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Some situations can cause stress VOL. 19 - (2) - OCTOBER 2009 The European Journal of Help them through it, Companion Animal Practice And because stress may cause dermatological and digestive disorders in animals, CALM formula is highly digestible and contributes to a healthier skin. CALM: a major and comprehensive innovation to help maintain the emotional balance of cats and dogs, which can also be recommended for use in conjunction with behaviour therapy. www.royal-canin.com THE EUROPEAN JOURNAL OF COMPANION ANIMAL PRACTICE - Vol. 19 - (2) - October 2009 To help manage the stress of cats and dogs under 15 kg when faced with certain situations, CALM contains natural actives, AlphaCasozepine and L-Tryptophane. NEW Photos : Arioko - Andreas Gradin - Illustration Cubedesigners - 08/2009 VETERINARY give them CALM Moving house, a new pet or baby in the household, going away on holiday ... ISSN 1018-2357 Clinical Cytology of Companion Animals: Part 3. Cytology of the lymph node 117 Folded flap palatoplasty for treatment of elongated soft palates in 55 dogs 125 Treatment of feline hyperthyroidism with radioactive iodine-131 156 The Recession and how it is affecting or may affect Vets in Practice 185 THE OFFICIAL JOURNAL OF FECAVA Federation of European Companion Animal Veterinary Associations www.fecava.org Volume 19 (2) October 2009 The Official Journal of the Federation of European Companion Animal Veterinary Associations (FECAVA). EDITOR Dr. Keith Davies 43, Hill Top Road - Newmillerdam GB-WF2 6PZ Wakefield Tel.: (44) 1924 250486 (UK) (33) 4 68 39 50 29 (F) Fax: (44) 1924 259572 E-mail: [email protected] PRODUCTION COMMITTEE Dr Andrew Byrne, FECAVA President Dr. Keith DAVIES, Editor Astrid M. BJERKÅS, Sub-Editor Dr. Joaquin ARAGONES Dr. Peter STERCHI Dr. Denis NOVAK Dr. Johan VAN TILBURG Dr. Monique MEGENS Dr Ellen BJERKÅS EDITORIAL BOARD (FOR NEW WORK) Dermatology Didier-Noël CARLOTTI (F) Anna TIDHOLM (S) Cardiology Internal Medicine Åke HEDHAMMAR (S) Orthopaedics Aldo VEZZONI (I) Surgery Simon ORR (GB) Imaging Ingrid GIELEN (B) Eiliv SVALASTOGA (DK) Reproduction Stefano ROMAGNOLI (I) Dentistry Peter FAHRENKRUG (D) Ophthalmology Ellen BJERKÅS (N) Neurology André JAGGY (CH) Endocrinology Mike HERRTAGE (GB) Oncology Jane DOBSON (GB) New Material should be sent to: Prof. Ellen BJERKÅS, Norwegian School of Veterinary Science, PO Box 8146-Dep, N- 0033, Oslo. E-mail: [email protected] ADVERTISEMENT BOOKINGS Sould be sent to: The Editor (see above) CIRCULATION All members of the Associations belonging to the Federation of European Companion Animal Veterinary Associations receive the European Journal of Companion Animal Practice as a part of their membership subscription (26,000 copies). PURCHASE OF COPIES For others interested in purchasing copies the price is 62 € per Volume (2 issues). Payment is only accepted by electronic transfer in euros. Orders should be sent to: FECAVA HQ, rue Defacqz 1, B-1000 Brussels EDITORS NOTE The language of EJCAP is English (UK). Where reprint papers have been translated, or where other versions of English were originally used, these have been translated to English (UK). THANKS The production Committee of EJCAP thanks: Dr. Tim Hutchinson Dr. Bob Gibbons Dr. Mike Herrtage Dr. Freddie Marshall Dr. John Houlton Dr. Sue Roberts who have spent time correcting the translations. PRINTED BY Roto Smeets GrafiServices, p.o. box 7052, 3502 KB Utrecht, The Netherlands. Tel +31 (30) 282 28 22 DISCLAIMER “The Federation of European Companion Animal Veterinary Associations and the Production Committee of the European Journal of Companion Animal Practice accept no responsibility for any omissions and/or errors in information printed in this journal.We specifically draw readers attention to the need to follow instructions of manufacturers products. In any specific situation readers are strongly advised not merely to rely on the material contained in the journal. Any views and opinions expressed are those of the writer and not the Federation or the Production Committee.” The European Journal of Companion Animal Practice (EJCAP) Contents The Federation of European Companion Animal Veterinary Associations (FECAVA) Editorial News 98 101 104, 208 CARDIOLOGY AND RESPIRATORY SYSTEM Blood Pressure in Small Animals - Part 3: Hypertension - Target organ damage, eyes and the CNS Diagnosis and treatment considerations B. Egner, P. Carr, T. Duke 111 GENERAL Clinical Cytology of Companion Animals: Part 3. Cytology of the lymph node E. Teske 117 EAR NOSE AND THROAT Folded flap palatoplasty for treatment of elongated soft palates in 55 dogs L. Findji and G. Dupré 125 ORTHOPAEDICS Diagnosis, treatment and prognosis of disc associated Wobbler syndrome in dogs S. De Decker, S. Bhatti, I. Gielen, L. Van Ham Treatment of degenerative joint disease of the hip with cementless and cemented total hip arthroplasty in a dog – a case report A. Eklöf, E. Eskelinen 133 141 GASTEROINTESTINAL SYSTEM Acute pancreatitis in dogs: a review article I. Kalli, K. Adamama-Moraitou, T. S. Rallis 147 ENDOCRINOLOGY Treatment of feline hyperthyroidism with radioactive iodine-131 I C. van Dijl, A.J. Hof 156 URINOGENITAL SYSTEM Dystocia: recognition and management I. M.Reichler, E.Michel 165 OPHTHALMOLOGY Hereditary retinopathies in the dog: genetic fundamentals and genetic tests C. Andréa, G. Chaudieu, A. Thomas, O. Jongh, J.-P. Jegou, S. Chahory, B. Clerc, P. Pilorge, O. Brenac 175 PRACTICE MANAGEMENT The Recession and how it is affecting or may affect Vets in Practice G. Little The Oxford Cat Clinic C. Blundell EJCAP 19(3) Dermatology Book Reviews Calendar of main European national meetings and other continuing education opportunities Secretariat or address to contact for information 97 185 193 163 199 204 206 The Federation of European Companion Animal Veterinary Associations (FECAVA) FECAVA Headquarter’s address: C/O Federation of Veterinarians of Europe rue Defacqz, 1 B-1000 Brussels Tel: +32 2 533 70 20 – Fax: +32 2 537 28 28 FECAVA Website: www.fecava.org Participating Associations: SKSAVA Slovak Small Animal Veterinary Association Director: Dr. Igor KRAMPL SASAP Serbia Association of Small Animal Practitioners Director: Dr. Denis NOVAK SSAVA Swedish Small Animal Veterinary Association Director: Dr Alexandra VILÉN SVK/ASMPA Schweizerische Vereinigung für Kleintiermedizin/Association Suisse pour la Médecine des Petits Animaux Director: Dr. Peter STERCHI SZVMZ Slovensko Zdruzenje Veterinariev Za Male Zivali Director: Dr. Bojan ZORKO TSAVA Turkish Small Animal Veterinary Association Director: Dr. Erkut GOREN USAVA Ukrainian Small Animal Veterinary Association Director: Dr. Vladimir CHARKIN VICAS Veterinary Ireland Companion Animal Society Director: Dr. Peter A. MURPHY VÖK Vereinigung Österreichischer Kleintiermediziner Director: Dr. Silvia LEUGNER AFVAC Association Française des Vétérinaires pour Animaux de Compagnie Director: Dr. Jean-François ROUSSELOT AIVPA Associazione Italiana Veterinari Piccoli Animali Director: Dr. Andrea VERCELLI APMVEAC Associação Portuguesa de Médicos Veterinários Especialistas em Animais de Companhia Director: Dr. José H. DUARTE CORREIA AVEPA Associación de Veterinarios Españoles Especialistas Pequeños Animales Director: Dr. Xavier MANTECA BASAV Bulgarian Association of Small Animal Veterinarians Director: Dr. Boyko GEORGIEV BHSAVA Bosnia and Herzegovina Small Animal Veterinary Association Director: Dr. Josip KRASNI BSAVA British Small Animal Veterinary Association Director: Dr. Wolfgang DOHNE CSAVA Czech Small Animal Veterinary Association Director: Dr. Jiri BERANEK CSAVS Croatian Small Animal Veterinary Section Director: Dr. Davorin LUKMAN DSAVA Danish Small Animal Veterinary Association Director: Dr. Hanne WERNER ESAVA Estonian Small Animal Veterinary Association Director: Dr. Janne ORRO FAVP Finnish Association of Veterinary Practitioners Director: Dr. Kaj SITTNIKOW GSAVA German Small Animal Veterinary Association Director: Dr.Dr. Peter FAHRENKRUG HSAVA Hungarian Small Animal Veterinary Association Director: Dr. Ferenc BIRÓ HVMS Hellenic Veterinary Medical Society Director: Dr. Katerina LOUKAKI LAK Letzebuerger Associatioun vun de Klengdeiere - Pracktiker Director: Dr. Katia DI NICOLO LSAPS Latvian Small Animal Practitioners Section of The Latvian Association of Veterinarians Director: Dr. Linda JAKUSONOKA LSAVA Lithuanian Small Animal Veterinary Association Director: Dr. Saulius LAURUSEVICIUS MASAP Montenegro Association of Small Animal Practitioners Director: Dr. Predrag STOJOVIC MSAVA Macedonion (Fyrom) Small Animal Veterinary Association Director: Dr. Pero BOZINOVSKI MVA Malta Veterinary Association Director: Dr. L. VELLA NACAM Netherlands Association for Companion Animal Medicine Director: Dr. Monique MEGENS NSAVA Norwegian Small Animal Veterinary Association Director: Dr. Stein DAHL PSAVA Polish Small Animal Veterinary Association Director: Dr. Roman ALEKSIEWICZ PVA Pancyprian Veterinary Association Director: Dr. Yiannis STYLIANOU RSAVA Russian Small Animal Veterinary Association Director: Dr. S. SEREDA SAVAB Small Animal Veterinary Association of Belgium Director: Dr. J. van TILBURG Associate Associations: European College of Veterinary Dermatology Contact: Dr. Dominique HERIPRET ECVS European College of Veterinary Surgeons Contact: Monika GUTSCHER ESAVS European School for Advanced Veterinary Studies (A part of the European Association for Veterinary Specialisation (EAVS)) Contact: Dr. Hans KOCH ESVC European Society of Veterinary Cardiology Contact: Dr. Nicole VAN ISRAËL ESFM European Society of Feline Medicine Contact: Claire BESSANT ESVCE European Society of Veterinary Clinical Ethology Contact: Dr. Sarah HEATH ESVD European Society of Veterinary Dermatology Contact: Dr. Aiden FOSTER ESVIM The European Society of Veterinary Internal Medicine Contact: Dr. Rory BELL ESVN European Society of Veterinary Neurology Contact: Dr. Jacques PENDERIS ESVOT European Society of Veterinary Orthopaedics & Traumatology Contact: Dr. Aldo VEZZONI EVDS European Veterinary Dental Society President: Dr. Olivier GAUTHIER EVSSAR European Veterinary Society for Small Animal Reproduction Contact: Dr. Gaia Cecilia LUVONI ECVD FECAVA Officers: Dr. Andrew BYRNE Dr Johan van TILBURG Dr. Simon ORR Dr. Jerzy GAWOR Eire Belgium UK Poland President Vice-President Secretary Treasurer Advisor to the board: Dr. Dr. Ellen BJERKÅS Norway Senior Vice-President Dr. Keith DAVIES 98 EJCAP Editor Editorial Development of Multi-resistant Bacteria and the Threat to Small Animal Practice There is now ample evidence that bacteria with multi-resistance to therapeutic antimicrobials are becoming more and more common both in animals and man. This is a consequence of increasing and ill-considered use of antimicrobials, particularly certain broad-spectrum agents, and there is growing pressure from the human field to restrict their use by veterinary surgeons. In his annual report for 2008, the Chief Medical Officer of England, Sir Liam Donaldson stated that “every inappropriate use [of antimicrobials] in medicine or agriculture is a potential source of harm or death in a future patient” and he made the specific recommendation that use of quinolones and cephalosporins in animals should be banned. Sir Liam was referring particularly to farm animal use but the close relationship between small animals and their owners and growing evidence of transfer of resistant organisms between animals and man is now focusing attention on small animal practice. It is clear that small animal practitioners need to take action not only to demonstrate that they can use antibiotics wisely but also to deal with the threat which well-recognised multi-resistant bacteria such as Escherichia coli, Pseudomonas aeruginosa and meticillin-resistant Staphylococcus aureus (MRSA), and more recently the emergence in Europe of multi-resistant Staphylococcus pseudintermedius (formerly known as S. intermedius) pose. Such organisms can be resistant to all licensed veterinary antibacterials, making treatment difficult or impossible, and can be carried by owners and veterinary staff leading to infection of in-contact people and animals. MRSA carriage amongst veterinary staff has been shown to be as high 27% in small animal referral hospitals and up to 10% of small animal practitioners sampled at a conference in Europe, whereas levels of carriage amongst the general public are typically 3% or less. Guidelines for hygiene and the use of antimicrobials in veterinary practice are available in certain countries and provide practical and effective ways of reducing the levels of nosocomial infection and the development of antimicrobial resistance. Typically, they focus on appropriate use of antimicrobials (use of sensitivity testing, selection of agents with maximum efficacy, use for minimum effective duration), cleanliness and disinfection, principles that are commonly taught at veterinary schools but too often not observed in veterinary practice. In the human field more rigorous implementation of such guidelines and effective publicity informing the public about rational use of antimicrobials has been associated with significant improvements; in Belgium, for example, high profile publicity during the autumn and winter months during 2000-2007, reduced outpatient prescription of antibiotics by 36% and erythromycin resistance in Streptococcus pyogenes, a common cause of tonsillitis, fell from 17% in 2001 to 2% in 2007. There is a need now for such guidelines to be actively put into place at the individual practice level by small animal practitioners throughout Europe, combining efficient use of antimicrobials, enhanced personal and practice hygiene, and client education. Such actions need to be combined with studies evaluating antimicrobial use and resistance levels in indicator pathogens, such as those listed above, demonstrating clearly that veterinarians can be trusted to handle these valuable agents. To facilitate these objectives the FECAVA Working Group on Hygiene and Use of Antimicrobials in Veterinary Practice is bringing together guidelines and recommendations from all member associations with the aim of establishing a unified approach that can be promoted to inform and educate both veterinarians and owners and provide a mechanism that will reduce inappropriate antimicrobial prescription, and decrease levels of antimicrobial resistance and nosocomial infection. The Working Group will present its initial studies in the FECAVA Symposium at the WSAVA/FECAVA/SVK-ASMPA Congress, Geneva, in June 2010. David H. Lloyd, Didier-Noel Carlotti, Katerina Loukaki, Ana Mateus, Peter A Murphy, Alexandra Vilen, FECAVA Working Group on Hygiene and Use of Antimicrobials in Veterinary Practice 101 FECAVA NEWS FECAVA NEWS Keith Davies, EJCAP Editor reports: FECAVA and G20 choose Baden-Baden for important meetings Why hold a FECAVA Council in BadenBaden? FECAVA holds two Council meetings every year and tries, where possible, to hold these in different Member countries. This March we were invited by the German Small Animal Veterinary Association to hold our Council, and other important FECAVA meetings, in association with the well-known ‘Spring Baden-Baden Small Animal Veterinary Congress’. The sceptical reader may think that this gadding around is an unnecessary and rather expensive perk for FECAVA Directors. Of course it is very pleasant to meet at different interesting venues all over Europe, but there is a very good reason why we do not choose always to meet at the most convenient and least expensive locations. In Baden-Baden we were able to meet a large part of the executive of GSAVA together with hundreds of their grass root members. It is important for both Officers and Directors to get the opinion of individual FECAVA members and Member Associations on how FECAVA is progressing and attempting to serve them. Council meetings not only remind FECAVA Directors what has been done but also what must be done and what may be done in the future. Quite a large proportion of the Council meeting is devoted to what “may be done”. This was especially important in Baden-Baden. It is L>>R Janne Orro, Tiina Toomet, Monique Megens and Lynda Davies took time off in the in the Caracalla Therme, Baden -Baden. Photo courtesy of Lynda Davies (not pictured). The Baden-Baden Council was a first for, Right>Left, new Directors Linda Jacusonoka (LSAP), Janne Orro (ESAVA), Stein Dahl (NSAVA), Ruth Bjerkås at one year old was certainly the youngest person to attend Council, although unlike the case of the other Directors, we preferred her in sleep rather than pro-active mode! impossible to be unaware of the current World financial crisis and developing recession. This has and will affect FECAVA. Interest on the financial reserves of the Federation has dropped dramatically, the reserves themselves also being worth less than they were. All this has happened outwith FECAVA’s control. Before the recession took us all by surprise, FECAVA had laid plans for many developments to serve better the needs of members. A few items can be highlighted: The improvement and expansion of our website, the development of EJCAP, plans to make FECAVA more politically effective by being proactive and liaising with both FVE and UEVP. At that time our reserves were good and provided a good financial cushion together with some interest. It was difficult for the FECAVA Council to decide how we should react to these times of recession. Some possible cuts to save money could be: • Placing a hold on our attempts,with the help of FVE and UEVP, to influence the EU decision making? This would certainly save costs in meeting travelling expenses, secretarial and 104 office help. • Leaving our website in its less than satisfactory state. • Should we delay further 3rd issues of EJCAP and cut down on commissioned papers in issues one and two? • Savings to Member Associations could be made by putting all 3 issues of EJCAP on-line as even though the Journal is largely self-funding, its distribution is costing member Associations a considerable amount of money. An on-line issue admittedly has all the information required and is easily accessible but it does not make FECAVA members aware of what FECAVA is doing and what material is available. To date, extensive questioning of FECAVA members indicates that even in the case of young, highly computer literate veterinarians, there is a feeling that whilst on-line is great and should continue, hard copies are still very much appreciated. Help to new emerging Associations could also be halted to save money. There is, of course, an alternative to making any of these cuts. The contribution paid by each member could FECAVA NEWS be increased. As a practical illustration of how this would affect FECAVA member’s pockets, if we all could forego a couple of pints of beer each year and be prepared to use that money to fund an increase in national associations’ membership dues, all these projects could go ahead. Do we want to draw back from trying to make sure the EU does not do things which are deleterious to our practices and our patients? Do we want to give up the idea of having hard copy Journals as tangible evidence of FECAVA in our clinics and homes? All these matters were discussed at length in Council and possible proposed membership increases were put forward. There was some opposition to the latter, particularly in the case of larger Associations who perhaps feel that they EJCAP - Vol. 19 - Issue 2 October 2009 agreed that some increase would be acceptable. A decision on the way forward, of course, cannot be taken until national representatives have had time to discuss all the points raised with their National Executives. It is at the FECAVA Council in Lille in November that we will make the final and important decisions. The Baden-Baden Kurhaus was the venue for the gala dinner. It was well chosen by GSAVA, and we were followed a week later by the G20 who also chose it to entertain Angela Merkel, Barack Obama, Nicolas Sarkozy, Gordon Brown and others at the same venue. already provide a very satisfactory service to protect and inform their members. It was, however, generally What are the views of FECAVA members and EJCAP readers? It will be immensely helpful if readers could take time to inform their national representatives, FECAVA Officers or EJCAP Editor of their feelings. E-mail addresses and names of those to contact are given on pages 98 & 206. The way forward is up to you. Please complain, suggest and praise as you think appropriate. When is a Congress International, European or National? The FECAVA Eurocongress is of course the key European Veterinary Companion Animal meeting in Europe. There can be no doubt of this. The next Eurocongress will be held in Lille, November 27th -29th and I am sure many readers will be there. What however is a European or National Congress? Is it ‘European’ or ‘International’ because it has a large number of international speakers lecturing in English or is it European because it has a high percentage of delegates attending are from outside the hosting country. The last FECAVA European Congress held in Dublin was a shining example of a successful European event in that 75 percent of its delegates came from countries other than Ireland and there was a high percentage of non Irish speakers. The recent BSAVA Congress could also claim some considerable success as a Congress for members outside the borders of the UK. At the last Congress in Birmingham, 190 delegates from outside the UK were present (8%). At the Voorjaarsdagen Congress in April there were many lectures given in English and a good range of speakers from countries other than The The International BSAVA Congress. From front, left, clockwise. Tina Toomet (Estonia), Keith Davies (UK) Merit Villemson-Kavak (Estonia) Wolfgang Dohne (Germany and UK- the incoming BSAVA Director to FECAVA), two delegates from Belgium, Yuri Kucherenko (Ukraine), Yvonne Man (UK and Hong Kong). 105 Netherlands. AVEPA recently rebranded its annual meeting as a Southern European Veterinary Congress. At the last of these events the number of delegates from outside Spain was 1278 and the total delegation 3288 (30% non Spanisch delegate). These statistics are interesting but more important, as FECAVA has said many times before is that FECAVA members should pursue their continuing education not only in their own countries, but at other European events. It is a very enjoyable and rewarding experience. FECAVA NEWS News from our more Eastern members from Tiina Toomet, our roving correspondent FECAVA, RSAVA and ESAVA join to help make the 17th International Moscow Congress a big success The first Veterinary Association in Russia was founded in St. Petersburg in 1846 and a second in Moscow in 1881. By the year 1912 there were no less than 30 Veterinary Associations in Russia. Veterinary Journals were published in Moscow, St Petersburg and Warsaw: The first Veterinary congress was held in 1874 in the province of Vyatka. Between 1903 and 1914 the annual congresses each had an attendance of almost a 1000 delegates. One of organizers of the Moscow and Warsaw Associations (at that time the present Poland was part of Russia), Dr. Sergei Jevsenko, is well known for his succinct observation “A human doctor is treats humans, but a veterinary surgeon treats humanity”. 1917 was the year of the revolution in Russia and after this there was initially little documented history until the Russian Veterinary Association was founded. This is an umbrella body for other veterinary associations (swine, poultry, equine companion animals etc.) Both practitioners and government Vets are members. In 1997 The Association of Veterinary Practitioners was founded. This is the section of The Russian Veterinary Association concerned with small and exotic animals, and it is this body that is a member of FECAVA. It is also called RSAVA (Russian Small Animal Veterinary Association). Prior this, in 1994, a small animal conference had already been organised. Nowadays there is an Annual International Veterinary Congress. The RSAVA The RSAVA joined FECAVA in 1998 and WSAVA in 1999 and represents companion and exotic animal practitioners. At its Annual Congress two prizes are awarded, “The Golden Scalpel” and “The Dr. Mitin Medal”. The former is awarded Tiina Toomet Dr Sergei Sereda (left) is President of RSAVA . Dr. Sasha Tkachov (right) represents RSAVA in FECAVA. for each year for excellence, which can be in a variety of fields (best clinic, best lecturer and teacher etc). Each regional division of RSAVA nominates candidates for the prize to the selection committee. The later, in recognition of excellence in oncology and surgery, was first awarded this year at the 17th International Moscow Congress held on 25th -27th of April. At this congress, there were no less than 3000 delegates participating in 6 different sections. Five of these were devoted to small animals. There were many lectures covering a wide range of subjects including dermatology, exotic pets, biochemistry, oncology, infectious diseases, laboratory work, anaesthesia, neurology, cat diseases, practice management, general surgery, cardiology, parasitology, nephrology, microchip identification and ophthalmology. Among speakers from abroad were Dr. P. Schrenk (Slovakia), Dr.D .Senior (USA), Dr. C. Eule (Germany) and many others. There was a ‘FECAVA Day’ supported by 106 FECAVA, ESAVA and the Estonian pharmaceutical company “Magnum Medical”. Four lecturers from Estonia presented papers on Practice Management (Dr.Tiina Toomet), Ophthalmology (Dr.Ulle Kell), Neurology (Dr.Ranno Viitmaa) and Dermatology (Dr. Sveta Belova). They lectured in the Russian language. Approximately 100 delegates took part in a quiz about FECAVA, the winners receiving free registration to the ESAVA summer seminar and the FECAVA Eurocongress in Lille. ESAVA grows in stature in partnership with FECAVA From its foundation, ESAVA has participated and benefitted from the FECAVA Eurocongresses. At the first FECAVA Congress in Paris (1994) there were 2 ESAVA members. ESAVA wasn’t even a year old itself and not yet a FECAVA member. It also had a member at the second FECAVA Congress in Brussels. ESAVA joined FECAVA in 1996 and since then the ESAVA delegation at Eurocongresses has gradually grown. In the early years due to our young country’s financial situation things were difficult. By the time of the 10th FECAVA Congress in Rhodes however, 10% of our membership were able to be present! Particularly popular were the Dublin and EJCAP - Vol. 19 - Issue 2 October 2009 ESAVA members relaxing in a break during the ‘Irish Day’ from the scientific content. It’s an idea we recommend to other FECAVA member Associations similar to our own. Three hundred delegate attend the USAVA Annual Congress in the Ukraine Prague congresses. Both had over 20 ESAVA participants. At the 14th FECAVA Eurocongress in Dublin we used a new registration procedure. Whilst we had taken advantage of cheaper group registration before, in Dublin, for the first time participants didn’t have to pay their fees to ESAVA straight away, but were allowed do it after the congress. As an additional incentive they were only asked to pay to ESAVA 50% of the registration fee if they prepared and presented a lecture, lasting 45 minutes, to the other members of ESAVA on an interesting subject or lecture which they had attended in Dublin. On 20th September last year we arranged an event which we called an ‘Irish Day’, which was incredibly popular. Of the 21 members who were at Dublin, 5 gave lectures attended by 50 of our members - that’s 1/3 of our association! The ESAVA lectures were on many different subjects: perineal hernias, babesiosis, diseases of exotic animals, oncology and suicide in the veterinary profession. During coffee breaks there was a large screen presentation of photos showing different places in Ireland and illustrating what an enjoyable time delegates had on pre- and post-congress tours. An excellent scientific and social programme was enjoyed by 300 delegates. Dr.Tiina Toomet repeated the lecture she had given in Moscow at the RSAVA Congress again in Uman. From L>>R Vladimir Charkin (FECAVA Director USAVA), Dimitri Berezhnoy, Vladlen Ushakov (President of USAVA ) with his wife Natalie Tkachenko and their 4 daughters, relaxing in the park at Uman during the USAVA Annual Congress It was such a success that we have already decided that we will most definitely host a similar day after the Eurocongress in Lille. We hope that these kind of the events will both tempt ESAVA members to take part in future FECAVA Eurocongresses and also enable members who can’t take part in the congress for financial or language reasons to benefit Astrid Bjerkås, Executive Assistant to FECAVA and EJCAP sub Editor reports FECAVA recognises the importance of animal assisted therapy and activities Katerina Loukaki (HVMS/Greece) gave a presentation on animal assisted therapy (AAT) and animal assisted activities The FECAVA Council has decided to form a working group on animal assisted therapy and animal assisted acitivities. Photo: Pixelio.de (AAA) at the recent FECAVA Council meeting in Baden Baden. She suggested that the veterinary profession has had little involvement in this area and they should be advocates in promoting the role of animals in the context of their value in family and social life. A recent questionnaire to Directors had indicated there was no official national veterinary association in Europe, which was involved in this work. It was unanimously agreed by Council that a Sub- committee for “AAT & AAA and Vets” should be formed under the umbrella of the group looking at the Socio-economic Importance of Companion Animals. The role of FECAVA should be: • To produce guidelines for all European countries regarding: 107 • • • • 1. Developing a health plan for animals involved in AAT and AAA programmes. 2. Specifying the role of vets in these programmes. To encourage cooperation with European Societies for AAT and AAA and Institutes for Social Learning with Animals. To encourage co-operation with our medial colleagues (Doctors, Psychologists and Nurses). To actively promote the introduction of projects in this field in the European Veterinary Schools and in Continuing Educations programmes. To encourage scientific presentations in co-operation with human doctors, nurses, psychologists and others during Congresses. FECAVA NEWS FECAVA report on the socio-economic importance of companion animals The FECAVA Council asks Directors to inform their national organisations about the report and to use it in their communication with policy makers and the public in their countries. Traditionally the main focus of the European Union regarding veterinary medicine has been on production animals and food safety. FECAVA feels that the importance of companion animals to humans should also be considered. A working group set up by the FECAVA Council (consisting of FECAVA Senior Vice President Ellen Bjerkås and Directors Katerina Loukaki (HVMS/Greece), Monique Megens (NACAM/Netherlands) reported to the recent FECAVA Council meeting in Baden Baden. They recommend that FECAVA should definitely become involved. The group have produced a report for FECAVA entitled “Health Benefits (Socioeconomic Value) of Companion Animals”. The report is based on a review of recent literature on the value of companion animals to humans. If readers have any questions or comments on the report, please contact FECAVA Senior Vice President, Ellen Bjerkås, by e-mail [email protected] According to the group this review shows that companion animals do indeed have an important socioeconomic value. An example of this is the resulting improved recovery shown in some cases following surgical trauma. This can in part be calculated directly as a reduced number of medical consultations and more rapid recovery after surgery for pet owners, and indirectly by improved quality of life and thus better function in society. The report can be downloaded from www.fecava.org In order to make the report easier to understand, it has been divided according to age groups: • Children pre- school to end of high school (babies are not included) • Adolescents • Adults • Elderly Each group is further divided according to : • Social and health benefits • Disadvantages and dangers At the end of each part there is a list of relevant literature. In addition, the reader is directed to the following websites: www.americanhumane.org www.deltasociety.org http://www.vet.cornell.edu/services/ companions/research.htm FECAVA has produced a report on the socio-economic importance of companion animals. The report is a review of recent literature on the value of companion animals to humans. Photo: Pixelio.de FECAVA President elected Vice-President of the UEVP Board FECAVA President Andrew Byrne has been elected Vice-President of UEVP. UEVP is the section of the Federation of Veterinarians of Europe (FVE) that represents practitioners. UEVP is in other words the European umbrella organisation of national veterinary practitioners’ associations. Marc Buchet past president of FECAVA retires this year from the UEVP board after six years of service. Marc was a member of the FEACVA Board for ten years and has made an enormous contribution to the work of both FECAVA and UEVP for which everyone in FECAVA is truly grateful. FECAVA develops a new website FECAVA has decided to develop a new website. At the recent Council meeting in Baden Baden a new Website Working 108 Group was set up consisting of Ian Mason (BSAVA), Stein Dahl (NSAVA), Katia di Nicolo (LAK) and Johan van Tilburg (FECAVA Vice President and SAVAB) to help the FECAVA Executive Assistant to develop proposals that will be presented to the FECAVA Council at their next meeting in Lille in November this year. The next steps to be taken should be to; • Agree on the goals and on the target groups • Agree on the time line. It was suggested that proposals for the website should be finished before the next Council meeting in Lille. • Form a working group to lead the project. • Finish the specifications for a new content management system. • Contact potential providers. • The Directors will be involved as the work progresses in order to develop the best possible FECAVA website. Have you read the EJCAP special issue on Zoonoses? Last December saw the publication of a special issue on Zoonoses - EJCAP 18(3). The articles are written by some of the leading experts in Europe. The EJCAP special issues are online issues only. Log on to www.fecava.org and download the articles free of charge. The topic of the EJCAP special issue of 2009 EJCAP 19(3) is Dermatology. In 2007 it was Ophthalmology [17(3)]. And finally, don’t forget Lille – hopefully you’re registered already The Congress programme has a true European feel. The congress is designed for general veterinary practitioners and final-year students. The main goal of the Congress is to promote contacts between generalists, students, and specialists. AVFAC (France), the two SAVAB Associations (Belgium) and LAK (Luxemburg) have worked hard to create an appealing programme with a true European feel. There is more information on the Web News, or visit http://www. fecavalille2009.com/ to find out more about the Congress! EJCAP - Vol. 19 - Issue 2 October 2009 Highlights from The 2009 Presidential report to the WSAVA Assembly The next WSAVA year will be even more exciting than this one has been. The 50th birthday celebrations will commence in Sao Paulo and conclude in Geneva in 2010 on the shores of Lac Leman, with the Mont Blanc massif providing the backdrop for a wonderful Congress Banquet. This year has seen a great deal of hard work by the various members of the Board and Committee Chairmen. The focus of the Executive Board has been formalising a number of WSAVA processes and exploring methods to more effectively manage the implementation of WSAVA’s growing initiatives. These discussions include registering the WSAVA as an incorporated, non-profit making association, a more central role in Congress planning and execution, strategic planning with member associations and assessing the benefits of utilising an outside association management firm. The WSAVA CE programme continues to go from strength to strength with over 5000 delegates at 34 meetings in 30 countries all being enthralled by the improvement to their post graduate education. I have said it before and I will repeat that CE is the cornerstone of WSAVA work – it entirely fits in with our vision to continue the development of global companion animal care and our mission to foster the exchange of scientific information between individual veterinary surgeons and veterinary organisations. The programme could not take place without the dedicated local organisers and the regional organisers, Luis Tello in South America, Roger Clarke in Asia, Lawson Cairns in Africa and Julian Wells in Eastern Europe. As well as our long term sponsors, Hill’s Pet Dr. David Wadsworth, WSAVA President. Nutrition, Bayer Animal Health, and Intervet-Schering Plough Animal health, we are grateful to the following associations who have all donated funding to support this venture – AFVAC, ASAVA, BSAVA, NACAM, NSAVA, HVMS, SVK, VOEK, DSAVA, FSAVA , CSAVA and SkSAVA. It is truly good to know that there are people with the vision to support the future of the profession. The Animal Welfare committee, another cornerstone of WSAVA work, continues to work hard at increasing the standards of animal welfare internationally. As veterinary surgeons we take it for granted that we are involved in animal welfare on a daily basis but there is so much more that can be achieved. Roger Clarke and Ray Butcher have organised programmes for the FASAVA Congress in Bangkok in November, for the WSAVA Congress in Sao Paulo and for the NAVC Congress in Orlando this year. They are in contact with other international welfare organisations and we hope that their efforts will continue to be effective in this field. 109 The Scientific Advisory Committee, under the chairmanship of Michael Day has strong ties with the academic world and our standardisation projects are reported annually to ACVIM and ECVIM. The committee is formed entirely of internationally renowned academic veterinary surgeons and gives advice on congress programmes, state of the art lectures, the prestigious WSAVA Awards and oversees the scientific integrity of standardisation project applications. We are grateful to all involved in the work of this committee. Many thanks to our sponsors, which include a close working partnerships with Hill’s Pet Nutrition who are the WSAVA Prime Sponsor for WSAVA Congresses, the GI, Hepatic and Renal standardisation projects, the website and news bulletin production and of course the long running and most valuable WSAVA Continuing Education programme. Bayer Animal Health who have provided invaluable assistance in the Renal Standardisation project, the website and News Bulletin production and the CE courses, and Intervet/ Schering-Plough Animal Health, the vaccine standardisation project and CE. We are extremely grateful to these companies whose aim is to work towards our shared goal of Continuing Veterinary Excellence. Future World Congresses: • Geneva, Switzerland – June 2-5, 2010 • Jeju. Korea – October 14-17, 2011 • Birmingham, England – April 12-15, 2012 FECAVA NEWS UEVP NEWS On May 21st, during the Annual Spring General Assembly held in Stockholm, a new board was elected to serve for the following 2 year term. From left >> right: Thierry Chambon (France) Vice- President, Anne Ceppi (Switzerland) Treasurer, Zsolt Pintér (Hungary) President, Andrew Robinson (UK) Secretary General, Andrew Byrne (Ireland) Vice-President. [Rens van Dobbenburgh (Netherlands) elected as vice-president was not present] UEVP and CPD It was about 6 years ago that a report on the result of an initial survey on CPD throughout Europe was given to EJCAP by Christophe Buhot (France), who was then General Secretary of UEVP. Since that time Christophe has served as President for UEVP for two terms. Under his leadership UEVP has compiled, discussed and then in 2007 adopted a paper on CPD. This gives us a great chance to achieve a strongly recommended and better harmonised CPD system throughout Europe. Earlier this year member countries were again questioned to ascertain an up to date assessment of the CPD situation and the outcome was reported at the May General Assembly of UEVP. I can now give a revised summary of these reports given to UEVP from 23 European countries: CPD exists in 19 countries, while the 4 without a CPD system were in favour of developing one in the future. In half of the countries with CPD, the system is mandatory and in half voluntary. Half of the countries use the number of hours engaged in CPD and the other half a points system to compile CPD records. Fourteen countries have national CPD committees, with members from Practicing Veterinarians, Academia and Statutory bodies. CPD recording and record keeping, if organised, was different in the countries. Mostly records are kept personally or by the Statutory body. In more than half of the countries CPD providers are evaluated, however only in 6 countries are they fully accredited. CPD providers are evaluated, however in only 6 countries are they fully accredited. In about 1/3 of the countries there is a link between CPD and the licence to practice. However in most of the countries there is no such link. Most countries accept CPD credits from other countries, some from all over the world, and others just from the EU and the US. The UEVP Board recommends that we should not to attempt to completely harmonise CPD, but rather to urge all our member countries to mutually accept CPD points and to ensure CPD is kept under veterinary control. As CPD is one of the core values of liberal professions UEVP will continue to maintain a strong co-operation on this issue with its member organisations and other European professional organisations. Dr. Zsolt Pintér President UEVP July, 2009 www.fecava.org Get the latest FECAVA news Sign up for the FECAVA Newsletter Download the FECAVA policy statments Download the EJCAP special issues Get access to the EJCAP archive 110 CARDIOLOGY COMMISSIONED PAPER Blood Pressure in Small Animals - Part 3*: Hypertension - Target organ damage, eyes and the CNS - Diagnosis and treatment considerations A.P. Carr(1), B. Egner(2) *INTRODUCTION This is the final paper in the series on hypertension in small animals which has covered assessment and target organ damage. In the previous two issues EJCAP 18(2) and 19(1) we published papers on the assessment blood pressure in small animals and target organ damage (TOD) to the heart and kidneys. To summarise, hypertension can have various causes including renal disease, hyperadrenocorticism, and hyperthyroidism. The predominant concern with hypertension is that target organ damage (TOD) can occur. The organs most affected by hypertension include the kidney, heart, (covered in EJCAP 19(1)) and eyes and brain which are discussed in this paper. Hypertension can be classified based on the risk of TOD (Table 1). The Eye and Hypertension Risk categories Although various organs are affected by hypertension, the eyes are the only organs where visual inspection can often be adequate to determine that TOD is occurring. A retinal examination is certainly indicated in all animals known to be hypertensive. Ocular examination including inspection of the retina is good idea in all patients, but especially in older patients where hypertension is more common. In some cases, documenting ocular damage is the reason a more thorough work up is initiated including blood pressure measurement and a biochemical profile. Finding evidence of TOD also eliminates white coat hypertension as a cause for an elevated blood pressure reading. In one study of cats with chronic renal disease, at initial presentation approximately 20% of cats were hypertensive with 70% having retinal changes consistent with hypertension. [1] It appears that in cats systolic hypertension is more predictive of ocular TOD than diastolic or mean arterial pressure. [2] Systolic Pressure Diastolic Pressure Risk for target organ damage I <150 <95 minimal II 150-159 95-99 mild III 160-179 100-119 moderate IV ≥180 ≥120 severe Table 1. Classification of hypertension based on the risk of TOD. Blood supply to the retina is via the choroidal and retinal arterioles. The retinal vessels supply nutrition to the inner retinal layer whereas the choroidal vessels supply nutrition to the outer retinal layers. [3] Retinal arteries have autoregulatory capability, as blood pressure increases, they vasoconstrict. With prolonged hypertension this will lead to pathologic changes in the arterioles resulting in ischemia and potentially rupture and haemorrhage (hypertensive retinopathy). This is not true of the choroidal vessels. Choroidal vessels have large fenestrations (1) Small Animal Clinical Sciences, Western College of Veterinary Medicine, 52 Campus Drive, Saskatoon, SK S7N 5B4 Canada E-mail: [email protected] (2) Clinical Centre for Small Animals, Hoerstein, Moembriser Str. 100 - Germany 111 Blood Pressure in Small Animals - Part 3*: Hypertension - Target organ damage, eyes and the CNS - A.P. Carr, B. Egner leads to vasoconstriction, ischemia and focal necrosis of the choriocapillaris. [4] This leads to infarction and degeneration of the retinal pigment epithelium (RPE). The blood-retina barrier is compromised leading to accumulation of fluid underneath the retina and serous retinal detachments. Clinical findings A variety of clinical signs related to the eye can be seen with hypertension, however it is important to remember that other diseases (hyperviscosity, bleeding disorders, vasculitis, neoplasia) can cause similar signs. With hypertension it is not unusual to have the patient present having either sudden blindness or a change in the appearance of the eye as the primary complaint. One manifestation of hypertension is hyphaema. Variable amounts of bleeding into the anterior chamber can occur. Initially haemorrhage will cause a uveitis, with persistence secondary glaucoma can result. [3] Unilateral or bilateral mydriasis with poor to absent PLRs may be seen as well as blindness. In older cats it is important to evaluate for iris atrophy as this too can result in abnormalities of pupil size or response to light. (Figure 2). Fig 1. Focal bullous retinal detachment with tortuous retinal vessels. which allow fluid to move freely into tissues. With hypertensive choroidopathy, severe bullous retinal detachments are more common (Figure 1). A hypertensive optic neuropathy can also be encountered. Hypertensive retinopathy can have various manifestations. With an increase in systemic blood pressure the retinal arterioles undergo vasoconstriction. This leads to compensatory changes in the vasculature including hypertrophy and hyperplasia of the tunica muscularis. If hypertension persists, sclerosis and potentially necrosis of the smooth muscle can develop. These changes lead to leakage of fluid and potentially blood into the retina. In the choroid the process leading to hypertensive choroidopathy differs from that which occurs with retinal arterioles. In the choroid, angiotensin II and norepinephrine Examination of the posterior segment is important when trying to evaluate for TOD from hypertension. A variety of lesions can be found. Initially retinal vascular tortuousity with a “box car” appearance can be seen. These lesions require experience with retinal examination to be easily identified. In fact these changes may be artefacts in acute disease, the narrowing is caused by retinal oedema. [4] In more advanced cases haemorrhages and detachments are seen. Haemorrhages can be intraretinal or vitreal (Figure 3). In some cases bullous detachments predominate and can lead to complete detachment (Figure 4). The optic nerve can also be involved with papilloedema being seen. Older lesions may be present such as retinal degeneration and retinal hyper-reflectivity (Figure 5). Prognosis for patients with indications of ocular TOD is variable. With early and mild lesions it is often possible to arrest and reverse hypertensive injury. Once extensive retinal detachments and haemorrhage are present the prognosis worsens considerably. Fig 2 Bilateral mydriasis and absent PLR in a cat with serous retinal detachments. Fig 3. Severe vitreal haemorrhage in a cat with hypertension. 112 EJCAP - Vol. 19 - Issue 2 October 2009 Fig 5. Diffuse retinal atrophy of the temporal tapetal retina. Fig 4. Complete bullous retinal detachment The CNS and Hypertension “sausage-string” appearance whereby the constricted portions are areas where autoregulatory constriction is still present whereas the dilated portions are areas where autoregulation is failing and the vessel is distending. [5] Eventually the over distended areas begin to leak protein and fluid (oedema formation). This will eventually lead to widespread dilation of the vessel and increased, diffuse cerebral oedema formation. Haemorrhages can also occur if the vessel ruptures. The most common area to develop oedema is the white matter, this has been documented in humans and cats. [6] Haemorrhage into the brain is irritating resulting in inflammation (meningitis, myelitis, encephalitis). Cerebral haemorrhages have been documented in cats with seizures and hypertension. [7] This same study Damage to the CNS can be seen secondary to hypertension, though often this is the most difficult type of TOD to recognize. Clinical signs are often vague and hypertensive encephalopathy is only suspected when severe manifestations are present. These signs develop when the brain’s ability to blunt the effects of high blood pressure are overwhelmed. The brain, just as the eye, has the ability to autoregulate blood flow to maintain steady blood flow to the brain as systemic blood pressure varies. In the brain, increased systemic pressure leads to vasoconstriction whereas hypotension leads to vasodilation. Sustained increases in systemic blood pressure cause the cerebral blood vessels to develop a Table 1 A Guide to common dosages used – Please check with manufacturer or cardiology specialist Medication Enalapril (1) (2) Cat Dosage Dog Dosage 0.25 to 0.5 mg/kg Orally twice daily same 0.25 to 0.5 mg/kg Orally daily same Ramipril 0.125 mg/kg Orally daily 0.125 to 0.25 mg/kg orally daily Amlodipine 0.625-1.25 mg/cat/day orally(0.13 to 0.3 mg/kg q24h) 0.05 to 0.4 mg/kg orally daily Atenolol 2 mg/kg Orally once or twice daily (6.25 to 12.5 mg/cat Orally twice daily 0.25 to 1.0 mg/kg Orally twice daily Acepromazine 0.05-0.1 mg/kg SC, IV same Hydralazine 2.5 to 5 mg/cat Orally twice daily (approximately 0.5 to 0.8 mg/kg) 0.5 to 3 mg/kg Orally q 12h Benazapril Phenoxybenzamine 0.25 to 0.5 mg/kg orally twice daily 0.25 to 1.5 mg/kg PO q 8 to 12h Prazosin 0.5 to 2 mg/dog orally two to three times daily None SC - Subcutaneous IV - Intravenous 1 Some suggest higher doses in dogs – up to 3.00 mg/kg twice a day, and favour the lower dose only in cats 2 some suggest a higher dose in cats of up to 1.0 mg/kg Generally with drugs to control blood pressure it is often ideal to start at the lower end of the dosage recommendation and titrate upward to effect. 113 Blood Pressure in Small Animals - Part 3*: Hypertension - Target organ damage, eyes and the CNS - A.P. Carr, B. Egner Treatment suggested that 11 of 24 cats hypertensive cats had some degree of neurologic involvement including seizures, nystagmus, decorticate posturing, and intermittent dragging of limbs. Other studies have suggested neurologic signs to be present in about 10% [8] to 25% [9] of hypertensive cats. With hypertension vascular changes in the brain are common as in the retina with the development of hypertrophy, hyperplasia and ischaemia. Although hypertension can cause damage to the brain it is important to remember that brain disease can lead to systemic hypertension as well via the Cushing reflex. If intracranial pressure increases there is a concomitant increase in systemic blood pressure to help maintain blood flow to the brain. [10] Treatment of hypertension has been described in Part 2 of this series of articles. Table 1 lists commonly used medications to control hypertension. With TOD of the brain or eye, use of medications that are known to drop blood pressure significantly is preferred. Amlodipine is the most commonly used medication for this purpose. When treating patients with hypertensive neuropathy it is important to avoid dropping blood pressure too rapidly. If this occurs, cerebral blood flow can be compromised leading to more severe damage to the CNS. In more severely affected animals, cerebral oedema may be severe. Treating this with a diuretic such as mannitol or furosemide may be of benefit. Clinical findings Clinical signs are relatively variable. The mildest signs noted are behaviour changes such as lethargy and depression. This can progress to include seizures, ataxia, salivation, cranial nerve abnormalities and potentially coma. It is difficult to be sure if the clinical signs noted are neurologic consequences of hypertension or not. In humans some common signs include headache, vomiting and visual disturbances, signs that might be difficult or impossible to detect in a small animal patient. [6] Other clinical signs that have been noted include polyphagia, abnormal vocalisation, photophobia, frequent blinking, head pressing, cortical blindness and extensor rigidity. [6] References [1] Syme HM, Barber PJ, Markwell PJ, Elliott J. Prevalence of systolic hypertension in cats with chronic renal failure at initial evaluation. J Am Vet Med Assoc. 2002; 220: 1799-1804. [2] Sansom J, Rogers K, Wood J. Blood pressure assessment in healthy cats and cats with hypertensive retinopathy. Am J Vet Res. 2004; 65(2): 245-52 [3] Maggio F, Davidson MG. The Eye as a Target Organ. In: Egner B, Carr A, Brown S: Essential Facts of Blood Pressure in Dogs and Cats, 4th Edition, pp.146-154. ISBN 978-3-938274-15-6, VBS GmbH, Babenhausen, 2007. [4] Crispin SM, Mould JRB. Systemic hypertensive disease and the feline fundus. Veterinary Ophthalmology 2001; 4: 131-140. [5] Johansson B, Strandgaard S, Lassen NA. On the pathogenesis of hypertensive encephalopathy: the hypertensive “breakthrough” of autoregulation of cerebral blood flow with forced vasodilation, flow increase and blood-brain barrier damage. Circ Res 1974; 34/35: 1167-1171. [6] Brown CA, Munday JS, Mathur S, Brown SA. Hypertensive encephalopathy in cats with reduced renal function. Vet Pathol. 2005; 42: 642-649 [7] Littman MP. Spontaneous systemic hypertension in 24 cats. J Vet Intern Med 1994; 8: 79-86. [8] Elliot J, Barber PJ, Syme HM, et al. Feline hypertension: clinical findings and response to antihypertensive treatment in 30 cases. J Small Anim Pract. 2001; 42: 122-129 [9] Maggio F, DeFrancesco TC, Atkin CE, et al. Ocular lesions associated with systemic hypertension in cats : 69 cases (1985-1998). J Am Vet Med Assoc. 2000; 217: 695-702. [10] Bagley RS. The Brain as a Target Organ. In: Egner B, Carr A, Brown S: Essential Facts of Blood Pressure in Dogs and Cats, 4th Edition, pp.163-175. ISBN 978-3-938274-15-6, VBS GmbH, Babenhausen, 2007. Images: All images are taken from Egner B, Carr A, Brown S: Essential Facts of Blood Pressure in Dogs and Cats, 4th Edition, pp.163-175. ISBN 978-3-938274-15-6, VBS GmbH, Babenhausen, 2007 with permission. 114 GENERAL COMMISSIONED PAPER Clinical Cytology of Companion Animals: Part 3. Cytology of the lymph node E. Teske(1) INTRODUCTION Of all indications for FNAB, the enlarged lymph node is the most rewarding. In general the peripheral lymph nodes are easy to fix with one hand and therefore easy to aspirate, the biopsy procedure is not painful, and the number of possible diagnoses is not high. It is thus not surprising that the history of the cytology of lymph nodes goes back to the beginning of the last century. In 1904 Greig and Gray used this technique to demonstrate trypanosomes and, after a publication by Guthrie in 1921, systematic diseases such as lymphomas were also diagnosed in this way. The cytologist who examines the FNAB of a lymph node should know whether the node was of normal size, possibly enlarged, or undoubtedly enlarged. A slight enlargement of the lymph node is difficult to confirm clinically. If the enlargement is dubious and no abnormalities are found cytologically, then the obvious conclusion is that the lymph node is normal. If the lymph node is unquestionably enlarged, then there must be a cause. The cytologist will then be more cautious about giving a negative report and will advise a follow-up histological examination. It can be very difficult to differentiate the cytological appearance of a normal lymph node from that of some welldifferentiated lymphomas. In addition, the cytologist should know whether the FNAB was performed in order to answer a specific question. If the patient is suspected of having leishmaniasis or tumour metastases, then a longer and more specific search will be made for parasites or for tumour cells. For the same reason it is important to know whether the lymph node enlargement is generalized or concerns only one node and, in the latter case, whether there is (or has been) a tumour in the area drained by this node. It is also important to know which lymph node has been aspirated. The mandibular lymph nodes are often reactive, because many animals have inflammatory processes in the mouth. If there is generalized enlargement of lymph nodes, the mandibular nodes are therefore not the most suitable for cytological examination. Finally, it is important for the cytologist to know what therapy has already been given. The administration of corticosteroids causes lymphocytolysis and suppression of the immune response. This can greatly distort the cytological appearance of the nodes. Normal appearance and benign changes majority (85-95%) of the cells are small B- and T-lymphocytes. These cells are characterized by little cytoplasm, round nuclei without nucleoli, and often slightly rough chromatin structure (Fig. 1). The size of these cells (about 10µm) lies between that of erythrocytes and polymorphonuclear granulocytes. The cytoplasm of lymphocytes is rather fragile and can be found in loose fragments throughout the smear, the so-called Although the normal lymph node is seldom aspirated, familiarity with the normal cytological appearance is necessary in order to recognize abnormalities. Mild antigenic stimulation also takes place in the normal lymph node and, in principle, all of the stages of B- and T-lymphocytes can be found. However, the (1) Department Clinical Sciences Companion Animals, Veterinary Faculty, Utrecht University PO Box 80.154, NL- 3508 TD Utrecht. E-mail: [email protected] 117 Clinical Cytology of Companion Animals: Part 3. Cytology of the lymph node - E. Teske Fig. 1 FNAB of a normal lymph node of a dog. Monomorphic population small lymphocytes. Pink material in between cells is nuclear material of streaked out damaged cells. Small blue fragments are lymph glandular bodies. Fig. 2 Cluster epithelial cells in acinic structure with a mucoid background. Normal salivary gland tissue. lymphoglandular bodies (Fig. 1). With the May-Grünwald Giemsa stain they are light blue. Lymphoglandular bodies are characteristic of lymphoid tissue and their presence can be useful in differentiating lymphoid cells from those of an undifferentiated small cell carcinoma. A normal lymph node also contains other developing stages of the lymphoid series, but never more than 5-10% of the total number of cells. Other nonlymphoid cells occurring in a normal lymph node include polymorphonuclear neutrophilic and eosinophilic granulocytes, macrophages, histiocytes, mast cells, erythrocytes, and monocytes. These cells are only present sporadically. An overview of the different types of cells in the normal lymph node is given in Table 1. shaped) structures. Lymphocytes and lymphoglandular bodies are absent. In obese animals it is possible to have the wrong impression that the lymph node is enlarged because it is surrounded by a thick layer of fat. An aspiration biopsy obtains mainly fat. It should be realized, however, that most fat tissue is dissolved in the fixation in alcohol, which is used in most staining methods. Reactive hyperplasia The most frequent cause of a generalized lymphadenopathy is reactive hyperplasia, via which the lymph node reacts to an antigenic stimulus. This can be the result of a viral, bacterial, or parasitic infection, or a reaction to tumour antigens, a foreign body, a skin disorder, or waste products of inflammation somewhere else. Reactive hyperplasia is characterized cytologically by an increase in the number of large blast cells, such as immunoblasts and centroblasts, in relation to the number of small, normal Non lymphoid tissue The most frequent cause of the wrong diagnosis of an enlargement of the mandibular lymph node is the mistaken palpation of a mandibular salivary gland, whether normal or enlarged (Fig. 2). In the dog and the cat the mandibular lymph nodes are rostral to the salivary gland and both are in principle readily palpated. Salivary gland cells are much larger than lymphoid cells, contain more cytoplasm, and form acinar (gland- Fig. 3 Cell pattern of a reactive lymph node of a dog. A mixed lymphoid cell population is seen with several mature lymphocytes, some blast cells and one plasma cell (top left). A long naked nucleus of a histiocytic (epitheloid) cell is also present. Table 1. Types of cells in a normal lymph node cell type frequency (%) small, mature lymphocyte 80-90 prolymphocyte 5-10 young, blast cells <5 plasma cells 0-5 eosinophilic granulocytes 0.3 neutrophilic granulocytes 0.1 mast cells 0.2 macrophages/histiocytes 0.4 118 EJCAP - Vol. 19 - Issue 2 October 2009 Fig. 4 FNAB of a reactive hyperplastic lymph node of a dog. Several plasma cells with Russell bodies are present. Fig. 5 Purulent lymphadenitis. Mixture of small lymphocytes and many neutrophils. In the background are some threads of degenerated nuclear material. lymphocytes. There are also more mitoses and the number of lymphoplasmacytoid cells (intermediate stage between immunoblast and plasma cell) and plasma cells is increased (Fig. 3). Sometimes so-called “Russell bodies” are seen in the cytoplasm of plasma cells (Mott cells). These are vacuoles filled with immunoglobulins (Fig. 4). Depending on the cause of the stimulation, there can also be increased numbers of other types of cells such as macrophages, polymorphonuclear granulocytes and, especially in skin disorders, eosinophilic granulocytes and mast cells. macrophages. The difference from a reactive hyperplasia is sometimes difficult to confirm, but can also be quite clear, as in bacterial lymphadenitis. In the latter case there are many polymorphonuclear granulocytes, necrosis, and sometimes bacteria (Fig. 5). Lymphoid cells can even be completely absent. An increase in eosinophilic granulocytes is seen mainly in allergic dermatitis and parasitic infections such as leishmaniasis (Fig. 6). If bacteria are present they will be found in granulocytes, while parasites will mainly be found in macrophages. Granulomatous lymphadenitis is also usually characterized by a slight reactive lymphoid picture and in addition includes an increase in macrophages, epithelioid cells, and multinucleated giant cells. Epithelioid cells are reticulum cells with an elongated oval nucleus, which is often indented at one end and which has a lightly granular chromatin pattern. Epithelioid cells often lose their cytoplasm in the preparation. Sometimes these cells occur in clusters and can then resemble carcinoma metastases. Granulomatous lymphadenitis is seen in toxoplasmosis, fungal and yeast infections, and certain bacterial infections (e.g., infections with Mycobacterium spp) (Fig. 7). Lymphadenitis The presence of many inflammatory cells in the lymph node is referred to as lymphadenitis. Differentiation into purulent and granulomatous lymphadenitis is made according to the types of inflammatory cells. Purulent lymphadenitis is characterized by the occurrence of many polymorphonuclear granulocytes, usually combined with a light reactive lymphoid population and a few Fig. 6 Dog with leishmaniasis. The amastigotes are present in the large macrophage, but are also individually in the background of the smear. Several plasma cells are present. Fig. 7 In this FNAB of a granulomatous lymphadenitis due to a mycobacterium infection in a cat, several large histiocytic cells with some unstained rod bacteria can be seen on the left side of the picture. 119 Clinical Cytology of Companion Animals: Part 3. Cytology of the lymph node - E. Teske Fig. 8. Dermatopathic lymphadenopathy in a dog. There are several brown-black melanin granules in the background, several mature lymphocytes and a large nucleus of an interdigitating cell. Fig. 9 Adencocarcinoma metastases of a mammary gland tumour in a prescapular lymph node in a dog. A dermatopathic lymphadenopathy is a granulomatous lymphadenitis which occurs with skin disorders in which pruritus, scaling of skin and skin damage are prominent. The cellular picture is characterized by the presence of many brownblack melanin granules and a few eosinophilic granulocytes. Interdigitating cells are also encountered. These are elongated histiocytes with a reticular nucleus and a characteristic indentation of the nucleus (Fig. 8). the malignancy characteristics of the “foreign” cells, before speaking of malignancy. It is also possible that in one aspirate both the primary tumour and the lymph node are aspirated, when which a metastasis would be suggested. This can occur if a supramammary lymph node is biopsied simultaneously with the most caudal mammary gland which contains tumour. In addition to abnormal cells, the cytological appearance of a lymph node with metastases can also be characterized by benign changes as a result of the reaction of the immune system to the tumour cells. The number of macrophages, plasma cells, and young large lymphoid cells is often increased when there are metastases in the lymph node. The cytological appearance of metastases in the lymph node depends very much on the histological type of the primary tumour. With an anaplastic carcinoma there are mainly separate cells of a type that does not belong to the lymph node and these can vary greatly in size. Mostly one encounters various cells that are many times more numerous than lymphoid cells and are easily recognized at low magnification. Many malignancy criteria, such as a variable N/C ratio, large nuclei, a high mitotic index, multiple and sometimes pathological nucleoli, can be found. With more differentiated carcinomas, such as adenocarcinomas, cell clusters and sometimes even acinar structures are encountered (Fig. 9). Aggregates or syncytia of macrophages and epithelioid cells can resemble a cluster of metastasized carcinoma cells and must not be confused with them. Another type of carcinoma that can usually be easily classified is the squamous cell carcinoma. With this tumour small clusters of small carcinoma cells with small amounts of deep blue cytoplasm are encountered beside cells with a large amount of cytoplasm in different stages of keratinization. Keratinization is recognizable in the May-Grünwald Giemsa stain by the uniform sky blue color of the cytoplasm, sometimes containing a few small “droplets”. A characteristic difference from normal keratinized epithelial cells is that, during keratinization, the nucleus of the carcinoma cells does not degenerate but remains present. A few mast cells are always found in a normal lymph node or one that has benign changes. According to the literature, however, the number never exceeds 3%. More mast cells are suggestive of a metastasized mast cell tumour or even mast cell leukemia. The mast cells can contain many purple-blue granules, sometimes so Malignant changes Lymph nodes filter the lymph drained from a particular part of the body and remove the foreign material it contains. Tumour cells can also reach the regional lymph node in this way. In the lymph node the immune system can recognize the specific antigens expressed by the tumour cell and then eliminate the tumour cell. Sometimes tumour cells escape this “immune surveillance” and multiply themselves right in the lymph node. From here, metastasis can occur to other parts of the body. In addition to metastases of tumour cells, the lymph node can become tumorous due to neoplasia of cells of the hematopoietic system which normally occur in the lymph node. In this part further attention will be given to these two categories of malignancy involving the lymph node. Metastatic malignancies A complete survey of metastatic malignancies in the lymph node is not worthwhile, for in principle all malignant tumours can metastasize via the lymphatic system. Some types of tumours do metastasize earlier than others to the regional lymph node. Sarcomas generally spread earlier by hematogenous than by lymphogenous routes. Carcinomas, melanomas, and mast cells tumours are often found to metastasize to the lymph node, although this also depends upon the histological subtypes. In principle, every cytological preparation from a lymph node in which there are cells that do not belong in a lymph node is suspicious of metastatic malignancy. One must, however, take into account that when an aspirate is obtained from the lymph node, some cells from the surrounding tissues can be aspirated also. Hence it is always necessary to first evaluate 120 EJCAP - Vol. 19 - Issue 2 October 2009 Fig. 10. Mast cell tumour metastases to a lymph node. Mast cells are numorous, differ in size and have prominent nucleoli. A binuclear cell can be seen. Fig. 11 Transformation scheme of normal lymphocytes (after Lennert) (from: Van Heerde (P.) - Malignant lymphomas and histiocytic tumours. Cytology and other diagnostic methods. Thesis, Uitg Rodophi, Amsterdam, 1984) numerous that they obscure the nucleus. The cell can, however, also be sparsely granulated or even nongranulated (Fig. 10). In the latter case, the mast cells are difficult to recognize as such. Another tumour that sometimes metastasizes to the lymph node is the malignant melanoma. This tumour cell is larger than the lymphoid cell, varies in form from round to spindleshaped, and has a slightly oval nucleus. Bizarre nuclear shapes and multiple nuclei are frequently observed in malignant melanoma. The nucleolus is not always visible. The cell is usually characterized by the occurrence of black to brown-black granules in the cytoplasm. There are, however, also amelanotic melanomas. These contain few or no melanin granules and are thus difficult to identify. Melanophages can be confused with melanocytes. Melanophages are phagocytizing cells which have taken up pigment and occur in the lymph node in large numbers especially with skin disorders associated with pruritus and damage to the skin. Usually the cells are recognisable because the cytoplasm is slightly vacuolated and contains other phagocytized material besides melanin. In addition, they have no malignancy characteristics. Lymphoid malignancies Primary malignant transformation of the lymph node usually involves cells of the lymphoid system. Such cells as epithelioid cells and histiocytes are seldom involved. In the dog and cat these lymphoid tumours are called malignant lymphoma or lymphosarcoma. They are comparable to non-Hodgkin’s lymphoma in man. Since Hodgkin’s lymphomas have never been convincingly demonstrated in the dog and cat, the lymphoid tumours in these animals are usually simply called malignant lymphomas. The cytological appearance of the malignant lymphoma can vary from patient to patient. One assumes that a lymphoid cell in each stage of its development can become malignant, whether by a blockage in further differentiation or by autonomous proliferation of a certain cell type (Fig. 11). The cell types which are encountered in malignant lymphoma thus do not differ in appearance from normal lymphoid cells. The cytological differentiation rests on the presence of a monomorphic cell population, while in a non-lymphomatous lymph node all different development stages of the lymphoid series are visible. Various classifications schemes have been developed for nonHodgkin’s lymphomas in man. The Kiel classification (Lennert, 1974) is based entirely on the transformation scheme for normal lymphocytes described and is very suitable for cytological purposes (Table 2) (Fig. 12). Table 2. Simplified classification of lymphomas by cell type, based on the Kiel classification according to Lennert, 1974 Lymphocytic Immunocytic Plasmacytic In the literature, this Kiel classification has been applied successfully to malignant lymphomas of dogs. There is as yet no information about the applicability of this classification to malignant lymphomas of cats. A detailed description of the various types of lymphomas is presented below for readers who are interested. This is of interest for scientific reasons and to illustrate the diverse forms in which the malignant lymphoma occurs but, under practical conditions, the diagnosis of malignant lymphoma and its subclassification into low- or highgrade lymphoma is usually sufficient. If the aspirated cell population consists mainly of characteristic blasts, the diagnosis of malignant lymphoma is not so difficult to make. However, there are also forms of lymphoma in which Centrocytic Centroblastic/centrocytic Centroblastic pure centroblastic anaplastic centrocytic polymorphic centroblastic Lymphoblastic Immunoblastic Other histiocytic ‘multilobated’ cell 121 Clinical Cytology of Companion Animals: Part 3. Cytology of the lymph node - E. Teske Fig. 12 Schematic drawing of malignant lymphoma cells according to Kiel claasification (after Lennert) (from: Van Heerde (P.) Malignant lymphomas and histiocytic tumours. Cytology and other diagnostic methods. Thesis, Uitg Rodophi, Amsterdam, 1984) the tumour cells are difficult to differentiate from mature lymphocytes, especially for the less experienced cytologist. This can be the case, for example, with the lymphocytic and centrocytic lymphomas. Problems can also occur when the lymphoma contains more than one cell type, as in the immunocytic or centroblastic/centrocytic lymphoma. In many of these cases, the cell combination of enlarged lymph node and nonreactive cellular appearance is decisive, especially if the cell population is monomorphic. If in doubtful cases there are a few more plasma cells or other inflammatory cells, more experienced help should be sought or the diagnosis should be confirmed by a surgical biopsy for histological examination. Sometimes the preparation consists almost entirely of individual degenerated nuclei and streaks of nuclear material. This can be the result of inexpert streaking out of the aspirate, but it can also be the result of necrosis. If such a preparation is carefully searched, in particular not neglecting the margins, then a location with intact cells may be found. Sometimes the majority of the loose nuclei in such a preparation contain definite remnants of nucleoli. This is suggestive of a malignant lymphoma, but it is risky to base the diagnosis on this alone. Fig. 13 Lymphoplasmacytoid lymphoma. Several small lymphoid cells with abundant cytoplasm and a slightly eccentrically placed round nucleus. Fig. 14 Plasmacytic lymphoma. Large, atypical plasma cells. 122 EJCAP - Vol. 19 - Issue 2 October 2009 Fig. 15 Centroblastic/centrocytic lymphoma. A mixed population of large centroblasts, small centrocytes (cleaved cells), and lymphocytes. Fig. 16 (Polymorphic) centroblastic malignant lymphoma. A monomorphous populations of round centroblasts (with multiple small nucleoli). A large starry sky macrophage with cellular debris ‘tingible bodies’ is also present. Morphology of canine lymphomas, classified by the Kiel classification Centroblastic/centrocytic lymphoma As the name indicates, this type of lymphoma consists of both centrocytes and centroblasts (Fig. 15). Centroblasts have a large, round nucleus with multiple nucleoli that often lie adjacent to the nuclear membrane. The cytoplasm consists of a thin, dark blue rim. Many mitoses can be found. If the percentage of centroblasts is higher than 30-50%, the lymphoma is called centroblastic. Lymphocytic lymphoma This type of lymphoma consists of a monotonic population of small, mature lymphocytes. The cytological appearance is often difficult to differentiate from a nonreactive, normal lymph node. If this picture is found in a definitely enlarged lymph node without any evidence of reactivity, the chance is great that this type of lymphoma is present. If the lymphocytic lymphoma consists of B-lymphocytes, which can only be confirmed with certainty by immunotyping, then the nuclei are usually round and have a slightly rough chromatin pattern. This is in contrast to the T-lymphocytic lymphoma in which the nucleus is slightly indented and has a dense chromatin pattern. Both types of lymphoma exhibit little cell multiplication. The lymphocytic lymphoma occurs infrequently in dogs. Centroblastic lymphoma The most important cell type is the centroblast, but a few centrocytes will often be present. There are two special forms. If there are immunoblasts in addition to centroblasts, the tumour is called a ‘polymorphic centroblastic’ lymphoma (Fig. 16). If there are more than 50% immunoblasts, the tumour is considered to belong to the immunoblastic lymphomas (see below). The other special form is the ‘anaplastic centrocytic’ lymphoma. Anaplastic centrocytes are large centrocytes with a large, irregularly formed nucleus. The cytoplasm is often more lightly stained than that of the centroblasts. In the dog, the centroblastic, polymorphic centroblastic, and anaplastic centrocytic lymphomas are the most frequently occurring types of lymphoma. Lymphoplasmacytoid / Immunocytic lymphoma The most important cell type here is the immunocyte, a small lymphoid cell with more cytoplasm than the cells of a lymphocytic lymphoma and a slightly eccentrically placed round nucleus. This cell type has developed a little farther in the direction of the plasma cell.The lymphoma is called lymphoplasmacytoid lymphoma (Fig. 13). In addition to this cell type, a few centrocytes, immunoblasts, and plasma cells can be found. The majority of the cells are, however, small lymphocytes. In this case the term immunocytic lymphoma is used. Lymphoblastic lymphoma The lymphoblastic lymphoma is infrequent in the dog. The lymphoblast is a medium-sized, round to oval cell with a thin rim of light to moderately basophilic cytoplasm that is sometimes vacuolated. The nucleus has a fine chromatin pattern with a few small nucleoli. Many mitotic figures can be present. In humans this type of lymphoma sometimes contains ‘starry sky macrophages” (Fig. 16), which are thought to be characteristic of a certain subtype, the so-called ‘Burkitt lymphoma’. In the dog, however, this type of macrophage (large, vacuolated macrophages that have phagocytized all kinds of material) is found in various types of lymphomas. Plasmacytic lymphoma The occurrence of plasmacytoma in lymph nodes is extremely rare (Fig. 14). In this type of lymphoma, mainly atypical plasma cells in diverse stages of development are found. Centrocytic lymphoma This lymphoma consists primarily of centrocytes. Centrocytes are small cells with an irregular, sometimes indented nucleus. The cytoplasm is often absent or is very pale. The chromatin pattern is fine and there are usually no visible nucleoli. Immunoblastic lymphoma If at least 50% of the cells in a preparation are immunoblasts, a diagnosis of immunoblastic lymphoma is made (Fig. 17). Immunoblasts are large cells with a large, round, often 123 Clinical Cytology of Companion Animals: Part 3. Cytology of the lymph node - E. Teske Fig. 18 FNAB of a lymph node with histiocytic sarcoma. Large cells sometimes with small cytoplasmic vacuoles and very irregular forms of nuclei. Phagocytosis and ring-shaped nuclei can also be present (not on this picture). Fig. 17 Immunoblastic lymphoma in a dog. Apart from some naked nuclei, a monomorphous population of immunoblasts is present, characterized by a large centrally located nucleolus. eccentrically located nucleus. This nucleus is characterized by one large, centrally located nucleolus. Immunoblasts have a thick margin of blue cytoplasm. In addition to the large immunoblast with a slightly eccentrically located nucleus and much cytoplasm, in the dog there is also a smaller type of immunoblast with a smaller nucleus located centrally in the cell. The common characteristic with the large immunoblast is the large and centrally located nucleolus. Letters to the Editor From Adam and Deborah Gow: 27th May 2009 Dear Editor, We read with interest the case report “Disseminated Mycobacterium avium in a young Basset Hound located in a suburban area in the United Kingdom” in the April issue of EJCAP.1 It was stated in the report that this was the first published case of M. avium in a dog in the UK. Other types Other types of lymphoma that occur incidentally are mycosis fungoides, histiocytic lymphomas (Fig. 18), and multilobated lymphomas. In view of their low frequency of occurrence, they are not discussed in this overview. Suggested Literature - - - - - - We would like to draw attention to our case report “Disseminated Mycobacterium avium complex infection in a dog” which was published as a short communication in The Veterinary Record on the 3rd of May 2008.2 This describes the infection in a cross-breed dog in the UK which was diagnosed in 2005. Fournel-Fleury C, Magnol JP, Guelfi JF. Colour atlas of cancer cytology of the dog and cat. Conference Nationale des Veterinaires Specialises en Petits Animaux, Paris, 1994, 221-321. Messick JB. The lymph nodes. In: Cowell RL, Tyler R.D, Meinkoth JH., Denicola DB .Diagnostic Cytology and Hematology of the Dog and Cat. 3rd Ed. Mosby Elsevier, St. Louis. 2008; p179-192. Mills JN. Lymph node cytology. Vet Clin North Am, Small Anim Pract. 1989; 19: 697-717. Teske E, Wisman P, Moore PF, van Heerde P. Histological classification and immunophenotyping of canine non-Hodgkin’s lymphomas. Unexpected high frequency of T-cell Lymphomas with B-cell morphology. Experimental Hematology. 1994; 22: 1179-1187. Teske E, van Heerde P. Diagnostic value and reproducibility of fine-needle aspiration cytology in canine malignant lymphoma. Veterinary Quarterly. 1996; 18: 112-115. van Heerde (P.) Malignant lymphomas and histiocytic tumours. Cytology and other diagnostic methods. Thesis, Uitg Rodophi, Amsterdam, 1984. Thrall MA. Cytology of lymphoid tissue. Comp Cont Ed Pract Vet. 1987; 9: 104-111. Zinkl JG, Keeton KS. Lymph node cytology - I., California Veterinarian. 1979; 33(1): 9-11. Zinkl JG, Keeton KS. Lymph node cytology - II., California Veterinarian. 1979; 33(4): 20-23. Zinkl JG, Keeton KS. Lymph node cytology – III, Neoplasia. California Veterinarian. 1981; 35(5): 20-23. Yours Faithfully Adam Gow BVM&S CertSAM MRCVS Deborah Gow BVM&S MRCVS Hospital for Small Animals R(D)SVS The University of Edinburgh Easter Bush Roslin EH25 9RG References: 1. Gerber, K., Hargreaves, J., Iveson, A., Worth, D. Disseminated Mycobacterium avium a young Basset Hound located in a suburban area in the United Kingdom. EJCAP 2009;19(1): 31-35. 2. Gow AG, Gow DJ. Disseminated Mycobacterium avium complex infection in a dog. Vet Rec 2008;162:594-595. 124 EAR NOSE AND THROAT REPRINT PAPER (A) Folded flap palatoplasty for treatment of elongated soft palates in 55 dogs L. Findji(1), G. Dupré(1) ABSTRACT Objectives – To evaluate the safety and efficacy of the folded flap palatoplasty (FFP), a new surgical technique addressing all components of the respiratory obstruction caused by elongated soft palates, and to evaluate the clinical outcomes associated with it. Methods – Medical records (2004-2005) of all dogs which underwent a FFP were reviewed and included in the study. Recorded information included breed, gender, age, weight, duration of hospitalisation, and presence or absence of postoperative tracheostomy. Respiratory grading scores (1-3) were used to record the severity of the disease, before and after surgery, and at a minimum follow-up time of 180 days by detailed telephone interviews with the owners. Results – No intraoperative complications were encountered. A temporary tracheostomy was performed in six cases (10.9%). Two dogs died postoperatively, from tracheostomy complications and unknown cause after unremarkable recovery, respectively. Follow-up (379 ± 142 days) could be obtained for 40 dogs. Thirty-nine dogs (97.5%) showed improvement of respiratory clinical signs after surgery. Improvement of respiratory clinical signs was observed within 15 days after surgery in 85% of cases. Clinical significance – The FFP can be recommended as a safe and efficient technique, particularly valuable for excessively thick elongated soft palates. Key words: Brachycephalic airway syndrome, elongated soft palate, soft palate hyperplasia, folded flap palatoplasty This paper originally appeared in: Vet. Med. Austria / still constitutes the cornerstone of its treatment. Up to 100% of brachycephalic dogs are reported to suffer from ESP [1, 3], which can cause laryngeal obstruction due to aspiration to the rima glottidis during inspiration. Elongated soft palates (ESPs) also commonly demonstrate excessive thickness, which is considered to cause narrowing and obstruction of the naso and oro-pharynx, further contributing to respiratory compromise in affected individuals. Conventional surgical techniques used for correction of ESP consist of its shortening by resection of its caudal aspect (staphylectomy). These techniques address the laryngeal obstruction but are unlikely to achieve significant relief of the nasopharyngeal and oropharyngeal obstructions [4]. Wien. Tierärztl. Mschr.* 95 (2008), 56 - 63 Introduction Elongated soft palate (ESP) is part of brachycephalic airway syndrome (BAS), a widespread condition in brachycephalic dogs. Although recent studies have demonstrated the high incidence of BAS-associated digestive lesions and the benefits resulting from their medical treatment regarding outcome and prognosis [1, 2], surgical relief of the upper airway obstruction (1) Centre Hospitalier Vétérinaire Frégis, 43 av Aristide Briand, F- 94110, Arcueil. Current adresses: Dr Findji-Veterinary Referrals Cancer and Critical Care, 1 West Mayne, Bramston Way, Southfields, Laindon, Essex GB- SS15 6TP. Dr Dupré-Klinik für Chirurgie und Augenheilkunde, Veterinärmedizinische Universität Wien, Veterinärplatz 1, Wien A-1210. Corresponding author: Laurent Findji E-mail: [email protected] & [email protected] * Presented by VÖK (Austria) 125 Folded flap palatoplasty for treatment of elongated soft palates in 55 dogs - L. Findji, G. Dupré Recently, a new surgical technique has been devised to address and relieve all the components of airway obstruction associated with ESP [4, 5]. The aim of this study was to assess whether FFP is suitable for treatment of ESP, and whether it is associated with good results and few complications. Materials and Methods Inclusion Criteria Medical records of all the dogs which had a folded flap palatoplasty (FFP) between March 2004 and October 2005 were reviewed. During this period, FFP was used exclusively for treating ESP. Recorded information included breed, age, weight, birth date, duration of hospitalisation and the requirement for temporary tracheostomy in the postoperative period. Whenever possible, detailed telephone interviews with owners, using a consistent questionnaire, were obtained with a minimum follow-up of 180 days. Clinical Assessment and anaesthesia Upon admission, clinical history was obtained from the owners. The severity of respiratory clinical signs was then graded by the admitting clinician using a 1 to 3 score, according to the scale established by Poncet and others [2] (Table 1). The degree of nare stenosis was subjectively evaluated. Food and water were withheld for a minimum of 15 hours before anaesthesia. Premedication included 0.05 mg/kg acepromazine (Calmivet; Vétoquinol), 0.2 mg/kg dexamethasone (Dexadreson; Intervet), 0.5 mg/kg metoclopramide (Primperid; Sanofi) and 0.01 mg/kg glycopyrrolate (Robinul; Vétoquinol), all administered intramuscularly. General anaesthesia was induced with intravenous thiopenthal (5-10 mg/kg IV) (Nesdonal; Merial) or propofol (3-5 mg/kg IV) (Rapinovet; Schering-Plough) and maintained with isoflurane (Aerrane; Baxter), in 100% oxygen. On induction, direct visual or endoscopic evaluation of the upper airway was carried out by the surgeon. The soft palate was examined with regards to its length and thickness by manipulation and palpation with forceps. The tonsils, the pharynx and the larynx were subjectively evaluated. Figure 1: Positioning of the dog for surgery. opening of the nasopharynx could be visualised. The retracted caudal edge was then applied to the ventral mucosa of the soft palate and the point at which the contact was made (usually 1 or 2 cm caudal to the palatine process of the palatine bone) was marked with an electrocautery cut. The ventral mucosa of the soft palate was then incised in a trapezoidal shape from this mark rostrally to the free edge of the soft palate caudally. Laterally, the sides of the trapezoid passed just medially to the tonsils (Figure 2). The soft tissues under the cut portion of the soft palate were excised together with the ventral mucosa of the soft palate, the palatinus muscles and part of the levator veli palatini muscle (Figure 3). The dissection ended when this portion of the soft palate was reduced to the nasopharyngeal mucosa and submucosa. The caudal edge of the soft palate was retracted rostrally to the rostral edge of the trapezoidal incision (Figure 4). The soft palate was then sutured folded on itself with interrupted monofilament absorbable sutures (glycomer 631, Biosyn; Tyco) (Figure 5). The mouth was then freed and closed. When stenotic nares were diagnosed, dogs subsequently underwent a vertical wedge Surgical Procedure The dog was placed in ventral recumbency. The head was restrained with the mouth kept open. The tongue was pulled rostrally and fixed with tape to allow better exposure of the oropharynx (Figure 1). After surgical preparation of the oral cavity, the caudal edge of the soft palate was grasped with forceps or traction sutures and retracted rostrally, until the caudal Table 1: Grading of respiratory clinical signs according to Poncet and others[2] Nature of respiratory signs Never Occasionally (<once monthly) Regularly (Once weekly) Daily (once daily) Grade 1 Grade 2 Grade 3 Snoring Inspiratory efforts Stress or exercise intolerance Syncope 126 Often (>once daily) Constantly EJCAP - Vol. 19 - Issue 2 October 2009 Figure 2: Incision line (frontal, sagittal and intraoperative views). Figure 3: End of dissection (frontal, sagittal and intraoperative views). Figure 4: Soft palate folding (frontal, sagittal and intraoperative views). Figure 5: Sutured flap (frontal, sagittal and intraoperative views). In cases considered at risk from life-threatening pharyngeal or laryngeal obstruction because of excessive secretions, vomiting or laryngeal collapse, a temporary tracheostomy tube was placed (Jackson double-lumen tracheostomy tube (Tracheostomy tube Rüschelit Biesalski, 7 and 8 mm, Rüsch, Kernen, Germany)). Additional postoperative care consisted of appropriate administration of dexamethasone, metoclopramide, or glycopyrrolate and intra-oral suction, chest percussion and tracheostomy tube care if needed. Dogs were discharged from hospital when no specific nursing care had been necessary for at least 12 hours. Duration of hospitalisation was recorded. resection rhinoplasty [6] during the same surgical procedure. At the time of the study, non absorbable monofilament sutures were still used for rhinoplasty, as previous attempts to use absorbable suture material resulted in more inflammatory wounds and poorer cosmetic results. Postoperative Care After surgery, the mouth and pharynx were washed to remove debris, clots and saliva, and a nasotracheal tube (Pediatric feeding tubes 40cm, 6 to 10 FG, Salva, Unomedical, Birkerød, Danemark) was placed for postoperative oxygen therapy (50 ml/kg/min). 127 Folded flap palatoplasty for treatment of elongated soft palates in 55 dogs - L. Findji, G. Dupré Table 2: Questionnaire for the owners’ interview at follow-up 128 EJCAP - Vol. 19 - Issue 2 October 2009 Clinical findings Grading was recorded for dogs whose follow-up could be obtained (Figure 6). Three dogs had undergone prior conventional staphylectomy 8 months, 1 and 4 years before surgery, respectively, but showed clinical signs of nasopharyngeal and oropharyngeal obstructions due to excessive thickness of the remaining soft palate that necessitated reintervention. Stenotic nares were diagnosed in 50 dogs (90.9%). One dog had already been treated surgically, and four dogs had normal nares. One dog suffered from laryngeal paresis and laryngeal saccule eversion. One dog had undergone prior lateralization of left arytenoid cartilage 3 months before surgery. Follow-Up Dogs which underwent a rhinoplasty were re-evaluated at the time of suture removal and an interview with the owners was conducted with a minimum of six month follow-up, using a consistent questionnaire (Table 2), for all dogs. Statistical analysis Categorical data (e.g. breed or gender) are reported as frequencies and percentages. Continuous data (e.g. age at presentation or hospitalisation duration) are reported as mean ± SD. Chi square analyses were used to study the distribution of males and females in the studied population, and to evaluate the significance of the changes in the repartition of the animals between grades before and after surgery. T-tests were used to evaluate whether the duration of hospitalisation was different for animals which underwent a tracheostomy compared to those which did not. The use of T-tests was possible after a Kolmogorov-Smirnov test indicated no significant deviation from normal distribution. For every statistical test, significance was established at P<0.05. All analyses were performed with commercial statistical software (SPSS for Windows 14.0, SPSS Inc., Chicago, IL). Surgical procedure All dogs underwent a FFP. No intraoperative complications were encountered. Rhinoplasty was performed in 50 dogs. In one dog, concomitant severe laryngeal collapse and laryngeal oedema required arytenoid lateralization and temporary tracheostomy in the early postoperative period. No other surgical procedures addressing the respiratory tract were performed concomitantly. Results Postoperative care and treatment A temporary tracheostomy was performed in 6 cases (10.9%). These 6 dogs were suffering from grade 3 respiratory clinical signs before surgery. All dogs had oxygen therapy provided through either the tracheostomy or a nasotracheal tube. Mean duration of hospitalisation was 1.6 ± 1.1 days (range 1 to 6 days). It was 1.3 ± 0.5 days (range 1 to 2 days) for dogs which did not have a tracheostomy performed and 4.4 ± 1.1 days (range 3 to 6 days) for dogs which did, which was significantly longer (P=0.003). Two dogs died perioperatively (3.6%). One dog had had a tracheostomy and died 16 hours after surgery from respiratory distress caused by excessive tracheal secretions, despite closed tracheal tube surveillance. The other dog died from cardiovascular Epidemiological data Fifty-five dogs underwent a FFP between March 2004 and October 2005 and were included in this study. Forty-five dogs were males (81.8%) and 10 were females (18.2%). Significantly more males were affected (P<0.001). Age at the time of surgery ranged from 6 to 105 months (mean 39 ± 22.6 months, median 34.6 months). Eight different breeds were represented: French bulldog (n=32, 58.2%), Pug (n=8, 14.5%), English bulldog (n=7, 12.7%), Boxer (n=3, 5.5%), King Charles spaniel (n=2, 3.6%), Norwich terrier (n=1, 1.8%), Sharpei (n=1, 1.8%) and Shi Tzu (n=1, 1.8%). Body weight at the time of surgery ranged from 6.5 to 46 kg (mean 14.9 ± 7.9 kg, median 12.3 kg). Figure 6: Distribution of respiratory grades in preoperative and postoperative periods, and at follow-up (*, ‡: significantly different, p<0.001; †: not significantly different, p=0.497) 129 Folded flap palatoplasty for treatment of elongated soft palates in 55 dogs - L. Findji, G. Dupré Figure 7: Time from surgery to improvement of respiratory signs No pharyngonasal regurgitations or nasal discharge were reported, either at time of suture removal or at follow-up. collapse of undetermined origin, 12 hours after surgery, after unremarkable recovery. Post-mortem examinations of these dogs were declined by the owners. All other 53 dogs (96.4%) were discharged from hospital without complication. Discussion Follow-up A minimum of six month follow-up could be obtained for 40 dogs. Thirteen dogs were lost to follow-up. Follow-up ranged from 183 to 715 days (379 ± 142 days). The evolution of respiratory grades between preoperative and postoperative periods and follow-up are illustrated in Figure 6. Respiratory grades were improved significantly between preoperative and postoperative periods (P<0.001), and between preoperative and follow-up periods (P<0.001). On the contrary, no significant difference was found in respiratory grades between postoperative and follow-up periods (P=0.497). The times from surgery to improvement of respiratory clinical signs are shown in Figure 7. Although seldom reported in the literature, excessively thick ESP has previously been mentioned [7, 8]. Its incidence seems to vary widely from one breed to another, but anatomical studies which could confirm this observation are lacking. In the absence of such studies or precise normal ranges, the diagnosis of excessively thick ESP remains subjective and can be made by ways of direct examination and palpation of the soft palate, or lateral radiographs (Figure 8, Figure 9), CT scan or MRI of the pharyngeal area. Ideally, imaging should be done without oral intubation, which is not without risks in brachycephalic dogs. It can also be made retrospectively, after surgical excision, by direct examination of the excised tissues. In this preliminary retrospective study, the thickness of the soft palate in pre and postoperative periods was not recorded. The assessment of the oro- and nasopharyngeal Figure 8: Lateral radiographic appearance of the pharyngeal region of a mesocephalic dog Note as both the nasopharynx (black arrow) and oropharynx (hollow arrow) are unobstructed by the soft palate (SP) Figure 9: Lateral radiographic appearance of the pharyngeal region of a brachycephalic dog Note as both the nasopharynx (black arrow) and oropharynx (hollow arrow) are reduced to a thin line of aeric density, as they are nearly completely obstructed by the excessively thick soft palate (SP) 130 EJCAP - Vol. 19 - Issue 2 October 2009 palate and to curl its caudal border downwards [14], which eases the air flow through the widened pharynx during breathing. It is possible that the shortening of the soft palate and the rostral position of the suture line, which is thought to widen the pharynx by pulling the caudal border of the soft palate rostrally and ventrally, achieves the same effect. No intraoperative complications were encountered, though the FFP appears subjectively more technically challenging and longer to perform than conventional techniques. The use of electrocautery is thought to ease the procedure. However, many authors recommend avoiding its use for soft palate surgery [11, 15], because it is expected to cause more postoperative oedema than scalpel or scissors, and that such oedema in the pharyngeal area could result in life-threatening airway obstruction. However, use of steroidal anti-inflammatory drugs in the perioperative period minimizes this risk [9, 16]. Besides, with the FFP, the surgical site is displaced rostrally and the possible postoperative oedema or bleeding is likely to be located rostrally in the mouth, away from the pharynx. Furthermore, it is likely that such an oedema would be clinically less significant standing in a greatly thinned soft palate. The FFP is then believed to be less susceptible to the consequences of a possible oedema than conventional techniques, and electrocautery was therefore used here in all cases. Figure 10: Excised portion of the soft palate after FFP obstructions would however have been of greater relevance but would have required advanced diagnostic imaging means (CR scan or MRI) and was not technically achievable in our hospital. In the absence of advanced diagnostic imaging, the most accurate assessment of the preoperative soft palate thickness is obtained retrospectively, after the FFP has been performed, and the soft palate has been dissected and excised (Figure 10). Over the study period, the FFP was used exclusively, regardless of the preoperative subjective assessment of the soft palate thickness, which is therefore facultative. Further studies including preand postoperative objective measurements of the oro- and nasopharyngeal volumes by means of CT scan or MRI would however be valuable. Some authors recommend performing a temporary tracheostomy before surgery to prevent postoperative airway obstruction caused pharyngeal by oedema [17, 18] or to decrease encumbrance of the pharyngeal area during surgery [15]. With the FFP, the surgical site is displaced rostrally, rendering the issue of intraoperative encumbrance of the pharynx and the risk for postoperative pharyngeal oedema of lesser importance. A temporary tracheostomy was therefore performed in only 6 dogs (10.9%), always postoperatively when considered required because of possible life-threatening complications. In accordance with some authors [15], we performed temporary tracheostomies as soon as we first considered it might have been necessary, as it is a low-risk procedure [19]. This might have made their incidence appear higher than considered necessary by some other surgeons. Despite this fact, our incidence compared similarly with previous reports of 5 to 27.9% [1, 9, 19, 20]. The FFP thins the soft palate by excising most of the connective and muscular tissues responsible for its excessive thickness, and thus relieves oropharyngeal and nasopharyngeal obstructions [4, 5]. This study is to date the first to report the outcome of a series of dog undergoing this surgical procedure. Previously described surgical techniques aim at shortening the ESP [9, 10] to relieve the laryngeal obstruction it causes. The FFP achieves the same effect as it shortens the soft palate by folding it on itself. However, with the FFP, the ESP is left shorter than usually recommended [6] to achieve thinning of the soft palate on its entire length; the nasopharyngeal opening is most often directly visible in the mouth after the procedure (Figure 5). Excessive shortening of ESPs is thought to expose to pharyngonasal regurgitations [3, 9, 11], as the soft palate is both reported to prevent them actively [12] and passively [13]. Furthermore, it is likely that the active movements of the soft palate are greatly diminished, if not suppressed, as most of its muscles are removed during the procedure. However, in this study, no episode of pharyngonasal regurgitation was observed nor reported. It is possible that, in brachycephalic dogs, after marked shortening of the soft palate, its obliterative role is passively carried out by the base of the tongue, pushed dorsally during the swallow reflex [12] (especially as many of these dogs are macroglossic) and the redundant pharyngeal mucosal soft tissues. Palatine muscles are also reported to shorten the soft Males were significantly more likely to be affected in our study (P<0.001). This differs from a study on BAOS conducted in Australia in which no sex predisposition is reported [20], but confirms the observation from a previous series in our centre, where 43 out of 61 dogs (78.7%) were males [1]. The perioperative mortality in our study (3.6%) compares with perioperative mortalities of 0 to 14.8% previously reported [1, 9, 20, 21], particularly as one death remained unexplained and may not be related to surgery. All but one dog (97.5%) showed improvement of their respiratory function after surgery. One dog was considered not to have shown any improvement, but its preoperative clinical signs were limited to constant snoring without any inspiratory efforts, stress or heat intolerance, or syncope. This dog carried 131 Folded flap palatoplasty for treatment of elongated soft palates in 55 dogs - L. Findji, G. Dupré on snoring but did not show any other respiratory difficulty. As in the other clinical studies on this topic [1, 9, 20-22], the concomitancy of another procedure addressing another component of BAS (here: rhinoplasty) renders impossible to distinguish between the respective participation of each procedure in this improvement. Furthermore, the sole clinical appreciation would probably be insufficient in evaluating the efficacy of each procedure, and dynamic measurements would certainly be required. Because most dogs diagnosed with BAS suffer from several of its components, it seems hardly feasible to design a clinical study in which correction of each of its components is separate and dynamic measurements are performed. Improvement was rapidly observed (immediately in 61.5% of cases, within 15 days in 87.1% of cases), and was durable since at a mean follow-up of 379 days, 82.5% of dogs had improved their respiratory score by at least 1 point. Notably, some dogs were considered to be improved by their owners but stayed in the same grading category, often because of persistent snoring despite improvement of other respiratory clinical signs. On the other hand, our results support the well spread conception that, although surgically treated and markedly improved, these dogs can rarely be considered normal as for their respiratory function: 35% and 10% of dogs were still graded 2 and 3 respectively for respiratory signs at time of follow-up. dogs. Am J Vet Res. 1986; 47: 2200-4 [9] Harvey CE. Upper airway obstruction surgery 2: Soft palate resection in brachycephalic dogs. J Am Anim Hosp Assoc. 1982; 18: 538544 [10] Clark GN, Sinibaldi KR. Use of a carbon dioxide laser for treatment of elongated soft palate in dogs. J Am Vet Med Assoc. 1994; 1779-1781 [11] Bright RM, Wheaton LG. A modified surgical technique for elongated soft palate in dogs. J Am Anim Hosp Assoc. 1983; 19: 288 [12] Herdt T. Movements of the gastrointestinal tract in Textbook of veterinary physiology, Cunningham J.; Philadelphia, 1997. Vol 1:272-289 [13] Evans H. The digestive apparatus and abdomen in Miller’s anatomy of the dog, Evans H. Philadelphia. 1993. Vol 1:385-462 [14] Hermanson J. Evans H. The muscular system in Miller’s anatomy of the dog, Evans H. Philadelphia. 1993. Vol 1:258-384 [15] Harvey CE, Venker-Von Haagan A. Surgical management of pharyngeal and laryngeal airway obstruction in the dog. Vet Clin North Am. 1975; 5: 515-35 [16] Davidson EB. et al. Evaluation of carbon dioxide laser and conventional incisional techniques for resection of soft palates in brachycephalic dogs. J Am Vet Med Assoc. 2001; 219: 776-81 [17] Orsher R. Brachycephalic airway disease in Disease mechanisms in small animal surgery, Bojrab M. Philadelphia. 1993. Vol 1:369370 [18] Hendricks JC. Brachycephalic airway syndrome. Vet Clin North Am Small Anim Pract. 1992; 22: 1145-53 [19] Harvey CE, O’Brien JA. Upper airway obstruction surgery 7: Tracheotomy in the dog and cat: Analysis of 89 episodes in 79 animals. J Am Anim Hosp Assoc. 1982; 18: 563-566 [20] Torrez CV, Hunt GB. Results of surgical correction of abnormalities associated with brachycephalic airway obstruction syndrome in dogs in Australia. J Small Anim Pract. 2006; 47: 150-4 [21] Lorinson D, Bright RM, White RAS. Brachycephalic airway obstruction syndrome - A review of 118 cases. Canine Pract. 1997; 22: 18-21 [22] Harvey CE. Overview of results. J Am Anim Hosp Assoc. 1982; 18: 567-569 During the study period, the FFP was used exclusively for treatment of elongated soft palate, and has shown to be safe and efficient regardless of the soft palate thickness. It can therefore be used for any ESP and will be most valuable if the soft palate appears, either pre or intraoperatively, to be excessively thick. Acknowledgements The authors would like to thank Prof Robert N White and Alexander Tichy for their most valuable help in reviewing our manuscript and with statistics, respectively, as well as Drs Cyrill Poncet and Valérie Freiche for their active involvement in the clinical aspects of this study References [1] Poncet CM. et al. Long-term results of upper respiratory syndrome surgery and gastrointestinal tract medical treatment in 51 brachycephalic dogs. J Small Anim Pract. 2006; 47: 137-42 [2] Poncet CM et al. Prevalence of gastrointestinal tract lesions in 73 brachycephalic dogs with upper respiratory syndrome. J Small Anim Pract. 2005; 46: 273-9 [3] Wykes PM. Brachycephalic airway obstructive syndrome. Probl Vet Med. 1991; 3: 188-97 [4] Dupré G, Findji L. La palatoplastie modifiée chez le chien. Le Nouveau Praticien Vétérinaire, 2004, 553-556 [5] Dupré G, Findji L, Poncet CM. The Folded Flap Palatoplasty: a new technique for treatment of elongated soft palate in dogs. 2005 ECVS annual meeting (2005). Lyon, France [6] Monnet E. Brachycephalic Airway Syndrome in Textbook of Small Animal Surgery, Slatter D.; Philadelphia, 2003, Vol 1:808-813 [7] Hendricks JC. et al. The English bulldog: a natural model of sleepdisordered breathing. J Appl Physiol. 1987; 63: 1344-50 [8] Amis TC, Kurpershoek C. Pattern of breathing in brachycephalic How to contact the FECAVA Office and Secretary Our secretarty is Ulrike Tewes. You can contact Ulrike: By phone : +32 (0)2 533 70 20 By e-mail : [email protected] The office is open from 8.30 am to 4.30 pm Monday to Friday. 132 ORTHOPAEDICS REPRINT PAPER (B) Diagnosis, treatment and prognosis of disc associated Wobbler syndrome in dogs S. De Decker(1), S. Bhatti,(2)I. Gielen, L. Van Ham(1) ABSTRACT Disc associated wobbler syndrome (DAWS) is the most prevalent and most typical wobbler syndrome in dogs. It is typically seen in the middle-aged Dobermann Pinscher. Caudal cervical spinal cord compression is caused by protrusion of the annulus fibrosus of the intervertebral disc into the spinal canal, sometimes in combination with ligamentum flavum hypertrophy and malformed vertebrae. Clinical signs vary from neck pain to tetraplegia. The diagnosis is generally made using myelography. There is a lot of controversy concerning the treatment of this disease. Many surgical techniques have been developed for it, but little is known about the results of conservative treatment. Objective data about the prognosis of this disease is scarce. middle-aged large breed dogs, in particular the adult Dobermann Pinscher. In DAWS, cervical spinal cord compression results from the protrusion of the intervertebral disc between the sixth and seventh cervical vertebrae (C6-C7) and/or between the fifth and sixth cervical vertebrae (C5-C6), and from generally mild vertebral malformations, frequently in combination with dorsal compression resulting from hypertrophy of the ligamentum flavum [Van Gundy, 1988]. Approximately 13 to 20% of dogs present with both C5-C6 and C6-C7 lesions at the time of initial diagnosis [Van Gundy, 1988; Sharp and Wheeler, 2005]. This article deals primarily with DAWS and reviews the diagnosis, treatment and prognosis of this specific type of wobbler syndrome. This paper originally appeared in: Vlaams Diergeneeskundig Tijdschrift*, 2008, 78 139 -146 Introduction Wobbler syndrome refers to a collection of disorders of the caudal cervical vertebrae and intervertebral discs of large breed dogs resulting in spinal cord compression [Van Gundy, 1988]. A large variety of lesions with different proposed aetiologies have been attributed to the wobbler syndrome and many synonyms are found in the literature, such as spondylolisthesis [Dueland et al., 1973], cervical spinal subluxation and spondylolisthesis [Gage and Hoerlein, 1973], cervical vertebral instability [Mason, 1977; Parker et al., 1973], cervical spinal stenosis [Wright et al. 1973], cervical spondylopathy [Denny et al., 1977], spondylomyelopathy [Read et al., 1983] and cervical malformation/malarticulation syndrome [Shores, 1984]. All these different clinical entities result in the same clinical signs of ataxia, paresis (predominantly affecting the hind limbs) and cervical pain. The term wobbler only refers to the characteristic ‘wobbling’ hind limb ataxia [VanGundy, 1988]. The most typical and predominant syndrome is the disc associated wobbler syndrome (DAWS). This is seen in Diagnosis Clinical presentation Animals affected with DAWS are usually 4 to 8 years of age, and Dobermann Pinschers are overrepresented. The most common presentation is a gait disturbance. The owners commonly report a gradual onset, although the symptoms can sometimes occur or become exacerbated more acutely. A slowly progressing hind limb ataxia and/or paresis of the pelvic limbs is usually noted. (1) Department of Small Animal Medicine and Clinical Biology (2 )Department of Medical Imaging of Domestic Animals –Faculty of Veterinary medicine, Ghent UniversitySalisburylaan 133, B-9820 Merelbeke. Corresponding author-E-mail: [email protected] * Presented by SAVAB (Belgium) 133 Diagnosis, treatment and prognosis of disc associated Wobbler syndrome in dogs - S. De Decker, et al A broad-based hind limb stance can be noticed [Seim, 2000; Wheeler and Sharp, 2005]. In dogs with apparently normal thoracic limbs, it is sometimes difficult to distinguish DAWS from a thoracolumbar lesion [McKee and Sharp, 2003]. Progression to thoracic limb involvement with a short stilted gait can also occur [Van Gundy, 1988, Sharp and Wheeler, 2005]. Affected dogs often show a characteristic ‘disconnected’ gait, in the sense that the thoracic and pelvic limbs seem to advance at different rates. Neck pain may be seen but is usually not overtly present: a history of neck pain is seen in approximately 40% of the cases [Seim, 2000]. Tetraplegia is uncommon [Sharp and Wheeler, 2005]. Figure 1. Survey radiograph of a 4-year-old Dobermann. Severe narrowing of the intervertebral disc space between C6-C7 (arrow). New bone formation is clearly visible on the ventral aspect of C6C7 (arrowhead). Malformation of the cranioventral border of C7. Survey radiography Survey radiographs may be indicative for the presence of DAWS, but they are not conclusive and do not precisely indicate the site of spinal cord compression. This non-invasive technique is useful to rule out potential differential diagnoses such as vertebral fractures, (sub)luxations, vertebral neoplasia and discospondylitis [Sharp and Wheeler, 2005]. General anaesthesia is necessary to obtain correct positioning of the dog. In dogs with DAWS, changes can be seen in the vertebral body, the vertebral canal and the intervertebral disc space. The altered shape of the vertebrae can range from varying degrees of loss of the ventrocranial border, to a triangularly shaped vertebra. Spondylosis deformans may be seen ventral to the intervertebral space, with associated changes in the opacity of the vertebral body. Narrowing of the intervertebral disc space is frequent and often corresponds to the site of cord compression, although there are exceptions to this [VanGundy, 1988; Lewis, 1991; Sharp et al., 1992]. The vertebral canal may be stenotic, with the cranial orifice being much narrower than the caudal orifice [Sharp, 1992] (Figure 1). Changes on survey radiographs do not always correlate with myelographic evidence of spinal cord compression [Seim and Withrow, 1982; Read et al., 1983, Lewis, 1991]. Some dogs with severe radiographic abnormalities will show no spinal cord compression on myelography and demonstrate no clinical signs [Lewis, 1991]. Conversely, survey radiographs may be normal in some dogs with DAWS, in which case spinal cord compression is only identified by myelography [Sharp et al., 1992]. Even when the main site of compression is obvious, secondary sites of compression cannot be identified using plain radiography. Figure 2. Lateral myelogram of the same dog as in Fig 1. Although the survey radiographs suggest a compressive lesion between C6 and C7, severe extradural spinal cord compression is noted between C5 and C6 (arrow). A smaller compressive lesion is noted between C6 and C7 (arrowhead). Figure 3. Myelogram of the same dog as in the previous figures while applying traction to the head. The severity of the compressive lesion reduces remarkably in size with traction. This is a clear example of a traction-responsive lesion. Myelography With myelography or contrast radiography, the spinal cord is outlined by a contrast medium injected into the subarachnoid space. Myelography is the diagnostic method of choice for identifying DAWS in the dog [Sharp and Wheeler, 2005]. In lateral views, abnormalities are seen both in the ventral and dorsal aspects of the vertebral canal (Figure 2). Ventral extradural compression related to the intervertebral disc is the most common finding. The ventral contrast column may be elevated or even arrested in some dogs. Multiple sites of compression are common [Sharp et al., 1992]. Dorsal compression caused by hypertrophy of the ligamentum flavum is seen in some dogs. This also frequently occurs at multiple sites. The degree of spinal cord compression caused and the clinical significance of this radiological finding are unclear, although some authors believe Figure 4. Myelogram of the same dog as in the previous figures while flexing the caudal cervical region. The severity of the compressive lesion reduces remarkably in size with flexion. Extension was not performed due to the potential risk of exacerbation of spinal cord compression. 134 EJCAP - Vol. 19 - Issue 2 October 2009 A B C Figure 5A. CT image at the level of the vertebral body of an adult Dalmatian without DAWS. The bony structures are clearly visible. The spinal cord (black) is not visible in this image. compression in dogs with DAWS [Sharp et al., 1992] (Figure 4). Flexion and extension views may be of particular interest in the evaluation of mild lesions, whose significance is unclear when myelography is performed in a neutral position [McKee and Sharp, 2003]. Positional studies are not without risk. The extension view can cause severe exacerbation of spinal cord compression and should be done either with extreme care or, in certain cases, not at all [Lewis, 1991]. Although myelography is the standard procedure to confirm the diagnosis of DAWS in dogs, this rather invasive procedure is not completely without risk [Sharp and Wheeler, 2005]. Seizures and transient neurological deterioration are the most important complications following myelography [Sharp et al., 1992]. A significantly higher incidence of postmyelographic complications in Dobermann Pinschers with caudal cervical spondylomyelopathy, compared to dogs suffering from other cervical lesions, was demonstrated in the study of Lewis and Hosgood (1992). Figure 5B. CT myelography image at the level of the intervertebral disc of the same dog as in Figure 5A. The subarachnoidal space is filled with a radiolucent contrast medium (white). Intervertebral disc (*). The spinal cord (dark) appears round and is surrounded by a subarachnoid space of relatively even diameter. Figure 5C. CT myelography image at the level of C5-C6 of the same dog as in Figures 1-4. Calcified disc material and a right sided protrusion of the intervertebral disc with severe spinal cord compression (arrow). The spinal cord has a flattened appearance and the ventral subarachnoid space is clearly attenuated. it is significant [Lyman, 1991]. The merit of applying stress during myelography by the use of traction, flexion or extension has been discussed extensively. The degree of spinal cord compression may change as the positions of adjacent vertebrae are altered. Lesions may be categorised based on whether or not compression changes in the ‘stressed’ positions of traction, flexion or extension. Lesions are termed static when the degree of compression remains the same, whatever the position of the neck, whereas dynamic lesions improve or worsen, depending on the different positions of the neck [Seim and Withrow, 1982]. Dynamic lesions can be further subdivided into tractionresponsive and positional lesions. This subdivision of lesion types can provide some information regarding the nature of the lesion and it helps the surgeon to decide on the best surgical procedure to perform [Sharp and Wheeler, 2005]. Traction views are performed by applying tension to the head in a forward direction and to the forelimbs in a caudal direction. Compressive lesions that improve with traction are termed ‘tractionresponsive’ [McKee and Sharp, 2003] (Figure 3). Traction usually decreases spinal cord compression caused by the annulus fibrosus or ligamentous structures [Rusbridge et al., 1998]. Therefore most dogs with DAWS will show traction-responsive lesions. These traction-responsive lesions can be expected to benefit from distraction-stabilisation surgery [McKee and Sharp, 2003]. The degree of compression can change as the neck is moved between flexed, neutral and gently extended positions [Sharp et al., 1992; McKee and Sharp, 2003]. These types of dynamic lesions are termed ‘positional’, as they are worsened by positions that reflect normal neck motion [Sharp and Wheeler, 2005]. Extension usually exacerbates and flexion usually relieves Computed Tomography and Computed Tomography myelography Computed tomography (CT) generates successive cross-sectional images with excellent detail, particularly of the bony structures, which can be reconstructed in different planes (Figure 5A). The reconstruction of these images, for example in a sagittal plane, can, however, be accompanied by a loss of detail [Thomson et al., 1993]. Because of its inability to delineate the spinal cord, conventional CT does not provide as much information as conventional myelography [Sharp et al., 1995]. When CT is used in combination with a subarachnoidal injection of contrast medium (CT myelography), good delineation of the spinal cord can also be obtained. An optimal CT myelography (CTm) image is obtained when a lower dose of contrast medium is used than in a conventional myelographic study [Yu et al., 1986]. The natural resorption and dilution of the contrast agent that occurs during a conventional myelographic procedure can be utilised and usually conventional myelography precedes CT myelography under the same anaesthetic episode [Sharp et al., 1992]. The normal canine cervical spinal cord has a somewhat round appearance and is surrounded by a subarachnoid space of relatively even diameter (Figure 5B). In dogs with DAWS the ventral subarachnoid space is attenuated and the spinal cord appears to be displaced from the floor of the vertebral canal (Figure 5C). These abnormalities are caused by the extradural soft tissue mass of protruding annulus fibrosus. CT myelography may also provide prognostic information by detecting spinal cord atrophy in diseases that cause chronic spinal cord compression. Spinal cord atrophy is characterised by a somewhat triangularly 135 Diagnosis, treatment and prognosis of disc associated Wobbler syndrome in dogs - S. De Decker, et al A B Figure 6A. T2-weighted sagittal MRI image of an adult Dobermann Pinscher without DAWS. Note the excellent soft tissue detail on this MRI image, compared with FIG 5A-C. The spinal cord (SC) is surrounded by the hyperintense subarachnoidal space (white). The subarachnoidal space is visible at each point and never interrupted. VB = Vertebral body. * = a normally hydrated intervertebral disc. Between C6 and C7: partial intervertebral disc degeneration, characterised as a partial loss of hyperintensity of the disc. Figure 6B. T2-weighted sagittal MRI image of the same dog as in Figures 1-4 and 5C. At the level of C5-C6 there is complete loss of the hyperintense CSF signal around the spinal cord with subsequent spinal cord compression. A hyperintense area in the spinal cord can be noted at this level (arrow). At the level of C6-C7 there is complete disc degeneration characterised as a total loss of hyperintensity of the disc (arrowhead). shaped spinal cord and a relative widening of the subarachnoid space, relative to the spinal cord [Sharp et al., 1995]. There is a strong connection between spinal cord atrophy in humans with cervical spondylotic myelopathy and a poor prognosis following surgery. When the transverse area of the spinal cord is less than 50% of the subarachnoid space, the prognosis is poor [Badami et al., 1985; Yu et al., 1986]. To date, not one single similar relationship has been studied in veterinary medicine. When used in the immediate postoperative period, CT myelography can be used to confirm adequate removal of a compressive lesion and may demonstrate possible spinal cord re-expansion [Sharp et al., 1992]. only a few reports on the use of Magnetic Resonance Imaging (MRI) in the diagnosis of DAWS [Penderis and Dennis, 2004; da Costa et al., 2006a; da Costa et al., 2006b]. MRI allows direct, non-invasive, multiplanar imaging without loss of detail and an excellent soft tissue characterisation with an absence of ionising radiation [Thomson et al., 1993; Lipsitz et al., 2001]. A distinct advantage is the ability to assess correctly the spinal cord parenchyma. Spinal cord compression, intervertebral disc degeneration, intervertebral disc protrusion and spinal cord signal changes are abnormalities that can be revealed in dogs with DAWS using MRI. Spinal cord compression can be evaluated on sagittal and transverse T2-weighted images as a loss of hyperintense cerebrospinal fluid (CSF) signal around the spinal cord or as a change in shape of the spinal cord from round to oval on the transverse image [Lipsitz et al., 2001] (Figures 6A and 6B). Intervertebral disc degeneration is characterised by a loss of hyperintensity of the disc on T2-weighted images. Abnormal spinal cord signal changes are classified either as hyperintense or as hypointense when they are compared to the normal spinal cord signal intensity adjacent to the abnormal area [da Costa et al., 2006b]. Hyperintense T2-weighted signal changes within the spinal cord are a common MRI feature of spinal cord diseases in humans. It is believed that they reflect a broad spectrum of spinal cord abnormalities such as oedema, inflammation, vascular ischaemia, gliosis and myelomalacia. The exact clinical and prognostic significance of spinal cord signal changes is not yet known [Suri et al., 2003] (Figures 7A and 7B). The possible complications associated with myelography do not occur with MR imaging, because this technique does not require the injection of a contrast medium into the subarachnoid space. Penderis and Dennis [2004] and da Costa and co-workers [2006b] demonstrated the application of traction during an MRI scan to differentiate between traction-responsive and tractionnonresponsive lesions. A possible disadvantage of MRI in the evaluation of the spine is the possibility of over-interpretation, which may result in false positive results. In a recent study [da Costa et al., 2006a], 16 clinically normal Dobermann Pinschers underwent MRI. Four of them had spinal cord compression, 12 of Magnetic Resonance Imaging Although this is the technique of choice for imaging humans with degenerative diseases of the cervical spine, there are Figure 7A. T2-weighted transverse MRI image at the level of C5-C6 of the same dog as in Figure 6A. The spinal cord (SC) has a somewhat round appearance. The spinal cord is surrounded by a hyperintense cerebrospinal fluid signal (*) of relatively even diameter. IVD = Intervertebral Disc. The spinal cord is surrounded by the bony (B) pedicles. Figure 7B. T2-weighted transverse MRI image at the level of C5C6 of a 10-year-old Dalmatian with neck pain and tetraparesis. The spinal cord has an abnormal shape caused by a rightsided extradural spinal cord compression (white arrow). The hyperintense ventral subarachnoid space is attenuated at this level. A B 136 EJCAP - Vol. 19 - Issue 2 October 2009 governing the choice of surgical procedure is the appearance of the spinal cord on imaging, in particular the traction views after myelography. Other factors include the number of sites of spinal cord compression, the degree of vertebral malformation and the presence of nerve root compression (thoracic limb lameness) [McKee and Sharp, 2003]. them had disc degeneration and, in addition, foraminal stenosis was detected in 11 of them. Mild disc protrusion or herniation was also detected in all of these clinically normal dogs. Spinal cord signal abnormalities, however, were not detected in them. Other disadvantages are the lack of general availability, the high cost and the long time required to complete this kind of study [Sharp and Wheeler, 2005]. Ventral Decompression Ventral decompression by a standard ventral slot technique is, according to several authors, appropriate for single, static lesions [Seim, 2000; McKee and Sharp, 2003; Sharp and Wheeler, 2005]. Ventral decompressive surgery can be very challenging for dogs with DAWS because of the possibility of vertebral malformations, limited access to the caudal cervical disc spaces and intraoperative bleeding due to possible adhesions between the hypertrophied annulus and venous plexus [McKee and Sharp, 2003; Sharp and Wheeler, 2005]. It is very important to remove all of the compressive dorsal anulus and dorsal longitudinal ligament. This can be very difficult to do in chronic compressive disorders like DAWS. The two main disadvantages of this surgical technique are the inability to perform surgery on two adjacent disk spaces and the inability to treat dorsal compression due to ligamentum flavum hypertrophy [McKee and Sharp, 2003; Sharp and Wheeler, 2005]. Short-term deterioration is common, even among dogs that have good long-term results [Rusbridge et al., 1998]. It is very difficult to interpret and compare reports on the results of ventral decompressive surgery due to the large differences in inclusion criteria and follow-up periods for the different authors. Chambers and colleagues [1982] only included dogs which had a survival of at least one year after surgery in their report. In this way they ignored the dogs that were destroyed in the first year after surgery due to lack of postsurgical improvement. They reached a 100% success rate in this study. In a later study they also included dogs that died postoperatively due to problems unrelated to DAWS. In this study they reached a success rate of 66% [Chambers et al., 1986]. In the study by Rusbridge and colleagues [1998], cases were excluded if a minimum follow-up period of 24 months after surgery could not be reached. For this reason, six dogs were excluded from the study and 4 of the remaining 14 dogs demonstrated a recurrence of clinical signs two years or more after surgery. This last piece of information demonstrates the most important complication in applying ventral decompression to dogs with DAWS. It is commonly believed that about 20% to 30% of the dogs undergoing single level decompression suffer a second episode of neurological signs within 2-3 years [Bruecker et al, 1989; Rusbridge et al, 1998]. The reason for this neurological deterioration is presumed to be a recurrence at the original site or the development of a compressive lesion at an adjacent disk space, which is called a domino lesion [Wheeler and Sharp, 2005]. This occurs independently of the surgical technique performed, and has been reported after distractionstabilisation techniques [Jeffery and McKee, 2001]. Treatment A lot of controversy and discussion exists concerning the treatment of DAWS and the type of surgery that is most likely to give the best results in each individual case [Jeffery and McKee, 2001]. Conservative treatment There is a lack of knowledge and objective data on the natural progression of DAWS and of the results of conservative treatment*. In the literature, DAWS is often defined as a progressive disease in which surgery is necessary to halt progression of symptoms [Sharp and Wheeler, 2005; McKee and Sharp, 2003]. The study by Denny and colleagues [1977] is often cited to provide evidence that conservative therapy is ineffective in the treatment of wobbler syndrome. This paper described 35 cases of cervical spondylopathy with follow-up records of 10 surgically treated and 25 untreated animals. In the group of untreated animals, only one dog could be suspected of having DAWS based on the signalment and radiographic abnormalities, and this animal was lost during follow-up. The study dealt almost exclusively with the specific type of wobbler syndrome that typically affects immature Great Danes and Dobermanns. This syndrome is associated with vertebral malformation-malarticulation and has a different aetiology and prognosis from DAWS. Although objective results are not available, it is possible that conservative treatment could be successful in certain cases. Conservative treatment would consist of cage confinement for several weeks in combination with anti- inflammatory drugs when needed. If the initial cage confinement is successful, the patient should gradually return to normal activity over the course of 4-6 weeks. Intermittent anti-inflammatory drug therapy may be necessary [McKee and Sharp, 2003; Sharp and Wheeler, 2005]. One study describes the successful application of physiotherapy as the sole treatment for three dogs with chronic disc associated compressive lesions of the caudal cervical spinal cord [Speciale and Fingeroth, 2000]. Surgical treatment Several surgical procedures have been described to treat DAWS. Although many authors claim their procedure has a success rate of between 70% and 90%, the large number of reported techniques reflects the difficulty of treating DAWS [Chambers et al., 1982; McKee et al., 1990; Dixon et al., 1996; Rusbridge et al., 1998; de Risio et al., 2002]. All surgical procedures for the treatment of DAWS have a high potential for morbidity and postoperative complications [VanGundy, 1988; Sharp and Wheeler, 2005]. There are three basic types of surgery: ventral decompression, vertebral distraction-stabilisation and dorsal decompression [Sharp and Wheeler, 2005]. The main factor Vertebral distraction-stabilisation The primary indications for a distraction-stabilisation procedure are the presence of a traction-responsive lesion on myelography and the presence of nerve root compression. A number of different techniques have been developed for this procedure, * See update at end of paper 137 Diagnosis, treatment and prognosis of disc associated Wobbler syndrome in dogs - S. De Decker, et al surgery for the treatment of DAWS, as it is not stated whether the compressive lesions treated were ventral or dorsal in nature [Lyman, 1991; De Risio et al., 2002]. such as vertebral distraction and stabilization with vertebral body pins or screws and bone cement [Bruecker et al., 1989], a screw and washer [McKee et al., 1989], a screw and double washer [McKee et al., 1990], interbody bone cement plug [Dixon et al., 1996] and the Compact Unilock System [Voss et al., 2005]. All of these different surgical techniques are based on the same principle. A ventral slot defect is drilled to a depth of three-quarters of the height of the intervertebral disk space. In this way the dorsal annulus is preserved and the vertebral canal is not entered into. Traction is applied to the adjacent vertebrae using vertebral distraction instruments or by manual traction on the head. The two vertebrae are then rigidly stabilised with an orthopaedic implant to maintain distraction. Linear traction provides immediate cord decompression by stretching the dorsal annulus, dorsal longitudinal ligament and ligamentum flavum. By stabilising the adjacent vertebral bodies, it is assumed that the hypertrophied soft-tissue structures would then be allowed to atrophy with time. The advantage of not entering the vertebral canal, as is done in direct decompressive surgical techniques, is offset partly by the risk of implant failure or other implant-associated complications such as loosening, migration or breaking of implants, vertebral end-plate fracture due to inadequate contact between the orthopaedic implant and the vertebral endplate, and the increased risk of surgical infection. Implant failure can be asymptomatic in some patients [Sharp and Wheeler, 2005]. As in other surgical techniques, it seems to be very difficult to perform surgery on more than one intervertebral disc space at the same time. Domino lesions occur with the same incidence with this technique as with ventral decompressive surgery. The two most recommended techniques are the interbody bone cement plug and vertebral body pins combined with bone cement [Seim, 2000; McKee and Sharp, 2003; Sharp and Wheeler, 2005]. Prognosis There is little objective data available on the prognosis of DAWS. Even though there is not a single specific report on the natural progression or medical treatment of dogs with DAWS, neurological and surgical handbooks do describe a generally guarded to unfavourable prognosis for patients treated medically [Seim, 2000; McKee and Sharp, 2003; Sharp and Wheeler, 2005]. In surgical reports, many authors claim a success rate of more than 70% or 80% immediately postoperatively [Bruecker et al., 1989; McKee et al., 1989; McKee et al., 1990; De Risio et al., 2002]. Conversely, overall long-term mortality rates vary from 19% to 43%, which suggests a less favourable prognosis [Dixon et al., 1996; Rusbridge et al., 1998, McKee et al., 1990; De Risio et al., 2002]. After both ventral decompressive and vertebral distraction-stabilisation techniques, a second episode of clinical signs is seen in about 20% to 30% of cases [Jeffery and McKee, 2001; McKee and Sharp, 2003, Sharp and Wheeler, 2005]. It is very difficult to compare the results of the different surgical techniques due to the differences in case selection, in the definition of a successful outcome and in the length and descriptions of follow-up [Jeffery and McKee, 2001]. Most surgical reports deal with the ‘wobbler syndrome in general’ and do not focus on DAWS in particular. This could give the false impression of a favourable outcome because the surgical treatment of the wobbler syndrome typically seen in young adult giant-breed dogs gives better results than the surgical treatment of DAWS [McKee and Sharp, 2003]. Generally, patients with multiple lesions have a guarded to unfavourable prognosis [Seim, 2000; Jeffery and McKee, 2001; McKee and Sharp, 2003; Wheeler and Sharp, 2005]. The most plausible reason is that, when employing one of the current surgical techniques, it is very difficult to perform surgery on two adjacent disc spaces at the same time. Other potential prognostic factors are the degree of neurological dysfunction, the duration of clinical symptoms before diagnosis and the rate of spinal cord compression [Jeffery and McKee, 2001; McKee and Sharp, 2003; Sharp and Wheeler, 2005]. Patients with severe neurological dysfunction and a long period of clinical signs may have a more guarded prognosis. In some cases, surgery will only halt the progression of the disease. In these cases, irreversible spinal cord damage has probably already occurred. Several authors suggest the use of advanced medical imaging, such as CT myelography and MRI, as a prognostic tool to diagnose spinal cord atrophy [Sharp et al., 1995; Jeffery and McKee 2001]. A possible correlation between the diagnosis of suspected spinal cord atrophy and a poor outcome has not yet been investigated in veterinary medicine. Dorsal decompression Dorsal decompression by dorsal laminectomy is normally used to relieve compression caused by dorsal lesions that do not respond to traction. Such compressive lesions are usually seen in young adult large-breed and giant-breed dogs suffering from a wobbler syndrome, in which the compression is caused by articular and periarticular tissue proliferations, often in combination with ligamentum flavum hypertrophy [McKee and Sharp, 2003; Sharp and Wheeler, 2005]. Although this technique is not often used in the treatment of DAWS, several authors have reported a continuous dorsal laminectomy extending from C4 to C7 for dogs with ventral lesions at multiple intervertebral spaces. In this way, spinal cord compression is alleviated by allowing the spinal cord to ride dorsally [Lyman, 1991; De Risio et al., 2002]. The major disadvantages of dorsal decompression are the invasiveness of the surgical technique, which can be associated with significant short-term morbidity, transient deterioration in neurological status and prolonged length of hospitalisation. Also, the technique does not allow the removal of ventrally located disc material [VanGundy 1988; De Risio et al., 2002]. A possible complication is the recurrence of clinical signs. This is not caused by a domino lesion but rather by the formation of a laminectomy membrane at the surgical site, which is also termed constrictive fibrosis [De Risio et al., 2002]. It is very difficult to interpret the reported results of dorsal decompressive Conclusion Disc associated wobbler syndrome is a relatively common cause of chronic spinal cord compression in adult large breed dogs. This disease can be very challenging, both for the referring veterinarian and even for the specialist. One of the key problems is the variation in definitions and the discrimination between this 138 EJCAP - Vol. 19 - Issue 2 October 2009 and other wobbler syndromes. Making a diagnosis is not always straightforward, and the advantages and disadvantages of the different diagnostic procedures should be considered. DAWS is considered a surgical disease, but the ideal surgical procedure still does not exist. Conversely, there is insufficient knowledge about the conservative treatment and natural progression of this disease. In addition, there is insufficient objective data available on the potential prognostic parameters of this disease. It seems quite clear that further studies are needed to deal with the aforementioned problems. of magnetic resonance imaging and myelography in 18 Doberman Pinscher dogs with cervical spondylomyelopathy. Vet Radiol Ultrasound. 2006b; 47: 523-531. Denny HR, Gibbs C, Gaskell CJ. Cervical spondylopathy in the dog. A review of thirty-five cases. J Small Anim Pract. 1977; 18: 117-132. De Risio L, Munana K, Murray M, Olby N, Sharp N.J.H, Cuddon P. Dorsal laminectomy for caudal cervical spondylomyelopathy: Postoperative recovery and long-term follow-up in 20 dogs. Vet Surg. 2002; 31: 418-427. Dixon BC, Tomlinson JL, Kraus KH. Modified distraction-stabilization technique using an interbody polymethyl methacrylate plug in dogs with caudal cervical spondylomyelopathy. J Am Vet Med Assoc. 1996; 208: 61-68. Dueland R, Furneaux RW, Kaye MM. Spinal fusion and dorsal laminectomy for midcervical spondylolisthesis in a dog. J Am Vet Med Assoc. 1973; 162: 366-369. Gage ED, Hoerlein BF. Surgical repair of cervical subluxation and spondylolisthesis in the dog. J Am Anim Hosp Assoc. 1973; 9: 385-390. Jeffery ND, McKee WM. Surgery for disc-associated wobbler syndrome in the dog – an examination of the controversy. J Small Anim Pract. 2001; 42: 574-581. Lewis DD, Hosgood G. Complications associated with the use of iohexol for myelography of the cervical vertebral column in dogs: 66 cases (1988-1990). J Am Vet Med Assoc. 1992; 200: 1381-1384. Lewis DG. Radiological assessment of the cervical spine of the Dobermann with reference to cervical spondylomyelopathy. J Small Anim Pract. 1991; 32: 75-82. Lipsitz D, Levitski RE, Chauvet AE, Berry WL. Magnetic resonance imaging features of cervical stenotic myelopathy in 21 dogs. Vet Radiol Ultrasound. 2001; 42: 20-27. Lyman R. Wobbler syndrome. Continuous dorsal laminectomy is the procedure of choice. Progr Vet Neurol. 1991; 2: 143-146. Mason TA. Cervical vertebral instability (wobbler syndrome) in the Doberman. Aust Vet J. 1977; 53: 440-445. McKee WM, Lavelle RB, Mason TA. Vertebral stabilisation for cervical spondylopathy using a screw and washer technique. J Small Anim Pract. 1989; 30: 337-342. McKee WM, Lavelle RB, Richardson JL, Mason TA. Vertebral distractionfusion for cervical spondylopathy using a screw and double washer technique. J Small Anim Pract. 1990; 31: 22-27. McKee WM. Intervertebral disc disease in the dog 2: Management options. In Practice. 2000; 22: 458-470. McKee WM, Sharp NJ. Cervical spondylopathy. In: Slatter (Editor). Textbook of Small Animal Surgery. 2nd Edition, W.B. Saunders Company, London; 2003. p. 1180-1193. Parker AJ, Park RD, Cusick PK. Cervical vertebral instability in the dog. J Am Vet Med Assoc. 1973; 163: 71-74. Penderis J, Dennis R. Use of traction during magnetic resonance imaging of caudal cervical spondylomyelopathy (‘wobbler syndrome’) in the dog. Vet Radiol Ultrasound. 2004; 45: 216-219. Read RA, Robbins GM, Carlisle CH. Caudal cervical spondylomyelopathy. Wobbler syndrome in the dog: A review of thirty cases. J Small Anim Pract. 1983; 24: 605-621. Rusbridge C, Wheeler SJ, Torrington AM, Pead MJ, Carmichael. Comparison of two surgical techniques for the management of cervical spondylomyelopathy in Dobermanns. J Small Anim Pract. 1998; 39: 425-431. Seim HB, Withrow SJ. Pathophysiology and diagnosis of caudal cervical spondylomyelopathy with emphasis on the Doberman Pinscher. J Am Anim Hosp Assoc. 1982; 18: 241-251. Seim HB. Diagnosis and treatment of cervical vertebral instabilitymalformation syndromes. In: Bonagura J.D. (Editor): Kirk’s Current Veterinary Therapy. XIII Small Animal Practice. 13th Edition. Update Since the original publication of this paper in Vlaams Diergeneeskundig Tijdschrift two retrospective studies have been published regarding the results of conservative treatment in dogs with cervical spondylomyalopathy / disc associated wobbler syndrome (DAWS): • da Costa R.C., Parent J.M., Holmberg D.L., Sinclair D., Monteith G. (2008). Outcome of medical and surgical treatment in dogs with cervical spondylomyelopathy: 104 cases (1988-2004). Journal of the Veterinary Medical Association 233, 1248-1290). • De Decker S., Bhatti S., Duchateau L., .A. Martlé A.V., Van Soens I., Van Meervenne S.A.E., Saunders J.H., Van Ham L.M.L. (2009). Clinical evaluation of 51 dogs treated conservatively for disc associated wobbler syndrome. Journal of Small Animal Practice 50, 136-142. The results of these papers suggest that conservative treatment can be applied in selected cases. Acknowledgements This literature review is part of a project supported by a Ph.D. grant from the Institute for the Promotion of Innovation by Science and Technology in Flanders (IWT Vlaanderen). References Badami JP, Norman D, Barbaro NM., Can C, Weinstein PR, Sobel DF. Metrizamide CT. myelography in cervical myelopathy and radiculopathy: correlation with conventional myelography and surgical findings. Am J Roentgenol. 1985; 144: 675-680. Bruecker KA, Seim HB, Blass CE. Caudal cervical spondylomyelopathy: Decompression by linear traction and stabilization with Steinmann pins and polymethyl methacrylate. J Am Anim Hosp Assoc. 1989; 25: 677-683. Chambers JN, Oliver JE, Kornegay JN, Malnati GA. Ventral decompression for caudal cervical disk herniation in large-and giant-breed dogs. J Am Vet Med Assoc. 1982; 180: 410-414. Chambers JN, Oliver JE, Bjorling DE. Update on Ventral Decompression for Caudal Cervical Disk Herniation in Doberman Pinschers. J Am Anim Hosp Assoc. 1986; 22: 775-778. da Costa RC, Parent JM, Partlow G, Dobson H, Holmber DL, Lamarre J. Morphologic and morphometric magnetic resonance imaging features of Doberman Pinschers with and without clinical signs of cervical spondylomyelopathy. Am J Vet Res. 2006a; 67: 16011612. da Costa RC, Parent J, Dobson H, Holmberg D, Partlow G. Comparison 139 Diagnosis, treatment and prognosis of disc associated Wobbler syndrome in dogs - S. De Decker, et al intramedullary signal changes on the surgical outcome of patients with cervical spondylotic myelopathy. Spine J. 2003; 3: 33-45. Thomson CE, Kornegay JN, Burn RA. Magnetic resonance imaging – a general overview of principles and examples in veterinary neurodiagnosis. Vet Radiol Ultrasound. 1993; 34: 2-17. Vangundy TE. Disc-associated wobbler syndrome in the Doberman Pinscher. The Vet Clin North Am Small Anim Pract. 1988; 18: 667-696. Voss K, Steffen F, Montavon PM. Use of the compact unilock system for ventral stabilization procedures of the cervical spine. Vet Comp Orthop Traumatol. 2005; 19: 21-28. Wright F, Rest JR, Palmer AC. Ataxia of the Great Dane caused by stenosis of the cervical vertebral canal: Comparison with similar conditions in the Basset hound, Doberman Pinscher, Ridgeback and the thoroughbred horse. Vet Rec. 1973; 92: 1-6. Yu YL, Du Boulay GH, Stevens JM, Kendall BE. Computed tomography in cervical spondylotic myelopathy and radiculopathy: visualization of structures, myelographic comparison, cord measurements, and clinical utility. Neuroradiology. 1986; 28: 221-236. Saunders Company, Philadelphia. 2000. p. 992-1000. Sharp NJH, Wheeler SJ, Cofone M. Radiological evaluation of ‘wobbler’ syndrome – caudal cervical spondylomyelopathy. J Small Anim Pract. 1992; 33: 491-499. Sharp NJH, Cofone M, Robertson ID, Decarlo A, Smith GK, Thrall DE. Computed tomography in the evaluation of caudal cervical spondylomyelopathy of the Doberman Pinscher. Vet Radiol Ultrasound. 1995; 36: 100-108. Sharp NJH, Wheeler SJ. Cervical spondylomyelopathy. In: Small Animal Spinal Disorders. Diagnosis and Surgery. 2nd Edition, Elsevier Mosby. 2005. p. 211-246. Shores A. Canine cervical vertebral malformation/malarticulation syndrome. Compend Contin Educ Pract Vet. 1984; 6, 326-333. Speciale J, Fingeroth JM. Use of physiatry as the sole treatment for three paretic or paralyzed dogs with chronic compressive conditions of the caudal portion of the cervical spinal cord. J Am Vet Med Assoc. 2000; 217: 43-47. Suri A, Chabbra RPS, Mehta VS, Gaikwad S, Pandey RM. Effect of 140 ORTHOPAEDICS REPRINT PAPER (FIN) Treatment of degenerative joint disease of the hip with cementless and cemented total hip arthroplasty in a dog – a case report A. Eklöf(1), E. Eskelinen(1) SUMMARY Chronic degenerative joint disease of the canine hip is commonly treated with total hip arthroplasty. The outcome of surgery is generally excellent and good pain management and mobility are achieved. The modular total hip system consists of three parts. The cup is implanted in the acetabular area and the combination of the head and the stem into the proximal femoral medullary canal. The implants are attached either with polymethylmethacrylate bone cement or without cement in the so-called cementless system. Both systems have advantages and disadvantages. This paper describes treatment of canine chronic degenerative joint disease of the hips with cementless and cemented total hip arthroplasty. initial mechanical attachment (press fit), a biological attachment is formed when the connective and bone tissues grow directly into the porous surface of the implant. [1,4] This paper originally appeared in: Suomen Eläinlääkärilehti * 2007, 113 (9) 7-13 Case Report Introduction A 7-year-old, mixed-breed male dog weighing 45 kg was brought to the veterinary clinic in September 2002 with a 2 month history of lameness. In the orthopaedic examination the mobility of the hip joints was impaired. The extension of both hip joints, particularly the left one, caused a painful response. The proprioception of the hind legs was normal. Bilateral osteoarthrosis of the hip joints was diagnosed by radiography. Nonsteroidal anti-inflammatory medication, meloxicam (Metacam® 1.5 mg/ml oral suspension, Boehringer Ingelheim Vetmedica GmBH) was initiated at 0.1 mg/kg once daily for two weeks after which the owner was instructed to give the medication as needed on week-long regimens or even continuously. Additionally, sodium pentosan-polysulphate injectable medication (Cartrophen® 100 mg/ml injection, Arthropharm Ltd) was administered to the dog at 3.3 mg/kg once a week, Total hip arthroplasty has been performed on dogs since the mid-1970s. Indications for surgery include all non-neoplastic and non-infectious diseases of the hip joints causing significant signs of lameness and pain. The most common indication is painful and advanced degenerative joint disease caused by hip dysplasia. Traditionally the prosthetic parts (the implants) have been attached with polymethylmethacrylate (PMMA) bone cement. This method is referred to as cemented total hip arthroplasty. In human as well as canine hip surgeries, noncemented systems have also been used, in which the implants are directly placed into accurately pre-drilled depressions and shaped grooves in the acetabulum and femur. The implants in the non-cemented systems are coated with titanium grains, for example, to make the bone contact surface porous. After the (1) Veterinary Clinic Apex, Kirkonkyläntie 15, FIN-00700 Helsinki E-mail: [email protected] *Presented by FAVP (Finland) 141 Treatment of degenerative joint disease of the hip with cementless and cemented total hip arthroplasty – A. Eklöf, E. Eskelinen surgery. The values were within normal ranges. The day before surgery the rear of the patient from the costal arch caudally was washed with a neutral shampoo and two fentanyl patches (Durogesic 50 µg/h, Janssen-Cilag) were applied. On the day of surgery the dog was first premedicated with levometadone (L-Polamivet® injectable, Intervet International B.V.), 0.3 mg/kg intramuscularly. Half an hour later, a cannula was inserted into a vein in order to administer diazepam 0.5 mg/kg (Stesolid Novum® 5 mg/ml injectable, Alpharma). Epidural administration of 15 mg of bupivacaine (Bicain® 5 mg/ml injection, Orion Pharma) and 4 mg of morphine (Morphin® 2 mg/ml injectable, Leiras) was performed. Anaesthesia was induced by administering propofol (Rapinovet® 10 mg/ml injectable, Schering-Plough Animal Health), 40 mg of which was administered intravenously. The patient was given cefuroxime (Zinacef® 1.5 g lyophilized injectable powder, GlaxoSmithKline) at 22 mg/kg intravenously during the induction phase of anaesthesia and additionally three times afterwards at 2-hourly intervals. The dog was also given gentamicin (Genta-kel 05® 50 mg/ml, KELA Laboratories, Belgium) during the induction phase and additionally twice afterwards with an interval of 12 hours. For maintenance of anaesthesia, 1.5% isoflurane-oxygen mixture was used. A dose of 80 mg of carprofen (Rimadyl® 50 mg/ml injectable, Pfizer Animal Health) was given intravenously during the latter part of the operation. for a total of 4 weeks. The owner was also advised that the dog could be given chondroprotective agents containing chondroitin sulphate and glycosamines orally. Additionally the owners were advised to consider total hip arthroplasty should conservative treatment prove insufficient. The dog was treated for approximately 3 years with physiotherapy, acupuncture, sodium pentosan-polysulphate injection regimens, nonsteroidal anti-inflammatory medication and a chondroprotective preparation (Cartivet, Biofarm). In March 2005 a partial tear in the anterior cruciate ligament of the left knee was diagnosed and treated surgically by extracapsular stabilisation of the stifle. The result was not satisfactory. Degenerative joint changes developed in the stifle. At the beginning of June 2005, when the dog was almost 10 years old, it was brought in for evaluation because the left leg was again very painful. Upon examination, extension of the left hip caused a severe pain response. The left stifle was not painful. The spine was not painful and proprioception of the limbs was normal. Non-cemented total hip arthroplasty was elected to treat the degenerative joint disease of the hip as it had not responded adequately to conservative treatment (figure 1). Preparations for surgery and anaesthesia A full blood panel (Check-up, Vet Med Labor), including packed cell volume and white blood cell count, was examined prior to The total prosthetic hip system For this patient, a cementless prosthetic hip system BXF (produced by BioMedtrix-company, New Jersey, USA), composed of three parts, a cup, a stem and a head, was used. The cup is made of ultrahigh molecular weight polyethylene. The metal backing of the cup is made of titanium alloy, which is coated with titanium grains of 250-300 µm diameter. The stem is made of cobalt chrome and 45% of its proximal portion is coated with titanium grains of 250-300 µm diameter (2). The prosthetic head is made of cobalt chrome. The diameter of the head is 17 mm. The neck of the stem portion of the prosthesis fits the hole of the head. Holes come in four different depths (0, +3, +6 and +9 mm) allowing adjustments to be made to the length of the prosthetic neck (hence, modularity). Figure 1 Severe osteoarthrosis of the hip joints, a ventrodorsal radiograph (DEX= right side) Cementless prosthetic hip surgery Cementless prosthetic hip surgery was performed by William D. Liska (Dipl. ACVS) together with the authors of this article. The left hip joint was approached craniolaterally in the conventional fashion.[5] The ligament of the Gluteus profundus muscle was partially cut, close to its point of insertion on the greater trochanter, and the muscle was split 3 cm along its length. An incision was made in the joint capsule in the direction of the femoral neck and was continued past the origin points of the vastus lateralis and intermedius muscles to reveal the femoral neck and metaphyseal region.[6,7] The ligamentum teres femoris was cut, allowing the femur to be rotated 90 degrees externally so that the femoral head could be dislocated from the acetabulum. Severe degenerative changes were noted in the hip joint. With this exposure maintained, ostectomy of the femoral head and neck was performed using a resection template to guide 142 EJCAP - Vol. 19 - Issue 2 October 2009 profundus and vastus muscles were closed with polydioxanone sutures (1 PDS®, Johnson & Johnson). Fascia lata, subcutaneous tissue and skin were closed in a routine manner. Postoperative care and result Acceptable implant positioning was confirmed in post-operative radiographs. Cephalexine (Kefavet® 500 mg, Orion Pharma) was given orally at 22 mg/kg twice a day for 1 week. Carprofen (Rimadyl® vet 50 mg, Pfizer Animal Health) was given as the anti-inflammatory pain medication on the day of surgery and for 2 weeks after surgery at 3.3 mg/kg once a day. Fentanyl patches were removed after 4 days. It was recommended that the dog should be handled with extra care during physical activity for a month. It was also recommended to avoid slippery surfaces and stairs. Mobility exercise for the operated hip was started 2 days after surgery. Minimal physical exercise was encouraged for a period of 2 months after surgery. When the sutures were removed, a mild loss of proprioception was noted in the operated limb. The dog dragged the toes of the left hind limb. The dog against the ground to some extent while walking. The problem was probably caused by mild neurapraxy of the sciatic nerve. On examination 2 months after the surgery the proprioception of left hind limb had recovered to normal and the left hip joint was painless on palpation. No abnormalities were observed on radiography. About 8 months later the dog was able to carry more weight on the operated left hind limb than on the right. Figure 2 Cementless hip prosthesis in a plastic bone model the oscillating saw. After this, reaming of the acetabular region was conducted by removing all remnants of joint cartilage, ligaments and connective tissue.[6,8] Reaming was carried out using a prosthetic cup-unit-shaped drill (reamer), which was kept at an angle of 15-20 degrees to the saggital plane and 45 degrees to the horizontal plane. Hence, the cup was seated 1520 degrees in retroversion with 45 degrees of lateral opening. [6] Osteophytes around the acetabular region were removed with bone rongeurs.[6,9] The biggest possible cup component relative to the size of the pelvis of the dog was implanted.[8,9] A BXF-cup with an outer diameter of 28 mm was implanted with the BXF acetabular cup positioner. A good mechanical attachment was achieved by lightly tapping with a hammer.[6] Cemented prosthetic hip surgery On clinical examination, 10 months after surgery on the left hip joint, the operated hind limb functioned normally but the degenerative joint disease of the right hip joint caused crepitus, severe pain and limitation in hip movement. No findings were noted on palpation of the spine. The proprioception of the hind limbs was normal. Due to the fact that the degenerative joint disease in the right hip caused severe signs and had not responded well to conservative treatment, it was decided that prosthetic surgery of the hip should also be performed on the right hip joint, 13 months after that of the left. The total hip arthroplasty operation was performed by Esa Eskelinen. A modular, cemented prosthetic system produced by Veterinary Instrumentation Company (Sheffield, England) was used. Preparation of the patient, premedication as well as postoperative treatment were the same as for the cementless procedure. Cefazoline (Kefzol® 1 g lyophilized injectable powder, Astro Pharma, Austria) at 20 mg/kg intravenously three times every 2 hours and gentamicin at 2.0 mg/kg intravenously three times every 12 hours were administered as the perioperative antibiotic medication. The cemented prosthetic hip surgery was performed in routine fashion as described by Olmstead.[8] The prosthetic cup, made of ultrahigh molecular weight polyethylene, was fixed in place using gentamicin-containing low-viscosity bone cement (CMW 3 with gentamicin, DePuy, Johnson&Johnson, New Jersey, USA). The prosthetic cup was of medium size. The large-sized prosthetic stem made of cobalt chrome was fixed in place with low-viscosity bone cement according to the second-generation cementing technique.[10] The prosthetic head of size ”15 mm long neck ball” was attached to the prosthetic stem and the new hip joint was reduced. The joint capsule, myotomy incisions The medullary cavity of the femur was opened using a drill, starting from the surface of the osteotomy. After this, the medullary cavity of the femur was expanded into shape so as to fit the prosthetic stem component, first with fluted reamers attached to the drill and then with femoral broaches which had the same shape as the prosthetic stem.[8] Broaches were tapped into and out of the medullary cavity with a hammer. As the operation proceeded larger broaches were utilized. The aim was to implant a prosthetic stem into the medullary cavity of the femur which would bring about a good mechanical attachment without risk of cracking the femoral diaphysis. When a cavity of adequate size was obtained, the right prosthetic stem (#10 BXF stem) was attached in a neutral position (no anteversion nor retroversion) by tapping with a hammer. Anteversion here is rotation of the head and stem components in a cranial direction relative to the femoral shaft; retroversion is rotation of the femoral component caudally.[9] Before the prosthetic head was selected a plastic tester head was used to establish the desired depth of the hole (in this case +0 mm) to provide the most suitable length of the prosthetic neck. The head was attached to the prosthetic stem and the new hip joint was reduced.[8] The joint capsule as well as the myotomy incisions on the gluteus 143 Treatment of degenerative joint disease of the hip with cementless and cemented total hip arthroplasty – A. Eklöf, E. Eskelinen DX Figures 3 and 4 Ventrodorsal and lateral radiographs taken after the cemented total hip replacement operation. Cementless hip prosthesis on the left side and cemented prosthesis on the right side. so good that 80 % of patients require only unilateral surgery. [11,12] Degenerative joint disease caused by hip dysplasia is the most common indication for prosthetic hip surgery. Other indications include severe fractures and unsuccessful surgical interventions of the hip joint, malunion or non union of the acetabulum or proximal femur, chronic luxation of the hip joint and avascular necrosis of the femoral head.[11,12] Good results have been reported in regard to both cemented and cementless total hip arthroplasty.[12] Previous surgical removal of the femoral head may make total hip arthroplasty difficult to perform, thus this can be regarded as a contraindication to prosthetic hip surgery.[7,12,13] Neoplastic diseases of the hip joint used to be regarded as absolute contraindications to total hip replacement,[9] however, prosthetic hip surgery has also been used for the treatment of neoplastic diseases of the hip joint region.[14,15] Severe radiographic changes alone are not a sufficient indication for canine total hip arthroplasty.[2,7,11,12] The patient must also have severe clinical signs. Other orthopaedic and neurologic diseases must be ruled out before considering prosthetic hip surgery. Simultaneous neurological disease (for example myelopathy, intervertebral hernia, spinal cord tumours and cauda equina syndrome) is regarded as a contraindication to surgery.[11,12] If the dog is diagnosed with another orthopaedic or neurological disorder, then that disorder should be treated as well as fascia lata, subcutaneous tissue and skin were closed as in the cementless operation. Postoperative radiographs indicated that the positions of the implants were good and implants were covered with an even layer of cement (figures 3 and 4). On clinical examination, 12 days after surgery, the patient was able to move normally but was limping slightly on the right hind limb. A mild loss of proprioception was noted. Two months after the cemented total hip arthroplasty, the patient was able to move without limping, the proprioception of the hind limbs was normal and the patient finally had the possibility and permission to move normally as in the period before degenerative joint disease developed in the hips. Physiotherapy, including underwater treadmill was initiated. In clinical examinations 9 months after the cemented total hip arthroplasty, the patient was able to move without limping and the joints were painless on palpation. Discussion Total hip arthroplasty is an efficient method for restoring the normal, painless function and mobility of the hip joint destroyed by degenerative joint disease. In 95% of total prosthetic hip surgery cases, a good or excellent prognosis is expected[11,12]. In most surgery cases the pain control and mobility achieved is 144 EJCAP - Vol. 19 - Issue 2 October 2009 the exothermic reaction of the bone cement.[7,12] It can also be caused by the lengthening of the limb from prosthetic hip surgery, leading to stretching of the sciatic nerve.[27] In the described case, this is the most probable cause of the neurapraxy observed in the left hind limb in conjunction with the cementless prosthetic hip surgery. A prosthetic head giving the shortest possible prosthetic neck (+0 mm) was selected for this patient. Still, this length of neck caused the joint to become rather tight and the reduction to be quite difficult. Recovery from neurapraxy takes an average period of 10 weeks.[12] before considering prosthetic hip surgery. A typical example is rupture of the anterior cruciate ligament of the stifle. In addition, infections such as dermatitis, urinary tract or orodental infections must be treated before prosthetic hip surgery in order to avoid potential cutaneous or blood-borne spread of infection to the prosthesis.[2,7,9,12] The patient must be at least 9-10 months old at the time of surgery to ensure that the growth in bone length has ended. There is no upper age limit for the operation.[9,11,12] Surgical complications Luxation is the most commonly encountered surgical complication.[3,12,16] It can be caused by improper positioning of the cup or stem, excessive physical strain on the joint after surgery, or trauma.[12,16] The position of the cup may be less critical as the cause of luxation than was earlier believed, whereas the abnormal movement of dysplastic hip joints are likely to be a more important factor.[17] If protruding osteophytes or severely thickened joint capsule are left around the acetabulum, they may act as a fulcrum when the dog walks and the prosthetic head may be levered off the prosthetic cup.[16] Also insufficient soft tissue tension around the artificial joint has been noted to predispose to luxation.[16,18] Significant muscle atrophy around the right hip joint was diagnosed in this patient, therefore, in order to decrease the risk of craniodorsal luxation, the prosthetic cup was cemented in a position where the lateral opening angle was left slightly smaller than usual. In aseptic loosening various mechanical and biological factors lead to loosening of the cement or the prosthesis from the bone as a result of osteolysis due to osteoclastic activity.[19,20] Initially, the reaction was believed always to be associated with the use of cement. Later, loosening of cementless prostheses were also reported, leading to a new term called particulate disease. [19] Studies have indicated that this is a foreign-body reaction, which can be initiated by bone cement, polyethylene or metallic particles.[21] It has been suggested that aseptic loosening is the most common surgical complication in the cemented system, although the exact prevalence is difficult to estimate as all loosenings do not cause clinical signs or necessitate corrective interventions.[22] Prosthetic cup displacement from the cement or bone is considered a separate clinical entity in contrast to aseptic loosening.[23] This complication is suspected to be of a purely mechanical nature and due to an unsuccessful implantation of the cup.[4,23] Infection is the most serious complication of prosthetic hip surgery. In dogs it is not encouraged to implant a new prosthesis after removal of an infected one. The situation after removal of a prosthesis is comparable to that after surgical removal of the femoral head.[24, 25] Prolonged surgery, major tissue trauma and earlier surgical operations performed in the hip region are factors predisposing to infection.[9,11,12] Femoral fractures are another serious complication. Approximately half of these occur intraoperatively, the rest have a traumatic aetiology.[7] In addition to technical factors, different bone diseases such as osteopathies and osteoporosis as well as aseptic loosening of the implants predispose to fractures.[2,26] Neurapraxy may be caused by stretching of the tissues or elevation of the femur during surgery or by heat released in Most complications can be avoided by a meticulous surgical technique, but the instrumentation is also an important factor. [18] Experience of the surgeon in performing the procedure has been determined to decrease the risk of complications significantly.[18,22] Cemented and cementless prosthetic systems for the hip joint The bone cement used in the cemented system, polymethylmethacrylate, is a plastic matter made of two components. A powder and a solution are mixed and the emerging mixture hardens in approximately 15 minutes through an exothermic reaction. The fumes released during the mixing process are toxic, necessitating their removal from the operating room through adequate ventilation or scavenging. The reaction produces so much heat that the surrounding tissues, including the sciatic nerve, have to be protected during the hardening of the cement. [9] The bone cement may predispose to infection, because bacteria can easily attach to the surface of the cement and form a polysaccharide glycocalyx, which protects the bacteria from the effects of antibodies and antibiotics.[24] Generally, antibiotics are added to the cement in order to decrease the risk of infection. Bone cements and cementing techniques have been developed to achieve a more durable and even cement layer. In the secondgeneration cementing technique used in this case with surgery, a polyethylene plug is placed in the medullary cavity of the femur in order to prevent the cement from spreading too distally and cement is injected with pressure into the medullary cavity starting distally near the polyethylene plug.[28] Cementless hip prosthesis systems were developed for human and canine surgery in order to avoid complications caused by acrylic cements.[3,29] The aim of developing the cementless systems has also been to extend the life spans of prostheses as bone grows into its porous surfaces.[1,29] The major biological attachment occurs during the course of the first year and the connection appears to get stronger with time.[4] Another advantage of the cementless system is the shorter surgical time since there is no need to wait for the cement to harden. In the cementless system described here, it is quite common for the femoral stem component to move distally up to several millimeters in the immediate post-operative period.[3,30,31] In canine patients this mobility appears to be linked to the process of the settling of the implants into the tissues, and it usually causes no adverse signs.[3] The most important factor in preventing postoperative mobility of the prosthesis is to achieve a firm mechanical bond between the bone and the implant. Postoperative mobility of the implant is more likely to occur if the implant is undersized.[30,31] 145 Treatment of degenerative joint disease of the hip with cementless and cemented total hip arthroplasty – A. Eklöf, E. Eskelinen The biggest obstacle to general use of the cementless prosthetic hip system in canine patients is the expense of the implants and the instrumentation.[13] Also, cementless implants are not available for all sizes of dogs and the cementless system is not suitable for patients with osteoporosis. Cementless prosthetic hip surgery is technically rather challenging because preparation of the acetabular region for prosthesis demands high precision, and possible errors in reaming this anatomical region cannot be corrected by adding cement.[2,6] It is also very difficult to remove a cementless femoral stem after bone ingrowth should this removal prove necessary for one reason or another.[29] [14] Liptak JM, Pluhar GE, Dernell WS, Withrow SJ. Limb-sparing surgery in a dog with osteosarcoma of the proximal femur. Vet Surg. 2005; 34: 71-7. [15] Sherrer W, Holsworth I, Goossens M, Schulz K. Coxofemoral arthroscopy and total hip arthroplasty for management of intermediate grade fibrosarcoma in a dog. Vet Surg. 2005; 34: 43-6. [16] Dyce J, Wisner ER, Wang Q, Olmstead ML. Evaluation of risk factors for luxation after total hip replacement in dogs. Vet Surg. 2000; 29: 524-32. [17] Cross AR, Newell SM, Chambers JN, Shultz KB, Kubilis PS. Acetabular component orientation as an indicator of implant luxation in cemented total hip arthroplasty. Vet Surg. 2000; 29: 517-23. [18] Warnock JJ, Dyce J, Pooya H, Schulz KS. Retrospective analysis of canine miniature total hip prostheses. Vet Surg. 2003; 32: 28591. [19] Dowd JE, Schwendeman LJ, Macauley W, Doyle JS, Shanbhag AS, Wilson S ym. Aseptic loosening in uncemented total hip arthroplasty in a canine model. Clin Orthop Relat Res. 1995; 319: 106-21. [20] Edwards MR, Egger EL, Schwarz PD. Aseptic loosening of the femoral implant after cemented total hip arthroplasty in dogs: 11 cases in 10 dogs (1991-1995). J Am Vet Med Assoc. 1997; 211: 580-6. [21] El-Warrak AO, Olmstead ML, Apelt D, Deiss F, Noetzli H, Zlinsky K ym. An animal model for interface tissue formation in cemented hip replacements. Vet Surg. 2004; 33: 495-504. [22] Bergh MS, Gilley RS, Shofer FS, Kapatkin AS. Complications and radiographic findings following cemented total hip arthroplasty. A retrospective evaluation of 97 dogs. Vet Comp Orthop Traumatol. 2006; 19: 172-9. [23] Hunter S, Dyce J, Butkus L, Olmstead ML. Acetabular cup displacement after polyethylene-cement interface failure: a complication of total hip replacement in seven dogs. Vet Comp Orthop Traumatol. 2003; 16: 99-104. [24] Dyce J, Olmstead ML. Removal of infected canine cemented total hip prostheses using a femoral window technique. Vet Surg. 2002; 31: 552-60. [25] Lee KCL, Kapatkin AS. Positive intraoperative cultures and canine total hip replacement: risk factors, periprosthetic infection, and surgical success. J Am Anim Hosp Assoc. 2002; 38: 271-8. [26] Liska WD. Femur fractures associated with total hip replacement. Vet Surg. 2004; 33: 164-72. [27] Pozzi A, Kowaleski P, Dyce J, Johnson KA. Treatment of traumatic coxo-femoral luxation by cemented hip arthroplasty. Vet Comp Orthop Traumatol. 2004; 17: 198-203. [28] Horne JG, Bruce W, Devane PA, Teoh HH. The effect of different cement insertion techniques on the bone-cement interface. J. Arthroplasty 2002; 17: 579-83. [29] Engh CA, Glassman AH, Suthers KE. The case for porous coated hip implants: the femoral side. Clin Orthop Relat Res. 1990; 261: 63-81. [30] DeYoung DJ, Schiller RA, DeYoung BA. Radiographic assessment of a canine uncemented porous-coated anatomic total hip prosthesis. Vet Surg. 1993; 22: 473-81. [31] Pernell RT, Gross RS, Milton JL, Montgomery RD, Wentzel JGW ym. Femoral strain distribution and subsidence after physiological loading of a cementless canine femoral prosthesis: The effects of implant orientation, canal fill and implant fit. Vet Surg. 1994; 23: 503-18. Epilogue After the THR operations the canine patient of this case report was painless and the ability to function was normal as far as the coxofemoral joints were concerned. Euthanasia of the patient was performed at the age of 12 years and 7 months, 2.5 years after the cemented THR operation, for reasons unrelated to the hip joints. References [1] Bouvy BM, Manley PA. Vascular and morphologic changes in canine femora after uncemented hip arthroplasty. Vet Surg. 1993; 22: 18-26. [2] Conzemius MG, Vandervoort J. Total joint replacement in the dog. Vet Clin Small Anim. 2005; 35: 1213-31. [3] Marcellin-Little DJ, DeYoung BA, Doyens DH, DeYoung DJ. Canine uncemented porous-coated anatomic total hip arthroplasty: Results of a long-term prospective evaluation of 50 consecutive cases. Vet Surg. 1999; 28: 10-20. [4] Schiller TD, DeYoung DJ, Schiller R, Aberman HA, Hungerford DS. Quantitative ingrowth analysis of a porous-coated acetabular component in canine model. Vet Surg. 1993; 22: 276-80. [5] Piermattei DL. An atlas of the surgical approaches to the bones and joints of the dog and cat. 3. painos. WB Saunders. 1993; 230-35. [6] DeYoung DJ, DeYoung BA, Aberman, HA, Kenna RV, Hungerford DS. Implantation of an uncemented total hip prosthesis. Technique and initial results of 100 arthroplasties. Vet Surg. 1992; 21: 16877. [7] Olmstead ML. Total hip replacement. Vet Clin Small Anim. 1987; 17: 943-54. [8] Olmstead ML. The canine cemented modular total hip prosthesis. J Am Anim Hosp Assoc. 1995; 31: 109-24. [9] Massat BJ. Canine cemented total hip arthroplasty. Waltham Focus. 1995; 5: 21-31. [10] Ota J, Cook JL, Lewis DD, Tomlinson JL, Fox DB, Cook CR ym: Short-term aseptic loosening of the femoral component in canine total hip replacement: effects of cementing technique on cement mantle grade. Vet Surgery. 2005; 34: 345-52. [11] Olmstead ML. Canine cemented total hip replacements: state of the art. J Small Anim Pract. 1995; 36: 395-9. [12] Tomlinson J, McLaughlin Jr R. Total hip replacement: the best treatment for dysplastic dogs with osteoarthrosis. Vet Med. 1996; 2: 118-24. [13] Denny HR, Butterworth SJ. A guide to canine and feline orthopaedic surgery. 4. painos, Blackwell Science. 2000; 484-90. 146 GASTEROINTESTINAL SYSTEM ORIGINAL WORK(GR) Acute pancreatitis in dogs: a review article I. Kalli(1) K. Adamama-Moraitou(1), T. S. Rallis(1) SUMMARY Canine acute pancreatitis is a relatively common disease, but it is often misdiagnosed. The most common causes of acute pancreatitis in dogs include malnutrition, drug administration, infection, trauma, reflux of duodenum contents into the pancreatic duct and ischaemia. Idiopathic causes have also been encountered. The clinical signs of the disease are not specific and are often associated with a number of life-threatening, severe systemic complications. Despite the continuing new knowledge of pancreatic pathophysiology, the aetiopathogenesis of canine pancreatitis is still unclear and subsequently treatment is supportive. Key words: Exocrine pancreas; Canine; Aetiology; Pathogenesis Outline of anatomy and physiology of the pancreas Definition and Incidence According to the Atlanta Symposium, acute pancreatitis (AP) is defined as an acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems [1]. The above definition refers to humans, but it also characterizes the disease in dogs. Based on the patient’s condition, it is classified as mild, moderate or severe, and non - fatal or fatal [2, 3]. Histopathological criteria for AP include pancreatic oedema and necrosis, infiltration of mononuclear and polymorphonuclear cells, peripancreatic fat necrosis and thrombosis, but without permanent disruption of the pancreatic architecture. In humans, AP is usually complicated by pancreatic pseudocyst formation, abscesses and acute intraabdominal fluid collection [2, 3], which are rather rare in dogs. Several terms related to AP have been replaced or abandoned in human medicine. Infected pseudocyst is replaced by pancreatic abscess, and persistent acute pancreatitis is replaced by interstitial or necrotizing pancreatitis. Haemorrhagic pancreatitis was abandoned, because most cases of pancreatic necrosis occur without gross intraglandular haemorrhage [4]. Although AP is a common disease in dogs, it is often misdiagnosed, especially in its mild forms, because of the lack of pathognomonic clinical signs, and diagnostic tests with high sensitivity and specificity [3]. The pancreas lies in the cranioventral abdomen and consists of right and left lobes with a small central body. The right lobe lies in contact or in close proximity to the descending duodenum and contains most of the pancreatic polypeptide-producing cells, while the left lobe lies between the greater curvature of the stomach and the transverse colon and contains glucagonsecreting cells. Each pancreatic lobule is composed mainly of acinar cells that synthesize the digestive enzymes in the form of proenzymes and store them in zymogen granules. The pancreas of the dog usually has two ducts by which secretions are transported from the organ to the descending duodenum [5]. The pancreas also contains endocrine tissue, the islets of Langerhans, accounting for one to two percent of the gland [3]. The main function of the exocrine pancreas is the secretion by the acinar cells of a fluid rich in digestive enzymes involved in the initial degradation of proteins, lipids, and polysaccharides [6]. Exocrine pancreatic proteases include trypsin, chymotrypsin, elastase, carboxypeptidase A and B, and Phosphpolipase A. The principal inorganic components of exocrine pancreatic secretions include water, sodium, potassium, chloride, bicarbonate. The exocrine pancreatic secretions facilitate delivery (1) Companion Animal Clinic (Medicine), Faculty of Veterinary Medicine, Aristotle University of Thessaloniki, 11 S. Voutyra Str., GR-546 27 Thessaloniki, Greece. E-mail: [email protected] 147 Acute pancreatitis in dogs: a review article - I. Kalli, K. Adamama-Moraitou, T. S. Rallis zymogens, which contributes to pancreatic inflammation, acinar necrosis and peripancreatic fat necrosis [9-11]. Normally, free plasma protease inhibitors inactivate the proteolytic enzymes released into the circulation. Consequently, a1-proteinase inhibitor, which serves as a transient inhibitor, passes the proteases on to a2-macroglobulins. Finally, the enzyme-macroglobulin complex is cleared from the plasma by the monocyte-macrophage system [9-11]. During an episode of AP, excessive trypsin causes depletion of the trypsin inhibitors in the pancreas and plasma [9, 11-13]. Furthermore the barrier, which normally inhibits the translocation of bacteria from the intestine into the systemic circulation, breaks down. Under condition of stress, such as acute inflammation, the pancreas becomes vulnerable to bacterial infections. In canine experimental pancreatitis luminal Escherichia coli translocates to mesenteric lymph nodes and remote organs [14]. These pathophysiologic events may produce systemic inflammatory response syndrome (SIRS), acute respiratory distress (ARDS) and multiorgan failure. In experimental pancreatitis in rats, activation of trypsin occurs within 10 minutes, and large amounts of trypsin and increased concentrations of trypsinogen activation peptide (TAP) accumulate within the pancreas [15]. TAP is produced when trypsinogen is activated to trypsin and serum or urine concentration of TAP correlates with the severity of pancreatic inflammatory response [16]. While enzyme synthesis continues, early blockage of pancreatic secretion may produce AP [4]. AP produces microcirculatory injury, leukocyte chemoattraction and release of cytokines, oxidative stress and bacterial translocation [4]. The release of pancreatic enzymes damages the vascular endothelium and the acinar cells, producing microcirculatory changes, vasoconstriction, capillary stasis, progressive ischaemia and oedema of the pancreas. Pancreatic damage may lead to the release of free radicals and inflammatory cytokines into the circulation, which could cause further multiorgan failure. In cases of AP, active granulocytes and macrophages release proinflammatory cytokines (TNF-a, IL-1, IL-6, IL-8), arachidonic acid metabolites (prostaglandins, PAF and leukotrienes) and reactive oxygen metabolites. These substances also interact with the pancreatic microcirculation and increase vascular permeability, which in turn induces thrombosis and haemorrhage (Figure 2) [4]. of digestive enzymes to the lumen of the duodenum and neutralize acidic content coming from the stomach [7]. Colipase, contained in the pancreatic fluid, facilitates the breakdown of fats by the pancreatic lipase [8]. The pancreatic juice also contains factors that enable the absorption of cobalamin (vitamin B12) and zinc, as well as antibacterial agents, and “trophic agents” for the small intestinal mucosa [9]. Several mechanisms protect the normal pancreas against autodigestion. The proteolytic enzymes are synthesized and secreted by the pancreas in an inactive form (zymogens) into the duodenum. The enterocytes lining the duodenal mucosa are responsible for the synthesis of an enzyme called enteropeptidase that converts inactive trypsinogen to active trypsin. Trypsin, in turn, activates the remaining digestive enzymes [9-11]. Another protective mechanism against early trypsin activity is the synthesis and secretion of pancreatic secretory trypsin inhibitor (PSTI) by the acinar cells [9-11, 12]. Moreover, blood plasma contains several antiproteases, such as a1-proteinase inhibitor, a2-macroglobulin and antichymotrypsin, which limit intrapancreatic proenzyme activation [10]. Additional protective mechanisms include the sequestration of pancreatic enzymes within the intracellular compartments of the acinar cells during synthesis and transport, and the separation of digestive enzymes from lysosomal hydrolases as they pass through the Golgi apparatus (Figure 1) [3]. Pathogenesis It is believed that AP develops because of premature activation of the digestive zymogens within the acinar cell (Figure 1). Premature activation of trypsin results in further activation of all Figure 1: Initiating events of acute pancreatitis. Aetiology d L RER G Z : : : : : : : Z1 – L1 : The inciting cause of canine AP usually remains unclear. However, the following trigger factors should be considered: Diet: low-protein, high-fat diets seem to induce pancreatitis probably by stimulating oversecretion [9-11]. It is still indefinite whether hyperlipidaemia causes AP or it is the result of AP [911, 17, 18]. Drugs: the drugs most commonly used in veterinary practice and suspected of causing canine AP are azathioprine, oestrogens, tetracycline, chlorthiazides, thiazide diuretics, furosemide, L-asparaginase, potassium bromide and organophosphates [9-12]. The role of steroids in the aetiopathogenesis of AP is controversial. It has been found that steroid administration is related with high serum lipase activity. However, there is still no evidence of steroids inducing pancreatitis [19, 20]. Duodenal fluid reflux: conditions, such as vomiting or Ductal Lysosomes Rough Endoplasmic Reticulum Golgi apparatus Zymogen Hydrolases Zymogen Granules Abnormal fusion of lysosomes and zymogen granules → activation of trypsinogen by lysosomal proteases → premature activation of digestive enzymes 148 EJCAP - Vol. 19 - Issue 2 October 2009 Trypsinogen (inactive) trypsin (active) enterokinase Kinins Proelastase Phospholipase A2 Lipase Vasoactive polypeptides Elastase Phospholipase A2, lecithinase Fat necrosis Hypotension, pancreatic oedema Capillary wall elastin disruption Membrane cell phospholipase hydrolysis Hypocalcaemia Shock Capillary injury Necrosis of parenchymal organs Haemorrhages, thrombosis Pulmonary oedema Heart Free radicals Inflammatory cytokines (TNF, IL-1, IL-6, IL-8) Prostaglandins, PAF, leukotrienes MDF Factor XII ARD SIRS DIC Figure 2. Pathophysiology of systemic complications of AP (neutralization of protective mechanisms). MDF: DIC: ARD: SIRS: TNF: IL: PAF: altered intestinal motility, disorganise the antireflux protective mechanism of the high-pressure system of the sphincter of Oddi and the pancreatic duct. Duodenal contents (active pancreatic enzymes, bacteria and bile) reflux into the pancreatic ducts contributes to the development of AP [9, 11, 12, 18]. Pancreatic trauma/ischaemia: intraabdominal surgical procedures and manipulations, including biopsy of the pancreas, or accidental trauma could be the inciting cause of AP [9-11, 18]. According to our experience, in a total of 47 cases, surgical pancreatic biopsies did not produce AP (unpublished data). Moreover, ischaemia of the pancreas due to shock, severe anaemia, and hypotension may also lead to the onset of AP [9, 11, 18]. Hypercalcaemia: it is a rather uncommon finding in dogs with AP. However, it is suspected to have a fundamental role in the pathogenesis of AP on a cellular basis. Exposure of acinar cells to free radicals causes increased calcium concentration. This abnormal increase can trigger trypsin activation, acinar cell damage and AP [21]. Infectious agents: while some infectious agents (Feline Infectious Peritonitis Virus, Toxoplasma gondii) and liver flukes are considered as potential causes of AP in cats [9, 18], there is no such evidence in dogs. However, canine babesiosis can cause AP either primarily or as a complication to SIRS [22]. Myocardial Depressant Factor Disseminated Intravascular Coagulation Acute Respiratory Distress Systemic Inflammatory Response Syndrome Tumor Necrosis Factor Interleukin Platelet Activating Factor History, Risk Factors and Clinical Signs Most affected dogs are middle-aged or older [23]. Miniature schnauzers, Yorkshire terriers and Skye terriers may be at increased risk of developing pancreatitis. Recent data suggest that mutations of PSTI gene might be associated with pancreatitis in Miniature schnauzers [24]. Males and neutered females appear to be in a high-risk group of developing the severe form of AP [23]. Concurrent diseases, such as diabetes mellitus, hyperadrenocorticism, hypothyroidism and epilepsy are related to a poorer prognosis [23]. However, epileptic dogs receiving a combination of potassium bromide and phenobarbital may be at high risk of developing AP [25]. Dogs with AP are usually presented with a sudden onset of widely varied clinical signs, such as pyrexia, anorexia, vomiting, weakness, and diarrhoea, as well as adoption of “praying” position that indicates cranial abdominal pain. In severely affected dogs, hemorrhagic diarrhoea, shock, and even sudden death may be seen. Most animals are mildly to moderately dehydrated and the palpation of a mass in the cranial abdomen may be 149 Acute pancreatitis in dogs: a review article - I. Kalli, K. Adamama-Moraitou, T. S. Rallis a possible clinical finding. Jaundice, bleeding disorders, ARDS, and cardiac arrhythmias, as a result of systemic complications of severe AP and multi-organ failure, may rarely be observed [9, 26]. Due to the vague clinical signs of AP, differential diagnosis should include all the conditions causing acute abdomen syndrome: – Acute enteritis or gastroenteritis (Parvo-virus, syndrome of acute gastroenteritis) – Exacerbation of inflammatory bowel disease – Intestinal obstruction, particularly due to foreign bodies or intussusception – Peritonitis – Acute renal failure – Acute hepatitis/acute hepatic failure – Pyometra – Ruptured abdominal organs – Acute prostatitis Coagulation abnormalities / SIRS/ Cardiac arrhythmia The extrinsic coagulation pathway is stimulated and DIC is established [27]. In a retrospective study, 61% of the dogs with severe AP showed prolonged partial thromboplastin time (PTT), and 43% prolonged prothrombin time (PT) [26]. Therefore, performing coagulation function tests is recommended in all dogs having or being suspected of having AP. Severe AP promotes bacterial translocation into the circulation resulting in septicaemia [27, 32]. It is the authors’ impression that this might be the same mechanism as the one that produces spontaneous peritonitis in humans. In the presence of AP, trypsin stimulates the formation of a bradykinin that increases vascular permeability, while acinar cells produce the myocardial depressant factor (MDF). The exact role of MDF is not known, but in experimental pancreatectomy in animals the amount of MDF was decreased [27]. Acute respiratory distress syndrome / Pulmonary oedema / Pleural effusion Monocytes and macrophages are believed to be the main source of TNF-a production, and in the presence of large numbers of alveolar macrophages the early development of ARD may be explained [27]. In addition, one of the main pancreatic enzymes involved in pulmonary surfactant degradation and development of ARD is considered to be phospholipase (lecithinase) [33]. Lecithin is an essential component for normal pulmonary function, and its degradation may be responsible for alveolar collapse in AP [28]. Pleural effusion may be present in patients suffering from AP due to altered vascular permeability [27]. Complications of acute pancreatitis The most commonly seen complications of AP are diabetes mellitus, diabetic ketoacidosis, intestinal obstruction, bile duct obstruction, renal failure and pulmonary oedema; rare complications of acute pancreatitis include pleural effusion, pancreatic abscess and pseudocyst formation, cardiac arrhythmia, disseminated intravascular coagulation (DIC), bacteraemia and acute respiratory distress (ARD) [27, 28]. Pathophysiology of systemic complications of acute pancreatitis Pancreatic abscess / pseudocyst formation Pancreatic abscess is defined as the collection of pus with little or no pancreatic necrosis, usually associated with superinfection of a pseudocyst by the enteric flora, from which bacterial cultivation is possible [34, 35]. Pancreatic pseudocyst is defined as the collection of sterile pancreatic juice surrounded by a capsule of fibrous or granulation tissue [34, 35]. Both pancreatic abscess and pseudocyst are uncommon complications of AP but should be suspected in any case where clinical signs do not resolve [35]. In the presence of severe AP, hyperproduction of proinflammatory cytokines, such as tumor necrosis factor-a (TNF-a) and interleukin (IL-6), is noticed, resulting in upregulation of the immune system. These substances, and especially TNF-a, stimulate the accumulation of neutrophils mainly at the site of inflammation (pancreatic tissue) and pulmonary parenchyma, which in turn are degranulated resulting in the secretion of proteolytic enzymes and oxidative substances causing endothelial damage, cellular dysfunction, DIC, formation of emboli and finally multiple organ failure syndrome (Figure 2) [17, 27-30]. Diagnostic approach to acute pancreatitis Diabetes mellitus / Diabetic ketoacidosis During an episode of AP, transient or permanent hyperglycaemia may be the result of progressive islet cell destruction. Alternatively, autoantibodies directed against insulin secreting cells might trigger generalized pancreatic inflammation. Diabetic ketoacidosis may also occur [28, 31]. It should be mentioned that human patients with diabetic ketoacidosis without suffering from AP might show signs of abdominal pain and increased values of serum glucose and amylase [28]. The diagnostic approach to a dog suspected of having AP should include a complete blood count (CBC), serum biochemistry profile, urinalysis and diagnostic imaging. However, the changes seen are non-specific. Complete blood count Evidence of dehydration with high packed cell volume (PCV) and plasma protein concentration is a common finding. On the other hand, anaemia is possible in some cases and can be explained either by the shortened life span due to azotemia and decreased production of the red blood cells in AP or due to the presence of bloody diarrhoea [18, 36]. Some dogs may have pancreatic ascites characterized by a serosanguineous fluid that may also contribute to the low PCV [36]. Leukocytosis characterized by a neutrophilia with a left shift is expected, especially in the Acute renal failure Aetiologic factors for acute renal failure are hypovolaemia / ischaemia, release of proteolytic enzymes from the inflamed pancreas and the presence of intravascular coagulopathy [28, 29]. 150 EJCAP - Vol. 19 - Issue 2 October 2009 cases where significant inflammation is present (i.e., peritonitis, pancreatic abscess) [18, 36]. Additional tests of haemostasis, e.g. PT, APTT, fibrinogen, D-dimer, and/or FDPs, must be performed in cases of thrombocytopenia in dogs having or being suspected of having AP. amylase and lipase activities are of limited clinical value in dogs with AP. Trypsin-like immunoreactivity (TLI) is specific for exocrine pancreatic function in dogs. According to experimental studies, TLI declines to the lower limit after pancreatectomy in dogs [43] and increases after pancreatic duct ligation [44]. It is suggested, that TLI is an early indicator of AP, because peak concentrations are noticed more rapidly than amylase and lipase [44, 45], but its early decline to normal values indicates that we cannot rule out AP if TLI concentration is normal [44]. Serum TLI concentrations are increased in experimentally induced pancreatitis. However, these elevations are observed in less than 40% of dogs with spontaneous pancreatitis, making it a suboptimal diagnostic test for pancreatitis in dogs [46]. According to recent data, the sensitivity of TLI appears to be approximately 34.8% [42]. Limitations in the sensitivity and specificity of TLI led to the development of a new diagnostic test. An enzyme-linked immunosorbent assay (ELISA) for the determination of canine pancreatic lipase immunoreactivity (cPLI) was developed [47]. The use of immunoassays allows for the specific measurement of lipase activity originating from the exocrine pancreas and is specific for assessing exocrine pancreatic function. Serum cPLI concentrations were significantly decreased in dogs with exocrine pancreatic insufficiency [48], while were found to be normal in 24/25 dogs with biopsy proven gastritis, indicating that serum cPLI concentration originates from the exocrine pancreas and is specific for exocrine pancreatic function determination. In another study serum cPLI was evaluated in dogs with experimentally induced chronic renal failure, where none of the dogs had serum cPLI concentrations above the cut-off value for pancreatitis [49]. Further studies showed that serum cPLI is sensitive (81.8%) for the diagnosis of AP in dogs [46]. Thus, serum cPLI is not only a specific marker for exocrine pancreatic function but is also highly sensitive for the diagnosis of canine pancreatitis. Trypsinogen activation peptide (TAP) is a small peptide that derives from further activation of trypsinogen that sometimes occurs during an episode of AP and therefore is measurable in plasma and urine [50]. Measurement of serum TAP and/or urine TAP to creatinine ratio (UTCR) seems to be of more importance in severe, necrotizing pancreatitis and may be a better prognostic than a diagnostic indicator of pancreatic inflammation [41, 50]. Peritoneal fluid lipase activity may be a more sensitive and specific marker than serum lipase activity. It is suggested that a two-fold increase of lipase activity in peritoneal fluid over serum activity may be indicative of pancreatic inflammation [51]. Controlled trials are needed to substantiate this hypothesis. Serum biochemistry profile Increased blood urea nitrogen (BUN) and creatinine concentrations in dogs unable to eat or drink may be due to prerenal azotemia, or it may be the result of acute renal failure [9, 11, 18]. Urine analysis, prior to fluid therapy, could help to differentiate prerenal and renal azotemia based on the urine specific gravity. Elevation of serum liver enzyme levels reflect hepatic inflammation either due to the close anatomical proximity of the pancreas or due to the inflammation caused by the pancreatic enzymes delivered from the pancreas in portal circulation or due to cholestasis [18]. Hyperbilirubinaemia usually indicates bile duct obstruction secondary to pancreatic oedema/inflammation [18]. Hyponatraemia and hypokalaemia are frequently seen and associated with anorexia, gastrointestinal electrolyte loss, osmotic diuresis and aldosterone stimulation secondary to hypovolaemia [18, 36]. During an episode of AP hyperglycaemia is expected and is associated with hyperglucagonaemia, hypoinsulinaemia due to islet cell destruction and elevation of gluconeogenic hormones (catecholamines and cortisol) [9, 18, 28, 36]. Proposed explanations for the hypocalcaemia seen in AP are hypomagnesaemia, calcium soap deposition, hyperglucagonaemia resulting in increased calcitonin secretion and decreased parathormone secretion [28, 36]. Dogs with AP are often hypoalbuminaemic and since approximately half of the circulating calcium is bound to albumin, total calcium measurements may be correspondingly low [26, 28, 36]. Ideally, ionized calcium should be measured to detect hypocalcaemia, or the total serum calcium should be corrected for the degree of hypoalbuminaemia based on the following formula: Corrected calcium (mg/dl)= Serum calcium (mg/dl) - Serum albumin (g/dl) + 3.5 Pancreas specific enzymes Classically, increased activities of serum amylase and lipase have been used as indicators of pancreatic inflammation in dogs. However, elevation of these enzymes may be observed in diseases of other organ systems or other disorders of the pancreas, such as renal failure, hepatic disease, GI neoplasia, pancreatic neoplasia-abscess and duct obstruction [37-39]. Serum lipase activity was found to be increased in young dogs with enteritis or gastroenteritis [40]. It has been shown that the sensitivity/specificity for amylase is 62%/57%, and for lipase 73%/55%, respectively [41]. In a recent study of 23 dogs with macroscopic and histological evidence of pancreatic inflammation, serum lipase had the lowest sensitivity (13%), followed by serum amylase activity (17.4%) [42]. Furthermore, corticosteroid administration may increase serum lipase activity up to five-fold without histologic evidence of pancreatitis [19, 20]. In contrast, the administration of corticosteroids appears to decrease serum amylase activity [19, 20]. In summary, serum Radiographic studies The main radiographic abnormalities associated with AP are increased radiopacity and loss of detail in the right cranial quadrant, gas filling and displacement of descending duodenum and/or stomach, widening of gastric/duodenal angle, and abdominal fluid leading to local increased opacity [37]. The described changes are not always present and are non-specific. However, abdominal radiographs are a valuable tool in ruling out other gastrointestinal diseases. 151 Acute pancreatitis in dogs: a review article - I. Kalli, K. Adamama-Moraitou, T. S. Rallis Ultrasonography Ultrasonographic findings associated with AP include hypoechoic pancreatic parenchyma, hyperechoic mesentery, pancreatic enlargement, peritoneal effusion, and identification of pancreatic cysts, pseudocysts, or masses [37, 52]. One study in dogs with fatal acute pancreatitis indicated that ultrasonographic examination supported a diagnosis of pancreatitis in 23/34 dogs (68% sensitivity) [26]. Conventional treatment • Parenteral administration of electrolyte solutions (44-66 ml/ kg + % dehydration x B.W. x 1000) ml • Correction of metabolic acidosis (bicarbonate 1-2 mmol/kg IV) • Correction of hypokalaemia (Scott’s scale) Serum K (mmol/L) mmol/L of administrated solution <2 80 2.1-2.5 60 2.6-3.0 40 3.1-3.5 28 >3.5 <5.0 20 • Antiemetic agents (metoclopramide [0.2 - 0.4 mg/kg SC every 6 to 8 hours or 1 mg/kg/day by continuous intravenous infusion], ondansentron [0.05 mg/kg IV every 8 to 12 hours], maropitant [1mg/kg SC every 24 hours]) • H2 blockers (ranitidine [2-4 mg/kg IV every 12 hours]) • Antibiotics (enrofloxacin [2.5-5 mg/kg SC every 12 hours, trimethoprim-sulphathiazine [15 mg/kg IV every 12 hours])* • Plasma or blood transfusion (10-20 ml/kg B.W.) • Analgaesics (meperidine hydrochloride [5-10 mg/kg IM or SC every 2 to 4 hours], butorphanol [0.2 - 0.4 mg/kg SC every 6 hours], morphine [0.5-2 mg/kg SC or IM every 3-4 hours], diadermic phentanyl patches) Computerized Tomography (CT) CT of the abdomen is a routine procedure for the diagnosis of AP in humans. In small animals the use of CT is limited because of the expense, the expertise skills required and the need for general anesthaesia; however there are sedation protocols that allow the performance of CT in dogs without the need for general anesthaesia [53]. Histopathology Pancreatic histopathological examination is considered to be the most definitive method for diagnosis of pancreatitis. In both clinical and experimental canine AP the macroscopic findings include generalized peritonitis, massive adhesions to adjacent organs, extensive necrosis, haemorrhage, fat necrosis and areas of abscessation [54]. Lack of macroscopic findings does not exclude histologic pancreatitis [55].The main histopathological findings are extensive necrosis of pancreatic acinar cells, haemorrhage, inflammatory cell infiltration of pancreatic tissue, pancreatic and peripancreatic fat necrosis, and saponification, acinar atrophy, and fibroplasias [54]. Pancreatitis lesions are often focal, and multiple sections of pancreas should be taken in vivo if AP is suspected. In a recent study pancreata were sectioned every 2 cm. In half of the dogs with pancreatitis evidence of pancreatic inflammation was found in less than 25% of all sections [55]. Treatment recommendations of questionable usefulness • Vasoactive agents (vasopressin, dopamine, terbutaline) • Pancreatic antisecretory agents - anticholinergic agents (atropine, propantheline) - other agents (glucagon, somatostatin, octreotide) • Pancreatic enzyme inhibitors (aprotimin) • Glucocorticosteroids (shock) • Peritoneal lavage • Surgical intervention (rarely and under certain circumstances) Treatment * The routine use of antibiotics in canine AP is not recommended since infectious complications are rather uncommon. However, in cases with evidence of pancreatic infection or in cases of AP failing to respond to supportive measures, antibiotic use is justified. Main treatment strategies of AP are listed in Table 1 and include: – Removal of the inciting cause, if known – Maintenance of fluid and electrolyte balance – Relief of pain – Management of complications – Constant monitoring Table 1. Treatment of acute pancreatitis In order to correct dehydration, hypovolaemia or shock, parenteral administration of balanced electrolyte solutions (e.g., Lactated Ringer’s) is proposed. The rate of administration depends on the estimated degree of dehydration and shock. Continuous monitoring of the patient is necessary and includes the control of body weight, urine output and careful auscultation in order to avoid pulmonary overhydration. Serum creatinine and/or blood urea nitrogen (BUN) should be monitored in order to evaluate renal function. Blood glucose monitoring is essential since hyperglycaemia is common. Serum potassium should be determined on a daily basis since anorectic, vomiting patients tend to be hypokalaemic, and supplemental potassium chloride should be added to the IV fluids as necessary (the rate of 0.5 mmol/kg/hour should never be exceeded) [9]. Correction of suspected acid-base imbalances with the administration of bicarbonate should not be blinded, without prior blood gas determination, since patients may be acidotic or alkalotic [9, 18]. In the presence of severe hypoproteinaemia the administration of plasma or another volume expander is required. Plasma transfusion is beneficial by replacing a1-antitrypsin and a2macroglobulin and by providing clotting factors in patients at high risk of DIC [9, 12]. Treatment recommendations in dogs suffering from AP traditionally included withholding food, water and per os medications for 24-48 hours, in order to reduce the stimuli for pancreatic enzyme synthesis and secretion. Results of recent studies have led to some changes in the former nutritional strategy. It is true that patients with pancreatitis should be offered nothing per os (NPO) if vomiting is profuse for a 152 EJCAP - Vol. 19 - Issue 2 October 2009 However, in cases with evidence of pancreatic infection or in cases of AP failing to respond to supportive measures, antibiotic use is justified [59,60]. Clindamycin, metronidazole, chloramphenicol, and ciprofloxacin are substances with high pancreatic tissue concentrations in canine models of AP [17]. The use of pancreatic antisecretory agents is not yet recommended. Administration of somatostatin, dopamine and octreotide in experimental AP cases in both dogs and cats seems to improve the severity of symptoms and duration of the disease [9]. The use of proinflammatory cytokines (TNFa/IL6) and free radicals inhibitors may aid in the future treatment of AP. Surgical treatment may be beneficial in cases of obstructive jaundice, intestinal obstruction or in the presence of pancreatic abscess and severe necrosis of the pancreas [59, 60]; however, further studies are warranted to evaluate the efficacy of surgical intervention in dogs with AP. Peritoneal lavage in order to remove toxic substances as trypsin and kinins is recommended in cases where exploratory laparatomy is performed or in patients that fail to respond to medical treatment [9, 10, 12, 17, 18]. However, there are no studies specifically evaluating the beneficial effects of peritoneal lavage in canine AP and given the potential risks (e.g. peritonitis), this procedure should be carefully considered. period of up to 48 hours. Current evidence in both dogs with experimental pancreatitis and humans with pancreatitis, suggest that enteral feeding is not contraindicated, and may even be beneficial; pancreatic secretion from enteral nutrients decreases as the feeding site moves down the bowel. Consequently, early institution of intrajejunal feeding may have beneficial effects in dogs with AP. This is attributed to the maintenance of intestinal integrity and reduced bacterial translocation from the intestine and a reduced systemic inflammatory response [56]. Oesophagostomy, gastrostomy, or jejunostomy (distal to the site of pancreatic stimulation) tubes are useful for nutritional management of anorectic dogs. In non-vomiting dogs feeding by naso-oesophageal or gastrostomy tube may be beneficial. In cases with signs indicative of severe abdominal pain, analgaesic therapy should be given to provide relief. Analgaesic agents recommended are meperidine hydrochloride, butorphanol tartrate, morphine or diadermic phentanyl patches [57]. Antiemetics, such as metoclopramide hydrochloride should be given only in cases with frequent and uncontrolled vomiting, since its cessation may indicate improvement of the patient’s condition [56]. In cases where metoclopramide administration is not effective, slow intravenous administration of ondansentron is recommended. A new antiemetic, maropitant, has recently become available and seems to have antiemetic efficacy in dogs [58]. Appropriate antibiotic therapy is based on the ability of the drug to penetrate the pancreas and on its effectiveness against bacteria known to cause pancreatic infection. However, the beneficial effects of antibiotic treatment in any case of AP are still controversial. In contrast to what has been demonstrated in humans with AP, infectious complications are rather uncommon in dogs with naturally occurring AP [59, 60, 61]. Consequently, the routine use of antibiotics in canine AP is not recommended. Prognosis Stratifying the severity of AP is necessary in order to decide how aggressive the medical and nutritional support should be. Mild pancreatitis often responds to symptomatic treatment and has a good prognosis, whereas severe pancreatitis requires aggressive therapy and prognosis is guarded. Early diagnosis and treatment of the disease and the absence of systemic complications are factors that result in a better outcome. A scoring system Table 2. Systems considered and criteria for compromise of organs, as used in the “severity of illness” score applied to spontaneous canine acute pancreatitis. System Criterion Laboratory reference range Lymphoid > 10% band neutrophils or white cell count > 24 x 109 /L 0.0 – 0.2 x 109 /L band neutrophils 4.5 – 17.0 x 109 /L WCC Renal Serum urea concentration > 14 mmol/L or creatinine concentration > 0.3 mmol/L 2.5 – 9.5 mmol/L urea 0.06 – 0.18 mmol/L creatinine Hepatic Any of ALP, AST or ALT > 3 x reference range 0 – 140 IU/L ALP 15 – 80 IU/L AST 15 – 80 IU/L ALT Acid/base bufferinga Bicarbonate concentration < 13 or > 26 mmol/L and/or anion gap < 15 or > 38 mmol/L Endocrine pancreasa Blood glucose > 13 mmol/L and/or β-OH butyrate > 1 mmol/L 15 – 24 mmol/L bicarbonate 17 – 35 mmol/L anion gap 3.3 – 6.8 mmol/L glucose 0.0 – 0.6 mmol/L β-OH butyrate The score is the total count of organ systems showing compromise under these criteria (Ruaux and Atwell 1998) a: if hyperglycaemia, butyrate and acidosis coexist, count as one system WCC: white cell count ALP: alkaline phosphatase AST: aspartate aminotransferase ALT: alanine aminotransferase 153 Acute pancreatitis in dogs: a review article - I. Kalli, K. Adamama-Moraitou, T. S. Rallis Disease severity Score Prognosis Mortality rate (%) Mild 0 Excellent 0 Moderate 1 2 Good to fair Fair to guarded 11.1 20 Severe 3 4 Poor Grave 66.6 100 Ruaux and Atwell 1998, Ruaux 2000 Table 3. Scoring system – prognosis and mortality rate (%) in canine acute pancreatitis cases according to the number of organ systems showing evidence of failure based on Table 2. [15] Nakae Y, Naruse S, Kitagawa M, Hirao S, Yamamoto R, Hayakawa T. Activation of trypsinogen in experimental models of acute pancreatitis in rats. Pancreas. 1995; 10: 306-313. [16] Bettinger JR, Grendell JH. Intracellular events in the pathogenesis of acute pancreatitis. Pancreas. 1991; 6: 52-56. [17] Holm JL, Chan DL, Rozanski EA. Acute pancreatitis in dogs. J Vet Emerg Crit Care. 2003; 13: 201-213. [18] Strauss JH. Pancreatitis. In: Bojrab (MJ), editor. Disease Mechanisms in Small Animal Surgery. Philadelphia: London, Lea&Febiger; 1993. p237-242. 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[33] Mansfield CS, Jones BR, Spillman T. Assessing the severity of canine pancreatitis. Res Vet Sci. 2003; 74: 137-144. [34] Rutgers C, Herring DS, Orton EC. Pancreatic pseudocyst associated with acute pancreatitis in a dog: ultrasonographic diagnosis. J Am Anim Hosp Assoc. 1985; 21: 411-416. [35] Coleman M, Robson M. Pancreatic masses following pancreatitis: Pancreatic pseudocysts, necrosis, and abscesses. Compend Contin Educ Vet. 2005; 27: 147-153. [36] Schaer M. A clinicopathologic survey of acute pancreatitis in 30 dogs and 5 cats. J Am Anim Hosp Assoc. 1979; 15: 681-687. [37] Ruaux CG. Diagnostic approaches to acute pancreatitis. Clin Techn in Small Animal Practice. 2003; 18: 245-249. [38] Quigley K, Jackson M, Haines D. - Hyperlipasemia in 6 dogs with pancreatic or hepatic neoplasia: evidence for tumor lipase production. Vet Clin Pathol, 2001; 30:114-120. [39] Strombeck DR, Farver T, Kaneko JJ. Serum amylase and lipase activities in the diagnosis of pancreatitis in dogs. 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[45] Williams DA, Melgarejo T, Henderson J, Kazacos E. Serum trypsinlike immunoreactivity (TLI), trypsinogen activation peptides (TAP), amylase and lipase in canine experimental pancreatitis. J Vet Intern Med (abstract). 1996; 10: 159. [46] Steiner JM, Broussard J, Mansfield CS, Gumminger SR, Williams DA. Serum canine pancreatic lipase immunoreactivity concentrations in dogs with spontaneous pancreatitis. J Vet Intern Med (abstract). 2001; 15: 274. [47] Steiner JM, Teague SR, Williams DA. Development and analytical validation of an enzyme-linked immunosorbent assay for the measurement of canine pancreatic lipase immunoreactivity in serum. Can J Vet Res. 2003; 67: 175-182. [48] Steiner JM, Rutz GM, Williams DA. Serum lipase activities and pancreatic lipase immunoreactivity concentrations in dogs with exocrine pancreatic insufficiency. Am J Vet Res. 2006; 67: 84-87. [49] Steiner JM, Finco DR, Gumminger SR, Williams DA. Serum canine pancreatic lipase immunoreactivity (cPLI) in dogs with experimentally induced chronic renal failure. J Vet Intern Med (abstract). 2001; 15: 311 [50] Mansfield CS, Jones BR. Plasma and urinary trypsinogen activation peptide in healthy dogs, dogs with pancreatitis and dogs with other systemic diseases. Aust Vet J. 2000; 78: 416-422. [51] De Arespacochaga G, Hittmair KM, Schwendenwein I. Comparison of lipase activity in peritoneal fluid of dogs with different pathologies - a complementary diagnostic tool in acute pancreatitis? J Vet Med. 2006; 53: 119-122. [52] Nyland TG, Mulvany MH, Strombeck DR. Ultrasonic features of experimentally induced, acute pancreatitis in the dog. Vet Radiol. 155 ENDOCRINOLOGY REPRINT PAPER (NL) Treatment of feline hyperthyroidism with radioactive iodine-131 I.C. van Dijl(1), A.J. Hof(1) SUMMARY Feline hyperthyroidism can be treated by thyroidectomy, anti-thyroid drugs, or radioactive iodine-131 (131I). The aim of this retrospective study was to evaluate the treatment of 83 hyperthyroid cats with 131I. The dosage of 131I ranged from 4 to 6 milliCurie (mCi). Prior to, ten days after, and several months after treatment, blood samples were collected and plasma concentrations of total thyroxine (TT4), urea, and creatinine were determined. In addition, arterial blood pressure was measured before and ten days after treatment. The median plasma TT4 concentration ten days after 131I treatment (27 nmol/L, 64 cats) was significantly lower than before treatment (123 nmol/L). The median plasma TT4 concentration several months after 131I treatment was 22.5 nmol/L (40 cats). Ten days and several months after 131I treatment, plasma TT4 concentrations had decreased below the upper limit of the reference range in 64 (77%) and 72 cats (87%), respectively. In four cats the plasma TT4 concentration had decreased below the lower limit of the reference range, but only two cats had symptoms of hypothyroidism. Plasma urea and creatinine concentrations were not increased ten days after 131I treatment, but the median plasma creatinine concentration was significantly higher several months after treatment when compared with before 131I treatment. Before treatment a high arterial blood pressure (>180 mmHg) was measured in 28 cats, whereas after treatment a high arterial blood pressure was measured in 25 cats. The results of this study indicate that 131I treatment is an effective therapy in most cats with hyperthyroidism. Keywords: adenomatous hyperplasia, arterial hypertension, cats, nuclear medicine, renal insufficiency. have been found in some cats [33]. Recent studies indicate that there might be a correlation between the number of cats diagnosed with hyperthyroidism and the consumption of canned food [9,18,23]. Clinical signs are caused by excessive production of thyroid hormones. The most common signs of hyperthyroidism are weight loss, polyphagia, hyperactivity, coat changes, polyuria, polydipsia, and gastrointestinal symptoms [5,34]. Signs of apathy, lethargy, anorexia, and weakness are occasionally seen [34,45]. Diagnosis can be made based on the cat’s clinical signs, palpation of a mass in the neck area, an increased plasma total thyroxine (TT4 ) concentration, and thyroid scintigraphy. Thyroid scintigraphy is the most reliable diagnostic tool for confirming the diagnosis [30], but this is only available in a This paper originally appeared in: Tijdschrift voor Diergeneeskunde* 133(2):54-62 Introduction Hyperthyroidism is the most common endocrine disorder in cats older than eight years of age. The pathogenesis is however still unclear. Immunological, infectious, nutritional, environmental or genetic factors are possibly involved [9,18,23,26,33]. Somatic mutations of the thyroid stimulating hormone (TSH) receptor gene [48] as well as the gene encoding for Gsα, a protein involved in the second messenger system of the TSH receptor, 1) Lingehoeve Diergeneeskunde Veldstraat 3a, NL-4033 AK Lienden, The Netherlands E-mail: [email protected] *Presented by NACAM (The Netherlands) 156 EJCAP - Vol. 19 - Issue 2 October 2009 few institutions. Enlargement of the thyroid(s) is detectable by palpation in over 80% of cases [5,45]. In most cases hyperthyroidism can be diagnosed by determination of an increased plasma TT4 concentration. Cats with mild hyperthyroidism or cats with other diseases can have a plasma TT4 concentration within reference range [5,31,37]. Both thyroid lobes are affected in approximately 70% of the cats, and in less than 10% of the cases ectopic thyroid tissue is involved [12,35,45]. On histological examination multinodular adenomatous hyperplasia is often found [28,35]. Carcinomas, by contrast, are rare [29,35]. Feline hyperthyroidism can be treated by thyroidectomy, antithyroid drugs, or radioactive iodine ( 131I). The 131I treatment is considered as the best choice, because of the effectiveness and minimal risk of complications [36,41]. One of the advantages of the 131I treatment is that it is minimally invasive procedures. Only one subcutaneous injection with radioactive iodine will be enough to convalescent euthyroidism in most cats. Compared to thyroidectomy there is no anaesthetic risk. Radioiodine treatment is also effective in cases of ectopic thyroid tumour tissue. One of the disadvantages is that the therapy is only possible in a few institutions. The laws governing the use of radioactive materials enforce exclusive constraints on the therapeutic use of radioactive iodine in animals [49]. Moreover, the cat becomes a temporarily source of radiation, which makes hospitalization in a special room during a determined period necessary. When the cat is allowed to return home the risks of radiation are not sufficiently diminished and precautions are necessary. The goal of this retrospective study was to investigate the results of the treatment of feline hyperthyroidism with radioactive iodine at a small animal clinic in the Netherlands. Hyperfunctional thyroid tumor tissue TT4 I dose 131 in nmol/L in mCi < 90 4.0 Unilateral > 90 4.5 Bilateral < 90 4.5 Bilateral > 90 5.0 Also ectopic < 90 5.5 Also ectopic > 90 6.0 Unilateral Table 1: 131I-dose estimation in mCi. (1 mCi = 37 MBq). Plasma TT4 concentration is represented in nmol/l. The term ‘also ectopic’ represents cats that had besides a unilateral or bilateral increased uptake also ectopic hyperfunctioning tumour tissue. Protocol Blood samples for determination of plasma thyroxine (TT4 ), urea, and creatinine concentrations were collected prior to, ten days after, and several months after treatment. The referring veterinarians took blood samples before and several months after treatment. Veterinary Clinic Lingehoeve took blood samples ten days after treatment. In addition, arterial blood pressure was measured before and ten days after treatment. A telephone survey was conducted on the cat’s owners. Seventyseven owners were willing to cooperate. The survey was held on average 14 months (median 16 months, range four months to three years) after treatment. On the day the cats were admitted to the hospital for radioiodine treatment, a complete physical examination was performed, the cat was weighed and arterial blood pressure was measured with an Ultrasone Doppler Flow Detector 811-Ba. The area proximal of the metacarpal footpad was shaved, on the first 45 cats. This was later found to be unnecessary when enough gel was applied. A cuff attached to a manometerb was placed below the elbow. Blood pressure was measured at least five times. The result was calculated as a mean of the final three measurements. Subsequently, an intravenous catheter was placed so that if necessary, the cats could be sedated with propofolc. Technetium99m was given intravenously (IV) or subcutaneously (SC) and after staying in the quarantine room for 30 (IV) to 45 (SC) minutes, respectively thyroid scintigraphy was performed using a gamma camerad. All radioiodine treatments took place between February 2004 and October 2006. The radioiodine dose was estimated empirically (see Table 1) and varied from 4 to 6 milli Curie (mCi). The final dose was estimated at the moment of injection using a callibratore. Materials and Methods Cats The age of the cats varied from five to seventeen years. The mean age at which the cats were treated was 12.8 years (median 14.3 years, range 5.3 – 17.9 years). The body weight ranged from 2.4 – 6.4 kg. Seventy-seven cats were European Shorthairs. Furthermore, there were one Norwegian Forrest Cat, one Russian Blue, one Persian Cat, and three Persian Crossbreeds. Forty-two cats were male and 41 female. Except for one male and one female, all cats were neutered. The diagnosis had been made by the referring veterinarians and was based on the clinical signs (anamnesis and physical examination) and the plasma TT4 concentration. The diagnosis was confirmed by thyroid scintigraphy with radioactive Technetium-99m (pertechnetate, 99mTcO4 -, mean dose 66 mCi, median dose 58 mCi, range 40 – 86 mCi) at Veterinary Clinic Lingehoeve. Of the 83 cats, 65 cats had been treated with antithyroid drugs before radioiodine treatment. The duration of treatment with antithyroid drugs ranged from two weeks to one year. Administration of antithyroid drugs was discontinued at least three days before radioiodine was administrated. Thyroid scintigraphy indicated that nine cats had ectopic thyroid tumour tissue. Of the remaining cats, 50 had bilateral and 24 unilateral hyperplasia. a b c d e Parks Medical Electronics inc, Aloha, Oregon. Riester Precisa n 0124, Germany. Rapinovet®, Schering Plough, Utrecht, The Netherlands. GE400A, GE Electronics, Great Brittan. Atomlab TM 100 Radioisotope Callibrator model 086-250, Biodex Medical Systems, New York. f Universitair Veterinair Diagnostisch Laboratorium, Utrecht, The Netherlands. g Vet Med Labor GmbH, Ludwigsburg, Germany. 157 Treatment of feline hyperthyroidism with radioactive iodine-131 - I.C. van Dijl, A.J. Hof During hospitalization the cats stayed in a special quarantine room. The hospitalization time was determined by measuring the radiation level of the cat. On the day the cats returned home blood samples were taken, the cat was weighted, and arterial blood pressure was remeasured. Reference range Blood analyses before and several months after treatment were mainly performed by the referring veterinarians in their own laboratories or by the Veterinary Diagnostic Laboratory of Utrecht University (UVDL) f. VetMedLaborg performed almost all blood analyses taken ten days after treatment. It should be noted that the laboratories used different reference ranges. The reference range of the plasma TT4 concentration used by the UVDL was 15 – 45 nmol/L and by VetMedLabor was 10 – 50 nmol/L. In this study a reference range of 10 – 50 nmol/L has been used. A short comment has to be made about the plasma urea and creatinine concentrations. VetMedLabor determined blood urea nitrogen (BUN) and the other laboratories determined plasma urea. The BUN results can be converted to plasma urea concentration using a conversion rate of 2.14. When the VetMedLabor BUN reference range (1.7 – 5.5 mmol/L) is converted to plasma urea (3.6 – 11.8 mmol/L), the reference range is lower when compared to the reference range used by the UVDL (6.1 – 12.8 mmol/L). In this study, a reference range for plasma urea concentrations of 3.6 – 12.8 mmol/L has been used. VetMedLabor uses a reference range for plasma creatinine concentrations of < 177 µmol/L and the UVDL 76 – 164 µmol/L. We used a reference range of < 177 mmol/L. The reference ranges of the equipment used by the referring veterinarians for blood analysis compared well with the instrumentation used at UVDL. Figure 1: “Box-and-whisker plots” of the plasma TT4 concentration before 131I treatment (TT4 before), ten days after treatment (TT4 after) and several months after treatment (TT4 later) in nmol/L. The horizontal lines represent the reference range (10 – 50 nmol/L). The asterisks represent the level of significance between the different groups (* P < 0.001). and several months after 131I treatment plasma TT4 concentration had decreased below 50 nmol/L in 64 (77%) and 72 cats (87%), respectively (Group I and II, Table 2). In five of the 83 cats, plasma TT4 concentration remained between 50 – 70 nmol/L (group III, Table 2) and in six cats it was above 70 nmol/L (group IV, Table IV). In four cats the plasma TT4 concentration decreased below 10 nmol/L (Group I, Table 2). Only two of these cats had clinical signs of hypothyroidism and were treated with l-thyroxine. Of the five cats of which the plasma TT4 concentration decreased to 50 – 70 nmol/L (Group III, Table 2), four cats had no clinical signs of hyperthyroidism at the time of this retrospective study. Statistical analyses Statistical analyses were performed using SPSS 12.0. The ‘one sample Student’s t-test’ and the ‘paired Student’s t-test’ were used for analysing the body weight. For all other analyses the ‘Wilcoxon signed rank test’ for paired, non-parametric variables was used. All values are reported as median and range. Differences were considered significant at P < 0.05. Results are summarized in ‘box and whisker plots’. The frames inside the ‘box and whisker plots’ indicate the 25th and 75th percentile, while the black line inside the box represents the median. The whiskers include the 95% interval. The small circles represent the outliers. The asterisks indicate the value of significance. Results Thyroxine The median plasma TT4 concentration ten days after 131I treatment (27 nmol/L, range 2 – 185 nmol/L, 64 cats) was significantly lower (P < 0.001) than that before treatment (123 nmol/L, range 31 – 320 nmol/L) (Figure 1). The median plasma TT4 concentration several months after 131I treatment was 22.5 nmol/L (2 – 152 nmol/L, 40 cats). There was a significant difference (P < 0.001) between the plasma TT4 concentration before treatment and several months after treatment. Ten days Group TT4 (nmol/L) TT4 ten days after 131I I < 10 6 cats 4 cats II 10 – 50 59 cats 68 cats III 50 – 70 6 cats 5 cats IV > 70 Total Last measured TT4 12 cats 6 cats 83 cats 83 cats Table 2: Overview of the plasma TT4 concentrations ten days after 131 I treatment and the last measured TT4 concentrations of all cats. In 83 cats blood analyses were performed ten days after treatment (third column). The fourth column represents the last measured plasma TT4 concentration of all cats. 158 EJCAP - Vol. 19 - Issue 2 October 2009 had also an increased plasma urea concentration ten days after treatment. One cat did still have clinical signs after treatment but the owner declined a second treatment. This cat had deceased at the time of this study. In two out of the five cats of group III, the final blood analyses were performed ten days after treatment and in one cat, two months after treatment. One of the six cats of the group with a plasma TT4 concentration above 70 nmol/L after treatment (Group IV, Table 2) was treated with radioiodine again. After the second treatment the clinical signs had decreased, but not disappeared. This cat was again treated with antithyroid drugs and the clinical signs resolved. In another cat from group IV, the plasma TT4 concentration decreased to less than 50 nmol/L ten days after treatment, but increased at a later stage. The clinical signs returned with the increase of the plasma TT4 concentration. At an even later stage the clinical signs had resolved and this was accompanied by a decrease of the plasma TT4 concentration to within the reference range. At the time of this retrospective study two cats of group IV had deceased. The clinical signs had completely resolved in the remaining two cats in group IV. Five out of the six cats with a plasma TT4 concentration above 70 nmol/L (Group IV, Table 2) had strongly enlarged thyroid glands on scintigraphy. In addition, these cats also had a large amount of irregularly shaped thyroid tumor tissue with variation in technetium uptake on scintigraphy. Creatinine The median plasma creatinine concentration ten days after radioiodine treatment (88 µmol/L, range 30 - 239 µmol/L, 64 cats) was significantly lower (P = 0.043) than before treatment (98 µmol/L, 44 - 187 µmol/L). The median plasma creatinine concentration several months after treatment was 143.5 µmol/L (85 - 267 µmol/L, 24 cats). The difference between the median plasma creatinine concentration before and several months after treatment was significant (P = 0.002). Ten days after treatment two cats had a plasma creatinine concentration above the reference range (< 177 µmol/L). One of these cats also had an increased plasma urea concentration. Of the three cats with a plasma creatinine concentration above the reference range before treatment, only one had this after treatment. This specific cat also had plasma urea concentrations above the reference range prior to as well as ten days after treatment. This cat died one month after treatment. Several months after treatment five cats had a plasma creatinine concentration above the reference range. One of these also had plasma urea concentrations above the reference range. Arterial blood pressure Blood pressure was measured in the 53 cats with plasma TT4 concentrations that decreased to within the reference range. The median arterial blood pressure ten days after treatment (180 mmHg, range 120 – 270 mmHg) did not differ significantly from that before treatment (190 mmHg, range 120 – 300 mmHg). Before treatment a high arterial blood pressure (>180 mmHg) was measured in 28 cats and after treatment a high arterial blood pressure was measured in 25 cats. Urea The median plasma urea concentration ten days after radioiodine treatment (9.0 mmol/L, range 4.7 – 16.5 mmol/L, 64 cats) did not differ significantly (P = 0.32) in comparison to the plasma urea concentration before treatment (8.8 mmol/L, 4.7 – 16.1 mmol/L). The median plasma urea concentration several months after treatment was 10.3 mmol/L (7.7 – 21.4 mmol/L, 22 cats). The difference between the median plasma urea concentration before and several months after treatment was not significant (P = 0.05). After treatment, seven cats had plasma urea concentrations above the reference range (3.6 – 12.8 mmol/L). From the six cats that had a plasma urea concentration above the reference range before treatment, only one had this after treatment. Several months after treatment five cats had a plasma urea concentration above the reference range. Two of these cats Body weight Bodyweight was recorded for 55 cats before and several months after treatment (range 3 – 31 months). The mean bodyweight several months after treatment (4.9 kg, standard deviation ± 1.2) was significantly higher (P < 0.001) than that before treatment (4.0 kg, standard deviation ± 1.0). Only four cats showed a decrease in body weight. Figure 2: “Box-and-whisker plots” of the plasma urea concentrations (left panel) and the plasma creatinine concentrations (right panel) before 131I treatment (Urea before, Creat before), ten days after treatment (Urea after, Creat after) and several months after treatment (Urea later, Creat later). The asterisks represent the level of significance between the different groups (* P = 0.04; ** P = 0.002). 159 Treatment of feline hyperthyroidism with radioactive iodine-131 - I.C. van Dijl, A.J. Hof Clinical features before treatment showed normal behaviour and gained weight (Figure 4). At the time of the telephone survey 16 cats were deceased. Six owners were unreachable. The probable diagnoses of the deceased cats were tumour (3 cats), heart failure (2), renal failure (2), neurologic signs (2), liver failure (1), inflammation (1), diabetes mellitus (1), car accident (1), and unknown (3). Of the 61 cats that were still alive, 58 had no clinical signs of thyroid disease, according to the owners. One cat received antithyroid drugs and two cats received thyroxine. Eight cats were treated for arterial hypertension, four cats were treated for kidney failure, and three cats received both treatments. The most common reason for choosing the radioiodine treatment was the fact that the cat did not respond well to antithyroid drugs. The side effects of the antithyroid drugs (gastro intestinal problems, anorexia and/or hematologic changes) affected the cats too much or it was not possible to give the cat the antithyroid drugs twice a day. The most mentioned advantage of the radioiodine treatment was that the cat did not have to undergo surgery. That the cat had to stay in a kennel for ten days without the possibility of the owners to visit, was a disadvantage of the radioiodine treatment mentioned by the owners. The cost was another disadvantage often commented upon. Number of cats (percentage of total) Weight loss 64 (83%) Polyphagia 35 (45%) Hyperactivity 21 (27%) Coat changes 18 (23%) Polydipsia 12 (16%) Anorexia/less appetite 6 (8%) Change in vocalisation 6 (8%) Other behavioural changes 5 (6%) Vomiting 4 (5%) Apathy 3 (4%) Diarrhoea 3 (4%) Dyspnoea 3 (4%) Heat intolerance 3 (4%) Aggressive behaviour 2 (3%) Not house-trained 2 (3%) Muscle weakness 2 (3%) ‘Wild look in the eyes’ 2 (3%) Discussion Table 3: Clinical signs before 131I treatment mentioned by the owners. The term ‘other behavioural changes’ represents behavioural changes that were noticed by the owners, but could not be specifically named by them. Follow up Table 3 shows the most important clinical signs observed by the owners before radioiodine treatment. Figure 3 shows the changes observed by the owners after the ten days hospitalisation period in which treatment occurred compared with the clinical signs before treatment. According to the owners, weight loss (83%) was the most important clinical sign before treatment according to the owners. In general, a hospitalisation period of ten days was not long enough to reach the same body weight as before the cat became hyperthyroid. The success of the radioiodine treatment was measured by almost all owners by the fact that their cat The results justify the conclusion that radioiodine treatment is a highly effective therapy for feline hyperthyroidism. In 72 out of 83 cats the plasma TT4 concentration decreased to less then 50 nmol/L. This corresponds with the results, 85 to 91%, found in other studies [6,36,39,42]. In four of these 72 cats the plasma TT4 concentration decreased below the lower limit of the reference range. In five cats the plasma TT4 concentration decreased to a value between 50 and 70 nmol/L (Group III, Table 2). In six cats the plasma TT4 concentration did not decrease below 70 nmol/L (Group IV, Table 2). Other studies indicate comparable percentages on which the therapy was not successful (1 – 8%) [6,25,36,38,42]. The clinical signs resolved completely in two cats of group III as well as two cats of group IV, despite the increased plasma TT4 concentrations. One possible explanation might be the fact that blood samples from these cats were only taken once or twice Figure 3: The owners’ reactions on the general state of the cat when returned home after 131I treatment. Figure 4: Time after treatment when all clinical signs of hyperthyroidism had disappeared according to the owners. 7% 1% Direct improvement 2% 1% Direct disappearance of all clinical features 10% No change Deterioration 56% 23% No clinical features before treatment Clinical features of hypothyroidism Unreachable 160 EJCAP - Vol. 19 - Issue 2 October 2009 before radioiodine treatment. If and how much this antithyroid treatment influenced the radioiodine treatment is hard to say. Different studies contradict each other [13,36,42]. The mean age (12.8 years) found in this study corresponds with the mean age found in other studies [5,36,45]. To determine the effect of the radioiodine treatment on the renal function, only the renal blood samples were reviewed from the cats whose plasma TT4 concentration decreased within the reference range. Only when the plasma TT4 concentration had decreased within the reference range, could a pronouncement be made about the effect of the radioiodine treatment on the renal function. Hyperthyroidism and renal insufficiency are both diseases of the older cat. They can appear separately, but often together. Hyperthyroidism increases glomerular filtration rate (GFR), renal perfusion, renal tubular reabsorption and secretion capacity in the kidneys. This results in a decrease of the plasma urea and creatinine concentrations [21]. Clinical and biochemical signs of renal failure can be masked in cats that suffer from hyperthyroidism as well as renal insufficiency. When a cat is treated for hyperthyroidism, renal perfusion and GFR decrease and the clinical signs of renal failure can come to light or become worse. Because it is difficult to predict the impact of treatment of hyperthyroidism on the renal insufficiency, it is advisable to treat cats with renal insufficiency with a reversible therapy (oral antithyroid drugs) until the effect of the restored thyroid function becomes clear [1,3,31]. No test exists which can predict if a cat will develop renal failure after radioiodine treatment [2,11]. If plasma urea and creatinine concentrations and urine specific gravity before treatment are within reference range, the chance of developing renal failure after treatment is small [8]. However, Elliot (2004) found a risk of 30% for developing uraemia after radioiodine treatment in non-uraemic cats [11]. Our study demonstrates that the median plasma urea concentration before treatment did not differ significantly from that ten days and several months after treatment. Other studies did demonstrate a significant difference between the plasma urea concentration before and after treatment [1,2,7,14]. One possible explanation can be that the increased urea production produced by the increased protein turnover in the body exceeds the increase in renal excretion [8,40]. The plasma urea concentrations are difficult to interpret, because in this retrospective study different laboratories were used, each with their own reference ranges. The significant increase of the median plasma creatinine concentration several months after treatment compared with before treatment did correspond with the results found in other studies [1,2,7]. The number of cats showing an increased plasma creatinine concentration before, ten days after and several months after treatment did not indicate that cats with a moderate renal function before treatment, had a greater chance of developing renal insufficiency after treatment. An increased systemic arterial blood pressure (> 180 mmHg) is a common complication in cats with hyperthyroidism. It results from the effects of increased β-adrenergic activity on heart rate, myocardial contractility, systemic vasodilatation, and activation of the rennin angiotensin aldosterone system. Hypertension caused by hyperthyroidism is usually clinically silent. Retinal hemorrhages and retinal detachment are the most common clinical complications of systemic hypertension in hyperthyroid shortly after treatment (ten days to two months) and were not repeated at a later moment. It can take up to several months before euthyroidism occurs [27,36]. Therefore it is possible that the plasma TT4 concentration decreased to within reference range at a later time. A striking observation was that five out of six cats of group IV (the group in which the plasma TT4 concentration did not decrease below 70 nmol/L) had a greatly enlarged thyroid gland on scintigraphy. In addition, these cats also showed a large amount of irregularly shaped thyroid tumour tissue with variation in technetium uptake on scintigraphy. Research in humans indicates that a greatly enlarged thyroid gland can be a possible explanation for an incomplete cure after radioiodine treatment [15,16]. One possible explanation is that more adenomatous cells have to be destroyed in comparison to the number of cells that have to be destroyed in cats with small tumors [36]. Besides this, a high turnover in the thyroid gland could be a possible explanation. In this case, the radioiodine would not stay long enough in the thyroid gland to achieve the desired cell destruction. The irregular uptake of Technetium99m might indicate that some thyroid cells also absorbed less 131I that resulted in an incomplete destruction. Another factor that may lead to an incomplete response to the radioiodine treatment is the presence of a thyroid carcinoma rather than adenomatous hyperplasia of the thyroid gland [47]. One of the risks of the radioiodine treatment is the development of hypothyroidism. The results mentioned in other studies vary from 2.1 up to 9% [6,25,36,38,42]. Nykamp et al (2005) found in their retrospective study an occurrence of 30%, but the conclusions were based solely on the plasma TT4 concentrations and did not take into account the clinical signs of hypothyroidism [32]. After radioiodine treatment low plasma TT4 concentrations without clinical signs of hypothyroidism frequently occur. Treatment is often not required [38]. The radioiodine dose was empirically estimated and varied from 4 to 6 milli Curie (mCi). A comparable method for radioiodine dose estimation has been used by Peterson and Becker (1995) [36]. They used a scoring system that was concurrently based on the severity of the clinical signs. The doses they administered ranged from 2.0 to 6.0 mCi. In another study the dose given varied from 1.1 to 2 mCi [17]. Another possibility is to give each cat a fixed dose of radioiodine [25]. Risks that can develop are that the cats with mild clinical signs can be overdosed and cats with severe clinical signs can be underdosed. With overdosing, the cat and caretakers will be exposed to unnecessary high doses of radiation [38]. The estimation of the radioiodine dose with tracer studies is a third method [24,25,39,46]. The disadvantage of this last method is that there can be a sophisticated difference between the calculated dose and the actual dose that reached the thyroid gland. In response to this study it is recommended that future studies also include the amount of hyperfunctioning thyroid tissue in the calculation of the radioiodine dose. The radioiodine can be administered orally, intravenously or subcutaneously. Oral administration usually demands higher doses, the risk of contamination of the environment increases and sometimes it can provoke vomiting [13,22]. A subcutaneous injection is easier to administer, less risky for the caretakers and even effective as intravenous administration [27,44]. Sixty-five cats got antithyroid drugs during at least two weeks 161 Treatment of feline hyperthyroidism with radioactive iodine-131 - I.C. van Dijl, A.J. Hof cats, but in general, lesions are not commonly identified in cats with hyperthyroidism [31]. Kobayashi et al (1990) found that 85% of the hyperthyroid cats had an increased arterial blood pressure [19]. Earlier studies indicate that a moderate increase in arterial blood pressure is common in hyperthyroid cats. Only in cases of renal failure severe hypertension was found [10,20]. Before treatment 28 cats (53%) had an arterial blood pressure above180 mmHg and after treatment 25 cats (47%). This indicates that in this study (effective) treatment with 131I did not result in significantly decreased arterial blood pressures ten days after treatment compared with before treatment. However, it cannot be excluded that the recovery of the blood pressure takes more than ten days. A study of Bewel et al (1999) indicates that comparable to what has been reported in humans cats can also suffer from ‘white coat hypertension’ [4]. This study shows that cats in a simulated office visit had significantly higher arterial blood pressures compared by measuring 24 hour values. In our study blood pressure measurement was repeated at least five times. The cats stayed in the room for at least ten minutes before the first measurement was started. Nevertheless, the question arises if the increased arterial blood pressures found in our study were caused by the effect of high circulating thyroid hormone concentrations, the ‘white coat hypertension’ or by another cause not related to hyperthyroidism [43]. Moreover, a human study on the effect of high circulating thyroid concentrations on the heart and vascular resistance indicates that an increase in plasma thyroid concentrations causes a decrease in systemic peripheral vascular resistance [19]. Vascular resistance can decrease by 50 – 70%, accompanied by a high increase in circulation of the skin, muscles, kidney, and heart. This could possibly also compensate much of the β-adrenergic influence on the heart. The question is if feline hyperthyroidism results in arterial hypertension. More research is necessary. In conclusion, the results of this study indicate that 131I treatment is a highly effective therapy in most cats with hyperthyroidism. Ten days and several months after 131I treatment, plasma TT4 concentration had decreased below 50 nmol/L in 64 (77%) and 72 cats (87%), respectively. Five out of six cats whose plasma TT4 concentration did not decrease below 70 nmol/L showed, in comparison to other cats, a greatly enlarged thyroid gland in scintigraphy. In addition, these cats also had irregularly shaped thyroid tumour tissue with variation in technetium uptake on scintigraphy. If this is related to the poor results of the radioiodine treatment is a point for further investigation. [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] Holm LE, Lundell G, Dahlqvist I et al. Cure rate after 131I therapy for hyperthyroidism. Acta Radiol Oncol. 1981; 20: 161-6. [17] Jones BR, Cayzer J, Dillon EA and Smidt KP. Radio-iodine treatment of hyperthyroid cats. N Z Vet J. 1991; 39: 71-4. [18] Kass PH, Peterson ME, Levy J, James K, Becker DV and Cowgill LD. Evaluation of environmental, nutritional, and host factors in cats with hyperthyroidism. J Vet Intern Med. 1999; 13: 323-9. [19] Klemperer JD, Klein I, Gomez M, Helm RE, Ojamaa K, Thomas SJ, Isom W and Krieger K. Thyroid hormone treatment after coronary bypass surgery. New Engl J Med. 1995; 333: 1522-7. [20] Kobayashi DL, Peterson ME, Graves TK, Lesser M and Nichols CE. Hypertension in cats with chronic renal failure or hyperthyroidism. J Vet Intern Med. 1990; 4: 58-62. [21] Langston CE and Reine NJ. Hyperthyroidism and the kidney. Clin Tech Small Animal Pract. 2006; 21: 17-21. [22] Malik R, Lamb WA and Church DB. Treatment of feline hyperthyroidism using orally administered radioiodine: a study of 40 consecutive cases. Aust Vet J. 1993; 70: 218-9. [23] Martin KM, Rossing MA, Ryland LM, DiGiacomo RF and Freitag WA. Evaluation of dietary and environmental risk factors for feline hyperthyroidism. J Am Vet Med Assoc 2000; 217: 853-6. [24] Meric SM, Hawkins EC, Washabau RJ, Turrel JM and Feldman EC. Serum thyroxine concentrations after radioactive iodine therapy Acknowledgements The authors would like to acknowledge the referral veterinarians and the owners of the cats for their cooperation. Special thanks goes to Mr. E.P.J.M. de Schrijver for his critical view and useful new ideas. References [1] [2] hyperthyroidism using 131I. Vet Radiol Ultrasound. 1997; 38: 2318. Becker TJ, Graves TK, Kruger JM, Braselton WE and Nachreiner RF. Effects of methimazole on renal function in cats with hyperthyroidism. J Am Anim Hosp Assoc. 2000; 36: 215-23. Belew AM, Barlett T and Brown SA. Evaluation of the white-coat effect in cats. J Vet Intern Med. 1999; 13: 134-42 . Broussard JD, Peterson ME and Fox PR. Changes in clinical and laboratory findings in cats with hyperthyroidism from 1983 to 1993. J Am Vet Med Assoc. 1995; 206: 302-5 . Chun R, Garrett LD, Sargeant J, Sherman A and Hoskinson JJ. Predictors of response to radioiodine therapy in hyperthyroid cats. Vet Radiol Ultrasound. 2002; 3: 587-91. DiBartola SP, Broome MR, Stein BS and Nixon M. Effect of treatment of hyperthyroidism on renal function in cats. J Am Vet Med Assoc. 1996; 208: 875-8. DiBartola SP and Brown SA. The kidney and hyperthyroidism. In: Bonagura JD. Ed. Kirk’s Current Veterinary Therapy XIII. WB Saunders, Philadelphia, 2000. pp 337-9. Edinboro CH, Scott – Moncrieff JC, Janovitz E, Thacker HL and Glickman LT. Epidemiologic study of relationships between consumption of commercial canned food and the risk of hyperthyroidism in cats. J Am Vet Med Assoc. 2004; 224: 879-86. Elliott J, Barber PJ, Syme HM, Rawlings M and Markwell PJ. Feline hypertension: clinical findings and response to antihypertensive treatment in 30 cases. J Small Anim Pract. 2001; 42: 122-9. Elliot J. Chronic renal failure in hyperthyroid cats: Diagnostic and therapeutic dilemmas. 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Changes in renal function in cats following treatment of 162 EJCAP - Vol. 19 - Issue 2 October 2009 [25] [26] [27] [28] [29] [30] [31] [32] [33] [34] [35] [36] in cats with hyperthyroidism. J Am Vet Med Assoc. 1986; 188: 1038-40. Meric SM and Rubin SI. Serum thyroxine concentrations following fixed-dose radioactive iodine treatment in hyperthyroid cats: 62 cases (1986-1989). J Am Vet Med Assoc. 1990; 197: 621-3. Merryman JI, Buckles L, Bowers G and Neilsen NR. Overexpression of c-ras in hyperplasia and adenomas of the feline thyroid gland: an immunohistochemical analysis of 34 cases. Vet Pathol. 1999; 36: 117-24. Mooney CT. Radioactive iodine therapy of feline hyperthyroidism: a simple method of dose estimation and comparison of intravenous and subcutaneous administration. J Small Anim Pract. 1994; 35: 289-94. Mooney CT. Hyperthyroidism. In: Ettinger SJ, Feldman EC. Ed. Textbook of Veterinary Internal Medicine: Diseases of the dog and cat. 6th ed. Elsevier Saunders, Missouri, 2005. pp 1544-60. Naan EC, Kirpensteijn J, Kooistra HS and Peeters ME. Results of thyroidectomy in 101 cats with hyperthyroidism. Vet Surg. 2006; 35: 287-93. Nap AM, Pollak YW, Van den Brom WE and Rijnberk A. Quantitative aspects of thyroid scintigraphy with pertechnetate (99mTcO4-) in cats. J Vet Intern Med. 1994; 8: 302-3. Nelson RW and Couto CG. Hyperthyroidism. In: Small Animal Internal Medicine, 3th ed. Mosby, Missouri, 2003. pp. 712-28. Nykamp SG, Dykes NL, Zarfoss MK and Scarlett JM. Association of the risk of development of hypothyroidism after iodine 131 treatment with the pretreatment pattern of sodium pertechnetate Tc 99m uptake in the thyroid gland in cats with hyperthyroidism: 165 cases (1990-2002). J Am Vet Med Assoc. 2005; 226: 16715. Peeters ME, Timmermans-Sprang EP and Mol JA. Feline thyroid adenomas are in part associated with mutations on the G(s alpha) gene and not with polymorphisms found in the thyrotropin receptor. Thyroid. 2002; 12: 571-5. Peterson ME, Kintzer PP, Cavanagh PG, Fox PR, Ferguson DC, Johnson GF and Becker DV. Feline hyperthyroidism: pretreatment clinical and laboratory evaluation of 131 cases. J Am Vet Med Assoc. 1983; 183: 103-10. Peterson ME, Becker DV. Radionuclide thyroid imaging in 135 cats with hyperthyroidism. Vet Radiol .1984; 25: 23-7. Peterson ME and Becker DV. Radioiodine treatment of 524 cats with hyperthyroidism. J Am Vet Med Assoc. 1995; 207: 1422-8. [37] Peterson ME, Melián C and Nichols R. Measurement of serum concentrations of free thyroxine, total thyroxine, and total triiodothyronine in cats with hyperthyroidism and cats with nonthyroidal disease. J Am Vet Med Assoc. 2001; 218: 529-36. [38] Peterson ME. Radioiodine treatment of hyperthyroidism. Clin Tech Small Anim Pract. 2006; 21: 34-9. [39] Puile M, Knietsch M, Spillmann T, Grünbaum E-G and Bauer R. Radioiodine treatment of feline hyperthyroidism in Germany. Nuklearmedizin. 2002; 41: 245-51. [40] Shirota T, Shinoda T, Yamada T and Aizawa T. Alteration of renal function in hyperthyroidism: Increased tubular secretion of creatinine and decreased distal tubular delivery of chloride. Metabolsim. 1992; 41: 402-5. [41] Slater MR, Komkov A, Robinson LE and Hightower D. Long-term follow-up of hyperthyroid cats treated with iodine-131. Vet Radiol Ultrasound. 1994; 35:204-9. [42] Slater MR, Geller S and Rogers K. Long-term health and predictors of survival for hyperthyroid cats treated with iodine. J Vet Intern Med. 2001; 15: 47-51. [43] Sparkes AH, Caney SM, King MC and Gruffyd-Jones TJ. Interand intraindividual variation in Doppler ultrasonic indirect blood pressure measurements in healthy cats. J Vet Intern Med. 1999; 13: 314-8. [44] Theon AP, Van Vechten MK and Feldman E. Prospective randomized comparison of intravenous versus subcutaneous administration of radioiodine for treatment of hyperthyroidism in cats. Am J Vet Res. 1994; 55: 1734-8. [45] Thoday KL and Mooney CT. Historical, clinical and laboratory features of 126 hyperthyroid cats. Vet Rec. 1992; 131: 257-64. [46] Turrel JM, Feldman EC, Hays M and Hornof WJ. Radioactive iodine therapy in cats with hyperthyroidism. J Am Vet Med Assoc. 1984; 184: 554-9. [47] Turrel JM, Feldman EC, Nelson RW and Cain GR. Thyroid carcinoma causing hyperthyroidism in cats: 14 cases (1981-1986). J Am Vet Med Assoc. 1988; 193: 359-64. [48] Watson SG, Radford AD, Kipar A, Ibarrola P, Blackwood L. Somatic mutations of the thyroid-stimulating hormone receptor gene in feline hyperthyroidism: parallels with human hyperthyroidism. J Endocrinol. 2005; 186: 523-37. [49] http://wetten.overheid.nl/kernenergiewet; Kernenergiewet, artikelen: 15, 15a, 28, 29, 29a, 30, 35, 37a. EJCAP special issue on Dermatology The ECJAP special issue 2009 is devoted to Dermatology. It will be an online issue only available on www.fecava.org in December 2009. If you have not already read the special issues of 2007 (ophthalmology) and 2008 (zoonoses), log on to www.fecava.org and download all the articles free of charge. www.fecava.org URINOGENITAL SYSTEM REPRINT PAPER (CH) Dystocia: recognition and management I. M.Reichler(1), E.Michel(1) SUMMARY The morbidity and mortality of bitches and queens and their offspring at parturition is significantly reduced by optimum veterinary care. Usually, the patient’s history already indicates that a parturition disorder may be present. If during physical examination a dystocia is confirmed, the cause of dystocia, the general condition of the dam and the foetal number and vitality are the cornerstones of the decision as to whether medical management or surgical therapy is indicated. As a consequence of scientific progress in veterinary medicine overall, and especially in veterinary anaesthesia, a caesarean section is the treatment of choice in a wide variety of conditions. Medical management of dystocia is indicated only if expulsion of all foetuses is possible via the birth canal without delay. If medical therapy fails, surgical intervention is mandatory. Keywords: abnormal parturition, dog, cat, obstetrics canine spermatozoa are capable of staying fertile in the female genital tract for a period of up to 7 days. Parturition date can be accurately predicted if the estimated date of ovulation at time of mating, using serum luteinizing hormone, or progesterone concentrations, is known: from the initial rise in preovulatory progesterone concentration, which is concurrent with the ovulatory surge in LH, gestation length in the bitch is 64-66 days [6,7]. Therefore a planned caesarean section should be scheduled on day 63. If ovulation timing has not been carried out, the first day of cytological dioestrus, and therefore whelping date, can be reliably estimated if daily vaginal cytologic smears are evaluated (table 1). This paper originally appeared in: Kleintierpraxis * 53(7) 2008 434-446 Introduction Dystocia is defined as the inability to expel the foetus through the birth canal without assistance. The incidence is around 5 per cent overall, but reaches almost 100 % in some breeds of dogs and 20 % in some breeds of cats [1-3]. Date of Delivery If the date of ovulation is unknown, estimation of parturition date using ultrasonography or radiology is recommended (table 1 and 2). In the second half of pregnancy the ability to determine the day of parturition within 2 days by measuring the biparietal diameter was 85% in bitches [8]. Ultrasonography and radiology are also suitable for estimation of date of delivery in the cat. Radiographic identification of teeth indicates that parturition will take place in the next 6 days [9]. Detection of foetal gastric rugal folds is first possible by ultrasound at day 5457 after mating [10]. Kittens with a skull diameter of 2.5 cm and A thorough knowledge of the physiology and endocrinology of normal parturition as well as an accurate prediction of the date of delivery is essential for the diagnosis and treatment of dystocia. In the cat, 94 % to 97 % of all deliveries take place between the 61st and 69th day of gestation, and the mean gestation length is 65 days [4,5]. Gestation and length, when timed from the first mating, is even more variable in the dog and can range from 57 to 71 days. This is because oestrus behaviour in the bitch is not necessarily most obvious at the time of ovulation and because (1) Small Animal Reproduction, Clinic of Reproductive Medicine, Vetsuisse-Faculty University Zurich, Winterthurerstr. 260, CH-8057 Zurich E-mail: [email protected] *Presented by SVK(Switzerland) 165 Dystocia: recognition and management - I. M.Reichler, E.Michel Method Parameter Ovulation timing Progesterone Days before Parturition (DbP) Increase from 0.3-0.8 to 0.9-3 ng/ml (preovulatory LH surge if progesterone continues to increase the next day) DbP = 63-67 3.4-6.6 ng/ml (ovulation) DbP = 61-65 Early pregnancy: >25 Days before Parturition Vaginal Cytology Degree of cornification of superficial cells, shift to dioestrus DbP = 51-60 Ultrasonography Crown-rump length (CRL in cm) DbP = 38-3xCRL Chorionic cavity diameter (CCD in cm) DbP = 45-6xCCD Late pregnancy: <25 Days before Parturition Ultrasonography Radiography Progesterone Drop in body temperature Biparietal diameter (BPD in cm) DbP = 45-(15xBPD) Body diameter at the gastric / hepatic level (BD in cm) DbP = 36-(7xBD) Biparietal diameter and body diameter (cm) DbP = 35-(6xBPD)-(3xBD) Mineralized pelvis DbP = 9-13 Teeth DbP = 3-8 4.5 ± 0.6 ng/ml DbP = 5 3.12 ± 0.4 ng/ml 40 - 32 hrs before parturition 1.19 ± 0.36 ng/ml 24 - 16 hrs before parturition 0.55 ± 0.07 ng/ml 12 - 8 hrs before parturition 1°C or more DbP = 0-1 Table 1: Criteria for Estimating Parturition Date in Bitches [6, 13, 41]. place in the last 24 hours prepartum, causes a transient rectal temperature drop (1°C or more) in many bitches. This temperature drop can be recognised by monitoring rectal temperature two to three times daily and is considered a trustworthy indicator of imminent parturition [13]. However, predicting onset of whelping/kittening by measuring rectal temperature in the bitch is not always possible [12] and in the cat is usually impossible. Increasing litter sizes are associated with a shorter gestation period [4,14]. Breed also affects gestation length: Korat cats a body diameter of 4 cm at the level of the liver are considered to be mature [11]. The rapid decline in serum progesterone is a reliable predictor of impending parturition (table 1 and 2). If signs of impending parturition are unclear, determining plasma progesterone concentration using commercial assay kits also used for estimating the time of ovulation is a suitable method of detecting onset of labour [12]. The decrease in serum progesterone, which takes Table 2: Criteria for Estimating Parturition Date in Queens (42-44) Method Parameter Days before Parturition (DbP) Mating date Ultrasonography DbP = 65 (61 - 69) Body diameter at the gastric / hepatic 2.0 cm level (in cm) 3.0 cm Biparietal diameter (in cm) Radiography Crown-rump length (in cm) DbP = 8 - 12 3.5 cm DbP = 4 - 8 4.0 cm DbP = 0 - 1 1.5 cm DbP = 21 - 25 2.0 cm DbP = 9 - 13 2.5 cm DbP = 0 - 1 13.0 cm DbP = 7 13.6 cm DbP = 5 14.5 cm Progesterone DbP = 18 - 22 DbP = 0 Molar teeth DbP= 2 - 9 4 - 5 ng/ml DbP =0 - 2 2 ng/ml DbP = 0 166 EJCAP - Vol. 19 - Issue 2 October 2009 Fig. 1: Bitch, first stage of parturition A: Closed cervix B: Beginning of cervical dilatation C: Liquifying of cervical plug D: Discharge of a cloudy mucus clinical examination and whether signs of dystocia are present. Questions asked should include the following: – Maternal well-being – Accurate mating date (first and last matings). Bitch: Has optimum mating date been determined? Is gestation prolonged? – Age of the dam (risk of uterne inertia and singleton pregnancy increases with increasing age of the dam) – Breed (brachycephalic breeds have a higher risk of dystocia) – Has pregnancy been confirmed, has the number of the foetuses been determined? (In singleton and twin pregnancies dystocia is much more common) [2,17]) – Number and course of previous parturitions – 41 % of all cases of dystocia are encountered in primiparous animals (the birth canal in primiparous animals is still narrow, so foetuses are often relatively oversized) – Any previous history of dystocia? – Are there any indicators that the dam has suffered a pelvic trauma since the last parturition? – Have any diseases, and especially metabolic disorders, been diagnosed during pregnancy? – Are there any signs that parturition has begun? – Bitch: Drop in rectal temperature – Vaginal discharge (Green vaginal discharge in the bitch and brown-reddish vaginal discharge in the queen before delivery of the first puppy / kitten indicate the beginning of placental separation. Haemorrhagic vaginal discharge is a sign of genital tract injury. Foul smelling vaginal discharge indicates a neglected, or overdue, birth.) – Passage of foetal fluids, straining. – Are there any neonates already delivered? When was the last one born? – Were any drugs given to the dam during pregnancy or parturition? (It is very common practice among breeders to administer oxytocin without seeking veterinary advice [3].) and German Shepherd dogs have the shortest gestation period compared to other breeds [4,14]. Stages of Parturition Parturition can be divided in three stages. The first stage, the “dilatation period”, lasts about 6 to 12 hours in the bitch (up to 24 hours in primiparous bitches), but usually less than two hours in the queen. It is characterised by the abrupt decline in progesterone, the concurrent onset of myometrial contractions which are not visible externally and cervical dilatation, which is recognisable by a cloudy mucous vaginal discharge (figure 1). The dam may be restless and seeking attention or seclusion. Maternal heart rate and respiratory rate increase. The second stage of parturition, the “expulsive period”, is characterised by strong myometrial contractions and the onset of abdominal straining. As the foetus enters the birth canal, the chorioallantoic membrane ruptures and a clear vaginal discharge is noted. About 60 per cent of all puppies / kittens are born in anterior, presentation the remaining 40 per cent in posterior presentation [13]. In the bitch, expulsion of the puppy should be achieved after 30 minutes of active straining. In the queen, expulsion of the kitten usually lasts 5 minutes, but, rarely, may be longer with the first kitten. The third stage of parturition, during which expulsion of the foetal membranes take place, follows 5 to 15 minutes after the delivery of each foetus. In polytocous species like the canine and feline, expulsion of one or two foetuses is followed by the passage of their placentae, as the foetuses are usually expelled alternately from the two uterine horns. Normally, the dam frees the neonate by licking the foetal membranes away and severing the umbilical cord. Rarely, but especially in canine brachycephalic breeds, the dam needs assistance. As eating of the placentae can induce vomiting in the dam, it is prevented by most breeders. In the bitch, a rest period of 0.5 to 4 hours between the expulsion of two puppies is not abnormal. In the queen, however, kittens are usually born in quick succession. Overall, parturition in the bitch lasts about 12 hours, and in the queen 6 hours. Increasing age of the dam tends to be associated with a longer expulsive period [2,15]. Anecdotally, the delivery of healthy puppies or kittens 37 to 48 hours after beginning of parturition has been reported [4]. Increasing delivery time is associated with a lower survival rate of the offspring [16]. Indicators of possible dystocia, which make an immediate veterinary examination imperative, are listed in table 3. As veterinary advice given on the telephone can sometimes be the subject of legal conflicts, one should minutely document the conversation and make sure that pre-existing disorders and treatment measures that have already been instituted are recorded. Critical parameters which make presentation of the dam mandatory have to be discussed with the owner. Full details, and the time of the conversation, must be noted in the case history. If any doubt remains that the parturition is progressing normally, the dam should be presented to a veterinarian. Evaluation and Diagnosis of Dystocia Usually, if an owner suspects dystocia, they will initially seek advice over the telephone. By taking a thorough history, the veterinarian will be able to decide whether the dam needs 167 Dystocia: recognition and management - I. M.Reichler, E.Michel Causes of Dystocia Bitch: Traditionally, dystocia is considered to be of either maternal or foetal origin (table 4), the former being more common [2,18-20]. Often however, a combination of different causes is responsible for dystocia, and one can rarely diagnose them purely by obstetric examination. To meet the needs of the clinician, it is more useful to differentiate between a dystocia which occurs before the delivery of the first puppy or kitten, and one which occurs after this (table 5). 1) Before delivery of the first puppy: a) More than 68 days from day of last mating, no signs of impending parturition b) More than 24-36 hrs from rectal temperature drop, no signs of impending parturition c) Rectal temperature has returned to normal, no signs of impending parturition d) Passage of foetal fluids before onset of abdominal straining e) Persistent abdominal straining for more than 30 minutes without delivery of a puppy f) Intermittent abdominal straining for more than 4 hrs without delivery of a puppy g) Green vaginal discharge (beginning of placental separation) Primary uterine inertia is defined as failure to induce expulsive contractions despite a completed period of dilatation and a non obstructed birth canal. In a study of dogs presented with dystocia, primary uterine inertia was the cause in 22.5% [21]. A breed predisposition seems to exist for the dachshund, some small terrier breeds, the chihuahua, the bulldog and the welsh corgi. In dolichocephalic cat breeds, primary uterine inertia is the most common cause of dystocia, accounting for 41 % of all dystocias. As cats of these breeds tend to be nervous, taking the queen to a quieter environment may help. If no additional causes of dystocia are present, one can try to treat primary uterine inertia conservatively. Secondary uterine inertia occurs when after initially normal labour activity the myometrium is fatigued and contractions stop. Possible causes are large litters, aged dam or obstruction of the birth canal. If obstruction of the birth canal can be excluded, only one or two foetuses remain to be delivered, and the dam is not exhausted, conservative treatment may be tried. 2) After delivery of the first puppy: a) More than 2 hrs since the birth of the last puppy b) Persistent abdominal straining for more than 30 minutes without delivery of a puppy 3) Abnormal: foul smelling,or haemorrhagic vaginal discharge 4) Presence of a puppy stuck in the birth canal 5) Maternal compromise (persistent whining or crying, abnormal posture, apathy, tremor, dyspnoea) Queen: One possible cause of obstructive dystocia is foeto-maternal disproportion. In brachycephalic breeds such as the scottish terrier and the welsh corgi, foeto-maternal disproportion is more common. Depending on the breed, either the foetal head or shoulders may be too large or the maternal pelvis too narrow [22-24]. In singleton or twin pregnancies, the foetus may be absolutely oversized and therefore cannot be delivered by the natural route. If a foetal malformation such as anasarca, schistosoma reflexum, hydrocephalus or conjoined twins is present, the foetus usually is too large for the birth canal and has to be delivered surgically. Dead foetuses may occasionally cause an obstructive dystocia, especially if the first foetus to be delivered is dead or if massive emphysema formation has already taken place. Further causes of obstructive dystocia are faulty foetal position such as transverse presentation, lateral or ventral deviation of the head or breech presentation (especially where the first pup in a primiparous dam is concerned). If manual reposition is not possible, caesarean section is indicated. Furthermore, obstructive dystocia may also be caused by pathological alterations of the soft or bony tissue of the birth canal (pelvic fractures, tumours, vaginal prolapse, congenital malformations of the uterus, the vagina, or the vestibulum). 1) Before delivery of the first kitten: a) More than 69 days from day of last mating with no signs of impending parturition b) Intermittent abdominal straining for more than 2 hrs without delivery of a kitten c) Haemorrhagic vaginal discharge d) Passage of foetal fluids before onset of abdominal straining e) Persistent abdominal straining for more than 5 minutes without delivery of a kitten 2) After delivery of the first kitten: a) More than 2 hrs since the birth of the last kitten b) Queen does not take care of her offspring c) Persistent abdominal straining for more than 5 minutes without delivery of a kitten 3) Abnormal: foul smelling, or hemorrhagic vaginal discharge 4) Presence of a kitten stuck in the birth canal (a kitten which protrudes from the vulva should be delivered within 3 to 5 minutes) 5) Maternal compromise Clinical examination Clinical examination consists of a general examination as well as a vaginal exploration (digitally performed with sterile gloves and vaginoscopically), which gives information about width and lubrication of the birth canal, relaxation of the vagina and Table 3: Indicators of Dystocia 168 EJCAP - Vol. 19 - Issue 2 October 2009 Foetus Dam Foetal oversize: – Singleton or twin pregnancy – Small litter size – Prolonged gestation – Genetic predisposition (breed / brachycephaly) – Broad shoulder / broad head Pelvic constriction: – Genetic predisposition (breed) – Age (juvenile) – Previous pelvic fractures – Neoplasia – Malformation of the pelvis – Diet-related Abnormal development: – Malformation of the head (hydrocephalus) – Malformation of the limbs (number, formation) – Anasarca / ascites – Foetal death – Schistosoma reflexum Abnormalities of the caudal reproductive tract – Cervix: – Inflammation – Hormonal – Congenital – Vagina Vestibule: – Stricture, Septum – Hypoplasia – Vagina duplex – Neoplasia – Trauma – Hyperplasia / prolapse – Inflammation / fibrosis – Vulva: – Stricture – Recessed vulva – Hormonal – Inflammation/Fibrosis Faulty foetal position: – Presentation: – Transverse presentation – Simultaneous presentation of two foetuses – Posture: – Lateral deviation of the head – Ventral deviation of the head Table 4: Foetal and maternal factors in dystocia [45] Disorders of expulsion (uterine causes) 1. Primary uterine inertia: – Genetic – Overstretching: large litter, locally: large puppy – Hormonal – Infectious – Hypocalcemia 2. Secondary uterine inertia: – Prolonged expulsive period – Dystocia 3. Abnormal position of the uterus: – Uterine herniation – Uterine torsion 4. Uterine rupture 5. Uterine neoplasia 6. Placentitis/adhesions sometimes about foetal position. If palpation (“feathering“) of the dorsal vaginal wall triggers an episode of involuntary straining, uterine inertia can be excluded as the cause of dystocia. The foetus can often be made palpable by the induction of abdominal contractions, and possible malpresentations can be diagnosed. If the foetus is out of reach, the abdominal wall can be lifted with one hand. If the cause of dystocia cannot be determined by palpation of the vagina, examination of the birth canal using a vaginoscope or pediatric proctoscope with a large diameter is performed. To get additional information, imaging methods can be used. Radiographic images must always be obtained in two radiographic planes to avoid misinterpretation (figure 2). They give information about the number of foetuses, the developmental stage, abnormal presentation, position or posture and foeto-maternal proportion. Depending on the breed, there are different pelvic constrictions which may cause dystocia [24, 25]. An assessment of whether birth via the natural route is possible can be obtained by calculating the ratio of the broadest transverse diameter of the foetal skull to the horizontal diameter of the maternal pelvis on a ventrodorsal radiograph. If the ratio is greater than one, the probability of vaginal delivery is reduced. If the ratio is greater than 1.25, vaginal delivery is highly unlikely [26]. Radiographically, foetal death cannot be diagnosed sooner Disorders of expulsion (extra-uterine causes): 1. Diaphragmatic hernia 2. Tracheal rupture 3. Pain 4. Fear 5. Drugs (progesterone, anaesthetic agents) 6. Muscle weakness 7. Obesity (excessive perivaginal fat) 169 Dystocia: recognition and management - I. M.Reichler, E.Michel Before birth of the first puppy/kitten Good general condition of the dam, foetal heart rate (HR) > 180/min → wait Cervix closed or incompletely dilated Bad general condition or HR < 150-180/min → caesarean section Lubrication, palpation → Initiation of abdominal straining, manual traction synchronous with abdominal straining, may use haemostatic forceps if foetus is dead Foetus has entered the pelvic canal, normal presentation Birth canal too narrow, only one foetus → episiotomy more than one foetus → caesarean section Tentative diagnosis: obstructive dystocia (abnormal presentation or posture, malformation, foeto-maternal disproportion) → caesarean section Amniotic fluid passed, strong abdominal straining, foetus has not yet entered the pelvic canal Secondary uterine inertia because of obstructive dystocia → caesarean section No abdominal straining, amniotic fluid passed, foetus has not yet entered the pelvic canal, cervix dilated No obstruction: • Primary uterine inertia (age, dead foetuses, unusually large litter, singleton pregnancy…) • Uterine rupture (oxytocin?) • Uterine spasm • Hypocalcemia • Stress, obesity Good general condition of the dam and ≤ 2 foetuses and HR>150-180/ min → try conservative management (infusion, lubricants, agents to relax the contracting pregnant uterus or udilated cervix, oxytocin) > 2 foetuses, or HR<150180/min or poor general condition of the dam → caesarean section After birth of the first puppy/kitten Strong abdominal straining, foetus has not yet entered the pelvic canal, cervix dilated Tentative diagnosis: obstructive dystocia (abnormal presentation or posture, malformation, foetomaternal disproportion) → caesarean section Secondary uterine inertia because of obstructive dystocia → caesarean section No abdominal straining, normal foetal position No obstruction: • Secondary uterine inertia (uterine fatigue, exhaustion of the dam) Good general condition of the dam and ≤ 2 foetuses and HR>150-180/min → try conservative management (infusion, lubricants, tocolytic agents, oxytocin) Table 5: Aids to decision making in managing dystocia 170 > 2 foetuses, or HR<150180/min or poor general condition of the dam → caesarean section EJCAP - Vol. 19 - Issue 2 October 2009 than six hours post mortem [1]. Radiographic signs of foetal death include, presence of gas within the foetuses and collapse of foetal skull bones. To determine foetal viability, foetal heart rate is evaluated ultrasonographically. Healthy puppies physiologically have a heart rate above 200 beats per minute, healthy kittens, possibly above 220 beats per minute. Heart rate can fall as a consequence of foetal distress, for example hypoxia caused by premature placental separation, but also during straining [1]. If the heart rate of a foetus is permanently below 180 beats per minute, the authors recommend a caesarean section. Laboratory examinations complete the assessment of maternal health status. Important parameters are packed cell volume, total protein, urea, glucose and calcium [27]. Management Obstetric procedures include conservative techniques such as delivery by traction, and surgical interventions such as episiotomy and caesarean section. If dystocia is diagnosed, surgical intervention is required in 60 to 80% of cases [17,18,28]. The incidence of dystocia is around 5% [1,4,5]. Overall, the probability of delivering all foetuses alive is significantly higher in elective caesareans than in emergency ones [29]. The reasons for the poorer outcome of emergency caesarean sections are that patients presented with dystocia have often been in labour for several hours, that maternal and/or foetal compromise have occurred, and that insufficient time and staff members are available for optimum management. Therefore, a caesarean section should be planned whenever preliminary examinations indicate that a normal parturition is not possible for anatomical reasons, for example foeto-maternal disproportion. In singleton pregnancies, the foetus is commonly grossly oversized, preventing a natural delivery. If a singleton pregnancy is recognised before the foetus has become too large, and if the ovulation date is known, induction of parturition with aglépristone, with or without additional oxytocin or prostaglandin, can be considered as an alternative to caesarean section [30-32]. Induction of parturition may also be indicated if gestation is prolonged and normal vaginal delivery is still possible [33]. The induction of a premature delivery can result in the expulsion of non-viable foetuses, and retention of foetal membranes is common. Therefore, an accurate prediction of the date of delivery – which is difficult in practice - is a prerequisite for inducing labour [34]. A thorough monitoring of the course of parturition, including evaluation of foetal heart rates, is strongly recommended, as surgical invervention is sometimes necessary. A dose of 15 mg/kg aglépristone was administered subcutaneously to Beagle bitches in which ovulation dates had been determined, on the 58th day of gestation. After 24 hours, an initial dose of either 0.15 IU/ kg oxytocin or 0.08 mg/kg alfaprostol were administered, and then repeated every two hours until all puppies were born. The combination of aglépristone and oxytocin was found to achieve better survival rates and result in fewer side effects [30]. The owner must always be informed about the risks of induction of parturition. Fig. 2: Queen presented with secondary uterine inertia: Radiographs have to be taken in two planes for assessing dystocia. A: Latero-lateral radiograph B: Faulty foetal position (transverse presentation is clearly visible). malformations can be ruled out. In addition to this, medical treatment may be considered only if the general condition of the dam and the offspring is still good (foetal heartrate > 180 beats per minute). If more than two foetuses remain to be delivered, the authors recommend a caesarean section. Before therapeutic measures are taken, clinical findings, treatment options, and their advantages and disadvantages must all be discussed with the owner. Medical Management of Dystocia is only indicated where the birth canal is fully dilated and faulty foetal position, absolute or relative foetal oversize, and birth canal constrictions or Medical management of dystocia is always performed while concurrently administering parenteral fluids, and includes the 171 Dystocia: recognition and management - I. M.Reichler, E.Michel application of drugs, and vaginal instillation of a warm substitute for foetal fluids, as well as manipulative delivery. Several different treatment protocols (with or without application of a tocolytic agent or calcium gluconate) and different oxytocin dosage schemes are described [17,27,35,36]. At the authors’ clinic, the dam is infused (Lactated Ringer’s solution at an infusion rate of 10 ml/kg/hr, for small patients 2.5 % glucose may be added), and a tocolytic agent (denaverin© 20-60 mg/ animal) is administered. About 20 minutes later a warmed substitute for foetal fluids is instilled into the uterus using a soft rubber catheter (NB: the volume instilled should not exceed the estimated volume of one foetus), and 1-2 IU oxytocin / animal is injected intramuscularly. If necessary, administration of oxtytocin can be repeated once to twice 20 to 30 minutes later. Alternatively, the dam can be infused for 20 minutes with a Lactated Ringer’s solution containing calcium gluconate and glucose (mix 250 ml of Lactated Ringer’s Solution with 12.5 ml of 50% glucose and 10 ml of 10% calcium gluconate) at an infusion rate of 10 ml/kg/hr, while the dam’s heart rate is monitored. If by palpating the dorsal vaginal wall abdominal straining can be initiated, insufficient contractions can be treated by intramuscular administration of oxytocin. No more than two doses should be given 20 minutes apart. The disadvantages of oxytocin treatment include the short duration of action, the risk of premature placental separation, and of tonic uterine spasm, (the latter being especially common if high or repeated doses of oxytocin are given). Uterine tetany, besides causing interruption of the placental blood flow and therefore foetal hypoxia, can result in uterine rupture. If failure of conservative treatment is likely, a caesarean section should be performed without delay to ensure optimum conditions for maternal health and viability of the offspring [1-4,37,38]. inspected for presence of cleft palate. The neonate is rubbed on warmed bedding until it is dry. By rubbing the perineal region, urination and defaecation, as well as respiration, are stimulated. The umbilical cord is ligated 0.5–1 cm from the abdominal body wall and disinfected (chlorhexidine gluconate 3%). In order to optimise oxygen supply, an oxygen tube is held in front of the neonate’s nose. If signs of asphyxia are present, a centrally acting respiratory stimulant can be given: (Cropropamid - Crotethamid 1–2 drops given on the oral mucosa or Doxapram 1(–5) mg/ animal sublingual, s.c. or i.v.). When examining the puppy/kitten, one should pay special attention to the presence of congenital malformations such as umbilical hernia, hydrocephalus externus and atresia ani [40]. References [1]. Linde-Forsberg C, Eneroth A. Abnormalities in pregnancy, parturition, and the periparturient period. In: Ettinger SJ, Feldman CE, editors. Textbook of Veterinary medicine. Philadelphia: Saunders, W.B.; 2000: p. 1527-38. [2] Stengel B. Untersuchung über Auftreten und Verlauf von Geburtsstörungen bei der Hündin. München: LMU; 1997. [3] Trautmann A. Retrospektive Untersuchung von Geburtsstörungen und der Notwendigkeit von Kaiserschnitten bei den Hunderassen: französische Bulldogge, Tecke, Boxer und Berner Sennenhund. Hannover: Tierärztliche Hochschule Hannover; 2003. [4] Sparkes AH, Rogers K, Henley WE, Gunn-Moore DA, May JM, Gruffydd-Jones TJ, et al. A questionnaire-based study of gestation, parturition and neonatal mortality in pedigree breeding cats in the UK. J Feline Med Surg. 2006; Jun;8(3):145-57. [5] Root MV, Johnston SD, Olson PN. Estrous length, pregnancy rate, gestation and parturition lengths, litter size, and juvenile mortality in the domestic cat. J Am Anim Hosp Assoc. 1995 SepOct;31(5):429-33. [6] Concannon P. Canine Pregnancy: Predicting Parturition and Timing Events of Gestation. Recent Advances in Small Animal Reproduction 2000. [7] Kutzler MA, Mohammed HO, Lamb SV, Meyers-Wallen VN. Accuracy of canine parturition date prediction from the initial rise in preovulatory progesterone concentration. Theriogenology. 2003 Oct 1;60(6):1187-96. [8] Beccaglia M, Luvoni GC. Comparison of the accuracy of two ultrasonographic measurements in predicting the parturition date in the bitch. J Small Anim Pract. 2006 Nov;47(11):670-3. [9] Haney DR, Levy JK, Newell SM, Graham JP, Gorman SP. Use of fetal skeletal mineralization for prediction of parturition date in cats. J Am Vet Med Assoc. 2003 Dec 1;223(11):1614-6. [10] Zambelli D, Caneppele B, Bassi S, Paladini C. Ultrasound aspects of fetal and extrafetal structures in pregnant cats. J Feline Med Surg. 2002 Jun;4(2):95-106. [11] Beck K, Bladwin C, Bosu W. Ultrasound prediction of parturition in queens. Vet Radiol 1990;31(1):32-5. [12] Veronesi MC, Battocchio M, Marinelli L, Faustini M, Kindahl H, Cairoli F. Correlations among body temperature, plasma progesterone, cortisol and prostaglandin F2alpha of the periparturient bitch. J Vet Med A Physiol Pathol Clin Med. 2002 Jun;49(5):264-8. [13] Johnston SD, Root Kustritz MV, Olson PN. Canine parturition Eutocia and Dystocia. In: Johnston SD, Root Kustritz MV, Olson PN, editors. Canine and feline theriogenology. Philadelphia: Saunders, W.B.; 2001. p. 105-28. [14] Okkens AC, Hekerman TWN, de Vogel JWA, van Haaften B. Influence of litter size and breed on variation in length of gestation Manipulative Obstetrical Procedures should be performed only using sterile gloves and lubricants, after thoroughly cleaning the perineal area. Usually, correction of faulty foetal position by retropulsion is possible only if diagnosis is not delayed. If a foetus is stuck in the birth canal, prompt treatment is required to save its life. After intravaginal instillation of sterile lubricants, for example using a soft feeding tube, the vaginal vault surrounding the foetus is manually dilated. Using one’s index and middle fingers, the head of the foetus is positioned in anterior presentation, the caudal body in posterior presentation. Careful traction is applied in a caudoventral direction in the bitch, and in a caudal direction in the queen. Using obstetric forceps or applying traction to a single limb generally results in severe injury, therefore these manoeuvres should be avoided. If the foetus cannot be extracted, episiotomy is indicated. If manipulative procedures are impossible due to a narrow birth canal, or if more foetuses remain to be delivered, a caesarean section is indicated. An episiotomy incision is begun at the dorsal commissure of the vulval lips and extended midline 1-2 centimetres towards the anal sphincter. After delivery is complete, the incision is closed in three layers: Vaginal mucosa (inverting pattern into the vaginal vault), subcutaneous tissues and finally the skin [39]. Immediately after birth, the neonates are held head downwards and freed from foetal membranes. By applying gentle suction, the upper airways are cleared of fluid. Concurrently, the oral cavity is 172 EJCAP - Vol. 19 - Issue 2 October 2009 in the dog. Veterinary Quarterly. 1993;15(4):160-1. [15] Münnich A. Geburtsstörungen bei der Hündin. In: AGRH, editor. Neues aus der Reproduktionsmedizin beim Hund; 2008; Giessen: AGRH; 2008. [16] Sohst S, Münich A, Grüssel T, Sohst E, Busch W. Auswertung der klinischen Daten von Katzen mit Geburtsstörungen - eine Patientenstatistik. Kleintierpraxis. 2003;48(12):725-92. [17] Stolla R, Dusi-Färberer B, Stengel B, Schmid G, Braun J. Geburtsstörungen bei der Hündin: eine retrospektive Studie. Wien Tierärztl Mschr. 1999;86:145-9. [18] Darvelid AW, Linde-Forsberg C. Dystocia in the Bitch - a Retrospective Study of 182 Cases. Journal of Small Animal Practice. 1994 Aug;35(8):402-7. [19] Gaudet DA. Retrospective Study of 128 Cases of Canine Dystocia. Journal of the American Animal Hospital Association. 1985;21(6):813-8. [20] Gaudet DA, Kitchell BE. Canine Dystocia. Compendium of Continuing Education for the Practicing Veterinarian. 1985;7(5):406-16. [21] Polster K-J. Untersuchungen zur Häufigkeit, zu den Ursachen und der Therapie von Geburtsstörungen bei den Hündinnen eine statistische Auswertung von Patientengut. Berlin: Freien Universität Berlin; 2006. [22] Freak MJ. The whelping bitch. Veterinary Record. 1948;60:295301. [23] Heath JS. Indications and complications in cesarean section in the bitch. J Small Anim Pract. 1962;4:289. [24] Linde-Forsberg C. Pelvimetry to diagnose dystocia in the bitch. http:/wwwvincom/Members/Proceedings; 2003. [25] Eneroth A, Linde-Forsberg C, Uhlhorn M, Hall M. Radiographic pelvimetry for assessment of dystocia in bitches: a clinical study in two terrier breeds. J Small Anim Pract. 1999 Jun;40(6):257-64. [26] Farrow CS. Maternal-fetal evaluation in suspected canine dystocia: a radiographic prospective. Can Vet J. 1978 Jan;19(1):24-6. [27] Gendler A, Borourman JD, Graf KE. Konservative und operative Behandlung der Dystokie beim Hund. Tierärztliche Praxis. 2008;36(K):55-64. [28] Ekstrand C, Linde-Forsberg C. Dystocia in the Cat - a Retrospective Study of 155 Cases. Journal of Small Animal Practice. 1994 Sep;35(9):459-64. [29] Moon PF, Erb HN, Ludders JW, Gleed RD, Pascoe PJ. Perioperative risk factors for puppies delivered by cesarean section in the United States and Canada. J Am Anim Hosp Assoc. 2000 JulAug;36(4):359-68. [30] Fieni F, Marnet PG, Martal J, Siliart B, Touzeau N, Bruyas JF, et al. Comparison of two protocols with a progesterone antagonist aglepristone (RU534) to induce parturition in bitches. J Reprod Fertil Suppl. 2001;57:237-42. [31] Arnold S, Hubler M, Reichler I. Weiblicher Geschlechtsapparat. In: Niemand H, Suter P, editors. Praktikum der Hundeklinik. Berlin Parey Buchverlag; 2006. p. 890-2. [32] Baan M, Taverne MA, Kooistra HS, de Gier J, Dieleman SJ, Okkens AC. Induction of parturition in the bitch with the progesteronereceptor blocker aglepristone. Theriogenology. 2005 Apr 15;63(7):1958-72. [33] Riesenbeck A, Klein R, Hoffmann B, Hospes R. Geburtsinduktion infolge einer verlängerten Gravidität bei einer Hündin unter Verwendung eines ANtigestagens. Tierärztliche Praxis. 1999;27(K):186-8. [34] Wehrend A, Gergiev P. Erfahrungen mit der Anwendung des Progesteronantagonisten Aglepriston bei der Hündin und der Katze. Terärztliche Praxis. 2006;34(K):409-14. [35] Biddle D, Macintire DK. Obstetrical emergencies. Clin Tech Small Anim Pract. 2000 May;15(2):88-93. [36] Cain JL. Drugs used to treat reproductive disorders. Vet Clin North [37] [38] [39] [40] [41] [42] [43] [44] [45] 173 Am Small Anim Pract. 1998 Mar;28(2):395-410. Moon PF, Erb HN, Ludders JW, Gleed RD, Pascoe PJ. Perioperative management and mortality rates of dogs undergoing cesarean section in the United States and Canada. J Am Vet Med Assoc. 1998 Aug 1;213(3):365-9. Shille V. Diagnosis and management of dystocia in the bitch and queen. In: Bojrab M, editor. Current Techniques in Small Animal Surgery. Philadelphia: Lea&Febiger; 1983. p. 338-46. Arnold S, Hubler M, Reichler I. Pathologie der Geburt. In: Suter PF, Kohn B, editors. Praktikum der Hundeklinik. 10 ed. Stuttgart: Parey Verlag; 2006. p. 887-2. Trasch K, Wehrend A. Versorgung der Welpen nach der Geburt. In: Wehrend A, editor. Neonatologie beim Hund Hannover: Schlütersche Verlagsgesellschaft; 2008. p. 45-50. Mattoon J F , Nyland TG. Ovaries and uterus. In: Nyland TG, Mattoon JF , editors. Small Animal Diagnostic Ultrasound p.231249 2ed. Philadelphia: Saunders; 2002. Johnston SD, Root Kustritz MV, Olson PN. Feline parturition. In: Johnston SD, Root Kustritz MV, Olson PN, editors. Canine and feline theriogenology. Philadelphia: Saunders, W.B.; 2001. p. 4317. Johnston SD, Root Kustritz MV, Olson PN. Feline Pregnancy. In: Johnston SD, Root Kustritz MV, Olson PN, editors. Canine and feline theriogenology. Philadelphia: Saunders, W.B.; 2001. p. 41430. Yeager AE, Concannon P. Ultrasonography of the reproductive tract of the female dog and cat. In: Kirk R, Bonagura JD, editors. Kirk’s current veterinary therapy XII. Philadelphia: Saunders, W.B.; 1995. p. 1040-52. Wykes P, Olson P. Normal and abnormal parturition. In: Slatter D, editor. Textbook of Small Animal Surgery. 3rd ed. Philadelphia: Saunders; 2003. p. 1510-6. OPHTHALMOLOGY REPRINT PAPER (F) Hereditary retinopathies in the dog: genetic fundamentals and genetic tests C. André(1), G. Chaudieu(2), A. Thomas(3), O. Jongh(4), J-P. Jégou(5), S. Chahory(6), B. Clerc(7), P. Pilorge(8), O. Brenac(9) SUMMARY This paper aims to give an overview on the genetic aspects of PRA in canines through the following topics: 1. Fundamentals in genetics; 2. Advantages of dogs to study genetics for both human and dogs; 3. How to search for genes and mutations involved in hereditary diseases; 4. Update on the genes and mutations identified, responsible for hereditary retinal diseases; 5. Genetic tests: Definitions of a mutation genetic test, and a linkage genetic test; Quality of a genetic test: the methods used, the numbers of dogs and the populations analysed inside a breed; 6. Update on available genetic tests; 7. The role of the veterinary ophthalmologist in fundamental genetic research: example of an X-linked PRA in the Border Collie; 8. The place of genetic tests in ophthalmology for the practitioner. Key words: dog, gene mutations, genetic tests, retina, retinitis pigmentosa, PRA. for breeders. Far from being a real advantage, this situation is very difficult to control, for veterinarians and breeders. Indeed, veterinarians need to have an excellent knowledge of these genetic tests so that they can precisely advise breeders and owners on the relevance of performing a particular genetic test on a particular dog belonging to a particular breed, then to find the relevant laboratory to perform the genetic test and finally to interpret the result. In addition, veterinarians are often asked to participate in research programmes, by sending samples to geneticists. Until now, ophthalmology has been the most relevant discipline to develop genetics since the number of hereditary ocular This paper originally appeared in: Prat Méd Chir Anim Comp* (2008) 43, 75—84 Introduction Canine genetics is a quite recent discipline with ongoing fundamental research started as recently as 15 years ago, and with the development in real time of genetic tests allowing the diagnosis and the prediction of hereditary diseases that are readily available for veterinarians but are also available online (1) Institut de Génétique et Développement, UMR 6061, CNRS/Université de Rennes1, Faculté de Médecine, 2 Avenue du Pr Léon Bernard, F-35043 Rennes. (2) Clinique Vétérinaire Beaulieu, 2 Place Beaulieu, F-63400 Chamalières. (3) Antagene, Laboratoire de Génétique Animale, Immeuble Le Meltem 2 Allée des Séquoias, F-69760 Limonest. (4) Clinique Vétérinaire, 2 Rue Jacques, F-69259 Neuville sur Saône. (5) Clinique d’ophtalmologie Vétérinaire, 39 Rue Rouelle, F-75015 Paris. (6)(7) Ecole nationale Vétérinaire, Unité d’ophtalmologie, 7 Avenue du général de Gaulle, F-94704 Maisons Alfort. (8) Clinique Vétérinaire, 70 Rue Papu, F-35000 Rennes. (9) Clinique Vétérinaire St-Cyr, 7 Avenue du Médoc, F-33320 Eysines. Corresponding author: G. Chaudieu(2) E-mail: [email protected] * Presented by AFVAC(France). We are indebted to Elsevier for allowing us to reprint this paper in EJCAP. 175 Hereditary retinopathies in the dog: genetic fundamentals and genetic tests - C. André et al Genetic methods in canines and humans are different since the two populations are very different. The canine species is divided into 350 breeds, which have undergone directed selection: thus, breeds can be considered as genetic isolates. Humans have undergone a natural selection: the human population is highly mixed and thus very heterozygous along the entire genome (in a given region, the paternal and the maternal alleles of one gene are different). The main consequence of this situation is that recessive diseases are frequent in dogs, whereas they are fewer in the human population. Indeed, in dogs, inbreeding increases the chance that the mutated allele segregates twice in a dog; this situation is very rare in humans, except in inbred populations. In dogs, a mutation occurring in one of the dogs having founded the breed will consequently rapidly spread within the entire breed. Thus, canine geneticists have hypothetized that a clinical defect diagnosed in several dogs from a given breed will most probably be the same disease in the entire breed, and will result from a single genetic defect. The other consequence is that the frequency of these diseases is very high, reaching more than 20% of affected dogs for some diseases in different breeds, while in humans, the most frequent hereditary diseases only reach some 0.1% of the population. Finally, inherited diseases in dogs are spontaneous and mostly breed-specific. diseases in different breeds is very high and on the rise, with more and more ongoing genetic research programmes and the growing availability of genetic tests. Moreover, the first genetic tests were developed in ophthalmology. In this article, we will focus on canine progressive retinal atrophies (PRA), which have been described in more than 100 dog breeds [1-3], but the number of different breed-related eye diseases is also very high. This breed specificity for inherited eye diseases in the dog, a consequence of breeding practices, is a unique opportunity for geneticists to unravel their genetic causes in a given breed. This article aims to examine and explain the different steps of genetic testing involving veterinary practice: - from clinical diagnosis to identification of the genes and their mutations (from the veterinarian to the researcher); - from the identified mutations to the genetic tests (from the researcher to the diagnostic laboratory); - then from the disease to the genetic test (from the veterinarian to the diagnostic laboratory and vice-versa). It must be mentioned that, although several genes and their mutations responsible for recessive PRA have been identified and show a perfect correlation between the genotype (the responsible mutation) and the phenotype (declared PRA), the more the research advances, the more this simple configuration is becoming rare. Indeed, the expressivity of the disease, within the same breed, may differ and the mutations are not always fully penetrant (the mutation/disease correspondence is not always observed). We must keep in mind that the light transduction process and the complex protein pathway involved in the phototransduction retinal mechanism, can be modified by environmental factors or other still unknown minor genes effects. Advantages of studying the genetics of inherited retinopathies, especially PRA, in dogs for both humans and dogs Dogs are a valuable population to identify the many genes responsible for diseases that are identical in humans but have different genetic causes. The more than 100 breeds segregating different retinopathies, such as PRA, provide a useful resource for the identification of new retinopathy-causing genes and a unique model for treatments for homologous human retinal diseases [8, 9]. The strong founder effect and genetic drift occurring during the breeding of dogs have significantly reduced the genetic heterogeneity of diseases in each breed, making it easier to identify causal mutations in dogs than in humans. Several genes responsible for canine PRA have already been identified (Table 1). PRA is a clinically homogeneous group of diseases characterized by a loss of night vision in the first few years of life (2 - 5 years), followed by a progressive loss of the peripheral visual field and finally a total loss of vision, involving an initial loss of rods and then cone photoreceptors [2, 3, 10]. In dogs, age-at-onset differs between breeds. PRA are highly heterogeneous genetically, with several modes of transmission and a large number of genes and mutations involved. At present, some 10 genes and their mutations have been involved in different breeds used to investigate canine PRA (Table 1). Each kind of PRA generally occurs in only one or a few breeds, PRA-prcd being a notable exception, since more than 20 breeds are affected [11, 12]. Two X-linked PRA have been described both involving the RPGR gene (Retinitis Pigmentosa GTPase Regulator) with two different mutations in exon 15 in different breeds: XLPRA1 causing an immediate premature stop in the protein in the Siberian Husky and Samoyed, XLPRA2 causing a change in the protein sequence in a mongrel dog [13]. Some fundamentals in genetics The canine genome is organized into 39 chromosome pairs: 38 autosomal pairs and chromosomes X and Y (the human genome has 22 autosomal pairs and chromosomes X and Y). The genome size is estimated to be slightly smaller than the human one: 2.4 gigabases (2.4 billion nucleotides) versus 3 gigabases. The number of genes is also slightly lower: the number estimated in the dog 19,000 genes versus 21,000 in humans. The year 2005 was very important for canine genetics since a map of the genome, placing 10,000 canine genes was produced [4] and the nearly complete sequence of all chromosomes except Y was also published [5]. This improved knowledge made it possible to produce a more precise annotation of the canine genome than is available for the human genome: the vast majority of genes are shared by the two species, except a few genes that are specific in one or the other species or that have undergone specific duplications [6]. This is the case for gene families, for example the olfactory receptor gene family, more numerous in dog than in human, with 1200 and 900 genes respectively [7]. Most of the canine genes are annotated on the canine genome owing to their human orthologous genes, but the functions of all of them are far from well known. Indeed, the identification of genes and their mutations in different diseases and different species give functional information on genes themselves. Taking the orthologous human and canine genes by pairs shows that there are great similarities maintaining the same function. 176 EJCAP - Vol. 19 - Issue 2 October 2009 Gene Chromosome Disease Affected breeds Mutation References PDE6B Phosphodiesterase subunit CFA3 Rod cone dysplasia Type 1 (rcd1 et rcd1a) Irish Setter (rcd1) Nonsense W807X (TGG -> TAG) Subber et al., 1993 [22] Sloughi (rcd1a) 8 nucleotide insertion Dekomien et al., 2000 in exon 21 [32] PDE6A Phosphodiesterase subunit CFA4 Rod cone dysplasia Type 3 (rcd3) Cardigan welsh Corgi Del A1939 Petersen-Jones et al.,1999 [33] RHO Rhodopsin CFA20 Dominant PRA English Mastiff Bullmastiff Missense T4R Kijas et al., 2002 [34] Kijas et al., 2002 [35] PDC Phosducin CFA7 Photoreceptors dysplasia (pd) Type A-PRA Miniature Schnauzer Missense R82G (CGA->GGA) Zhang et al., 1998 [36] RPGR Retinitis Pigmentosa GTPase Regulator CFA X X-Linked Progressive Retinal Atrophy 1 (XLPRA1) Samoyed Siberian Husky Deletion GAGAA in exon 15 Zhang et al., 2002 [13] X-Linked Progressive Retinal Atrophy 2 (XLPRA2) Mongrel Deletion GA in exon 15 CNGB3 Cyclic Nucleotide Gated channel 3 CFA29 Achromatopsia-3 Alaskan Malamute Deletion removing all exons (Del 140kb) German Shorthaired Pointer Missense D262N in exon 6 Sidjanin et al., 2002 [24] RPE65 Retinal Pigment CFA6 Epithelium-specific protein 65kDa CSNB Congenital stationary night blindness Briard Deletion AAGA in exon 5 Veske et al., 1999 [37] NHEJ1 CFA37 NonHomologous EndJoining factor1 CEA Collie Eye Anomaly 8 breeds (1) 7.8 kb deletion in intron 4 Lowe et al., 2003 [38] Parker et al., 2007 [39] PRCD Progressive Rod Cone Degeneration CFA9 PRCD Progressive Rod-Cone 22 breeds (2) Degeneration C2Y Missense TGC ->TAC in exon 1 Zangerl et al., 2006 [11] RPGRIP1 RPGR Interacting Protein 1 CFA15 CORD1 Cone Rod Dystrophy 1 Miniature Longhaired Dachshund 44 nucleotide insertion Mellersh et al., 2006 [40] BEST1 (VMD2) Bestrophin 1 CFA18 CMR Canine Multi-focal Retinopathy English Mastiff, Bullmastiff, Dogue de Bordeaux, Great Pyrenees Cmr1 C73T Guziewicz et al., 2007 [26] Cotton de Tulear Cmr2 G482A (1) Australian Shepherd, Border Collie, Lancashire Heeler, Longhaired Whippet, Nova Scotia Duck Tolling Retriever, Rough Collie, Shetland Sheepdog, Smooth Collie. (2) List of breeds harbouring the prcd mutation, as listed in the Optigen web site (optigen.com): American Cocker Spaniel, American Eskimo Dog, Australian Cattle Dog, Australian Shepherd, Australian Stumpy Tail Cattle Dog, Chesapeake Bay Retriever, Chinese Crested Dog, Cockapoo, English Cocker Spaniel, Entelbucher Mountain Dog, Finnish Lapphund, Golden Retriever, Kuvasz, Labradoodle, Labrador Retriever, Lapponian Herder, Miniature and Toy Poodle, Nova Scotia Duck Tolling Retriever, Portuguese Water Dog, Spanish Water Dog, Swedish Lapphund. Table 1: Genes involved in canine retinopathies including Collie Eye Anomaly, specifying the affected breeds and mutations. Up-dates of this Table can be found on the web page of the CNRS : www-recomgen.univ-rennes1.fr/doggy.html genetic potential, as it has facilitated the identification of a number of dog genes and invaluable candidates for the homologous diseases in humans [17, 18]. This applied to retinal diseases and PRA in particular, with the example of the identification of a new canine gene (PRCD), responsible for PRAprcd in different dog breeds: recently, a mutation in this gene has also been identified in a human patient from Bangladesh affected with RP [11]. PRA are naturally occurring retinal diseases in dogs, and have a phenotype similar to that of Retinitis Pigmentosa in humans. Retinitis Pigmentosa (RP) is the most prevalent group of inherited retinopathies in humans, affecting about one in 3600 individuals [14, 15]. Until now, 54 loci for non-syndromic RP have been mapped, for which 39 genes have been identified [16]. Those genes account for an estimated 50% of RP cases [14]. In the last decade, the canine model has showed considerable 177 Hereditary retinopathies in the dog: genetic fundamentals and genetic tests - C. André et al How to search for genes and mutations involved in hereditary diseases ? genealogical and clinical data (Figure 1). This pedigree, delineating affected dogs, unaffected dogs and any obligate carriers, provides a hypothesis of the transmission mode. Practitioners are encouraged to perform pedigrees themselves, with the help of the breeder, to determine the type of transmission. This first confirms whether the disease is familial; if so, the transmission can be: - monogenic: one gene is involved in the development of the disease and the segregation follows Mendelian laws, with expected proportions of affected dogs according to the hypothesized transmission mode ; - multigenic: several genes are involved together to produce the disease and there are no expected proportions of affected dogs; - X-linked: X-linked transmission is the most frequent, males are predominantly affected, rare cases of females can be affected. Males are either affected or healthy, they cannot be carriers. These are the most frequent and easy to detect transmission modes (for details, see [19, 20]), but others can also be observed: - a maternal transmission (only females are affected) when the gene is carried by the mitochondrial genome; - incomplete penetrance (a proportion of dogs do not present the phenotype): this might stem from environmental causes and/or other unknown genes; - co-dominant situation, where 2 mutated genes are coexpressed and give an intermediate phenotype. For a monogenic transmission mode, the disease can be recessive, the most frequent case in dogs, or dominant. Depending on the mating, different proportions of affected and unaffected dogs are expected. In the case of a recessive disease, the disease may not be observed at each generation, since affected dogs must have both mutated alleles of the responsible gene; if only one allele is mutated, the dog is a carrier ; it will not be affected but Briefly, the first step consists in collecting samples: blood, to extract DNA and any tissue relevant for the study, to analyse gene expression. With the clinical and genealogical data, the construction of pedigree is followed by formulating a hypothesis on the transmission mode. The molecular genetics analyses generally involve taking several samples and a lot of expensive experiments followed by statistical analyses. Finally, when a gene and its mutation have been discovered, the correspondence between the mutation and the affected status must be checked on a large number of dogs of the same and different breeds, to ensure that this mutation is not a simple polymorphism possibly shared by several animals of several breeds. The ultimate experiments leading to the proof that the observed mutation is the real cause of the disease can take a long time, but are necessary to precisely understand the pathophysiology of the gene and its mutation in the disease. Sample collection and pedigree analyses Blood samples are needed for DNA extraction (to analyze the gene sequences) and any other tissue (e. g. retina) for RNA extraction (to analyse gene expression). All samples must be accompanied by the veterinary certification of the tattoo or/ and microchip number of the dog sampled, the clinical data (with relevant examinations: ophthalmoscopy, electroretinography [ERG], fluorescein angiography…) and the genealogical data. Any complementary analyses, for example histopathology of the retina in PRA, help understand the pathophysiology of the disease, and thus will help in the definition of metabolic candidate genes. The first step of the molecular analysis of a disease in a breed will consist in establishing a precise pedigree from all available Figure 1 : Example of the design of a pedigree, for an autosomal recessive transmission mode : use of Cyrillic software [41]. Males Females Affected dogs Carrier dogs Unaffected dogs 178 EJCAP - Vol. 19 - Issue 2 October 2009 Update on the genes and mutations identified that are responsible for hereditary retinal degeneration will transmit the disease. A dominant disease will show affected dogs in all generations and no carrier, since affected dogs have only one mutated allele out of two. Molecular genetic analyses to identify the causative gene(s) and mutation(s) Several methods can be used, depending on the transmission mode, the ability to collect families or unrelated cases and controls, the size of the breed, the pathophysiology of the disease, the knowledge of candidate genes, etc. Thus, prior to undertaking such investigations, it is important to know the pathophysiology, the transmission mode, the breed history, etc. These methods aim to identify a region on the chromosome which will be systematically associated with the “affected” status of the dogs. This region will then carry the gene and the responsible mutation. This research can be done through a family linkage approach, or a case-control approach. The family linkage approach analyses a set of 400 polymorphic markers (microsatellites) regularly spaced on the genome, on the members of a large family including three generations, with affected and unaffected dogs. The case-control approach consists in the analysis of a set of markers, at least 400 microsatellites or 10,000 Single Nucleotide Polymorphism (SNP) markers on cases (affected dogs) and controls (unaffected dogs), which are unrelated at the grandparent level, or as far as possible. The actual methods tend to use chips containing several thousands of SNP markers in a high throughput genotyping experiment. These analyses, while very rapid and powerful, are still extremely expensive. These approaches determine the physical links between markers whose positions are known on the chromosomes and the responsible gene. The region identified by the markers is called a locus. Several statistical treatments of the genotyping results are possible depending on the method and the population used [21]. The family linkage approach uses the LOD score value, which calculates the logarithm of the probability of linkage / probability of no linkage. If the linkage between the disease and a given marker gives a LOD score value over 3, it means that linkage is a 103-fold more probable than no linkage. The case-control approach uses p values, with theoretical significant values being over 10 -5. Other molecular genetics steps are then necessary to identify, in the locus, the precise sequence (a gene or a regulation sequence) and its mutation leading to the phenotype. At that time, good knowledge of the pathophysiology of the disease, any results obtained on gene expression in the adequate tissue, histopathology, and immunostaining results, and the knowledge of the causative gene in another species will help in defining candidate genes. These genes or chromosomal regions will be sequenced in healthy and affected dogs to determine the mutation. In dogs, more than 100 breeds are specifically affected by PRA, and each breed or group of breeds can have many genes involved in light transduction and retinal development. The list of genes given in Table 1 shows the presently known genes involved in inherited retinopathies and in the Collie Eye Anomaly (CEA), most of them segregating on a recessive mode [2, 3]. In each breed, incidence can be high, for example more than 5 % for PRA-prcd-affected English Cocker Spaniels, with some 15% carriers (Thomas A et al, unpublished data). For each clinical description in each breed [10], one may suspect a novel gene is being identified. However, the correlation between genotypes and phenotypes (age of onset, severity of the disease, etc.) is not always perfect: these situations are to be taken into consideration by practitioners and encourage researchers to pursue fundamental research on such diseases. A few examples of retinopathies for which the genetic test alone is not sufficient are listed below to exemplify the importance of a clinical examination and the problems sometimes encountered interpretating the results of a genetic test. These examples also show that when a genetic test has been developed, care must be taken in selecting the population used to validate the test. Rod and cone dysplasia type1 (rcd 1): The mutation originally identified in the Irish Setter responsible for rod and cone dysplasia (rcd1) corresponds to a point mutation in the PDE6B gene [22]. This mutation has been, at least in France, very rare in the Irish Setters population (1 case report in a 25-year period ; Chaudieu, unpublished data). However, another rare PRA segregates in this breed, with typical lesions of the fundus found around three to five years old [10] or later [23]. This situation illustrates that a clinical diagnosis is required and the existing genetic test is not sufficient. Progressive rod and cone degeneration (PRA-prcd): The Figure 2 : Rod-cone degeneration (Labrador Retriever, six years old) : right eye showing obvious signs of PRA-prcd including tapetal hyperreflectivity, narrowed blood vessels and pale optic disc; this dog is homozygous for the PRA-PRCD mutation. Validation of the mutation Once a mutation is found in the collected samples from affected dogs and not in healthy dogs from the collected samples, the perfect correspondence (total penetrance) of the mutation must be validated. This is done by the sequence of the mutation in the greatest number of dogs from the same breed and in dogs from other breeds, to rule out a possible polymorphism associated with the disease, but not causative of the disease. 179 Hereditary retinopathies in the dog: genetic fundamentals and genetic tests - C. André et al specified breeds. This means that a genetic test is to be used for and only for the specifications given by the diagnosis laboratory. Genetic tests will be used, either to confirm the diagnosis if the clinical examination needs to be completed or for prediction in a general breeding selection. - Genetic tests based on the mutation Today, most genetic tests are based on the search for the mutation in the appropriate genomic region. The mutations can differ from one disease to another, involving a nucleotide change of one or several nucleotides or a deletion of one or several bases up to large chromosomal segments. Depending on the mutation type, the surrounding sequence and the number of tests to perform, several techniques can be used. - Genetic tests based on the linkage Few genetic tests are still based on the detection of a linkage between the gene (usually still unknown) and one or several markers. The reliability of the test depends on the distance between the gene and the markers. The diagnostic laboratory proposing such tests must give an estimate of the reliability, after having analysed a large cohort of dogs from the same affected breed. Currently, the genetic test for the Schapendoes PRA is the only linkage test (Bochum University, Germany). Figure 3 : Rod-cone degeneration (Golden Retriever, 4 years old): right eye showing similar signs of PRA-prcd; this dog is not homozygous for the PRA-PRCD mutation. prcd point mutation (Figure 2) discovered in a yet unknown gene, thus called PRCD, recently published by G. Aguirre et al. [11, 12], presently concerns 21 dog breeds. However, in some breeds, the penetrance does not appear to be complete. This is the case for the English Cocker Spaniel in which, out of several hundreds dogs genetically tested, few dogs of french origin were homozygous for the PRCD mutation and did not declare the disease, even though they were more than 10 years old and having a normal ERG trace. Nevertheless, some of the descendants of such dogs have declared the disease at the usual onset times. Such situations show that for yet unknown reasons, the expressivity of the disease might differ within a breed and the practitioner can encounter unexpectedly late ages of onset (Thomas et al, unpublished data). On the contrary, in french Labrador Retrievers, 15% of dogs, clinically diagnosed with PRA-prcd signs are not homozygous for the PRA-PRCD mutation (Thomas A et al, unpublished data). This situation suggests that an other form of PRA might be present in this breed, due to a different mutation in the prcd gene or in another gene. The same situation is encountered in France in the Golden Retriever, in which the rare clinically diagnosed dogs with PRA-prcd signs (Figure 3) are neither homozygous not heterozygous for the PRA-PRCD mutation (Thomas A et al. unpublished data). Cone Dysplasia : this day blindness has been attributed to two different mutations in the same gene (CNGB3) in two different breeds: a point mutation in German Shorthaired Pointer dogs and a deletion of the entire gene in the Alaskan Malamute dogs from the USA [24]. Recently, the mutation was not found in affected Alaskan Malamute of australian origin [25]. This situation suggests that, inside a breed, populations from different countries might differ genetically. The advantages of genetic tests Genetic tests have several advantages. They : - are easy to perform, from a blood or a cheek swab sample; - are done on puppies or even on the sires and dams, such as a prediction test; - provide the same result throughout the life of the animal; - identify affected dogs, before they develop clinical signs (particularly important for late-onset genetic diseases such as PRA); - identify carriers (heterozygous, for a recessive inheritance mode). This information is crucial for breeders to differentiate dogs that will never transmit the disease allele (healthy dogs homozygous normal) from those, clinically healthy, but carrier, who will transmit the disease allele to half of the litter. Limits of a genetic test Present genetic tests only interrogate the (known) genetic defect of one gene, for one or several specified breeds. If a similar disease exists in a breed, caused by unknown mutations in the same gene or in another gene, these genetic defects will not be tested by the genetic test considered valuable for this breed. This happens when the ophthalmologist diagnoses a PRA in individuals of a breed that present a clear result (homozygous normal) for the known PRA genetic test in this breed: other than a technical error in the process from the sample to the genetic test result, this would indicate that another genetic cause is also responsible for another PRA type in this breed. Of course, genetic tests do not test for any acquired cause of the disease or for another eye disease; these are major reasons why clinical ophthalmological examination is required in purebred dogs. Genetic tests The aim of a genetic test Genetic tests aims to determine the status of the dog for one disease, by searching for one mutation in one gene, in one or several Practically : sampling the dogs The genetic test must be done on a sample from an identified animal: the veterinary practitioner must certify the sample to 180 EJCAP - Vol. 19 - Issue 2 October 2009 certify the truth of the identification of the dog, to prevent any error. Samples can be either blood on EDTA anticoagulant tubes, or cheek swabs, or any tissue containing enough nucleated cells to extract DNA. These sample types ensure a sufficient quality and quantity for the actual molecular genetics methods used (for example, hair bulb samples are not guaranteed, because of possible contaminations from another dog). Cheek swab sampling must be done to collect enough epithelial cells from the inside of the cheek and not only saliva. It is therefore important to brush the oral mucosa inside the cheek in a rotating movement for at least 10 s. An oral brush must be used and cotton tips are not possible. The brush is then placed in a tube of alcohol, mixed and kept at room temperature (alcohol preserves the DNA and avoids degradation and contaminations). Samples should be sent by ordinary mail, in a few days for the blood, a few weeks for the cheek swab. research. Then, it is a question of cost for the development of each test and of market price of the puppy for the breeder. In the near future, it could be anticipated that several genetic tests in a given breed could be analysed in one experiment. Update on available genetic tests Table 2 presents the state of the art on the available genetic tests for PRA. The indication of genetic tests for diagnosis and for prediction and their limitations have been discussed so as to give the best information, in terms of feasibility, reliability, validity, and interpretation. It is important to recall that presently, a genetic test is made for one disease in one breed at least, and it only tests the presence of one mutation, after it has been validated in a given population. This Table was updated in March 2008 and and includes a list of the genetic tests available with a list of the main diagnostic laboratories proposing these genetic tests in Europe and the United States. Carrying out the genetic test From these samples, the diagnosis lab extracts the DNA, and the mutation-carrying regions are amplified by Polymerase Chain Reaction (PCR). Then, several techniques are specifically applied: either another PCR, precisely targeting the mutation, or classical sequencing, or other dedicated methods, the aim being to determine the presence or absence of the mutation on both alleles. At present, these methods require dedicated techniques and equipment, which must be performed in a diagnosis laboratory. The reliability of a genetic test is analysed by the laboratory itself, by testing the reproducibility of the method and testing a large number of dogs in the same breed and in different countries, so that the frequency of the mutation in the breed and the penetrance of the disease (proportion of dogs carrying the mutation, that are clinically affected) can also be estimated. The role of the veterinary ophthalmologist in fundamental genetic research: example of an X-linked PRA in the Border Collie This section provides a rapid overview of the present research project led by the CNRS of Rennes, Gilles Chaudieu and the Antagene laboratory, on the genetic basis of a PRA in the Border Collie breed, whitin a context where four loci (RP6, RP23, RP24, RP34) and only two genes (RPGR and RP2) have yet been identified for X-linked human Retinitis Pigmentosa (RP), the equivalent human disease to canine PRA [26, 27]. Other genes causing human X-linked RP remain to be identified, even if known genes and loci involved in these diseases have already been excluded in several families [28]. To complete the list of canine genes potentially involved in human X-linked RP, we searched the genetic causes of PRA segregating with a high frequency in the Border Collie in France. This retinopathy has been described by Chaudieu in 2001 [29] in this breed as having a probable X-linked transmission mode. This PRA does not seem to be linked to CEA (excluded by genetic testing) and is not Central Progressive Retinal Atrophy (CPRA). In the present study, the clinical examination by indirect ophthalmoscopy of 487 Border Collie dogs from France demonstrated the highfrequency occurrence of PRA in the breed. Over 250 Border Collie blood samples were collected, most of them could be connected through a 375-dog pedigree. Segregation analysis suggested an X-linked mode of transmission. We excluded the possibility of the molecular cause of this PRA being a known mutation, by carrying out the genetic tests for XLPRA1 and XLPRA2. This result suggested that this PRA in Border Collies might correspond to a new form of X-linked PRA [30]. A genetic family linkage on a 159-dog pedigree, using a chromosome X genome scan with 100 microsatellite markers is ongoing. Genetic tests results When receiving the results, the veterinarian can interpret them with the breeder or/and the owner. A genetic test used for prediction will serve to plan selection, to anticipate breeding, etc. It is advised to breed only healthy dogs (homozygous normal dogs). However, in the case of carrier dogs (heterozygous dogs) presenting interesting or unique characteristics that the breeder wants to keep, or in cases of a small population, a heterozygous dog can be bred, but it should be bred with a healthy dog; the obtained litter should be tested and only healthy animals (homozygous normal) should be kept. This procedure will progressively diminish the prevalence of the disease in the breed, without excluding interesting dogs. Moreover, especially in small populations, one must be careful not to overly restrict genetic diversity by excluding lines of dogs. Indeed, the rapid exclusion of too many dogs will diminish the remaining genetic diversity, leading to the emergence of other genetic diseases. In conclusion, the practitioner should keep in mind that genetic tests are useful for confirmation of a diagnosis or for prediction to advise the breeder, but they should be complementary to clinical examinations. Will every disease in every breed, benefit from a genetic test? This depends first on the ability to perform fundamental 181 Hereditary retinopathies in the dog: genetic fundamentals and genetic tests - C. André et al Inherited Eye Disease Breeds Collie Eye Anomaly (CEA) Australian Shepherd, Border Collie, Longhaired Whippet, Lancashire Heeler, Nova Scotia Duck Tolling Retriever, Rough Collie, Shetland Sheepdog, Smooth Collie. Rod and cone dysplasia type 1 - rcd1 Irish Setter Rod and cone dysplasia type 1a – rcd 1a Sloughi Rod and cone dysplasia - rcd3 Cardigan Welsh Corgi Dominant Progressive Retinal Atrophy - RHO Mastiff, Bullmastiff X linked Progressive Retinal Atrophy XLPRA Siberian Husky, Samoyed –(RPGR) Cone dysplasia (day blindness, achromatopsia) Alaskan Malamute (CNGB3) Cone dysplasia (day blindness, achromatopsia) German Shorthaired Pointer (CNGB3) Progressive Retinal Atrophy progressive rod American Cocker Spaniel, American Eskimo Dog, Australian Cattle Dog, Australian cone degeneration (PRA-prcd) Shepherd, Australian Stumpy Tail Cattle Dog, Chesapeake Bay Retriever, Chinese Crested, Cockapoo, English Cocker Spaniel, Entelbucher Mountain Dog, Finnish Lapphund, Golden Retriever, Kuvasz, Labradoodle, Labrador Retriever, Lapponian Herder, Miniature and Toy Poodle, Nova Scotia Duck Tolling Retriever, Portuguese Water Dog, Spanish Water Dog, Swedish Lapphund. Photoreceptor dysplasia (Type A PRA) Miniature Schnauzer Cone Rod Dystrophy (crd1) Miniature Longhaired Dachshund Congenital stationary night blindness (csnb) Briard Canine Multifocal Retinopathy (CMR) Mastiff, Bullmastiff, Dogue de Bordeaux, Coton de Tulear, Great Pyrenees This list is not comprehensive and only contains the main laboratories proposing these genetic tests in Europe and the united States, updated March 2008. The number of such diagnosis laboratories is rapidly expanding. Up-dates of this Table can be found on the web page of the CNRS : www-recomgen.univ-rennes1.fr/doggy.html AHT (UK): www.aht.org.uk Antagene (F) : www.antagene.com Genindexe (F) : www.genindexe.com Laboklin (DE): www.laboklin.de Optigen (USA): www.optigen.com PennGen (USA): w3.vet.upenn.edu/research/centers/penngen/services/deublerlab/index.html Table 2 : List of the genetic tests available for PRAs and Colly Eye Anomaly, available in the following list of diagnosis laboratories. The place of genetic tests in veterinary practice References [1] Genetic tests for diagnosis or prediction should be not taken lightly. Practitioners should not simply propose the least expensive test available on the internet, but should propose and advise a genetic test either as part of a whole diagnosis process or for prediction. In this context, the role of the veterinarian is central in: - alerting the geneticist to a new hereditary disease: practitioner’s clinical examinations feed the researcher’s work; - being the authorized professional for the certification of the sample taken for research purposes or for carrying out a genetic test; - bringing together the breeder/owner and the diagnostic laboratory. The clinical examination remains the first act in investigating PRAs, then a genetic test can be proposed if it is relevant for the disease and the breed presented. [2] [3] [4] [5] [6] 182 Patterson DF. Companion animal medicine in the age of medical genetics. J Vet. 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Targeted Identification of New Genes and Gene Losses in the Domestic EJCAP - Vol. 19 - Issue 2 October 2009 [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] Dog Genome. Genome Research Submitted. Quignon P, Kirkness E, Cadieu E, Touleimat N, Guyon R, Renier C et al. Comparison of the canine and human olfactory receptor gene repertoires. Genome Biol. 2003; 4: R80. Acland GM, Aguirre GD, Bennett J, Aleman TS, Cideciyan AV, Bennicelli J et al. Long-term restoration of rod and cone vision by single dose rAAV-mediated gene transfer to the retina in a canine model of childhood blindness. Mol Ther. 2005; 12: 1072-1082. Le Meur G, Stieger K, Smith AJ, Weber M, Deschamps JY, Nivard D et al. Restoration of vision in RPE65-deficient Briard dogs using an AAV serotype 4 vector that specifically targets the retinal pigmented epithelium. Gene Ther. 2007; 14: 292-303. Chaudieu G. Affections oculaires héréditaires ou à prédisposition raciale chez le chien. 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Djajaniningrat-Laanen SC, Boevé MH, Stades FC and Van Oost BA. Familial non-rcd 1 generalised retinal degeneration in Irish Setters. J Small Anim Pract. 2003; 44: 113-6 Sidjanin DJ, Lowe JK, McElwee JL, Milne BS, Phippen TM, Sargan DR et al. Canine CNGB3 mutations establish cone degeneration as orthologous to the human achromatopsia locus ACHM3. Hum Mol Genet. 2002; 11: 1823-1833. Seddon JM, Hampson EC, Smith RI, Hughes IP. Genetic heterogeneity of day blindness in Alaskan Malamutes. Anim Genet. 2006; 37: 407-410. [26] Guziewicz KE, Zangerl B, Lindauer SJ, Mullins RF, Sandmeyer LS, Grahn BH et al. Bestrophin gene mutations cause canine multifocal retinopathy: a novel animal model for best disease. Invest Ophthalmol Vis Science. 2007; 48: 1959-1967. [27] Hardcastle AJ, Thiselton DL, Zito I, Ebenezer N, Mah TS, Gorin MB et al. Evidence for a new locus for X-linked retinitis pigmentosa (RP23). Invest Ophthalmol Visual Science. 2000; 41: 2080-2086. 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[33] Petersen-Jones SM, Entz DD, Sargan DR. cGMP phosphodiesterasealpha mutation causes progressive retinal atrophy in the Cardigan Welsh corgi dog. Invest Ophthalmol Vis Science. 1999; 40: 16371644. [34] Kijas JW, Cideciyan AV, Aleman TS, Pianta MJ, Pearce-Kelling SE, Miller BJ et al. Naturally occurring rhodopsin mutation in the dog causes retinal dysfunction and degeneration mimicking human dominant retinitis pigmentosa. Proc Natl Acad Sci U S A. 2002; 99: 6328-6333. [35] Kijas JW, Miller BJ, Pearce-Kelling SE, Aguirre GD, Acland GM. Canine models of ocular disease: outcross breedings define a dominant disorder present in the English mastiff and bull mastiff dog breeds. J Hered. 2003; 94: 27-30. [36] Zhang Q, Acland GM, Parshall CJ, Haskell J, Ray K, Aguirre GD. Characterization of canine photoreceptor phosducin cDNA and identification of a sequence variant in dogs with photoreceptor dysplasia. Gene. 1998; 215: 231-239. [37] Veske A, Nilsson SE, Narfstrom K, Gal A. Retinal dystrophy of Swedish briard/briard-beagle dogs is due to a 4-bp deletion in RPE65. Genomics. 1999; 57: 57-61. [38] Lowe JK, Kukekova AV, Kirkness EF, Langlois MC, Aguirre GD, Acland GM et al. Linkage mapping of the primary disease locus for collie eye anomaly. Genomics. 2003; 82: 86-95. [39] Parker HG, Kim LV, Sutter NB, Carlson S, Lorentzen TD, Malek TB, Johnson GS, DeFrance HB, Ostrander EA, Kruglyak L. Genetic structure of the purebred domestic dog. Science. 2004; 304: 1160-1164. [40] Mellersh CS, Boursnell ME, Pettitt L, Ryder EJ, Holmes NG, Grafham D et al. Canine RPGRIP1 mutation establishes cone-rod dystrophy in miniature longhaired dachshunds as a homologue of human Leber congenital amaurosis. Genomics. 2006; 88: 293301. [41] CyrillicSoftware http://www.cyrillicsoftware.com/. 183 PRACTICE MANAGEMENT COMMISSIONED PAPER* The Recession and how it is affecting or may affect Vets in Practice G. Little (1) SUMMARY As veterinarians in practice we continually find ourselves in the predicament of balancing the overriding desire to do our very best for patients and their owners and yet at the same time, those of us who are practice owners, need to keep a watchful eye on turnover, cash flow and profit. There needs to be enough of the latter to reward the practice team, to invest in equipment, to fund CPD and to provide a return to owners in recognition of their investment, input and level of risk. Our clients’ behaviour is no different from our own in the current economic climate. Research carried out by Onswitch in March this year with groups of dog and cat owners revealed that those with cash are less adversely affected as are those who never had credit. Those individuals who are feeling the real or perceived effects of the downturn are shopping around where “commodity items” are concerned, e.g. vaccinations, neutering, wormers and flea products. Some are trading down from premium to less expensive alternatives; others are staying with the products they have always purchased but are shopping around for a more competitive price; the temptation is for pet owners to increasingly seek advice from sources other than veterinary practices, e.g. pet shops and the internet. Never before has it been more important to maximise each and every interaction with our clients to ensure client footfall (number of potential clients who visit the practice), the health of our patients and indeed our practices. It is important for readers to bear in mind the title of this article and to appreciate its focus is on the business side of practice. It should be taken as read that finances should at no time override our professional desire and duty to do the best for our patients and their clients. Having said that, we need to remain profitable, thereby ensuring we are here in the future for our patients and their owners and that we are in a position to offer them the best possible care. Introduction have an extremely good idea as to how the current situation is impacting, or will impact on them and / or their businesses. Too many others will have no idea until they see their next set of annual accounts. They may well have perceptions based on gut feel, the number of free appointment slots, a downturn in number of operations, etc. etc. Those forecasts may well alter from one month to the next as they have a good or bad month followed by a reversal in fortunes the next. This in turn may well result in a series of knee jerk reactions. No country has escaped the effects or perceived effects of the global downturn and no doubt there will be practices out there which will have been or will shortly be adversely affected. There will be others where there will be minimal effect. Perception and fear have a good deal to answer for in where we find ourselves to-day. The trouble is that perception is the truth until proved otherwise and we have no choice but to deal with perceptions. And just like our clients, some practice owners will (1) 9 Thorn Road,Bramhall,Stockport, Cheshire,SK7 1HG E-mail: [email protected] * Geoff Little MVB MRCVS is a Veterinary Business Advisor and was, until 5 years ago, a general practitioner in the UK. He recently lectured on the subject of this paper to Veterinary Ireland , the parent association of FECAVA member, VICAS 185 The Recession and how it is affecting or may affect Vets in Practice - G. Little The truth is, when it comes to our businesses, there are factors which are outside of our control and some we can influence. In this article we will look at those we can directly affect and being the eternal optimist, can I suggest we should regard the ‘recession’ as a wakeup call or even an opportunity, to look at areas of our businesses which perhaps, because things have been stable in the past, we have neglected? We can see from the above, from a cost perspective we are far better concentrating on promoting existing services and products to clients we currently have. And where do the majority of new clients come from? As recommendations from existing clients who have been well looked after. And with that in mind, in this economic climate we need to be pulling out the stops to exceed clients’ expectations, not just matching them. The Challenges Turnover, Cash Flow Profit, and People What are the challenges we face? Each and every practice will face its own particular set of challenges. The truth is they always have done; it’s just that in the current situation, these have been brought into focus. And having been highlighted and brought into clear focus we would be very foolish to ignore them and not take action. When it comes to practice finances there is a limit to what owners have control over. In simplistic terms net profit is what is left after all the overheads have been accounted for. When it comes to maximising profit one must always have an eye on reducing overheads, but we must be careful in our paring away at the flesh that we do not hit an artery and bleed to death! The Fort Dodge Indices1 (FDI) have tracked the performance and activities of a significant number of UK practices for some years now and their latest quarterly report for the period ending March 2009, which compares results with the equivalent quarter for last year shows the following: Maximum results are always more likely to come from addressing the big numbers and in veterinary practice those are always going to be Purchases and Labour. It is always worth while shopping around to get the best deal, but that should not be based on price alone. Availability of products and quality of service are just as important, if not more so. And remember, you cannot sell what you haven’t got! • Turnover Growth has decreased to 0.7% from 1.1% • Transaction Volume Growth has decreased to -0.7% from -0.3% • Active Clients per vet has reduced to 984 • Active Patients per vet has reduced to 1499 • Average Transaction Value (ATV) has increased by 10.7% As has been commented on earlier, our clients are no different from ourselves. An important lesson here is, when clients are also phoning around for prices, as they will do in the current economic climate, we must provide them with more than price on which to make comparisons. There are a limited number of services and products that clients will phone around about. Typically that will include neutering and vaccinations. Because neutering is a common and routine procedure it is often regarded by clients as a simple process and because of that, maybe one that clients think should be inexpensive. To simply provide a quote or an estimate over the phone will probably result in the owner going for the cheapest option. Encouraging team members to talk about a hysterectomy (I wouldn’t normally encourage the use of medical jargon, but everybody is familiar with that term) immediately elevates the spay to a new level in terms of complexity and importance. If the receptionist goes on to talk about the monitoring of the anaesthetic by a qualified nurse, the provision of pain relief etc. etc. the inquirer now has a great deal more on which to base their decision. Your practice may not be the cheapest for the procedure, but the caring pet owner now knows you have qualified nurses who will be looking after their family member and that pain relief will be provided after the operation. They will wonder if the other practice they phoned that was cheaper will provide a similar level of care. And if you were to follow up the telephone conversation with a personalised letter the same day about your practice and the procedure, they will have something tangible. Another good reason to choose your practice over the others in your area. The overall message that comes out of the FDI is that the future is less optimistic in terms of practices being able to produce the 6 – 7% annual growth rate necessary to maintain growth above veterinary inflation. There are basically three main ways to achieve growth in business: • Increase the number of clients • Increase the number of visits per client • Increase the Average Transaction Value In simplistic terms we can see from the above that for the practices taking part in the FDI survey they have fewer clients with fewer pets but they are maintaining growth through a significant increase in the ATV; they are selling more services and products to a shrinking market. Looking at the challenge and the possible solutions from another perspective, the chart below shows the relative costs when it comes to services and products, existing and new clients: Sell existing services and products to existing client € 4 Sell existing services and products to new clients € 16 Sell new services and products to existing clients € 8 Sell new services and products to new clients € 32 Coming back to overheads. Whereas purchases will be the most significant overhead in monetary terms in large animal practice, labour will no doubt be the greatest in small animal practice. What can be done to reduce labour costs? I suggest this is not the time, except in extreme cases, to seek to reduce labour Relative costs of providing services and products to the market 186 EJCAP - Vol. 19 - Issue 2 October 2009 product ranges. It is well worth considering what the effect is of reducing margins further. costs. It may be a time to restrict the increase in costs, but people will always be a practice’s main asset. This is a time when people, both clients and team members are very precious and this is a time to look after them as we have never done so before. It is a time to invest in our teams in terms of training; it is a time to motivate them, encouraging them to promote our services and products. Generally speaking, the lower the margin the greater the number of additional products that will have to be sold to achieve the same level of profit. If for example the current margin is 25% on a particular item and you decide to drop your prices by 10%, how many more products will you have to sell to maintain the same level of overall profit? The answer is 66.7%. The Role of the Leader We are told that we need good leaders to find solutions to the world recession. Likewise, practices need good leaders, who once they have understood the challenges and opportunities can formulate a plan, and more importantly can convey that plan to the rest of the team, to ensure results, and will lead from the front. As your margin reduces and your generosity increases the numbers you have to sell becomes unrealistic as the table below demonstrates: Drop Your Price By: It has been said that many practices have bosses; some have leaders and even fewer have effective leaders. Good leaders require many qualities which they need to employ with varying degrees and combinations when faced with differing challenges; those who only have a hammer in their toolbox tend to see everything as a nail, often with disastrous results. What are the leadership qualities that are particularly useful in the present economic climate? 15% 20% 30% 40% You have to sell this much more to break even: 5% 50% 33.3% 20% 14% 10% 200% 100% 50% 33.3% 300% 100% 60% 15% Effect on sales of reducing margin Having the detailed information at your fingertips allows you to make informed decisions. Without the information it’s down to fortune. When times are good, fortune may smile on you, but when times are hard you need more than good fortune. Vision is the first one, in terms of being able to analyse the business to ascertain what is happening. Where is the profit made? Where are the losses occurring? Vision also in terms of formulating a plan for the future and vision to monitor the progress. When it comes to pricing products, too many practices still work on mark-up, taking the invoice price of an item and then apply a percentage increase to arrive at the selling price. It is much more relevant to look at margin instead. Margin is the percentage of the final selling price that is profit. One key thing to remember when calculating margin is to remember that our more business minded competitors, e.g. supermarkets and pet superstores may well have greater buying power (but not always) and they will be using their net net price (cost price less both manufacturer’s and wholesaler’s discounts) as their starting point when it comes to calculating the selling price. If we want to compete in selling the same products we too need to start from the same relative point. Key Areas of Lost Profit What are the most likely key areas of lost profit in practice? • • • • When your current margin is: Incorrect pricing structure Failure to convert inquiries into appointments Failure to rebook appointments Undercharging or not charging for services and products Correct Pricing Structure is the subject of an entire article in itself but in summary, a veterinary practice should understand where its profit is coming from. Turnover should be allocated to Profit Centres, with the sum of the individual profits from those centres providing us with the cumulative profit for the business. Only when the turnover is broken down into its component elements can you look at numbers of transactions and their unit prices to assess the effect of change. Having that information allows a business to budget for the coming year and if that information is available in an interactive spreadsheet, it allows you to ask the “What if?” questions. For example, when it comes to the sale of a particular products one view might be to reduce prices to sell more. The counter view could well be that in current times “We are going to sell less anyway and therefore we should increase, not decrease our prices to maintain profit”. Role of the Team Let’s assume there is an intelligent pricing structure in place that covers both services and products and that the budget has been set for the following period. What next? The Leader, having set the strategy and decided on the tactics must lead from the front and set a good example. He or she must first of all share their vision with the other practice drivers, because it will fall on their shoulders too, to put the plan into action. But if the vision has not been shared, if the message has not been conveyed properly or if the team members cannot see the benefits to them, the clients and their pets from sticking to the plan, this is where the other key areas of lost profit will come into play to wreak havoc with the best made plans. Over the last few years, where increased competition has been a factor, practices have already had to reduce margins on certain 187 The Recession and how it is affecting or may affect Vets in Practice - G. Little Were offers of appointment made? When it comes to perishable items, we would probably regard food products as being pretty high upon the list, if not at the top. However, that block of cheese or piece of fruit which is not sold to-day may well sell tomorrow; and if it is not sold within three days, there will be a queue to buy it when it goes on the shelf with all the other ‘bargains’. Airline seats along with consulting and operating slots are even more perishable. Once the door shuts on that aircraft, the empty seat, on that flight can never be sold again. Similarly, if the three empty appointment slots currently available for tomorrow afternoon remain vacant, they can never be filled once that time has elapsed. If, in a particular practice the Average Transaction Value is €40, and if for some reason, the last appointment of the day is always empty, that is equivalent to lost turnover in the region of €12,000 per annum. Belgium Footfall In order for us to provide services and products to our clients we must maintain and increase footfall. Although some practices may provide some products over the internet, most practices require clients to cross the threshold to transact business. Germany Onswitch2 is a UK based business that mystery shops veterinary practices. Practices which use their services do so in order to acquire an objective opinion on their businesses. The mystery shopper contacts the practice over the phone or calls in with a particular concern or query, for example a scratching cat or a dog with diarrhoea or to say they have just acquired a new puppy or kitten. The practice owner receives feedback as to how the queries were dealt with. In the vast majority of cases, clients are dealt with in a very polite and professional manner; they have their questions answered but in the vast majority of cases are not offered an appointment to see the veterinarian or a nurse. The queries are such that one would generally agree an appointment should be made for the client to visit the practice. Perhaps it is because of our desire to help clients and solve their problems, that there is a willingness to do so without inconveniencing the client by asking them if they would like to attend the practice. Ireland UK Apart from the adverse financial consequences of seeking to solve problems without seeing the patient, statistically there will be the cases that really should have been seen on clinical grounds. Whatever the reasons for not offering appointments, it seems to be a phenomenon that is not confined to the UK. Onswitch have carried out mystery shopping in a number of European countries. In a particular survey, mystery shoppers contacted practices seeking advice concerning a recently acquired pet. In the majority of cases the phone was answered promptly and generally speaking clients were dealt with in a polite and efficient manner. However, when it came to clients being offered appointments the results were generally very poor as was the perceived level of interest in the client and their new pet as expressed by the practice. There were differences between the different countries as seen below: Netherlands The average conversion of telephone inquiries to appointments made is 30%. We will look at training later in this article, but Onswitch have seen a 6 – 7% improvement in conversion rates following training. The equally worrying finding has been the attitude of practice personnel towards mystery shoppers; not in terms of their 188 EJCAP - Vol. 19 - Issue 2 October 2009 efficiency but in the perceived level of interest they had in the owner and their pet. And like it or not, interest is directly converted by callers into the level of care they perceive they would subsequently receive from the practice. We must remember Veterinarians do not have a monopoly when it comes to pet care. Clients of practices which take part in the FDI visit their practices, on average 6.0 times a year, with patients’ visits as follows: Those findings are as follows: Canine visit frequency 4.5 times / year Feline visit frequency 3.6 times / year Rabbit visit frequency 2.8 times / year The perceived interest of practice personnel in owners and their pets in different countries How often do these same clients visit the supermarket of their local pet shop? Clients are promiscuous when it comes to using veterinary services, with a significant number of owners using more than one practice for their pets. Hardly surprising when we probably have the same attitude when it comes to, for example, looking after our cars. We may take our car to a main dealer for servicing or if we suspect it has a major problem, but are probably quite happy to go elsewhere, based on price, for tyres, batteries and exhausts, because those are not too important and the main dealer is bound to be more expensive. How many clients have the same attitude towards vaccinations, pet food, wormers and flea control products? Belgium “We make more money on days when we’re quiet!” One of the consequences of the recession or economic downturn is likely to be a reduction in footfall, which in turn may well result in fewer consultations. One of the major drawbacks of short appointment times is the temptation to hijack the consultation. Research on the human medical side has shown that general practitioners interrupt their patients, on average 18 seconds after asking them an opening question3. Before we become too smug, unfortunately recent research with veterinarians has revealed a similar picture, although with communications training, the length of time has been extended. This interruption is no doubt stimulated by the fear that if we allow patients or clients too much freedom within the consultation it may never end! If we want to develop that all important relationship with clients, a bond that will encourage them to keep coming back, and indeed lead them to recommending us to their friends, we need to invest the time to demonstrate genuine interest in them and their pet. Germany Ireland There are a number of ways in which we can communicate with our clients, e.g. brochures, newsletters, web sites, telephone, etc. but face to face contact is by far the most powerful and should be used to maximum effect. The one thing all of us have in common is 24 hours in our day. Because of that, it is not always possible, as veterinarians, to spend as much time as we would like, or should with our clients. This is where the other team members come into their own. The greatest attraction as far as our nurses is concerned, when it comes to their jobs, is working with animals; often, like our clients, they are animal lovers and that love comes across to owners which can make them great communicators. We need to make more use of our nursing team to bond clients to the practice. The FDI results for the last quarter shows that: • Nurse consultations contribute 6.7% of turnover • Leveraged sales (non veterinary surgeon sales) contribute UK Netherlands 189 The Recession and how it is affecting or may affect Vets in Practice - G. Little and most will be aware of the daily takings. But that will probably be the extent of their financial knowledge. How many will be aware of how much of the turnover is profit? How many are aware of the consequences of failing to charge for an item, or the effect of charging a repeat consultation fee when it should have been a full consultation? On interrogating a practice’s management system, it is not uncommon to find a significant number of ‘Re-examine no charges’ that should have been charged differently, or a large number of ‘re-examine small furry’ with a complete absence of ‘examine small furry’ charges. 29% to practice turnover • Leveraged sales make up 38.5% of practice transactions However, it is unfair and counterproductive to ask team members to play an active role in client care without adequate training, both in clinical and communication skills. Educating the Team As a rule practices spend very little on CPD when it comes to their support staff. Receptionists in general receive the least training of all and yet their’s is probably one of the most, if not the most important role in the practice when it comes to ensuring a busy and successful business. As a profession we are not very good at marketing to our clients; the sad fact is that we are probably even worse at our internal marketing; at communication with the rest of the team. It is the receptionist or receptionist/nurse who generally answers the phone and who greets the client when they enter the practice. Again, they are generally the team members who take payments, make the subsequent appointments and who provide the farewell greeting to the clients. Speaking of that farewell greeting and the making of subsequent appointments, another common fault seen in practice, this time practised by veterinarians is the comment, “Bring him or her back if he or she is no better”. What message does that send out to the client? It may well be the patient has been suffering from otitis externa and the veterinarian has just examined the ear through an otoscope, informing the client that “the ear is much better, almost back to normal”. The client is then being asked to make a clinical decision and to come back if the condition isn’t subsequently resolved. Surely we should be seeing that patient until we can assure the client that the problem has been resolved. Practice owners would be well advised at this particular economic time to share some high level financial information with the rest of the team. I’m not suggesting owners should divulge what they are earning. My experience is when you ask team members how much of the €1150 that goes into the till ends up in the owners’ pockets, the answer is seldom less than €800. Not everybody appreciates there are taxes, wholesalers, utilities, motoring costs, insurances, etc. etc, to pay. A very useful exercise is to show the entire team a pie chart which depicts where the €1,150 does go to. You can decide how much information you want to reveal. You may decide it is okay to share with the rest of the team the level of Team Profit as a percentage of the €1,500 as in the example below: When it comes to practice finances the majority of the team probably has very little understanding of the structure that has been put in place, a system that needs to be adhered to in order to hit budget. And whose fault is that? Are they aware, for example, that the practice has to sell X amount of this and Y amount of that, within a certain period, at the correct prices? Probably not. And whose fault is that? My submission is that it is almost certainly the Leader’s. As has already been stated, one of the key responsibilities of the practice Leader is to share the Vision with the team members and to motivate them. Just as Pricing Structure is the subject of another article, so is motivation; in fact it has been the subject of many books. Suffice it to say, it is not really possible to motivate anybody. People motivate themselves. Leaders can only strive to understand what makes each individual tick, bearing in mind that different things motivate different people and that different things motivate the same individual at varying times in their career. Where does the money go? It is only when individuals understand the consequences of their actions, how those actions impact on others and the benefits from changing, will they alter their ways. In this article we have looked at some factors that can affect practice profitability. I have purposely confined the comments to factors which practice owners have control over. I suggest the next stage is to find time to take a critically constructive look at your business to see where improvements can be made. Irrespective of the individual and the particular stage of their career, we know for certain that one of the main de-motivators for everybody and at all times is lack of communication. Can I suggest, in the first instance you find an easy winner. For the team, success is a great motivator. From the practice finance aspect it is important to see things from the team’s perspective. For example, all team members are aware of the price list and what they should be charging, 1 Fort Dodge Index March 2009 2 Onswitch.co.uk/vet/shop 3 Beckman and Frankel 190 PRACTICE MANAGEMENT The Oxford Cat Clinic* INTRODUCTION The Oxford Cat Clinic opened its doors in March 2006, after four years of dogged determination to see it established. Obstacles had included those common to any new business – especially location and finance - but also there was a need to convince friends, colleagues and above all the financial backers why this business would be unique, and how a cat-only practice could thrive in the face of competition and increasing financial challenge. The one group who needed no persuasion were cat-owners themselves; they saw the benefits for their pets immediately and were keen for the venture to start, providing encouragement to keep going when the going got tough. The challenges and rewards of a cat only practice now residents of Oxfordshire, they wished to make their vision a reality in the region. Martha wished to apply her specialist and referral skills within a cat-only environment, but outside of the University this was not easily accommodated. The seeds of the Oxford Cat Clinic were sown in 1998 when Martha Cannon and Caroline Blundell first met and collaborated as post-graduate-clinicians at The Feline Centre, part of the faculty of Veterinary Medicine at Langford, University of Bristol. Martha had accepted the post of Feline Advisory Bureau Scholar in Feline Medicine and Caroline was already The Fort Dodge Feline Fellow. With Langford regarded as a centre of excellence in many aspects of veterinary medicine, the Feline Centre had assumed a special renown under the guidance of Professor Tim Gruffydd-Jones, whose passion and research in feline medicine had done much to advance the profession’s understanding and application of this subject within the UK and elsewhere over the previous decades. Established private referral practices had evolved to focus on the presenting complaint and were not geared to considering cats as a separate entity from dogs. This reflected in the roles of staff, since specialists in internal medicine and the qualified nurses that supported them were required to work equally with cats and dogs. A truly “cat-centric” referral centre was still rare or non-existent outside of the Universities. The exterior of the practice, showing the large viewing windows. Admiration of cats and enthusiasm for feline medicine led both Martha and Caroline to join Tim’s team. Their interests were turned into a truly deeper knowledge and understanding within this environment, but the ultimate treasure was to understand the cat as a unique medical speciality, moulding the way they worked with and thought about this fascinating species. By the time Caroline and Martha left the University in 2000, first opinion Cat-Only practice, although familiar throughout the USA, was still fairly uncommon in the UK, with only six firstopinion cat-only clinics. By this stage Martha had passed her Diploma and achieved the Royal College of Veterinary Surgeons Specialist Status in Feline Medicine. Caroline had completed postgraduate qualification in small-animal medicine. They knew that a cat-only practice had a lot of benefits to offer its patients. Both * For correspondence contact Caroline Blundell The Oxford Cat Clinic 78a West Way, Botley, Oxford GB-OX2 9JU E-mail: [email protected] 193 The Oxford Cat Clinic It was with this background that Caroline and Martha first began to discuss the possibility of establishing a cat-only referral and first opinion clinic. The comprehensive service was part of the overall financial business plan; despite an anticipated demand for the referral service it was unclear if a purely cat-only referral facility could generate sufficient revenue to finance the relatively high investment costs of a referral practice. However it was felt that referral work income would help support cash flow in the early days of a start-up practice, and that first opinion practice provides plenty of opportunity to work up medical cases to referral standard, and thus the two arms of the business would happily compliment each other. Luckily the pair were in contact with a progressive and forward thinking mixed practice in Oxfordshire. The Larkmead Veterinary Group welcomed the couple’s ideas and expertise within their own practice, and supported a cat-focused referral and first opinion service based under the umbrella of their well-equipped state of the art surgery. This opportunity allowed Martha and Caroline a chance to explore public and professional response to their proposal and to check the financial soundness of the proposition, without the financial exposure and difficulties of a practice start-up. The nursing and veterinary team. From L>>R Front row: Jo Mercado dip. VN (med), Linda Robinson VN, Caroline Blundell MRCVS. Back row: Liz Howes VN, Martha Cannon MRCVS, Amanda Horton MRCVS, Jo Whittle student VN (standing). Kate Mulcahy-Hawes (not pictured). Happily the model appeared to work well. Local veterinary practices soon began to appreciate the referral service for more complex feline cases. First opinion clients also benefited from a referral-class service, with both practitioners able to offer extensive experience and paying attention to keeping up to date with any new developments in feline medicine. However, the one thing that was still not offered to the patients was a hospital of their own! Despite a well designed and private cat-holding area within the Larkmead Hospital, all the other hospital facilities were shared with other species – and in particular with dogs. So the hunt for new premises began – a challenging period of false starts and expenses, but culminating in success in March 2006, when the Oxfordshire Cat Clinic at Larkmead finally shut its doors to re-open in Oxford as the Oxford Cat Clinic. The prep area. Å Downstairs layout The Oxford Cat Clinic The Oxford cat clinic occupies 2 stories of a detached commercial building on the western perimeter of Oxford. Oxford is a University City in the South East of England, west of London. It enjoys a favourable economic outlook, with higher than average income and less than average rates of unemployment. Figures from the 2001 census indicate a population of 250,000 within a 10-mile radius of the practice. Trying to satisfy the demands of both primary and referral work the site was chosen for three main benefits; for primary clients, the excellent local demographics, with good connections to the more populated city centre and the generally affluent outer villages; for referral clients, the excellent road links to the major road networks running to London, the south coast and the midlands, while avoiding the traffic congestion associated with the inner-city; and for all clients the provision of parking at the front of the building, since our patients are always carried to the front-door! È Upstairs layout The cat-clinic caters for both first opinion and referral cases. It is open seven days a week, accepting referrals in feline internal medicine from Monday to Friday, and offering daily appointments 194 EJCAP - Vol. 19 - Issue 2 October 2009 to bonded clients. As part of the referral service, a fax and phone feline advice service is offered to referring veterinary surgeons, allowing them to discuss potential referrals or challenging cases. There are three veterinary surgeons: Martha Cannon, a RCVS recognised specialist; Caroline Blundell, who holds a certificate in small animal medicine; and Amanda Horton, who offers 21 years of experience in small animal medicine, with a cat-only focus for the last 18months. They are assisted by a team of four nurses, including a diploma-holder in medical nursing, and two receptionists. Occupying approximately 160 square meters over two floors, the area is compact. A lot of planning went into making most efficient use of space (see floor plan) while keeping the building cat-friendly. The feline-focus begins from the moment a patient enters. The reception area is relatively quiet and of course free from the noise or smell of dogs. Owners are offered raised resting areas for the cats within reception to increase their sense of security. Both consulting rooms have perching areas for the cat. The consulting rooms were also designed with perching places for cats, where they can sit quietly while the vet and client talk. Another unusual feature of the practice is a clear window at the front, allowing the public a clear “no-secrets” view of the consulting room. There is a second more private consulting room for use when required. An unexpected benefit of the “room with a view” is how the cats respond to it – happily perching and indulging in street surveillance from the consulting table or window seat, while the vets busy themselves around them with stethoscopes and blood pressure monitors etc. Within the consulting area are a (washable) upholstered window seat and a wicker-type chair. Both cats and owners are relaxed by the provision of these comfy places. The original wooden parquet Bedding is tailored to the individuals preference. Comfy chairs in the consulting room put our visitors at ease. flooring was sealed and retained in this area. Since there is rarely wet contamination associated with cats this still allows efficient cleaning and disinfection of the floor surface. Cattery design includes warm, non-reflective polypropylene kennels, offset and placed at 90 degrees to each other – directly facing another cat would be very stressful for the occupant. Cats are offered individual beds according to their preferences (covered, non-covered etc). The cattery is unconventionally located at the centre of the building. We made this decision so that close observation of patients at all times could be a cornerstone of our care. If transmissible disease is suspected the case is transferred to isolation cages sited in the upstairs area. Recent expansion has allowed us to start to use a large room separate to the main building, so there may be the option for isolation facilities in this area in the future. Patients are induced and prepared for diagnostic and surgical procedures in the main “prep” room, which leads directly to the lab, imaging area and surgical theatre. Hospital facilities include dentistry, radiology, ultrasound, electrocardiography, endoscopy 195 The Oxford Cat Clinic and soft-tissue surgery amongst others. Recovery occurs within the preparation room, ensuring that cats are continually observed during this most-critical period of anaesthesia. Animals recover within a clear-sided incubator. We are always mindful of the large surface area to body mass ratio of our patients, and bodytemperature management is considered vital throughout any procedure and also peri-operatively. Critical patients will also be pre-warmed and pre-oxygenated. All surgical patients benefit from the provision of circulating water-heating pads, air-blankets or heat mats, and wrapping extremities with bubble wrap is the norm. Warmed fluids, continuous temperature monitoring and thermo-vent devices are also standard during anaesthesia. in our patients, for example helping to “cure” our anorexic cats even before restorative medical treatment has begun. We recognise that how cats are housed and handled during examination, recovery from surgery or when being hospitalised in the clinic for medical treatment can have a major influence on their overall wellbeing. Just like humans, cats and other species will recover more comfortably and more rapidly in an environment that offers a feeling of peace and security, free of strange smells and noise. Why owners prefer a cat only clinic We try to ensure the owner’s experience of a visit to the vets will be a positive one. We are very aware that an anxious cat inevitably results in an anxious owner, and vice versa. As well as any concern over their pet’s health, much owner-anxiety is generated by the actual process of getting the cat to the vet, including concerns of how the cat will behave once it arrives, and the worry of potentially deleterious effects on the cat from the experience. All parts of the journey may be stressful for the owner, from loading the cat into the carrier, the travel experience itself and the encounter at the final destination. We are very aware of these issues and try and make the process better for both the cat and owner at every step. As well as providing advice on the benefits of different types of carrier we provide leaflets describing methods of familiarising the cat with the cage and advice on how to relax it during the journey. Pheromone diffusers run throughout the building – aiming to further relax an anxious cat. Why cats prefer a cat only clinic Just as the anatomy of dogs and cats is different, so is their temperament and behaviour. Any visit to a vet is stressful for a cat. Some cats may appear bomb-proof, appearing to cope with any situation, but the majority are creatures who like routine and being within their own comfort zone. The experience of being confined within a cat carrier and subjected to a journey is bad enough. If compounded by further stress at the destination the cat will become increasingly reluctant to visit the vet. A cat that has to sit in a waiting room full of unfamiliar noise and smell is likely to become alarmed, especially in the presence of dogs. Being both predators and prey, cats will exhibit both attack and fearful behaviour, and may respond with aggression if challenged. Even where cat and dog waiting rooms are separate the cat will still be aware of the presence of dogs in the shared environment. A stressed cat is more difficult to examine and physiological factors e.g. heart rate and blood pressure may become affected. The results of laboratory tests e.g. Cortisol and blood sugar levels, will also be altered. Being feline-specific allows us to better accommodate our patients in a relaxing way. Away from the hustle, bustle, smell and barking of mixed practice the Cat Clinic generally has a quiet, calm atmosphere that patients, clients and colleagues appreciate. Once the cat arrives the practice is designed to reduce the stress associated with a visit. The reception is calm and welcoming, with friendly staff. Attractive cat-themed art-works are placed in all of the public areas, continuing the feline-friendly mood. Once in the consultation room the cat is allowed to exit the cage in its own time. For animals that are too cautious to exit from the carrier we recommend carriers where the top will lift up or even ideally off, to avoid the situation where a cat has to be forcefully squeezed through a narrow exit. Cat owners are very quick to notice good “cattitude”, and detect cat-lovers Reception is kept bright, calm and welcoming. Feline artwork is on display. The consulting area is designed to be as unthreatening as possible. We will often place the basket on the ground or table, open the door and wait for the cat to emerge and explore while we are taking the history from the client, diverting attention away from the cat. Those cats that want to be the centre of attention will soon come and find it! Cats are slightly secretive by nature – and this seems equally true in their attitude to illness. Their clinical signs are often subtle and frequently non-specific. In addition to hiding illness for long periods of time, cats also specialise in sudden deterioration; chronic murmurs turn into congestive heart failure; inappetance into acute pancreatitis or hepatic lipidosis etc. By recognising that cats work to a different time scale to dogs we have adjusted our own procedures accordingly. Consultations are longer and nurses are encouraged to take time to pet and hand-feed the patients. This is time-consuming and may seem rather a “soft” version of veterinary medicine – but these extra steps are observed to make an enormous difference 196 EJCAP - Vol. 19 - Issue 2 October 2009 nearly as quickly as their pets do. The positive attitude of all our staff and their great cat-handling skills is frequently commented on. They respond positively to the fact we are all cat-owners – we can all empathise with their concerns. In particular we receive feed-back on the patience of the staff - allowing the cat to acclimatise before examination – perhaps not considered of great importance medically, but mentally noted by owners. It is very rewarding to hear a client comment that they have never seen their cat behave so well at the vets before, or is now much less fearful of the vets or the journey. In the future we hope to offer a mobile clinic to eliminate some of these issues further. reference source for all things cat: advice on catteries, groomers, carriers, behaviour, bedding, feeding, collars, holiday care etc. Our experience is that the clients relish the differentiation and choice, and happily take their dog to another local vet – confident in their skills in this other particular area. Recruitment - Why our vets and vetnurses prefer a cat only clinic An unexpected benefit of our speciality is that our staff have specifically sought us out when we have recruited (and sometimes when we have not been recruiting!) – attracted by the combination of feline speciality and the possibility of following through each medical case at referral level. We therefore benefit from a very committed and able team. Because of their genuine love of cats, nursing care is exemplary, and cats will be quietly offered warmed tit-bits, comfy bedding, gentle grooming and tender petting whenever time allows. It is apparent by the way that the cats respond that there is a huge medical benefit from this quiet attention. The veterinary surgeons benefit from working with fantastic cat-handlers, which, as any vet will confirm, makes a huge difference to the way the day runs. Our For those cats that are ill, owners recognise and respect the years of cat-care experience we offer. They inform us that they experience peace of mind, feeling that they have brought the cat to the right place. They are re-assured that we will have a very thorough understanding of cat disease and all treatment options because of our feline-focus, and also that we will have the gentle touch their sick-cat requires. We offer 20 minute consultations as standard for our first opinion work, up to 60 minutes for referral appointments. These appointment times are generous, but we hope this allows our clients sufficient time to ask questions and feel comfortable with treatment options offered. Of course this service has to be cost effective, but we find that by ensuring we have time to examine and discuss each case very thoroughly the owners perceive the value of the work we can offer and are more inclined to engage with suggested investigations or treatment. The pace of work is particularly suited to feline practice. It sometimes seems that dogs may present with a higher percentage of uncomplicated medical complaints and specific signs e.g. cuts, bites, trauma, foreign bodies in eyes, ears, pads, acute self-limiting vomiting caused through indiscriminate eating. This is in contrast with cats, where the disease is often obscured, presenting with non-specific signs such as anorexia, lethargy and weight loss. Disease also often presents at a later stage. Therefore the illness may take more time to unravel and more time to correct. If the animal is admitted the owners will receive a daily phone-call regarding their pet’s condition. At discharge an appointment is made with a vet or the vet-nurse in charge of the case. The owners will receive verbal and written instructions regarding the treatment plan. A follow up visit is usually arranged for 48 hours after discharge. In the case of referral patients this may be with the original referring vet. The referring vets are updated on the day a case is discharged by Fax and a referral letter is sent within the following week. More complicated cases are discussed with the referring Vet on the phone. The clinic has attracted a highly skilled and dedicated nursing team. nurses also get to work with vets who genuinely like and will slow down for cats, and who are interested in all the nursing observations of eating, sleeping, pain assessment etc. Visiting colleagues frequently comment that the “Vibe” is different in feline practice. Although days can be frantically busy there seems to be a different pressure – a feline “resonance” perhaps! Much of this is to do with the absence of noisy dogs – although our Bengals and Siamese do their best in the vocal stakes. Once a diagnosis has been made we still focus on the fact that the patient is a cat – and that patient compliance is a major issue. We place great emphasis on ease of medication, and where any drug choice is equivocal the “easy-to-give” medicine will always win out. Taking advantage of the fact that we only need to store feline diets we also choose to stock several manufacturers, hoping to be able to offer a prescription diet the cat actually enjoys; for example for renal patients we can offer a selection from seven wet diets and three dry diets Outside of medical advice, clients know that we can be used a Cats present a daily medical challenge; as well as their narrow repertoire of presenting signs and the challenge of hidden disease, late presentation and small body size mean that cats can decompensate quickly, so we learn to stay alert, ready for sudden alterations. Emphasis is placed on frequent monitoring 197 The Oxford Cat Clinic and preservation of body warmth, hydration status, assisted feeding methods etc. Feline medicine is also a rapidly developing field, with new developments keeping the topic fresh and interesting. had treated dogs as well, and was essentially high with the specification of equipment required for referral work. However the practice has performed in line or above expectations. Caseloads are variable. Occasionally a busy referral load will compliment a quiet time in first opinion or vice versa, but more commonly they both get busy together, resulting in busy times for all. Working in a one-species facility means that all medications and protocols can be tailored to cats. There is accelerated experience in the area of interest, and this encourages familiarity with more specialised treatments and diagnostics. Blood pressure measurement, duodenal endoscopy, cardiac ultrasound, bronchoalveolar lavage, thoracocentesis, blood typing and transfusion become familiar procedures. Endoscopes and ultrasound probes are size-appropriate. In addition a lot of emphasis is placed on continuing education, which is now better than ever in the feline field, so that newer, often off-licence, medical drugs are introduced and can be used confidently. We are committed to continue to incorporate new veterinary learning and technology for the benefit of our patients. Knowledge is pooled and shared within the group. Challenges facing a cat only clinic In a time when the number of pets is falling and the number of veterinary surgeons is rising one has to consider carefully the business implications of a one-species clinic. Although the percentage of cat owners is steadily overtaking that of dog owners, single-species selection will mean that a cat-only clinic requires a larger population size from which to draw its primary client-base. In addition potential clients who own species other than cats may choose another vet because of the refusal to see their other pets. Furthermore sales profits from drug and food are likely to be less than in a general clinic, since the gross value sales is smaller (a 10-day course of antibiotics for a Rex is much less expensive than a 10 day course of antibiotics for a Retriever. Quantities of diets are of course much smaller). Additionally routine surgery on cats, in particular neutering, may bring in less income than the same surgery on dogs. The benefits of equipping a cat only clinic The advantage of equipping a cat-only practice is that domestic cats come in a limited and smaller size range, so that equipment such as endoscopes, ultrasound probes, x-ray plates, anaesthetic circuits and endotracheal tubes, together with facilities such as kennels and tables can be selected or designed to accommodate this narrower range. Sadly for us, other than a few items and actual floor space, this aspect is only marginally financially significant. There is little equipment available in a mixed small animal practice that does not need to be replicated in a cat-only practice, and we have additional costs related to our referral requirements. Most equipment (dental x-ray, x-ray, ultrasound machine) is equivalent to that used in any small animal practice with similar cost and specifications. Reduced size is rarely correlated with reduced cost; Small non-standard consulting tables/operating tables are often more expensive than standard veterinary tables: smaller endoscopes suitable for exploring a cat duodenum are more expensive than the dog equivalent. In addition, where we may not need to carry such a large range of sizes we will often carry extensive stock associated with referral work. For example with urinary catheters we carry a large variety of types, with at least 5 different styles in various catgauges for specific indications. We also have a large range of assisted feeding tubes, thoracotomy tubes etc. and a generally high level of investment in technical equipment e.g. anaesthetic monitoring equipment etc. to satisfy the demands of referral medicine. Continuing education for all our staff is another area in which we invest heavily. Happily we have found that we attract clients from a large area because of our speciality, and the majority quickly become well-bonded for the same reason. In line with new edicts we deliberately apply low mark-ups on drugs and charge fairly for our services. The fact that we are a highly specialised practice ensures that our clients are committed and willing to spend money on their pets and the services we provide. Our average transaction value (ATV) for services compares favourably with other practices. The referral work influences the ATV to an amount probably higher than the average small animal practice. Referrals make up approximately one third of the practice’s workload, and were a huge help in maintaining cash flow in the early days. Along with Martha’s lecturing, they also help to raise awareness of the practice. In Conclusion Species specialisation has allowed a focus in one area of veterinary medicine, enabling us to dedicate the time and equipment required to solve complicated problems. The benefit of cats-only practice spreads three ways. We find it is good for the cat, the owner and for the veterinary surgeons – both those working within the clinic and those who refer to us. We have had lots of positive feedback from referral vets regarding the quality of the service we provide – and we are grateful to these vets for their ongoing support. Our experience also suggests that the primary clients who are attracted to a feline-only practice also want a high quality service, taking it on trust that as a cat-only clinic we will provide an educated and thoughtful response to their problems and a gentle touch with their best friends. There are savings to be made on drug stocks, with only the smallest size of each medication being needed, but we tend to carry a high number of “special” medications, including off licence chemotherapy agents, hopefully required less frequently, but reflected by relatively high stock costs and increased stock holding days. Overall costs of fitting out the practice was no less than if we 198 BOOK REVIEWS BSAVA Manual of Canine and Feline Wound Management and Reconstruction, Second Edition Edited by John Williams and Allison Moores Published by BSAVA Distributed by Wiley-Blackwell (April 2009) 250 pages, Illustrated, Paperback ISBN: 978-1-905319-09-1 € 89.90 £70 Available from www.wiley.com/go/vet. BSAVA members should order from www. BSAVA.com for member prices. The book is divided into int 12 Chapters embracing basic as well as more advanced knowledge in wound management. The first one, on biology of wound healing, is a nice summary of current know-ledge. Well-illustrated it will be useful both for teachers and students. The chapter entitled “decision-making in wound closure” actually deals with patient assessment, initial stabilisation, basic closure technique and basic principles of oncological surgery. A chapter dedicated to the most appropriate method of closure (decisionmaking or how to close THIS wound) would have been helpful to the clinician. In the management of open wounds the author mentions the newest as well as the oldest methods (Honey and Maggots). The properties of different wound dressings are well described. Drains and drain techniques are described in a very conventional manner. In the chapter on tension-relieving techniques and local skin flaps the author used cadavers to illustrate some techniques. A more complete description of other local flaps is found at the end of the chapter in the operative techniques section. Some inconsistencies are apparent: The pouch flap, a distant flap per se, is illustrated in the local skin flap chapter. In the same chapter, although the author mentions that a ½ ratio is a good guideline, a massive transposition flap with an approximate 1/5 Basis/Length ratio is used to cover a postmaxillectomy defect and distal necrosis can be seen. Concise and simple examples of local skin flaps would have been useful to the practitioner. In the axial pattern flap chapter the author deliberately uses tables and drawings instead of text. These are very helpful. Some severe flap complications are depicted making the practitioner aware of these. The chapter on pedicled muscle flaps is certainly the best in the manual. The text is concise and many references are listed. High quality illustrations are provided, tables are clear and support or replace the text. At the end most known muscle flaps are mentioned and well illustrated. Although it is beyond the possibilities of most practitioners not to say surgeons, the chapter on Microsurgery is also a nice summary of what can be achieved. At the end of the manual a chapter is dedicated to special considerations in wound management. This chapter is pretty confusing. Amongst paragraphs on surgical management of stick injuries, bite and burn wounds, the author brings in some information on medical treatment of peri-anal fistula. In this chapter conditions as different as skin fold dermatitis, anal sacculectomy, mammary gland surgery and omentum transposition are all considered. In this manual many clinical cases are brought to illustrate the different techniques at our disposal; therefore making the actual content aesthetic is quite challenging. The choice of the pictures on the cover page (a bloody surgical field and an inappropriate flap design with distal necrosis) could be questioned. This however should not discourage the practitioner from buying this manual. Many tables that summarise the current knowledge together with nice drawings and many good tips and useful information will be found in its pages. Professor Gilles Dupré (A) BSAVA Manual of Rodents and Ferrets Edited by Emma Keeble and Anna Meredith Published by BSAVA Distributed by Wiley-Blackwell (March 2009) 360 pages, Illustrated, Paperback ISBN: 978-1-905319-08-4 € 94-90 £75 Available from www.wiley.com/go/vet. BSAVA members should order from www. BSAVA.com for member prices. This is another in the excellent series of BSAVA manuals, although it is really two manuals rolled into one as the first 192 pages are entirely on rodents and the rest is entirely on ferrets. The chapters on rodents cover them as a group rather than separating the different species. There are a total of 199 31 chapters, each of which have a separate author and cover a particular subject, such as: diagnostic imaging; clinical pathology; dentistry; therapeutics; ophthalmology; dermatoses; and digestive disorders. The manual extends the information contained within the manual of exotic pets, which I have always found a useful but limited resource due to the wide range of species that it inevitably covers. The publication of the manual of rodents and ferrets completes a series of manuals that covers the majority of the species range from the original manual of exotic pets. As usual in the manuals there is a compliment between practical advice and detailed information on different diseases and conditions. The field of rodent veterinary medicine has in the past relied heavily on information gained from laboratory animals and the available detailed reference books have previously been directed at this area. This manual is an extremely useful step to approaching pet rodents that are presented in practice, although I still feel that a small amount of the disease information is truer of laboratory animals. However some of the authors have clearly had a greater practical exposure to the range of species in the general practice situation and this is reflected in the chapter content. On reviewing this generally excellent book, I have been found some minor distractions, such as the picture of a Merino guinea pig labelled as a Peruvian; and I am concerned at the recommendation to breed guinea pigs as young as 6 -12 weeks! The chapters on ferrets are an excellent guide, and contain sufficient information in a practical context to treat these animals. In view of recent developments there is some up to date practical advice on the reproductive management of this species. The manual should find a niche in the practice library and prove a valuable resource. The chapters on rodents are probably the best publication that covers these species in a general practice situation and only rivalled by one other publication that is devoted entirely to them and therefore this manual would be my recommendation for the majority of practices that do not have a particular interest in ferrets. Owen Davies MSc BVSc MRCVS(UK) BOOK REVIEWS BSAVA Manual of Canine and Feline Abdominal Imaging Edited by Robert O’Brien and Frances J Barr Published by BSAVA Distributed by Wiley-Blackwell (April 2009) 252 pages, 472 Illustrations paperback ISBN: 978-1-905319-10-7 € 84 £ 75 Available from www.wiley.com/go/vet BSAVA members should order from www. BSAVA.com for member prices BSAVA Manual of Canine and Feline narians who want to keep in touch with radiology and who want get an idea of what kind of imaging modalities they can request. Practitioners and radiologists will enjoy the illustrated text and nice images. Certainly regarding radiographic diagnosis of the abdomen, the book will be helpful in small animal practices. The book fulfills its purpose in comprehensively describing the clinical role of imaging of the abdomen and pelvis. I would grade this as an excellent book, and the experience of many authors comes through well in the text. This book will find a useful place in the library of most clinics and radiology departments. Ingrid Gielen DVM, MSc, PhD (B) and self-assessment tests. At over 500 pages the book is extremely comprehensive and the authors are to be applauded for their meticulous attention to detail. The book follows the dissection of a dog as traditionally undertaken in preclinical classes and every stage is illustrated by colour photographs, line drawings and (where appropriate) radiographs and advanced imaging scans. There are ten chapters: the first covers the surface and skeletal anatomy of the whole animal, and the following eight chapters cover each anatomic region (head, neck, forelimb, thorax, abdomen, hindlimb, pelvis, spine). The final chapter considers the comparative anatomy of the cat. Color Atlas of Veterinary Anatomy – Volume 3 the Dog and Cat, 2nd edition In their preface the authors hope that in addition to the target audience of veterinary students and practitioners, the book may appeal to “dog and cat enthusiasts”. However, I suspect that the placing of photographs of the (overtly) fit, healthy and very much alive greyhound adjacent to what appears very much to be the same dog, but skinned and embalmed, would be off-putting to most people outside the veterinary sphere! Abdominal Imaging Stanley H. Done,Peter C. Goody, Susan A. Evans, Neil C. Stickland Edited by Robert O’Brien and Frances Barr The BSAVA manual of Canine and Feline Abdominal Imaging is a textbook on all topics of imaging modalities in the abdomen. It has an extremely practical layout, is easy to read and there are high-quality illustrations. The emphasis of the book is put mainly on radiology and ultrasound investigation for solving clinical problems. Besides an overview about general abdominal radiography and ultrasound, there are 15 chapters in this book, each one devoted to a specific region in the abdomen and pelvis. Each chapter is well structured: normal anatomy, technique and diseases. The spectrum of disease patterns is well demonstrated. Excellent schematic diagrams support the understanding of the text. Some chapters contain good drawings, and the topics are well illustrated with radiographic and ultrasonographic images. The main emphasis remains radiography and ultrasound. Other possible imaging techniques are however described in most chapters. A small remark is, that the use of CT could be described in more detail as a valuable tool in abdominal imaging. Most chapters have been contributed by radiologists with specific experience in the areas being discussed and all authors are drawn from reputed institutions. The book is a reference text that provides advanced information on most topics. In addition to students and residents, this book will also be useful for clinical veteri- Published by Mosby Elsevier ( www.elsevierhealth.com), (2009); 540 pages, 1550 Ilustrations, Paperback, ISBN: 978-0-7234-3415-3 € 111 £ 77 99 How times have changed! Twenty years ago our standard anatomy texts were tough-going wordy tomes in which the anatomical structures were described in great detail, but only illustrated by occasional line drawings. I remember, vividly, drooling over human anatomy atlases in which dissections were portrayed in explicit colour photographs; this is a volume that seeks to redress that balance. If I had to make a criticism of this work (and it is a shame to have to criticise such a magnificent effort), it is that the dissections make exclusive use of embalmed cadavers. The authors acknowledge this criticism, but feel that the embalmed tissue better demonstrates the topographical relationship of structures and also reproduces better in photographs than fresh tissue. Whilst there is some truth in this, the constant barrage of embalmed flesh becomes repetitious and one feels oneself longing for the glistening vitality of a surgical atlas. However, this is a minor criticism and I would foresee that this book will be an essential purchase of all veterinary pre-clinical students and should also find its way onto the shelves of most practice libraries. Tim Hutchinson BVSc CertSAS MRCVS (UK) Small Animal Oncology An Introduction Susan M. North and Tania Ann Banks Volumes one and two of this series dealt with the ruminant and horse. In this third volume the authors (all from the Royal Veterinary College) turn their attention to the dog and cat. This second edition has expanded considerably its predecessor and the main differences are the frequent use of radiographs, CT and MRI scans, brief clinical notes to highlight the more significant areas and also access to an on-line resource 200 Published by Elsevier Saunders (www.elsevierhealth.com) (2009); 304 pages, 200 Ilustrations ,Hardback, ISBN: 978-0-7020-2800-7 € 89.99 £62.99 Oncology is undoubtedly the most rapidly developing interdisciplinary speciality and this textbook, written by devoted special- BOOK REVIEWS ists, is an excellent way to learn how to approach cancer patients using all aspects of modern medicine, from purely medical to psychological, moral and socio-ethical. The content of the book clearly shows the open-mindedness and wide knowledge of the authors who present readers, whether specialists in other disciplines, practicing vets, residents, interns or students, with all necessary information to guide them through history taking; clinical examination; diagnostic procedures, therapy decision making and good first line therapy. Interestingly authors recommend rectal examination in dogs over 5 years of age, which points to their belief that sophisticated medical machines cannot replace a good, thinking doctor. The book starts with 12 introductory chapters which concisely describe the human – animal bond, cancer biology, diagnostic procedures, treatment modalities, emergencies, paraneoplastic syndromes, cancer pain and nutrition. Introductory chapters do not go beyond the scope of the book and they successfully achieve the authors’ goal of motivating the reader to pursue additional reading. A systems approach follows, including virtually all tumours of companion animals, which is distinctly different to the approach of similar textbooks from the last decade. The authors’ honestly admit that it was sometimes difficult to decide where to include a specific tumour. The approach to tumours reflects the experience of the authors; even a beginner is safely guided through clinical signs, clinical evaluation, diagnostic work-up, staging, prognostic evaluation and treatement. Grading of tumours is clearly emphasised all through the text. Controversies in diagnostics, prognosis and treatments are clearly pointed out, supported by rationally selected references, with tips from the great experience of authors, especially Dr. Susan North, interwoven into the text. Clear example of this is seen with lymphoma, where all possibilities are listed, supported by references, but the advice to a treating vet is to take into account all factors, including the capabilities of the treating vet, equipment available, the character of the patient, the social and material status of the client, treatment being tailored accordingly. Dr. North is one of just a few veterinary radiation oncologists practising in Europe with an in-house linear accelerator, giving her first hand experience to recommend the possibility of multi-modality treatment all through the text, especially in relation to surgical treaments which can be considerably reduced in terms of surgical dose where radiation treatment is available. The text is equally understandable and guiding for a student with a special interest in oncology and useful for an experinced clinician. Much new data can be found in thepages and recent controversies and dabatable information regarding less frequent or rare tumours are discussed. The book was an enjoyable read. It is strongly recommended as an excellent source of up-to-date information for enthusiastic students, general clinicians as well as for those devoted specifically to veterinary oncology. Professor Janoš Butinar, DVM, Ms, PhD(Slovenia) Veterinary Reproduction and Obstetrics, 9th Edition Edited by David E. Noakes – Timothy J. Parkinson – Gary C.W. England Published by Elsevier Saunders (www.elsevierhealth.com), (2009); 950 pages, Illustrated ,Hardback, ISBN: 978-0-7020-8 €147 £103 The first edition of this now standard reference textbook on reproductive medicine was published in 1938 by Professor Franz Benesch (Head of the Clinic of Obstetrics at the Vienna University of Veterinary Medicine, Austria). His book “Veterinary Obstetrics (equine and bovine)” was translated into English by J.G. Wright. Among the editors of subsequent editions are J.G. Wright, G. Arthur, H. Pearson, D.E. Noakes, T.J. Parkinson and G.C.W. England. All chapters in the 9th edition have been completely revised and adapted to today’s comprehensive knowledge of the discipline. Some chapters are completely new 201 containing the most recent developments. Specialists from eight different countries are contributing authors to this book making it a truly international overview of veterinary reproduction and obstetrics. The book is organised into eight sections: Normal cyclical ovarian activity and its control; Pregnancy and parturition; Dystocia and other disorders associated with parturition; Operative interventions; Subfertility and infertility; The male animal; Exotic species; and Assisted reproduction. These eight parts comprise a total of 35 chapters covering farm animals such as cattle, horses, gilts and sows, ewes and does (female goat); herd management; dogs and cats; pet small mammals (rodents, rabbits, guinea pigs, chinchillas, mice, rats, gerbils, sugar gliders) as well as Camelidae and buffalos. The 17 authors of the book provide the reader with their personal experience in reproductive medicine focussing on farm animals. Numerous full-colour and blackand-white illustrations and many graphics contribute to a deeper understanding of normal veterinary reproduction and obstetrics as well as reproductive disorders and diseases in the common and less common domesticated species. Information on reproductive medicine in the dog and cat is included in each chapter. Physiological considerations and the use of hormones is contained in Part One, while disorders associated with parturition and their treatment options (provided a correct diagnosis has been made) are discussed in Part Three by Prof. David Noakes. The comprehensive sections on fertility and subfertility of the bitch and queen together with a description of surgical interventions in their genital tracts are a contributed by Prof. Gary England. Part Six provides relevant information on reproductive issues in the male animal, discussing physiological reproduction, fertility, subfertility and infertility as well as artificial insemination. This part has been revised and adapted by Prof. Timothy J. Parkinson from New Zealand. In Part Seven, dedicated to exotic species, Ms. Sharon Redrobe gives a review of physiological and pathological reproductive medicine in small pet mammals. For all those already working in veterinary reproductive medicine or those planning to specialise in this field, and also for students, this book represents a valuable and complete overview of the discipline making it an indispensable work of reference in the library of every veterinarian. Dr. Hans-Klaus Dreier (A) Calendar of main European National Meetings and other continuing education opportunities WSAVA & FECAVA Congresses (Red) Principal annual meetings (blue) A list of the addresses and telephone numbers of the Secretariat or person holding information is attached. 2009 2-4 October AVEPA Barcelona AVEPA Annual Congress /SEVC - Southern European Veterinary Conference English, Spanish, French, German, Polish 10-11 October VÖK Kufstein CE GI Diseases German 10-11 October AIVPA Modena National Congress-Neonatology and Paediatric diseases - new possibilities Italian/English 17 October VÖK Vienna Emergencies Seminar German 17 –18 October LSAPS Riga WSAVA CE lectures - Emergency medicine English 20 October BSAVA BSAVA HQ, Gloucester CE Clinical Nutrition English 22 October BSAVA Thorpe Park Hotel & Spa GIT II English 23-24 October VÖK Leoben VÖK/VSK-Joints-Workshop German 23-24 October TSAVA Istanbul 4th TSAVA Anadolum Congress Turkish/English 23-25 October PSAVA Lublin Annual Congress: Small Animal Medicine Polish/English /French 23-25 October SASAP Belgrade Annual Symposium Serbian/English 24-25th October AIVPA -CELEMASCHE Legnaro (Padova) Practical and theorical course - Radiographic diagnosis of congenital/genetic diseases of the skeleton (HD, ED, SP, WS) DNA analysis Italian 24-25th October AIVPA -AIVPAFE Grugliasco (Torino Haematology and cytology of the dog and cat (Theoretical Italian & Practical 26-30 October ESAVS Berne(CH) Neuropathology – Intensive Course for Pathologists, Neurologists and MRT Users English 5-6 November SSAVA Uppsala Annual Veterinary Congress (Neurology) Swedish, English 7-8th November AIVPA Pisa Basic Dermatology of the dog (Theoretical & Practical) Italian 13-14 November DSAVA Aarhus Annual Meeting Danish/English 14-15 November VÖK Steyr Ultrasound Seminar German 15th November AIVPA-CARDIEC Bologna Seminar - The critical patient: from anaesthesia to awakening Italian 16-20 November ESAVS Halmstad (S) Dentistry IV Oral Surgery (course with wet lab) English 16-27 November ESAVS Utrecht (NL) Internal Medicine English 17 November BSAVA BSAVA HQ, Gloucester CE Neurology English 19 November BSAVA Thorpe Park Hotel & Spa, Leeds CE Haematology English 21-22 November VÖK Krems X-Ray Seminar German 22nd November AIVPACELEMASCHE Varese Seminar -Diseases of the hip, elbow and stifle Italian 26-29 November FECAVA/AFVAC/ LAK/SAVAB Lille 15th FECAVA/AFVAC/LAK/ SAVAB Eurocongress www.fecavalille2009.com French, English 28 November VÖK Vienna Patella Seminar German 30 November4 December ESAVS Lisbon (PT) Internal Medicine and Emergency Care Course English 1-5 December ESAVS Halmstad (S) Oral Surgery Course English 2-4 December VÖK Leoben VÖK/VSK-Spine-Workshop German 5-6 December SkSAVA Smolenice Castel Orthopaedics English/Czech 7-12 December ESAVS Lisbon (PT) Ophthalmology and Neurology English English 2010 11-13 March, SAVAB-Flanders Antwerp GI congress 19-20 March HVMS Athens 9th Annual Congress(FECAVA Day 19th.) Greek, English 8-11 April BSAVA Birmingham Annual Congress English* 22-24 April NACAM Amsterdam Voorjaarsdagen Dutch/English 14-15 May EVSSAR Louvain - La Neuve (B) 7th Biennial congress English 2-5 June FECAVA /WSAVA /SVK Geneva 16th FECAVA/34th WSAVA/SVK-ASMPA Congress English and others 204 18-20 June ESFM Amsterdam (NL) ESFM Feline Congress - Feline Dentistry & Feline pain management English 1-3 July ECVS Helsinki (Fi) 19th Annual Meeting English 15-18 September ESVOT /VOS Bologna(I) World Veterinary Orthopaedic Congress English 23-25 September ESVD-ECVD Florence (I) Annual congress English 25-26 September VÖK Salzburg 25th Annual Meeting German 1-3 October AVEPA Barcelona AVEPA/SEVC Annual Congress English, Spanish, French, German, Polish 12-13 November DSAVA Aarhus Annual Meeting English, Danish 10-12 December AFVAC Paris Annual Congress French * 60 Veterinary surgeons or 70 Nurse registrations required for simultaneous translation to be provided ADVANCE NOTICE 2011 BSAVA 31 March-3 April Annual Congress SVK/ASMPA Interlaken 18-21 May VÖK Salzburg 17-18 Sept AFVAC 2 to 4 December Annual Congress Lyon Voorjaarsdagen 28-30 April FECAVA/TSAVA Istanbul 7-11 September EuroCongress, AVEPA, 30 September - 3 October Barcelona, AVEPA/SEVC Annual Congress 2012 FECAVA/WSAVA/BSAVA Birmingham 12-15 April Voorjaarsdagen 26-28 April 2013 Voorjaarsdagen 25-27 April 205 Secretariat or address to contact for information (Full Association names are given at the front of the Journal) Contact Address for Information Secretariat: 40 rue de Berri – F-75008 Paris Tel/Fax Tel: (33) 1 53 83 91 60 – Fax: (33) 1 53 83 91 69 AIVPA Secretariat: AIVPA - Medicina Viva, Via Marchesi 26D - I-43100 Parma, Italy. Director: Andrea Vercelli. First contact use Director. Tel: (39) 0521-290191 – Fax: (39) 0521-291314 APMVEAC Director: Dr. José H. Duarte Correia/ Secretariat: Rua Américo Durão, 18D, 1900-064 Lisboa, PORTUGAL Secretariat: Paseo San Gervasio 46-48, E7, E-08022 Barcelona Spain Director: Dr. Boyko Georgiev, Institute of Biology and Immunology of Reproduction, Tzarigradsko shousse 73 Sofia 1113, Bulgaria Contact: Dr. Josip, Krasni - Avde Hume 6, 71000 Sarajevo – Bosnia and Herzegovina Secretariat: Woodrow House 1 Telford Way, Waterwells Business Park Quedgeley, Gloucester GB-GL2 2AB Director: Dr. Jiri Beranek, University of Veterinary and Pharmaceutical Sciences – Palackého 1/3 – 612 Brno Czech Republic Director: Dr. Davorin Lukman, Specijalizirana Ambulanta Varazdin Trnovecka 6, 42000 Varazdin, Croatia Secretariat: Emdrupvej 28 A, DK 2100 Copenhagen Director: Dr. Tiina Toomet, Vabriku 45 Tallinn, EE- 10 41.Estonia Director: Dr. Kaj Sittnikow, Ykskoivuntie 32, FIN-23500 Uusikaupunki Tel: +351 218 404 179 – Fax: +351 218 404 180 AFVAC AVEPA BASAV BHSAVA BSAVA CSAVA CSAVS DSAVA ESAVA FAVP GSAVA PSAVA PVA RSAVA SAVAB SkSAVA Secretariat: Dr. Birgit Leopold-Temmler, Gneisenaustr. 10, D- 30175 Hannover Director: Fereac Biró, Isvan u. 2 Budapest H-1078 Director: Dr. Katerina Loukaki, Protopapa 29, Helioupolis, GR- 163 43 Athens DIirector :Dr. Katia Di Nicolo, Médecin Véterinaire, 36 rue des Redoutes, L-6476 Echternach Director: Dr.Linda Jakušenoka, Meža iela 4 – 76, Tukums, LV-3101 President: Dr. Lita Konopore, Dïka iela 4 – 1, Rïga, LV–1004 Contact: Dr. Saulius Laurusevicius, Tilzes 18, LT-47181 Kaunas President: Dr Predrag Stojovic Ul.Ilije Plamenca lamela 103 bb, (Montvet), 81000 Podgorica, Montenegro Director: Marin Velicovski, Ul. Lazar Ppo Trajkov 5-7 Skopje, Fyrom Director: Dr. C.L. Vella, Blue Cross Veterinary Clinic Msida Road, Birkirkera, Malta Secretariat: NACAM, KNMvD, PO box 421, 3990 GE, Houten, The Netherlands Secretariat: SVF v/Dr. Ellef Blakstad, PO Box 6781 St. Olavs Plass N-0130 Oslo Director: Dr.Roman Aleksiewicz, Secretariat PSAVA 20-934, Lublin Director: Dr. Yiannis Stylianov, PO Box 5284, 1308 Nicosia Cyprus Contact: Dr. A. Tkachov-Kuzmin, V-Kojinoi, 23 – 121096 Moscow, Russia Director: Dr. J van Tilburg, Ernest Claeslaan 14 B-2500 Lier Belgium Director: Dr. Igor Krampl, Sibirska 41, 83102 Bratislava, Slovak republic SASAP Director: Denis Novak, Dr Ivana Ribara 186/30, 11070 Belgrade, Serbia HSAVA HVMS LAK LSAPS LSAVA MASAP MSAVA MVA NACAM NSAVA SSAVA Director: Dr. Alexandra Vilén, Regiondjursjukhuset i Helsingborg, Bergavägen 3, Box 22097, S-250 23 Helsingborg, Sweden SVK/ASMPA Director: Dr. Peter Sterchi, Mühlegrund, CH-3807 Iseltwald SZVMZ Director: Dr. Zorko Bojan, Veterinary Faculty, Gerbiceva 60, SLO-1000 Ljubljana, Slovenija TSAVA President: Erkut Goren, Vali Konagi Caddesi Akkavak Sokak. No. 11/3 Nisantasi, Istanbul, Turkey USAVA Director: Dr. Vladimir Charkin, 8 Filatova str., Apartement 24, Odessa 65000, Ukraine Tel: (34) 93 2531522 – Fax: (34) 93 4183979 Tel: (359) 888 272529 – Fax: (359) 2 866 44 50 E-mail/Website www.afvac.com [email protected] [email protected] www.aivpa.it andrea.vercelli@ ambulatorioveterinario.com or [email protected] [email protected] www.apmveac.pt www.avepa.org [email protected] Tel +387 61 133 368 – Fax 387 33 235 333 [email protected] Tel: (44) 1452 726700 – Fax: (44) 1452 726701 Tel: (420) 603 272 796 – Fax: (420) 549246974 [email protected] www.bsava.com [email protected] Tel/Fax: (385) 42 331 895 [email protected] Tel: (45) 38 71 08 88 – Fax: (45) 38 71 03 22 Tel: (372) 6413 11 – Fax: (372) 641 3110 Tel: (358) 2 844 2580 Fax: (358) 2 844 2589 Mob (358) 0400 602 081 Tel: (49)511-85 80 60 0r 99 Fax : (49)511-85 80 45 [email protected] [email protected] [email protected] Tel: (36) 305950750 Tel/Fax: (30) 2109932295 [email protected] [email protected] Tel: (352) 691711795 [email protected] Tel: (371) 26575228 – Fax: (371) 63122510 [email protected] Tel: (370) 698 45876 – Fax: (370) 373 63490 Tel: 00382 69 014 726 – Fax: 00382 81 662 584 [email protected] [email protected] Tel: (389) 91 115 125 – Fax: (389) 91 114 619 Tel: (356) 225 363 – Fax: (356) 238 105 [email protected] [email protected] Tel : (31) 30 63 48 900 – Fax: (31) 30 63 48 909 [email protected] www.gggknmvd.nl [email protected] Tel: (47) 22 994600 – Fax: (47) 22 994601 Tel: (81) 44 56 158 Tel: (357)99603 499 Tel/Fax: (7) 095 921 6376 Tel: (32) 3 489 2309 – Fax: (32) 3 480 1942 Tel: (421) 905 511971 [email protected] Tel: (46) 421 68 000 – Fax: (46) 421 68 066 www.pslwmz.org.pl [email protected] [email protected] [email protected] [email protected] www.savlmz.org [email protected] www.smasap.org.yu [email protected] Tel: (41) 33 845 11 45 Tel: (386) 14779277 – Fax: (386) 647007111 [email protected] [email protected] Tel/fax: (381) 11 2851 923; (381) 11 382 17 12; TEL: +90 212 351 71 41 – FAX: + 90 212 352 69 73 [email protected] www.tsava.org Tel.: (380) 503369810 - Fax: (380) 482 606726 v.charkin.hotmail.com or [email protected] www.usava.org.va VICAS Director: Dr. Peter A. Murphy, Summerhill Veterinary Hospital, Wexford, Tel: (353) 5391 43185 – Fax: (353) 5391 43185 [email protected] Co. Wexford Ireland by request www.veterinary-ireland.org VÖK Director: Dr. Silvia Leugner, Schönbrunnerstraße 291/1/1/3, A-1120 Wien Tel. (43) 664/8212318 or (43) 1 8791669 - 18 or (43) [email protected] [email protected] www.voek.at 1 8132983 - Fax (43) 1 8791669 - 7033 Associate members ESAVS Contact: ESAVS Office Birkenfeld, Schadtengasse 2, D-55765 Birkenfeld Tel: (49) 6782 2329 – Fax: (49) 6782 4314 ewelina.skrzypecka@esavs. or [email protected] www.esavs.org ECVD Contact: Dr. Dominique Héripret, Clinique Vétérinaire Frégis 43, avenue Tel: (33) 149 85 83 00 – Fax: (33) 149 85 83 01 [email protected] Aristide-Briand F-94110 Arcueil www.ecvd.org Tel: (41) 44 635 84 08 – Fax: (41) 44 313 03 84 ECVS Contact: Executive Secretary – ECVS Office Vetsuisse Faculty University [email protected] Zürich Winterthurerstrasse 260, CH-8057 Zürich www.ecvs.org ESFM Contact: Claire Bessant, Taeselbury, High Street, Tisbury, Wiltshire, GB Tel: (44) 1747 871872 - Fax: (44) 1747 871873 [email protected] or SP3 6LD, UK [email protected] ESVC Contact: Dr.Nicole Van Israël, Rue Winamplanche 752, Tel: +32-(0)87-475813 – Fax + 32-(0)87-776994 [email protected] B-4910 ,Theux, Belgium www.acapulco-vet ESVCE Contact: Dr. Sarah Heath, 10 Rushton, Upton, Chester GB-CH2 1RE Tel: (44) 1244 377365 – Fax: (44) 1244 399288 [email protected] or admin@ brvp.co.uk ESVD ESVD President, Dr Aiden P. Foster, VLA Shrewsbury, Kendal Road, Tel +44 (0) 1743 467621 – Fax +44 (0)1743 441060 [email protected] Harlescott, Shrewsbury, Shropshire, SY1 4HD UK www. esvd.org ESVIM Tel: (+44) 141 330 5848 - Fax: +44 141 330 3663 Contact: Dr. Rory Bell, Department of Veterinary Clinical Studies [email protected] University of Glasgow, Bearsden, Glasgow, GB- G61 1QH ECVIM-CA For Congress: Sharon Green Avenue du Guéret 1 B-1300 Limal Tel: (+32) 10 400 603 - Fax: +32 10 400 703 www.ecvimcongress.org [email protected] ESVN Tel: (44 )141 330 5738 - Fax: (44) 141 330 3663 Contact: Dr. Jacques Penderis, Division of Companion Animal Sciences, [email protected] Faculty of Veterinary Medicine, University of Glasgow, Bearsden, www.esvn.org Glasgow, GB- G61 1QH ESVOT Contact: Dr. Aldo Vezzoni, via Massarotti 60/A, I-26100 Cremona Tel: (39) 0 372 23451 - Fax: (39) 0 372 20074 www.esvot.org EVDS President: Jerzy Gawor, UL. Chlopska 2A 30 - 806 Krakow, Poland Tel: (+48) 12 6588 365 [email protected] EVSSAR Contact/President: Dr Gaia Cecilia Luvoni, Dept Veterinary Clinical Tel: +39 02 50318147 - Fax: (+39) 02 50318148 [email protected] Sciences, Obstetrics and Gynaecology,University of Milan,Via Celoria10, I-20133, Milan 206 STOP PRESS! FECAVA NEWS ESFM (European Society of Feline Medicine) and ABCD (Advisory Board on Cat Diseases) Karin de Lange reports from the ESFM Congress in Dubrovnik June 2009 prevention of feline panleukopenia, feline herpesvirus and calicivirus infections, FeLV, FIV, rabies, feline infectious peritonitis, Chlamydia/Bordetella infections and H5N1 avian influenza in cats. Swedish researcher Jonas Wensman wins the ABCD & Merial Young Scientist Award 2009 The ABCD and Merial Young Scientist Award 2009 was presented to Jonas Wensman, from the Swedish University of Agricultural Sciences (SLU, Uppsala), on 20 June in Dubrovnik, on the occasion of the congress of the European Society of Feline Medicine. Jonas Wensman (33) received the award for his work on Borna virus infection in cats and in particular the development of a real-time RT-PCR diagnostic assay. “Borna virus infection or staggering disease is a fatal, progressive, neurological disorder which also affects cats. At present, the tentative diagnosis is made clinically by excluding other causative agents and on the basis of history and epidemiology, he recalled. The need for sensitive and specific diagnostics has led to he development of a real-time RT-PCR assay, which is currently under evaluation. The award was presented by Professor Marian C. Horzinek, Chair of the Advisory Board on Cat Diseases (ABCD) and of the award jury, who congratulated the laureate. “The standard of the applications we received was very high, but the entire jury agreed on the quality of the work of Dr Wensman. This may well be the first of a number of awards he will collect in his career!” Dr Jean-Christophe Thibault, Merial’s Technical director for biologicals (Europe, Middle East and Africa), added, “True to Merial’s mission statement of being an innovation-driven leader in animal health, we are very proud to have made this European award possible. Initiatives such as these, in association with renowned scientific bodies like the ABCD, highlight promising young researchers and the teams to which they belong.” Both Professor Horzinek and Dr Thibault agreed that Jonas Wensman, under the tutorship of Professors Mikael Berg and Sándor Belák (SLU, Uppsala), has contributed lasting insights into an enigmatic feline infectious disease. Jonas Wensman, laureate of the 2009 ABCD & Merial Young Scientist Award, flanked by Jean-Christophe Thibault from Merial (left) and Marian Horzinek from the ABCD (right). The ABCD and Merial Young Scientist Award, created in 2008 and worth 1000 €, is funded by Merial and is presented to a young scientist in veterinary or biomedical science, who has made an original contribution in the field of feline infectious diseases and/or immunology. Applications for the 2010 award are now being invited (deadline 1 December 2009). Applicants should have published their findings in a journal listed in PubMed or Web of Science or have had them accepted by another recognised assessing body. Candidates should be based in Europe, have completed a veterinary or biomedical curriculum, and be under 35 years of age at the time of application. Application forms and detailed rules can be downloaded from the ABCD web site (www.abcd-vets.org) For further information, please contact Karin de Lange, ABCD secretary, karin. [email protected] Guidelines from ABCD on major infectious cat diseases now available At the Annual Congress of the European Society of Feline Medicine, in Dubrovnik (Croatia), on June 18th The Advisory Board on Cat Diseases (ABCD) launched its guidelines and fact sheets on the 10 major infectious cat diseases. A comprehensive and illustrated synopsis of the guidelines was published in the July 2009 issue of the Journal of Feline Medicine and Surgery. These are also available online (www.abcd-vets.org). Pre-publication Prepublication copies here were distributed at the launch. In addition to making vaccination recommendations, the guidelines cover the pathogenesis, management and 208 Fact sheets: educating the owner At the guidelines launch, a complete set of fact sheets were also made available. These fact sheets are intended for use by veterinary practitioners for quick and easy reference during vaccination consultations or telephone queries. They contain illustrations to help educate the cat owner in disease prevention and management. Fact sheets exist in several European languages, and copies can be downloaded from www.abcd-vets.org. The vaccination interview The launch reception in Dubrovnik was held immediately after an interactive forum organised by Merial entitled ‘The Vaccination Interview - from routine to customised vaccination’. During this event, actors played out various commonly encountered ‘vaccination issues’ in veterinary practice, including cat owners questioning the practice’s vaccination protocol, those that doubt the need for vaccination and how to handle ‘overdue’ boosters.
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