Companion Animal Practice The European Journal of give them CALM

Transcription

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
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maintain the emotional balance
of cats and dogs, which can also
be recommended for use in conjunction with behaviour therapy.
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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.
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
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!
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
(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
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
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
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
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
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
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
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
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
Table 2: Questionnaire for the owners’ interview at follow-up
128
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
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
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
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
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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
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
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
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
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
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
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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).
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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).
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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
*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
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
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
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
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
[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
[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
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
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
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
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
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
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.
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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
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
*Presented by NACAM (The Netherlands)
156
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
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
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
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
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.
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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.
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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).
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
*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
0.55 ± 0.07 ng/ml
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
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
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
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
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
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
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].
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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
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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
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
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
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
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
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
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
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.
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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
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
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
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
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
193
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 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
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
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
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
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.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.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
2013
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.

Companion Animal Practice The European Journal of give them CALM

Transcription

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