyone was very friendly and helpful, with so many invitations to see different procedures. All in all, whether you are looking to improve your skills, renew your enthusiasm, or just try something different, I would definitely recommend applying for this opportunity – it is well worth it! Big thanks to CAV and all the surgeons, residents and interns at Massey. l

CAV is pleased to acknowledge that the A Week With … grant is now sponsored by RxVet so that support can be offered to two recipients in 2017

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

WSAVA UPDATE

Taking a look at the WSAVA Hereditary Disease Committee The World Small Animal Veterinary Associationâ&#x20AC;&#x2122;s (WSAVAâ&#x20AC;&#x2122;s) Hereditary Disease Committee was formed to offer small animal clinicians clinically relevant information on the diagnosis and management of hereditary diseases and genetic predispositions to disease in dogs and cats. Its key achievement is the creation of an online DNA database on hereditary diseases. Committee members also offer educational seminars to improve the genetic health of companion animals worldwide. Committee chair Professor Urs Giger from the University of Pennsylvania offers this update on its work. Where are we now?

Incredible progress has been made in understanding hereditary diseases which have become recognised as a key clinical issue in small animal practice worldwide. Hereditary diseases are seen both in purebred animals and in mixed-breed dogs and domestic cats, but in-breeding practices certainly favour the more frequent occurrence of specific hereditary defects in specific breeds (e.g. anaemia caused by PK deficiency in West Highland White terriers and Abyssinian cats but also other breeds). Some are present at birth; others become evident as puppies and kittens grow, while yet others cause disease only in adult animals. Genetic defects can affect any organ system and include malformations, inborn errors of metabolism, and genetic predispositions to infections, immune diseases, drug reactions, cancer, and degenerative diseases. We donâ&#x20AC;&#x2122;t know the exact number of hereditary diseases affecting dogs and cats because some are poorly defined, while others are caused by different mutations in the same or different genes. Progressive retinal atrophy, for instance, is a very heterogeneous group of blinding disorders based upon clinical onset, disease progression, and molecular defects. Similarly, epilepsy is expected to be caused by different gene defects, but little is currently known about the molecular basis. Overall, cats may be affected by few hundred hereditary

Photo courtesy of Pixabay.com

diseases while around one thousand are likely to affect dogs. Most of the hereditary diseases are known to be inherited by an autosomal recessive trait. This means affected animals are homozygous for a specific gene mutation; its parents appear clinically unaffected but are carriers. Less common are those with an x-chromosomal or dominant mode of inheritance. Predispositions to disease are being recognised to have frequently a complex inheritance pattern: more than one mutation is responsible (polygenic) and disease expression is further influenced by the environment. Examples include hip and elbow dysplasia, cryptorchism, allergies and cancer predispositions. The completion of the canine and feline genome sequences and the development of sophisticated and

affordable genetic laboratory tools have led to rapid progress in our understanding of health and disease at the molecular genetic level. Currently more than two hundred disease-causing mutations have been identified in dogs and approximately three dozen mutations in cats. These are typically breed-specific, but some are ancestral, causing disease in many different breeds. In general, DNA mutation tests for established diseases in specific breeds are the most accurate and precise diagnostic tests available in clinical practice.

Treatment and control of hereditary diseases

Treatment for hereditary diseases and genetic predispositions is often limited clinically but some diseases can be cured or well controlled. For instance, hereditary cobalamin malabsorption seen in several canine breeds can be treated with cobalamin injections every two-four weeks. Bleeding due to von Willebrand disease, haemophilia and other coagulopathies can be treated with plasma transfusions. One type of cystinuria seen in many breeds can be cured by castration. However, many diseases can only be managed with supportive care and are still progressive. This makes the key issue the genetic control of these hereditary diseases in future generations. While it is simple to stop breeding affected animals and carriers, this can result in a further

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

reduction in the narrow gene pool of a breed. It is important to remember that carriers with excellent breed characteristics can be safely used when DNA tests are available so long as they are bred to clear/normal animals and offspring considered in future breeding are tested.

How the WSAVA Hereditary Disease Committee helps For the practitioner, keeping up with the immense recent progress can be overwhelming as the spectrum and information available on genetic traits continues to accumulate. Thus, it is a daunting task to diagnose and manage patients with hereditary diseases in each breed and to give sound advice to breeders. The WSAVA Hereditary Disease Committee helps by providing readily accessible and comprehensive resources in various forms on hereditary disease testing and management. In 2012, we launched a web search tool and database, allowing clinicians to search for information on the DNA tests which exist for specific hereditary diseases, breeds, and the labs that test for them. This database is one of the most frequently accessed resources on the WSAVA website freely accessible to veterinarians, breeders and pet owners: http://www.WSAVA.org/ HereditaryDefects.htm

The emerging issues related to hereditary disease include: Genetic disease counselling

Clinicians should play a crucial role in guiding their clients – pet owners and breeders – regarding the diagnosis, management and control of hereditary diseases. Objective measures as to the tests for wellness and disease screening of puppies and kittens need to be developed. Because the onset and severity of the disease, diagnostic tests, therapeutic options, and mode of inheritance vary, specific recommendations are needed. Sound recommendations are particularly challenging to formulate for complex disease traits. There is no animal completely free of any deleterious genes.

Breed club recommendations and laws A number of national breed clubs and associations have implemented strict guidelines for breeding healthy animals. Informed responsible breeding

should be implemented for the welfare of animals. We welcome these developments and encourage clinicians to utilise these sources and specific guidelines in their region.

Laboratories offering specific DNA tests

There has been an increase in laboratories offering DNA tests and other genetic traits. DNA tests specific for a particular mutation are generally robust but there are no accreditation processes currently in place to assure quality in each laboratory. We aim to set standards for laboratories which may restrict testing to laboratories using the best techniques as well as appropriate controls. The move toward new affordable chip and other technologies will further change testing from single disease tests to panel testing.

Prevalence of diseases and registries

Until now, it has been difficult to make a reliable assessment of the prevalence of diseases in a breed and region. Samples submitted to laboratories are biased and often driven by the discovery of affected and carrier animals and breeder participation. Furthermore, with a good test and follow through by breeders, the disease and carrier prevalence may rapidly decline, for instance copper toxiciosis in Bedlington terriers. The frequency may also vary between countries based upon breeder participation and popular sires used in breeding. Registries, such as OFA are good sources, but they are based on voluntary disclosures. CERF and PennHIP are two examples of registries containing every tested animal.

Patents for DNA tests

Until recently DNA mutations could be patented which restricted the availability of tests to licenced laboratories – and thereby also made them more expensive. However, as these are naturally occurring mutations and not innovations and their discoveries are supported by federal funds, they can no longer be patented in the USA, and DNA tests are now becoming more readily available after peer-reviewed publication.

Panel screening in breeds and species

Mixed-breed and purebred DNA tests have been available for a few years. They are based on microchip technology and assess multiple alterations in the

genome (SNPs – single nucleotide polymorphisms). This and other technologies have been recently applied to hereditary disease mutations. In fact, it is now possible and more affordable to screen for multiple diseases with one sample in one laboratory. Panel screening can make testing simpler but interpreting the vast data information is more complicated. No animal will be found to be perfect, particularly if its entire genome is sequenced and analysed. It is also a concern that a certain disease-causing mutation in a breed may not clinically manifest the same way in another breed as modifying genes may be improve or worsen the condition as much as environmental influences.

Distribution of updated information

It is a major task to collate and keep up-to-date the ever-growing resource of information on hereditary diseases and genetic predispositions. This is particularly challenging as molecular genetics is not (yet) the regular vocabulary of clinicians, therapeutic opportunities are limited, genetic counselling is different for each disease and can be time consuming. Thus, it will also be important to educate breeders and show judges to improve the genetic health of animals. To spread genetic information, the theme for this year’s WSAVA World Congress 2017 is Hereditary Diseases. During Congress, global experts will update delegates on practical tools and recommendations. WSAVA World Congress takes place from September 25–28, 2017 in Copenhagen. Early bird booking rates end in May 2017: www. wsava2017.com.

What is the WSAVA?

The WSAVA aims to enhance the quality of veterinary care for companion animals and to create a global community of veterinarians, working together for the benefit of both animals and people. Its members and affiliates comprise 101 veterinary organisations from around the world. As a CAV member, you are automatically a member of the WSAVA. The WSAVA Hereditary Disease Committee sincerely appreciates the generous support of its educational partner, Waltham and Mars Veterinary. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

CAV SPECIALIST PROFILE

Devon Thompson

BVSc(Dist), MVS (Hon), MANZCVSc (Radiol), DipECVDI The Specialist Profile is a regular feature that aims to provide an insight into the path New Zealand veterinarians have taken to achieve specialisation.

THIS ISSUE TONI ANNS TALKS TO DEVON THOMPSON WHO IS A REGISTERED SPECIALIST IN VETERINARY RADIOLOGY BASED AT VETERINARY SPECIALISTS GROUP IN AUCKLAND.

What is your specialty, and how many years have you been practicing as a registered specialist? I am a registered specialist in Veterinary Radiology and have been since October 2013.

Where did you obtain your veterinary degree, and did you move directly into a residency from there?

I obtained my BVSc at Massey University and then spent two and half years in general practice, predominantly doing companion animal work at mixed animal practices in rural New Zealand including Gore, Te Awamutu, Wairoa and Napier.

What drove you to specialise, and why did you choose radiology?

I tend to be a perfectionist and found working as a general practitioner somewhat frustrating and unrewarding. When I eventually realized that I was not cut out for general practice, I felt disillusioned and was uncertain of what to do next. I decided to investigate the possibility of post-graduate study and discovered an advertisement for a new residency in Veterinary Radiology at Massey University. I had never considered specialisation prior to this and certainly had not had a particular affinity for radiology as a general practitioner,

Photo courtesy of D. Thompson.

however I greatly admired the radiologists at Massey University at that time (Drs Angela Hartman and Mark Owen) and decided to apply.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

Explain the process you took to become a registered specialist (briefly include duration, location, how you found the experience, challenges).

I completed a three-year residency at Massey University during which I had the opportunity to complete externships at several other specialist hospitals in the UK, Europe and Australia. I then moved to a private multidisciplinary specialist practice in Perth, Australia where I worked alongside three other radiologists whilst preparing and completing my European Board exams. Although I had supportive mentors, family and friends, I found the experience very challenging. Completing the residency and preparing for the Board exams required considerable effort and discipline, and the stress involved is not something I wish to experience again, but I have no regrets and am very pleased to be where I am now.

What do you like most about your job?

I thoroughly enjoy working closely with other specialists to try and obtain diagnoses in those really tricky/difficult cases. Case discussions and journal clubs are just some of the benefits of working in a multidisciplinary specialist centre such as VSG. Radiology also gives you the flexibility of being able to work as a tele-radiologist virtually anywhere in the world, well as long as you have access to high speed internet!

What is the worst part of your job?

In previous positions I was required to discuss the imaging results directly with the client, however at VSG this is left up to the primary clinician, whether that be a general practitioner or other specialist. Not being so emotionally involved in case management seems to suits my personality.

What is the most challenging part of your job?

Tele-radiology! Although this service has the potential to greatly assist and improve veterinary care in this country, the quality of radiographs produced in practice (both analog and digital) is sometimes disappointing and often does not allow accurate interpretation.

What advice would you give to someone thinking of specialisation?

Achieving good grades at vet school is likely to provide you with greater opportunities for post-graduate study. In addition, publications (even if they are only case reports) and attaining Membership of the Australian and New Zealand College of Veterinary Scientists in your field of interest, will greatly increase your likelihood of obtaining a residency. Spending time with a specialist, to gain mentorship and make contacts, may also help you through the application process.

What do you think about veterinarians specialising later in their careers, after a significant period of time in general practice? Go for it! As long as you have considered the potential impacts of reduced pay, long hours and the stress it may put on your relationship and/or family.

Do you think NZ needs more specialists, and if yes, in what areas?

There has been a recent influx of New Zealand specialists returning to the country, however there are still shortages in many important fields including cardiology, neurology, ophthalmology, oncology and even radiology. With the increased uptake of pet insurance in recent years there is sure to be more opportunities for clients to seek specialist care in the future.

What are your passions outside of work?

Spending time with family and friends, drinking good coffee, and arts and crafts. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

Companion Animal Health Foundation Update WE NEED YOUR HELP! CAHF has funded some wonderful projects related to companion animals in NZ in the past, but weâ&#x20AC;&#x2122;d love to see more research undertaken, especially projects relevant to New Zealand companion animals.

CATH WATSON, CAHF Chair, www.healthypets.org.nz Pets are subjected to many diseases, injuries and abuse. However, while there are several charities devoted to the prevention of cruelty to pets, few are concerned with the improvement of companion animal health through improved medical care, surgery, and an understanding of sociological issues related to pets in New Zealand. The Foundation supports and assists veterinarians and veterinary nurses to undertake investigations into the problems associated with companion animals; medicine, surgery, and investigations on the relationships between animals, pet owners and the veterinary profession. The goal of the CAHF is to help veterinarians to help pets enjoy longer and healthier lives.

More research projects needed

We have funds available, and are keen to hear from researchers, practitioners and vet nurses alike. If you have a project or research related to companion animals in NZ that requires some funding assistance, please contact us at cav@vets.org.nz to discuss your needs, or visit healthypets.org.nz to download an application form.

Can you raise $500? Support the future of pet health by donation to the CAHF

We are asking for the support of all practices in New Zealand and individual veterinarians to raise at least $500 each, a sum which would secure the future of the Foundation and ensure it works as planned to help our pets enjoy better and healthier lives. Every dollar will be used to help combat health and welfare problems encountered by companion animals in New Zealand. 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 http://www.healthypets.org.nz/ help/donate for details. Supporting the Foundation will clearly demonstrate to your staff, your clients and your suppliers that you invest in the health of pet companion animals and that you support the veterinary profession through the Foundation. If you wish to register your practice as an annual $500 practice supporter for the CAHF use the online registration form on the website www.healthypets.org.nz l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 28 No 2 | June 2017

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 28, No. 2 | June 2017

VOLUME 28 NO 2 JUNE 2017

A review of femoral head and neck ostectomy

A case of a nasal turbinate cyst in a pug

Go Slow: a foodborne disease of dogs

Juvenile laryngeal paralysis and polyneuropathy in Rottweilers

A week with.....the surgeons at MUVTH