CAS Newsletter Vol26 no1 March 2015

NZVA COMPANION ANIMAL SOCIETY NEWSLETTER

Volume 26 No 1 March 2015

In This Issue ...

• Haemangiosarcoma in dogs • Management of traumatic brain injury • Intra-occular prostheses • Managment of insulinoma-induced hypoglycaemia – case study • Update on Feline Leukaemia Virus • Highlights from ECVIM Conference 2014

VOLUME 26 NO 1 MARCH 2015

Newsletter

Volume 26 No. 1 March 2015 ISSN No. 1173-6941

EXECUTIVE COMMITTEE 2015 President

Contents

Catherine Watson

cath@vetservices.co.nz

Editorial................................................................................................................... 2

Secretary

From your society...................................................................................................6

Rochelle Ferguson rochellemf@hotmail.com

Grants & Scholarships............................................................................................ 8

Treasurer

Article of the Issue winner..................................................................................... 10

Aimee Brooker ollyaimee@gmail.com

Apology to Imex.................................................................................................... 10

Committee Members

Haemangiosarcoma in dogs.................................................................................. 12

Kate Hill

Deepti Deshpande, Boyd R Jones

K.Hill@massey.ac.nz

Helen Beattie

Management of a cat with traumatic brain injury...................................................20

Helen.Beattie@op.ac.nz

Tania Krupitza

Brendon Bullen

brendonbullen@gmail.com

Intra-ocular prostheses for end-stage eye diseases..............................................28

Hannah Bain

Craig Irving

hannah.bain@merck.com

Warren Stroud

Prolonged survival time following medical management of insulinoma-induced hypoglycaemia...............................................................................................32

stroud@wellpet.co.nz

Pauline Calvert

Neil Stuttle

pcalvert@xtra.co.nz

EDITORAL COMMITTEE

An update on Feline Leukaemia Virus....................................................................38

Sarah Fowler (Editor) Genevieve Rogerson Angus Fechney Craig Irving Christine Moloney (Advertising) Janice Thompson Simon Clark

Dr Pru Galloway

Practitioner on sabbatical report...........................................................................44 Kate Heller

Highlights from the 2014 European College of Veterinary Internal Medicine Conference, Mainz, Germany.........................................................................45

Address for submitting copy/ correspondence etc.

Dr Pru Galloway

Sarah Fowler

Subject Index: Vol 25: 2014...................................................................................48

15 Salisbury Ave Terrace End Palmerston North 4410 Ph H:(06) 353-6253, W:(06) 358-8675, Mob: 027-358-4674 Email: sarah.fowler@gmail.com

Massey Home Page..............................................................................................50 Continuing Education Calendar............................................................................. 51 Guidelines for Authors...........................................................................................52

Advertising Manager Christine Moloney

25 Manchester St, Feilding Telephone: 06 323 6161 Fax: 06 323 6179 Email: christine.moloney@totallyvets.co.nz

Cover Photograph

Koko and Gypsy who belong to Kylee & Paul Scotney-Hopkins.

Photo by Catherine Holmes

NZVA Website

http://www.nzva.org.nz

CAS Website

http://cas.nzva.org.nz

Cover Design & Newsletter Setting

The whole of the content of the CAS Newsletter is copyright, CAS/New Zealand Veterinary Association Inc.

Penny May Aorangi Print Email: penfriend@xtra.co.nz

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

Disclaimer: The CAS newsletter is a non peer reviewed publication. It is published by the Companion Animal Society (CAS), 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 CAS newsletter, the CAS executive, the NZVA, and neither CAS nor the editor endorses any products or services advertised. CAS 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 CAS 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 CAS, 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.

March 2015

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Editorial Dangerous dogs & rampaging cats Dog attacks, SPCA prosecutions for welfare breaches, cat hoarders and community cat colonies all seem to be gaining increasing attention in the media in recent times.

Whether this is because incidences are on the rise, or it has just become a ‘popular’ topic, the outcome is more public discussion about responsible pet ownership.

Increasingly pet owners are being held to account for the behaviour of animals under their care. And when that behaviour is poor, prosecution with increasingly severe consequences are starting to result. NZ has one of the highest pet ownership figures in the world, but is this at risk? Is all this negative media attention going to drive people away from pet ownership? What role do vets have in this?

Personally, I don’t think it matters if the overall numbers go down if those that do choose to have a pet, do so with a good understanding of what is required of them to ensure their pets health and welfare is optimal. They are also more likely to make sensible decisions when choosing an appropriate companion for their lifestyle. At the end of the day, this is the client we want to see through our clinics because they are motivated and prepared to do the best by their pet!

Maybe it is wishful thinking that every patient we see is an insured, well socialized, healthy weight individual, free of preventable and inherited diseases, and comes with an educated, rational owner that considers the science and understands welfare implications of their decisions. But wouldn’t it be good

if we could even increase the percentage of these patients?

Achieving this is not up to ‘someone else’ though. It is something every one of us can tackle, both on an individual front and a collective front.

Individually vet clinics can play a very important role in helping to educate prospective pet owners to make appropriate choices when it comes to choosing a suitable pet. Do you offer pre-purchase consults for your clients? If not, this would be a really good place to start.

We are good at advising on medical and surgical problems when presented to us, and OK at promoting vaccinations (though still rely on catteries and kennels to drive people to us), but we’re far less effective on wellness care messages about things like nutrition, and when it comes to advice on behavioural problems, most of us like to duck for cover and refer to ‘someone else’.

Why? Have confidence in your ability!

You’d be surprised how much you do know compared to the average pet owner when it comes to normal behaviour. Problem behaviours are one of the most common reasons for euthanasia, so it is an area that has huge potential benefits for both the pet and the family they live with. Even just being able to identify those ‘special edition’ puppies that don’t behave like 90% of others early and discussing expectations with owners can go a long way to managing future problems and saving lives and lifestyles – animal and human.

Newsletter Design Phone: 06 323-4516 Fax: 06 323-3156 Mobile: 021 255-1140 Address: 125 Campbell Rd, RD 5, Feilding 4775 Email: print@aorangi.co.nz

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Editorial Is it our role individually to educate owners about what is best for their pet at every opportunity? Yes! And I’m sure we all try to do that, even if the client is not always receptive. Perhaps our communication efforts could do with some attention from time to time too.

But what about our collective role? What role should CAS & the NZVA as a whole be taking in public education about what responsible pet ownership actually means?

In keeping pets and people safe? In legislation?

CAS and the NZVA have developed policies on responsible cat and dog ownership, as well as dangerous dogs, which can be found on the NZVA website and are worth familiarizing yourself with: http://www. nzva.org.nz/policies. These policies are reviewed every three years, or sooner if required, so if you think we’ve got it wrong or a policy is outdated, then please don’t hesitate to offer assistance. These policies help direct our media releases too.

But we need more than just policies and media releases to educate people and manage the current problems with stray cats and dangerous dogs.

On the cat front in particular, there is no legislation to make anyone responsible for the stray cat population. DOC manages the cats on conservation land as with other pests, but for the ‘urban’ strays there is nothing. The SPCA, whether you are agreement with their methods or not, have taken it upon themselves in the past to trap, neuter and rehome or release stray cats when no one else would, but this is not their core function. And for an organization that relies on donations, it puts a huge strain on resources.

Given that there is no legal framework to cover this, a forum of NZVA, CAS,

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(Continued)

Auckland SPCA and the Auckland City Council has been developed with the aim of developing and implementing sustainable solutions to humanely manage the cat population, and promoting responsible pet care in communities as a collaborative effort. Its called the Collaborative Cat Management Forum (CCMF), and has been meeting for around 18 months now to try to establish a workable formula in Auckland between the Council, SPCA and vets that can then be rolled out around the country.

NZVA and CAS are also key stakeholders in the NZ Companion Animal Council who are in the process of reassessing their strategic plan, with the aim of gaining greater visibility. This organization, as discussed in the September editorial, has the aim of being a true representation of all organisations involved in companion animal health and welfare, including vets. The public education opportunities through a forum like this have enormous potential for the future, so ‘watch this space’.

CAS still continues to look at opportunities specifically for vets through the Wellness project. This project has taken many twists and turns to date, but is starting to evolve into a project we can get our teeth into and promote the profession at the same time.

Another ‘watch this space’!

So there is a long way to go on the public education front to happier and healthier pet friendly communities, but every little bit helps. There are some outstanding contributors already leading the way, but they need our support. Ideas and offers of assistance are always welcome, but don’t forget you as an individual can make a difference by helping just one family – have that conversation today! n

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From your society Summary CAS Executive Committee Meeting Held NZVA Offices, Wellington on 13 November 2014 Attendance: Catherine Watson, Aimee Brooker, Rochelle Ferguson, Kate Hill, Helen Beattie, Brendon Bullen, Sarah Fowler, Hannah Bain, Gill Taylor, Pauline Calvert. Apologies: Warren Stroud, Viv Lintott.

Matters arising from previous minutes and correspondence: We agreed to put Pauline Calvert forward to represent CAS on the NZVA AMR working group. Recent member surveys showed that around 1/3 of members would be happy to receive their CAS newsletter in an electronic format and would support a private members only CAS Facebook page. Plans were made to work on improving NZVA prepurchase advice for puppies and kittens and update the current NZVA euthanasia policy.

President’s report – Cath Watson: Cath updated us from the WSAVA congress. We discussed how we would engage with this global forum and the preference was to support Australia with an Oceania presence as the expense required to exert NZ’s limited influence on WSAVA outweighs the benefits.

Newsletter Editor’s report – Sarah Fowler: Discussion revolved around publishing the newsletter in an electronic format. It is very important the advertisers and members are happy with any changes.

CAHF and CAS Grants Update: Educating the Educators awarded $9,000 this year with $7000 being distributed. The sponsor of the Practitioner on Sabbatical Grant has withdrawn. CAS will offer a 2 week sabbatical for 2015 and then decide how best to support practitioners with their CPD in the future.

The speaker’s kit appears to be poorly utilised by regional branches so we plan to find out why with a view to reinvigorating this in 2015 and tie it into the webinar project.

Guests – Andy David and Stevenson Stevenson from Zoetis: Andy presented Zoetis’ promotional material on antibiotics that they plan to release next year in conjunction with a roadshow. The material is based on Australian guidelines produced by the Australian Infectious Disease Advisory Group (AIDAP).

They will be releasing a 4mL vial of convenia. He emphasized the following: Zoetis are interested in scientific outreach, scientific research and stakeholder outreach. Along with ADIDAP they are also involved with responsible use of AB in agriculture (RUAA). They take antimicrobial resistance (AMR) seriously – globally, regionally and at country level. They are committed to the maintenance of veterinary professional discretion in the prescription

of antibiotics. Controls and restrictions should be evidenced based – both evidence for the mandate and evidence that the desired outcome the mandate was made for is being achieved. The ultimate goal is the preservation of antibiotic utilisation for human health. Discussion following the presentation included the point that this document may cause confusion for practising veterinarians as some recommendations are different to the FECAVA guidelines that CAS has previously circulated. CAS will collate our concerns and provide feedback to Zoetis but will also note our appreciation in being given the opportunity to comment.

Guest – Janet Molyneux – Directory Veterinary Teaching Hospital: Janet gave us an overview of the building project at Massey. It is expected to be completed in 2020 at a cost of $100 million. There are plans to increase the number of veterinary students trained each year with a plan to reach 120–140 in 2016. They have done some modelling to workout the workforce requirements and don’t believe that the increased intake will result in an oversupply. The new vertically integrated curriculum is now in its second year and Janet updated us with recent staff changes.

Guests – NZVA – Julie Hood, Peter Benstead, Callum Irvine, Leanne Fecser and Shannon Leader. We were updated on initiatives for marketing the profession, a new coordinated approach to AMR in association with MPI across both animal and human health, and the NAWAC submission on inherited diseases of cats and dogs, along with a draft CPD calendar for 2015.

The animal welfare act is set to pass early next year and doesn’t eliminate tail banding.

Guests – World Animal Protection (WAP) – Wayne Ricketts and Bridget Vercoe: WAP are launching a website in February 2015 to help owners of pets make preparations for them in a disaster. They emphasised that owners need to be educated to realise that they are legally responsible for their animals in the event of a disaster – this obligation is only negated if the situation threatens their own life. Following the Christchurch earthquake MPI now have the overall responsibility for animals during a disaster. They thought that we should be presenting this information to owners of new puppies and kittens and this website will provide support that can be included in clinic’s new owner packs.

Inherited disorders – Brendon reported back from a meeting with NZKC and the NZVA that there was willingness from NZKC to work with vets to improve animal health. NZKC were concerned about accessing specialist vets for eye testing and wondered if we could explore the option of a limited specialist registration for a veterinarian to certify eyes for breeding purposes Next meeting date February 2015.

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NZVA CAS members are encouraged to apply for these Grants and Scholarships:

The New Zealand Veterinary Association Companion Animal Society

Hill’s Pet Nutrition/CAS Educating the Educators Scholarship This scholarship provides assistance for veterinary educators to attend advanced level continuing education events outside New Zealand. We recognise the importance in supporting our leading veterinarians’ participation in international conferences to ensure they remain up to date. With the terms of the scholarship we also encourage the dissemination of this knowledge to the wider CAS membership through articles in the CAS Newsletter and presentations to regional branches.

This scholarship is open to both CAS members and non-members – with CAS members being more generously supported. Applications are considered at the end of March and September each year but can also be made on a case by case basis. The scholarship provides $10,000 per annum to be divided between applicants. We are very grateful to Hill’s Pet Nutrition as the principle sponsor along with support from Massey University Institute of Veterinary, Animal and Biomedical Sciences and VetLearn.

Please email the CAS Secretary Rochelle Ferguson cas@vets.org.nz for more information or see our website.

Thanks to Hill’s Pet Nutrition for their ongoing support

CAS/CAHF Annual Project Grant 2015 Sponsored by Virbac The Companion Animal Health Foundation (CAHF) is a charitable trust established by the Companion Animal Society to fund research projects that will enhance companion animal health and welfare.

The CAHF website has a list of the projects that have been supported by the CAHF and details of the papers published following this research. Applications are invited from CAS members each March and September for funding towards research projects that meet the aims and objectives of the CAHF. Application details along with the terms and conditions are also available from the website or by contacting the CAS Secretary Rochelle Ferguson on cas@vets.org.nz

CAS Practitioner on Sabbatical Grant 2015 The NZVA Companion Animal Society (CAS), welcomes applications from CAS members with at least three years’ experience in Companion Animal practice for the Practitioner on Sabbatical (POS) Grant 2015.

If you wish to develop a particular skill in an area of interest, or are studying for post-graduate qualifications, this grant will help you achieve your goals. The grant will support the successful candidate by paying $1250 for each week of the sabbatical as well as a payment of $250 each week to the hosting practice.

Create a CPD course tailored to your own specific interests and requirements. Spend two weeks working on a project, preparing for relevant examinations, participating in distance learning or upgrading your skills.

Previous candidates have furthered their interests in orthopaedic surgery and ultrasonography by spending time with specialists in private practices and at the Massey Veterinary Teaching Hospital.

The sabbatical is flexible – take a full fortnight or two weekly periods to best suit you and your practice’s schedule.

On completion of the sabbatical, CAS would like you to share your experience (including skills learnt and knowledge gained) with the wider veterinary profession via: 1) a formal report, 2) an article to be published in the CAS Newsletter and 3) by delivering a presentation to your regional NZVA branch.

Further details and application forms can be obtained from the CAS Secretary Rochelle Ferguson by emailing cas@vets.org.nz Applications for 2015 close on 31st March 2015.

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Apology Due to a computer gremlin the heading of the advertisment for Imex Medical Technology in the December 2014 issue of the CAS Newsletter was missing a line. It should have read: “The heart of a good X-Ray system is your X-Ray unit”.

We unreservedly apologise for this mistake.

EYEVET Services Limited

Joonbum Seo & Hania Klubokowska December 2014, Volume 25(4), Pp28–32

Article of the Issue Winner Paper: “An intrathoracic bleeding peripheral nerve sheath tumour.”

Helpful hint:

HOW TO GET THE BEST POSSIBLE RESULTS FOR PRESENTATION OF FIGURES IN YOUR ARTICLE

Send any pictures separately rather than part of the word document within the article you have written. When figures are combined as part of a word document they do not transfer with the best possible quality and lose some definition. It is therefore better to send the figures separate to the text but put the captions to the figures at the end of the text.

CASE REPORTS Have you seen an interesting case recently? Been considering writing it up for the Newsletter? This is why you should:

A payment of $150 is now paid for every published report (i.e. articles submitted by practitioners not as part of requirements for receiving a CAS grant)

Guidance on preparing case report manuscripts is now available on the CAS website or by emailing the editor (sarah.fowler@gmail.com)

Deepen your understanding, share your knowledge and skills with your colleagues, see your name in print!

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Haemangiosarcoma in dogs Deepti Deshpande1 BVSc & AH, MVS and Boyd R Jones2 BVSc, FACVSc, DECVIM-Ca, MRCVS Introduction

This review of haemangiosarcoma in dogs should revise your knowledge about the pathobiology of the neoplasm, its diagnosis and treatment and importantly, provide some information about recent research and potential diagnostic and therapeutic options for the future.

Haemangiosarcoma is a malignant neoplasm originating from multipotential bone marrow-derived stem cells, with their differentiation arrested at the haemangioblast or angioblast stage (LameratoKozicki et al., 2006). This tumour accounts for 5% to 7% of the total neoplasms in dogs (Schultheiss, 2004).

The German shepherd, Labrador retriever and golden retriever are over represented and show a genetic predilection to HSA (Schultheiss, 2004). Alterations in the expression of a few heritable genes such as the up-regulation of Vascular Endothelial Growth Factor Receptor 1 (VEGFR I), down-regulation of Major Histocompatibility Complex (MHC I) and downregulation of Thrombospodin-3 (TSP-3) predispose individuals of the breed to these tumours (Tamburini et al., 2009).

The other primary aetiology of HSA is from novel genetic mutations (Yonemaru et al., 2007). Mutations of tumour suppressor genes play an important role in the pathogenesis of HSA. The presence of a mutation in the p53 gene has been associated with angiosarcoma in humans (Naka et al., 1997 as reviewed by Yonemaru et al., 2007) but this finding has been challenged

by Yonemaru et al. (2007), who suggested that it is an alteration of the p16-cyclin D1-retinoblastoma pathway rather than a p53 mutation that is associated with HSA. The mutant protein stimulates transition from G phase to S phase of the cell cycle, increases resistance to apoptosis and may contribute to accumulation of additional mutations resulting in tumour progression. Deletion of the Phosphatase and Tensin homolog (PTEN) gene from chromosome 10 has been proven to increase the susceptibility to HSA in dogs and these deletions also play a role in the pathogenesis and behaviour of these tumours (Dickerson et al., 2005). The PTEN mutation results in increased cell proliferation, decreased apoptosis and increased angiogenesis (Dickerson et al., 2005).

Genetic mutations thus play a vital role in tumour progression and metastasis.

An obvious association between HSA and exposure to radionuclides was established in beagles exposed to inhalant radionuclides with over 40% of the dogs developing neoplasms in their lungs, liver and bone (Benjamin et al., 1975). HSA in humans has been associated with exposure to vinyl chloride, thorium dioxide and arsenicals (Falk et al., 1981). There is no evidence that carcinogens are a potential cause of HSA in dogs but the role of environmental carcinogens in the development of HSA is open.

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Cutaneous HSA is common in lightly pigmented and sparsely haired breeds such as beagles, bloodhounds, white bulldogs, English pointers, salukis, Dalmatians, and whippets. The increased occurrence of cutaneous HSA in the ventral glabrous skin folds of the above mentioned breeds suggests an association with exposure to solar radiation (Calmon, 2002).

Clinical presentation

The most common site for primary visceral HSA in dogs is the spleen (Brown et al., 1985) but not all dogs with splenic enlargement have haemangiosarcoma!

Primary tumours also occur frequently in the right atrium (25%), subcutis (13%), liver (5%), and other organs (1–2% in kidney, urinary bladder, bone, tongue, prostate). Five to nine per cent of HSA occurs in the liver-spleen-atrium simultaneously (Nelson and Couto, 2009). HSA is highly malignant with 80% of dogs having distant metastasis at the time of their first examination (MacEwen, 2007).

HSA commonly metastasizes to the liver, omentum, mesentery, lungs and brain by either a haematogenous route or by transabdominal implantation after rupture of the primary tumour (MacEwen, 2007). Because metastasis develops early in the disease the prognosis is often poor for most dogs. HSA overexpresses a growth factor for angiogenesis which results in extravasation of the tumour cells in the vasculature (Clifford et al., 2000) an event which aids in the development of distant metastasis and thus multifocal disease. These neoplastic cells seed in different organs and rapidly develop into large tumours (Bergman, 2012). HSA affects the normal function of the organ containing the primary tumour and organs such as the lungs and heart – common sites of metastasis. The different anatomical locations of HSA result in a wide spectrum of clinical signs and presentations. The clinical signs of HSA are often vague and vary according to location of the tumour (MacEwen, 2007). Sometimes the clinical manifestations are very nonspecific such as anorexia, vomiting, weakness or lethargy. Most dogs are presented due to episodes of collapse as a result of rupture of an abdominal tumour mass. Some dogs collapse due to acute blood loss and hemoperitoneum.

The dog may recover without medical intervention after reabsorption of red blood cells from the peritoneal cavity or “autotransfusion”. In other cases haematological and haemostatic abnormalities may lead to disseminated intravascular coagulation (DIC) or pericardial and thoracic effusions which can lead to cardiac tamponade and death. Such varied clinical presentations make definitive diagnosis a challenge (MacEwen, 2007).

Diagnosis

Haematology, biochemistry and imaging techniques aid in identifying the primary body system involved and also assist staging the tumour which is an

Veterinarian, Acumed Veterinary Speciality, Kandivali East, Mumbai, India Professor Emeritus Massey University, Palmerston North

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important part of HSA diagnosis. Staging is crucial to determine the prognosis and to determine whether treatment is warranted (MacEwen, 2007).

Anaemia and spontaneous bleeding are common with HSA regardless of the primary location or stage.

Anaemia is associated with intracavitary bleeding or microhaemangiopathic haemolysis with bleeding associated with DIC or thrombocytopenia. There is a wide range of haematological and haemostatic changes including anaemia, thrombocytopenia, the presence of nucleated red blood cells (RBC) and evidence of RBC fragmentation (schistocytes, acanthocytes). Anaemia, schistocytosis and acanthocytosis are more common in dogs with HSA of the spleen, atrium or viscera. There is often abnormal coagulability with thrombocytopenia.

Haematological as well as haemostatic abnormalities make some dogs inappropriate candidates for surgical biopsies thus making definitive diagnosis difficult.

HSA cells can be identified in tissue aspirates or smears but are not easily identified in effusions. The probability of a confirmed diagnosis from cytology of effusions is less than 25% (Nelson and Couto, 2009).

Imaging techniques such as radiography, ultrasound, echocardiography and computed tomography may identify unique imaging patterns of HSA and can locate the site of the primary tumour and/ or of metastases. Ultrasound is the most reliable technique for the diagnosis of cardiac and abdominal HSA. Tissue-enhanced contrast ultrasound, with use of bubble contrast agents, aids early detection of metastatic hepatic haemangiosarcoma nodules (Webster and Holloway, 2008). CT or MRI may be indicated for selected cases.

However, histopathology remains the only available confirmatory diagnostic tool. HSA cells can be identified and histochemically are positive for von Willebrand’s factor in 90% of cases. Deepseated or intracavitary tumours require surgical biopsy (MacEwen, 2007). Fine needle aspiration is contraindicated in these tumours, due to the risk of haemorrhage and the potential for seeding neoplastic cells and inducing metastasis.

With the non-invasive diagnosis of HSA being a challenge and risks involved with surgical biopsy, current research is focused on methods of accurate pre-surgical diagnosis. Some of the angiogenic growth factors are overexpressed in HSA and the detection of these factors may become useful for early diagnosis.

Increased plasma concentration of Vascular Endothelial Growth Factor (VEGF) and elevated urine concentration of basic Fibroblast Growth Factor (bFGF) have been observed in dogs with HSA. The serum cardiac troponin I concentration was higher in dogs with HSA compared to concentrations determined in other cardiac diseases (Shaw et al., 2004). It has been reported that the serum collagen XXVII peptide concentration in dogs with many metastatic HSA masses was 9.5-fold higher than in healthy dogs and thus identification of this peptide can be used as a supportive diagnostic test for HSA (Kirby et al., 2011). Recent studies have also aimed at increasing the specificity and sensitivity of diagnostic tests for diagnosis of HSA. Immunohistochemistry has

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been employed to identify specific HSA biomarkers (Sabattini and Bettini, 2009). These different markers help to identify the neoplastic HSA cells accurately.

Claudin-5, Factor VIII and CD31/PECAM are immunohistochemical antibody assays that have been used to diagnose HSA (Jakab et al., 2011).

Concentrations of the molecular signature proteins such as retinoblastoma protein (Rb), phosphor-Rb and cyclin D1 are higher in HSA patients than those measured in healthy dogs (Yonemaru et al., 2007).

These different biomarkers and molecular signature proteins have great potential as additional tests for the early detection of HSA. The refinement of biomarker diagnosis of HSA will occur in the future and assist early diagnosis of HSA, especially in predisposed breeds.

Treatment

Although surgery remains the primary treatment of choice for HSA, the aggressive nature of this tumour often warrants combination therapy. Adjunct chemotherapy and palliative radiation therapy have been undertaken with variable success. Therapeutic trials with immunotherapy, biological response modifiers, a novel allogenic canine HSA vaccine and antiangiogenic therapy are new and in the initial investigation phases (Bergman, 2012).

Different stages of HSA have a different prognosis and survival times. Thus it is crucial to stage each dog with HSA as the treatment plan (or decision not to treat) is determined by the stage (Ogilvie et al., 1996). Staging of HSA uses the findings of the diagnostic techniques mentioned above. The following staging system is used in canine HSA (Table 1, MacEwen, 2007).

Table 1.

Staging for canine haemangiosarcoma

T primary tumour T0

No evidence of tumour

T1

Tumour less than 5 cm in diameter and confined to primary site

T2

Tumour 5 cm or greater or ruptured: invading subcutaneous tissues

T3

Tumour invading adjacent structures, including muscle

N regional lymph nodes N0

No regional lymph node involvement

N1

Regional lymph node involvement

N2

Distant lymph node involvement

M distant metastasis M0

No evidence of distant metastasis

M1

Distant metastasis

Stages I

T0 or T1, N0, M0

II

T1 or T2, N0 or N1, M0

III

T2 or T3, N0, N1 or N2, M1

A more practical staging system for HSA which is easier to follow and is more commonly used by clinicians classifies HSA into three stages based on the gross appearance (Table 2).

Table 2.

Classification of HSA based on gross appearance

Stage I

Primary tumour only

Stage II

Primary tumour with splenic rupture or lymph node involvement

Stage III

Primary tumour with splenic rupture or lymph node involvement and evidence of distance metastasis

Since HSA affects the function of vital organs, the mean survival time of the patient is often very short but reports show that early diagnosis and treatment

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of HSA, especially in stages I and II, can significantly increase the mean survival time (MacEwen, 2007).

Surgery remains the treatment of choice; the gold standard therapy for HSA (Bergman, 2012). It should be as aggressive as possible, removing all the local affected tissue. However, in spite of complete surgical resection with clear margins, micro-metastasis can, and often has occurred (Clifford et al., 2000).

An exception is primary cutaneous HSA without hypodermal invasion, which has a good prognosis after surgical resection with a mean survival time of 780 days (Bergman, 2012).

Post-surgical adjuvant chemotherapy is recommended and a choice should be made based on staging and the clinical findings in each individual case (Clifford et al., 2000). Chemotherapeutic protocols using doxorubicin, doxorubicin with cyclophosphamide, vincristine with cyclophosphamide and doxorubicin, and dacarbazine with vincristine have been used (Bergman, 2012). The survival time varied according to the stage of tumour and according to which protocol was followed. There was an increased survival time over surgery alone. The presence of metastases was not a negative prognostic factor for the three drug VAC (vincristine, doxorubicin and cyclophosphamide) protocol but survival time was short; median 140 to 200 days (Alvarez et al., 2007, cited by Nelson and Couto, 2009.) Palliative radiation therapy has successfully reduced the size of retroperitoneal HSA tumours (Hillers et al., 2007).

Metronomic chemotherapy (continuous low-dose oral chemotherapy with standard chemotherapy drugs) has been applied successfully in order to reduce the adverse effects of high dose chemotherapy with equivalent survival times (Lana et al., 2007).

A different aspect of chemotherapy has been exploited which targets angiogenesis in HSA. HSA is known to be associated with overexpression of angiogenic factor. Hence, antiangiogenic chemotherapeutics such as tetracycline and the analogue minocycline used in combination with antineoplastic drugs resulted in marginally increased survival time (Sorenmo et al., 2000).

In spite of all the different therapeutics available, the prognosis of HSA remains guarded. Immunotherapy and biological therapies have recently gained favour.

Macrophage-activating agents such as liposome-encapsulated muramyl tripeptidephosphatidylethanolamine (L-MTP-PE) appear to have tumouricidal activity (Vail et al., 1995). A novel allogenic tumour lysate vaccine for HSA in conjunction with doxorubicin therapy can slightly prolong survival time (U’Ren et al., 2007). An oncolytic virus (parvovirus MVMp) has been investigated as a vector to deliver the therapeutic transgene IP-10 in HSA tumour cells in mice, a process which may have future therapeutic potential for dogs.

The observed survival time of patients following diagnosis of HSA is often not more than six months to one year. Elaborate surgical procedures, with adjuvant chemotherapeutic and other therapeutic options have not been able to extend this mean survival time beyond 220 days (Clifford et al., 2000).

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During my 40 years in practice (BJ) there have been few significant advances for treatment of this neoplasm. The lack of diagnostic techniques for the early diagnosis of HSA, limited treatment options and the short survival time with any treatment is concerning for all veterinarians. Elaborate research is being conducted throughout the world to attempt to find better ways to manage this neoplasm. Watch this space!! Jon Bray, at IVABS, Massey University, has a major research interest in sarcomas, their diagnosis and treatment, including HSA. Jon is interested in referral of dogs with HSA. I hope he can help!

Summary comments

• HSA is a common neoplasm in middle-aged and older dogs.

• There is a breed predilection: German shepherd, golden retriever and others.

• The most common organs of origin are the spleen (50%), right atrium (25%), skin and subcutaneous tissues (13%).

• Not all dogs with splenic enlargement have HSA (50%)!

• Clinical signs depend on the location of the tumour.

• Intracavitary bleeding, especially leading to abdominal distension after rupture of an intraabdominal tumour(s), is common.

• HSA is highly malignant and metastasis has occurred in most dogs at the time of first diagnosis (80% cases).

• Anaemia, acanthocytosis, schistocytosis and thrombocytopenia are supportive of a diagnosis of haemangiosarcoma. You have to do a blood smear.

• Coagulopathies and DIC are present in some cases.

• A diagnosis can be made on cytological and histopathological findings.

• Imaging is essential to identify the primary tumour and the presence and location of metastases and for staging.

• In the future the application of specific biomarkers for diagnosis will allow early and specific diagnosis.

• Surgery is the gold standard treatment but results are poor and depend on the stage (1 year survival <10%).

• The exception is primary dermal HSA where surgery has better results.

• The results of surgery and adjuvant chemotherapy or radiation therapy are marginally better than surgery alone but survival is still very short (median 140–200 days).

• Biological response modifiers and antiangiogenic agents may be treatment options in the future.

References

Benjamin SA, Hahn FF, Chiffelle TL, Boecker BB, Hobbs CH, Jones RK, Snipes MB. Occurrence of Hemangiosarcomas in Beagles with Internally Deposited Radionuclides. Cancer Research, 35(7), 1745–55, 1975 Bergman PJ. Haemangiosarcoma. In: SJ Ettinger and EC Feldman (Eds.), Textbook of Veterinary Internal Medicine (7th ed., Vol. 2). Saunders Elsevier, St Louis, USA, 2012 Brown NO, Patnaik AK, MacEwen EG. Canine hemangiosarcoma: retrospective analysis of 104 cases. Journal of the American Veterinary Medical Association, 186(1), 56–8, 1985

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Calmon, JP. Solar dermatosis. Part 2: tumours induced by UV rays. Pratique Medicale et Chirurgicale De L Animal De Compagnie, 37(4), 269–79, 2002 Clifford CA, Hughes D, Beal MW, Mackin AJ, Henry CJ, Shofer F, Sorenmo KU. Plasma Vascular Endothelial Growth Factor Concentrations in Healthy Dogs and Dogs with Hemangiosarcoma. Journal of Veterinary Internal Medicine, 15(2), 131–35, 2001 Clifford CA, Mackin AJ, Henry CJ. Treatment of Canine Hemangiosarcoma: 2000 and Beyond. Journal of Veterinary Internal Medicine, 14(5), 479–85, 2000 Dickerson EB, Thomas R, Fosmire SP, Lamerato-Kozicki AR, Bianco SR, Wojcieszyn JW, Modiano JF. Mutations of Phosphatase and Tensin Homolog Deleted from Chromosome 10 in Canine Hemangiosarcoma. Veterinary Pathology Online, 42(5), 618–32, 2005 Falk H, Herbert J, Crowley S, Ishak,K, Thomas L, Popper H, Caldwell G. Epidemiology of hepatic angiosarcoma in the United States: 1964–1974. Environmental Health Perspectives.

41, 107–13, 1980 Hillers KR, Lana SE, Fuller CR, LaRue SM. Effects of Palliative Radiation Therapy on Nonsplenic Hemangiosarcoma in Dogs. Journal of the American Animal Hospital Association, 43(4), 187–92, 2007 Jakab C, Halasz J, Kiss A, Rusvai M, Galfi P. Claudin-5 protein is a new differential marker for histopathological differential diagnosis of canine hemangiosarcoma. Histology and Histopathology, 24, 801–13, 2009 Lamerato-Kozicki AR, Helmb KM, Jubalaa CM, Cutterc GC, Modianoa JF. Canine hemangiosarcoma originates from hematopoietic precursors with potential for endothelial differentiation. Experimental Hematology, 34(7), 870–78, 2006 Lana S, U’ren L, Plaza S, Elmslie R, Gustafson D, Morley P, Dow S. Continuous Low-Dose Oral Chemotherapy for Adjuvant Therapy of Splenic Hemangiosarcoma in Dogs.

Journal of Veterinary Internal Medicine, 21(4), 764–69, 2007 MacEwen EG. Chapter 32 – Miscellaneous Tumors. In: Withrow SJ, Vail, DM (Eds.), Withrow and MacEwen’s Small Animal Clinical Oncology (Fourth Edition). Pp 785–823. W.B. Saunders, Saint Louis, USA, 2007 Naka N, Tomita Y, Nakanashi et al. Mutation of the P-53 tumour suppressor gene in angiosarcoma. International Journal of Cancer, 71, 952–955, 1997 Nelson RW, Couto CG. Selected Neoplasms in Dogs and Cats, In: Small Animal Internal Medicine, pp. 1195–1197. Mosby Elsevier, St Louis, USA, 2009.

Ogilvie GK, Powers BE, Mallinckrodt CH, Withrow SJ. Surgery and Doxorubicin in Dogs With Hemangiosarcoma. Journal of Veterinary Internal Medicine, 10(6), 379–84, 1996

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Sabattini S, Bettini G. An Immunohistochemical Analysis of Canine Haemangioma and Haemangiosarcoma. Journal of Comparative Pathology, 140(2–3), 158–68, 2009 Schultheiss PC. A Retrospective Study of Visceral and Nonvisceral Hemangiosarcoma and Hemangiomas in Domestic Animals. Journal of Veterinary Diagnostic Investigation, 16(6), 522–6, 2004 Shaw SP, Rozanski EA, Rush JE. Cardiac Troponins I and T in Dogs with Pericardial Effusion. Journal of Veterinary Internal Medicine, 18(3), 322–4, 2004 Sorenmo K, Duda L, Barber L, Cronin K, Sammarco C, Usborne A, Shofe F. Canine Hemangiosarcoma Treated with Standard Chemotherapy and Minocycline. Journal of Veterinary Internal Medicine, 14(4), 395–8, 2000 Tamburini BA, Trapp S, Phang TL, Schappa JT, Hunter LE, Modiano JF. Gene Expression Profiles of Sporadic Canine Hemangiosarcoma Are Uniquely Associated with Breed.

PLoS ONE, 4(5), e5549, 2009 U’Ren LW, Biller BJ, Elmslie RE, Thamm DH, Dow SW. (2007). Evaluation of a Novel Tumor Vaccine in Dogs with Hemangiosarcoma. Journal of Veterinary Internal Medicine, 21(1), 113–20, 2007 Ward,H, Fox LE, Calderwood-Mays MB, Hammer AS, Couto CG. Cutaneous Hemangiosarcoma in 25 Dogs: A Retrospective Study. Journal of Veterinary Internal Medicine, 8(5), 345–8, 1994 Webster N, Holloway A. Use of contrast ultrasonography in the diagnosis of metastatic feline visceral haemangiosarcoma.

Journal of Feline Medicine and Surgery, 10(4), 388–94, 2008 Wiley JL, Rook KA, Clifford CA, Gregor TP, Sorenmo KU. Efficacy of doxorubicin-based chemotherapy for nonresectable canine subcutaneous haemangiosarcoma.

Veterinary and Comparative Oncology, 8(3), 221–33, 2010 Wood CA, Moore AS, Gliatto JM, Ablin LA, Berg RJ, Rand WM. Prognosis for dogs with stage I or II splenic hemangiosarcoma treated by splenectomy alone: 32 cases (1991–1993). Journal of the American Animal Hospital Association, 34(5), 417–21, 1998 Yonemaru K, Sakai H, Murakami M, Kodama A, Mori T, Yanai T, Masegi T. The significance of p53 and retinoblastoma pathways in canine hemangiosarcoma. The Journal of Veterinary Medical Science, 69(3), 271–8, 2007 Yonemaru K, Sakai H, Murakami M, Yanai T, Masegi T. Expression of Vascular Endothelial Growth Factor, Basic Fibroblast Growth Factor, and Their Receptors (Flt-1, Flk-1, and Flg-1) in Canine Vascular Tumors. Veterinary Pathology Online, 43(6), 971–80, 2006

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Management of a cat with traumatic brain injury Tania Krupitza, BVSc, Small Animal Veterinarian Abstract Traumatic brain injury (TBI) is relatively commonly seen in first opinion practice. Immediate treatment is critical in maximising survival and good outcome in these cases. Treatment focuses on minimising secondary brain injury, which is a cascade of cellular responses subsequent to the initial physical insult.

Many TBI cases suffer concurrent injuries predisposing them to hypotension and hypoxia, and these are two of the most important factors which worsen secondary brain injury. Thus provision of circulatory (intravenous fluid therapy) and respiratory support (oxygen therapy) are the treatment priorities.

Coma scales are used in neurological assessment to characterise injury severity and monitor progression.

This informs treatment decisions, in particular the use of agents which decrease intracranial pressure (ICP).

Regular monitoring is of utmost importance. Other important considerations are treatment of concurrent injuries, choice of anaesthesia and provision of pain relief.

In recent years the practice of giving corticosteroids has been discontinued. TBI is an active area of research and changes in knowledge and treatment recommendations in the last 10–20 years have led to a dramatic improvement in outcomes in human medicine. As few studies have been done in veterinary medicine, guidelines have been extrapolated from the huge body of research in human medicine.

Case management History and physical examination A 9-year-old desexed male Abyssinian cat weighing 5.2 kg was presented immediately after a road traffic accident (RTA). The cat was laterally recumbent and appeared unaware of his surroundings. He was moderately dyspnoeic and had extensive facial swelling, abrasions, mild bilateral exophthalmos, and asymmetry and swelling of the lower jaw. A brief major body system (MBS) assessment at this time showed his mucous membranes (MM) were pale pink, capillary refill time (CRT) was 1 second and heart rate (HR) was 240 bpm. He was panting and appeared moderately dyspnoeic. His mentation appeared abnormal; he was semi-comatose. He was put into an oxygen tent immediately and pain relief was administered (1.5 mg intramuscular morphineA.) After 10 minutes his panting had stopped and he was re-examined. His MM were pink and his CRT was 1 second. HR was 210 bpm; his heart was difficult to auscultate due to increased respiratory noise.

Dyspnoea had improved and there were harsh lung sounds on auscultation. He remained in lateral recumbency and semi-comatose, but he responded

to tactile stimulation and had positive withdrawal reflexes in all four limbs. Due to marked periocular swelling we were unable to assess his pupil size, shape or reactivity. He had negative deep pain sensation to the tail but a positive anal reflex. Rectal temperature was 37.8°C. Gentle abdominal palpation revealed no obvious abnormalities.

Prioritised problem list The most serious problems were considered to be traumatic brain injury and thoracic trauma. Brain injury was considered moderate to severe as he was semi-comatose and had only minimal responsiveness to outside stimuli. Thoracic trauma was most likely to be pulmonary contusions and/or pneumothorax.

This was likely to be mild as dyspnoea was moderate and had improved significantly after a brief period of oxygen therapy. It was also possible that the increased respiratory effort and harsh lung sounds were due to pain or stress, or to neurogenic oedema.

Cardiovascular assessment indicated normal perfusion or mild hypovolaemia.

Other less immediately life threatening potential problems were traumatic injury to the caudal spinal cord, tail paralysis, multiple skull fractures and jaw fracture or dislocation.

Diagnostics and treatment Cardiovascular and respiratory support are considered crucial to successful treatment of TBI so initial diagnostics and therapy were aimed at these systems.

Stressful procedures were kept to a minimum.

A lateral chest radiograph showed no major abnormalities. An intravenous (IV) catheter was placed. Lactated Ringers Solution B was started at a maintenance rate of 10 ml/hour. A 10 ml bolus of pentastarchC was given slowly IV. DexamethasoneD 5 mg was given slowly IV. Oxygen therapy was continued for one hour. After one hour the cat had improved markedly. He was alert and able to sit sternally, but he was unable to stand or walk. His heart rate was 200 bpm and his respiratory rate was 50 breaths per minute.

Orthopaedic assessment showed instability of the mandibular and maxillary symphyses with abnormal jaw occlusion. Repeated thoracic radiography (lateral and DV views) was unremarkable. Intravenous fluids were continued at maintenance rates. Morphine was given as a continuous rate infusion at a dose rate of 0.1 mg/kg/hour.

The following day the cat’s mental status appeared normal. He was able to sit sternally and walk stiffly.

Cardiovascular and respiratory parameters and rectal temperature were within normal range. His eyelids were still swollen and he appeared to have bilateral pupillary dilation but due to the swelling this was very Compound sodium lactate: Baxter Health Care Starquin 200 10%: Biomed Ltd D Dexadreson 2 mg/ml: Intervet B

C A

Morphine sulfate 15 mg/ml: Hospira

Shore Vets, Devonport, taniakru@xtra.co.nz

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difficult to assess. His right eyelid did not appear to close properly.

The cat was anaesthetised with ketamineE/diazepamF and isofluraneG and radiographs were taken of his jaw, skull, lumbar spine and pelvis. Radiographs revealed fractures of the mandibular and maxilliary symphyses and of the left angular process of the mandible and sacrococcygeal separation.

The TBI was resolving and the major problem at this stage was loss of bladder control. However an intact anal reflex suggested that his prognosis for return of bladder function was good. Subsequent therapy focused on stabilization of the jaw fractures, maintenance of hydration and nutrition, pain control and supportive care of bladder function. The cat was anaesthetized a second time and the multiple jaw fractures repaired as follows; The mandibular symphysis was stabilized with a loop of cerclage wire encircling the mandible caudal to the canine teeth, the maxillary fracture was stabilized with a figure of eight wire encircling the maxilliary canines and the mandible and maxilla were wired together to immobilize the fracture of the left ramus of the mandible. To ensure adequate nutrition, an oesophagostomy tube was placed before the jaws were wired closed.

Over the next few days intravenous fluids (Lactated Ringers Solution with 20 mEq/L potassium chlorideH) were continued at maintenance rates. Hills a/dI diet was fed via the oesophagostomy tube. Analgesia consisted of a fentanyl 25 ug/hourJ dermal patch applied after jaw surgery and buprenorphineK 0.06 mg SC for approximately 12 hours (expected onset of efficacy of the fentanyl patch). A five-day course of amoxicillin-clavulanic acidL (50 mg PO twice daily) was given to prevent infection of facial and jaw injuries. Ocular lubricant was applied regularly to both eyeballs.

His bladder was catheterised for two days. He started urinating spontaneously after catheter removal. He was sent home with MeloxicamM at 0.25 mg PO once daily.

Four days after the injury swelling of the eyelids had reduced and eye examination was now possible. He had anisocoria, with mydriasis of the right pupil.

Bilateral direct pupillary light reflexes (PLR) were present, but consensual PLR was difficult to assess.

He had a bilateral positive menace reflex. The oesophagostomy tube was removed after two weeks and mandibular symphyseal wires were removed after four weeks. This cat has done remarkably well. He still has anisocoria but his owner reports he is a happy cat and his behaviour has not altered significantly compared to before the accident.

Discussion

TBI is commonly seen in small animal practice.

Causes include RTA, falls or trauma caused by humans or other animals.

G

H

I

J

K

L

M

E F

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Ketamine 100 mg/ml: Phoenix Pharm Pamlin 5 mg/ml: Parnell Technologies Attane: Bomac Laboratories Ltd Potassium Chloride: Astra Zeneca Hills Pet Nutrition, Inc Durogesic 25: Janssen-Cilag Temgesic: Reckitt Benckiser NZ Ltd Clavulox 50mg tablets: Pfizer Metacam oral suspension for cats: Boehringer Ingelheim

A large number of TBI cases also have concurrent injuries of other organ systems, as in this case. There is controversy regarding the optimal treatment for TBI cases in veterinary medicine, and this partly because very few veterinary studies exist. Most of the studies have been carried out in human medicine or in animal models.1 (Because the pathophysiology of TBI in dogs and cats closely resembles that of human TBI, these animal models can also be at least partially extrapolated to veterinary medicine.2) It is widely recognized that the early treatment of TBI cases is crucial to maximizing chances of a successful outcome. Thus the first veterinarian to see these cases is in the best position to influence outcome. This will often be in first opinion practice. 3 Pathophysiology of TBI TBI is divided into primary and secondary injury.1,4,5,6 Primary injury is due to mechanical trauma and includes concussion (the mildest form of injury with no histological changes), contusion, haematoma, lacerations and haemorrhage. The veterinarian has no influence on primary injury.4,5 Secondary brain injury is due to a variety of biochemical processes initiated by the initial insult. Treatment in TBI cases is focused on minimising these processes by rapid identification and treatment of factors which may exacerbate them.

Pathophysiology of secondary brain injury Brain cell injury results in the release of large amounts of excitatory neurotransmitters, primarily glutamate.

Glutamate has direct and indirect toxic effects on brain cells.6 Massive cell membrane depolarisation leads to ATP depletion, which in turn leads to failure of cell membrane pumps. Sodium and calcium ions accumulate in the cells. Cell oedema occurs, followed by cell damage and possibly cell death.1,5,6 Inflammatory and coagulation cascades are activated, resulting in further damage. The blood-brain barrier (BBB) is disrupted and various chemicals such as nitrous oxide (NO) are produced, leading to altered cerebral vasoreactivity.1 The pathophysiology of brain injury can thus be seen to consist of a large number of interconnected pathways; disruption of any part will lead to exponentially increasing cell damage in a cascade of multiplying effects.

The normal brain has a high and constant demand for oxygen and glucose to maintain energy pumps and metabolic energy production and the integrity of the whole system. 5,6 This becomes even more critical in the injured brain. In the normal brain the constancy of oxygen and energy supply is ensured by cerebral autoregulation. This maintains a constant cerebral blood flow (CBF) over mean arterial pressure (MAP) between 50â&#x20AC;&#x201C;150 mmHg. Trauma can result in loss of this autoregulating ability, making the brain highly sensitive to abnormal systemic blood pressure. Small decreases in MAP can cause significantly decreased cerebral blood flow which can lead to ischaemic or hypoxic cell injury and possibly cell death.1,5 Preventing ICP from rising too much is also critical to outcome in TBI. Increased ICP will initially also cause decreased CBF and possible cell death. If ICP continues to rise brainstem compression may result which can quickly be fatal. The Monro-Kellie

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hypothesis sees the brain as three compartments of variable volume encased by a rigid structure (the skull). These are the brain, blood and the CSF. An increase in one must be accompanied by a decrease in another or there will be increased ICP.1 The traumatized brain is also more sensitive to tissue acidosis, hypoxaemia and hypercapnia or hypocapnia.

Tissue acidosis increases the production of reactive oxygen species, which cause oxidative damage to the neurones. Alterations in carbon dioxide levels can cause either inappropriate vasodilation or vasoconstriction, further compromising CBF.1 Thus the priority in TBI cases is to optimize cerebral blood flow and oxygenation.

Patients with TBI often have co-existing hypovolaemia due to haemorrhage, or hypoxaemia due to pulmonary trauma. So it is vital to provide respiratory and circulatory support if needed, as soon as possible. It has been shown that even brief periods of hypotension and hypoxia worsen TBI.7 In this case, after a very brief clinical assessment, it was judged best to provide immediate oxygen support before undertaking a more thorough examination, or performing any stressful procedures such as IV catheterisation. Morphine was also given at this time.

Pain relief is important in reducing cerebral metabolic rate and thus oxygen demand.7 It would have been better to delay this until an initial neurological exam had been carried out as it can interfere with reflex interpretation and neurological assessment. The cat’s head was slightly elevated but a better option would have been elevation of the whole body at an angle of 15–20 degrees, which decreases ICP.4,8,9 After 10 minutes in an oxygen cage the cat appeared calmer and was given an MBS assessment. He showed some signs of respiratory trauma and was still considered unstable so only a brief lateral chest radiograph was taken. (A DV radiograph would have been a better option as it would have caused less physical compromise.)

Cardiovascular examination indicated that there was only moderate if any hypoperfusion and there was no sign of external or internal bleeding. Better assessment of perfusion would have been possible with blood pressure measurement, pulse characterisation and also PCV/TS testing at time of catheterisation.

An initial blood glucose level would have also been valuable. Both hypoglycaemia and hyperglycaemia can worsen TBI.1 Initial treatment consisted of provision of oxygen and intravenous fluids. Crystalloids were started at maintenance rates and then reassessed after one hour. As the cat was not judged to be suffering from significant hypovolaemia, care was taken not to overload the cardiovascular system with fluids thus predisposing to increased ICP. A bolus dose of colloids was also given. There is controversy in the literature regarding the relative advantages of colloid compared to crystalloid administration in TBI cases.

Colloids persist for longer in the vascular system than crystalloids, providing longer acting support for cerebral perfusion. It is questionable whether this bolus dose of colloids was useful in this case. If the BBB was disrupted, as is often the case with TBI, leakage of the colloid particles into the extravascular

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space may worsen cerebral oedema.1 Colloids are also contraindicated in the presence of severe pulmonary contusions, as they may worsen lung oedema.10 Most recent studies suggest that hypertonic saline (HTS) – with colloid to prolong its effects – is the fluid treatment of choice for severe TBI. Several human studies have shown improved outcomes in patients with severe TBI treated with HTS.11 HTS provides rapid volume resuscitation with a minimal volume of fluid and promotes exit of water from the cells, decreasing ICP and reducing the risk of brain cell damage. 3,4,5 It may also improve brain oxygenation.12 The (human) Brain Trauma Foundation, which reviews current medical research on a regular basis, recommends isotonic crystalloid solutions for hypotensive patients, and HTS for severe TBI cases. Interestingly BTF considers that there is not enough evidence to support the use of HTS in cases of traumatic increased ICP.14 The severity of traumatic brain injury (TBI) can be graded according to the Modified Glasgow Coma Scale (MGCS), which is a variant of a human scoring system for TBI. This assesses three separate categories: level of consciousness, motor activity and brainstem reflexes (pupil size, position and reactivity). Each category is scored out of 6 and higher scores indicate less serious signs.8,13 There have been relatively few studies looking at correlation of MCGS scores with survival; however one recent study in dogs showed an almost linear progression of survival at 48 hours when plotted against coma scale values.13 The MCGS can be used as an objective tool to chart progression as well as providing some prognostic information, though more studies are needed.4 In this cat the initial MGCS findings were (taken after 10 minutes): level of consciousness; 2 (semi comatose, responsive only to repeated noxious stimuli) and motor function; 5 (tetraparesis). As we could not see the pupils we could not assess brainstem reflexes at this time. (Total MGCS score: 7/14.) One hour later his level of consciousness had improved markedly to 5 (depression or delirium, capable of responding but response may be inappropriate). Motor function remained at 5. (MGCS score improved to 10/14.) The 10 minute MGCS assessment in this cat indicated the TBI was severe enough that HTS was indicated.

Unfortunately there was none in the clinic.

Mannitol is an alternative treatment to HTS for severe or deteriorating TBI, and may also have been useful in this case. It works both as an osmotic diuretic and it also has a direct effect on the cerebral vasculature to decrease ICP. Possible side effects include hypotension and ischaemia so it should not be used in hypovolaemic animals. Electrolyte values must be watched closely.9,13 Monitoring in this cat would have been improved with blood pressure monitoring and pulse oximetry. MAP should remain above 100 mmHg and pulse oximetry values above 95%.

This cat shuld not have received dexamethasone.

Corticosteroids have been used in the treatment of TBI in human patients for many years, but they are now absolutely contraindicated. The Corticosteroid Randomization After Significant Head Injury (CRASH) study was a randomised, placebo-controlled, multicentre trial of early use of corticosteroids in over 10,000 human adults with head injury conducted

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during the early 2000s. The trial was stopped early due to a significant increase in mortality in the steroidtreated subjects. The authors were unsure as to why.

The major limitation of this study was that one very high dose of methylprednisolone (IV) was used in all cases. There is no information on the use of lower doses.15 One possible cause of increased mortality is that the cells of the hypothalamic-pituitary axis (HPA) are particularly vulnerable to traumatic injury, and an intact HPA is essential in mounting a suitable stress response in the face of severe illness. Corticosteroids may exacerbate cell death in the HPA, thus worsening an already damaged stress response and leading to increased mortality.16 A better choice of anaesthetic would have been diazepam/propofol.N Though propofol causes respiratory and cardiovascular depression, this can be minimised by monitoring oxygenation and MAP. Propofol also has some neuroprotective function.

Diazepam is useful as it is a safe drug in TBI and also decreases the amount of propofol required.

Ketamine has traditionally been considered a bad choice of anaesthetic agent for TBI. It stimulates the sympathetic system and may increase ICP, and it has been shown to increase cerebral oxygen consumption.7 However this belief has recently been challenged. It is now well recognised that it has some neuroprotective benefits. A recent study showed it reduced ICP and increased cerebral perfusion pressure.17,18 However, more research needs to be done before its use can be recommended.

TBI causes a hypermetabolic state and a recent human study showed that severe undernutrition was linked to increased mortality rates.14 It is logical to assume that early provision of high quality nutrition increases recovery rates.

This case illustrates the evolving nature of TBI research and shows that treatment guidelines are constantly changing. It is likely that previously held assumptions will be challenged in the future, as was the case with corticosteroid use. This case, though initially presenting as a fairly severe TBI, did very well.

6. Leonard SE, Kirby R. The role of glutamate, calcium and magnesium in secondary brain injury. Journal of Veterinary Emergency and Critical Care 12(1), 17–32, 2002 7. Armitage EA, Chan MA, Wetmore LA, Chan DL. Anaesthetic management of the head trauma patient. Journal of Veterinary Emergency and Critical Care 17(1), 5–14, 2007 8. Platt SR. Evaluation and treatment of the head trauma patient. In Practice 27(1), 31–35, 2005 9. Platt, S. Coma Scales. In: Silverstein D and Hopper K (eds).

Small Animal Critical Care Medicine. Pp 410–413. Saunders Elsevier, St Louis Mi, USA, 2009 10. Hughes D, Boag AK (in press). Fluid therapy with Macromolecular plasma volume expanders. In Di Bartola S (ed.) Fluid, Electrolyte, and Acid Base Disorders in small Animal Practice, 4th edition. Pp 20 – 22. Saunders Elsevier, St Louis, Mi, USA, in press.

11. Tyagi R, Donaldson K, Loftus CM, Jallo J. Hypertonic saline: a clinical review. Neurosurgical Review 30 (4), 277–289, 2007 12. Pascual JL, Maloney-Wilensky E, Reilly PM et al.

Resuscitation of Hypotensive Head-Injured Patients: Is Hypertonic Saline the Answer? American Surgeon 74(3), 253–259, 2008 13. Platt SR, Radaelli ST, McDonnell JJ. The Prognostic Value the Modified Glasgow Coma Scale in Head Trauma in Dogs.

Journal of Veterinary Internal Medicine 15 (6), 581–584, 2001 14. Guidelines for the management of severe traumatic brain injury, 3rd edition – Brain Trauma Foundation, 2007 15. LeCouteur RA. Glucocorticoids in Veterinary Neurology/ Neurosurgery: The Good, the Bad and the Ugly. In: Small animal and exotics. Proceedings of the North American Veterinary Conference, Volume 20, pp: 717–719. Orlando, Florida, USA. 2006 16. Chen Xin, Zhang Bin, Chai Yan. Methylprednisolone exacerbates acute critical illness-related corticosteroid insufficiency associated with traumatic brain injury in rats.

Brain Research 1382, 298–307, 2011.

17. Nemergut E. Ketamine: still learning its secrets after 45 years. Journal of Neurosurgery 4 (1), 37–8, 2009.

18. Bar-Joseph G, Guilburd Y, Tamir A, Guilburd J. Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension. Journal of Neurosurgery 4 (1), 40–46, 2009.

n

Acknowledgements to AEC (Animal Emergency Centre, Mt Albert, Auckland) for their care of the cat for several days after jaw surgery, and to Dez Hughes, Associate Professor (BVSc, Dip. ACVECC) and lecturer of Massey MVM paper Emergency Medicine in 2011.

N

Repose 10mg/ml: Norbrook

Reference list

1. Sande A, West C. Traumatic brain injury: a review of Pathophysiology and management. Journal of Veterinary Emergency and Critical Care 20(2), 177–190, 2010 2. Finnie JW. Animal models of traumatic brain injury: a review. Australian Veterinary Journal 79(9), 628–633, 2001 3. Platt SR. Treatment options for head trauma patients.

In: Gething M, Jones, B. (eds). 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland. Pp 498– 500. 2008 4. Beal MW. Approach to the head trauma patient. In: Smith, R.A. (ed). Proceedings of the North American Veterinary Conference, Volume 22, Orlando, Florida, USA. Pp 247–251, 2008 5. Syring R. Assessment and treatment of central nervous system abnormalities in the emergency patient. Veterinary Clinics of North America Small Animal Practice 35(2), 343– 358, 2005

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Intra-ocular prostheses for end-stage eye diseases Craig Irving, BVSc, MACVSc, CertVet Ophthal, Registered Specialist Veterinary Ophthalmologist As an Ophthalmologist where our efforts are directed primarily toward saving an eye and maintaining vision, inevitably one is faced with the prospect of eye removal.

For many ocular conditions we deal with, the eye can be retained even if there is no vision, as I would be the first to agree that a companion animal “looks better” with two eyes.

In a number of situations where there is unrelenting pain or the presence of the eye constitutes a grave risk to the general health of the animal, eye removal or as an alternative, an intra-ocular prosthesis can be used.

Some of the indications for prosthesis insertion are: 1) Some cases of intra-ocular infection, for example, cat scratch injuries.

2) Extreme trauma with scleral and/or lens rupture.

3) Some intraocular tumours.

4) Non-controlled glaucoma.

5) Ongoing and non-controlled uveitis (Figure 1).

6) An eye which has sustained severe trauma internally and is starting to shrink (phthisis bulbi).

Facts

• Owner’s expectations these days are for choices or a number of solutions to their animal’s problems.

Undoubtedly eye removal does give an instant solution to a problem, but the cosmetic effect is variable especially if there is no attempt to prevent sagging of skin at the position of the original lid aperture. This may be less obvious in long-haired dogs but becomes more obvious in the short coated breeds. (Figure 2) • An intraocular prosthesis gives symmetry to the head and there is normal eyelid and ocular movement (Figures 3, 4). Additionally the cornea will change in colour and becomes an overall grey, which will not look a lot different from the

Figure 1. A six-year-old Fox terrier 3 months after ocular prostheses were implanted bilaterally. This dog initially presented with very high intraocular pressures and dislocated cataractous lenses due to bilateral retinopathy causing secondary cataract formation and ultimately lens-induced uveitis with secondary glaucoma. At this stage, the corneal colour is still settling down as there is the normal reaction to the prosthetic insert. In a few months time the redness will disappear and a blue and black appearance will predominate.

original eye, especially if there were corneal changes associated with the disease process that necessitated the surgery e.g. associated keratitis or the corneal oedema of glaucoma.

• The surgery (Figure 5) involves the removal of the entire uveal tract, vitreous, retina and lens, so that one is just left with scleral shell within which the silicon ball is placed. At that point the initial sclera incision is closed under a conjunctival flap.

• In the event of there being buphthalmia (enlarged eye) from a previous glaucomatous episode, correction can be made in the size of the silicone implant so there is symmetry between the two eyes.

a)

b) Figure 2.

Two cases, a) a welsh springer spaniel and b) a Burmese cat, in which both eyes have been removed due to primary glaucoma.

Both have a good quality of life following surgery.

Eyevet Services, craigeyevet@clear.net.nz

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Figure 3.

The two mid-aged terriers shown in this figure both have prosthetic implants in their left eyes. In both cases uveitis caused blockage of aqueous outflow pathways leading to glaucoma. Both have a very good cosmetic result and a comfortable eye with no long-term treatment needed.

Figure 4.

Five-year-old spaniel with an intra-ocular prosthesis in the right eye.

• Postoperatively there is a requirement for several weeks of anti-inflammatory/pain relief medication as well as a precautionary 4 to 5 days of broadspectrum antibiotic cover.

• In my hands, the cost of doing this procedure is marginally greater than eye removal, which I consider a more difficult procedure. I stage it this way to encourage people to take advantage of this procedure.

• The consistent feedback I get from owners is an overwhelming satisfaction for the result and in many cases, sincere thanks for being talked into going along with my advice on the benefits of this procedure.

• I have a short hand-out on the procedure which I give the owners prior to the surgery and this helps immeasurably with the decision-making.

• There are few contraindications for prosthesis insertion. Undoubtedly severe intraocular infection would make it difficult, but I have used them in catscratch injuries where there is a localised area of infection in the vitreous which is eliminated with the presurgical uveal/vitreal removal. Some of the readily identifiable intraocular tumours in dogs e.g. ciliary body adenocarcinomas and melanomas of the iris, are recognised as being well localised and rarely metastasise; these eyes can be candidates

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Figure 5. The instruments used for implantation of an intraocular prosthesis. From L to R; measuring calliper, silicon ball and introducer.

for prostheses. In the case of severe ocular trauma where the sclera or cornea is ruptured, repair of these areas along with insertion of the prostheses can still end up with an excellent result.

• As is the case with eye removal, relief from the intractable pain associated with some ocular diseases becomes obvious within a few days with animals starting to play and interact with the owners in a way they had not recently witnessed.

• In a situation such as glaucoma, topical medical management is difficult and one never really knows just how comfortable the animal is. Additionally the costs for maintaining animals on a therapeutic regime steadily rise and in the long term surpass the cost of this surgery.

• The surgery is applicable for dogs, cats and the equine and has been performed in all of these species For any veterinary surgeons involved in cases which may benefit by this surgery, feel free to contact me as quite a few of the cases are elective and could be assessed prior to a decision being made by myself during my regular trips around New Zealand.

Alternatively some pictures and discussion by e-mail would be adequate.

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Prolonged survival time following medical management of insulinoma-induced hypoglycaemia Neil Stuttle BVSc Case history Poppy, a 6-year-old spayed Tibetan terrier was presented in December 2011 for occasional episodes of periodic weakness and disorientation. On clinical exam Poppy was bright, alert and responsive with no significant findings. A blood sample was taken for inhouse serum biochemistry (Spotchem EZ Chemistry Analyzer). Mild hypoglycaemia was present (serum glucose 2.9 mmol/L, reference range 3.6–6.7 mmol/L).

Liver enzymes (ALP, ALT), total protein, urea, and creatinine were within normal limits.

Poppy was re presented 7 weeks later. The episodes of weakness were now occurring weekly and becoming more prolonged. The episodes appeared to worsen during exercise and improve following rest and feeding.

Poppy again was bright and alert on clinical exam with no abnormalities detected. Blood glucose (Accu chek Advantage glucometer, Roche Diagnostics) was measured at 1.9 mmol/L. A blood sample was taken for a complete blood count (CBC) and biochemistry profile. No significant abnormalities were detected.

Based on the history, hypoglycaemia and lack of other clinical abnormalities, an insulinoma was suspected.

Poppy was started on 0.25 mg/kg prednisone, PO, SID for two weeks (Apo prednisone, 5 mg tablets, Apotex NZ Ltd) to counteract the action of excessive insulin.

No further episodes were noted while Poppy was receiving prednisone however they returned a few days after treatment stopped. Further blood tests (taken 20 weeks after initial presentation) revealed a serum insulin level of 11.3 MIU/L (<5 mIU/L – >20mIU/L) with concurrent blood glucose of 2.6 mmol/L. (Accu Chek Advantage glucometer, Roche Diagnostics) The elevated insulin level with concurrent hypoglycaemia and clinical history of episodic weakness supported a tentative diagnosis of insulinoma (pancreatic beta cell neoplasia). Referral for further diagnostic work-up (e.g. ultrasound) and potentially surgical removal of identified tumours was declined. An abdominal ultrasound examination was performed 21 weeks after the initial presentation at the primary care clinic. No abnormalities of the pancreas were detected (Figure 1). However, a presumptive diagnosis of insulinoma was made based on the clinical signs, persistent hypoglycaemia, insulin levels and response to prednisone. Treatment for presumptive insulinoma was initiated. This consisted of frequent (3–4 times daily) meals of a high fibre diet and restricted exercise to maintain steady blood glucose levels and prednisone (0.5 mg/kg every 48 hours) to promote gluconeogenesis and thus raise blood glucose levels.

Ten months later Poppy began having episodes of weakness again.

Her serum fructosamine (261 umol/L) level confirmed persistent hypoglycaemia, (prolonged hypoglycaemia is indicated by levels < 300 umol/L). Her prednisone dose was increased to 0.5 mg/kg, SID. Hypoglycaemic episodes were managed

Figure 1.

Ultrasonographic image of pancreas

by applying honey (a source of glucose) topically to the gums.

Seventeen months after the initial presentation Poppy started having episodes of weakness once to twice weekly. Her serum fructosamine level (223 umol/L) again confirmed persistent hypoglycaemia.

At this point starting treatment with diazoxide was discussed with the owner but this was declined due to cost. Instead the prednisone dose was increased to 0.5 mg/kg, BID and 0.5 mg/kg, SID on alternate days. This was again increased four months later to 0.5 mg/kg, BID due to increasing exercise intolerance and lethargy. Feeding frequency was increased to 5–6 times daily. A good response was reported by the owner.

An abdominal ultrasound examination in March 2014 (27 months after initial presentation) revealed a 0.76 cm x 0.85 cm hyperechoic nodule in the right limb of the pancreas (Figure 2). As Poppy was experiencing an increasing number of lethargic episodes, her prednisone dose was again increased (to 1 mg/kg BID).

Figure 2. Ultrasonographic image of pancreas hyperechoic nodule (labelled ‘Tumour’)

with

Vet Services Hawkes Bay Ltd, Hastings 4120. Neil.Stuttle@vshb.co.nz

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Poppy was euthanized in September 2014 due to severe lethargy and weakness which was now unresponsive to prednisone (2 mg/kg, BID) and frequent feeding. It had been 33 months (990 days) since Poppy was first presented for this condition. Necropsy revealed a 5 x 4 cm cream lobular mass in the right limb of the pancreas (Figure 3) along with multiple raised cream nodules throughout the liver parenchyma. Histology of the pancreatic mass confirmed an endocrine tumour most suggestive of an insulinoma. Immunohistochemical stains which would have provided a definitive diagnosis were not performed.

Figure 3. The pancreas at necropsy. A 3 cm x 5 cm creamcoloured lobular mass involving the right limb of pancreas is seen on the left in this image. The mass has been incised to reveal its interior appearance.

Discussion

Blood glucose levels are primary regulated by two peptide hormones; insulin, released from the beta cells in the pancreatic islets and glucagon, released from the alpha cells in the pancreatic islets. Insulin is released in response to an increase in blood glucose (typically post-prandially) and acts to reduce blood glucose by moving glucose into cells. Insulin also has anabolic effects promoting synthesis of glycogen and protein and reducing fat metabolism (Kahn, 2005). Glucagon is released in response to a decrease in blood glucose and acts to increase blood glucose levels by promoting breakdown of stored glycogen (Kahn, 2005). Growth hormone, glucocorticoids, catecholamines and possibly thyroid hormones also act in along with glucagon to raise blood glucose (Herrtage, 2009).

Poppy was first presented with non-specific signs of weakness and lethargy which had resolved by the time of examination. No immediate treatment was needed to correct the hypoglycaemia. In moderate hypoglycaemia the patient may present weak and disorientated. The first line of treatment is oral glucose either through feeding or application of honey or golden syrup to the gingival mucosa. If the hypoglycaemia is severe patients may present collapsed or seizuring and parenteral treatment with dextrose or glucose is needed. This involves giving an intravenous bolus of 50% dextrose (1 ml/kg) slowly over 5–10 minutes (Mooney and Peterson, 2004). The goal of treatment is to control the clinical signs of hypoglycaemia but not necessarily to return the blood glucose to normal.

(Mooney and Peterson, 2004). It should be noted that in patients with insulinomas, giving an intravenous bolus of dextrose can be dangerous. In this situation

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dextrose may cause marked insulin release which in turn causes a rebound hypoglycaemia. A vicious hypo-hyperglycaemic cycle can form which can be very hard to break and potentially fatal (Schoeman, 2011).

The most common clinical signs associated with insulin-secreting tumors in dogs are seizures and episodic weakness. Other clinic signs include collapse, ataxia, posterior weakness and muscle fasciculations, polyphagia and weight gain. Peripheral neuropathies have been observed in dogs with insulin-secreting tumours leading to proprioceptive deficits, depressed reflexes and muscle atrophy (Nelson and Couto, 1998).

Insulin-secreting tumours typically affect middleaged to older dogs (mean age 9.5 years, range 3–14 years). A breed predisposition may exist in standard poodles, boxers, fox terriers, German shepherd dogs and Irish setters. There is no sex predilection (Nelson and Couto, 1998). Over a five-year period at Davies Veterinary Specialists (UK), 89% of the dogs diagnosed with insulinoma were diagnosed during the summer. Insulinomas are very rare in cats (Tilley and Smith, 2004).

Differential diagnoses for hypoglycaemia include starvation, sepsis, hypoadrenocorticism, hepatic disease, exogenous insulin excess, xylitol toxicity, uraemia, extrapancreatic neoplasia and insulinoma (Tilley and Smith, 2004). The history and clinical examination ruled out exogenous insulin overdose, starvation and xylitol toxicity.

The CBC and serum biochemistry results showed no evidence of sepsis, hepatic or renal disease.

Classical hypoadrenocorticism was unlikely as serum sodium and potassium levels were within normal limits.

Atypical hypoadrenocorticism (defects of the adrenal cortex causing decreased cortisol secretion but not affecting the electrolytes) was possible. An ACTH stimulation test was needed to rule out atypical hypoadrenocorticism but was not performed in this case.

A tentative diagnosis of insulinoma was made based on the following criteria (Whipple’s triad, Herrtage, 2009): 1. The presence of neurological signs typical of hypoglycaemia, such as weakness, lethargy, confusion or collapse, which may be precipitated by exercise or excitement.

2. Hypoglycaemia (plasma glucose < 3 mmol/L) at the time of the clinical signs.

3. Resolution of clinical signs following feeding or administration of glucose.

Definitive diagnosis of insulinoma is based on serum insulin concentrations of > 20 mIU/L with concurrent hypoglycaemia (blood glucose < 2.7 mmol/L, Schoeman, 2011; Nelson and Couto, 1998). Samples for insulin measurements should be treated carefully in order to ensure accurate results. Samples should be collected into a fluoride oxalate tube, centrifuged, and the serum collected and frozen or chilled during transport to the laboratory. Haemolysed samples should not be used as this results in erroneous insulin values and may also give inaccurately high glucose values. Human insulin assays are valid for canine samples. Measured insulin levels have been used to predict the probability of a beta cell tumour where insulin ranges of >20 mIU/L, 10–20 mIU/L, 5–10mIU/L and <5mIU/L predict the probability as

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high, possible, low and ruled out respectively (Feldman and Nelson, 2004). In this case, Poppie’s serum insulin level was 11.3 mIU/L with a blood glucose of 2.6 mmol/L, indicating that is was “possible” that she had an insulinoma. It should be noted that in this case the blood glucose value taken at the time that insulin was measured was obtained using a hand-held glucometer (Accu Chek Advantage, Roche Diagnostics). Blood glucose measurements taken by glucometers can vary in accuracy by 10% when compared to plasma glucose measured by automated chemistry analyzers (Johnson, 2009).

An initial abdominal ultrasound examination in this case revealed no significant findings. Pancreatic masses may be detectable by ultrasonography as hypoechoic nodules. However in 25% of insulinoma cases the mass may be too small to visualise.

Insulinomas can also be present diffusely within the pancreas. Ultrasonography may also be used to detect metastases which in the case of insulinomas commonly occur within the liver and spleen (Mooney and Peterson, 2004). The sensitivity of ultrasonography is also highly dependent on the resolution of the equipment and the experience of the operator. A definitive diagnosis of an insulinoma can be made on supportive blood results alone. Ultrasonography is used to investigate equivocal blood results or as pre-surgical assessment following confirmatory blood results.

Treatment for insulinoma is either surgical removal of the mass, medical management of chronic hypoglycaemia or a combination of the two approaches (Herrtage, 2009). Surgical removal offers the only chance of cure. The majority (90%) of beta cell tumours are malignant (Fossum, 1997) and 50% of affected dogs have detectable metastatic lesions (regional lymph nodes, liver) at the time of surgery (Fossum, 1997). Fifty percent of all dogs that do not have evidence of metastasis at the time of surgery will be normoglycaemic for at least one year after partial pancreatectomy (Fossum, 1997).

Complications of surgery include persistent hypoglycaemia (due to incomplete tumour resection or unrecognised metastases), pancreatitis, diabetes mellitus, epilepsy and diffuse polyneuropathy. Transient hyperglycaemia can occur in up to one third of dogs following surgery due to suppression of normal beta cells by insulin from the tumour cells (Fossum, 1997).

Medical management can provide good symptomatic control (does not slow tumour growth) and standard treatment consists of dietary management, glucocorticoids and diazoxide (Herrtage, 2009).

Feeding frequent small meals of a diet high in protein, fats and complex carbohydrates acts to decrease postprandial hyperglycaemia which reduces stimulation of the tumour cells, resulting in a lower insulin release (Mooney and Peterson, 2004). Prednisone (0.2–1.0 mg/kg PO BID) increases blood glucose levels by inhibiting the action of insulin and stimulating glyconeolysis (Herrtage, 2009). Diazoxide is a non-diuretic benzothiadiazide antihypertensive agent often successful in controlling hypoglycaemia in patients which are not responding to diet and prednisone alone (Mooney and Peterson, 2004). Diazoxide inhibits insulin secretion, enhances hepatic glycogenolysis and gluconeogenesis and

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inhibits glucose uptake by peripheral tissues (Mooney and Peterson, 2004). Treatment with octreotide (a growth hormone analogue) and streptozotocin (a cytotoxic chemotherapy) have also been used in cases that are refractory to the usual symptomatic therapy (Herrtage, 2009).

The long-term prognosis for a patient with an insulinsecreting tumour is guarded. The mean survival time in one study was 365 days following partial pancreatectomy and 75 days with medical treatment alone (Tobin and Nelson, 1999). A more recent study based on 28 dogs showed an overall mean survival of 547 days (Polton, 2007). Dogs that had a partial pancreatectomy had a mean survival time of 785 days.

Dogs that had a partial pancreatectomy followed by prednisone on relapse of hyperglycaemia had a mean survival of 1316 days (Polton, 2007). The reason for euthanasia/death in most cases was uncontrollable hypoglycaemia. In this case Poppy survived 990 days with prednisone and dietary therapy alone which is markedly longer than the mean survival times from these studies would predict.

Conclusion

Surgical treatment (partial pancreatectomy) has been shown to extend survival times in cases of insulinoma.

However this individual case report highlights that medical management with prednisone and dietary/ exercise management alone can also provide a substantial period of quality life when managing insulinoma-induced hypoglycaemia.

References

Kahn CR, Weir GC, King GL, Moses AC, Smith RJ, Jacobson AM. Joslin’s Diabetes Mellitus 14th edition. Lippincott Williams & Wilkins, Baltimore, USA, 2005 Feldman and Nelson, Canine and Feline Endocrinology and Reproduction 3rd Edition, Saunders 2004 Fossum TW. Surgery of the Endocrine System. In: Small Animal Surgery, TW Fossum (ed), Pp 421–424, Mosby, St Louis, USA, 1997 Herrtage ME. How I Treat Canine Insulinoma, In: Proceedings of the 34th World Small Animal Veterinary Congress WSAVA, Sao Paulo, Brazil, 2009 Johnson BM, Fry MM, Flatland B, Kirk CA. Comparison of a human portable blood glucose monitor, a veterinary portable blood glucose meter, and an automated chemistry analyzer for measuring canine blood glucose concentration. Journal of the American Veterinary Medical Association, 235, 1309–13, 2009 Mooney CT, Peterson ME. Diagnosis and Treatment of Insulinoma. In: BSAVA Manual of Canine and Feline Endocrinology 3rd ed, Pp 200–204, British Small Animal Veterinary Association, Gloucester, UK, 2004 Nelson RW, Couto CG. Disorders of the Endocrine Pancreas . In: Small Animal Internal Medicine 2nd ed, Pp 766– 771 Mosby, St. Louis, USA, 1998 Polton GA, White RN, Brearley MJ, Eastwood JM, Improved survival in a retrospective cohort of 28 dogs with insulinoma.

Journal of Small Animal Practice 48, 151–6, 2007 Schoeman JP. Endocrine Emergencies, In: Proceedings of the 36th World Small Animal Veterinary Congress WSAVA, Jeju, Korea 2011 Tilley LP, Smith Jr FWK. The 5 Minute Veterinary Consult Canine and Feline third edition, Pp 712–713, Lippincott Williams & Wilkins, Baltimore, USA, 2004 Tobin RL, Nelson RW, Lucroy MD, Woolridge JD, Feldman EC. Outcome of surgical versus medical treatment of dogs with beta cell neoplasia: 39 cases (1990–1997), Journal of the American Veterinary Medical Association, 215, 226–30, 1999

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An update on Feline Leukaemia Virus Dr Pru Galloway, BVSc MANZCVS FANZCVS, Registered Specialist in Feline Medicine Feline Leukaemia Virus (FeLV) is uncommon in New Zealand, but I have recently confirmed a small number of cases in young sick stray/rescue cats from South Wairarapa and the Kapiti Coast.

These cats were positive for the FeLV p27 capsid antigen in plasma by a rapid point-of-care lateralflow immunochromatography assay and had clinical findings consistent with the disease, such as severe non-regenerative anaemia. Owing to the low positive predictive value of diagnostic tests when disease prevalence is low (i.e. the likelihood of an animal with a positive test, truly harbouring the disease), infection was confirmed with a test with a higher specificity, in these cases a fluorescent antibody (FA) test on a blood smear. A positive FA test identifies FeLV antigen within leukocytes and platelets and is consistent with persistent bone marrow infection.

Traditionally FeLV infection has been classified into three stages; regressor infection, transient viraemia with latent infection, and persistent viraemia. However polymerase chain reaction (PCR) has identified a new group of cats that are PCR-positive for FeLV in blood but p27 antigen-negative. This has contributed to a change in FeLV nomenclature; the three types of FeLV infection are now known as abortive, regressive and progressive (see Tables 1 and 2).

Table 1.

FeLV nomenclature

Old FeLV nomenclature

New FeLV nomenclature

Regressor infection

Abortive infection

Transient viraemia, then latent infection

Regressive infection

Persistent viraemia

Progressive infection

Abortive infection: virus replicates in oropharyngeal lymphoid tissue, but an effective immunity prevents the development of viraemia.

Regressive infection: viraemia occurs but is short lived (usually 3–6 weeks, but can be up to 16 weeks) and infection is contained before or shortly after bone marrow infection. Cats are infectious while viraemic.

If bone marrow infection occurs, proviral DNA is incorporated into bone marrow stem cells (this stage was formerly known as latent infection, but is now considered a stage of regressive infection).

Features of regressive infection: • Negative for p27 antigen in plasma/serum but positive by PCR for FeLV DNA provirus in blood (PCR detects FeLV DNA integrated in the feline genome).

• FeLV ‘carriers’ i.e. there is no active viral Table 2.

replication. They don’t shed virus in saliva so under natural circumstances they are not infectious to other cats. However they may transmit the virus via blood (so blood donors should be PCR tested for FeLV).

• Are at low risk of developing FeLV related disease but may develop sequestered infections and contribute to some cases of FeLV antigen-negative myelosuppressive disease and haematopoietic/ lymphoid malignancy.

• Reactivation of infection can occur in ~10–15% of cases, as the genes for making a complete virus particle are still present. Reactivation is more likely closer to the time of infection, and becomes increasingly unlikely 1–2 years post infection.

Immunosuppressive doses of corticosteroids can cause reactivation. Reactivated infections have low infectivity to other cats (they may excrete virus in urine and faeces, but not saliva).

Progressive FeLV infection: widespread viral replication occurs in lymphoid tissue, bone marrow, plus mucosal and glandular epithelial cells. Viraemia is persistent and virus is shed in high numbers, especially in saliva. Young and immunosuppressed cats are most at risk and most cats die of FeLV-related disease within three years. Regressive and progressive infections can be distinguished by repeat tests for viral antigen in plama/serum, with the former testing negative for FeLV antigen 16 weeks post-infection at the latest and the latter remaining persistently positive. (Table 2) FeLV vaccination In cats experimentally infected with FeLV: • Vaccination does not prevent regressive infection, provirus integration into the genome or reduce risk of reactivation.

• Vaccination does reduce risk of progressive infection and FeLV associated disease/death.

FeLV prevention: Antigenaemic cats shed large amounts of virus in saliva and to a lesser extent faeces, urine and milk. They should always be separated from FeLV negative cats.

Close contact is required for FeLV to be transmitted, such as sharing food bowls, litter trays and mutual grooming or via biting. Test and removal polices have been instrumental in reducing FeLV transmission and prevalence in breeding catteries and rescue shelters, but logistically this is more challenging in stray/feral cats.

Features of FeLV infection

Infection type

p27 Ag in blood

IFA

PCR [DNA in blood]

RT-PCR [RNA in blood]

FeLV Abs

FeLV shedding

Clinical outcome

Progressive

+ve

+ve [21d]

+ve [high]

+ve

-ve or low

Yes

Regressive

-ve

-ve

+ve [low]

-ve

high

No

Usually healthy, but reactivation possible

Abortive

-ve

-ve

-ve

-ve

high

No

Healthy, protected

FeLV associated disease

Catmed Ltd, Hill’s Pet Nutrition Adjunct Senior Lecturer in Feline Medicine, Massey University

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The risk of transmission in vet clinics is low as the virus is environmentally labile, surviving only minutes outside the host and is susceptible to routine disinfectants.

Routine cleaning and sterilisation of equipment (e.g. dental equipment, endotracheal tubes) plus hand washing and thorough cleaning of food bowls, litter trays and bedding should prevent transmission in the hospital environment. Progressively infected cats should be kept separate from other cats, but they should not be housed in an isolation ward with other contagious cats, such as those with upper respiratory tract infections.

Vaccination should be considered for at-risk naive cats (e.g. young, outdoor, in known at-risk areas. If you haven’t been testing for FeLV, doing so will help establish if it is a problem in your locality). Cats should be tested for FeLV p27 antigen in serum/plasma by ELISA or lateral-flow immunochromatography prior to vaccination; as this is an antigen test maternal antibodies will not give false positives. Given the age related resistance to FeLV, arguably vaccination could continue for the first few years of life only. The latter along with vaccinating subcutaneously as distally as possible in the left hind limb (Left for Leukaemia), may help ameliorate concerns over vaccine associated sarcoma.

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Closing comments

• With the advent of PCR, we now know that ELISA and lateral-flow immunochromatography antigen tests underestimate the true prevalence of FeLV. • The AAFP recommends that the FeLV and FIV status of every cat should be known.

• Although FeLV is considered an uncommon infection in NZ, if it is on the rise, we should be proactive. With the premise of “if we don’t look we’ll never find it” I believe we should be testing kiwi cats for FeLV, while recognising the potential for false positives with low disease prevalence.

References and further reading

Hartmann K. Role of PCR in Feline Leukaemia Virus Infection.

ECVIM-CA Proceedings, Mainz, Germany 2014 Hartmann K. Feline Leukaemia Virus Infection. In: GE Greene (ed), Infectious Diseases of the Dog and Cat, 4th Edition. Pp 108–136, Elsevier, 2012 Hofmann-Lehmann R. Feline leukaemia virus infection: where do we stand? Second International Society for Companion Animal Infectious Diseases Symposium; 2012 2013 American Association of Feline Practitioners Feline Vaccination Advisory Panel Report. Journal of Feline Medicine and Surgery, 15, 785–808, 2013

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PanPac in Brisbane, May 2015 This year the New Zealand Veterinary Association (NZVA) and the Australian Veterinary Association (AVA) bring you the Pan Pacific Veterinary Conference – the largest veterinary gathering in Australasia, being held in Brisbane, Australia from 24–29 May. NZVA’s Companion Animal Society Education Committee has been actively involved with our Australian colleagues in developing an extensive programme incorporating 15 veterinary disciplines with over 130 speakers and 200 scientific sessions over eight consecutive streams.

The Small Animal Stream

Keynote speaker Dr Daniel Chan, Royal Veterinary College Senior Lecturer in Emergency and Critical Care and Clinical Nutrition, will address major critical care challenges, including haemorrhage, the collapsed patient, major trauma and fluid therapy, as well as feeding critical patients and the debate around raw food diets.

Dr Meghan Herron, Assistant Professor and Head of the Behavioural Medicine Clinic at Ohio State University, will address behavioural issues including training puppies and kittens, feline elimination, cognitive dysfunction in dogs and management of the aggressive patient.

Other topics in the Small Animal Stream include: • Anaesthesia presented by Roz Machon • Cruciate and elbow surgery presented by Kyle Clark • Oral tumours presented by Rod Straw • Discussions on aggression presented by Robert Holmes • A series on varying imaging techniques presented by Zoe Lenard • Cancer therapy presented by Maurine Thomson.

The conference includes streams relevant to small animal clinicians including behaviour, practice management, dental and acupuncture.

Dr Michelle Tilghman, contributing author to Veterinary Acupuncture: Ancient Art to Modern Medicine will address the acupuncture stream. She will discuss diagnosis and treatment of common canine lamenesses, multimodal treatment of osteoarthritis, neurological classification of disc disease and trigger point therapy.

Our own Dr Chris Thomson will underpin these presentations with a lecture on the neurophysiological basis of acupuncture.

Plenary sessions for everyone

Nobel Prize winner and immunologist Professor Peter Doherty, an internationally acclaimed Queensland veterinary graduate (1963), opens the conference on the Monday with “From vet school to the Nobel prize and beyond”.

Tuesday’s plenary session is delivered by Annabel Crabb, renowned journalist and political commentator.

Her topic – “Having it all doesn’t mean doing it all”.

On Wednesday economist Michael Knox will discuss “Why economists matter”.

“One health and superbugs: The ever-growing threat that includes our food supply” is Thursday’s Ben Cuneen Memorial Plenary (named in honour of the Australian veterinarian who died in in 2008 of Hendra virus contracted while treating a sick horse). This will be presented by infections disease physician and microbiologist Professor Peter Collignon.

Forums, workshops, field trips and networking The member forum “Convincing the public to pay vets what they’re worth! Shaping your association” facilitated by Jane Caro, a social commentator, writer and lecturer based in Australia, is strongly relevant to all veterinarians – and one you won’t want to miss.

There is also a forum on animal welfare on the Sunday before the conference. It is facilitated by Mark Strom, a well-known Australian strategic thinker and storyteller.

The conference also offers a variety of breakfast sessions, workshops and field trips. There is a packed programme with dozens of local speakers, the largest veterinary trade exhibition in the region and a complete social programme giving you plenty of chances to connect with your colleagues.

Register now to take advantage of the early bird rates This is a conference you won’t want to miss.

Head to www.panpac2015.com to view the full programme and register. Register before 20 April to take advantage of the early bird rates at www.panpac2015.com.

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Practitioner on sabbatical report Kate Heller, BVSc, Mixed animal practitioner I was lucky enough to be awarded the 2014 MSD Practitioner on Sabbatical Grant. For my sabbatical I had the privilege of being able to work alongside Chris Warman and his radiology team at the Veterinary Specialist Group in Auckland. I spent two weeks in the clinic there during which time I saw a large variety of interesting cases, both outpatient ultrasounds and also cases from within the specialist practice.

I decided to spend the majority of my time there focusing mainly on the ultrasonography aspect of radiology as my practice has recently invested in a new ultrasound machine and I have a particular interest in developing my skills and utilising this diagnostic tool more within the practice. I think ultrasound is often a much under-utilised tool in our armour of diagnostics when investigating and working up cases. Its use can be many and varied but also has its limitations which it is important to be aware of. Throughout my time with Chris, I observed how ultrasound was used to diagnose intestinal foreign bodies through to potential neoplastic disease processes and cardiac disease.

The staff were all very helpful, informative and even inspiring, making my time there enjoyable and definitely educational. I would like to thank Chris and the nursing staff at VSG for sharing their extensive knowledge as well as practical expertise and also allowing me to even practice with their machine to form a logical approach to basic abdominal ultrasound.

I also wish to thank CAS and MSD for providing me with this fantastic opportunity.

I would encourage anyone who has a particular area of interest they want to develop to apply for this sabbatical, and take the opportunity to further your

skills and also improve the service you are able to provide your patients! I have enjoyed coming back to work and practicing some of the things I learnt as well as being better equipped to make use of our ultrasound machine.

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Tauranga Vets, Tauranga, etak_vet@hotmail.com

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Highlights from the 2014 European College of Veterinary Internal Medicine Conference, Mainz, Germany Dr Pru Galloway BVSc MANZCVS FANZCVS, registered Specialist in Feline Medicine I was fortunate enough to be awarded a Hill’s Pet Nutrition CAS Educating the Educators Scholarship to assist in attending the European College of Veterinary Internal Medicine Companion Animal (ECVIM-CA) conference in September. ECVIM-CA is a veterinary specialty organisation established in June 1994 by the European Society of Veterinary Internal Medicine.

It was formed in response to a growing demand for specialised veterinary care for companion animals and a need to harmonize the certification of specialists within Europe. Their annual conference is Europe’s ‘must attend’ continuing education event for small animal internal medicine Specialists.

Here’s a selection of topics relevant to kiwi small animal vets, some in short note format in the interests of being concise. In addition I have added some ‘tidbits’ from the 2013 American College of Veterinary Internal Medicine conference.

The Microbiome in Health and Disease; J Scott Weese, Canada Microbiota = microflora = individual’s microbial population • Any site with exposure to external environment; e.g. gut, nose, skin • Microbial cells outnumber host cells by ~ 10:1 • < 1% culturable Microbiome = genetic composition of microbiota • 100–1000x host DNA • Each site [e.g. gut, nose, skin] has its own microbiome • Gut microbiome is complex, diverse and dynamic Transcriptome = sum of all gene expression, mostly non-host cellular functions • up to 1/3 of small molecules in human blood are from gut microbiota Microbes = important cause of disease but often broader than ‘one-bug, one-disease’ • complex and continuous interaction between microbiota and immune system ‘Normal’ gut microbiota is essential for pathogen exclusion, digestion, vitamin formation and a complex array of immune interactions including immune tolerance. Early development of the gut microbiome is critical, infants born via caesarean aren’t exposed to the maternal vaginal flora and this may affect development of their gut microbiome.

‘Abnormal’ gut microbiota play a potential role in diverse health issues including infections, allergy, metabolic disease, obesity, neoplasia and neurocognitive disorders.

The microbiome can be modified by antibiotics, vaccination, diet, prebiotics, probiotics and biotherapy (e.g. faecal microbial transplantation]).

Background to Faecal Microbial Transplantation (FMT) In 2000, hypervirulent strains of Clostridium difficile colitis appeared in humans. C.difficile currently causes ~ 300 deaths per day in people in the USA. As its name suggests it is hard to treat; only ~ 20% respond to antibiotics but 80–100% respond to FMT (F+ via enema).

Aim of FMT: reset normal balance of flora, not to remove bacteria of concern. If successful, the recipient responds very rapidly in 24–72 hours.

• FMT faecal donor: Healthy 1–7 y/o adult of the same species who in the last 6 months has had no gastrointestinal disease, antibiotics or raw animal based treats/diet. Their diet should be as close to the recipient’s as possible and they need to be screened for enteric pathogens. Obtain 5–10 grams fresh F+ from colon, mix with 30 mls saline, blend and sieve. In future synthetic freeze dried poop may be available.

• FMT recipient: Chronic idiopathic colitis/ enterocolitis (i.e. biopsy proven inflammatory bowel disease (IBD)) with all known causes of IBD excluded such as food sensitivity and enteropathogens. Sedate for ~ 45 mins, administer a warm water enema, then 10 ml/kg F+ solution via red rubber tube instilled high into colon, leave tube in for a few mins, then remove. Turn onto opposite side half way through. If colitis; instil into colon. If enteritis (small bowel) give oral and via colon (ideally instil 3 mls/cat into duodenum via endoscope, or oral and pre-treat with omeprazole).

Biofilms: J Scott Weese, Canada • Biofilms are complex sessile bacterial populations imbedded in a self-produced extracellular polymeric substance (EPS or ‘slime’) of carbohydrates, proteins and DNA. • Develop by a continuous process and are ~ 10% bacteria and 90% EPS ‘slime’.

• EPS slime; provides adherence, cohesion, physical protection, and an opportunity for gene transfer (e.g. antibiotic resistance genes). Avoids host immune response, reduces antibiotic penetration and increases virulence.

• Clinical examples of biofilms include; dental plaque, valvular endocarditis, infections of foreign material (e.g. surgical implants, foreign bodies & catheters), osteomyelitis, UTIs, otitis externa and respiratory infections [including secondary bacterial infection associated with feline viral upper respiratory tract disease].

• Not all biofilms are bad, if they harbour beneficial bacteria they may prevent colonisation by pathogens e.g. in the gut.

• Bacteria commonly associated with biofilms in domestic animals include Staphlococcus

Catmed Ltd, Hill’s Pet Nutrition Adjunct Senior Lecturer in Feline Medicine, Massey University

March 2015

Companion Animal Society Newsletter

45

pseudintermedius, Pseudomonas aeruginosa and Malassezia pachydermatis.

• Infections with biofilms are harder to treat and a high local concentration of antimicrobial is needed.

Rather than minimum inhibitory concentration (MIC), ideally antibiotic selection is based on a MIC in the biofilm = MIBC. It is important to remove the primary cause [e.g. infected implant] and a combination of local and systemic therapy is often needed. Combine antibiotics with drugs to help breakdown the biofilm. Examples of the latter include tris EDTA and low dose macrolides (even if the bacterium is resistant to it) e.g. azithromycin or clarithromycin.

Angiotension II receptor blockers [ARBs]; Amanda Coleman, USA ARBs are a promising new family of drugs used for management of proteinuric chronic kidney disease (CKD), congestive heart failure and systemic hypertension. They are one of the fastest growing medications for managing hypertension in people and have a very good safety profile.

‘Traditional’ angiotensin converting enzyme inhibitors (ACE-Inhibitors): have a modest effect on lowering blood pressure, only block angiotensin (AT) synthesised by ACE, and AT/aldosterone break through is common (so they can lose efficacy over time).

ARBs: block all AT regardless of source at the AT1 receptor, while preserving the physiologically beneficial AT2 [see diagram below].

Telmisartan (Semintra; Boehringer-Ingelheim) is a new veterinary ARB; hepatic excretion, long acting • Licensed in cats in Europe for reducing proteinuria assoc with CKD, at 1 mg/kg PO SID. • Preclinical use by Coleman et al. in cats at 3 mg/kg and dogs at 1 mg/kg PO SID; more effective and longer lasting blockade of exogenous AT1 induced hypertension than benazepril (cats), enalapril (dogs) and placebo and losartan (cats and dogs).

PCR testing pitfalls and future perspectives: Iain Peters, UK • PCR allows rapid screening of large sample numbers without the need for pathogen viability.

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• Can be sensitive and specific but must interpret results in light of clinical signs and other diagnostic tests.

• Negative result does not necessarily rule out infection.

Definitions: • Amplicon: Gene target which is detected via exponential copying.

• Reverse transcriptase PCR (RT-PCR): converts RNA to a complimentary DNA strand before amplification.

• Conventional PCR: amplicon detected by gel electrophoresis, qualitative (positive or negative result), performed in an open tube so potential for lab contamination (false positives).

• Real-time quantitative PCR (QPCR); amplicon detected in real time using fluorescent reporters.

Uses sealed tube without risk of amplicon contamination at the lab.

False positives: • To prevent cross contamination extreme care must be taken when collecting samples in the clinic and during processing at the lab. This is particularly important where the organism is present in high copy numbers. e.g. Mycoplasma hemofelis can have 105 copies per µl of blood. To minimise equipment contamination in the lab, it is recommended that EDTA blood for M.hemofelis is submitted in a separate tube from haematology.

• Many PCRs detect genes that are highly conserved across species thus can inadvertently detect environmental contaminants or irrelevant organisms e.g. pan species and genera assays such as pan-bacterial 16S rDNA detect a wide range of bacterial pathogens and due to environmental contamination often produce false positive results.

• Recent vaccination with modified live (inactivated) vaccines may also lead to false positives.

False negatives: • To minimise false negatives, collect the correct sample i.e. from where the pathogen is most likely present in highest numbers. Blood is simple to collect but many bacteria/viruses have transient viraemia/bacteraemia.

• Potential PCR inhibitors: blood (especially heparinised), faeces and culture media.

• Recent antibiotics.

• Operator error • Formalin: cross links and fragments DNA, reduces yield of amplifiable material.

• Labs can (but don’t always) reduce false negatives by using internal controls to detect amplifiable DNA and PCR inhibitors

Tips from the ACVIM conference 2013 Pancreatic biopsy in 44 cats: Jorg Steiner, USA • Feline specific pancreatic lipase (fPLI) measured pre and 24 hours after pancreatic biopsy with a 4mm biopsy punch • Hemostasis: most pressure alone, +/– hemostasis powder or a single suture

Companion Animal Society Newsletter

Volume 26 Number 1

• Cats without histological evidence of pancreatitis had a significant increase in fPLI post-biopsy but did not exhibit any clinical signs of pancreatitis • Cats with histological evidence of pancreatitis on biopsy, had no significant increase in fPLI post biopsy • Conclusion; pancreatic biopsy safe in this cohort, follow up study will monitor fPLI at 72 hours Multi slice CT scanner: C Reinero, USA • University of Missouri has a 64 slice CT (= 64 detectors).

• Can scan awake/sedated cats in 5 seconds – they sit in sternal recumbency in a Perspex tube with padding on top so they can’t turn around.

• Much higher sensitivity for pulmonary metastases than x–rays.

• Can create 3D images, e.g. ‘virtual tracheobronchoscopy’.

• Wouldn’t we all love one of these!

Feline Aortic Thromboembolism = FAT cat study: D Hogan et al., USA • 72 cats with cardiogenic aortic thromboembolism (ATE), who had survived 1–3 months.

March 2015

• Prospective, randomised, double blinded.

• Two groups of 36 cats followed for 12+ months (1 cat withdrawn from each group).

• Randomly assigned to 81 mg aspirin PO q3d or clopidogrel, ¼ of 75 mg PO q24h.

• Primary end point = recurrence of ATE. • Median survival for recurrence of ATE at 1 year; 192 days for aspirin; > 365 days for clopidogrel, p = 0.021.

• Median survival for total study period; 192 days for aspirin; 443 days for clopidogrel, p = 0.019.

• Median time to ATE recurrence or cardiac death; 128 days for aspirin; 346 days for clopidogrel, p = 0.028.

• Clopidogrel at this dose and in this cohort of cats significantly improved survival compared to aspirin.

Clopidogrel is usually well tolerated in cats but V+, anorexia reported. Giving with food may reduce this. In humans major haemorrhage reported in 2% of patients on clopidogrel [Plumb, 7th Ed, 2011].

Anecdotally GI haemorrhage and epistaxis seen in one cat each in NZ [Galloway P and Gear R, pers comm. 2013].

Companion Animal Society Newsletter

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Subject Index: Vol 25: 2014 Accredited breeders scheme (NZKC)

No 2 … Pp 44

ACVIM Forum 2014 conference report:

No 4 … Pp 36–44

AGM 2014 American College of Veterinary Surgeons Symposium conference report:

No 2 … p 58 No 1 … Pp 46–48

American Veterinary Dental Forum 2013 conference report:

No1 … Pp 42–44

Antifungals in Dermatology Part 1

No 2 … Pp 24–25

Antifungals in Dermatology Part 2: Malassezia in dogs

No 3 … Pp 28–30

Antimicrobial use posters

No 2 … Pp 51–53

ANZCVS Science Week: Derm Chapter 2013 conference report:

No 1 … Pp 50–51

Aortic Thromboembolism, feline

No 1 … Pp 14–20

Australisan Exotics Conference 2013 conference report:

No 2 … Pp 48–49

Behaviour – dog,

No 2 … Pp 38–42

Canine Hip Dysplasia: management in immature animals

No 1 … Pp 26–28

CHD management with Juvenile pubic symphysiodesis

No 2 … Pp 26–29

Conference report: ACVIM Forum 2014

No 4 … Pp 36–44

Conference report: American College of Veterinary Surgeons Symposium

No 1 … Pp 46–48

Conference report: American Veterinary Dental Forum 2013

No 1 … Pp 42–44

Conference report: ANZCVS Science Week: Derm Chapter 2013

No 1 … Pp 50–51

Conference report: Australisan Exotics Conference 2013

No 2 … Pp 48–49

Conference report: NZVA Conference 2014 Part 1

No 3 … Pp 50–51

Conference report: NZVA Conference 2014 Part 2

No 4 … Pp 46–50

Conference report: WSAVA Conference 2014: Management of DM

No 4 … Pp 52–53

Dermatological conditions 1 – sterile suppurative necrolytic dermatitis of miniature schnauzers.

No 4 … p 34

Disease Watchdog

No 3 … Pp 48

Elbow dysplasia surgery – PAUL procedure

No 1 … Pp 20–24

Exocrine pancreatic insufficiency – What is your diagnosis?

No 2 … Pp 12, 54–56

FECAVA Antimicrobial use posters Hyperadrenocorticism, diagnosis of

No 2 … Pp 51–53 No 2 … Pp 14–20

Hill’s healthy weight protocol

No 2 … Pp 32–36

Hypoadrenocorticism – What is your diagnosis?

No 1 … Pp 10, 54–55

Intrathoracic, peripheral nerve sheath tumour

No 4 … Pp 28–32

The NZKC Canine Health Committee Hill K

Worth A

Gorman G Graham D Graham D FECAVA

Graham G Jones B Rana TL

Hurley R Baker C Soo M Hill K

Worth A

Gorman G Graham G Rana TL Field H

Watson C Bain H

Orbell G

Travers C Worth W Soo M

Jones B Phil Toll

McMeekin C

Seo J and Klobukowska H

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Companion Animal Society Newsletter

Volume 26 Number 1

Juvenile pubic symphysiodesis for management of CHD

No 2 … Pp 26–29

Kennel Cough – What’s new?

No 2 … Pp 46

Lecture, The

No 4 … Pp 14–16

Leifsonia aquatica in a dog bite injury

No 3 … Pp 20–22

Letter to a client re: MEBO ointment

No 1 … p 40

Letter to the Editor: re: Antibiotics staphylococci and canine pyoderma

No 1 … p 38

Nephroblastoma – What is your diagnosis?

No 3 … Pp 14, 52

Nerve sheath tumour

No 4 … Pp 28–32

NSAIDs for chronic pain in dogs – review

No 3 … Pp 42–46

NZKC Accredited breeders scheme

No 2 … Pp 44

NZVA Conference 2014 report – Part 1

No 3 … Pp 50–51

NZVA Conference 2014 report – Part 2

No 4 … Pp 46–50

PAUL procedure for canine elbow dysplasia

No 1 … Pp 20–24

Pet insurance – an overview

No 1 … Pp 34–37

Potassium homeostasis review

No 3 … Pp 32–36

Practitioner on Sabbatical report

No 1 … p 28

Rabbit nutrition

No 2 … Pp 30–31

Tarsocrural OCD – What is your diagnosis?

No 4 … Pp 12, 54–55

Tetanus: a post operative complication

No 3 … Pp 24–26

Tooth fractures

No 2 … Pp 22–23

Transdermal medication in cats

No 4 … Pp 18–26

Traumatic injuries of farm dogs

No 3 … Pp 38–40

Ultrasound guided isolation of a grass seed

No 1 … Pp 30–31

What is your diagnosis? Hypoadrenocorticism

No 1 … Pp 10, 54–55

What is your diagnosis? Exocrine Pancreatic Insufficiency

No 2 … Pp 12,54–56

What is your diagnosis? Nephroblastoma

No 3 … Pp 14, 52

What is your diagnosis? Tarsocrural OCD

No 4 … Pp 12, 54–55

Writing a scientific paper

No 3 … Pp 16–19

WSAVA Conference 2014 report: Management of DM

No 4 … Pp 52–53

WSAVA Pain Guidelines – summary

No 4 … p 26

Soo M

More G

Jones B Vaastra B and Gilchrist V Clark S Bell A

Bray S

Seo J and Klobukowska H Stevenson S

The NZKC Canine Health Committee Field H

Watson C Worth W

Watson C

Littlewood K Baker C Rana T

Visser J

Stuttle N

Gorman G Hill K

Sheard H

Anderson A

McMeekin C Soo M

Bray S

Visser J

Jones B Bain H

Gieseg M

n

March 2015

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Massey Home Page â&#x20AC;&#x201C; March 2015 Massey University Pet Emergency Centre

It has now been 1.5 years since the Massey University Veterinary Teaching Hospital (VTH) opened its 24/7 emergency and critical care clinic, the Massey University Pet Emergency Centre (MUPEC). The centre is staffed round the clock by trained veterinarians and nurses and is supported by specialists in surgery, internal medicine, emergency and critical care, anaesthesia and diagnostic imaging, ensuring a high standard of patient care at all times.

The facility contains state of the art equipment, including a critical care ventilator. This is an advanced machine that is used in human hospitals, and is different to that used during anaesthesia. It can either assist or control the patientâ&#x20AC;&#x2122;s breathing, and is recommended for significant respiratory disease or injury where the patient cannot maintain critical O2 or CO2 levels, or is at risk of respiratory arrest due to the effort required to breath. These conditions include diseases of the lungs (e.g. pneumonia, pulmonary contusions, pulmonary edema), chest wall, or neurological dysfunction.

MUPEC works in conjunction with the other speciality departments within the VTH, and patients which require specialist surgical or medical procedures are internally referred as required. Because of this, we can accept a wide variety of cases. Essentially, anything that may require urgent care. No case is too big or too small!

Other news from the MUVTH

Dr Janelle Wierenga, a boarded emergency and critical care specialist heads the service, and Dr Julia Giles joined the service late last year as an emergency and critical care clinician. Six interns rotate through the service, gaining valuable training in critical care medicine. This year Massey will also start training undergraduate veterinary and veterinary technology students in emergency and critical care medicine.

When the 24/7 centre first opened, its service primarily consisted of patients from the Manawatu. However, we are now actively encouraging referrals New Zealand-wide to MUPEC. Please feel free to contact us for initial stabilisation or travel advice if you think that you have a patient who could benefit from advanced care.

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Dr Arnon Gal has joined the internal medicine team as a clinician and academic.

Arnon graduated from the Koret School of Veterinary Medicine, Jerusalem with a DVM before working in private practice in Tel Aviv and a rotating internship at his alma mata. He undertook residency training in small animal internal medicine at the University of Illinois then a second residency there in Anatomic Pathology. He also has a PhD also from Illinois and is a Diplomat of the American College of Veterinary Internal Medicine and a Diplomat of the American College of Veterinary Pathologists. He has clinical interests in endocrinology, herpetology, immunology and infectious diseases. He will provide a strong link between the clinic and the realms of pathology which will be a great asset to our undergraduates.

For more information contact the MUVTH Tel: (06) 350 5329 or 0800 PET EMERGENCY (738 363) n

Companion Animal Society Newsletter

Volume 26 Number 1

www.nzva.org.nz/events

Calendar 2015 ...

2015 January–December January–December February 10–Dec 8 March 10–12 April 7 April 14–16 April 6–May 17 April 17–18 May 4–June 13 May 5 May 8–10 May 24–29 June 15–July 26 June–November June 29–August 9 July

August 17–Sept 18 August 24–October 4 October 19–Nov 19

December 3 (Auck) and

4 (Chch)

Vetscholar Online Course: Animal welfare and law: living up to expectations – 5 modules to be completed at your own pace. Tutor: Ian Robertson NZVA Leadership Intelligence series – six online modules to be completed at your own pace. Presenters: Sue Crampton and Rosie Overfield NZVA Leadership Series Live Webinars – monthly one hour webinars. Presenters: Sue Crampton, Tania Small, Mark Hardwick and Rosie Overfield NZVA Regional Roadshow – South Island. Theme: veterinarians, NZVA, VCNZ and ACVM working together on professional standards, veterinary medicines and NZVA career pathways.

NZVA Webinar – Making your medical records legal (1 hour). Tutor: Ian Robertson NZVA Regional Roadshow – North Island. Theme: see above.

Vetscholar course: Seize the Day: Mastering seizure management in small animals, Module 1 – Christopher Mariani Vetlearn Workshop – Companion Animal Abdominal Ultrasound Workshop, Massey University, Palmerston North. Tutors; Angela Hartman, Karon Hoffmann, Mark Owen, Chris Warman and Paul Wightman Veterinary Refresher Scheme for Companion Animal Practice – online course. Module 1: Anaesthesia and Critical Care – Sandra Forsyth NZVA Webinar – Making your informed consent legal (1 hour) Tutor: Ian Robertson Leadership and People. Veterinary Business Administration course offered to Master of Veterinary Medicine students in conjunctions with Massey University’s MBA programme. (2-day block course held in Christchurch) AVA and NZVA Pan Pacific Veterinary Conference, Brisbane, Australia, registrations open in January 2015. See www.panpac2015.com for more information.

Vetscholar course – Mindfulness: helping you thrive in your veterinary work – Angela Baker.

VetLearn Case of the Month Online Webinars for companion animal practice. First Tuesday of every month.

Veterinary Refresher Scheme for Companion Animal Practice – online course. Module 2: Surgery – Andrew Worth Master of Veterinary Medicine distance programme courses, starting July 2015 – Massey University Canine and Feline Neurology – Christopher Mariani and Chris Thomson Opthalmology in Small Animal Practice – Mark Bilson Canine and Feline Orthopaedic Surgery – Andrew Worth Principles of Veterinary Epidemiology – Naomi Cogger Online Vetscholar Course in avian medicine: Mastering medicine for our feathered friends (module 1).

Tutors: Lisa Argilla and Janelle Ward.

Veterinary Refresher Scheme for Companion Animal Practice – online course. Module 3: Medicine and Practical Pharmacology – Kate Hill Veterinary Refresher Scheme for Companion Animal Practice – online course. Module 4: Clincal Pathology – Tutor TBANovember 13–15 Marketing. Veterinary Business Administration course offered to Master of Veterinary Medicine students in conjunctions with Massey University’s MBA programme.

(2-day block course held in Christchurch) NZVA Workshop: Vision And Decision: The Importance Of Dental Radiology. Tutors: Angus Fechney and Anthony Caiafa.

For further details on these courses and other seminars and online courses please refer to the Vetlearn Updates or the following websites:

http://www.nzva.org.nz/eventcalendar

http://www.massey.ac.nz/massey/learning/colleges/college-of-sciences/students/mvm/mvm-home.cfm CAS publishes this list of national and international small animal veterinary meetings as a member benefit. The Editor takes no responsibility for the accuracy of this information and suggests you contact the organising association directly if you are interested in registration details for any meeting listed.

March 2015

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Instructions for Authors Submitting Articles to the CAS Newsletter Sarah Fowler (Editor), for the CAS Newsletter Editorial Committee The CAS newsletter is published quarterly in first week of March, June, September and December of each year. The printing costs are covered by the advertisements. There is therefore a limit of about 55â&#x20AC;&#x201C;60 pages to the size of each issue.

There is a balance between political issues, articles for continuing education and other news.

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

Articles

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

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

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

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

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

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

Proof reading

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

Articles and conference reports from recipients of grants and scholarships

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

References

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

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

Figures

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

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

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

Articles will be published as soon as possible after submission.

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

Depending on when the articles are received, the size of that particular issue and the need for refereeing, at the editorâ&#x20AC;&#x2122;s discretion articles may be held over for a later issue.

Refereeing

Articles may be sent to appropriate people in that field of expertise for refereeing/proof reading if the editorial committee deems this is necessary. This is to ensure accuracy within the text to protect readers, the authors CAS and the clients and the patients of veterinary practitioners.

SciQuest and NZVA website

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

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

Article of the issue and student article

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

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

There is a separate undergraduate student article competition.

Planning a case report? Some hints as to how do so!

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

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

Introduction, History, Clinical signs, Materials and methods

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

Results of investigations (e.g. laboratory results, radiography, ultrasonagraphy)

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

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

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Timing of article submission and publication

Discussion, Conclusion, Acknowledgments, References

Companion Animal Society Newsletter

Volume 26 Number 1

NZVA COMPANION ANIMAL SOCIETY NEWSLETTER

Volume 26 No 1 March 2015

In This Issue ...

• Haemangiosarcoma in dogs • Management of traumatic brain injury • Intra-occular prostheses • Managment of insulinoma-induced hypoglycaemia – case study • Update on Feline Leukaemia Virus • Highlights from ECVIM Conference 2014

VOLUME 26 NO 1 MARCH 2015