CAS Newsletter Vol26 no3 September 2015

NZVA COMPANION ANIMAL SOCIETY NEWSLETTER

Volume 26 No 3 September 2015

In This Issue ...

VOLUME 26 NO 3

• Pancreatitis – the diagnosis: is it that simple?

• Rubber jaw syndrome in a Cavalier King Charles Spaniel • Extraction complications: how to avoid that “Oh @%&$” moment • Clinical evaluation of pruritus and lesions in Atopic Dermatitis • Conference report: North American Veterinary Dermatology Forum 2015 • WSAVA 2015 Highlights • Specialist Profile: Pru Galloway • Book review: Kirk’s Current Veterinary Therapy XV

SEPTEMBER 2015

Newsletter

Volume 26 No. 3 September 2015 ISSN No. 1173-6941

EXECUTIVE COMMITTEE 2015 President

Contents

Catherine Watson

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

cath@vetservices.co.nz

From your society...................................................................................................4

Secretary

Rochelle Ferguson

Grants & scholarships............................................................................................. 6

rochellemf@hotmail.com

Article of the Issue winner.......................................................................................6

Treasurer

Aimee Brooker

CAS Executive News............................................................................................... 8

ollyaimee@gmail.com

What is your diagnosis?........................................................................................ 10

Committee Members

Barry Hedgespeth

Helen Beattie

Helen.Beattie@op.ac.nz

Pancreatitis – the diagnosis: Is it that simple?...................................................... 12

Brendon Bullen

Boyd R Jones

brendonbullen@gmail.com

Hannah Bain

Rubber jaw syndrome in a Cavalier King Charles Spaniel...................................... 16

hannah.bain@merck.com

Judith Visser

Warren Stroud

Extraction complications and how to avoid them: Or that “Oh @%&#” moment..........................................................................................................22

stroud@wellpet.co.nz

Pauline Calvert

Craig Hunger

pcalvert@xtra.co.nz

John Munday

The clinical evaluation of pruritus and lesion severity in Canine Atopic Dermatitis.......................................................................................................32

j.munday@massey.ac.nz

EDITORAL COMMITTEE

Duncan Graham

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

Conference report: North American Veterinary Dermatology Forum 2015............36 Duncan Graham

Conference report: WSAVA 2015 .........................................................................38 David Smith

Address for submitting copy/ correspondence etc.

CAS Specialist Profile – Pru Galloway...................................................................40 Book review: Kirk’s Current Veterinary Therapy XV...............................................42

Sarah Fowler

66 Callum Brae Drive Rototuna Hamilton 3210 Ph H:(07) 845-7455 Mob: 027-358-4674 Email: sarah.fowler@gmail.com

Highlights from NZVJ: Volume 63, Issue 5, 2015..................................................44 What is your diagnosis: The answer......................................................................46 PanPacific Conference 2015.................................................................................48 Massey Home Page..............................................................................................50

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

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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.

September 2015

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Editorial NZVA’s new aspirational goal for antimicrobial resistance is that ‘By 2030 New Zealand Inc. will not need antibiotics for the maintenance of animal health and wellness’ Development of antimicrobials has been one of the major developments in medicine.

Antimicrobials have allowed for major medical advances such as surgery and chemotherapy, and have significantly improved human and animal welfare over the last 70 years since the discovery of antibiotics. But with resistance increasing and a void of new antibiotic discovery for over 30 years, many institutions such as the World Health Organisation are now warning that the post antibiotic era is near, where we will no longer be able to rely on these drugs to treat many common ailments.

While most of the news headlines are concerned with human pathogens, maintaining the effectiveness of antimicrobial agents is critically important for our companion animal patients.

No-one wants to see commonly treated ailments becoming life threatening again without the availability of effective antibiotics. While we might also consider that the use of antimicrobials in production animals by far outweighs the contribution from companion animal medicine, there is increasingly strong evidence that the use of antibiotics in pets creates resistant bacteria and that these bacteria are readily transferrable to the humans who care for and cohabitate with them.

With medical knowledge doubling roughly every 3.5 years, the 15 years until 2030 is a long time in medical terms. It is likely there will be many treatment advances to assist us in this transition into the post antibiotic era. But time is just a number, and these medical advances will not occur on their own without a concerted effort across multiple industries. This will require some adjustments in mindset about the usage of antibiotics and the growing risk and importance of antimicrobial resistance.

Companion animal veterinarians have an educational role in this change of mindset in our clients. Taking time to discuss antimicrobial resistance concerns and positioning your practice as a guardian of these critical RVM’s is likely to be rewarded with greater understanding of the difference between viruses and bacteria, why clients don’t always leave the consult room with a bag of pills, or why you are prescribing oral medication rather than a more convenient long acting injection. It is also a chance to discuss the importance of wellness and proactive healthcare.

Our approach to antimicrobial use as clinicians is also vitally important. Before prescribing antibiotics for a case we need to ask whether they are required, what the most appropriate first line choice would be and whether there are alternative treatment modalities. Responsible prescribing involves using the right antibiotic for the right period of time, and making use of culture and sensitivity results where indicated. It also involves monitoring your prescribing choices at a clinic level and educating your colleagues, staff and clients around judicious use. As much as possible we should be discussing new treatment modalities amongst ourselves and sharing new ideas throughout the profession.

This is an opportunity for NZ to lead the way in responsible antimicrobial use. We have always punched above our weight on the world stage, and NZ is already estimated to be the world’s third lowest user of antibiotics in animals. By taking the front foot on this issue, we can position ourselves as leaders at the interface between companion animals, their owners and the environment they share, and preserve the availability and efficacy of these vital medications for as long as possible.

Brendon Bullen CAS President

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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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Companion Animal Society Newsletter

Volume 26 Number 3

September 2015

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From your society Summary of minutes Executive Committee Catch up held 7 May via Google Hangouts Attendance: Catherine Watson, Aimee Brooker, Rochelle Ferguson, Helen Beattie, Brendon Bullen, Hannah Bain, and John Munday Apologies: Pauline Calvert, Warren Stroud.

Practitioner on Sabbatical: Plan to rework this grant and offer it next year with a more defined structure and new name.

Membership benefits: Suggestion to NZVA to make these clearer and easy to find on the website and look at benefits that have wide appeal such as discounted petrol. Also will recommend to NZVA that more support is given to regional branches as this is an area where members are most likely to have contact with the NZVA. Leslie Lyon’s Presentation: Good quality presentation to interested CAS students at Massey – attracted an audience of around 50 people.

Veterinary Refresher Scheme: With lower registrations this year it was decided to withdraw tutor support of the forum and adopt the model we currently use for

the Australian students. Regular review of the course content is required to ensure it remains relevant.

Massey Meeting arrangements: Agreed to hold our AGM in the evening of our two day meeting at Massey in July.

CAS Resource Position: NZVA to report back to us on costs to administer the position.

TradeMe’s Breeders Code: Currently in draft form with TradeMe discussing it further with SPCA and MPI, will require a communication plan with members when TradeMe go live with it later this year.

NZCAC update: Peter Verhoek is resigning and Ross Blanks will represent the NZVA. President’s report – Cath Watson: Discussion about progressing work with NZKC to improve their breeds.

Suggestion has been made to consider them breed by breed rather than as a whole. Bulldogs have been mooted as the first breed we should tackle via breeder education and look at getting support from NAWAC to add more weight to our initiative.

Treasurer’s report – Aimee Brooker: Accepted with no changes.

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Companion Animal Society Newsletter

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September 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

EYEVET Services Limited

Article of the Issue Winner Geoff Orbell June 2015, Volume 26(2), Pp 36-37

Paper: “Unusual dermatological conditions – role of pathology in achieving a diagnosis.

Part 2: Necrotising fasciitis in a dog”

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Companion Animal Society Newsletter

Volume 26 Number 3

September 2015

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CAS Executive News New Zealand Companion Animal Council Update Significant changes to the structure and vision for the New Zealand Companion Animal Council (http:// www.nzcac.org.nz) have recently occurred. Informal discussions at forum meetings revealed a general feeling that more could and should be achieved by the NZCAC. This is turn, lead to a formal retreat in Queenstown, and development of these ideas by way of a strategy consultant.

The concept of the NZCAC was launched 25 years ago and its inception driven by Bob Kerridge, whose vision was to create “A forum to facilitate relationships between animals, humans and the environment.”

It has functioned as such and the relationships and networking of people from all parts of the companion animal sector have been advantageous, with annual conferences being a highlight.

However, there was a strong response from both the strategy workshop group, and via a member survey, that the outputs and tangible benefits of the NZCAC were lacking. This has resulted in a freshening of the vision, goals and strategic direction of the NZCAC, including embedding an executive board structure, and an operational role to provide outputs. The executive board is made up of representatives from the NZVA, CAS, RNZSPCA, NZKC, NZ Cat Fancy and four open positions for which applications were made.

Acknowledgement to Arnja Dale (UNITEC) and Barry Helem (Canterbury SPCA) for the huge amount of voluntary work they contributed to making this restructure happen.

Helen Beattie CAS Executive Member and NZCAC Board Member



Allan Bell awarded Life Membership of NZVA CAS would like to extend our congratulations to Dr Allan Bell who has been awarded Life Membership of the New Zealand Veterinary Association for services to companion animal veterinary medicine.

The award was presented to Dr Bell by Cath Watson, the outgoing CAS president at the AGM of the Companion Animal Society held recently in Palmerston North.

Dr Bell has played a significant role in the New Zealand veterinary profession right from the beginning of his long and busy career. He was a member of the first class of students to graduate from Massey University in 1967. He began practice in Christchurch, spent some time overseas then returned to companion animal practice in Auckland. His interest in dermatology developed from the weighting of cases he was seeing in general practice.

Dr Bell studied to achieve Membership of the Australian and New Zealand College of Veterinary Scientists in Canine Medicine in 1981, then commenced specific training with Dr Ken Mason towards Fellowship (in Veterinary Dermatology) of the Australian and New Zealand College of Veterinary Scientists which he achieved in 1995. He became (and remains) the only registered Veterinary Dermatology specialist in New Zealand.

Dr Bell has had a significant impact on the animals and clients under his professional care. His interests include infectious disease, clinical dermatology and immunology. In particular Dr Bell has been outspoken on issues of appropriate antibiotic usage and the development of antimicrobial resistance, particularly here in New Zealand.

Dr Bell has made major and significant contributions to veterinary CPD in New Zealand. He regularly presents at both local and international conferences and has been an examiner and co-examiner for the Fellowship examination in Veterinary Dermatology since 1996. He has published in peer-reviewed veterinary journals and written many articles for the CAS Newsletter as well as VetScript. He has acted as a mentor for other veterinarians interested in dermatology throughout his career, and in 2011 he received the Companion Animal Society Annual Service Award.

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Companion Animal Society Newsletter

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What is your diagnosis?

Barry Hedgespeth B.S. (Hons), BVSc, Companion Animal Intern An overweight, 7-year-old, castrated male cat named Tuck was presented to the after-hours emergency service for a suspected urethral obstruction. He was found earlier in the day under the house by his owners, where he was reluctant to move, hunched in pain, and emitting an odour of urine. He was recumbent upon presentation and a large, firm bladder was palpable.

Tuck was previously brought to the clinic with a similar presentation one month prior to this episode. During this previous hospitalisation, a cursory abdominal ultrasound examination revealed a small, hyperechoic mass within the bladder, but this was not investigated further. A decompressive cystocentesis was performed before he was deobstructed and managed with an indwelling urinary catheter; no further clinical signs developed until the current episode.

An ultrasound examination of Tuck’s bladder during the current presentation revealed the following image:

Figure 1.

Sagittal ultrasonographic image of Tuck’s urinary bladder Distance “A”: 39.4 mm; Distance “B”: 18.6 mm

A heterogenous mass was visualised on the dorsal mucosal bladder wall. The mass had smooth, mildly irregular, well– defined margins, and measured 39.4 mm x 20.0 mm x 18.6 mm in sagittal, transverse, and dorsal planes, respectively.

The mass was fixed to the mucosal surface, with its position unalterable even when the patient was placed in sternal recumbency. The mass did not exhibit appreciable colour flow signal, indicating a lack of vascularity.

1. List differential diagnoses for the observed mass, and the prognosis that each carries.

2. Describe procedures that could be useful in investigating a mass such as the one depicted, and the risks associated with each procedure.

(Answer on Page 46) Massey University Veterinary Teaching Hospital. B.A.Hedgespeth@massey.ac.nz

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Companion Animal Society Newsletter

Volume 26 Number 3

September 2015

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Pancreatitis – the diagnosis: Is it that simple?

Boyd R Jones, BVSc, FACVSc, DECVIM-Ca, Emeritus Professor Recently, a question from a specialist veterinarian was posted on the Comparative Gastroenterology Society list-serve. The specialist had been asked by a colleague to explain why a dog admitted for dental prophylaxis had no ultrasonic evidence of pancreatitis despite having a serum lipase of 4000u/L (reference interval 200–1800 u/L) and a spec cPL of 1000 µg/L. There were no clinical signs of pancreatitis. The serum lipase and spec cPL remained high but the dog was healthy.

The specialist said ‘I don’t know the answer’. There was a variety of feedback from members including: • There must be smouldering pancreatitis • We have all seen cases like this and we don’t know the reasons • Is there a connection with salivary secretion?

• A similar syndrome is recognised in humans • Treat the dog not the lab values!

The last comment is getting there, and one has to ask why either the lipase or the spec cPL were measured in the first place in a healthy dog! The question was not answered as to why, without pancreatitis, the serum lipase and spec cPL would be elevated.

In the last 8–10 years the diagnosis of pancreatitis has been investigated extensively and useful, specific diagnostic tests have been developed. The problem is that no test has a sensitivity and specificity that will allow interpretation or a diagnosis in every case, especially when we request measurement of spec cPL when no (or marginal) clinical signs of pancreatitis are present.

Jane Armstrong presented a paper on aspects of pancreatitis at the 2014 New Zealand Veterinary Association Conference. A review of the diagnosis of pancreatitis in the March 2015 issue of Vetscript (Brandt, 2015) provided a documentary approach to diagnosing pancreatitis with few recent references to support the options for diagnosis or the criteria for selection of a diagnostic test by a clinician. There are, in fact, some excellent recent reviews of the diagnosis of pancreatitis by Mansfield (2012), Mansfield (2013), Armstrong (2014) and Xenoulis (2015). The January 2015 issue of the Journal of Small Animal Practice focused on canine and feline pancreatitis with five review and two additional papers on aspects of pancreatitis including diagnosis. The editorial by Watson (2015) states: ‘Diagnosis of pancreatitis in dogs and cats remains a challenge, as it is in humans.’

That statement is correct and the more we know the more confusing the diagnosis can become. Here is a summary of my understanding of the diagnosis of pancreatitis. Above all, diagnostic tests used must be practical, available and value for money. Furthermore, a positive or negative test result should influence what we do regarding treatment or a decision for further diagnostic investigation, or there is no point doing the

test. If you have made a clinical diagnosis of suspected pancreatitis a test result received 2–4 days later is no use, so why request it? You can freeze and save serum for later analysis if you have to! Readers who have a particular interest in pancreatitis are referred to the references below for more detailed information, particularly to Mansfield (2013).

What tests are available and how can they help?

Serum lipase and amylase Each analyte is part of a routine biochemistry panel.

Neither enzyme is pancreas specific. Lipase can be elevated in dogs with acute enteritis, liver disease or impaired renal function. Steroid administration can elevate the serum lipase up to 5 times normal, without pancreatic pathology. The values of both enzymes can be normal in dogs with pancreatitis (20–50% cases). If you have a middle aged obese bitch with vomiting and right upper quadrant abdominal pain and the lipase is elevated more than 3 times normal you are probably right – pancreatitis. But recognise the limitation of interpreting values of these enzymes, whether high or low.

Canine pancreatic lipase (cPL) The use of this laboratory test is widespread. It measures lipase of pancreatic origin. The assays available commercially are the sandwich ELISA specific canine pancreatic lipase (spec cPL) and the ‘in clinic’ SNAP-cPL rapid semi-quantitative assay.

There should be concordance beween the spec cPL and the SNAP-cPL but manufacturers recommend that a positive SNAP-cPL test be followed by a quantitative spec cPL. A spec cPL value of >400 µg/L is consistent with pancreatitis and values <200 µg/L are expected in healthy dogs.

There are a number of studies that have determined the sensitivity and specificity of spec cPL with most relying on histological evidence of pancreatitis as confirmation of disease. There is no doubt that spec cPL is a specific test (80–97.5%) but its sensitivity is worrying as it ranges from 21–88% in different studies. In many of the post-mortem-based studies it is not apparent whether the animals had clinical signs of pancreatitis, and the diagnosis was only based on histology. The sensitivity is higher in acute onset disease and in severely affected dogs where significant pancreatic parenchymal damage is present.

In chronic pancreatitis the test has little merit as there is less damaged pancreatic parenchyma from which the enzyme can leak. Not a good test for chronic pancreatitis.

Some recent studies also signal caution in interpretation of the spec cPL and SNAP-cPL. In one study dogs with hyperadrenocorticism (HAC) had higher spec cPL concentrations and more positive SNAP-cPL results than healthy dogs with normal

Massey University, Palmerston North

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ACTH stimulation test results (Mawby et al., 2014).

These authors warned that SNAP-cPL and spec cPL results should be interpreted cautiously in dogs with HAC to avoid false diagnosis. In another study dogs in the more advanced stages of mitral insufficiency and congestive heart failure had elevated spec cPL values (>400 µg/L) when pancreatic circulation was impaired (Han et al., 2015). Furthermore, a study by Haworth et al., (2014) showed that the SNAP-cPL and spec cPL may provide a false diagnosis of pancreatitis in up to 40% of dogs presenting with acute abdominal disease.

The overall agreement between the two tests was good but 4 of 38 dogs in their study had a positive SNAPcPL and normal spec cPL (≤ 200 µg/L). If a dog has clinical signs that strongly indicate acute pancreatitis: vomiting, abdominal pain etc, a positive SNAP-cPL and spec cPL > 400 µg/L, pancreatitis is very likely but there is always doubt. Ultrasonography is always indicated.

Canine pancreatic lipase is the best laboratory test we have in New Zealand and is most easily interpreted when negative, to determine that dogs don’t have pancreatitis. Dogs with a negative SNAP-cPL and a negative spec cPL (< 200 µg/L) are unlikely to have acute pancreatitis. If you have a negative SNAPcPL you know you must recruit imaging techniques (ultrasonography/radiography) or other investigations to help understand what is happening in the abdomen.

Remember that for chronic pancreatitis there is no test, apart from histopathology, that is reliable.

In Europe, serum pancreatic elastase (CPE-1) is available as an alternative to spec cPL. It has a sensitivity around 78% (specificity 92%) when dogs with acute pancreatitis are assessed. There is close equivalence with canine pancreatic lipase for the diagnosis of acute pancreatitis (Mansfield et al., 2012). CPE-1 may be less affected by renal clearance than spec cPL too. This test is not available in New Zealand.

Diagnostic imaging Imaging must complement laboratory diagnostic investigations of a cat or dog with suspected pancreatitis.

Radiography is of little value for the diagnosis of pancreatitis as findings are frequently normal or nonspecific (Xenoulis, 2015). However, radiography is a logical initial approach as a ‘rule out’ for disorders that can cause similar clinical signs, e.g. gastrointestinal foreign body.

Abdominal ultrasonography is the imaging method of choice and can be completed before laboratory blood test results are received. The method can also rule in or out disorders other than pancreatitis.

Most studies confirm the value of ultrasonography.

The published sensitivity of abdominal ultrasound examination is about 68% in dogs with acute pancreatitis and 11–67% in cats with pancreatitis.

However, most of the published studies date from 1998–2003. The detection of pancreatitis is highly dependent on the skills of the ultrasonographer, the equipment used and the stage of the disease.

Equipment has improved as has the expertise of ultrasonographers. A diagnosis of pancreatitis made by an experienced ultrasonographer is highly reliable in my experience. In the last few years ultrasonographic

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results can be obtained before spec cPL can be completed. If there is ultrasonographic evidence of pancreatitis, a concurrent positive SNAPcPL offers a high probability that a diagnosis of pancreatitis is correct. Treat accordingly! Do you need a spec cPL? Probably not in this case.

A recent study in cats (Williams et al., 2013) that used serum fPL as a diagnostic indicator showed that ultrasonography had a sensitivity of 84% and specificity of 75% for diagnosing pancreatitis.

Ultrasonography is essential for the diagnosis of abdominal disease including pancreatitis; importantly, expertise and experience in using it are needed. Improve your ultrasound skills or refer.

Ultrasonography in the right hands is as useful as laboratory testing for diagnosing pancreatitis.

Xenoulis (2015) reviews current literature on ultrasound and pancreatitis.

Feline pancreatitis Measurement of the fPL concentration is the most sensitive serum marker for feline pancreatitis. Sensitivity is higher for severe pancreatitis but much less sensitive for cats with mild or chronic disease (which is most of them!).

There is an association between pancreatitis and inflammatory bowel disease but the previously reported association with cholangiohepatitis as well, is now challenged.

Cholecystitis and cholangitis can co-exist with pancreatitis but not cholangiohepatitis (Mansfield 2014). Azotaemia does not appear to affect serum values. There is a feline SNAP-fPL test that is equivalent to the SNAP-cPL, with manufacturers reporting 80–90% agreement between a SNAP-fPL and spec fPL. A negative SNAP-fPL should be a good indicator that pancreatitis is not present as the specificity is high. However, as with dogs, a diagnosis of pancreatitis cannot be based on the results of a SNAP-fPL alone.

The references provided with this article give more in depth information on validation studies and on specific factors that affect interpretation of the tests in cats.

Conclusions – dogs

• A negative spec cPL or SNAP-cPL means acute pancreatitis is unlikely • There is good overall agreement between the spec cPL and SNAP-cPL test results • SNAP-cPL and spec cPL may give false positive results for the diagnosis of pancreatitis in up to 40% of dogs with acute abdominal disease • A positive spec cPL must be interpreted in conjunction with supportive clinical signs and diagnostic imaging to confirm acute pancreatitis is the cause of clinical signs • Chronic pancreatitis is difficult to diagnose with laboratory testing or diagnostic imaging • Abdominal imaging (radiographs, ultrasound) is essential to rule out causes other than pancreatitis in dogs with acute abdominal disease • Ultrasound may support a diagnosis of acute pancreatitis

Companion Animal Society Newsletter

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Conclusions – cats

• A diagnosis of acute pancreatitis is best made with a combination of suggestive clinical signs, elevated feline pancreatic lipase and supportive abdominal ultrasound findings • There is a high association between chronic pancreatitis and inflammatory bowel disease in cats • The sensitivity for spec fPL and SNAP-fPL is low in chronic pancreatitis which is the most common form • The spec fPL has no place in a screening biochemistry panel unless clinical signs are indicative of acute pancreatitis and there is a high index of suspicion of acute pancreatitis • Amylase and lipase concentrations are of no value for diagnosing pancreatitis in cats

References

Armstrong J. Canine pancreatitis: diagnosis. Proceedings NZVA Annual Conference 2.19.2–4, 2014 Brandt L. Diagnosing pancreatitis in dogs: testing options explained. Vetscript 27, 36–9, 2015 Han D, Choi C, Hyun C. Canine pancreatic specific lipase concentrations in dogs with heart failure and chronic mitral valve insufficiency. Journal of Veterinary Internal Medicine 29, 180–3, 2015 Haworth MD, Hosgood G, Swindells KC, Mansfield CS. Diagnostic accuracy of the SNAP and spec canine pancreatic

September 2015

lipase tests for pancreatitis in dogs presenting with acute abdominal disease. Journal of Veterinary Emergency and Critical Care 24, 135–43, 2014 Mansfield CS, Watson P, Jones BR. Specificity and sensitivity of serum canine pancreatic elastase-1 concentration in the diagnosis of pancreatitis. Journal of Veterinary Diagnostic Investigation 23, 691–7, 2011 Mansfield C. Acute pancreatitis in dogs: advances in understanding diagnostics and treatment. Topics in Companion Animal Medicine 27, 123–32, 2012 Mansfield CS. Practical interpretation and application of exocrine pancreatic testing in small animals. Veterinary Clinics of North America: Small Animal Practice 43, 1241–60, 2013 Mansfield CS. Triaditis in Cats – does it exist. Proceedings World Small Animal Veterinary Association Congress 2014, p111. www,WSAVA2014.net.files/basichtml/page111 Mawby DI, Whitemore JC, Fecteau KA. Canine pancreaticspecific lipase in clinically healthy dogs and dogs with naturally occurring hyperadrenocorticism. Journal of Veterinary Internal Medicine, 28, 1244–50, 2014 Watson P. Canine and feline pancreatitis: a challenging enigmatic disease. Journal of Small Animal Practice 56, 2–3, 2015 Williams JM, Panciera DL, Larson MM, Were SR. Ultrasonographic findings of the pancreas in cats with elevated serum pancreatic lipase immunoreactivity. Journal of Veterinary Internal Medicine 27, 913–8, 2013 Xenoulis PJ. Diagnosis of pancreatitis in dogs and cats. Journal of Small Animal Practice 56, 13–26, 2015

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Rubber jaw syndrome in a Cavalier King Charles Spaniel Judith Visser, DVM, Companion Animal Intern Introduction

Chronic kidney disease (CKD) is the most common type of kidney disease in dogs and cats. The prevalence of CKD in the population dogs and cats varies worldwide from 0.5% to 1.5% (Polzin et al., 2005). It is a slowly progressive, chronic disease characterised by loss of functioning nephrons and decreasing glomerular filtration rate (GFR). Secondary hyperparathyroidism is a common complication of CKD with an incidence of 84% (Barber and Elliot, 1998). Renal secondary hyperparathyroidism develops early in the disease process, when serum phosphorus concentration rises due to decreasing GFR. High serum phosphorous suppresses the production of calcitriol (the active form of vitamin D) by the renal tubular cells and therefore removes the inhibition on parathyroid hormone (PTH) production. High levels of PTH in CKD induces translocation of bone calcium stores to the circulation. Hence, bone demineralisation and fibrosis of the supporting bony stroma result. This process is termed fibrous osteodystrophy. Clinical features of fibrous osteodystrophy are more likely to happen in young, growing animals with renal disease and include proliferative bone lesions and bowing of the bones. Softening and swelling of the bones is more commonly observed in adult animals. The full clinical spectrum of fibrous osteodystrophy is not commonly observed in adult dogs with CKD.

Clinical history and clinical findings

A 5-year-old female spayed Cavalier King Charles Spaniel was presented to the Massey University Pet Emergency Centre for anorexia of a 4-day period. The dog’s clinical history included a 5-week consumption of soft food, polyuria and polydipsia (PU/PD) of several months duration, and a recent development of ataxia and stiffness in both hind limbs. The dog was fed a commercial diet all its life and was recently switched from dry food to wet food.

On physical examination the dog was quiet, alert and responsive. Temperature, heart rate and respiratory rate were within normal limits, while mucous membrane were tacky and capillary refill time was approximately 1 second. The dog’s ambulation was characterised by hindlimb stiffness. The dog’s face had asymmetry in the sagittal plane, and saliva was drooling mainly from the right side of the mouth (Figure 1).

On closer inspection of the mouth, the dog had no pain or crepitus during passive movement of the jaw, and the temporomandibular joint had a normal range of motion. Minor periodontal disease and moderate gingivitis and plaque build-up were also noted.

Marked loosening and instability of the teeth in of both the mandibula and maxilla were present. A thorough orthopaedic exam was performed and indicated mild asymmetrical muscle atrophy in the hind limbs.

Figure 1.

Frontal appearance with marked asymmetry of the jaw

The flexibility of the jaw and instability of the teeth suggested metabolic bone disease. The main differential diagnoses included primary hyperparathyroidism, secondary nutritional hyperparathyroidism and secondary renal hyperparathyroidism.

Since the dog was fed a commercial diet nutritional hyperparathyroidism seemed unlikely. In primary hyperparathyroidism there is an autonomous production of PTH by the parathyroid glands which is independent of ionised calcium level. In dogs this is usually caused by an adenoma and occasionally by a carcinoma (Feldman, 2005).

A complete blood count indicated that the dog had a non-regenerative anemia with hematocrit of 0.24 L/L (reference range: 0.37–0.55 L/L). Other abnormalities included mild thrombocytosis of 646 x109/L (ref 200– 500 x109/L).

Clinicopathologic abnormalities in serum biochemistry are presented in Table 1 and included marked azotemia, mild hypoproteinemia, mild hyperamylasemia, mildly increased total calcium, moderate hyperphosphatemia and mild hypochloremia.

Radiographs of the skull were taken and evaluated (Figure 2). These showed that the bone density of the maxillae and mandibles was severely reduced. An ill-defined periosteal reaction was present along the dorsal aspect of the cranium with adjacent ill-defined cortical thinning.

Massey University Veterinary Teaching Hospital, j.visser@massey.ac.nz

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Table 1.

Serum biochemistry results

Parameter CK AST ALP ALT BIL TP ALB GLO URE CRE AMY CA CHOL CL K LIP NA PO4 GLU

Result 386 26 31 25 2 51 32 19 53.9 699 2089 3.04 5.4 98 4.9 144 144 7.14 6.0

Reference range (0–609 U/L) (0–79 U/L) (0–185 U/L) (0–75 U/L) (0–6 μmol/L) (52–75 g/L) (26–44 g/L) (17–39 g/L) (3.6–11.4 mmol/L) (53–123 μmol/L) (30–1020 U/L) (2.20–3.00 mmol/L) (3.0–9.0 mmol/L) (105–121 mmol/L) (3.5–5.6 mmol/L) (13–200 U/L) (139–153 mmol/L) (1.00–3.00 mmol/L) (3.9–6.1 mmol/L)

failure with secondary renal hyperparathyroidism was made based on the presence of marked azotemia, hyperphosphatemia and osteopenia. Because of financial constraints and the severity of the disease combined with a grave prognosis, the owner did not wish to pursue any treatment and the dog was euthanised.

Necropsy revealed that while fractures were not present, the mandibles, maxillae and ribs were severely pliable and easy to bend. Multifocal calcium deposits were present on the parietal pleura, the kidneys were small and pale, and the parathyroid glands were severely enlarged. Histopathological examination of the ribs uncovered multiple subperiosteal areas in which osteoid has been replaced by fibrous connective tissue (i.e. fibrous osteodystrophy).

The renal proximal convoluted tubules were severely dilated and had mineralised basement membranes. The glomeruli were reduced in number, occasionally mineralised and the Bowman’s capsule was severely thickened.

The pulmonary alveolar walls had multifocal areas of calcification, and the gastric submucosa had multifocal areas of mineralisation as well. A diagnosis of chronic end-stage renal failure with severe metastatic calcification and fibrous osteodystrophy was made.

Figure 2. Dorsoventral (a) and left lateral (b) radiographic views of the skull. Note periosteal reaction along the dorsal aspect of the cranium (black arrowhead) and adjacent cortical thinning (white arrow).

A dorsoventral view of the entire body was also taken.

This revealed that the cortices of the radius and ulna were noticeably thinned.

Due to financial constraints an ionised calcium level was not done in this dog, but the markedly elevated phosphorous level made primary hyperparathyroidism unlikely. A provisional diagnosis of end-stage renal

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Figure 3.

Whole body dorsoventral radiograph

Discussion

This case describes an unusual onset of mandibular fibrous osteodystrophy (i.e. ‘rubber jaw’) in an adult dog, as a result of renal secondary hyperparathyroidism that was induced by CKD. While not all aspects

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of the diagnostic workup have been fulfilled due to financial constraints, namely measurement of ionised calcium and serum PTH, other findings strongly support this diagnosis, including mandibular fibrous osteodystrophy, metastatic calcification in several organs, diffuse parathyroid gland enlargement, non-regenerative anemia, azotaemia and hyperphosphatemia.

In renal secondary hyperparathyroidism, there is aberrant regulation of calcium homeostasis. In a normal animal, serum calcium level is dependent on regulation of calcium and phosphorous by PTH and calcitriol. PTH increases the absorption of calcium and loss of phosphorous in the renal tubules, promotes translocation of calcium from the bone, and induces the renal conversion of the vitamin D precursor to calcitriol, the active form of vitamin D. Calcitriol increases intestinal calcium and phosphorous absorption and inhibits PTH synthesi (Stillion and Ritt, 2009). The key physiologic alteration in renal secondary hyperparathyroidism is the decreased production of calcitriol by the kidney because of chronic kidney disease. The decrease in calcitriol level removes the negative feedback regulation on PTH production.

Fibrous osteodystrophy of bones is associated with renal secondary hyperparathyroidism. The increased PTH acts directly on bone tissue to stimulate osteoclastic activity to elevate serum calcium level.

The lamina dura of the dental alveolar bone, the cancellous bone of the mandible, and the maxilla to a lesser extent are very sensitive to the increase in osteoclastic activity caused by elevated PTH. Increased calcium resorption from bone will lead to replacement of bone by fibrous stroma and connective tissues (Huang et al., 2015). Bone demineralisation can rarely cause jaw fractures (Proctor et al., 2005).

The crown of the teeth is not affected by osteoclastic activity and therefore remains intact (Roux, 2007), but the anchoring of the teeth into the alveolar bone by fibres is completely lost, which explains the loosening of the teeth (Harvey and Emily, 1993). Young, growing animals have high skeletal metabolic rates compared to adult dogs, therefore in young animals with secondary hyperparathyroidism bowing of the bones can occur due to proliferative bone lesions. In older animals this decalcification results in fibrous osteodystrophy leading to softening and swelling of the bone.

While fibrous osteodystrophy is caused by high level of PTH, metastatic calcification contributes to development of renal secondary hyperparathyroidism (i.e. increased PTH production) by lowering extracellular calcium level. In metastatic calcification there is precipitation of calcium and phosphorous in the connective tissues such as arteries, gastric mucosa, kidney, and pulmonary alveolar walls.

Precipitation of calcium and phosphorous in chronic kidney disease is driven by rising phosphorous level, however, the extracellular calcium level is often low.

Extracellular calcium level decreases in CKD due to three main reasons. The first is a global increase in renal tubular flow rate by the remaining nephrons in compensation for ongoing nephron loss. Because the majority of renal calcium handling is maintained by the thick ascending limb of Henle where calcium is passively absorbed, increase in tubular flow rate results in renal calciuria and calcium loss. The second reason is precipitation of calcium with phosphorous (i.e. metastatic calcification). This is a mass effect mediated by rising levels of phosphorous. The third mechanism is phosphorous-mediated inhibtion on calcitriol production by the rising phosphorous level; low level of calcitriol in turn results in a decrease in

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calcium absorption from the intestine. Therefore, decrease in the extracellular calcium level stimulates the parathyroid glands to produce PTH and hence contributes to renal secondary hyperparathyroidism.

Extracellular calcium regulates PTH production and secretion through its action on the calciumsensing receptor in the parathyroid gland. Blood calcium (often measured as total calcium) consists of 3 fractions: ionised (approximately 50%), protein bound (approximately 35%) and calcium that is bound to organic anions (approximately 15%). The ionised fraction in the blood is the biologically active portion of calcium and hence the one of clinical importance.

Serum ionised calcium (iCa) concentration varies widely from serum total calcium concentration.

Because serum total calcium does not adequately reflect serum iCa, it is important in patients with CKD to measure iCa when calcium status needs to be evaluated. It has been shown that total serum calcium underestimates hypocalcaemia by 56% (Kogika et al., 2006).

The long-term prognosis for CKD is poor, but in the short term, dogs can have a good quality of life as the disease progresses slowly. Hyperparathyroidism develops early in the disease process, and if recognised the progression can be slowed. Early recognition of renal disease and correction of abnormal calcium and phosphorous balance are important factors of preventing development of hyperparathyroidism.

Phosphate binders and limiting dietary phosphorus intake are important in lowering PTH levels (Stillion and Ritt, 2009). Clinical signs of secondary hyperparathyroidism start to show only in end-stage renal failure and usually are not clinical apparent in adult dogs. As the prevalence of this complication is so high in dogs with CKD, it is important to recognise hyperparathyroidism so appropriate management can be initiated to try and give these animals a good quality of life.

Acknowledgements

Special thanks to Dr. Angus Fechney for his help with this case and to Dr. Arnon Gal for his help preparing this article for publication.

References

Barber P, Elliot J. Feline chronic renal failure: calcium homeostasis in 80 cases diagnosed between 1992 and 1995.

Journal of Small Animal Practice 39, 108–116, 1998 Feldman EC. Disorders of the parathyroid glands, In: Ettinger SJ, Feldman EC, Textbook of Veterinary Internal Medicine 6th Edition, p.1437–1465. Elsevier Saunders, St.Louis USA. 2005 Harvey CE, Emily PE. Atlas of oral pathology of the dog and cat, In: Small Animal Dentistry 1st Edition, p.49–89 Mosby Jan 1993, Michigan USA Huang R, Zhuang R, Liu Y, Li T, Huang J. Unusual presentation of primary hyperparathyroidism: report of three cases. BMC Medical Imaging 15, 23, 2015 Kogika MM, Lustoza MD, Notomi MK. Serum ionized calcium in dogs with chronic renal failure and metabolic acidosis, Veterinary Clinical Pathology 35, 441–445 2006 Polzin DJ, Osborn CA, Ross S. Chronic Kidney Disease, In: Ettinger SJ, Feldman EC, Textbook of Veterinary Internal Medicine 6th Edition, p.1756–1785. Elsevier Saunders, St.Louis USA. 2005 Proctor R, Kumar N, Stein A, Moles D, Porter S. Oral and Dental Aspects of Chronic Renal Failure, Journal of Dental Research 84, 199–208, 2005 Roux PH. Fracture mandibulaire chez un Lhassa Apso avec hyperparathyroidie secondaire rénale, Schweizer Archiv für Tierheilkunde, 149, 157–159 2007 Stillion JR, Ritt MG. Renal secondary hyperparathyroidism in dogs. Compendium of Continued Education for Veterinarians 31, E8,2009

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This article was written as part of the requirements for receiving the CAS/Hills Pet Nutrition Educating the Educators scholarship.

Extraction complications and how to avoid them: Or that “Oh @%&#” moment Craig Hunger, BVSc, MANZCVS Small animal dentistry and oral surgery Introduction

Tooth extraction is a very common procedure performed daily to weekly in most small animal practices. Extractions can be required for multiple reasons including severe periodontal disease, fractured teeth, traumatic malocclusions, persistent deciduous dentition or tooth resorption. Extractions are a surgical procedure which require skill and patience, and complications can occur. Being aware of the possible complications and how to prevent or treat them is important.

Prevention or minimisation of extraction complications begins with having the correct equipment and skills, and knowledge of the proper techniques. Even then complications will happen if you extract enough teeth.

Complications can occur in either the peri or postoperative periods.

Dental training is available in New Zealand and overseas. I would highly recommend attending a dental wet lab or practical workshop. Last year I was lucky enough to attend the 2014 Veterinary Dental Forum in Atlanta, Georgia, USA. This is an annual threeday veterinary dental conference for veterinarians and nurses. There were four streams of lectures, many wet labs and a large exhibitors hall with an amazing array of dental equipment and instruments. Last year there were over 600 veterinarians and 200 veterinary nurses in attendance. The lectures and labs range from the fundamental through to the advanced.

Wet labs cover extractions, oral fracture repair, orthodontics, root canal therapy and rabbit dentistry to name but a few. The Veterinary Dental Forum this year is in Monterey, California, USA and I would highly recommend it to any veterinarian wanting to increase their dental knowledge and skills. I would also encourage veterinarians to consider sitting the MANZCVS exams in small animal dentistry and oral surgery.

The most important tool to prevent extraction complications is dental radiography. Radiographs give you a wealth of information, allowing you to discover and diagnose hidden intra-oral pathology and aid in the planning of the extraction and your ability to address any likely issues. If there is evidence that the extraction will be difficult then you can offer the client referral or inform the owner of the increased risks prior to proceeding. If you do have a complication and the client has been informed of the risks prior, then you are in a much better position. The comparison is attempting to repair a fractured limb without the benefits of preoperative radiographs. People routinely have dental radiographs taken when they go to their own dentist and so think it is normal for their pets to receive the same.

Perioperative complications Retained Root Fragments/Fractured roots Fractured tooth roots can be secondary to trauma or root resorption but the most common cause is iatrogenic. This is a common complication that will happen to everyone. “If you haven’t fractured a tooth root, then you haven’t extracted enough teeth”. The most common reasons are excessive force, non-surgical extraction techniques and the use of extraction forceps too early in the process. Preventing fractured roots is via the use of dental radiographs, surgical extraction techniques, good visualisation, and the appropriate equipment.

Pre-extraction dental radiographs will help you plan your surgical approach and identify pathology such as hooked or dilacerated roots, ankylosis, and tooth resorption that may hinder the extraction. For teeth that do not have severe periodontal disease, I will almost always perform a surgical extraction. This involves creating a muco-gingival flap, which is then elevated off the bone with a sharp periosteal elevator to allow good exposure (Figure 1). Multi-root teeth are then split at the furcation angle, into their individual roots. Removal of the buccal alveolar bone will make extraction of the tooth easier and is essential for extraction of the canines and carnassial teeth. Some vets will use a small round burr to create a gutter to allow introduction of the dental elevator or luxator into the periodontal ligament space. It is important to have a good knowledge of oral anatomy, to know where to place flaps, to avoid important structures and the location and size of the various roots (Figures 1, 2, 3, 4).

Figure 1.

Correct location for triangular flap for extraction of a maxillary canine.

Pet Doctors at Animates Takanini, Auckland, craig.hunger@gmail.com

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elevators that follow the curve of the tooth, elevate the tooth and also tear the periodontal ligament.

Figure 2. Correct location for flaps to extract the maxillary canine and 4th maxillary premolar. Note location of infraorbital foramen and that the sutures will be overlying bone rather than the defect.

Figure 3.

If you are worried about causing further damage or harm when trying to remove the root tips, think about offering referral. It is much easier to remove the roots at the time, rather than later on.

If roots are left behind then you need to document this and inform the owner. If you do not and there is a problem later on, then legally it is difficult to defend your position. â&#x20AC;¨If there is no apical disease and the apical blood supply is intact, the retained root is less likely to become infected. This is not an excuse to leave roots behind. Conversely, for this reason, it is important that teeth with complicated fractures or other endodontic disease have complete removal of the tooth root. Do not wait and see. The other case where it is hugely important to remove every bit of root is for cats with chronic gingivostomatitis. Even a small amount of root can allow the inflammation to continue.

Visualisation is markedly improved by good lighting (head lamp, LED light on high speed drill), magnification (loupes, bifocals, reading glasses etc.), and Minnesota lip retractors, stay sutures or an assistant to hold the lip, flap or soft tissue out of the way.

To remove retained root tips, first take a dental radiograph to work out the location and size of the root fragment and to identify any possible pathology. If not already done, create a large mucogingival flap, with releasing incisions to allow good visualisation. Remove the overlying buccal alveolar bone using a round bur, with a light feathering motion. The buccal bone can be removed to the level of the apex of the tooth, if required. Create a moat around tooth root using a small #1 round burr. This allows access to the periodontal ligament space with a fine elevator or root tip pick. Place the tip of the elevator into the periodontal space, being careful not to displace the root into the maxillary sinus or mandibular canal. Rotate the elevator around its long axis and hold for 15â&#x20AC;&#x201C;30 seconds to stretch and tear the ligament. Continue elevating around the root tip until it is mobile and then carefully remove it with extraction forceps or a root tip pick.

Appropriately sized, sharp instruments are vital for successful extractions. Order the correct instrument for the job and the size of your hand.

Sharpen them daily and replace them regularly.

Feline dental elevators are a must if you perform feline dentistry.

I personally prefer winged

Clinical signs suggesting the presence of retained roots are swelling over the area, a visible sinus tract or abccessation. If this occurs then either offer referral or be prepared to surgically explore the area. Again dental radiographs will be your best friend in this situation (Figures 5 and 6).

Figure 4.

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A canine skull showing the correct location to raise a flap to extract the 1st mandibular molar. Note location of mental foramen for when extracting the mandibular canine.

Even doing all of the above, fractured root tips can still happen. It is usually obvious at the time due to auditory and visual cues. Visually, the apex of the root should be rounded and smooth, and if the root has been completely extracted the socket will usually fill with blood. If unsure whether there is a fractured root tip you can confirm with dental radiographs.

Attempted atomisation of roots should be avoided as this can cause further damage to the surrounding bone and neurovascular structures, e.g. the mandibular canal, and is unlikely to remove all the root remnants. Atomisation has been associated with displacement of root fragments, bone necrosis, emphysema and air emboli (Holmstrom etâ&#x20AC;&#x201A;al., 2004).

Image of correct flap placement for buccal approach for extraction of a feline mandibular canine. Note the removal of the buccal bone overlying the canine.

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Haemorrhage Haemorrhage is a rare complication that will usually stop with direct, digital pressure. The exception is if a major vessel is damaged. Haemorrhage can occur due to damage from high-speed burrs, hand instruments or incorrect flap placement. You can use gel foam and other haemostatic agents but they are usually not necessary. Good closure of the gingiva over the alveolus will allow clot formation. If inappropriate haemorrhage persists post-operatively then consider checking for bleeding disorders such as Von Willebrands, etc.

Figure 5.

Figure 6.

Image showing a soft tissue swelling and sinus tract over maxilla. Note gutta percha cone in tract

Dental radiograph of dog shown in Figure 5 showing retained root fragment of the maxillary first molar (arrow head) and gutta percha cone.

Root tip displacement Root tips can be displaced into the nasal sinuses, the nasal cavity or the mandibular canal. It is usually due to a combination of severe periodontal disease or periapical lysis (due to endodontic disease) and overly aggressive extraction techniques. This is most commonly seen with the mesio palatal root of the maxillary 4th premolar. To help prevent root tip displacement, angle the dental elevator at 60 degrees to the hard palate for the mesio palatal root.

Treatment involves, dental radiographs to confirm the position and size of the root tip. Either attempt to extract or suture the flap closed and refer. Avoid further harm by blindly attempting to extract any remaining root. Extraction is via increasing your exposure, and removal of the overlying buccal bone until the root is exposed. Magnification, good lighting, and suction make the job a lot easier. Know your anatomy of the area. You may need to perform a rhinotomy to remove the displaced root (Taylor etâ&#x20AC;&#x201A;al., 2004.)

If you are unable to extract the root tip then cover with antibiotics and monitor for signs of nasal discharge, sneezing, oral pain, and draining sinus tracts, etc. The best chance to successfully remove the displaced root, is at time of it happening, before the root becomes entrapped in fibrous tissue.

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The infraorbital and inferior alveolar arteries can be damaged during creation of flaps for the extraction of the maxillary 4th pre molars and mandibular canines respectively. The vessel itself quite often retracts and is not amenable to ligation. The infraorbital artery is vulnerable where it emerges from the infraorbital canal apical to the distal root of the maxillary third premolar. To stop the bleeding, raise a flap and gently remove the outer wall of the infraorbital canal starting rostrally (like a dorsal laminectomy), until the vessel can be grasped and ligated. (See Figure 2 for position of infraorbital foramen).

The middle mental artery is vulnerable where it emerges from the mental foramen along with the neuro-vascular bundle (Figure 3). It can be accidentally transected when raising a buccal flap for extraction of the mandibular canine. Avoid this by being aware of your anatomy, watching the position of your vertical releasing incisions, carefully raising the flap and visualisation of the neuro-vascular bundle. If you do sever the middle mental artery, you will need to extend your flap to allow adequate exposure and then ligate the vessel.

Iatrogenic mandibular fracture Iatrogenic mandibular fractures are most commonly associated with the first mandibular molars and the mandibular canines. A fracture through the site of the mandibular first molar is not uncommon, especially with severe periodontal disease in older, small breed dogs. This occurs due to severe periodontal bone loss, leaving minimal bone that may have osteoporosis and infection and the use of simple extraction techniques, in the mistaken belief that the tooth will be easy to extract as it is mobile. In small breed dogs the amount of bone left at the ventral cortex of the mandible can be toothpick-thin. Pathological fractures can occur from normal chewing activity or mild trauma (Figures 7 and 8).

In the case of the mandibular canines, each tooth root makes up 30% of the strength of the lower jaw and is surrounded by minimal bony support. The lingual alveolar bone may be only 2â&#x20AC;&#x201C;3 mm thick in small dogs and cats. The tooth root is curved and premature rotation of the tooth with forceps can cause a fracture of the alveolar bone on the lingual aspect of the tooth. This will be seen as an instability, between the two mandibles. If both mandibular canines need extracting, I would stage the procedure with two months between each extraction. Another reason for the mandible to fracture is where there is ankylosis

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extraction techniques. Pre-extraction radiographs allow us to warn the owner of an increased risk of fracture due to severe loss of bone or the shape of the roots. It is always better to have warned the client of the increased risk, prior to, rather than after the fracture occurs. A viable alternative to extraction of fractured mandibular canines and mandibular first molars is standard root canal therapy (RCT).

This is less traumatic, maintains the strength of the mandible and we are left with a functional tooth. Root canal therapy can be performed on a fractured tooth of any age. There needs to be a closed apex. The goal is to remove all pulpal material via mechanical and biological debridement, to prevent any further bacterial growth, and then fill and seal the pulp canal.

If this is successful the periapical infection will resolve with antibiotics. Root canal therapy is not suitable for teeth with severe periodontal disease.

Figure 7.

Dental radiograph of 1st mandibular molar, showing severe bone loss, with a risk of mandibular fracture.

Note the fractured crown and periapical lysis, evidence of endodontic disease. Image courtesy of Anthony Caiafa.

Treatment of iatrogenic fractures initially involves applying a tape muzzle for temporary stabilisation.

Definitive treatment involves the use of intra-oral splints, wires, a tape muzzle, or a partial rostral mandiblectomy. We can expect reduced healing due to the bone loss and periodontal infection and they will have a guarded prognosis. You may end up with a functional malunion. See Textbook of Oral and Maxillofacial Surgery in Dogs and Cats (Verstraete and Lommer, 2012) for more details.

Instrument slippage Slipping with hand instruments or the high-speed drill can cause damage to the raised mucogingival flap or the surrounding soft tissues. More severe damage can occur, including ocular penetration (Smith et al., 2003) To prevent the damage caused by slipping with hand instruments, use controlled force and the correct instrument grip. The elevator or luxator should be held with a palm grip, with a finger stop. This involves the tip of the forefinger held just below the tip of instrument. (Figures 9 and 10). This will stop the instrument from slipping any more than a few millimetres. Use appropriately sized instruments (for example a stubby handle for smaller hands, Figure 10) for your hand and the size of the tooth.

Figure 8.

Post-operative dental radiograph from same case as shown in Figure 7. Image courtesy of Anthony Caiafa

between the tooth and the alveolar bone. Excessive rotation can then cause a fracture through the alveolar process.

The chance of iatrogenic mandibular fractures is decreased by the use of dental radiographs and surgical extraction techniques. Always support the jaw with your other hand while elevating around the tooth. With the mandibular canine you want to avoid elevating the tooth except along the long axis of the tooth root. There are plenty of textbooks and journal articles that go through the correct surgical

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Figure 9. Image of correct use of a winged dental elevator.

Note the maxilla being supported with the other hand and the finger stop to prevent instrument slippage.

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Figure 10. Image of correct position of dental instrument. Note the end of the instrument is supported in the palm and the tip of the index finger provides a finger stop to prevent slippage.

Prevention of soft tissue injuries due to the high-speed drill can be achieved with good exposure and lighting.

The use of large mucogingival flaps and retractors, stay sutures or an assistant will help to keep soft tissue out of the way.

Treatment will vary from a few sutures to an eye enucleation, if you are unlucky. Prevention is always preferable.

Post-operative complications Pain Prevention is via dental nerve blocks, adequate multi modal pain relief, gentle tissue handling, and alveoplasty. Suturing of extraction sites will prevent dry socket and decrease pain but this is not universally agreed upon. Dental nerve blocks are simple to perform, have minimal risks, decrease the level of gaseous anaesthesia required, and provide pre-emptive pain relief. Extractions should receive an opioid in the perioperative period and go home with NSAIDs if the animal is a suitable candidate.

Flap breakdown or non-healing extraction sites Wound or mucogingival flap breakdown is usually always due to tension or poor flap design. This can be prevented with the use of periosteal releasing incisions, alveoplasty and a properly designed flap where the base is wider than the apex and the releasing incisions are situated at the line angle of the adjacent teeth, so that the sutures are over bone not over the defect (Figures 1, 2, 3 and 4). Alveoplasty is the use of a round burr on a high-speed hand piece to remove any sharp edges of bone. Periosteal releasing incisions are created by carefully using a scalpel blade or iris scissors to release the flap from the underlying periosteum. Releasing the periosteum will free the flap so that it can be closed with minimal tension.

This is a vital step and will be the difference between success and failure.

If an extraction site is not healing, consider the possibility of infection, osteitis, bone necrosis or neoplasia, especially in cats. Biopsy of the affected site is the next step. Infection in the mouth is a rare complication, but can occur (Reiter et al., 2004).

Oronasal fistulas Oronasal fistulas are seen most commonly with the maxillary canine, either caused iatrogenically, due to

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rotation of the maxillary canine during removal or due to pre-existing severe, periodontal disease. Look for bleeding from the nostrils. If unsure you can flush sterile saline into the alveolus and look for presence at the nostril. Avoid excessive elevating or leveraging on the palatal surface of the maxillary canine. If an oronasal fistula is present it will require treatment, otherwise it will not heal. You will need to remove any diseased tissue, by curettage and flushing of the socket. Perform an alveoplasty to remove any diseased bone and incise any diseased gingiva. Close the fistula with a single or double flap under minimal tension. Don’t forget to release the periosteum! Avoid lifting the lip in the post-operative period and cover with systemic antibiotics.

Mandibular canine impingement After extraction of the maxillary canine, the mandibular canine can impinge on the upper lip.

This is more commonly seen in cats. To prevent this complication, consider performing standard RCT on maxillary canines if possible, instead of extraction. Warn clients of the possibility of this occurring. It may resolve with time or treatment may be required. This is either by extraction of the offending mandibular canine or crown amputation with a vital pulpotomy.

Conclusion

In conclusion, tooth extraction is a common procedure, but one that is not without risks and it does require skill and diligence. Complications can and will happen and being aware of the possibility and how to manage them appropriately will decrease the number of “@%&#!” moments. Extractions are a significant surgical procedure and should be treated as such. Pain relief and anaesthetic support including IV fluids and patient warming are a must. We need to be providing a good service and charging appropriately for our time. Having the correct instruments and equipment including lighting, dental radiographs and a highspeed dental base make the job a lot more successful and enjoyable.

References

Holmstrom SE, Frost-Fitch P, Eisner ER. Exodontics in Veterinary Dental Techniques for the Small Animal Practitioner 3rd ed. Pp 322–323. Philadelphia: Saunders, 2004 Smith MM, Smith EM, La Croix N, Mould J. Orbital Penetration associated with Tooth Extraction. Journal of Veterinary Dentistry 20, 8–16, 2003 Reiter AM, Brady CA, Harvey CE. Local and systemic complications in a cat after poorly performed dental extractions. Journal of Veterinary Dentistry 21, 215–221, 2004 Taylor TN, Smith MM, Snyder L. Nasal Displacement of a tooth root in a dog. Journal of Veterinary Dentistry 21, 222–225, 2004 Verstraete FJM and Lommer MJ. Oral and Maxillofacial Surgery in Dogs and Cats. Pp 153–158, Sanders, 2012

Recommended further reading

American Veterinary Dental Society: http://avds–online.org • Foundations Compendium (from Journal of Veterinary Dentistry) • Step-By-Step Compendia, Volume 1 and Volume 2 (from Journal of Veterinary Dentistry)

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This article has been submitted as part of the requirements for receiving the CAS/Hills Pet Nutrition/ Educating the Educators scholarship

The clinical evaluation of pruritus and lesion severity in Canine Atopic Dermatitis Duncan Graham, BVSc, BSc (Hons), Animal Dermatology NZ In 1999, the task force on Canine Atopic Dermatitis (CAD), comprised of eight board-certified dermatologists, began its review of this disease. This culminated in the 2001 publication of their findings (Olivry et al., 2001) They defined atopic dermatitis (AD) as a genetically-predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features. It is associated most commonly with IgE antibodies to environmental allergens. The specific allergens can be identified with either an intradermal test or with serum IgE levels. However these tests are not used to make the diagnosis but to identify specific allergens. The diagnosis of CAD is a clinical diagnosis, based on the typical clinical presentation and history of the disease in each individual animal.

Certain areas of the animal’s body are commonly affected, and in the Prelaud (Prelaud et al., 1998) system of evaluation, both this typical distribution of lesions and the evidence of pruritus are used as part of the diagnostic criteria. They found that a check list of the following major criteria gave an 80% specificity and sensitivity. The patient must have three out of five features: 1. Corticosteroid-responsive pruritus 2. Pinnal erythema 3. Bilateral cranial erythematous pododermatitis 4. Cheilitis 5. Appearance of the first signs between the ages of 6 months and 3 years Thus we know that Canine Atopic Dermatitis (CAD) is a common disease characterised by pruritus, with a characteristic distribution of pruritus and inflammatory lesions, which may also show signs of chronicity. It has been established that for erythema and pruritus, although they usually co-exist in the same animal, their severity is not always correlated.

For this reason, atopic skin lesions and pruritus should always be evaluated or graded independently.

Because making the diagnosis depends in part on the response to treatment (corticosteroid) and on the distribution and evaluation of lesions, in the last 15 years, there have been a number of efforts to produce both a pruritus grading system and a lesion scoring system. An owner-evaluated pruritus Visual Analogue Scale (PVAS) was validated by Peter Hill and his colleagues (Hill et al., 2007). They designed a scale which assesses the severity of a dog’s pruritus by allowing the owner to act as a proxy informant for their animal. A follow-up study by the same group in 2008 showed that normal dogs (without dermatological disease) scored less than 2 on the scale. The PVAS is a vertical line that starts at 0: normal dog, itching is not a problem and ends in 10: extremely severe itching. In the latter instance, the dog is scratching, licking, chewing almost continuously, regardless of what is happening around it. You have the owner, at the beginning of each consultation, mark where on the continuous line they feel their dog’s itching falls, between those two extremes. The lead author, Peter Hill has provided a pdf file on the web so that veterinarians can download

the scales. Go to http://www.cliniciansbrief.com/sites/ default/files/CaninePruritisScale.pdf.

His instructions are as follows: “1. Print out the first sheet on a plain piece of paper and have it laminated. This can then be used repeatedly in the examination room with a whiteboard (non-permanent) marker pen. It is best if the client is guided through the use of the scale, so that they are clear about what to do. We usually give the scale to the owner and ask them first to read the instructions at the top. Then we specifically remind them that they should read the descriptions starting from the bottom (the scale doesn’t make sense if it is read from the top down).

We also emphasise that they can place a mark anywhere on the vertical scale and not just next to the words. We find it helps to actually demonstrate putting a mark on the line somewhere, so that they know what to do.

2. The second sheet (with the numbers on it) needs to be printed on to a plain piece of paper, and then photocopied onto a transparency. This sheet is then placed over the top of the first sheet, after the client has made their mark, allowing the numerical score to be read off and recorded. The laminated sheet can then be wiped clean and used again.

3. Do not be tempted to use the second sheet as the actual scale. We have tested this and owners always place their mark next to whole or half numbers, which reduces the continuous nature of the scores that are obtained when using the visual analogue scale.”

I have started using this system and it works very well for establishing the level of pruritus at the beginning and end of treatments, which makes response to treatment a much more reliable component of the diagnostic approach (as long as you don’t use two medications at the same time).

As well as needing to evaluate pruritus in canine atopy, both as part of the diagnostic approach, and to assess the response to treatment, it is necessary to have a somewhat objective, replicable way of grading lesions.

It has been shown, as mentioned previously, that the primary lesions of canine atopic dermatitis, erythema and pruritus, coexist in the same animal, but aren’t always correlated. There may be severe pruritus, but scant erythema, and vice versa. For this reason they must be treated as separate parameters. Clinical trials particularly need a validated grading system so the response to therapy can be reliably evaluated Thierry Olivry and his colleagues have been working on this problem since 1997. In that year, they produced the Canine Atopic Dermatitis Extent and Severity Index (CADESI)-1 which evaluated erythema, excoriation, and lichenification at 23 different body areas using a scale of 0 = none to 3 = severe. In 2002, the CADESI-2 scale increased the number of sites evaluated to 40 but kept the same lesion and severity guides. In 2007, the CADESI-3 scale increased the body regions evaluated to 62, and added self-induced

duncan@animaldermatology.co.nz or http://www.animaldermatology.co.nz/

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alopecia to the lesions evaluated. It also widened the severity score to 6 grades where 0 = normal, mild = 1, moderate = 2–3, and severe = 4 or 5. This scale satisfied many of parameters needed to conduct clinical trials and, as it was the only validated disease scale, it was recommended for use in clinical trials evaluating medications for atopic canines.

The major drawback of the CADESI-3 scale was that because of the large number of body sites and lesions to evaluate (it required 248 separate evaluations), it was very time consuming to use and impractical in a clinical setting. In 2012, to provide a reliable and validated scale to evaluate lesions that was less time consuming to administer Jon Plant and his colleagues designed and validated the Canine Atopic Dermatitis Lesion Index (CADLI, Plant et al., 2012).

They reiterated that the assessment of changes in the severity of the lesions is best way to evaluate the efficiency of CAD treatment, both in clinical practice and in clinical trials. They simplified the disease measurement scale by limiting the evaluation to regions of the atopic dog most commonly affected. To decide which areas to use, they took advantage of the excellent 2010 study by Favrot et al. which identified the most commonly affected areas in 843 atopic dogs.

They grouped the lesions into those that respond within days to treatment (erythema, excoriation and erosion) and those chronic lesions that are slow to respond, taking weeks to change (alopecia, lichenification and hyperpigmentation). They decided on a 6 point ordinal scale (0–5) with 0= no lesions, 1 = mild, 2–3 = moderate, and 4–5 = severe and extensive lesions.

The five body areas chosen were the head and pinnae, forefeet, hind feet, and the ventral thorax and axillae.

They found that the CADESI-3 took 12.6 minutes to complete while the CADLI took 1.9 minutes, making it much more likely to be used in clinical practice.

Plant and his colleagues validated the new scale for reliability, internal consistency, responsiveness to change and convenience.

An example of the form that can be printed and laminated for easy use is found at: www.vetrespit.com/ resources/caldi_1219.pdf In 2014, Olivry and his group developed and validated a fourth version of the CADESI that was simpler and easier to administer than the previous CADESI scales (Olivry et al., 2014). Using the same Favrot et al.

(2010) study, they reduced the number of sites to 20, less than 1/3 the number of the previously validated CADESI-3. Their study found that the CADESI-3 took a median time of 12 to complete, the CADESI-4 took 4 minutes, and the CADLI took 1 minute.

International members voted anonymously to use a grading scale similar to the CADESI-3, i.e. 0–3 (none, mild, moderate and severe). The study concludes that “If investigators wish to include a larger number of body sites and a four-point categorical scale, they should select the CADESI-4. If shorter and quicker assessment is required, but with a six-point scale, then the CADLI would be preferable. The International Committee on Allergic Diseases of Animals (ICADA) recommends either, based on the individual clinician’s preference and goals.

The CADESI-4 grading sheet and lesion grading atlas (which can be laminated and reused) can both be found as part of the online article at: http://onlinelibrary. wiley.com/doi/10.1111/vde.12107/suppinfo In general practice, and in referral practice, time is always short so I have used the CADLI more often than the CADESI-4. I do find it easy and quick to use, and gives a semi objective point that I can refer back to when we are pondering how much the dog has improved.

Selected references

Olivry T, Saridomichelakis M, Nuttall T, Bensignor E, Griffin CE, Hill PB. Validation of the Canine Atopic Dermatitis Extent and Severity Index (CADESI)-4, a simplified severity scale for assessing skin lesions of atopic dermatitis in dogs.

Veterinary Dermatology 25, 77–e25, 2014 Hill PB, Lau P, Rybnicek J. Development of an owner-assessed scale to measure the severity of pruritus in dogs. Veterinary Dermatology 18, 301–8, 2007 Plant J D, Gortel K, Kovalik M, Polissar NL, Neradilek MB. Development and validation of the Canine Atopic Dermatitis Lesion Index, a scale for the rapid scoring of lesion severity in canine atopic dermatitis. Veterinary Dermatology 23, 515– e103 2012 Olivry T, DeBoer DJ, Griffin CE, Halliwell REW, Hill PB, Hillier A. The ACVD task force on canine atopic dermatitis: forewords and lexicon. Veterinary Immunology and Immunopathology 81, 143–146, 2001 Prélaud P, Guaguere E, Alhaidari Z, Faivre N, Heripret D, Gayerie A. Re-evaluation of diagnostic criteria of canine atopic dermatitis. Revue de Medecine Veterinaire, 149, 1057– 1064, 1998

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Calling all Veterinary Students The CAS Newsletter is a non-peer reviewed publication that publishes quality articles on a variety of topics of interest to companion animal veterinarians in New Zealand. Articles include a variety of formats such as case studies, reviews, and scientific studies.

We would welcome articles from veterinary students to be considered for publication in the CAS newsletter. These may be related to exemplary case reports and so will probably require only small amounts of work prior to publication. Guidelines to writing articles for the CAS Newsletter are published in each edition of the magazine and additional guidance can be obtained by contacting the Editor or John Munday, the Massey CAS representative. We suggest you consult with your lecturer and have the article reviewed prior to submission.

Being published looks great on your CV when applying for internships or post-graduate study and all undergraduate articles selected for publication will receive a $50 award, with the best student article published during the year winning a prize of $400, kindly donated by VetEnt. Please submit your article electronically to the Editor, CAS Newsletter, Sarah Fowler at sarahfowler@ gmail.com

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This article has been submitted as part of the requirements for receiving the CAS/Hills Pet Nutrition Educating the Educators scholarship.

Report on the North American Veterinary Dermatology Forum – Nashville, April 2015 Duncan Graham, BVSc, BSc (Hons), Animal Dermatology NZ Veterinary dermatology is coming of age. Next year, in 2016, from 31st May to June 4th, the 8th World Congress of Veterinary Dermatology will be held in Bordeaux, France. Four years later it will be held in Sydney, Australia. This infant discipline will then be 31 years old as the first world congress was in Dijon France in 1989. Several of the founding fathers have retired or died in the past year, but the ranks of veterinary dermatology are swelling. In Nashville, at the recent North American Dermatology Forum, I discussed cases with dermatologists from France, Spain, Australia and, of course, the USA. There were over 400 attendees at the mammoth Gaylord Convention Centre, on the outskirts of Nashville. Luckily Kate Hill had warned me of its confusing and expensive nature and suggested staying nearby, which I did for one third the cost, staying at the Fiddlers’ Arms, an easy 10-minute walk through park-like environs (once I got past the acres of parking lots.)

There was a heavy emphasis on pruritus – the itchy dog doctor’s staple problem: the presenters covered its pathogenesis, evaluation and treatment. To some extent this is being driven by the release by Zoetis of oclacitinib (Apoquel) to the general veterinarian in the US. They presented further research on that product. Candace Sousa gave a good overview of the pathways of pruritus, and discussed the mediators of pruritus. Considerable research is being done on cytokines, small protein signalling molecules that promote intercell communication. Both interleukin 2 (IL-2) and interleukin 31 (IL-31) have been shown to have pruritogenic activity. Binding of IL-31 to its receptor activates several signalling pathways, one of them involving Janus kinases. Oclacitinib is, of course, a novel Janus kinase inhibitor. Many recent studies have shown that oclacitinib provides a targeted therapy that selectively inhibits JAK1-dependent cytokines involved in allergy, inflammation, and pruritus and suggest that these are the mechanisms by which oclacitinib effectively controls clinical signs associated with allergic skin disease in dogs. Sadly, due to supply issues, the release of oclacitinib in New Zealand has been delayed yet again, and it won’t be reaching us in 2015 so I won’t dwell further on that drug. However there is another treatment modality that shows great promise.

Zoetis presented three papers on the use of a monoclonal antibody to treat atopic disease in dogs.

In humans, IL-31 and its receptors are overexpressed in skin affected by atopic dermatitis lesions. Therapy with anti-IL-31 monoclonal antibodies has been shown to reduce or eliminate the pruritic effects of IL31 in laboratory dogs. The first study identified and characterised a monoclonal antibody that neutralised IL-31 pruritus in Beagles. The second study worked out the most effective dose of the monoclonal antibody that reduced IL-31 produced pruritus. The final study by Zoetis that looked at the efficiency and

safety of an anti-IL-31 monoclonal antibody dosed twice subcutaneously at a 14–day interval. The study showed that these patients had a significant reduction in pruritus with no serious adverse events and no hypersensitivity.

Candace Souza included a discussion of the use of the owner-evaluated Pruritus Visual Analogue Scale (PVAS) that was validated by Peter Hill and his colleagues in 2007. A follow up study by the same group in 2009 showed that normal dogs (without dermatological disease) scored less than 2 on the scale.

I will discuss the clinical evaluation of pruritus and lesions in canine atopic dermatitis in a future article.

As usual some of the most interesting information came from the short scientific presentations and the residents’ projects. Here are some snippets: Elizabeth Mauldin and her colleagues presented a series of nine Boston terriers with zinc-responsive dermatosis. This is not a breed that we typically associate with zinc-responsive dermatosis although it has been reported previously in one Boston. Syndrome I zinc-responsive dermatosis is seen in the Arctic breeds; malamutes and huskies primarily. It appears to be associated with defective intestinal absorption of zinc. Syndrome II zinc-responsive dermatosis is seen in rapidly growing puppies or young adults that are fed zinc-deficient diets, or diets high in calcium that interferes with zinc absorption. Hyperkeratotic plaques form over areas of repeated trauma or the nasal planum and foot pads. In this series of Boston terriers, the median age of onset was 3.5 months with a range of 1 to 24 months. Alopecia with thick scale or hyperkeratotic plaques were seen on the dorsal muzzle in 5 out 9 cases, the margins and concave pinnae in 8 out 9, and pressure points in only 3 out 9 cases.

The histology was very suggestive of zinc responsive dermatosis with marked parakeratosis and serum lakes. Only five dogs were treated with zinc, given the retrospective nature of the study, with four responding to treatment.

Another disease that had a retrospective study done on it was canine epidermolysis bullosa acquisita, a sub-epidermal immune-mediated blistering disease.

Although it is classed as a rare disease, Petra Bizikova and colleagues described it in 20 cases, with young male dogs mainly affected (9 out 20 developed lesions before 1 year of age). Most interestingly, 11 out 20 dogs were Great Danes. A complete remission of skin lesions was obtained in 14 dogs, with either glucocorticoids alone or with other medications. The median dose of prednisone was 3 mg/kg/day. This is a more favourable prognosis than was previously assumed. Six dogs were euthanised (if you are American, euthanased if you are a Kiwi or Australian.)

We all have those dogs with recurrent Malassezia otitis externa, some with other symptoms of canine

duncan@animaldermatology.co.nz or http://www.animaldermatology.co.nz/

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hypersensitivity but there is a sub-population of dogs with no other skin disease. I am dealing with two as I write this. Doug DeBoer from the University of Wisconsin took blood samples from 21 dogs with at least three episodes of Malassezia otitis externa within 18 months and no other skin disease. A large percentage of these dogs had a positive Heska serum IgE test against allergens. Twenty-nine percent of the dogs (six of 21) had high serum IgE levels against Malassezia. The next step will be to evaluate the intradermal reactivity to Malassezia antigen and the dogs’ response to allergen specific immunotherapy.

These dogs are a source of frustration to owners if they are expecting a “cure”. I think it is appropriate even at the first presentation to warn them that there is a possibility that ongoing management may be needed.

It also highlights the need for further work-up for hypersensitivity even in cases that are presenting only with Malassezia otitis externa.

It is a common recommendation, when dogs treated with ciclosprin (Atopica) vomit, to place the Atopica capsules in a household freezer to decrease this likelihood. However whether or not this freezing impacted on the ciclosporin stability was unknown. A study by Rod Rosychuk’s group at Colorado showed that there was no effect on Atopica capsules stored at -20 degrees for up to one month.

Two separate studies illustrated the benefits of adding in polyunsaturated fatty acids to the treatment of canine atopics. One was a prospective, randomised, doubled-blinded, placebo-controlled trial on 36 atopic dogs treated with, and stable on, ciclosporin. Dogs were treated with either a placebo or with a combination of omega 3/omega 6 fatty acid supplementation for three months. The results of this study indicate a ciclosporin-sparing effect of omega 3 and 6 fatty acid supplementation.

The other study, another prospective, randomised, double-blinded, placebo-controlled trial that evaluated the effects of omega 3 fatty acid on atopic dermatitis in 72 dogs with a clinical diagnosis of atopy. Thirty-three were treated with fatty acid, 35 with placebo. On days 42 and 84, there was a significant reduction in pruritus scores of the fatty acid supplemented dogs.

Probably the most interesting hour was the workshop that I attended on microbial hypersensitivities, both bacteria and yeast, and dander hypersensitivities led by Valerie Fadok. The workshops are informal discussions of topics by 10–15 dermatologists, moderated by an expert in the field. As Valerie noted “…atopic dermatitis with associated relapsing staphylococcal pyoderma and/or Malassezia dermatitis is a common disease in dogs. For some dogs, we can reduce the relapses of pyoderma …

But many patients continue to break with pyoderma or yeast infection in spite of therapy that specifically addresses their allergies. One potential reason for these relapses is an allergic reaction to the microbes themselves. In the past, prior to the emergence of methicillin resistance and multidrug resistance in Staphylococcus pseudintermedius, these patients were treated with pulse antibiotic therapy. While this is still done in some parts of the country, it is becoming more difficult due to the selection of resistant strains of bacteria. Now we try to use bathing strategies and the use of lipid barrier repair products to help reduce pyoderma recurrence. Malassezia relapses can be

September 2015

prevented with pulse antifungal therapy and topical therapy.”)

First the workshop discussed Staph hypersensitivity which is well documented in human literature, with IgE directed against staphylococcal enterotoxins (superantigens).

Unfortunately the situation is less well documented in dogs. However everyone agreed that a history of frequent relapse, with an associated complete resolution of pruritus and lesions with antibiotics alone (another reason to use antibiotics without corticosteroids) is suggestive of hypersensitivity. Staph lysate is used as a therapeutic agent when staphylococcal hypersensitivity is suspected. Unfortunately Staph lysate is no longer available in New Zealand.

Over half of the group recognised Malassezia hypersensitivity as relapsing infections with yeast that are highly inflammatory and incredibly itchy. The point was made that even low numbers of yeast are relevant and should be treated. For management of these patients long term, pulse antifungal therapy and topical therapy are used to prevent relapse. Many participants are using the same protocol that we use in New Zealand, using Malassezia allergens in their intradermal testing protocols and as immunotherapy.

IgE against Malassezia can be identified with serum testing as well, although the sensitivity may be lower than that for intradermal testing. Like the New Zealanders, most people are either adding Malassezia allergen to their allergenic extracts, and some (as we are) are following Dan Morris’s protocol using it as monotherapy by mixing the allergen: saline or allergen:diluent 1:10 (1 ml of Malassezia 20,000 IU + 9 ml diluent). I have never used human dander as part of the intradermal testing regime, but do test for cat dander. A number of participants in the workshop include human dander in their testing regime, with a reported reaction rate of 20–30%. Based on this information, I have added human dander to my testing regime.

Shelley Rankin in her lecture “The Fast Track to Multidrug Resistance” introduced new research that dealt with the response of bacteria that are exposed to sub-therapeutic levels of antimicrobials.

Specifically, she discussed the difference between antibiotic resistance and “persister cell” tolerance to antimicrobials. Persistence refers to the phenomenon in which a small subpopulation of microbes survives the lethal effects of a drug. Persistence is distinct from resistance in that, unlike resistant mutants, persister populations do not expand in the presence of the toxic compound, and population growth resumes only once the drug has been removed. Furthermore, upon retreatment, the subcultured organisms are drug sensitive, suggesting unlike resistence, persistence is not heritable.

Persisters represent a small subpopulation of cells that spontaneously enter a dormant, non-dividing state. When a population is treated with a bactericidal antibiotic, ordinary cells die but persister cells survive because antibiotics need active metabolising cells in order to kill them. Dealing with persister cells is a difficult problem as no antibiotics are effective against dormant persisters. Some antibiotics like fluorquinolones may promote the formation of persisters by causing DNA damage, which then leads to dormancy.

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Highlights from the 2015 World Small Animal Veterinary Association World Congress (WSAVA 2015) Bangkok, May 15â&#x20AC;&#x201C;18, 2015

David Smith, BSc, BVSc(dist.)

In May this year, I was fortunate to attend the 2015 WSAVA conference in Bangkok, Thailand as the CAS representative. Accommodated in the busy shopping district of Pratunam, 2,500 people attended four days of lectures, workshops and social events. Choosing what to report on was a challenge, but here are some of my highlights.

WSAVA Guidelines for recognition, assessment and treatment of pain:

Established by WSAVA, the Global Pain Council has developed pain assessment and treatment guidelines, to improve confidence and competence in applying pain treatments. Launched at the conference in Bangkok, and endorsed by 52 member associations from around the world, including CAS, the guidelines provide a reference for pain recognition and management, easily implemented in clinical practice.

Information is provided on product and procedure modalities including pharmacology, mechanism of action, indications, contraindications, dosing, and practical clinical notes to help guide the reader to design their therapeutic approach to the needs of the individual patient.

Aligning well with the recent Animal Welfare Amendment Act (no. 2) 2015, the guidelines are well worth a read. The guidelines are available from http://www.wsava.org/guidelines/global-pain-councilguidelines

What do we know? nutraceuticals?

and (3) 300 mg ASU PO once daily. Analysed knee joint fluid prior to supplementation and then monthly throughout the study, to measure transforming growth factor b1 and b2 (TGF-b1, TGF-b2). TGF-b is a stimulator of extracellular matrix production (type II collagen, proteoglycan) in chondrocytes. At both doses, ASU increased both TGF-b1 and TGF-b2 compared to the control.

Is there evidence for

Ross Palmer from the USA gave a passionate lecture on nutraceuticals. Palmer shared findings from human, canine, and feline research for the use of avocado soybean unsaponifiables (ASU); ASU combined with chondroitin sulfate (CS) and glucosamine (Glu); and omega-3 fatty acids.

Avocado Soybean Unsaponifiables (ASU) Human medicine has shown good evidence for efficacy of ASU in osteoarthritis (OA) treatment. The result was a significant reduction in pain, functional impairment, and NSAID reliance in human OA in knees and hips. Activated chondrocytes incubated with ASU showed reduced: pro-inflammatory cytokines interlukin-1b (IL-1b) and tumour necrosis factor-a (TNF-a), enzyme expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX2) to levels similar of non-activated chondrocytes.

Similarly, activated monocyte/macrophage like cells incubated with ASU, showed a reduced TNF-a and IL-1b expression.

The author with the certificate endorsing the WSAVA Guidelines for Recognition, Assessment and Treatment of Pain

Canine study 1: Healthy young adult dogs: groups: (1) Control, (2) 300 mg ASU PO every 3 days,

Canine study 2: A CCL transection study found the group supplemented with ASU, showed reduced development of early OA cartilage and subchondral bone lesions (macro and microscopic), compared to placebo controls.

Combined ASU, Chondroitin sulfate (CS), and Glucosamine (Glu) Synovial lining surrogate cells treated with ASU and CS in combination inhibited levels of IL-1b, TNF-a and expression of PGE2 better than either agent alone.

When activated with IL-1b, canine chondrocyte cell culture cells showed a ~70% increase in PGE2 production.

Pre-incubation with ASU+CS+Glu combination decreased PGE2 production when activated to ~60% below that of non-activated control cells. Similar effects have been shown in activated feline chondrocyte cell cultures.

Epigallocatechin gallate (EGCG), is an antioxidant found in green tea. When this was combined with

Waikiwi Vet Services Ltd, 299 North Rd, Invercargill

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ASU+CS+Glu, there was an anti-inflammatory effect. A study of hound dogs with chronic induced stifle OA, were treated with Glu+CS+ASU+EGCG. The dogs showed increased peak vertical force similar to that seen in various NSAIDs. Although the study had some limitations, it shows potential.

Omega-3 fatty acids Dietary supplementation with fish oil omega-3 fatty acids in OA dogs has been shown to significantly improve weight bearing peak vertical force. The magnitude of improvement (+5.6%) was comparable to the magnitude reported in NSAID trails. Eighty two percent of OA dogs improved on omega-3 supplemented diet compared to 38% fed the control diet. Another study showed omega-3 fatty acid supplementation allowed for more rapid reduction in carprofen dose in OA dogs compared to dogs fed low omega-3 diet.

Diabetes mellitus: when the insulin doesnâ&#x20AC;&#x2122;t seem to be working

David Church from the UK gave an interesting lecture on diseases complicating the management of diabetes mellitus. The focus of the lecture was acromegaly in cats as other topics such as hyperadrenocorticism and diabetic ketoacidosis was covered in other lecture streams.

Feline acromegaly, although thought to be underdiagnosed, is an uncommon disease. UK data measured insulin-like growth factor-1 (IGF1) concentrations in 158 cases of variably controlled

September 2015

diabetic cats.

Fifty-nine (32%) had markedly increased IGF-1 concentration. Eighteen of the 59 underwent pituitary imaging, confirming diagnosis of acromegaly in 17/18 cases. Virtually all the cats had a normal physical appearance (with none having the classic sign of agromegaly â&#x20AC;&#x201C; prognathia inferior). They commonly presented with persistent hyperglycaemia with elevated fructosamine and concurrent weight gain rather than weight loss. Other clinical signs vary vastly due to wide range of effects the disease has on the body but tend to only be seen late in the disease process.

The medical management of acromegaly with somatostatin analogues has been evaluated in few cats with limited to no success. Growth hormone receptor antagonists are not reported in cats but have 90% response rates in humans. Dopamine agonists (L-deprenyl) had no effect on reducing insulin requirements in cats and in people typically was only 10â&#x20AC;&#x201C;20% effective. Aggressive insulin therapy, of up to 45 IU three times a day, may be effective in managing cats. Radiotherapy of the pituitary gland had limited response. Professor Church also described surgical excision of the pituitary in 25 cats. Twenty-two of the 25 cats no longer required insulin after the surgery and 3 died due to surgical complications. Following surgery, cortisone, L-thyroxine, +/- desmopressin were required to compensate with loss of pituitary function.

References are available on request via the WSAVA app (android or itunes).

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CAS Specialist Profile – Pru Galloway

The CAS Specialist Profile is a new feature we plan to run regularly in the CAS Newsletter, aiming to provide an insight into the path New Zealand veterinarians have taken to achieve specialisation.

Pru Galloway is a registered specialist in Feline Medicine, she lives in Wellington where she runs a feline referral service, CatMed. She has been a registered specialist since 1997.

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

I studied at Massey University for my BVSc. I then spent two and a half years in a small animal practice in Christchurch after graduation.

What drove you to specialise, and why did you choose feline medicine? I have tremendous respect for vets in general practice, but for me I felt I was a ‘jack of all trades’ and master of none. Specialisation has allowed me to delve deep in a narrow field.

Feline Medicine was a natural choice; I like cats’ independent nature and love working with them.

Although I won the Small Animal Surgery prize in my final year at Massey, I was never bold enough to be a surgeon; ‘do no harm’ was always playing loudly in my head. Feline Medicine combines my love of problemsolving with my affinity for cats.

Explain the process you took to become a registered specialist. I completed a two-year Residency in Feline Medicine at Bristol University, which I believe at the time was the only vet school in the world offering a feline-only position. I was lucky to have great supervisors, and that all the cases were referrals, so I saw a lot of really interesting cases.

Living in the UK was great; the clinical part of Bristol’s vet school is in Langford, a small rural village south of Bristol. I lived on the top floor of a stone manor house that had belonged to Winston Churchill’s family. It was a beautiful park like setting, quintessentially English with huge trees, a sweeping drive and wrought iron gates.

After completing my Residency I returned to small animal practice in Christchurch and gained Membership of the Australian and New Zealand College of Veterinary Scientists (ANZCVS) in Feline Medicine by examination. New Zealand’s big outdoors was a real draw-card for me and might have distracted me from sitting my ANZCVS Fellowship exams, but an injury while sea-kayaking left me with a prolapsed cervical disc and I was unable to work for a year. I could of course still study, so I did. Passing Fellowship involved having papers published in peer-reviewed veterinary journals, submitting a comprehensive case-log and passing written and oral examinations.

It was a huge academic challenge and the first time I had attempted something that I wasn’t confident I would pass. If Membership was climbing Mt Cook, Fellowship was my Mt Everest. It has opened many career doors for me and allowed me to apply for registration as a Specialist in Feline Medicine.

What do you like most about your job? I like lots of things about it, but the main two are: • Making a difference. How many jobs are there where every day you are thanked for the difference you make?

• Being self-employed.

An owner has told you they can’t have children and that their cat is their ‘baby’, it is a young cat which proves to have FIP. Some owners can be challenging, but most just need empathy and time for all their questions and concerns to be addressed (the receptionists might disagree with me about this! They often comment that my clients Dr. Prue Galloway, BVSc, are high maintenance). MANZCVS, FANZCVS, Registered What is the most Specialist in Feline Medicine challenging part of your job? Compassion fatigue. I am now better at compartmentalising work and home life.

What advice would you give to someone thinking of specialisation? Check out all your options carefully, and get good grades as residency positions are competitive. Think about where you want to live postspecialisation and if that is New Zealand, what the job prospects are.

What do you think about vets specialising later in their careers, after a significant period of time in general practice? Each to their own, if it is your dream then follow it. Specialist training is not a walk in the park and it is expensive in lost earnings, time and sometimes relationships. Be prepared to put other parts of your life on hold.

Do you think New Zealand needs more specialists, and if yes, in what areas? At least one of every specialist in small animals would be great, wouldn’t it?! It would be good to have a New Zealand cardiologist (we do have Fiona Campbell visiting Massey now), an oncologist, a small animal neurologist. But we need to be realistic about the size of our population and how many specialists it can support.

Apart from Catmed, what other ‘work’ roles do you have? I am on the chapter examination committee of the feline branch of the ANZCVS and the editorial board of the Journal of Feline Medicine and Surgery.

I am also the Hill’s Pet Nutrition Senior Adjunct Lecturer in Feline Medicine at Massey University.

How many cats do you own? One…..I am not a crazy cat lady! I am a greenie at heart and am very aware of the impact cats have on our indigenous fauna.

What are you passionate about?

At work: Improving the wellbeing of cats and vets.

Outside work: Friends, family, the NZ outdoors, conservation and chocolate.

What is the worst part of your job? I’ll set the scene.

Pru can be contacted at Catmed, 70 Pharazyn St, Lower Hutt. Tel 04 569 8830 or pru.catmed@clear.net.nz

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Companion Animal Society Newsletter

Volume 26 Number 3

September 2015

Companion Animal Society Newsletter

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Book review: Kirk’s Current Veterinary Therapy XV

By John Bonagura and David Twedt Published by Saunders, December 2013

Part 1: by Chris Welland*, BVSc, MACVS

My first introduction to CVT was in 3rd year at Massey when I purchased CVT XI. Most of the class was ordering Ettinger. My initial reaction to the book was disappointment – I wanted a text with a moderate amount on everything but ended up with a text with everything on a moderate amount. CVT does not claim to be an all-encompassing medical tome. In this age of VIN and online journals, a lot of texts become dust gatherers but this is certainly not the case with CVT. The contents page reminds me of going to a great restaurant, perusing over a tantalising menu and not knowing what to order (read) first. CVT remains a source for learning new things which quickly become part of your clinical repertoire – examples of this from previous editions include: • CVT XII – my first introduction to Jody Lulich’s voiding urohydropropulsion technique.

• CVT XIII – looking out for hepatoportal microvascular dysplasia/portal vein hypoplasia (updated in CVT XV).

• CVT XIV – the exotically named feline aqueous humour misdirection syndrome and an introduction to pulmonary hypertension (both updated in CVT XV).

Kirk’s Current Veterinary Therapy XV does not disappoint on providing new information either. For example I did not know that the depletion of B12 levels in cats with GI disease is very quick (T1/2 = 5 days). This is completely different in people where the presence of a binding protein means that depletion may take several years. There is also an updated chapter on critical illness-related corticosteroid insufficiency. This is a major cause of death in critical human patients and is probably very significant in our very sick animals – could this mean a return of the infamous steroid injections which we used to administer in liberal doses to our ‘shock’ patients???

One of my other new favourite chapters in the XVth edition is number 52 – ectopic ACTH syndrome and food-dependent hypercortisolism in dogs. Cushings is now no longer just an adrenal or pituitary-based tumour. Now we have to add ectopic ACTH secretion from a nonpituitary/adrenal tumour and increased cortisol production due to ectopic adrenal receptors stimulated by food to our differential list!

CVT XV also has a Kiwi flavour to the contents.

Marion Wilson and Fiona Hollinshead provide an excellent chapter on endoscopic transcervical insemination. Rhian Cope of the Environmental Risk Management Authority contributed to the toxicology section. His chapter titled ‘Pesticides: New Vertebrate Toxic Agents for Pest Species’ was a fascinating read.

The anti-1080 brigade will be interested to know that scientists are working on some new posions to combat our pest species. This includes a novel toxin derived * ‡

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from our native poisonous plant – tutu. It is a little ironic that I have to read an American text to find out what is going on in our neck of the woods.

Criticisms of Kirk’s Current Veterinary Therapy XV: 1. The name – When Dr Kirk’s first edition was printed in 1964 the word ‘current’ would have been very appropriate. Information is disseminated so quickly these days that by the time a book is published some of the contents are already outdated. One example of this from CVT XV is the chapter on exocrine pancreatic insufficiency.

A recent study has revealed that some dogs showing classical clinical symptoms have normal cTLI, BUT abnormal cPLI-deficiency in lipase alone. This recent information is not included in this chapter. Possibly RVT (Recent Veterinary Therapy) may be a better name…

2. The format of the additional electronic chapters (e-chapters). It would have made more sense to have updated chapters from the previous edition as exclusively e-chapters. New chapters should have been in the text alone rather than a combination on new and updated chapters in the text book.

3. Minor printing error(s)? – only found one!

CVT continues to be my ‘go to’ text and the current addition continues along the tradition of providing excellent information in detailed, readable and interesting chapters. I would certainly recommend this book to fellow clinicians and those who are studying for Membership or Fellowship exams.

Part 2: by Duncan Graham‡, BVSc, BSc (Hons), Animal Dermatology NZ

I will concentrate on the dermatological and otic disease section of Kirk’s Current Veterinary Therapy XV, although I did get some very good information from this edition about canine colitis and antibioticresponsive diarrhoea. A German shepherd with severe recurrent inguinal, perivulvar and perianal pyoderma and concomitant diarrhoea responded completely to metronidazole. Next we trialed tylosin at 25 mg/kg once daily as suggested by CVT XV. For the past 6 months the dog has remained normal.

The dermatological section starts off with an article on Diagnostic Criteria for Canine Atopic Dermatitis by Claude Favrot and a chapter on Treatment Guidelines for Canine Atopic Dermatitis by Thierry Olivry and Pascal Prelaud. All three authors are leaders in the field on these topics but have published similar information elsewhere. In fact, each section is written by dermatologists that have published widely on the

Halifax Veterinary Centre, Nelson, Chris@halifaxvet.co.nz dgg@clear.net.nz or http://www.animaldermatology.co.nz/

Companion Animal Society Newsletter

Volume 26 Number 3

subject. For example the excellent section of cutaneous granulomas in dog and cats is authored by Janet Fyfe and Richard Malik, both of whom have done an immense amount on the micro-organisms responsible for granulomas. I enjoyed the sections on toxicoses of various types. Being out of general practice for a while meant that specifics of some toxicoses were new to me.

For example, the toxic agent in Vitis species (grapes and raisins) hasn’t been identified. Many dogs do not develop signs of toxicosis after ingestion of grapes or raisins. It is not clear whether this is because the toxin isn’t always present or that some dogs are not sensitive.

There is anecdotal evidence that cooked raisins are not toxic.

Other good section was the one on dermatophytosis

by Karen Moriello and Doug DeBoer, confirming that terbinafine and itraconazole are the best treatments for that disease in both cats and dogs. The main

problem with terbinafine is that at 30 mg/kg you are giving 1 tablet for every 8 kg so a 30 kg dog would need 4 tablets. The generic itraconazole Itrazole might be a better choice for larger dogs although even then a 30 kg dog might need two capsules at the recommended dose of 5–10 mg/kg once daily for 7 days on then 7 days off. The perennial question of what to do about dermatophytosis in the cattery situation is well covered in Karen Moriello’s second chapter entitled Dermatophytosis: Investigating an Outbreak in a Multicat Environment.

The section on flea control in flea allergy dermatitis was disappointing in that several of the newer flea products like afoxolaner (Nexguard, Merial) and fluralaner (Bravecto, MSD Animal Health) weren’t mentioned.

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Companion Animal Society Newsletter

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Highlights from NZVJ Volume 63, Issue 5, 2015

Sarah Fowler, BSc, Msc, PhD, BVSc, CAS Newsletter Editor Remember, even if you are not a subscriber to the print version of NZVJ, all NZVA members have free online full-text access to the NZVJ at http:// www.sciquest.org.nz/nzvj

How accurate is your refractometer?

Comparison of specific gravity analysis of feline and canine urine, using five refractometers, to pycnometric analysis and total solids by drying Tvedten HW, Ouchterlony H & Lilliehöök IE Pages 254–259 Why they did it Measurement of urine specific gravity is a rapid, inexpensive diagnostic test performed in-house in most veterinary clinics. In order to assess the reliability and accuracy of refractometers used to measure USG the authors compared the performance of five refractometers using urine samples from cats and dogs.

What they did Starting with urine samples from 27 cats and 31 dogs submitted for routine analysis, the authors determined USG with five different refractometers.

They then compared these results to those obtained with two different reference methods: they dried the urine and estimated the USG from the weight of total solids and also measured the density of the urine with a pyncnometer.

What they found The five refractometers gave clearly different measurements for the USG of the urine samples.

These measurements were generally less than that estimated from total solids or measured with the pyncnometer and this was especially true for refractometers designed specifically to measure cat urine.

Take-home message The authors recommend that veterinarians should not use the precise cut-off values such as 1.030 or 1.035 for evaluating renal concentrating ability in cats and dogs.

Which approach to castration – caudal or prescrotal, is better for repair of perineal hernias in dogs?

Comparison of caudal and pre-scrotal castration for management of perineal hernia in dogs between 2004 and 2014 Snella WL, Orshera RJ, Larenza-Menziesb MP & Popovitcha CA Pages 272–275 Why they did it The most commonly used castration technique used concurrent with perineal hernia repair is pre-scrotal castration. This requires the patient to be positioned on their back for the castration then turned over for the hernia repair. In contrast, caudal scrotal castration is performed with the patient in sternal recumbency and so no repositioning is required. This study compared.

What they did This study compared the rate of peri- and postoperative complications for caudal scrotal castration + hernia repair to that for prescrotal castration + hernia repair. This was a retrospective study that reviewed medical records for 142 dogs undergoing these surgeries in Pennsylvania, USA between 2004–2014.

What they found There were no recorded perioperative or major post-operative complications in either group.

There was no difference in the rate of minor postoperative complications between the two groups (6% in the CSC group and 7% in the PSC group).

The most common minor complications were heat, erythema and swelling associated with the incision site and scrotal swelling.

Take-home message The authors recommend that caudal castration is the preferred approach when an orchiectomy is performed concurrent with perineal hernia repair. This is because caudal scrotal castration eliminates the need for repositioning and to prepare and drape a second site and is not associated with more peri/post-operative complications relative to the standard pre-scrotal castration. n

* sarah.fowler@gmail.com

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Companion Animal Society Newsletter

Volume 26 Number 3

September 2015

Companion Animal Society Newsletter

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“What is your diagnosis?” The answer (From page 10)

1. –Neoplasia: Although bladder neoplasia occurs rarely in cats, the most commonly described bladder neoplasm of cats (and dogs) is transitional cell carcinoma (TCC). This tumour often develops in the trigone region, making it poorly amenable to surgical excision. Mean survival time for cats with TCC treated with surgery, chemotherapy, NSAIDs, or a combination is 8.5–12 months.

–Cystotomy: This surgery makes direct visualisation of the bladder contents and excision of any masses possible, with the most common complications arising from anaesthesia or the development of uroabdomen. The latter manifests as depression, vomiting, or metabolic derangements such as azotaemia, dehydration, metabolic acidosis, and hyperkalaemia.

Less commonly reported bladder neoplasms include squamous cell carcinoma, lymphoma, leiomyo(sarco)ma, adenocarcinoma, and haemangiosarcoma.

–Thoracic and abdominal radiographs/ultrasound: An imaging series should be considered to identify possible neoplastic metastases, which may worsen the patient’s prognosis.

–Haematoma: Trauma to the bladder, either iatrogenic (e.g. cystocentesis, catheter tip trauma) or as a result of partial rupture, may result in the formation of a haematoma. If complications such as uroabdomen and prolonged haemorrhage are avoided, the prognosis is excellent. Mucosal defects generally heal within 5 days, while fullthickness defects heal within 14–21 days.

–Serial ultrasonographic imaging: The shape and size of the mass may be monitored through this non-invasive imaging modality, but requires multiple revisits as well as access to an ultrasound machine. The mass may continue to grow in the meantime, possibly giving rise to distant metastases or recurrent urethral obstruction.

–Polypoid cystitis: Inflammatory polyps occur uncommonly as a result of chronic irritation due to cystic calculi or lower urinary tract disease.

Polypectomy is not often necessary, as removal of the inciting cause often results in resolution of the polyp within 4–6 weeks.

2. –Complete blood count, serum biochemistry: While azotaemia or chronic inflammation may be revealed on bloodwork, a specific diagnosis is rarely achieved with these tests alone. Nonetheless an adequate minimum database may assist in ruling out concurrent disease or overt organ dysfunction.

–Urine sediment exam: A sediment exam may help to differentiate among infection, inflammation, and neoplasia. A lower urinary tract infection may be identified by the presence of erythrocytes, leukocytes, and most importantly intracellular bacteria. Inflammation (e.g. idiopathic cystitis) may appear similar to infection on sediment exam; however, there will be a distinct lack of intracellular bacteria (assuming there is no concurrent infection).

Exfoliated neoplastic cells are seen in up to 30% of urine sediment samples from patients with a primary bladder tumour; care must therefore be taken when interpreting these results as this test is poorly sensitive and specific for neoplasia.

Tuck was re-evaluated 3 and 12 days after initial discharge, with ultrasonographic images (Figures 2 and 3) collected at those times: The mass had reorganised into a smaller, segmented, pedunculated mass, eventually reducing in size so dramatically that it was barely visible. The bladder wall appears diffusely thickened in both images, possibly indicating a degree of ongoing cystitis, though true mural thickening cannot be appreciated unless the bladder is fully distended. Given the

–Urine culture and sensitivity: Lower urinary tract infection should be ruled out as this may predispose to the formation of benign inflammatory polyps. Urine for culture should be collected via cystocentesis while avoiding aspiration of a mass.

–Fine needle aspiration (FNA) of the mass: Although FNA may be useful in directly harvesting cells adequate for a cytological diagnosis, reports have been made of tumours being seeded throughout the abdominal cavity following this procedure.

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Because a hyperechoic mass has been visualised one month prior to Tuck’s presentation, there was concern that a malignant process was occurring in his bladder.

Tuck was deobstructed without cystocentesis, and no obvious physical obstruction was encountered during catheter placement. Serum biochemistry was unremarkable, while his urine sediment contained erythrocytes, fat droplets, neutrophils, and no crystals.

He was managed with an indwelling silicone urinary catheter for 2 days. After Tuck’s recovery from this episode, his owners opted for repeat ultrasonographic evaluation of the mass to monitor its development, with eventual cystotomy and excision should it continue to grow in size.

Figure 2. Ultrasonographic image of Tuck’s bladder, 3 days after discharge

Companion Animal Society Newsletter

Volume 26 Number 3

Acknowledgments

Tuck and his family Julia Giles BVSc, MVM, Small Animal Emergency/ Critical Care Veterinarian Paul Wightman BVSc, Veterinary Diagnostic Imaging Resident

Resources

Figure 3. Ultrasonographic image of Tuck’s bladder, 12 days after discharge

recurrence of Tuck’s obstruction, the lack of obvious physical urethral obstruction, and unremarkable serum biochemistry, his condition has been attributed to idiopathic cystitis. The bladder mass was likely a haematoma that developed either due to a partial rupture or iatrogenic trauma. It is unknown whether this mass is related to the one visualised one month prior to presentation. Tuck has since made a full recovery, with no subsequent episodes of cystitis or urethral obstruction, and no further bladder abnormalities visualised on ultrasonographic exam.

September 2015

Berent A. Endoscopic Polypectomy and Laser Ablation for Benign Urinary Bladder Lesions. In: Weisse C, Berent A (eds). Veterinary Image-Guided Interventions. Pp. 383–8.

John Wiley & Sons Ltd, Oxford, 2015 Cannon CM, Allstadt SD. Lower Urinary Tract Cancer.

Veterinary Clinics of North America: Small Animal Practice, 45(5), 807–24, 2015 Lipscomb VJ. Chapter 116: Bladder. In: Tobias K, Johnston SA (eds). Veterinary Surgery: Small Animal. Pp 1978–92. Elsevier Saunders, St. Louis, USA, 2011

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PanPacific Conference 2015

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Companion Animal Society Newsletter

Volume 26 Number 3

PanPacific Conference 2015

September 2015

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Massey Home Page – September 2015 Staff First veterinary oncologist to work in New Zealand.

It is with great excitement that the Massey University Veterinary Teaching Hospital can introduce Valerie Poirier to New Zealand. Valerie is from Quebec and graduated from the University of Montreal in 1998. Valerie undertook a residency programme at the University of Wisconsin and became a Diplomat of the American College of Veterinary Internal Medicine (Oncology) in 2003. From there, she moved to Switzerland and began work at the University of Zurich in 2003 working as a Medical and Radiation Oncologist and acquired a second Diploma from the American College of Veterinary Radiology (Radiation Oncology) in 2006. In 2007 she moved to Australia and joined the team at Brisbane Veterinary Specialist Centre and helped built the first radiation facility for pets in the southern hemisphere. She moved to Guelph in August 2012 and was part of the animal cancer centre as a radiation oncologist. She has joined Massey as an academic and clinician within the VTH. This is the first time we have had a double-boarded medical/radiation oncologist on staff, in fact it is a first in NZ to have a specialist oncologist within a referral setting. She will be a major asset to our patrons and their clients. Together with Jonathan Bray, Valerie will be further establishing a radiation oncology service in Palmerston North. Currently we can offer palliative protocols and the intention is to increase the range of protocols on offer over time. Combined with access to multiple forms of imaging (Eklin DR radiography, fluoroscopy, ultrasound, CT and MRI), in-house radiologists and anaesthesiologists and specialist surgeons, the VTH can truly offer a comprehensive oncology service. We welcome your referrals.

Robert (Bob) Bahr, Diplomat of the American College of Veterinary Radiologists, has joined the imaging department for a locum period. He will support Ron Green in a teaching and clinical role. Paul Wightman, our resident in diagnostic imaging, is temporarily leaving us for a year at the University of Melbourne Vet School. With in-house MRI this will be an exciting year for Paul as he completes his training prior to sitting his speciality examinations. We wish him well.

There are two new interns in the VTH rotating through the services and MU-PEC (MU Pet Emergency Centre). Nadia Vather, originally from South Africa, is a Melbourne Vet School graduate and spent a few months in mixed rural practice before coming to MU. Phil Hyndman grew up in Auckland and completed his BVSc at Massey. He spent the last 3 years in mixed practice in central and north Otago. We also have a new resident in small animal surgery. Malcolm Jack is originally from the UK but completed vet school in Melbourne. He has completed general and surgical internships and is joining us for a 3–4 year residency program as part of a European College of Veterinary Surgeons training programme.

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Becca Leung, a recent Massey BVSc graduate has commenced a residency in Small Animal Nutrition, supervised by Dr Nick Cave and sponsored by Hills Pet Nutrition. Becca will consult on cases with special dietary requirements as well as improve the nutritional surveillance of our in-hospital cases.

Congratulations

Sarah Hill, second year resident in Small Animal Medicine, passed Membership Examination of the Australian and New Zealand College of Veterinary Scientists. This is the first part of her credentialing for sitting Fellowship examination in the future. Well done Sarah, as any member of the ANZCVS knows, these are significant examinations and it’s a great feeling to become a member of the college.

Andrew Worth completed his PhD, which looked at degenerative orthopaedic disease of German shepherd police dogs. His studies involved canine hip dysplasia and lumbosacral disease.

Australian and New Zealand College of Veterinary Scientists Science Week

Massey was well represented in the small animal streams of Science Week with Jonathan Bray speaking in the surgical forum on soft tissue sarcoma and reconstructive surgery for mandibular neoplasia using custom titanium implants. Nick Cave was speaking on nutrition, and Andrew Worth spoke in the Welfare chapter on the Student Outreach programme in Samoa (desexing charity work), which is a joint project between MU, World Animal Protection, NZ Aid and the Animal Protection Society of Samoa. Kat Crosse won a young Speaker prize in the surgery forum presenting her research on the histology of enlarged soft palates in brachycephalics. Several Massey staff were involved as examiners.

Buildings

The car-park outside the IVABS entrance is gone and in its place the foundations for the new Wildlife unit are rapidly being erected. We have relocated our isolation unit and reception area and are successfully working with minimal disruption.

Clinical Trials

We are keen to receive referrals for a number of clinical trials underway: • Novel L7/S1 stabilisation for degenerative lumbosacral stenosis (cauda equine syndrome) using custom titanium implants.

• Angular limb deformity correction using computer assisted surgical solutions that allow internal fixation and one stage correction.

• Condylar fractures in working dogs.

• Talo-crural instability/luxation in working dogs – trialling a new form of stabilisation.

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Volume 26 Number 3

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