Foodstuffs toxic to small animals - a review

Transcription

VOL. 20 - (1) - APRIL 2010
ISSN 1018-2357
The European Journal of
Companion
Animal Practice
Modified functional end-to-end stapled intestinal
anastomosis: technique and clinical results in 15 dogs
75
The FECAVA Pain Symposium
54
The In-House practice Laboratory
31
THE OFFICIAL JOURNAL OF FECAVA
Federation of European Companion Animal Veterinary Associations
www.fecava.org
VOL. 20 - (1) - APRIL 2010
ISSN 1018-2357
Companion
Animal Practice
Modified functional end-to-end stapled intestinal
anastomosis: technique and clinical results in 15 dogs
75
54
31
THE OFFICIAL JOURNAL OF FECAVA
Federation of European Companion Animal Veterinary Associations
www.fecava.org
Volume 20 (1) April 2010
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. Johan VAN TILBURG, FECAVA President
Dr. Keith DAVIES, Editor
Astrid M. BJERKÅS, Sub-Editor
Dr. Joaquin ARAGONES
Dr. Peter STERCHI
Dr. Denis NOVAK
Dr. Monique MEGENS
Dr Ellen BJERKÅS
EDITORIAL BOARD (FOR NEW WORK)
Dermatology
Didier-Noël CARLOTTI (F)
Cardiology
Anna TIDHOLM (S)
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. Rob Goggs
Dr. Tim Hutchinson
Dr. Alexander Campbell
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.”
Companion Animal Practice (EJCAP)
Contents
The Federation of European Companion Animal
Veterinary Associations (FECAVA)
Editorial
5
News
8
CARDIOLOGY AND RESPIRATORY SYSTEM
Imaging features of exogenous lipoid pneumonia in a dog
J.J. Labruyère, S. Murphy, R. Dennis
17
URINOGENITAL SYSTEM
Post-partum pathological conditions in the bitch - Part 1
D.C. Orfanou, H.N. Ververidis, C.M. Boscos, G.C. Fthenakis
21
GENERAL
Urs Gilli
31
Foodstuffs toxic to small animals - a review
S. Handl, C. Iben
36
CRITICAL CARE
Traumatic Haemoabdomen
N. Sigrist, D. Spreng
53
54
Diagnosis of chronic pain in small animals
Alessandra Bergadano
55
Locoregional anaesthesia in small animals
Alessandra Bergadano
61
Acute pain management in the peri-operative period
F Roux
69
GASTEROINTESTINAL SYSTEM
Modified functional end-to-end stapled intestinal anastomosis:
technique and clinical results in 15 dogs
R.N. White
75
PRACTICE MANAGEMENT
Cyprus and the Pancyprian Veterinary Association
Yiannis Stylinou
83
Notes for Contributors
86
Book Reviews
88
Calendar of main European national meetings and other continuing
education opportunities
92
Secretariat or address to contact for information
95
1
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
AMVAC The Association of Veterinarions for Pets from Romania
President: Dr. Nicolae VALENTIN
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. Milǒs URBAN
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. Oili GYLDEN
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. Vytautas MACIJAUSKAS
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:
ECVD
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
FECAVA Officers:
Dr Johan van TILBURG
Dr. Simon ORR
Dr. Monique MEGENS
Dr. Jerzy GAWOR
Advisor to the board:
Dr. Andrew BYRNE
Dr. Keith DAVIES
2
Belgium
UK
Poland
President
Vice-President
Secretary
Treasurer
Eire
Senior Vice-President
EJCAP Editor
Editorial
2009 has been a difficult year, the worldwide crisis affecting all of us personally and professionally.
FECAVA has also had to face problems brought about by this crisis.
Even though the FECAVA Eurocongress in Lille was successful, all Congress organisers are facing more
and more difficulties to balance their budgets.
We are also in a situation where our member associations are thinking twice before spending every penny
The EJCAP journal is the most known FECAVA brand and valued in all corners of Europe. Its
distribution is however costing more and more each year. Also the distribution costs are different for
each country. Achieving a uniformity of costs in Europe has still a long way to go. Because of these facts
Council decided that EJCAP should go online only as soon as existing printer and advertiser contracts
and other practicalities allow. This will undoubtedly give some financial relief to many associations,
but only at the possible expense of a diminished product for our readers.
We will need to redefine EJCAP as a brand for FECAVA in other ways after 20 successful years in a hard
copy format. We are grateful that Keith Davies the EJCAP Editor is determined that the new online
only EJCAP will still remain a premier European Journal reflecting the work of veterinary
surgeons all over Europe.
Difficult times sometimes require painful decisions which often eventually turn out to bring positive
improvements .We are working hard on our future as a united profession all over Europe and will
continue in the same way developing our strategic plan with a Board that has always worked works as
a TEAM and as a TEAM so we will continue.
We have been working closely with the FVE and UEVP for a few years now enabling us jointly to exert
a larger political influence on behalf of the small animal practitioner. We are constantly building and
improving our strong links with these two organisations.
FECAVA also co-operates closely with the WASVA and will continue to do this by working alongside
them in promoting continuing education in Europe. The flagship of this synergy is the combined
FECAVA/WSAVA Congresses, the next being in GENEVA Switzerland in June 2010
2010 will hopefully see a U-turn in the global crisis for FECAVA and also, at a more personal level,
for all readers clinics.
Johan van Tilburg, FECAVA President
5
FECAVA NEWS
FECAVA NEWS
Johan van Tilburg – our new President
Belgium has a reputation for being
at the political centre of Europe,
and for FECAVA it is the only
member country to have supplied
two of our Presidents. Brussels has
an enviable but sometimes difficult
role in the EU. We all tend to lay
the blame for EU policies we do not
like on ‘the politicians in Brussels’.
When I recently spoke to Johan it
was clear that he was very aware of
the difficult decisions which have
to be made in the times we are
living in, but it was equally clear
that he intends not to take the easy
way out, but to choose the best long
term path for the future even if
necessary decisions are at first
unpopular.
Johan was born in Zaire, Africa,
moving to Belgium and graduating
in 1975 at the University of Ghent.
Initially he stated a small practice,
also working part time for a
Laboratory involved in
prophylactic disease control in poultry. In
1982 he started to work totally in Small
Animal Practice developing one of the
first Small Animal clinics in Belgium. For
the last 22 he has worked in the
Algemene Dierenkliniek Randstad (ADR
) Clinic where he is both senior partner
and Clinic manager. A profile of the clinic
was featured in EJCAP 14(1) April 2004
professional fields choose to spend
a significant part of their free time
working for the benefit of rest of
our profession. FECAVA has been
lucky in this respect, having been
led by several dedicated Presidents.
Johan followed this tradition
joining the FECAVA Council as the
representative for Belgium in 1999.
Prior to this he had been both a
SAVAB Board member and
President, during which time he
was President of the organising
committee of the 2nd FECAVA
Congress held in Brussels in 1995.
In FECAVA he has held Office as
both Treasurer and Vice President,
in addition to being instrumental
in the development of the FECAVA
Website
Johan has a special interest in
orthopaedic and neurosurgery. In
addition to this he believes strongly in the
importance of good practice management
which he feels benefits not only the
Veterinarian, but also helps raise the
standard of patient care.
It often seems surprising that
veterinarians who are busy in so many
Our President relaxes at his home in France.
Johan is married and has three
daughters, Barbara, Sarah and
Ellen – Ellen also being a
veterinarian. He has the added
responsibility of 5 soon to be six
grandchildren! Fiston the dog and 3 cats
– all re-homed from the practice, are also
important family members.
Together with his wife Maryke, he is a
keen golfer, both of them also sharing a
passion for modern art, visiting
exhibitions and travel .With such a busy
professional life it can be difficult to find
time for hobbies. FECAVA must never
forget the sacrifices and support given by
the wives and families of those who work
for the Federation.
Readers are perhaps wondering how
Johan will change FECAVA. I think the
Editorial in this issue gives us some clues.
The global recession is having an effect
on all of us, not least FECAVA . Difficult
decisions have to be made and a strong
leader is needed. FECAVA is lucky to
have such a person in Johan van Tilburg.
Keith Davies Editor EJCAP
8
EJCAP - Vol. 20 - Issue 1 April 2010
Simon Orr, FECAVA Vice President reports:
The value of membership
of FECAVA
and administrative help for the Board is
engaged efficiently on a part time
professional basis.
What does FECAVA do for you?
FECAVA has come a long way in the last
twenty years from its humble beginnings
as a body whose raison d’être was to to
harmonise the activities of its thirteen
founding members. The production of
the European Journal of Companion
Animal Practice (EJCAP) was soon added
to its brief. Today, it does much, much
more:
Harmonisation
FECAVA is the organisation that unifies
and represents the national companion
animal veterinary associations of Europe
and provides a conduit through which
the common objectives of its members are
pursued. FECAVA works closely with
UEVP and FVE in a focussed and
co-coordinated manner to ensure strong
representation of the issues.
Voice
FECAVA provides a voice for companion
animal issues and ensures inclusion of
relevant topics on the European political
agenda.
Focus
The focus of EU policy had traditionally
been on food safety and therefore food
animal issues. The importance of food
safety within the European community
suggests prioritisation of these aspects of
veterinary activity, which can work to the
detriment of the companion animal arm
of the profession. However there is
increasing recognition of the importance
of companion animals in the physical and
mental well being of European society.
In addition to zoonotic diseases the
sociological and economic importance of
companion animals must be promoted.
Current working groups include standing
committees and special projects working
groups:
• EJCAP Production Sub-committee
• Financial Advisory Sub-committee
Working groups:
• FECAVA Eurocongress Protocols
Review
• Constitution Review
• Continuing Education Accreditation
• Hygiene and the Use of Antimicrobials
in Veterinary Practice
• Continuing Education in Eastern
Europe
• Socioeconomic Value of Companion
Animals
Sub-committee on Animal Assisted
Therapy and Animal Assisted
Activities
• Website Development
How does FECAVA carry out its
work?
The Council is the main structure of
FECAVA comprising one director from
each of our 37 member associations and
is the forum through which all objectives
are proposed and policy ratified. The
Council establishes Working Groups to
concentrate on the implementation of
projects initiated by Council. The Board
of Officers works as a close knit team to
lead and implement objectives defined by
Council. In addition the Managing
Editor of the European Journal of
Companion Animal Practice coordinates and delivers a high quality
European journal. Executive assistance
Some areas that are currently
receiving special attention
Medicines
Maintaining availability of medicines for
use in companion animal practice in
Europe is an ongoing challenge essential
to the practice of high quality veterinary
care. This is not only an issue for smaller
member states but in the future will
remain an important issue for larger
member countries where continued
availability of products must be
protected. Medicines legislation is under
review by the European Commission and
FECAVA plays an active role in the FVE
Medicines Working Group where the
particular challenges both present and
future are kept on the agenda.
Animal Health Legislation
European common animal health laws
and strategy are under review with
legislation and policy being drafted for
implementation between 2011 and 2014.
The remit of the EU Commission in
relation to animal health has focussed on
the protection of consumers of animal
derived food and the food sector
economy. Yet the definition of community
health refers to the social and mental
wellbeing of the community. Companion
animals contribute significantly to this
wellbeing. This sector also makes a large
contribution to the economy of Europe
which is often over looked. FECAVA is
active in collating information to support
this fact and promoting this to the
9
European Commission, the European
Parliament and the public.
Education
FECAVA provides input into the
visitation of veterinary schools in
conjunction with UEVP through ECCVT.
It is well placed to contribute to debate on
the future strategies for education of
veterinary undergraduates ensuring a
reasonable balance of integration that
includes appropriate attention to
companion animal aspects of
undergraduate education. Continuing
education is supported by its programme
for CE in Eastern European regions and
of course through the FECAVA
Eurocongresses which provides a forum
annually for veterinarians across Europe
to come together in a pan European
congress.
The Blue Dog Project – the education of
young children to the benefits (and
potential dangers) of dog ownership is
pivotal in developing the next generation
of companion animal owners and
ensuring responsible pet ownership.
Veterinary Nursing Education
FECAVA liaises with the Veterinary
Nursing profession. It has worked closely
with VETNNET, the European network of
veterinary Nursing educators and
nursing associations. FECAVA has been a
project partner in several European
funded education projects with
VETNNET including DASVENT which
led to the formation of ACOVENE (the
Accreditation Committee for Veterinary
Nursing Education in Europe). It is also a
project partner in the Leonardo
supported PEPAS project to develop a
European OSCE examination protocol for
veterinary nurses to facilitate the
assessment of practical competences of
trainee veterinary nurses.
Liaison with other Veterinary
Organisations
FECAVA enjoys a productive and close
working relationship with other key
veterinary organisations such as UEVP,
FVE (including its sections and working
groups) and WSAVA.
Communications
EJCAP - The European Journal of
Companion Animal Practice is
published three times a year. Two hard
copy issues and one on-line issue,
dedicated to a particular discipline, are
FECAVA NEWS
produced. The journal continues to
emphasise the reprint of peer reviewed
papers especially from non-English
language publications to bring
information to a wider readership across
Europe. In addition, original work and
commissioned papers are published
together with news, editorial comment,
book reviews and calendar information
on CE in Europe, producing a
comprehensive and varied journal. This
is a high quality production with a strong
multi-cultural European flavour that is
sent to each and every member of
FECAVA. It is included as part of
FECAVA membership and represents
exceptional value for money to the
individual veterinarian.
We believe that EJCAP augments existing
national publications and provides
additional resources to all European
veterinarians. Existing veterinary
journals published by our member
associations should have continued
confidence in their own journals safe in
the knowledge that their own Federation
adds diversity and a European flavour to
their members reading through EJCAP.
Website - www.fecava.org provides an
information resource and promotion of
FECAVA activities and projects.
Electronic Newsletters
Regular electronic newsletters are
published and sent to each member
association for distribution to every
member. We are proud that every
member of FECAVA can be kept up to
date on all activities. Distribution of this
newsletter through the member
associations is essential and from
feedback we know that it has been very
successful in generating awareness and
ideas.
Promotion of Member Association
Educational Events - members CE events
are advertised through the calendars in
the Journal and on the website.
Policy Statements
Member associations find FECAVA Policy
Statements useful when lobbying national
government agencies. Suggestions for
policy and appropriate statements can be
received by the Board at any time from
individual member associations.
FECAVA Eurocongress Protocols
Review
Congress protocols have been reviewed to
provide comprehensive guidelines and
Standard Operating Procedures (SOPs)
for FECAVA Eurocongresses. These
protocols will be reviewed at regular
intervals to keep them current.
Constitutional Review
A review of the constitutions is underway
to ensure it meets the needs of today.
Continuing Education Accreditation
A working group has been established to
explore the development of accredited
modular C.E. that is achievable by
practitioners. FECAVA have been liaising
with the other veterinary organisations
and have reached agreement on a
multi-organisation working group,
including FECAVA, FVE (UEVP), EAEVE,
Statutory Bodies and EBVS, to bring this
concept forward.
Hygiene and the Use of Antimicrobials
in Veterinary Practice
This working group is reviewing
information on resistant microorganisms
relevant to companion animal practice and
will develop protocols and guidelines for
infection control practices and protocols
for use of antimicrobials in companion
animal practice. FECAVA is liaising with
UVEP and FVE on this matter.
Continuing Education in Eastern
Europe
FECAVA provides support to member
associations in Eastern Europe to assist
with C.E events. These events have been
very successful and many have attracted
collaboration and participation from
neighbouring countries. As time
progresses some countries no longer
require assistance and so funds are
redirected as appropriate.
Socio-economic Value of Companion
Animals
This working group is expanding to
include a sub-committee on Animal
Assisted Therapy and Animal Assisted
Activities and will collate information
and explore how the veterinary
profession may work with and assist
groups providing such services. It is
important to collate evidence and
promote the value of companion animals
both in economic and social terms. The
effects of such efforts are not seen
immediately but are a long term
investment in the development and
promotion of the relevance of companion
animal welfare and healthcare in Europe.
Cultural Benefits.
It is easy to overlook the obvious but
important cultural benefits that arise at
all levels from a strong pan-European
10
Federation that joins 37 countries in the
common goals of furthering the quality
companion animal veterinary care and
welfare and protecting the integrity of
the veterinary profession. As in all walks
of life participation and engagement is
the key to fulfilment - the more you take
part the more you benefit. This is true
from committee and working group level
to participation in European CE events,
reading and exchanges.
Cost and Value
FECAVA Officers and Council members
are all volunteers. As activities increase
there will be an increasing need for
professional secretarial help. In order to
remain active the Federation needs
income to fund the costs of running a
professional and effective organisation.
It is important that the future of FECAVA
activities is sustainable.
In the beginning, the first volume of
EJCAP was purchased at 2.6 ECU per
member and the second at 2.2 ECU per
member and they were distributed to
each member of the founding national
associations. In 1992, the Federation dues
were agreed at 1.8 ECU payable twice a
year. Allowing for inflation, the 3.6 ECU
payable in 1992 is approximately
equivalent to 5.48€ today. So in real
terms, the membership fee increase to
6.40€ per member, which will be
implemented over the next two years,
represents only a 0.92€ increase in
nineteen years..
The voluntary Board of FECAVA remains
ever mindful of costs and value for
membership and continues to monitor
expenditure on its activities carefully.
However it is also intent on securing the
activity level of FECAVA which relies
heavily on the voluntary commitment of
colleagues to enable it to function
efficiently.
Self Help and Solidarity
FECAVA relies on the generous
contribution of energy and time from its
member associations’ representatives on
Council and the Board. It also relies on
the financial contributions from each
individual member through their
associations. In addition the solidarity of
the 37 member associations who bring
diversity of needs and diversity of talents
and ideas is of paramount importance.
Every individual member association,
large and small, benefits from the
existence and activities of the professional
community that is FECAVA
The Costs of FECAVA
Membership
At the recent Council meeting in Lille, the
FECAVA Council agreed to a phased
increase in membership dues from the
present 4.4€ per annum per member to
6.4€ per annum per member. This
represents a 1€ increase in 2010 followed
by 1€ plus inflation increase in 2011.
Thereafter, the dues will undergo an
inflationary increase annually. As
already mentioned in the ‘Benefits of
membership section’ above, this increase
will represent a real increase of only 0.92€
per member in the last 18 years. A very
significant factor, which contributed to
the agreement was the decision, already
reported on on p ?? that EJCAP would go
online as soon as possible, probably from
April 2011 .
The subject of the FECAVA membership
dues has been the subject of frequent and
sometimes difficult debate over recent
years. This has resulted in delays in
agreeing the necessary increases which
have been compounded by delays in
implementing the agreed increases.
FECAVA has evolved into a much more
active organisation when compared to the
original European harmonisation body
founded in 1990, which in the early days
did little more than produce a European
reprint journal, the European Journal of
Companion Animal Practice.
Successive Honorary Treasurers have had
to propose and Council has had to accept
deficit budgets since 2006 and as a result
of this and the more recent economic
downturn, the Federation’s reserves have
increasingly come under pressure.
Fortunately, the effects on the reserves
have been ameliorated by the Treasurer’s
success in collecting outstanding dues
payments from some members and also
outstanding advertising revenues from
EJCAP.
The 2010 Budget also shows a deficit,
which the Board had hoped to avoid by
implementing the full 2€ plus inflation
increase in 2010. However, at the Council
meeting, it became increasingly apparent
that some member associations might
have difficulty with its members if the
full increase was implemented in one go,
before EJCAP goes online and member
associations no longer have to pay the
distribution costs of a hard copy journal.
For this reason, the Board proposed the
staged increase of dues over two years,
which was more palatable to the majority
of member associations.
Only time will tell us whether these
decisions, relating to the membership
dues and the move to an online journal,
will be entirely beneficial to the wellbeing
of the Federation. However, the Board
and the Editor of the Journal are
committed to ensuring the continued
success of all aspects of FECAVA’s activity
and hope that they will be able to report
favourably during the next two years.
The new FECAVA Board
At the recent FECAVA Council meeting in
Lille, an election was held for the new
FECAVA Board.
The following Officers were elected for
two years until the next election due to be
held at the FECAVA/TSAVA
Eurocongress in Istanbul in 2011:
President
Dr. Johan Van Tilburg (Belgium)
Vice President
Dr. Simon Orr (United Kingdom)
Honorary Secretary
Dr. Monique Megens (The Netherlands)
Honorary Treasurer
Dr. Jerzy Gawor (Poland)
Advisor to the Board
Senior Vice President
Dr. Andrew Byrne (Republic of Ireland)
Due to a family bereavement, our new
President, Dr. van Tilburg was unable to
attend the Council meeting in Lille or to
give his acceptance address, which was
transmitted to the Council members after
the meeting:
“Dear Friends
Even in difficult times, I’m very happy to be
elected and thank you all for the confi dence
given.
I want to thank first of all Andrew (Byrne)
and the other members of the Board for the
tremendous work that has been done in the last
two years. Remember: FECAVA work is
teamwork and this will continue under my
Presidency for the next 2 years (even if I have
had to let you all down this weekend)
FECAVA has influenced my daily life,
professional as well as private.
It is good to have the feeling that all of us, as
members of FECAVA, have influenced the
actions of the veterinary profession in a positive
way. We must all to remember that our goals
must be to help animal and owner by providing
the best possible advice and also to improve the
human-animal bond. Our profession is not
purely scientific but also has a very social
aspect. Whether we are in the North or South
of Europe, East or West; whatever religion we
have: Protestant, Catholic, Muslim etc. WE
DO HAVE THE SAME PROFESSION and
THE SAME GOAL
During the years I have served as a FECAVA
Director and Board member, I have had the
opportunity to visit different countries and
make a lot of friends. It has been an enriching
experience.
I intend to ensure that the Board will continue
to work as a team for the future of FECAVA
and the veterinary profession.
I hope that both myself and other Board
members can visit many of you in the next two
years. You all know that we are practitioners
with a busy calendar. If possible I would like to
hold some of our Board meetings at one of your
congresses as this will improve contacts
between directors, grass roots FECAVA
members and the Board.
I don’t have to emphasize the value of
FECAVA, this has been done in a document
circulated by the Board very recently, but the
written word must be continued in the fi eld.
With the help of every one of you, we will
succeed. Thank you”
Johan van Tilburg
The retiring FECAVA Board
as portrayed by Zebranie
Gawor, whilst the Board were
meeting at the home of Jerzy
Gawor our Treasurer.
From Left > Right
Jerzy Gawor, Simon Orr,
Johan van Tilburg,
Ellen Bjerkås
11
FECAVA NEWS
Keith Davies, Editor EJCAP reports:
15th EuroCongress in Lille a triumph for FECAVA,
AFVAC, SAVAB and LAK
It’s hard to believe that the recent
FECAVA EuroCongress held in Lille was
the 15th to be held since FECAVA was
founded in 1990.The first FECAVA
Congress hosted by CNVSPA (now
AFVAC), was held in1994 in Paris, and 15
years later it is appropriate that the 15th
Congress was also in France, hosted
jointly by three of our member
associations, AFVAC (F), SAVAB(B) and
LAK (Lux).
It was equally appropriate that FECAVA
should choose to honour its first and
founder President Didier Carlotti,
making him the first Honorary Member
of the Federation.
Didier has worked tirelessly for FECAVA
for 20 years. This year he has been very
active, despite his battle against cancer, in
helping produce the Dermatology on line
issue 19(3), currently available for
FECAVA members on our Website
www.fecava.org.
Didier-Noël Carlotti receives Honorary
FECAVA Membership from Andrew
Byrne, the outgoing FECAVA President
Eric Guaguère, AFVAC President, at the
Opening ceremony
Also at the Congress opening ceremony
AFVAC was proud to award its prestigious
medal to Patrick Benard, Didier-Noël
Carlotti, Emmanuel Delaporte, Francis
Fieni, Gérard Faure and David Wadsworth
and the Special AFVAC Prize to Roger
Guerre. The SAVAB FLANDERS AWARD
2009 was presented to Jos Vandelaer.
region of 300 veterinary surgeons came
from clinics in 33 mainly European
countries in addition to those from france,
choosing to pursue lifelong learning at the
FECAVA EuroCongress. The excellent
communications to Lillle by air and using
high speed trains (TGV and Eurostar)
proved their worth. There were 97
exhibitors in the very impressive
commercial exhibition. Hill’s Pet Nutrition
and Virbac were Platinum Partners and
Bayer HealthCare, Merial and Royal
Canin Gold Partners, all sponsoring the
Congress generously.
The breeder-veterinarian meetings were a
great success, with 140 canine breeders
and 64 feline breeders attending.
The ten-stream scientific programme was
devoted to cats and smaller companion
animals, including children’s and more
exotic Pets.
As one may expect when the
EuroCongress is organised in France, this
15th event was a tremendous success.
Every effort possible was made to promote
the brand ‘FECAVA EuroCongress’
The now well known ‘FECAVA
Symposium’ this year was well attended
covering the topic of ‘Pain in Companion
Animals’ Papers based on 3 of the lectures
will published in EJCAP. In this issue turn
to pages 54 to 73 where you will find a
Symposium introduction and these
papers. Three papers not featured will
appear in EJCAP 20(2). The full
symposium proceedings will be available
on www.fecava.org shortly.
There were 3263 delegates, including
veterinary nurses, speakers, veterinary
students and commercial exhibitors. Of
the scientific programme delegates, almost
1/3 came from outside France. In the
Of course no Congress where AFVAC is
involved could fail to have an outstanding
social programme. In Lille for the Soireé
du Congrès the organising committee had
the inspired idea of giving tickets for the
With 10 streams, 270 speakers and translation into English and
French when needed, the Scientific programme was impressive.
The commercial exhibition with 97 exhibitors was clearly not to be
missed.
12
FECAVA NEWS
The superb Lille National Orchestra was conducted by Roberto
Minczuk.
The copious supply of canapés and wines served in Le Palais des
Beaux Arts left no one hungry.
evening as part of the registration fee. All
delegates could enjoy the evening
together, not just a small elite. Judging by
the fact that there seemed to be at least
2000 people in the concert hall it certainly
showed how delegates of all ages and
tastes could enjoy an evening together.
For me the most memorable piece in the
concert programme was Respighi’s ‘The
pines of Rome’. It is seldom possible to
enjoy live so massive an orchestra in full
flow. A substantial section of wind
instruments were sited to the rear of the
auditorium for some sections, giving the
performance a stupendous all round
sound. At the end of the first half of the
concert, following an excellent
performance of the Concerto de
Aranjuez(Rodrigo), the FECAVA EJCAP
awards were presented as follows:
Dr Erik TESKE. Prize for the best
original paper in EJCAP 2007 to 2009
awarded for the papers ”Clinical Cytology
of Companion Animals.
Dr Silke SCHMITZ. Prize for the best
reprint article in EJCAP Volume 18(2)
October 2008 and Volume 19(1) April 2009
awarded for the paper “Gastric emptying –
physiology, pathology, diagnostic procedures
and therapeutic approaches in the dog”.
All the FECAVA Past Presidents were present in Lille. It proved impossible to find all
seven of them at the same time in Le Palais des Beaux Arts. Above from left to right: Ray
Butcher, Marc Buchet, Didier Carlotti, Simon Kleinjan, Andrew Byrne and Ben Albalas.
Ellen Bjerkas could not be found!
Erik Teske (Centre) winner of the prize for
best new work paper in EJCAP with Keith
Davies, Editor EJCAP(left) and Simon Orr
Vice President FECAVA Photo taken at le
Palais des Beaux Arts.
Silke Schmitz winner of the prize for the
best reprint paper in EJCAP with Andrew
Byrne, outgoing President of FECAVA
and the Editor of EJCAP.
13
FECAVA NEWS
The Romanian Small
Animal Veterinary
Association becomes the
37th member of FECAVA
Dr. Nicolae Valentin (President) and Dr.
Andrei Timen (Vice President) of the
Asociatia Medicilor Veterinari pentru
Animale de Companie (AMVAC), also
known as the Romanian Small Animal
Veterinary Association (RoSAVA)
attended the FECAVA Council meeting in
Lille on Saturday 28th November 2009 to
present an application for membership.
Dr. Timen explained that AMVAC was
founded in 1999, initially with 23
members. Its goal is to unite small
animal veterinarians within Romania
and to promote quality and
professionalism in the veterinary field.
FECAVA votes to become
an Associate Member of
Vet 2011
Prof. Jean-François CHARY, President of
the Vet2011 Animation and Coordination
Committee, was invited to give a
presentation on the Vet2011 project to the
FECAVA Council meeting in Lille on
Saturday 28th November 2009.
Professor Chary told Council that the
world’s first veterinary school was
founded in Lyon, France, in 1761, shortly
followed by the Alfort Veterinary School,
near Paris, in 1764, both of them at the
initiative of French veterinarian Claude
Bourgelat. By setting up the world’s first
veterinary training institutions,
Bourgelat created the veterinary
profession itself. This means that 2011
will mark not only the 250th anniversary
of veterinary education but also the 250th
anniversary of the veterinary profession.
Publication of Veterinary research
commences
The world’s first Veterinary School in Lyon
On November 24-25th, 2007 the 1st
AMVAC Symposium was organized with
70 participants. In March 2008, the 2nd
AMVAC Congress had 130 participants,
in November 2008, the 3rd AMVAC
Congress had over 500 participants and
in November 2009, the 4th AMVAC
Congress had over 600 participants.
Today, AMVAC proudly has 550 active
members. Its future goal is to increase
the number of members as well as to
develop more workshops for
veterinarians and veterinary nursing
technicians.
To ensure the best education for
members, AMVAC would greatly
appreciate the support of FECAVA in
recommending the most qualified
lecturers and speakers and would try to
benefit from FECAVA’s experience in
organizing aspects of these events.
The establishment of the
earliest Veterinary Schools
FECAVA Council unanimously voted to
accept AMVAC as a member.
14
Bourgelat’s influence did not stop there.
As a result of his collaboration with
surgeons in Lyon, he was also the first
scientist to suggest that studying animal
biology and pathology would help to
improve our understanding of human
biology and pathology. So 2011 will also
mark the 250th anniversary of the
concept of comparative pathobiology,
without which modern medicine would
never have emerged.
Vet 2011 has proposed that 2011 should be
declared “World Veterinary Year” and
aims to promote the veterinary
profession in all its aspects throughout
the world.
Vet 2011 proposes:
• symposia on veterinary science and
research,
• conferences on the future development
of the veterinary profession,
• symposia in relation to animal issues
(wildlife, pets, animal welfare etc),
• veterinary conferences concerning
animal-related events (dog shows,
horses or farm animals shows etc),
• television and radio coverage on :
o the history of the profession and
veterinary science,
o veterinary education,
o the various forms of professional
practice,
o the role of veterinarians in :
• reducing global hunger,
• controlling zoonoses,
• monitoring food quality and
safety,
• biomedical research,
• promoting animal welfare,
• protecting the environment and
biodiversity ;
• the issuing of a postage stamp
bearing the portrait of Claude
Bourgelat,
• sessions commemorating the birth
of the profession, with a press
conference in each veterinary
event held in 2011.
Professor Chary invited FECAVA to
become an Associate Member of Vet 2011.
FECAVA Council voted unanimously to
accept this invitation. There is a lot more
interesting information to be found on
the Vet 2011 website www.vet2011.org .
UEVP NEWS
Report on the General Assembly of the Union of European Veterinary Practitioners
The last GA took place in Brussels on the
12th November 2009 and was well
attended by the twenty five countries
which comprise the UEVP. We were also
able to welcome Romania as an observer
and prospective new member.
Our aim is to represent the interests of
veterinary practitioners irrespective of
the work that they carry out. This means
working closely with the FVE and the
other Sections - EVERI which represents
education, research and industry; UEVH
representing veterinary hygienists and
public health workers; and EASVO – state
veterinary officers.
As the work of veterinary practitioners is
so varied so are the topics we aim to
cover. We regularly attend meetings
organised by FVE on education,
medicines and animal health. To help us
understand the issues being raised in
Brussels by the Commission, Council and
Parliament we have for several years
engaged the services of Euralia who
provide monthly updates on legislation
which affects the profession.
At the last meeting we discussed the
problems of Q fever in the Netherlands
where goats over the last three years have
become a source of this zoonotic
infection. The disease is of concern to the
Veterinary profession not only because
of our role in its prevention in the host
species, but also because of our
responsibility to miminise the risks to
veterinarians and the local population.
We received an update from Declan
O’Brien on the work of EPRUMA, an
organisation that facilitates the various
stakeholders involved in the responsible
use of antimicrobials. In 2007 they
produced a document expounding the
responsible use of antimicrobials in food
producing animals which has now been
translated into several European
languages.
Concern was expressed over the lack of
investment in the production of new
classes of antibiotics and so we need to
keep those we have and to try to avoid
the build up of resistance. The
Commission is due to survey the
amounts of antibiotics used and the
problem of resistance.
The British Veterinary Association
announced that it has just produced a A3
wall poster for its members advocating an
eight step approach to the responsible use
of antibiotics in both food and companion
animals.
One of our vice presidents, Rens Van
Dobbenburgh ,gave a financial update on
how the recession has affected practices.
He gave details from small animal
practices in the UK (Fort Dodge Indices)
and from all types of practice in the
Netherlands and France. There were
15
large variations but all figures showed a
decrease from just a few % in small
animal up to 40% for horse work in the
Netherlands.
Ross Tiffin who has written many articles
over many years on the working of the
profession and is the editor of the Society
of Practising Veterinary Surgeons’
‘Annual Review’ gave two presentations.
The first was on the expansion of
corporate practices and the various types
existing in the UK; but also on the
changes affecting the provision of
veterinary services in the Netherlands
and Switzerland.
His second talk was on ‘Customers in the
Veterinary Marketplace’ where there
appears to be a discrepancy between the
expectations of the profession in relation
to an improved work-life balance and the
consumer, who wishes to experience a
positive purchasing experience.
If you would like to know more about
UEVP then please visit our website on
uevp.org or fve.org
Andrew Robinson
General Secretary UEVP
FECAVA NEWS
WSAVA 2009 Sao Paulo
Congress Highlights
Close to 3,500 attendees from 55 countries
representing every continent but
Antarctica came together in the bustling
and cosmopolitan city of Sao Paulo, Brazil
to learn and celebrate the collegiality of
veterinary medicine in the largest
WSAVA World Congresses ever held. In
addition to the scientific programme that
featured over 80 world-renowned
veterinary lecturers covering over 30
disciplines in 9 simultaneous session
streams, including 5 State-of-the-Art
Lectures (SOTALS), there was a WSAVA
Animal Welfare stream, a WSAVA
Hereditary Diseases stream, a North
American Veterinary Conference stream,
and 3 Pre-Congress Forums.
WSAVA New Board
Members
Prof Peter Ihrke joins the WSAVA
Executive Board in the Vice President
position and Dr. Veronica Leong joins
with a portfolio that incorporates WSAVA
Public Relations activities as well as the
new WSAVA Editor role.
WSAVA members in Sao Paulo, Brazil
WSAVA Hills Excellence in Veterinary
Healthcare Award: Professor Peter J
Ihrke VMD, DACVD, DECVD
Dear Colleagues and Friends,
On behalf of the Swiss Society of Small
Animal Medicine, I am really pleased to
invite you to the WSAVA 2010 world
meeting in Geneva on June 2 to 5. We are
planning to offer you a stimulating
scientific meeting as well as a large and
attractive social programme. The
FECAVA and the FAFVAC will be
associated to our congress and hold their
annual symposium. Parallel to the main
meeting in English, German and French
streams will be organised. Geneva is a
living postcard with a long history of
warm and generous host reception,
dating back to the 17th century. All
sessions will be held at the Palexpo, near
the airport, with a direct train connection
to the main railway station of Geneva,
downtown near the lake and all facilities
of the city centre.
Waiting to see you there.
WSAVA President’s Award: Didier-Noel
Carlotti, Doct-Vet DECVD.
Chris Amberger, Chairman of the Local
Organising Committee
For more information on the 2008 WSAVA
Congress, including a photo gallery,
Award winners, and access to the
Congress Proceedings, visit the
Homepage of the WSAVA website at
www.wsava.org.
WSAVA will celebrate its 50th
Anniversary in Geneva – please come
and join us!
2009 WSAVA Award
Winners
WSAVA WALTHAM International Award
for Scientific Achievement: Professor
Robert Washabau VMD, PhD,
Diplomate ACVIM (Internal Medicine)
WSAVA INTERVET/SCHERING
PLOUGH International Award for Service
to the Profession: Dr Larry G Dee DVM
DABVP (Canine and Feline)
WSAVA HILL’S Mobility Award: Duncan
X Lascelles BVSc, PhD, DACVS,
DECVS, RCVS CertVA
(Anaesthesiology and Small Animal
Surgery
Peter Ihrke and Veronica Leong new
WSAVA Board members
WSAVA/FECAVA World
Congress Geneva 2010
Update
An invitation from Dr. Christophe
Amberger, Congress Organizing
Committee Chair
16
Future Congresses
Geneva, Switzerland – June 2-5, 2010
(WSAVA/FECAVA)
Jeju, South Korea – October 14-17, 2011
Birmingham, UK – April 12-15, 2012
(WSAVA/FECAVA)
Christchurch, New Zealand – March, 2013
CARDIOLOGY AND RESPIRATORY SYSTEM
ORIGINAL WORK (UK)
Imaging features of exogenous
lipoid pneumonia in a dog
J. J. Labruyère (1) S. Murphy(1) R. Dennis(1)
SUMMARY.
Exogenous lipoid pneumonia (ELP) is recognized as occurring secondary to aspiration of exogenous lipidcontaining material. Diagnosis is based on radiographic examination and clinical signs but is most supported
by an accurate history. To the authors knowledge this is the first report to describe the clinical, radiographic and
ultrasonographic features of a dog with ELP, with confirmed histological evidence of lipid aspiration.
Introduction
Thoracic radiographs were taken under general anaesthesia
with the lungs manually inflated and revealed a homogeneous
soft tissue opacity involving the caudal part of the left cranial
lung lobe, sharply demarcated from normal lung. Several air
bronchograms were seen but there was no mediastinal shift or
change of volume of the affected lung lobe, suggesting lobar
consolidation (figure 1, 2, and 3).
Intercostal ultrasonography of the consolidated area of the
left cranial lung lobe revealed pairs of branching lines with
an anechoic centre, consistent with “fluid bronchograms”,
surrounded by uniformly hyperechoic lung tissue (figure 4). An
ELP has been observed most commonly in cats in which mineral
oil is used as treatment for hairballs, and in horses following
incorrect passage of a stomach tube when administering
mineral oil for treatment of gastrointestinal disorders [1-3].
There is only a single case report in the veterinary literature
of lipid pneumonia in the dog, and the authors were unable
to definitively determine whether it was the exogenous or
endogenous form [4]. In that case, supportive evidence that it
was an exogenous form included the presence of muscle fibrelike structures in one bronchoalveolar lavage sample, suggesting
the possibility of food aspiration. Here we report the first case of
ELP in a dog with evidence of oil aspiration.
Figure 1: Initial
examination.
Ventrodorsal
projection.
Homogeneous
soft tissue opacity
involving the caudal
part of the cranial
left lung lobe. Air
bronchograms are
visible, compatible
with lobar
consolidation. Some
infiltrates also
involving the right
middle lung lobe are
seen.
Case History
An eight-year-old, male neutered Labrador was presented to the
oncology referral service at the Animal Health Trust. The patient
had a history of increased respiratory noise and coughing over
the last three weeks, partly responsive to two weeks treatment
with antibiotics and corticosteroids. At the time the problem
started, cod liver oil had been administered with a spoon by
mouth on a daily basis as a food supplement for a period of
one month.
Clinical examination revealed a reduced state of nutrition. There
was increased respiratory noise on auscultation, which was
more severe on the left side. Serum biochemistry and routine
haematological examination revealed only a mild neutrophilia
17.80 K/µl ( 2.00 – 12.00 ).
(1) Animal Health Trust, Lanwades Park, Newmarket, Suffolk, GB-CB8 7UU.
(2) Corresponding author E-mail [email protected]
17
Imaging features of exogenous lipoid pneumonia in a dog - J. J. Labruyère, S. Murphy, R. Dennis
Figure 2: Initial radiographic examination: Left lateral recumbent
projection. An increased soft tissue opacity is superimposed over
the cardiac silhouette. Air bronchograms are visible.
Figure 5: H&E staining x40
Extracellular blue globules of fatty material are visible.
ultrasound-guided aspirate was taken at the level of the left 7th
intercostal space for cytology and bacteriology. The haematoxylin
and eosin (H&E) staining of the sample showed the presence of
foamy macrophages, many of them containing intracytoplasmic,
smooth, blue-green material and extracellular globules of
this fatty material was also seen (figure 5 and 6). Globules of
similar appearance were observed after haematoxylin and eosin
(H&E) staining a drop of pure liver oil (figure 7). This confirmed
the suspicion of cod liver oil aspiration based on the history,
nevertheless cod liver oil cannot be distinguished from other oils
based on H&E staining. Special stains for fat and glycogen (oil
red O and PAS respectively) were also performed and confirmed
the presence of lipid in this material. No evidence of infection,
inflammation or neoplasia was noticed, supported by negative
aerobic and anaerobic bacteriological culture. This was consistent
with aspiration of fatty material, and a diagnosis of ELP was
made. The dog was treated with enrofloxacin (Baytril; Bayer)
5mg/kg and prednisolone (Prednicare; Animalcare Limited)
1mg/kg administered orally for three weeks. Three weeks
later the dog was admitted for re-examination. The dog was
Figure 3: Initial examination. Ventrodorsal projection. Close up
Figure 6: H&E staining x100
Note the presence of foamy macrophages, some of which contain
smooth, intracytoplasmic material.
Figure 4: Initial examination. Ultrasonography.
Ultrasonography performed through an intercostal window. Note the
fluid-filled bronchus, appearing as an anechoic branching structure
(so called “fluid bronchogram”).
18
Figure 9: Repeated examination three weeks later. Left lateral
projection.
No significant changes in the radiographic appearance of the lungs.
Figure 7: H&E staining x 10: Cod liver oil
asymptomatic. There was however no change in the thoracic
radiographic lesions previously observed in terms of severity
and location (figures 8 and 9). On ultrasonography, the caudal
part of the left cranial lung lobe was diffusely hypoechoic with
scattered hyperechoic foci randomly distributed throughout
the parenchyma (figure 10). Ultrasound-guided fine needle
aspirations were taken and submitted for cytology and revealed
unchanged cytologic changes. Enrofloxacin was stopped after
three weeks and the dog weaned off prednisolone. One month
after cessation of treatment the owner reported the dog to be
well with good exercise tolerance.
lungs [1, 5]. It is further classified as exogenous or endogenous
on the basis of the source of lipid. Endogenous lipid pneumonia
(EnLP) occurs when cholesterol and other lipids are released
into the alveoli following breakdown of pulmonary cell walls
[6]. The pathogenesis is multifactorial, including obstructive
bronchopulmonary disease. ELP results from the inhalation or
aspiration of vegetal, mineral or animal oil. The severity and type
of pathologic lesion in the lung is dependent on the origin of the
lipid. Vegetal oils do not emulsify and therefore do not trigger an
inflammatory response and are removed from the lung largely by
expectoration. In contrast, mineral oils and lipids of animal origin
such as cod liver oil initiate a local cell-mediated inflammatory
response that eventually leads to fibrosis [6]. Fish oils have
recently gained the attention of nutritionists, veterinarians and
pet owners for their positive effects in management of a variety
of diseases. In the present case it is believed that the mode of
administration led to aspiration of the oil, the reluctant dog being
forced to swallow with the help of a spoon. The bland nature
Discussion
Lipoid pneumonia is a type of irritant pneumonia characterised
by a chronic inflammatory response to the presence of oil in the
Figure 8: Repeated examination three weeks later. Ventrodorsal
projection
No significant changes in the radiographic appearance of the lungs.
Figure 10: Repeated examination three weeks later.
Ultrasonography.
Hypoechoic appearance of the lung parenchyma, but with multiple
hyperechoic foci which represents trapped air.
19
Imaging features of exogenous lipoid pneumonia in a dog - J. J. Labruyère, S. Murphy, R. Dennis
of oil makes it non-irritating to mucosal surfaces and therefore
less likely to lead to reflex inhibition of aspiration. The gradual
accumulation of cod liver oil in the alveoli produced pathologic
changes characteristic of chronic foreign body pneumonia with
extensive macrophage response and fibrosis.
Radiographic changes with lipoid pneumonia are variable, and
do not help to provide a specific diagnosis. The radiographic
pattern is similar to that of aspiration pneumonia with lobar
consolidation involving the dependent part of the middle lung
lobes [7]. In the present case the radiographic findings were
typical but the differential diagnoses after the first radiographic
examination included a long list of possibilities such as lobar
pneumonia, neoplasia, haemorrhage, and lung abscess. This
illustrates the limit of radiography with regard to the lack of
specificity of an alveolar lung pattern. An alveolar pattern may
change its appearance relatively quickly, particularly when it
reflects fluid accumulation in the lung. If pulmonary oedema is
the cause, a marked decrease in infiltrate will become apparent
after 12-hour diuresis, whereas with bronchopneumonia, the
radiographic lesions may improve only after several days of
appropriate treatment [8]. The second radiographic examination
in this case was helpful to narrow the differential diagnostic
list, because improvement was not observed. This suggested a
chronic alveolar disease due to a granulomatous or foreign body
reaction, in the present case caused by oil aspiration.
Lung lobe consolidation may also be assessed using
ultrasonography when it occurs at the periphery of the lung.
Because the alveoli are no longer filled with air, the lungs
become more hypoechoic and take on an echotexture similar
to that of the liver. Fluid bronchograms may be seen as a pair of
branching lines with anechoic centre with a lack of flow shown
using Doppler ultrasonography [9]. In the present case, the
ultrasound findings with three weeks interval differed. The first
examination showed fluid bronchograms surrounded by lung
tissue with a uniform liver-like echotexture, whereas three weeks
later the lung parenchyma was homogeneously hypoechoic
with multiple hyperechoic foci of air throughout. This change
in appearance could be explained by more aeration of the
affected lung lobe possibly following decrease in the amount of
fish oil within the lung lobe, after administration of the oil had
been discontinued three weeks ago. Thoracic ultrasonography
showed improvement of the condition that was not detected
on radiography, suggesting that ultrasonography might be more
sensitive for such changes.
The clinical features of lipoid pneumonias can vary markedly
and are probably influenced by the volume of oil in the lungs,
severity of pneumonia and duration of the illness [2]. Many cases
of ELP are asymptomatic; however as granulomatous pulmonary
reaction becomes more severe, dyspnoea, cough and fever
may become evident [1]. In the present case it is interesting to
notice that at follow-up the patient was asymptomatic despite
radiographic persistence of the infiltrate. Haematology and
biochemistry assays are usually unremarkable but leucocytosis
can occur with complicating infections [2].
Treatment includes discontinuation of mineral oil administration.
If respiratory distress is significant, treatment with corticosteroids, bronchodilators, and oxygen may be necessary. The use
of antibiotics is suggested in patients with fever, leucocytosis,
mucopurulent nasal or oropharyngeal discharge, and radiographic
evidence of consolidating densities with air bronchograms [1].
Based on previous reports the prognosis is guarded for cats,
horses and human patients with lipoid pneumonia, [2]. It can
be influenced by several factors such as the amount of lipid
aspirated, the presence of secondary infections, the severity
of the inflammatory response (which is related to the nature
of oil) and the chronicity of aspiration. The prognosis for this
particular dog is good, but in some humans with ELP, malignant
transformation to bronchogenic carcinoma has been reported
[10]. It is not known if the lipids themselves are carcinogenic, or
if the secondary pulmonary inflammation and fibrosis predispose
to cancer. Therefore periodic re-examination was advised for
this dog.
Conclusion
To the author’s knowledge, this case report presents for the first
time radiographic and ultrasonographic features of a confirmed
exogenous lipoid pneumonia in a dog. Aspiration of cod liver
oil was responsible for a chronic alveolar disease, which was
non-specific clinically. This condition showed no progression
radiographically and this is believed to be an important feature
of any pulmonary granulomatous/ foreign body reactions.
Thoracic ultrasonography proved to be a useful diagnostic
tool, in particular to allow fine needle aspiration. In this
report ultrasonography demonstrated better sensitivity for the
detection of early improvement in a consolidated lung lobe.
Acknowledgments
The authors would like to acknowledge Andy Sparkes for his
contribution in reviewing the manuscript
References
[1] Tams TR. Aspiration pneumonia and complications of inhalation
of smoke and toxic gases. Vet Clin North Am Small Anim Pract.
1985; Sep; 15[5]: 971-989.
[2] Scarratt WK, Moon ML, Sponenberg DP, Feldman B. Inappropriate
administration of mineral oil resulting in lipoid pneumonia in three
horses. Equine Vet J. 1998; Jan; 30[1]: 85-88.
[3] Bos M, de Bosschere H, Deprez P, van Loon G, de Vriese SR,
Christophe AB, et al. Chemical identification of the (causative)
lipids in a case of exogenous lipoid pneumonia in a horse. Equine
Vet J. 2002; Nov; 34[7]: 744-747.
[4] Corcoran BM, Martin M, Darke PGG, Anderson A, Head KW,
Clutton RE, et al. Lipoid pneumonia in a rough collie dog. Journal
of Small Animal Practice. 1992; 33: 544-548.
[5] Ettinger SJ, Feldman EC. Textbook of Veterinary Internal Medicine.
6 ed. Saunders WB, editor 2005.
[6] Norris CR. Lipid pneumonia. In: Saunders WB, editor. Textbook of
respiratory disease in dogs and cats. 2004; p. 456-60.
[7] Suter PF. Text atlas thoracic disease of the dog and the cat.
SWITZERLAND PFSC, editor.
[8] Thrall DE. Textbook of Veterinary Diagnostic Radiology. 4 ed.
Saunders WB, editor 2002.
[9] Tidwell AS. Ultrasonography of the thorax (excluding the heart). Vet
Clin North Am Small Anim Pract. 1998; Jul; 28[4]: 993-1015.
[10] Felson B, Ralaisomay G. Carcinoma of the lung complicating lipoid
pneumonia. AJR Am J Roentgenol. 1983; Nov; 141[5]: 901-907.
20
URINOGENITAL SYSTEM
REPRINT PAPER (GR)
Post-partum pathological conditions
in the bitch- Part I
D.C. Orfanou(1), H.N. Ververidis(2), C.M. Boscos(2), G.C. Fthenakis(1)
SUMMARY
Various disorders, some of which are life-threatening, can develop in bitches during the puerperium. In this article,
a detailed review of the literature on puerperal pathological conditions, along with excerpts from the authors’
clinical experience and photographs, is presented. Initially, a brief account of the physiological processes during
the puerperium is presented. The hormonal changes, the changes in the genital system and the behavioural changes
taking place as the genital system progressively returns to the non-pregnant state, are described. Subsequently,
the various disorders, which are categorised as systemic diseases, diseases of the mammary glands and diseases
of the uterus, are reviewed. Systemic disorders that are manifested during the puerperium, are the puerperal
hypocalcaemia and the abnormal maternal behaviour. If hypocalcaemia occurs, it is usually after whelping, as
calcium requirements of the bitch are increased due to milk production. The disorder is due to the increased
calcium requirements coupled with either a decreased intake of calcium (primary) or an inability to absorb it from
the intestine or mobilise it from the bones (secondary). Abnormal maternal behaviour can be the result of factors
causing nervousness, pain or disturbance of the bitch. Factors, such as genetic predisposition, caesarian section,
young age or even the puppies themselves, may also trigger this condition. The puerperal mammary diseases are
mastitis, agalactia and galactostasis. Mastitis is a disease of bacterial aetiology (Escherichia coli, Staphylococcus spp.
and Streptococcus spp.) occurring as either an acute or subacute-chronic form. Agalactia is the inability for milk
production and can be either primary or secondary; it is defined as full agalactia or hypogalactia. Galactostasis
refers to impaired passage and expression of milk from the teats, resulting in increased accumulation into the
mammary glands. The pathological conditions of the uterus include post-partum metritis, uterine prolapse, retention
of foetal membranes, foetal retention, subinvolution of the placental sites and uterine haemorrhage. Post-partum
metritis is caused by bacteria (mainly E. coli) invading the uterus during or immediately after whelping and occurs
with systemic and genital signs. Uterine prolapse (full or partial) is usually the consequence of vigorous foetal
manipulations or intense tenesmus of the bitch. Foetal retention is the consequence of dystocia or of misuse of
long-acting progestagens. Subinvolution of the placental sites is the consequence of the erosion of the uterine wall
by trophoblast-like cells; often, this erosion involves the entire mucosa and may even invade the myometrium.
Puerperal haemorrhage occurs more frequently in bitches with pre-existing disorders of blood coagulation factors.
All the above pathological conditions may cause serious problems to the affected bitches. For successful treatment,
early and correct diagnosis is important. For each condition, the clinical signs and the paraclinical findings are
described and the procedure for accurate diagnosis is discussed. Finally, the recommended conservative or surgical
treatment for each condition is reviewed. It should be noted that in every case, appropriate measures for the welfare
of puppies also needs to be taken. Measures for a frequent and efficient post-partum monitoring of bitches and
puppies are proposed, in order to prevent development of the various pathological situations.
Keywords: bitch, puerperium, post-partum period, metritis, mastitis, review. Part II of the paper will be published in
EJCAP 20(2) October 2010 and the above summary relates to both Parts I a II.
This paper originally appeared in: The Journal of The Hellenic Veterinary Medical Society* (2008), 59(2): 126-138.
Parts I & II were in the same paper.
(1) Veterinary Faculty, University of Thessaly, GR- 43100 Karditsa, Corresponding Author G.C. Fthenakis E-mail: [email protected]
(2) School of Veterinary Medicine, Aristotle University of Thessaloniki, GR- 54124 Thessaloniki, Macedonia, Greece
* Presented by HVMS (Greece)
21
Post-partum pathological conditions in the bitch- Part I -D.C. Orfanou, H.N. Ververidis, C.M. Boscos, G.C. Fthenakis
Figure 2: Lateral radiographic image of a bitch two days after
whelping: uterus imaged as a radio-dense U-shaped structure
(marked with #) at the caudal abdomen.
prolactin and oxytocin, i.e. hormones directly associated with
milk production. In contrast, luteinising hormone (LH) and
follicle-stimulating hormone (FSH) are in basal concentrations.
Similarly, progesterone concentration does not exceed 2 ng ml-1.
Concentrations of oestrogens vary; a possible increase would
not be associated with signs of oestrous, but only with transient
changes in cytological findings in vaginal smears [Knight et al.
1977, Concannon et al. 1978, Fieni et al. 1999, Johnston et al.
2001].
Prolactin controls milk production and regulates maternal
behaviour. Its concentration in the blood increases sharply
before whelping, from 41 ng ml-1 to 117 ng ml-1 and remains
increased throughout the puerperium [Concannon et al. 1978].
Prolactin production does not have a circadian pattern [Gobello
et al. 2001] and decrease of its concentration is associated with
a reduction in milk production [Jochle 1997]. Five weeks after
whelping, its concentration was found to be <20 ng ml-1 and
two weeks later <10 ng ml-1 [Graf 1978].
Oxytocin is responsible for milk let-down from the mammary
glands and contributes to uterine involution. It promotes
contraction of myoepithelial cells of the mammary glands,
resulting to exit of milk into the sini lactiferi of the mammary
glands and finally let-down of milk. Its concentration in blood
is increased throughout lactation [Kustritz 2005]. Johnston and
others (2001) have found that, as a result of continuous oxytocin
secretion during lactation, no exogenous administration of the
hormone was necessary for uterine involution.
Steinetz and others (1987) reported presence of relaxin in small
concentrations in the blood of lactating bitches. During the first
week of the puerperium, that was found to be >0.6 ng ml-1,
progressively reducing to the basal concentration (<0.4 ng ml-1)
five weeks after whelping.
Figure 1: Perineal area of a bitch two days after whelping (left
lateral recumbency): discharge of normal mucohaemorrhagic
secretion from the vulva, lactating inguinal mammary glands.
Introduction
The puerperium is the period from completion of whelping to
weaning of puppies. During that period, the genital system of the
animal progressively returns to the pre-gravid size and function.
The puerperium is an important phase of the reproductive cycle
of the bitch. During that period, various pathological conditions
may develop, some of which can be life-threatening for the
bitch. Early diagnosis is paramount, as some of these disorders
require immediate veterinary attention. One should also note
that in all these disorders, as well as providing treatment for the
bitch, care is required for the puppies.
The disorders of the puerperium can be classified as follows:
systemic disorders (puerperal hypocalcaemia, abnormal maternal
behaviour), disorders of the mammary glands (mastitis, agalactia,
galactostasis) and disorders of the uterus (post-partum metritis,
uterine prolapse, retention of foetal membranes, foetal retention,
subinvolution of the placental sites, uterine haemorrhage).
In this (part I) of the series, initially the normal puerperium of the
bitch is briefly reviewed. This is followed by a literature review
of systemic disorders and of disorders of the mammary glands,
along with excerpts from the authors’ experience. Relevant
photographs from the authors’ records are included.
Changes in the genital system
As the bitch is a seasonally mono-oestrous species, whelping
is followed by an anoestrous period, the beginning of which
coincides with the puerperium. During the puerperium, the
corporae lutae of pregnancy are converted to corporae albicans,
The puerperium in the bitch
Endocrinological changes
In bitches, the puerperium is primarily under the influence of
22
Figure 3: Normally involuting uterus (28 days post-partum):
diameter of uterine horns 0.9-1.2 cm, with six equally-sized (1.1
cm) placental sites.
Figure 4: Normally involuting uterus (40 days post-partum):
diameter of uterine horns 0.8-1.1 cm, with five equally-sized (0.6
cm) placental sites.
the size of which is progressively reduced. At whelping, the
corporae lutae have a diameter of approximately 4.0 mm, whilst
three months later they have been converted to corporae albicans
with a diameter of 2.5 mm [Noakes 2001]. The puerperium mainly
refers to the uterine involution, achieved through contractions
of the myometrium. Contractions last for only a few days after
whelping and assist in the expulsion of all fluids and residual
tissues from the uterus, as well as to reduce bacterial numbers
in the genital tract. For a period of three to four weeks, fluids
are discharged from the genital tract in progressively reduced
quantities (Fig. 1). During the first week after whelping their
quantity is copious, but thereafter their quantities are reduced
and are discharged sporadically. Immediately after whelping,
canine vulval discharge has a characteristically green colour, due
to presence of uteroverdin. Twelve hours after whelping, the
genital discharge becomes muco-haemorrhagic [Noakes 2001].
The size of the vulva and the diameter of the vagina return to
normal progressively within four to six weeks. The size of the
uterus decreases progressively: the diameter of the uterine body
immediately after whelping is 4 cm and reduces to 3.3 cm,
2.6 cm, 2.0 cm and 1.3 cm on the 3rd, the 7th, the 14th and
the 21st day after whelping, respectively (Figs 2, 3 and 4). Full
reduction of the size of the uterus takes place within the next
two months [Ferri et al. 2003], whilst restoration of histological
structure requires at least three months [Al-Bassam et al.
1981]. Simultaneously with the above changes, regeneration of
the endometrium also takes place during the 12 weeks after
whelping. Placental sites can be seen (Figs 3 and 4) for at least
four weeks after whelping, as lumps symmetrically arranged on
the uterine horns [Noakes 2001]. Caesarean section does not
appear to affect the progress of puerperium [Ferri et al. 2003].
In smears of uterine content, it was found that the majority
(>80%) of the cells were normal epithelial cells. Leucocytes were
observed very rarely [Gunzel-Apel et al. 1999]. Swab samples
from the vagina or the uterus may yield a variety of bacteria,
however their numbers are reduced over time [Gunzel-Apel et
al. 1999]. The majority of microorganisms have been identified
as Pasteurella multocida, Escherichia coli, Staphylococcus spp.,
Streptococcus spp. or Bacteroides spp. [Allen and Dagnall 1982,
Gunzel-Apel et al. 1999, Munnich et al. 2000].
Behavioural changes
Maternal behaviour is regulated by oxytocin and prolactin
[Whitman and Albers 1995] and depends upon genetic and
hormonal factors. The experience from previous whelpings, as
well as olfractory, visual and auditory stimuli from the newborn
puppies play an important role. Maternal behaviour is also
affected by the health of the bitch and her puppies, by the
environment, the relationship with the owner and the breed.
Usually, bitches have a strong maternal instinct. One week
before whelping, they select and prepare a relatively isolated
area (“nest”), in order to pre-arrange care for their puppies.
During the course of whelping and up to its completion, they
usually do not allow sucking by the newborns [Kustritz 2005].
However, the newborn puppies must suck within the first 8 to
12 hours after birth to increase survival probabilities. Usually, a
bitch will place the newborns on her teats, in order to facilitate
sucking. After sucking, they would groom the abdomen of
their puppies, in order to instigate urination and defaecation.
These behavioural patterns take place up to the third week after
whelping, i.e. a period during which newborns have restricted
mobility. Thereafter, the frequency of sucking is reduced, as
consumption of solid feed starts and progressively increases
[Kustritz 2005]. However, it is noteworthy that behavioural
patterns in dogs during the puerperium have not been studied
extensively.
Systemic post-partum pathological
conditions
Puerperal hypocalcaemia
Puerperal hypocalcaemia (eclampsia, puerperal tetany) can occur
in the final stages of pregnancy or, more frequently, immediately
after whelping, at which stage calcium requirements of the
bitch are increased due to milk production. Cases occur more
23
frequently in bitches of small-size breeds, especially if suckling a
high number of puppies [Burke 1977, Drobatz and Casey 2000];
it is often associated with peak milk production, i.e. between
the second and the fourth week of lactation. In some rare cases,
the disease may occur even after 40 days post-partum [Wheeler
et al. 1984].
The largest proportion (99%) of calcium in animals is present in
the bones. Remaining calcium can be found in cell membranes
and the endoplasmic reticulum (0.9%), as well as in extracellular
fluids and blood serum (0.1%) [Rossol et al. 1995]. In extracellular
fluids and blood serum, calcium is present as biologically active
ionised calcium (50%), anion-bound calcium (5%) and proteinbound calcium (45%) [Rossol et al. 1995]. Hypocalcaemia occurs
due to the combination of increased calcium requirements and
reduced calcium availability, which is the consequence of reduced
calcium intake (primary aetiology) or reduced absorption from
the intestine / mobilisation from the bones (secondary aetiology).
In cases of hypocalcaemia, there is increased permeability of the
cell membrane of neurons, which leads to a lower threshold
for depolarisation [Capen 2004]. Thus, neurological signs are
caused by continuous, repeated depolarisation of neurons.
At the early stage of hypocalcaemia, which may not be detected
by the animal owner, the animal is restless, dyspnoeic and crying;
it develops excess salivation and itching of the head. Usually the
condition deteriorates quickly. At that stage neurological signs,
such as tetanic posture, mydriasis and seizures, may develop
[Thebault 2005]. Then, high fever (>40.5 oC) and signs of
cardiac dysfunction (arrhythmia) become evident, so death can
be imminent [Capen 2004]. Even after a seemingly successful
treatment, seizures may reoccur up to three weeks after the first
signs [Drobatz and Casey 2000].
Clinical diagnosis is based on history (post-partum period,
high calcium requirements) and clinical findings. Confirmation
is based on the results of biochemical tests (total calcium
concentration in blood serum is <8 mg dl-1) [Austad and Bjerkas
1976, Kaufman 1986, Drobatz and Casey 2000]. In general,
total calcium concentration in blood serum correlates with that
of ionised calcium. Nevertheless, in cases of hypoproteinaemia
when the proportion of protein-bound calcium is reduced,
the following formulae can be used for accurate calculation of
total calcium concentration: CTCa =(ΤCa-ΤALB)+4 [Sodikoff 2001]
or CTCa =(ΤCa-[0.4×ΤTP])+3.3 [Meuten et al. 1982], where CTCa :
corrected total calcium concentration, ΤCa: calcium concentration
(mg dL-1), ΤALB: albumin concentration (g dL-1), ΤTP: total protein
concentration (g dL-1).
Differential diagnoses include seizures of other aetiology (e.g.,
hypoglycaemia, meningoencephalitis), as well as toxicoses
with neurological signs (e.g., caffeine-, strychnine-, lead-,
metaldehyde-poisoning) [Johnston et al. 2001].
Measurement of glucose concentration in blood is necessary
for differential diagnosis between hypocalcaemia and
hypoglycaemia. One should note that occasionally glucose
concentration in hypocalcaemic bitches may be lower than
normal due to the intense muscular contraction [Kaufman
1986]. Phosphorus and magnesium concentrations are within
the normal range.
Treatment should start immediately based on history and
clinical findings, without waiting for laboratory confirmation.
Treatment includes administration of 10% calcium gluconate or
borogluconate intravenously at a dose of 3 to 20 ml (5 to 15
mg kg-1 bodyweight (bw)), depending on the severity of the
clinical condition. Calcium administration should be slow (up to
1 ml min-1 and completed within 10 to 20 min); it should be
interrupted if cardiac arrhythmia, severe bradycardia or vomiting
occurs. Usually, response to treatment is immediate. Following
that, calcium should be administered subcutaneously (same total
dose, divided into two equal quantities at different sites of the
body, in order to minimise potential irritant effects of calcium).
Subcutaneous administration should be repeated every 24 hours
[Wallace and Davidson 1995] or even more frequently (e.g.,
every 6 to 8 hours), depending on recurrence. One should note
that some cases of hypoglycaemia respond to administration
of calcium gluconate or borogluconate, because gluconates
can contribute partially to energy requirements of the animal.
Nevertheless, in cases of confirmed hypoglycaemia intravenous
administration of 10 to 20% dextrose solution at a dose of 5 to
20 ml is preferred. Administration of glucocorticoids is contraindicated, because they reduce calcium absorption from the
intestine and increase excretion in the urine [Johnston et al.
2001] and do not contribute to improvement of the animal’s
condition.
After improving and stabilising the general condition of the
animal, calcium should be given per os, specifically calcium
carbonate or calcium gluconate (dose 50 mg kg-1 bw, twice
daily) or bicalcium phosphate (dose 125 mg kg-1 bw, thrice daily),
as well as vitamin D (dose 10000 to 25000 IU, daily) [Kaufman
1986, Boscos and Samartzi 1996]. In order to achieve quick
clinical recovery, puppies should be removed from their dam for
12 to 24 hours. In cases of relapsing disease, they should be
permanently taken away from the bitch. In that case, cessation
of lactation can be achieved by using prolactin-inhibitors (e.g.,
cabergoline (dose 2.5 to 5 µg kg-1 bw, daily, per os, for 4 to 6
days), metergoline (dose 0.2 µg kg-1 bw, daily, per os, for 4 to 8
days) or bromocryptine (dose 10 µg kg-1 bw, daily, per os, for 10
days)) [Bastan et al. 1998]. Furthermore, appropriate nursing care
should be provided for the newborn puppies [Hoskins 1995].
Prevention of the disease is best achieved by feeding a
balanced diet during pregnancy and lactation. Ideally, the
calcium:phosphorus ratio therein should range from 1:1 to 1.2:1
[Martin and Capen 1980]. Usually, commercially available dog
feeds of type “high energy for adult dogs” or “puppy growth”
fulfil these requirements. Pre-emptive administration of calcium
during pregnancy does not seem to benefit the animals. In
contrast, it may cause reduction in parathormone production
and thus predispose rather than prevent the disease [Boscos and
Samartzi 1996, England 1998]. However, animals which have
suffered from hypocalcaemia in previous post-partum periods,
especially if they have a large litter, should receive calcium per
os starting immediately after whelping. Furthermore, owners
should be informed regarding the possibility that their animal
may develop the disorder and they must be alert for immediate
veterinary care.
Abnormal maternal behaviour- cannibalism
Various factors causing nervousness, pain or disturbance of
the bitch, which include medical disorders (especially in cases
of eclampsia, metritis or mastitis [Kustritz 2005]), a hostile
environment, frequent visits from unknown people and attempts
24
Figure 5: Acute mastitis: enlargement of affected mammary gland.
Figure 6: Mammary abscess: discharge of purulent exudate.
to foster puppies, can lead to abnormal maternal behaviour.
This behaviour becomes evident with abandonment of puppies,
with rejection of puppies or even with cannibalism [Kustritz
2005]. Other factors leading to abnormal maternal behaviour
are genetic predisposition, caesarean section, inexperience of
the dam and even the puppies themselves if they were crying
continuously [Linde-Forsberg 2005]. Furthermore, a bitch may
choose to neglect puppies with abnormalities (i.e., subnormal
bodyweight, cleft palate) or fading ones [Boscos and Samartzi
1996, England 1998]. Although the selecting behaviour is
considered to be abnormal, one may suggest that the dam, by
sacrificing some puppies, attempts to guarantee the survival of
the other puppies [Kustritz 2005]. There are occasions when
the dam herself can harm her own puppies; examples include
ulcerations in the feet from excessive grooming [England 1998]
or evisceration from umbilical chewing [Boscos and Samartzi
1996]. Finally, neglect of the whole litter is usually a sign of a
pathological condition in the dam.
In such cases, puppies should be removed from their dam
temporarily and until her behaviour returns to normal.
Subsequently, they could be placed with her again, in order
to evaluate her attitude. If she continues to show abnormal
behaviour, puppies should be removed from her [Boscos and
Samartzi 1996]. In that case, prolactin-inhibitors (details above)
should be administered to the bitch, in order to stop milk
production.
For prevention of abnormal behaviours, the parturient bitch
should be allowed to select the whelping area (“nest”) in a
quiet place. Only people whom she may accept should come in
contact with her. The animal must be observed discreetly, but
regularly, in order to detect early signs of nervousness resulting
from external stimuli and to recognise aggressive behaviour
early. After a caesarean section, the puppies are placed next to
their dam, with the fresh odour of foetal fluids. Administration
of sedatives should be avoided, because their effects in lactating
animals have not been fully evaluated. Finally, bitches which
have shown abnormal maternal behaviour in the past must
be closely monitored after subsequent whelpings to recognise
abnormal behaviours and to protect the newborns. In cases of
repeated abnormal behaviour, the animals should be excluded
from reproduction.
Post-partum pathological conditions of
the mammary glands
Mastitis
Mastitis is a disease of bacterial aetiology caused mainly by
Escherichia coli, Staphylococcus spp. (S. aureus, S. intermedius,
coagulase-negative Staphylococci) and Streptococcus spp.
[Wheeler et al. 1984, Johnston et al. 2001, Jung et al. 2002, LindeForsberg 2005]. The disease develops in one or more mammary
glands of lactating bitches, more frequently immediately after
the death or weaning of puppies, during mammary involution.
Bacteria enter into the mammary glands usually through the teat
duct. The possibility of mammary infection through scratches
or injuries of the skin [Boscos and Samartzi 1996] or even
haematogenously [Linde-Forsberg 2005] has been reported.
Various factors, including dirty, hot and humid environment,
mammary congestion immediately after whelping, injuries of
the teats, small litter size, early (before 5th week post-partum)
or abrupt removal of puppies from the bitch, severe stress of
the bitch (stressful and/or long whelping process, malnutrition
etc.) and presence of metritis, have been reported as factors
predisposing to the disease [Boscos and Samartzi 1996, LindeForsberg 2005].
Usually, the disease has an acute course and can be lifethreatening [Dernell and Kreeger 1992]. The general condition
of the animal changes and can show inappetance, restlessness,
fever (>40 oC) and indifference for the puppies [Wheeler et al.
1984]. Affected mammary glands are painful, hot, enlarged
and oedematous (Fig. 5). Mammary secretion becomes thick,
yellow, green, red or brownish and frequently contains flakes
or clots [Wheeler et al. 1984, Linde-Forsberg 2005]. Abscesses
may develop in the parenchyma of the affected mammary
glands (Fig. 6). More rarely, necrosis may develop in a part of
the affected mammary gland, consequently leading to sloughing
(Fig. 7).
25
Figure 7: Mastitis: demarcation of necrotised mammary tissue and
cyanosis of overlying skin.
Figure 8: Long-standing mastitis: shrinkage of affected mammary
gland.
In long-standing or subclinical cases of mastitis, no severe clinical
signs are evident. One may suspect the disease if puppies do
not appear to suck often, look hungry and do not thrive [Olson
and Olson 1986, Linde-Forsberg 2005]. Sometimes, the disease
may lead to septicaemia and death of the neonates [Sager
and Remmers 1990, Schafer-Somi et al. 2003, Schafer and
Breitenfellner 2006]. In long-standing mastitis, the mammary
gland may appear shrunken (Fig. 8). In other cases, fibrous tissue
develops in the affected mammary glands and can be palpated
as small (0.5 to 2 mm) hard nodules. Some of these, can cause a
recrudescence of the disease, with signs of acute mastitis in the
subsequent lactation or in cases of pseudopregnancy.
There is only one experimental study of mastitis in bitches
described in the international literature and the results are
presented in detail below [Ververidis et al. 2007]. The right
caudal abdominal mammary gland of six bitches was inoculated
on day 8 after whelping with S. intermedius to induce mastitis;
adjacent mammary glands were used as controls. Clinical
examination, bacteriological and cytological (Whiteside
Test, Giemsa) examination of mammary secretion, as well as
haematological tests were performed from 5 d before until 34
d after challenge. Mastectomy was sequentially performed 1,
2, 4, 18, 26 and 34 d after challenge in each of the bitches,
in order to carry out a pathological examination of mammary
glands. All animals developed clinical mastitis: challenged glands
became painful, hot, enlarged and oedematous; secretion was
brownish, purulent, with flakes or clots, subsequently becoming
yellowish and thick. Staphylococci were isolated from all
inoculated glands (up to 22 d). The Whiteside Test was positive
in 41/46 samples from inoculated glands and 66/138 samples
from control glands; neutrophils predominated during the
acute stage. Blood leucocyte counts increased, whilst platelet
counts decreased. Gross pathological findings initially included
congestion, purulent discharge and subcutaneous oedema
(Fig. 9A); then abscesses, brownish areas and size decrease
were seen. Salient histopathological features were neutrophilic
infiltration, haemorrhages, destruction of mammary epithelial
cells and alveoli (Fig. 9B), and later as infiltration by lymphocytes,
shrunken alveoli, loss of glandular architecture and fibrous tissue
proliferation.
The researchers concluded that in bitches, intramammary
inoculation of S. intermedius could induce clinical mastitis,
followed by subclinical disease. The disorder was characterised
by bacterial isolation and leucocyte influx in the challenged
glands, by leucocyte presence in adjacent mammary glands,
by increased blood leucocyte counts and by destruction of
mammary parenchyma.
Diagnosis of clinical mastitis is easy, based on the signs.
Bacteriological examination of mammary secretion is useful to
isolate and identify the aetiological agent. This would help to
choose the appropriate antimicrobial drug for treatment. Acute
mastitis should be differentiated from galactostasis, injuries and
dermatitis in the area of the mammary glands (very common
during lactation), as well as from inflammatory-type mammary
tumours. In cases of chronic mastitis, clinical differentiation of
Figure 10: Results of Whiteside test: coagulum formation in
mammary secretion from a gland with mastitis (left slide) or
absence of coagulum in milk from a healthy gland (right slide).
26
Figure 9A: Acute mastitis - gross pathological findings: brown
area in mammary parenchyma and purulent exudate.
Figure 9B: Acute mastitis - histopathological findings: diffuse
leucocytic infiltration (Η&Ε stain, ×100).
mammary nodules from similar findings in neoplastic mammary
lesions is not easy. For the diagnosis of subclinical mastitis,
the only reliable method is the combination of bacteriological
and cytological examination. The Whiteside test is reliable
in detecting presence of increased number of leucocytes in
milk [Ververidis et al. 2007]. Five drops of mammary secretion
(approximately 0.1 ml) are deposited on a clean glass slide
and then a drop of sodium hydroxide solution is added. The
mixture is swirled with a bacteriological wire. The resulting clot
formation (Fig. 10) is scored according to Schalm and others
(1971). Additionally, secretion films can be made by directly
smearing 20 µl from each sample on a microscope slide and
stained by the Giemsa method. The percentage of the various
leucocyte subpopulations may be determined by distinguishing
types present in the films (Fig. 11). Measurement of haptoglobin
concentration in serum samples, has also been reported as a
diagnostic test for subclinical mastitis [Dzieciol et al. 2006].
Treatment should start immediately after diagnosis and should
include systemic administration of antimicrobial agents for at
least 7 to 10 days. The results of bacteriological examination of
mammary secretion and of antimicrobial susceptibility testing, if
available, can support administration of the appropriate drug.
Otherwise, one should administer broad-spectrum antimicrobial
agents, e.g. β-lactams (Wallace and Davidson 1995) every 8 to
12 hours. If there is no improvement of the condition of the
animal within three days, the treatment regime should be
modified. In order to choose the most appropriate antibacterial
agent, one should also take into account that antibiotics are
excreted in the milk and therefore, uptaken by the puppies.
Hence, administration of tetracyclines, fluoroquinolones and
chloramphenicol is contra-indicated, as these drugs may cause
various adverse reactions in puppies [Johnston et al. 2001].
Non-steroidal anti-inflammatory drugs may be used adjunctively
to the antimicrobial treatment, in order to reduce fever, mammary
oedema and pain during acute mastitis and consequently to
provide relief for the animal. There are no specific reports in
the literature regarding their use in canine mastitis; however,
their efficacy in the control of mastitis in ruminants has been
documented [Dascanio et al. 1995, Fthenakis 2000, Mavrogianni
et al. 2004, Smith 2005].
Treatment also includes the care of puppies of the affected bitch.
In cases of mild mastitis, in which composition of milk has not
been altered and the general condition of the health of the bitch
would allow, newborns should suck their dam normally. In more
severe cases involving one or two mammary glands, cover-up of
the affected glands (in order to stop sucking from those glands)
would be adequate. In very severe cases, newborns should be
removed from the bitch and special care should be taken for
artificial feeding [Hoskins 1995]. In such cases, the secretion of
the affected mammary glands should be removed regularly; cold
compresses should also be applied. If an abscess develops in an
affected mammary gland, it should be opened (Fig. 6). If there is
extensive tissue necrosis, one may also perform surgical cleaning
and debridement of the mammary tissue. When systemic signs
are present, general support of the animal should be applied
Figure 11: Mammary secretion film from a gland with acute
mastitis: increased numbers of neutrophils (Giemsa stain, ×400).
27
[Johnston et al. 2001]. Finally, prolactin-inhibitors should be
administered in order to stop lactation (details above).
Treatment of long-standing mastitis is more difficult, because
in such cases there would be limited distribution of the
antimicrobial drugs into the mammary gland. Diffusion depends
on lipophilicity and pH of each antimicrobial agent; erythromycin,
iodide penethamate, clindamycin and lincomycin are antibiotics
with suitable pharmacokinetic properties in the mammary
gland [Ziv 1980]. For selection of the appropriate antibiotic, the
aetiological agent of the disease and the results of susceptibility
testing should also be taken into account.
causes contraction of myoepithelial cells and milk let-down
and is thus beneficial. In cases of nervousness, phenothiazines
(acetylpromazine, per os, dose: 1 to 2 mg kg-1) can also
contribute; these drugs also support prolactin secretion, as they
are dopamine antagonists. Continuous presence of the owner
is also encouraged, especially in cases of nervous, primiparous
bitches [Johnston et al. 2001], unless of course the owner is a
stress factor for the animal. In every case of agalactia, due care
should also be taken for feeding the puppies of the affected
bitch. Teat seeking and sucking should be encouraged and
supported 10-15 minutes after oxytocin administration. It is
noteworthy that after sustained attempts, secondary agalactia
can be resolved and normal milk production can start even after
3 to 4 days post-partum.
Agalactia
Agalactia is defined as unavailability of milk from the dam either
because of lack of milk production or because of impaired letdown to the ducti lactiferi and the teats. The disorder can be of
primary or secondary aetiology [Johnston et al. 2001]. Primary
agalactia is rare and is due to absence of various anatomical
structures of the mammary gland, which leads to problems of
synthesis, secretion or let-down of milk. Secondary agalactia
is the consequence of inadequate prolactin secretion, reduced
responsiveness of teat receptors to tactile stimuli or of increased
stress, which result in malfunctioning milk let-down reflex
[Johnston et al. 2001]. Secondary agalactia develops after
premature whelping, in cases of stress of the bitch, during
various pathological conditions (e.g., metritis, septicaemia), after
progestagen administration, in cases of hormonal imbalance or
even after inadequate nutrition of the pregnant bitch [Wheeler
et al. 1984]. Temporary agalactia may also develop after
administration of sedatives or anaesthetics. Primiparous bitches
may also develop temporary agalactia in the immediately postpartum period, usually as a consequence of fear or nervousness
[Olson and Olson 1986, Johnston et al. 2001]. According to Olson
and Olson (1986), cases of “true” agalactia are those related
to anatomical problems of the mammary gland or to hormonal
imbalance of the animal, in contrast to cases of impaired
milk let-down. “Complete agalactia” and “hypogalactia” are
distinguished depending on the quantity of milk produced
[Lorin 1975].
Suspicion of the disease may arise if the puppies are nervous
and crying. The disease can be diagnosed based on clinical
examination of the mammary glands of the bitch. The
examination would reveal improper development of the
mammary glands and/or impaired milk let-down by the animal.
Ideally, the examination should be performed at least one hour
after withdrawal of the puppies from the bitch and 5 to 10 min
after oxytocin (2 iu) administration.
Treatment includes control of possible post-partum
reproductive (mastitis, metritis) or systemic disorders (eclampsia,
hypoglycaemia, dehydration), in conjunction with neurohormonal stimulation of milk synthesis, secretion and letdown. It is effective only in cases of full development of the
mammary glands (secondary agalactia). Treatment also depends
on the identification and correction of the aetiological factor
causing the disorder. Subcutaneous or oral administration of
metoclopramide (dose: 0.1 to 0.5 mg kg-1 every 6 to 8 hours,
for 5 days) supports prolactin production [Linde-Forsberg
2005]. Furthermore, administration of oxytocin (dose: 0.5 to 2
iu, at least 8 times per day, for 1 to 5 days) [Davidson 2003]
Galactostasis
Galactostasis refers to delayed or difficult let-down of milk,
which results in its accumulation in the mammary glands.
Usually, it is the consequence of anatomical problems of the
bitch, which impede exit of milk. It may also be observed after
death of a puppy or abrupt weaning of puppies, as well as when
puppies cannot take up all the available quantity of milk, e.g.
small litter size [Johnston et al. 2001].
The mammary glands, more frequently the inguinal pair,
become oedematous and enlarged [Linde-Forsberg 2005]. The
skin of the inguinal area is stretched and the animal shows signs
of discomfort and local pain. Exit of milk is difficult or even
impossible. Galactostasis may accompany or progress to mastitis
[Johnston et al. 2001], as milk accumulating in the mammary
glands is an excellent substrate for bacterial growth.
It is noteworthy that some degree of galactostasis occurs even
after normal weaning of the puppies. However, as under natural
conditions, weaning takes place progressively over a period of
days or weeks, the condition does not have obvious clinical
manifestations. Furthermore, intermittent and usually subclinical
galactostasis develops in cases of a small litter and refers mainly
to those mammary glands that are sucked little or not at all.
Differential diagnosis includes bacterial mastitis (in which
case other signs of inflammation are present) and primary or
secondary agalactia (in which case no mammary enlargement
is present).
Treatment of galactostasis includes mild massage of the
mammary glands - always under strict hygiene - in order to
achieve partial exit of milk and relief of the glands. In bitches,
which are not suckling puppies, the administration of prolactin
inhibitors is indicated (details above). Furthermore, the quantity
of feed and water should be reduced. Possible administration
of diuretics may be beneficial to reducing mammary oedema
[Wheeler et al. 1984].
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Fthenakis GC. Field evaluation of flunixin meglumine in the supportive
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Heterogenity of circulating prolactin in the bitch. Reprod Nutr
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incidence, differentiation and microbiology of canine mastitis.
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Therapy in Theriogenology. 1986; 2nd edition, pp. 511-512.
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29
GENERAL
COMMISSIONED PAPER
The In-House Practice Laboratory
U Gilli (1)
INTRODUCTION
The in-house laboratory is an important tool for the practice of today. It enables practices to complete clinical
findings, to rule out differential diagnoses and to pursue the course to a final diagnosis. Many clinical suspicions
can only be confirmed by additional laboratory examinations, so there is a need for every practice to organise their
own in-house laboratory.
Technical innovations over the last few years and the development of equipment and tests designed specifically
for “in-house” testing have enlarged the possibilities for the practice of today to perform a variety of analyses and
examinations which would have been reserved for external laboratories in earlier times. However, some testing
which exceeds the capability of a normal practice in relation to technical and personal resources must still be given
to external specialised laboratories.
This article will focus on general considerations on how to establish an in-house laboratory and to what level of
sophistication a laboratory might be organised. Additionally some analytical departments will be discussed to show
the possibilities of examination from the simple to the more complex testing.
General Considerations
run an in-house laboratory in parallel with other daily routines.
Education and continuing education for veterinary assistants in
laboratory techniques is widely available.
The decision on how to organise a laboratory and to what level
of sophistication, must be made by each practice individually.
It is mainly dependant on the personnel, infrastructure and
financial resources available. The following points are worth
considering:
• Complexity and frequency of testing
Optimal in-house testing should be fast, everyday and easy to
perform, inexpensive and give accurate results. If a test proves
to be time consuming and difficult it is worth thinking of
outsourcing. Analyses which are performed infrequently may
result in a lack of acquired experience and give rise to mistakes.
However there are a many techniques and analyses optimised,
proven and designed for in-house testing.
• Importance of a parameter
It is obviously vital to establish laboratory examinations when
results are needed urgently in an emergency situation in order to
be able to initiate a correct treatment. The result of these tests is
vital in a life or death situation. A good example of this is the inhouse determination of certain critical serum and haematological
parameters such as blood urea nitrogen, creatinine, AP or GPT
(AST) and haematocrit or leucocyte count.
• Time delay
As mentioned above, a time-delay in sending samples away
for external testing might not be acceptable for important
parameters in life-threatening conditions. Other analyses
without this high priority might be outsourced. A time delay
is not acceptable in the case of certain critical samples such as
urine, which tend to degrade over time.
• Personnel and training
If a practice is a one-man-show, there is little capacity to perform
laboratory testing in time. However, since most practices have
more employees, a skilled veterinary assistant should be able to
(1) DIAVET Labor AG, Schlyffistrasse 10, CH- 8806 Bäch. E-mail: [email protected]
31
The In-House Practice Laboratory - U Gilli
• Reliability of tests
One must clearly know the reliability of one’s own In-house
testing. Most analytical equipment has its own inbuilt controls
and calibrators which will guarantee accurate results. Some
rapid and simple tests however might give unclear or debatable
results. In such situations it is a good idea to have back-up in
the form on an external laboratory which can confirm or reject
debatable results or even ensure reliable results from suboptimal
materials (such as lack of material or degraded samples like
haemolysed or lipaemic sera).
The field of hormone analyses today is mostly still in the hands
of external laboratories, since the test frequency in the practice
of such tests is not very high and the analytical equipment is
both very specialised and expensive. An exception is the analysis
of Thyroxin, which is made available for in-house diagnostics
and is very helpful in the diagnosis and follow-up of Feline
Hyperthyroidism.
Haematology
A minimum of haematocrit and haemoglobin determination,
leucocyte count and leucocyte differentiation should be
established in every practice. This can be done by trained
personnel either by using traditional techniques such as a cell
counting chamber, the use of a hematocrit centrifuge, Diff Quick
colouration and microscopic examination of blood smears, or
by using fully automated equipment. However, the technique
of investigating blood smears by microscope should not be
neglected, since the human eye is able to detect a lot more
anomalies than any automated equipment (such as normoblastic
cells, blood parasites, inclusion bodies or differentiation between
banded and segmented neutrophils). Other examinations, such
as reticulocyte counting or determination of clotting factors, are
still the work of specialised laboratories, since special equipment
and techniques are needed.
• Surrounding infrastructure
This point highlights the surroundings in which a practice is
situated. If there is no access to external laboratories such as in
remote regions and no fast transportation system, a practice is
forced to establish most laboratory examinations in-house. If a
practice is situated in a well populated area with many external
laboratories at hand, which might even pick up samples directly
with a courier service, it is easier to decide which analyses to
outsource.
The following section of this paper will focus on different
analytical departments and discuss the options for in-house
testing in the practice.
Clinical Chemistry
Parasitology
Today, it is undoubtedly essential to analyse parameters of
clinical chemistry in- house. Different producers offer a variety of
analytical equipment (Fig.1) with narrower or broader analytical
ranges, which can be operated by trained personnel. A minimal
programme should enable the analysis of blood urea nitrogen,
creatinine, AP, GPT (AST), GOT (ALT), glucose, total protein and
albumin to enable the diagnosis of severe and acute stages of
diseases. The analysis of potassium, sodium and chloride is also
helpful in endocrine and generalised disorders.
Search profiles and non-critical conditions might be examined
in-house, or for cost-saving reasons, outsourced to external
testing, since many external laboratories offer broad search
profiles at very competitive prices (Fig.2).
Parasitology provides a broad field of activity for the in-house
laboratory. The techniques are quite easy, and the determination
of parasites depends on the training and experience of the
personnel but is very rewarding.
Ectoparasites such as fleas, lice and certain mites may be
collected using a comb or by the scotch tape technique and
when immobilised and with the help of a reference book,
should not raise problems of identification (Fig. 3). Demodex
and sarcoptes mites might only be found by scraping technique
and KOH digestion, in cases of a doubtful diagnosis it might be
useful to use an external laboratory as a back-up.
The sedimentation/flotation technique is used to detect
Fig. 1) Small scale analyser for clinical chemistry for daily use at
the veterinary practice.
Fig. 2) Large scale analyser for clinical chemistry in a reference
laboratory.
32
Fig. 4) Tubes containing samples for parasitological examination
with sedimentation/flotation technique.
Urine might be incubated to find certain classes of bacteria to
intitate specific antibiotic treatment (also refer to the section on
microbiology).
Fig. 3) Dermanyssus gallinae found and immobilized with scotch
tape technique.
Infectious agents
helminthic endoparasites (Fig. 4). The technique is not
complicated and it is most rewarding for the personnel of the
practice to find and identify pathogens. With some training
and routine daily practice the major helminth classes such as
Trichuris, Capillaria, Taenia, Ascaridia and hookworms should
be distinguished without a problem. The diagnosis of other
endoparasites such as Giardia can also be done in practice, by
direct microscopical finding or by using rapid tests. However,
Giardiosis is not always detected with these techniques, since
the infestation must be quite high. In critical cases or unclear
results, it might be better to use the service of an external
laboratory, using the much more sensitive ELISA technique.
If the practice encounters the challenge of parasitological
examinations of exotic animals such as birds, reptiles or
amphibians, it is better to leave it to an external laboratory or
specialist with an appropriate expertise, since the diagnosis of
exotic parasites is difficult without respective experience and
also some sophisticated techniques must be applied to find
special pathogens such as amoebas or protozoans.
The significance of infectious agents in small animals is not to be
underestimated. Well known pathogens still play an important
role in generalised disorders (e.g. FeLV, FIP, Leishmania). New
pathogens may also arise (e.g. Babesia) due to the animal
travelling or because the pathogen has migrated into new
territories as a result of climate changes. A variety of pathogens
in this category exist such as protozoa, viruses, bacteria and
helminths and it is important that these be diagnosed in the
small animal practice. Some need to be treated specifically,
some will have a poor prognosis and some are recognised as
zoonoses (e.g. Leishmania). Therefore, the direct, fast and reliable
diagnosis of these pathogens is important to the practitioner of
today. A variety of older and newer techniques exist to confirm
the existence of pathogens.
Fig. 5) A selection of fast tests for detection of blood groups and
infectious agents for daily use in the practice.
Urine samples
The field of urine analysis is a good example of demonstrating
that the in-house laboratory can achieve a lot of useful diagnostic
information with relatively little effort. Since urine samples tend
to degrade quite rapidly, this kind of sample is always worth
analysing right on the spot and in-house. The equipment is simple
consisting of urine tubes, a centrifuge, slides and cover slips,
a microscope and urine sticks. By microscopic examination of
the sediment and analysis using urine dip sticks, the practitioner
gains direct information on several urological disorders, such as
urolithiasis and the composition of crystals, the severity of the
disorders by assessing associated cells (erythrocytes, epithelial
cells, leucocytes) and possible underlying bacterial cystitis.
33
The In-House Practice Laboratory - U Gilli
Fig. 6) Biochemical reaction pattern for differentiation of bacterial
strains.
Fig. 7) Necropsy with macroscopic findings in a deceased rabbit
(liver infiltration with taeniidae cysts).
Agents which are located in the blood (in erythrocytes or
leucocytes) may be seen directly in blood smears, such as
Babesia in erythrocytes, Anaplasma in neutrophils, Haemotropic
mycoplasmas or microfilaria in the blood stream. However for this
to be possible there needs to be quite a high infestation in the
blood. Agents too small to see (e.g. viruses) are not detectable
in the blood directly but their presence might be revealed by
formation of antibodies or secretion of specific antigens in the
blood. A lot of quick tests (“Speed tests”, “SNAP tests”; (Fig. 5))
have been developed to identify markers for infectious agents.
The technique is quite simple and can be done by using some
drops of anticoagulant blood or serum. The reliability of the
tests in terms of specificity and sensitivity is very good. With the
help of “fast” tests, pathogens like FeLV, FIV, FIP, Leishmania,
Dirofilaria, Borrelia, Ehrlichia and Brucella can be identified. Of
course, because of possible decisions relating to treatment and
the sometimes poor prognosis it is recommended to confirm
such critical results using an external laboratory with different
methods such as ELISA, IFAT, CFT or PCR.
the correct testing for antibiotic resistance also requires special
knowledge and techniques. For these reasons, microbiology
should still stay in the hands of specialised laboratories.
Necropsy and Histology
Necropsies can be done in the normal practice, if an adequate
location and equipment is available. However, for reasons
of sanitation and disease control it may not be allowed to
be undertaken by private practitioners in some countries.
Necropsies are a useful and fast tool to confirm clinical suspicions
if macroscopic alterations can be found such as masses or
traumatised organs (Fig. 7). In some cases when nothing obvious
can be found, histology or microbiology may still point the way
to diagnosis, but these cases would be better left to the expert.
The technique of histology and interpretation of histological
preparations is a specialised science which is reserved for
qualified and trained pathologists. Cytological preparations have
nearly as much diagnostic value as histological preparations, but
the sampling and processing is less difficult and may be done
easily by a trained practitioner.
Microbiology
Fig. 8) Work space for the daily sample processing at the veterinary
practice.
The options for microbiological examinations in the in-house
laboratory are more restricted than in the sections already
discussed above. This is for several reasons: firstly, simple and
fast tests for in-house microbiology are not widely available.
Some “dip-media” such as Urocult or Uriline tubes do exist, but
bacteria in tissues such as wounds or otitis cannot be cultivated
in them.
Secondly, the installation of a state-of-the-art microbiological
laboratory would clearly exceed the capacitiy of a traditional
practice. A lot of specialised equipment is needed such as
incubators and agar plates for cultivating bacteria, special
selective agar to identify delicate pathogens, gram stain and
biochemical identification kits (Fig. 6) to properly define bacterial
strains and so on.
Thirdly, the interpretation of the findings is difficult since it is
necessary to differentiate between the normal flora of tissues and
pathogenic flora. To find potential pathogenic germs in cultures of
mixed flora requires considerable microbiological experience, and
34
Conclusion
The innovations and developments available nowadays allow
much more diagnostic techniques to be done “in-house” than
in previous years. Modern practitioners should be encouraged to
establish competence in at least minimal laboratory techniques
since it enriches the daily routine and is very rewarding and
satisfying to personnel as well as enhancing the prestige of the
modern practice. The degree of in-house testing is dependant
on several factors and on individual decision. A small work space
for sample processing (Fig. 8) and for diagnostic equipment (Fig.
9) should fit into almost every practice and even a minimum of
trained personnel can achieve reliable results in useful time to
increase the diagnostic repertoire of the modern practice.
Suggested literature
Kraft W, Dürr U M. Klinische Labordiagnostik in der Tiermedizin,
Schattauer Stuttgart/New York
Suter P F, Kohn B. Praktikum der Hundeklinik, Parey Buchverlag c/o
Medizinverlage Stuttgart GmbH & Co. KG, Stuttgart, 10. Auflage
2006; p.96-113.
Feldman B F, Zinkl J G, Jain N C, Schalms Veterinary Hematology,
Lippincott Williams & Wilkins, 5th Edition 2000
Jain N C, Essentials of Veterinary Hematology, Lea & Febiger Pennsylvania, 1993
Fig 9) Work space for identification of endo- and ectoparasites,
examination of urine sediment and blood smears at the veterinary
practice.
35
GENERAL
REPRINT PAPER (A)
Foodstuffs toxic to small animals –
a review
S. Handl(1), C. Iben(1)
SUMMARY
Several foodstuffs that can be safely consumed by humans are harmful to pets and can be even lethal. This article
reviews case reports about intoxications with coffee and cocoa products, onions and garlic, grapes and raisins,
avocado fruits, macadamia nuts, hops, salt and xylitol. The pathological mechanisms are described, as far as they
are known, and therapies are suggested. The authors recommend to strictly avoid feeding foodstuffs containing
potentially harmful ingredients to pets and to store them inaccessible to animals. Veterinarians are requested to
inform pet owners about these risks, to continually educate themselves on the topic and to publish such cases to
make them generally known.
warning of the potential toxicity of theobromine and caffeine.
In their review, the authors clearly distinguished between
by-products of chocolate production, which still include all
the natural contents of the cocoa plant, and the residues of
theobromine extraction. They considered the former a danger
to animal health and even proposed regulations on their sale,
whilst the latter were regarded as harmless to animals, but
devoid of nutrients and therefore should not be marketed as
animal feed. Further, the authors reported the case of seven
army horses, which had died after being fed cocoa husks and
which were diagnosed with a disease pattern similar to caffeine
intoxication.
When after the Second World War animal feed was scarce,
cocoa husks were frequently fed to farm animals and several
cases of poisonings in pigs and poultry occurred [2,3,4]. The
first case report of cocoa intoxication in a dog was published by
Clough in 1942 [5]. Six dogs died after their owner had fed them
a homemade diet containing about 0.2-0.22 % theobromine.
Clinical signs prior to death included diarrhoea, hyperactivity
and increased vocalization. Several other case reports followed
[6,7,8]. Cocoa husk mulch is occasionally used in horticulture
and landscaping and some dogs apparently find it very palatable
and will ingest amounts large enough to result in methylxanthine
intoxication [9,10].
To the authors’ knowledge, cases of coffee or tea poisoning
are not published in veterinary literature. However, drugs for
human consumption containing caffeine can be dangerous to
animals as well [11,12]. Also soft drinks and herbal remedies
This paper originally appeared in: Vet. Med. Austria /
Wien. Tierärztl. Mschr.* 95 (2008), 235 - 242
Introduction
Several foodstuffs, which are not or only in very high doses
harmful to humans, can cause severe or even lethal intoxications
in animals. Although the toxicity of some of those substances
has been known for a long time, the food industry constantly
puts new food additives on the market, which might have a yet
unknown detrimental effect on pets. Pet owners might not be
aware of this fact, and may thus feed their pet potentially toxic
substances believing that if they are healthy for themselves, they
would not be harmful to animals.
In this review we describe the intoxications with chocolate and
other cocoa products, caffeine, onions, salt, hops and related
plants, grapes and raisins, avocados, macadamia nuts, salt and
xylitol.
Coffee, tea, cocoa
The potential use of cocoa by-products as animal feed had already
been discussed by the end of the 19th century. Marchadier &
Goujon [1] published a review on this topic in 1919. While some
experts of that time named cocoa by-products a nourishing
feedstuff considered to have beneficial effects, others gave
(1) Institute of Nutrition, Department for Farm Animals and Veterinary Public Health, University of Veterinary Medicine Vienna, Veterinärplatz 1,A-1100
Vienna, E-mail: [email protected]
* Presented by VÖK (Austria)
36
may contain caffeine. Ooms and co-workers [13] reported 47
cases of dogs that had ingested an herbal remedy containing
guarana (Paullinia cupana) and ma huang (Ephedra sinica). They
showed hyperactivity, tremor, seizures and changes in behaviour,
additionally with vomiting, tachycardia and hyperthermia.
Seventeen percent of these dogs died or had to be euthanized.
The lethal dose of theobromine in the dog is in the range 100250 mg/kg BW, the oral LD50 between 250-500 mg/kg BW
[14,15]. Those observations indicate that as little as 30 g of
baking chocolate could be lethal to a dog of 5 kg BW. Mild signs
of intoxication (vomiting, diarrhoea, polydipsia) could already
be seen after ingestion of 20 mg/kg BW, cardiotoxic effects
occurred at 40-50 mg/kg BW, seizures at 60 mg/kg BW [16].
Toxic principle
The active ingredients of coffee and cocoa are the methylxanthines caffeine (1,3,7-trimethylxanthine) and theobromine
(3,7-dimethylxanthine). Methylxanthines are almost completely
absorbed in the gastrointestinal tract. They are able to pass the
blood-brain barrier, cross the placenta and pass into the mammary
glands. Metabolism occurs in the liver by demethylation followed
by conjugation reactions. The enterohepatic recirculation
of methylxanthines has been described. About 10 % of the
ingested methylxanthines are eliminated unchanged in the urine.
The elimination of methylxanthines from the body is slower
in dogs compared to other species (plasma half life is 17.5 h
compared to 6-10 h in humans). This is the reason why dogs are
particularly sensitive to intoxication [14]. Methylxanthines cause
an increase in intracellular cyclic adenosine monophosphate
(cAMP) by inhibition of phosphodiesterase, as well as in
calcium concentration, caused by an enhanced influx into the
cell and a reduced uptake into the endoplasmic reticulum. This
results in increased contractility of skeletal muscles. The central
adenosine receptors are also competitively inhibited, causing
central nervous excitation, enhanced diuresis and tachycardia
[15].
Symptoms
Clinical symptoms of methylxanthine poisoning include
excitation, ataxia, weakness, seizures, hyperthermia, vomiting,
diarrhoea, abdominal pain, polyuria, incontinence, tachypnoea,
dyspnoea, tachycardia and arrhythmias. Deaths may occur
owing to cardiac or respiratory arrest.
Diagnosis
The case history as reported by the owner or the presence
of chocolate in vomit or gastric lavage contents will provide
indication of methylxanthine poisoning. Methylxanthines can be
detected in gastric contents, blood, urine, or in the liver using
high pressure liquid chromatography (HPLC). Post mortem
findings are not specific, although remainders of chocolate
might be found in the gastrointestinal tract [8].
Therapy
Therapy is mainly symptomatic (fluids, diazepam, lidocaine,
metoprolol). Further absorption of theobromine or caffeine can
be inhibited by administration of activated charcoal, enemas,
laxatives or a gastric lavage. Steroids and erythromycin should
be avoided, since those drugs might slow down the elimination
of methylxanthines from the body [14].
The caffeine and theobromine contents of various products are
given in tables 1 and 2.
Onions & Garlic
According to Carson [14], the minimum lethal dose of caffeine
in the dog varies between 110 and 200 mg/kg bodyweight
(BW), the LD50 is 140 mg/kg BW. Albretsen [15] states that the
minimum lethal dose of caffeine in the dog is about 140-150
mg/kg BW. The mimimum lethal dose for cats is quoted as 80150 mg/kg BW [14].
The association between onion feeding and damage to the
erythrocytes was already described in dogs in 1930 [17].
Onions were experimentally used as prophylaxis for niacin
deficiency and Heinz bodies were discovered as an incidental
finding. Since then, numerous cases of onion poisoning in dogs
Table 2: Average caffeine content of various coffee and cocoa
products [13,14,15,16]
Table 1: Average theobromine content of various cocoa products
[14,15,16]
product
theobromine content
product
caffeine content
cocoa beans
10.6-53 mg/g
coffee beans
1-2 %
guarana
3-5 %
filter coffee
40-150 mg/cup
coca husks
5.3-9 mg/g
coca husk mulch
2-32 mg/g
instant coffee
30-90 mg/cup
cocoa powder
14-26 mg/g
decaffeinated coffee
2-4 mg /cup
instant cocoa
4.8 mg/g
black tea
20-90 mg/cup
baking chocolate
13.8-15.9 mg/g
Cola soft drinks
40-60 mg/can
dark chocolate
4.8 mg/g
cocoa powder
0.18-1.5 mg/g
instant cocoa
0.5 mg/g
milk chocolate
1.6-2.1 mg/g
baking chocolate
1.2 mg/g
white chocolate
0.009 mg/g
milk chocolate
0.2 mg/g
37
Foodstuffs toxic to small animals – a review - S. Handl, C. Iben
counts and reduced glutathione and potassium in their serum
are more sensitive to onion poisoning then others (that includes
the Japanese breeds Akita and Shiba). Feline erythrocytes are
generally very susceptible to oxidation since feline haemoglobin
contains eight sulfhydryl groups (all other mammal species have
just two). Additionally, the spleen of the cat is inefficient at
filtering damaged erythrocytes from the blood stream [31].
Diagnosis
Diagnosis of onion intoxication can be made by asking the
owner about a possible ingestion of onion-like vegetables and
by the detection of Heinz bodies in blood smear (see figure 1).
Therapy
Decontamination of the gastrointestinal tract should be
considered. Otherwise symptomatic therapy is indicated,
including oxygen therapy or blood transfusions if necessary.
Antioxidants like vitamin E and acetylcysteine can be given
supportively.
Figure 1: Blood smear of a dog with onion intoxication (new
methylene blue stain, x1000) showing Heinz-bodies in several
erythrocytes [24]
have been published [18,19,20,21]. The disease pattern could
be demonstrated in experimental settings [22,23]. Also the
Catalan spring onion, which is grown covered in soil to avoid
photosynthesis and can be safely consumed in vast quantities by
humans, may cause intoxication in dogs [24]. The first case report
of onion intoxication in cats was published by Kobayashi in 1981
[25]. Two cats had shown Heinz bodies in all erythrocytes 9 h
after eating onion soup. Four days after onion ingestion their
plasma haemoglobin level increased and haemoglobinuria was
seen. These findings could be reproduced by feeding cats raw
onions, incubated in ether for 17 days at room temperature [25].
From July 1995 to February 1996, 13 cases of onion poisoning in
cats occurred in the USA, caused by baby food containing onion
powder. These incidents could be reproduced experimentally
[26].
Besides the onion (Allium cepa), other representatives of the
genus Allium, like garlic (Allium sativum) [27] and Chinese
chive (Allium tuberosum) [28], may also cause haemolytic
anaemia. Poisonings with leek (Allium porrum), chives (Allium
schoenoprasum), wild garlic (Allium ursinum) or shallots (Allium
ascalonium) are not published in veterinary literature, but are
conceivable.
Grapes & Raisins
The first article about the potential toxicity of grapes and raisins
was published in 2001 [32] from the database of the Animal
Poison Control Center (APCC) of the American Society for the
Prevention of Cruelty to Animals®. A total of ten dogs had
shown some of the following symptoms after the ingestion
of grapes or raisins: vomiting, diarrhoea, anorexia, lethargy,
painful abdomen, hypercalcaemia, hyperphosphataemia,
elevated serum creatinine and blood urea nitrogen (BUN).
Five of the dogs developed anuria. Two dogs died, three
needed to be euthanized, the other five survived thanks to
intensive therapy. Histopathological evaluation revealed only
mild damage of the renal epithelia that could not explain the
fatal outcome. Investigations for mycotoxins and heavy metals
proved negative. Therefore, the authors suspect either a
contamination of the grapes and raisins with some undetected
toxin (mycotoxin, pesticide, environmental toxin) or the presence
of a currently unknown toxic mechanism to be responsible for
the intoxication.
Since then, several more cases of azotaemia and renal failure
in dogs after grape or raisin ingestion have been published
[33,34,35]. The APCC was informed about 43 cases between
1992 and 2002 [36], the Veterinary Poison Information Service
(VPIS) in Great Britain came to know about 23 cases in the years
2003 to 2005 [37]. The intake reached from 2.8 to 57 mg/kg
BW of raisins and grapes intended for human consumption, raw
or cooked, fresh or spoiled, as well as pomace. No breed, age or
gender predisposition could be found.
Of all the cases of grape or raisin uptake that were reported
to the APCC and VPIS, 40 % of the dogs did not show any
symptoms [36,37].
Symptoms
Allium-exposed animals showed symptoms that are typical for
an intoxication (poor condition, anorexia, vomiting, diarrhoea)
as well as for haemolytic anaemia (pale mucous membranes,
haemoglobinuria, tachypnoea, tachycardia, weak pulse, anaemic
heart murmur). Heinz bodies are present in blood smears,
accompanied by a shift of the haemoglobin to the edge of the
erythrocyte (eccentrocytosis).
Toxic principle
Plants of the genus Allium contain reactive organothiosulphates,
which oxidize haemoglobin to methaemoglobin. Since
methaemoglobin is less soluble, it will clot together resulting
in Heinz body formation or precipitates at the cell walls of the
erythrocyte. This increases the fragility of the erythrocyte cell wall
causing intravascular haemolysis [22,29]. Yamoto and Maede
[30] found out that dogs with hereditary elevated erythrocyte
Symptoms
The initial symptom of grape or raisin intoxication is always
vomiting, which occurred in all described cases between
6 and 24 h after ingestion, followed by anorexia, lethargy,
diarrhoea, painful abdomen, and oliguria or anuria. Later
38
Avocado
The avocado (see figure 2) (Persea americana, P. gratissima, P.
nubigena) grows as trees to a height of 15 metres in tropical
areas. It belongs to the family Lauraceae and is native of South
and Central America. The egg-shaped fruit, technically a large
berry, is consumed by people all over the world. The leaves and
other parts of the plant were tested as feed for farm animals,
and first reports on their toxicity were published in the 1940s
[38,39]. Non-bacterial mastitis occurred in cows, goats and
rabbits; canaries died after the ingestion of avocado fruits, and
all fish in a pond were found dead after avocado leaves had
fallen into the water. In 1994, two dogs in Namibia, which were
known to like eating avocados, died of acute cardiomyopathy
[40]. Birds seem to be particularly sensitive to avocado poisoning.
Hargis and co-workers [41] described cases of acute dyspnoea
and death in canaries and cockatiels after avocado ingestion.
The researchers experimentally administered mashed avocados
in different dosages to canaries (0.7 ml every 4 h or every 2 h)
and to budgerigars (1 ml every 4 h or every 2 h). All birds were
lethargic and showed ruffled plumage and dyspnoea. Six of the
eight budgerigars and one of the eight canaries (from the group
with the more frequent application) died within 48 h, the other
birds recovered. Subcutaneous oedema, hydropericarditis and
congestion of all organs, especially the lungs, were found on
post-mortem. In an experiment carried out by Shropshire and
others [42], the application of a total of 1000 mg of avocado
(four times 250 mg at intervals of 90 min) resulted only in
excitation and feather picking in two budgerigars. A flock of 120
young ostriches was driven into an avocado plantation to graze
in the district Oudtshoorn, South Africa. On the next day eight
birds showed weakness, dyspnoea and swollen necks. They died
within a short time; another ostrich needed to be euthanized.
The fruits and leaves of this plantation were experimentally
administered to ten hens (5-25 g/kg BW) and eight ostriches
(15 g/kg BW twice a day up to 20 mg/kg BW five times a day).
The hens showed no clinical symptoms, while the ostriches all
died. In both species, signs of cardiomyopathy were found on
post-mortem [43].
Figure 2: All parts of the avocado tree (Persea sp.) can be toxic to
animals. (Photo from © Astrid - Borrower @ pixelio.de)
hyperphosphataemia,
hypercalcaemia,
elevated
serum
creatinine, elevated BUN and azotaemia might be seen. Death
may occur due to acute renal failure.
Toxic principle
Despite the high number of published cases, the toxic principle
of grapes remains unknown.
Symptoms
Lethargy, weakness, ruffled plumage, tachypnoea, tachycardia,
arrhythmia, dyspnoea, and oedema of neck and chest can be
seen in avocado intoxicated birds. Death from heart failure is
possible. In lactating mammals decreased milk yield, elevated
cell counts and flaky milk as well as oedema of the mammary
gland may occur.
Diagnosis
The diagnosis of grape or raisin poisoning is only possible by
interviewing the owner for the patient history and by identifying
grapes or raisins in vomit, faeces or gastric lavage.
Therapy
Because of the high mortality of 50-75 %, every dog that has
eaten grapes or raisins or is suspected to have done so, should be
hospitalized and intensively treated [37]. Decontamination of the
gastrointestinal tract with emetics, laxatives or a gastric lavage is
indicated. If vomiting persists, antiemetics and gastroprotectants
should be given. Aggressive intravenous fluid therapy and
constant monitoring of renal function and blood electrolytes is
recommended, enhanced diuresis with mannitol or furosemide
and enhancement of renal perfusion with dopamine might be
indicated. Peritoneal dialysis can be tried. If anuria persists for
several days, the prognosis is very poor.
Toxic principle
Oelrichs et al. [44] identified a component named persin ([Z,Z]1-[acetyloxy]-2-hydroxy-12,15-heneicosadien-4-on) as causative
agent for necrosis in the epithelium of the mammary gland and
the myocardium. Only the R-isomer seems to be active, but the
toxic mechanism remains unknown. The degree of toxicity varies
between the different cultivars of the avocado plant (Columbian,
Mexican, Guatemalan, and hybrids). As these varieties cannot
be distinguished morphologically, the authors strongly advise
against feeding any part of the avocado plant to animals.
39
found. On the next day, however, the dog had fully recovered
and was discharged from the clinic. The only treatment the
animal had received was an intravenous drip with Ringer’s
solution (132 ml/h).
Symptoms
Symptoms typical for macadamia nut poisoning are lethargy
and weakness, particularly in the hind legs, as well as ataxia,
vomiting, muscle tremor and elevated body temperature.
Toxic principle
The toxic mechanism of macadamia nuts is currently unknown.
Diagnosis
The patient history and the presence of macadamia nuts in
vomit can point towards macadamia nut intoxication.
Therapy
In most cases, no medical therapy is required. To reduce the
uptake of toxic substances, vomiting can be induced and/or
activated charcoal can be applied. The prognosis is very good,
no fatalities due to macadamia nuts are known to the authors.
Figure 3: Macadamia nuts are a healthy snack for humans, but can
cause mild intoxication in dogs. ©[email protected]
Hops
Diagnosis
There are currently no diagnostic procedures known to prove
avocado intoxication.
Hops have been used for beer brewing since the middle ages
to give beer its typical bitter taste and to reduce growth
of microorganisms. The term ‘hops’ refers to the female
flower cones of the hop plant (Humulus lupulus), which is a
climbing perennial belonging to the genus Hops of the family
Cannabaceae.
Pets seldom have access to brewery waste. Duncan et al. [46]
describe the case of two dogs whose owner had brewed beer
for home consumption and had disposed of the waste on the
compost pile accessible to the dogs. Three hours later, one of
the dogs was restless and panting, had a painful abdomen,
tachycardia and tachypnoea. The body temperature increased
rapidly to 41°C. All attempts at treatment – with butorphanol,
diazepam and prednisolone – were ineffective. When the dog
was anaesthetized for an exploratory laparotomy, the body
temperature climbed to 42 °C within 5 min and the dog died.
On post-mortem, a large quantity of hops was found in the
stomach. The other dog from the same household started to
develop similar symptoms 6 h after the assumed ingestion of
hops. Vomiting was induced with apomorphine, gastric lavage
and enemas were performed and activated charcoal was
administered. In this patient, the body temperature also rose
during anaesthesia, but the dog recovered under intensive care.
Three more cases of hops poisoning in dogs were reported to
the APCC from 1994 to 1997 [46]. The affected animals showed
panting, seizures, dark urine and a body temperature > 41°C 2-8
h after hops ingestion. All of them died despite intensive care
treatment.
Therapy
Therapy of avocado intoxication can only be symptomatic. If
heart and lungs are involved, the prognosis is uncertain, and
long-term consequences cannot be ruled out. If the mammary
gland is the primarily affected organ, animals will recover, but
the milk yield will remain impaired for some time or might even
cease completely.
Macadamia nuts
A total of ten species belongs to the genus Macadamia, family
Proteaceae, three of them yielding edible fruits (M. integrifolia,
M. tetraphylla and M. ternifolia). Originally from Australia, these
plants are nowadays mostly cultivated in Hawaii. Macadamia
nuts are merchandized as snacks for human consumption (see
figure 3), either fresh, roasted and salted, or in combination
with chocolate. Hansen [45] published a summary of 48 cases of
macadamia nut intoxication in dogs, which had been reported
to the APCC between 1987 and 2001. The dogs mentioned in
these cases had ingested dosages ranging from 2.2 to 64.4 g/
kg BW. The initial symptoms were lethargy and weakness (most
notably in the hind legs), followed by vomiting, ataxia, muscle
tremor and elevated body temperature. A slight elevation of
serum lipase, serum triglycerides and alkaline phosphatase could
be seen in four dogs after experimental application of 20 g
macadamia nuts/kg BW [45]. In June 2006, a three year old male
Golden Retriever was presented at the Clinic for Small Animals
and Horses of the Veterinary Medicine Department, University
of Vienna, that had ingested the entire contents of a bag of
macadamia nuts stolen from his owner the previous evening.
He was unable to stand or walk, and the spinal reflexes in his
hind limbs were absent; apart from that, no abnormalities were
Symptoms
Excitability, tachycardia, and tachypnoea were described in hops
poisoning. The most typical symptom is the severely elevated
body temperature. Hare [47] further mentions enhanced
vocalization and reddened mucous membranes.
40
Toxic principle
Duncan et al. [46] suspect a mechanism similar to the malignant
hyperthermia syndrome. Since four of the five affected dogs
happened to be Greyhounds, hops seem to trigger a malignant
hyperthermia hereditary in this breed. The toxic principle of action
is not known, but the symptoms point towards an uncoupling of
oxidative phosphorylation. Hops contain a variety of substances
that could be considered responsible for this effect, like essential
oils, phenols, resins, and active nitrogen compounds.
gastrointestinal tract causing ulcers that tend to bleed [49]. The
central nervous system is especially sensitive to hypernatraemia:
Dehydration, tissue shrinkage and damage to blood vessels
cause haematomas, bleeding and infarcts. Sodium is able to
pass the blood-brain-barrier and inhibits, if present in excess,
the anaerobic glycolysis and thus the energy production in the
neurons. If the sodium level in the brain decreases again, water will
flow into the cerebrospinal fluid causing cerebral oedema [50].
Whether the dilatative cardiomyopathy in the case described by
Pouzot et al. [51] was caused by the hypernatraemia or whether
it had already existed subclinically before the incident, remains
unclear.
Diagnosis
Diagnosis of hops intoxication is only possible by identification of
hops material in vomit or gastric lavage effluent. The owner must
be questioned exhaustively about possible hops ingestion.
The minimum toxic dose of NaCl is considered to be 2 mg/kg
BW, the minimum lethal dose 4 mg/kg BW [50]. Commonly
used play dough consists of two parts of flour, one part of water
and one part of salt. One teaspoon of salt equals about 8 g, one
table spoon about 15 g and one cup about 300 g.
Therapy
Treatment is symptomatic though decontamination of the
gastrointestinal tract must be carried out as soon as possible.
The body temperature must be monitored carefully, and the
animal must be cooled if necessary. Dantrolene sodium could be
used to reduce the body temperature by relaxation of peripheral
muscles [46,47].
Diagnosis
The diagnostic symptom for excessive salt ingestion is
hypernatraemia without signs of dehydration. The owner should
be questioned about the potential for exposure to salt.
Salt (NaCl)
Therapy
If the salt ingestion has occurred less than 30 min ago,
vomiting could be induced. Activated charcoal is not effective
in salt poisoning. As long as the animal does not show any
clinical symptoms, offering drinking water frequently and in
small amounts is the only measure that needs to be taken. If,
in contrast, several hours have already passed since the salt
ingestion occurred and/or the patient is in bad condition,
intensive therapy needs to be started right away. Elimination of
excess sodium from the body is the primary goal. Infusion with 5
% dextrose solutions is recommended; diuretics like furosemide
enhance sodium excretion and help prevent oedema [50].
Blood electrolytes and blood pressure need to be monitored
carefully. Antiemetics and gastric protection are indicated due
to the ulcerative effect of NaCl. If seizures should occur, they
can be controlled by the administration of diazepam. In case of
hyperthermia, cooling of the patient might be necessary.
Hypernatraemia caused by excessive salt intake is rarely seen in
pets. In 1969, Chew [48] published a case report of a Boxer bitch,
which used to drink huge amounts of salt water while swimming
in the ocean and regularly vomited afterwards. When the owner
one day did not offer her drinking water after swimming, she
died having epileptiform convulsions. Khanna et al. [49] reported
one and Barr et al. [50] a total of 14 dogs that had ingested play
dough containing NaCl. Their symptoms ranged from lethargy,
vomiting and diarrhoea to polyuria, polydipsia, ataxia and
confusion, and even to seizures and death. At least three of the
15 dogs died. Also the application of salt as an emetic can lead
to salt poisoning [51]. A five year old Doberman Pinscher bitch
was caught eating chocolate and was therefore given 100 g
of salt by her owner. She showed vomiting and diarrhoea, and
one hour later had ataxia, seizures and coma. Subsequently, she
developed clinical symptoms of renal insufficiency and dilatative
cardiomyopathy. After ten days all her symptoms had resolved
and she could be discharged from the clinic; only the dilatative
cardiomyopathy was irreversible. The Animal Antipoison Centre
in Lyon (France) recorded a total of 260 cases of salt poisoning
in dogs before the year 2007 [51].
Xylitol
Xylitol is a pentavalent sugar alcohol that occurs naturally in
many fruits and vegetables as an intermediate product of
glucose metabolism. As it tastes about as sweet as sucrose, but
only provides two thirds of its nutritional energy, xylitol is used
as a sweetening agent in human nutrition (E 976). Due to its
plaque-reducing properties [53] and its cooling effect on the
tongue, xylitol is often added to tooth pastes, chewing gums
and lozenges.
The first case of xylitol intoxication in a dog was reported by
Dunayer in 2004 [54]. A nine months old Labrador Retriever had
eaten about 100 pieces of a sugar-free chewing gum containing
70 % xylitol (which equals a dosage of about 3 g/kg BW).
When the dog was presented at the clinic, it was non responsive
and in lateral recumbency. Severe hypoglycaemia (37 mg/dl)
was detected. After intravenous infusion of Ringer’s solution
Symptoms
Lethargy, vomiting, regurgitation, diarrhoea, polyuria,
tachycardia, tachypnoea, coughing, dyspnoea, hyperthermia,
ataxia, myoclonia, tremor and seizures have all been described in
small animals with salt poisoning. Fatal outcomes are possible.
Toxic principle
Salt intake or infusions with hypertonic sodium solutions
elevate the osmotic pressure in the body. Water leaves the cells
resulting in hypervolaemia. If the body is not able to cope with
this additional volume, oedema will develop [52]. Additionally,
sodium chloride irritates the mucous membranes of the
41
containing 50 % dextrose the dog recovered rapidly. Dunayer
and Gwaltney-Brant [55] describe eight more cases of xylitol
poisoning from the APCC database. In addition to lethargy and
vomiting, five of the eight dogs also showed bleeding tendency
(petechiae, ecchymosis, gastrointestinal bleeding). Laboratory
blood testing revealed hypoglycaemia, elevated liver enzymes,
hyperbilirubinaemia, hyperphosphataemia, thrombocytopenia
and prolonged clotting times. Two of the dogs died, three
had to be euthanized. Post-mortem was performed on the
euthanized animals revealing severe necrosis of the liver tissue.
The number of cases of xylitol ingestion in dogs reported to the
APCC has increased constantly over the past years. After only
three cases in 2002, 20 occurred in 2003, 82 in 2004, and 193
in 2005; in the first half of 2006, already 138 cases had been
registered [55]. Todd and Powell [56] reported the case of a
English Springer Spaniel that had ingested half a loaf of bread
containing xylitol (dosage: 3.7 g/kg BW). Besides hypoglycaemia,
this dog also showed signs of liver failure (dramatic elevation of
all liver enzymes, severe coagulation dysfunction). It was treated
with intensive care (including several blood transfusions) and
was saved.
hospitalizing all dogs that have ingested more than 0.1 g xylitol/kg
BW and to monitor their blood glucose level and liver function. A
‘liver protection therapy’ including N-acetylcysteine, S-adenosylL-methionine, silymarin as well as vitamin E and C can support
recovery and should best be started early.
Discussion
Although the toxic effects of some foodstuffs on animals have
been known for a long time, cases of intoxication in pets still occur
frequently, either because they are fed by owners unaware of
the danger, or because the animals have unauthorized access to
these substances. In the majority of the cases, dogs are affected.
It seems that human food is not attractive to cats, who are
known for their distinctive eating behaviours. Such intoxication
cases can be expected to gain even more importance in the
future, since pets are living closer and closer to their owners
providing a substitute for human companions.
Besides the cases of intoxications described above, we would
further like to mention that several other human foodstuffs may
also cause adverse reactions in pets. Adult mammals have a
low lactase activity, which means that large amounts of dairy
products containing lactose will lead to osmotic diarrhoea.
While puppies can digest up to 5 g of lactose/kg BW/day,
an adult dog only tolerates 2 g/kg BW/day, which equals 20
ml of cow’s milk [59]. Fermented dairy products like cheese,
curd cheese or yoghurt, however, are more digestible. Snacks
made from dairy products also need to be considered in this
respect. Additionally, raw egg white contains not only trypsin
inhibitors that impair protein digestion, but also avidin, which
inhibits the absorption of biotin and can therefore cause biotin
deficiency. As a consequence, eggs (a valuable protein source
for cats and dogs) should only be fed when thoroughly cooked.
The stones of fruits belonging to the genus Prunus (apples,
pears, plums, apricots, peaches, nectarines, cherries) contain
the cyanogenic glycoside amygdalin. If the stones are cracked
open and swallowed, the digestive enzymes will break down
the amygdaline releasing hydrocyanic acid. Fitzgerald [60]
indicates that already five to 25 stones can cause hydrocyanic
acid poisoning. Raw manioc (cassava/yucca root) also contains
cyanogenic glycosides. For diagnosis and therapy of hydrocyanic
acid poisoning we would like to refer the reader to current
literature. Beans of the genus Phaseolus (common bean, runner
bean) are not suitable for raw feeding either, since they contain
a variety of detrimental components (lectins, tannins, trypsin
inhibitors, cyanogenic glycosides), which may cause indigestion
and damage to the gastrointestinal wall.
In January 2008, a case of a dog from Austria hit the press.
He had shown ‘symptoms like a drunk person’ after ingestion
of half a kilogram of raw yeast dough. The blood alcohol level
was measured and found to be 1.6%. It seemed that the
fermentation of yeast in the gastrointestinal tract had produced
enough amounts of ethanol to cause an intoxication. A similar
case was described by Suter in 1992 [61].
Eating habits and their effects on well-being have become a
popular topic both in human medicine and popular scientific
literature. Pet owners in Europe started to base their judgement
of pet food on recommendations for human nutrition. They
disapprove of commercial diets as being similar to ‘fast food’
Symptoms
Possible clinical symptoms of xylitol intoxication are lethargy,
unconsciousness, seizures, vomiting, epistaxis, melaena,
hypoglycaemia, elevated liver enzymes, coagulopathy, and
death due to liver failure.
Toxic principle
Research on xylitol was initiated in the 1960’s and 1970’s for its
potential use in nutrition for human diabetics. It was then found
that in dogs, contrary to humans, intravenous xylitol injection
causes insulin secretion followed by a decrease of blood
glucose level [57]. The mechanism leading to necrosis of liver
cells is not known. Dunayer and Gwaltney-Brant [55] propose
two theories. When xylitol is metabolized, phosphorylated
intermediate products are formed that use up all the adenosine
monophosphate (AMP), adenosine diphosphate (ADP) and
phosphorous within the liver cells. In addition, nicotinamide
dinucleotide is produced causing the formation of reactive
oxygen species in the mitochondria. One of these mechanisms,
or the combination of both, might be the reason for hepatocyte
necrosis.
In the cases described above, the dosage of xylitol ingested by
the dogs was 0.15 to 16 g xylitol/kg BW. An association between
the dose of xylitol and the severity of the symptoms could not
be established [55].
Diagnosis
The presence of hyperglycaemia of unknown cause in a dog
should make the veterinarian ask the owner about a possible
intake of xylitol containing substances.
Therapy
To avoid aspiration pneumonia, vomiting should only be induced
as long as the patient is fully conscious. Since hypoglycaemia can
develop as soon as 30 min after xylitol intake [54], intravenous
dextrose infusion should be started right away. Activated charcoal
is not effective [58]. Dunayer and Gwaltney-Brant [55] recommend
42
and feel the need to prepare ‘fresh and healthy’ food for their
pet. This development carries not only the risk of malnutrition,
but also the danger that potentially toxic substances might make
their way into the food bowl. In addition to that, more and more
exotic foodstuffs and novel food additives are brought to market,
that might have a yet unknown toxic effect on some animal
species. It is the duty of the veterinarian to inform pet owners
about those hazards. Foodstuffs that are known or suspected
to contain harmful substances must not be fed to pets and
have to be stored inaccessible to them. Veterinarians are further
requested to publish such cases to make them known to their
colleagues.
[22]
[23]
[24]
[25]
[26]
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44
CRITICAL CARE
REPRINT PAPER (CH)
N. Sigrist(1), D. Spreng(1)
SUMMARY
Traumatic haemoabdomen
Haemoabdomen is an important differential diagnosis for canine and feline abdominal trauma. The diagnosis is
made by aspiration of blood from the abdomen by abdominocentesis. Spleen and liver are the most likely sources of
traumatic bleeding. Patients are stabilized with appropriate fluid therapy, oxygen supplementation and analgesia.
With ongoing haemorrhage, serial measurement of abdominal and venous haematocrit can be helpful in making
the decision between surgical and medical therapy. Most patients with traumatic haemoabdomen can be treated
medically. Surgical therapy should be reserved for patients that cannot be stabilized despite medical intervention.
The surgical approach should be thoroughly planned in order to minimize further abdominal blood loss and blood
transfusions should be readily available.
Key words: haemoperitoneum, dog, cat, diagnostic procedures
Case discussion
This paper originally appeared in:
A two-year old male Labrador is presented 30 minutes after being
hit by a car. At presentation, primary survey revealed lethargy,
tachycardia (180 beats per minute), pale mucous membranes and
a prolonged capillary refill time (CRT) of 2 seconds. Respiratory
rate was 40 breaths per minute and bilaterally increased lung
sounds could be auscultated. Abdominal palpation was painful
and the clinician noticed a possible fluid wave. Orthopaedic
and neurologic examinations were within normal limits. The
initial CBC and biochemical profile showed a venous PCV of
44 %, total solids (TS) of 50 g/l (reference 57-75 g/l), normal
leucocyte and thrombocyte numbers, albumin 25 g/l (normal
27-38 g/l), creatinine 100 µmol/l (reference 53-120 µmol/l), ALT
6306 IU (reference 24-124 IU), AST 8284 IU (reference 20-73
IU), GLDH 268 IU (reference 2-10 IU) and normal electrolytes.
PT was 14.6 seconds (s) (reference 6.3-8.5 s) and aPTT 8.6 s
(reference 9.6-16.1 s). Indirect systolic blood pressure was 128
mmHg with a mean arterial blood pressure (MAP) of 78 mmHg.
Simultaneously with the venous blood collection the abdomen
Kleintierpraxis* 53(12) 2008 777-786#
Introduction
Haemabdomen or haemoperitoneum describes the pathologic
accumulation of blood in the abdomen. Causes of haemoabdomen
can be traumatic or non-traumatic. Blunt abdominal trauma is
common in trauma patients, but the prevalence of traumatic
abdominal bleeding is unknown and depending on the severity,
haemoabdomen can be clinically nonsignificant.
The diagnosis of haemoabdomen necessitates the differentiation
of active versus inactive bleeding which is often difficult.
However, immediate diagnosis and adequate stabilisation
are mandatory for the successful treatment of patients with
abdominal bleeding. The treatment of haemoabdomen includes
emergency surgery as well as medical therapy [Mongil et al.,
1995; Sigrist and Spreng, 2007].
(1) Department of Clinical Veterinary Medicine, Vetsuisse Faculty of Bern, Langgass-Strasse 128
CH - 3012 Bern Corresponding author E-mail: [email protected]
* Presented by SVK/ASMPA(Switzerland)
# Copyright permission gratefully received from www.vetline.de/kleintierpraxis
45
Traumatic Haemoabdomen - N. Sigrist, D. Spreng
was tapped. Serosanguinous fluid was aspirated. Abdominal
fluid showed a PCV of 42 %, TS of 43 g/l and creatinine of 96
µmol/l. A presumptive diagnosis of haemoabdomen was based
on these results.
Stabilization of the dog included nasal oxygen supplementation,
a bolus of 10 ml/kg Plasmalyte® (Baxter AG) as well as 5
ml/kg hydroxyethyl starch (Voluven®, Fresenius Kabi AG),
followed by lactated Ringer’s solution (Fresenius Kabi AG) at
2ml/kg/h, Voluven® at 1 ml/kg/h, amoxicillin-clavulanic acid
(Augmentin®,GlaxoSmithKline, 20 mg/kg i. v. q 8 hours), analgesia
[initially methadone (Methadon Streuli®, Streuli Pharma AG) 0.1
mg/kg i. v. q 2 hours followed by buprenorphine (Temgesic®,
Essex Chemie AG ) 0.01 mg/kg i. v. q 8 hours]. Monitoring
included hourly measurement of heart rate, respiratory rate,
mucous membrane color, CRT and blood pressure.
palpation. Depending on the amount of fluid accumulation
and body configuration a fluid wave may be palpable. At least
40 ml/kg of fluid is needed for a clear fluid wave to occur on
abdominal palpation [Crowe and Devey, 1994]. Occasionally
umbilical and peri-testicular skin discoloration may be observed
when significant intra-abdominal haemorrhage dissects
through the abdominal muscle planes and subcutis [Crowe
and Todoroff, 1982]. A normal physical exam does not exclude
traumatic haemoabdomen since haemoabdomen, as well as
other traumatic injuries to the abdomen may not be recognized
reliably [Crowe and Crane 1976; Davies et al., 1976].
Differential Diagnosis
Differential diagnoses for traumatic haemoabdomen include
all other traumatic injuries such as bladder or urethral rupture,
peritonitis following intestinal or bile duct injuries, traumatic
pancreatitis or traumatic shock [Crane 1980]. These traumarelated injuries might also be seen in addition to traumatic
haemoabdomen and have to be excluded during diagnostic
workup of the patient. Causes of non-trauma-related
haemoabdomen include neoplasia, coagulopathy and splenic or
liver torsion. Other differential diagnoses in patients presenting
with signs of an acute abdomen are peritonitis, intestinal
obstruction, pancreatitis or neoplasia.
On chest radiographs, the dog showed lung contusions and a
small pneumothorax. Ultrasonic examination of the abdomen
revealed large amounts of free fluid, signs of liver rupture with
haematoma formation, evidence of a blood clot in the bladder
and signs of pancreatic oedema and/or haematoma.
Two hours after presentation the venous PCV had decreased to
26 %. The abdominal PCV measured at the same time was 40 %.
Four hours after presentation, the dog showed a venous PCV of
22 % while the abdominal PCV was 41 %. Eight hours later the
venous PCV stabilized at 23 % and concurrent abdominal PCV
was 40 %. The dog remained haemodynamically stable. Venous
PCV increased to 25 % the following day and normalized within
a couple of days. The dog remained stable and went home 3 days
later without further diagnostic or therapeutic procedures.
Diagnostic approach
In human medicine, the diagnostic evaluation of blunt abdominal
trauma combines clinical evaluation, abdominal ultrasound,
computed tomography (CT) evaluation and analysis of abdominal
effusion retrieved by abdominocentesis or diagnostic peritoneal
lavage (DPL) [Hoff et al., 2002].
Aetiology
Laboratory evaluation
Traumatic haemoabdomen is a potentially live-threatening
complication of blunt or penetrating abdominal trauma and is
most often seen after motor vehicle accidents. The spleen and
liver have been described as common sources of haemorrhage
in human as well as veterinary patients [Clarke et al., 2002;
McKenney et al., 2001]. Due to its location and fragility, the liver
is the most common source of haemorrhage.
Acute bleeding leads to a similar loss of erythrocytes and plasma.
PCV and total solids (TS) will therefore not change in the first few
minutes following trauma. The decreased intravascular volume
then leads to splenic contraction with subsequent release of
sequestered red blood cells (dog >> cat) and to a shift of water
from the interstitial into the intravascular compartment, leading
to a lower TS compared to the PCV value. PCV may therefore
be normal with acute haemorrhage. A significant decrease in
PCV and TS values may be seen only after fluid therapy directed
at normalizing intravascular volume [Crane 1980]. Regular PCV
checks are therefore mandatory during resuscitation. Blood gas
analysis and lactate measurements may help in interpretation of
perfusion status, with metabolic acidosis and hyperlactataemia
being suggestive of cellular hypoxia [de Laforcade and Silverstein,
2008]. Increases in liver enzyme activities may commonly be seen
after trauma and are not associated with the cause of abdominal
haemorrhage. Additional laboratory evaluation including
complete blood count, biochemical profile and urinalysis is
often normal but may be helpful in excluding other concurrent
diseases or trauma-related organ dysfunction. Depending on
the history and physical exam results, coagulopathy as a cause
of non-trauma-related haemoabdomen should be ruled out.
Physical examination
Clinical symptoms may vary from patient to patient and
depend on other trauma-related abnormalities such as shock,
respiratory distress and other abdominal or extra-abdominal
injuries. After initial stabilisation of respiration and perfusion,
a complete physical exam is indicated in all patients. Clinical
signs of abdominal bleeding may appear several hours after
trauma. Depending on the amount of blood loss, signs of
hypovolaemic shock such as pale mucous membranes (MM),
prolonged capillary refill time, tachycardia and a weak femoral
pulse as described in the above case description may be seen.
During the compensation phase of hypovolaemic shock, animals
may present with red mucous membranes and a short capillary
refill time [de Laforcade 2008]. Abdominal bleeding as well as
other trauma-related injuries will lead to pain and patients will
present with signs of an acute abdomen and pain on abdominal
46
Diagnostic imaging
not specific for the diagnosis of haemoabdomen however and
identification has to be followed by abdominocentesis and fluid
analysis. Computed Tomography is the standard diagnostic
and monitoring tool used in human patients presenting with
haemoabdomen [Baron et al., 1993]. In veterinary medicine,
CT imaging is not widely available and the advantage over DPL
remains controversial in human medicine [Blow et al., 1998].
Abdominal radiographs in the presence of abdominal effusion
are of questionable diagnostic value, as the free abdominal fluid
will lead to decreased abdominal detail. Abdominal radiographs
may though be helpful to exclude severe haemoabdomen in
trauma patients and may detect other trauma-related injuries
[Brockmann, 2000]. Thoracic radiographs may be indicated in
trauma patients in order to identify or exclude pneumothorax,
haemothorax, diaphragmatic rupture or rib fractures that would
require additional treatment. Abdominal ultrasound is helpful
in the identification of abdominal effusion and possibly in the
identification of its cause [McKenney et al., 1998]. Scanning
defined abdominal locations using “focused assessment with
sonography for trauma” (FAST) shows a high sensitivity and
specifity for the diagnosis of haemoabdomen in trauma patients
[Scalea et al., 1999; von Künsberg et al., 2003]. FAST, used as a
scoring method, may help to estimate the extent of abdominal
effusion and may be used as a parameter to decide if a surgical
approach is required. A positive FAST result in haemodynamically
unstable human patients is an indication for laparotomy, while
a positive FAST result in stable patients requires CT evaluation in
order to identify the cause of abdominal haemorrhage [Scalea
et al., 1999]. In human studies, the specifity of this method is
71-78% [Ma et al., 1995; Huang et al., 1994].
Abdominocentesis
Any finding or suspicion of free abdominal fluid accumulation
should prompt abdominocentesis and fluid analysis.
Abdominocentesis is a sterile procedure and is most simply
done under ultrasound guidance using an 18-22 G hypodermic
needle with attached syringe. Blind paracentesis following the
4-quadrant rule is another option (figure 1). A hypodermic
needle with or without an attached syringe is introduced into
the abdomen paramedian either cranially or caudally to the
umbilicus [Walters, 2003]. Depending on abdominal palpation
results (cranial organomegaly versus large bladder), initial
paracentesis is done either caudally or cranially to the umbilicus
at the most gravity-dependent location. If no fluid is retrieved,
another quadrant is tried. Using the aspiration technique,
omentum may occlude the needle, requiring open paracentesis
and collection of fluid from the needle hub [Walters, 2003]. The
accuracy of abdominocentesis for detection of haemoabdomen
is 50-62% [Crowe and Crane, 1976; Kolata et al., 1976]. The
use of a peritoneal dialysis catheter increases the sensitivity up
to 100 % [Crowe and Crane, 1976; Crowe, 1984]. False-positive
results may be seen after aspiration of liver, spleen or abdominal
vessels [Crowe and Bjorling, 1993]. This can easily be ruled out
if the aspirated blood does not clot, as blood in contact with
abdominal serosa is depleted of fibrinogen and thrombocytes
[Prasse and Duncan, 1976].
Diagnostic peritoneal lavage (DPL) can be performed when
A FAST protocol has been developed for dogs and showed
a sensitivity of 96% and a specifity of 100% in terms of
identification of an abdominal effusion [Boysen et al., 2004].
With the patient in left lateral recumbency, the abdomen is
screened for free abdominal fluid at the following locations:
immediately caudal to the xiphoid process, on the ventral midline
over the bladder, over the right flank (gravity-independent
region) and over the most gravity-dependent area of the left
flank [Boysen et al., 2004]. The presence of abdominal fluid is
FIGURE 1A and 1B: Abdominocentesis using 4-quadrant aspiration.
The abdomen is punctured para¬median 2-3 cm from the midline. Depending on the sus¬pected disorder, the first puncture is done cranially
or cau¬dally to the umbilicus (figure 1A, “X”). The puncture is repeated in one quadrant after the other, until fluid can be retrieved.
Aspiration is best done using an 18-22 G hypodermic needle attached to a 5-10 cc syringe after surgical preparation of the site. If no fluid can
be aspirated, puncture is tried without aspiration.
Figure 1A
Figure 1B
47
paracentesis techniques do not provide a positive diagnosis
and ultrasound is not available [Crowe, 1984]. Warm sterile
0.9% saline is infused into the peritoneal cavity through the
DPL catheter (20 ml/kg) and the fluid is allowed to mix with
fluid present in the abdominal cavity for 15 minutes. The fluid is
collected by gravity flow into a sterile closed collection system
and analyzed. DPL allows the identification of as little as 0.8 ml/
kg blood [Crowe and Crane, 1976]. PCV values higher than 2-5%
in DPL fluid are associated with severe haemoabdomen [Crowe,
1993; Dye, 1999]. Unfortunately, neither abdominocentesis nor
DPL allow differentiation between active and inactive abdominal
bleeding [Bilge and Sahin, 1991]. With increased availability
of sonography, DPL has been largely replaced by ultrasoundguided abdominocentesis.
[Revell et al., 2003; Prough et al., 1991]. On the other hand,
attention must be given to maintaining an adequate blood
pressure until haemostasis has occurred. The concept of “low
volume resuscitation” is accomplished by maintaining a mean
arterial blood pressure (MAP) of 60 mmHg [Sondeen et al.,
2003]. Fluid therapy is carried out with intravenous boluses of
10-20 ml/kg of an isotonic crystalloid fluid such as 0.9% NaCl
or lactated Ringer’s solution and 5-10 ml/kg of a colloid such
as hydroxyethyl starch (Voluven®). Hypertonic saline (4 ml/kg)
together with smaller boluses of crystalloids and colloids would
be another option [Varicoda et al., 2003]. The volume expansion
with hypertonic saline may be difficult to control and hypertonic
saline should therefore be reserved for severely hypotensive
animals. Hypotonic solutions such as DW5 or glucose-NaCl
combinations should not be used in hypovolaemic shock. With
severe haemorrhage, whole blood transfusions may be necessary
in order to maintain oxygen carrying capacity and haemostasis.
Paracentesis fluid is collected into EDTA, heparin and sterile
serum tubes. EDTA-fluid is used for the determination of PCV/
TS and cell count and for cytological evaluation. Creatinine or
bilirubin can be determined from heparinized blood if indicated.
If the PCV of the abdominal fluid matches the venous PCV or is
even higher, the diagnosis of a haemoabdomen can be made.
Abdominal fluid with a lower than venous but still substantially
high PCV is indicative of abdominal bleeding in combination
with another effusion and may necessitate measurement of
abdominal and venous creatinine to rule out uroabdomen.
Higher creatinine concentrations in the abdominal fluid are
indicative of uroabdomen [Schmeidt et al., 2001]. According to
this approach, an increased abdominal bilirubin concentration is
indicative of bile peritonitis. Cytology is used to rule out septic
peritonitis [Conally, 2003].
Oxygenation: Oxygen supplementation is indicated for
hypovolaemic shock as well as additional lung dysfunction
in trauma patients. Oxygen supplementation during the
stabilization process is easiest achieved using a mask or flow-by
oxygen. Should continued oxygen supplementation be required,
a nasal oxygen catheter can be placed and oxygen supplied at 2-5
l/min. Arterial oxygen saturation should be at least 95% in order
to ensure sufficient tissue oxygenation. Anaemic patients should
have a higher saturation (SpO2 99-100 %) and maintaining
sufficient oxygenation may require transfusion therapy.
Transfusion therapy: Loss of oxygen-carrying erythrocytes will
lead to tissue hypoxia. Hypovolaemia and resulting hypoperfusion
will increase this effect. There is no real transfusion trigger [Day,
2000; Jutkowitz, 2004]. The decision to administer a red blood
cell transfusion or a blood substitute solution (Oxyglobin®)
should be considered when clinical signs compatible with severe
anaemia and haemorrhagic shock (tachycardia, tachypnoea,
bounding pulses, collapse) are seen, when required fluid therapy
will lead to a declining PCV or when PCV declines below 2025% [Herold et al., 2008; Jutkowitz, 2004]. The choice of blood
product depends on availability and the presence of coagulation
factor deficiencies. With severe haemorrhage, loss and dilution
of erythrocytes as well as coagulation factors may require
transfusion of fresh whole blood. The whole blood transfusion
must be fresh (<6 hours) in order to provide coagulation factors.
Isolated anaemia with normal coagulation times can be treated
with a pRBC transfusion and coagulation factor deficiencies
leading to haemoabdomen but only mild anaemia may be treated
with plasma alone. Detailed descriptions of transfusion therapy
are available elsewhere [Sigrist, 2005, Hohenhaus, 2000].
Therapy
Depending on the cause of haemoabdomen, patients are treated
surgically or non-surgically after initial stabilization [Hoff et al.,
2002; Nagy et al., 1995]. Severe abdominal haemorrhage that
needs immediate surgical intervention should be suspected in
patients that cannot be stabilized. Smaller abdominal bleeding
is usually self-limiting and patients may not show any clinical
symptoms. In any case, the patient must be stabilized prior to
any diagnostic or surgical interventions.
Stabilization
Stabilization of a patient with haemoabdomen follows the
ABC. Fluid therapy and analgesia are important therapeutic
interventions in all patients, regardless of medical or surgical
management.
Fluid therapy: Patients with abdominal bleeding will present
in hypovolaemic shock. Aggressive treatment of hypovolaemic
shock increases survival [Gallerani-Santibanez et al., 2001]. Fluid
therapy therefore is an important step in the stabilization of
the patient and aims to normalize tissue perfusion and oxygen
delivery while minimizing further bleeding. A combination of
isotonic crystalloids and colloids is advised [Sigrist, 2005]. With
haemorrhage, there is a risk of further bleeding with normalization
of perfusion. If blood pressure is increased substantially prior
to definitive haemostasis, further haemorrhage may occur
Autotransfusion: Catastrophic abdominal bleeding may require
autotransfusion of shed abdominal blood. Autotransfused
blood may be live-saving as it is readily available and presents
no risk of transfusion reaction. The abdominal blood is collected
aseptically and mixed with an anticoagulant solution [Crowe
1980, Jutkowitz, 2004]. Anticoagulation is carried out with
sodium citrate 3.8% (ratio 1:9) or CPDA (ratio 1:7). Blood can
also be collected directly into commercially available blood
collection bags. The advantages of autotransfusion must be
48
evaluated in light of potential side effects such as potential
induction of disseminated intravascular coagulation by cell
debris and transfusion of bacteria from potential abdominal
contamination. Autotransfusion is contraindicated if abdominal
blood is contaminated with tumor cells, urine or bacteria from
gastrointestinal rupture [Crowe 1980]. The authors recommend
autotransfusion only if insufficient blood products are available.
All blood products are administered using a filter.
Analgesia: NSAID’s are contraindicated in hypovolaemic
animals with decreased renal perfusion; therefore opioids are
the analgesics of choice in patients with haemoabdomen.
Short-acting, pure µ-agonists such as fentanyl (2-10 µg/kg/h)
or methadone (0.1-0.2 mg/kg q 1-2 h) are preferred as the
dose can be adjusted and they can be antagonized if necessary.
Intravenous lidocaine has analgesic and antioxidant properties
and is a good choice in combination with an opioid (fentanyl
CRI) in animals with abdominal pain. Lidocaine is given as a
bolus of 2 mg/kg (cats 0.5 mg/kg) followed by a CRI of 30 µg/
kg/min (≈ 2 mg/kg/h) [Valverde et al., 2004].
Figure 2: Comparison of venous and abdominal PCV.
Abdominal bleeding is determined to have stopped when serial
measurements of concurrent venous and abdominal PCV values
show trends in opposite directions. After fluid resuscitation, the
venous PCV value is suspected to decrease due to haemodilution.
The abdominal fluid PCV is expected to decrease in a similar
manner as the venous PCV if bleeding is continuing, whereas it is
suspected to stay stable or increase due to fluid reabsorption if the
bleeding has stopped
Arresting further haemorrhage
Arresting further haemorrhage requires normalization of
haemostasis while maintaining adequate perfusion without
hypertension. Abdominal counterpressure using an abdominal
bandage may help to stop abdominal bleeding and increase
survival [McAnulty and Smith, 1986]. A modification of this
technique describes the incorporation of the pelvic limbs into
the counterpressure bandage. Care must be taken to avoid the
compartmentalization of blood in the pelvic limb vasculature
and to avoid occluding the caudal abdominal vena cava [Crowe,
1988]. Our own experience shows that these bandages may be
painful and difficult to safely apply. Abdominal counterpressure
is contraindicated in patients with pelvic or femoral fractures,
respiratory distress due to pneumothorax, pleural effusion
or diaphragmatic rupture or with head trauma. Abdominal
counterpressure can potentially lead to abdominal compartment
syndrome with subsequent hypoperfusion of abdominal organs
[Nieman et al., 1983; Chang et al., 1995] and are therefore rarely
indicated in our opinion.
abdominal bleeding that require surgical control was shown to
increase with time [Clarke et al., 2002]. Other problems that
require surgical intervention should be ruled out as soon as
possible [Mongil et al., 1995, Prasse and Duncan, 1976].
However, patients with vague signs might pose a diagnostic
challenge to the emergency clinician. Clinical, biochemical,
haematological parameters, diagnostic imaging results as
well as response to treatment have been suggested as aids
to deciding if surgical intervention is necessary for the control
of haemorrhage but did not prove to be helpful [Holt, 1978].
Clinical evaluation alone was shown to miss 59% of injuries in
blunt trauma patients [Bivins and Sachatello, 1978; Smith et al.,
1996]. In a retrospective study of 28 dogs and cats with severe
haemoabdomen, no clinical parameters that differentiated
between the surgically and medically treated groups could be
identified [Mongil et al., 1995].
The initial venous PCV prior to fluid therapy has not been helpful
in the evaluation of active bleeding [Snyder, 1998] and a normal
PCV does not always indicate medical therapy is appropriate
[Paradis et al., 1997; Snyder, 1998].
Since neither repeated venous PCV measurements nor the
determination of a single abdominal PCV identifies active
bleeding, comparing abdominal fluid and serum PCV values
continuously might be more useful in the selection of therapy
[Sigrist and Spreng, 2007]. If abdominal bleeding has stopped,
serial measurements of concurrent venous and abdominal PCV
values will show trends in opposite directions, as venous blood
will be diluted by fluid therapy while the abdominal PCV will not
change. With continuous bleeding, the venous PCV will decrease
and not stabilize with fluid therapy and the abdominal PCV will
slowly decrease due to continuous bleeding with a lower venous
PCV (see figure 2). This approach differs from an experimental
study showing that using DPL, increasing PCV values in the DPL
solution are associated with severe haemorrhage [Thomson
Medical versus surgical therapy
Depending on the cause and the progression of disease, surgery
may be required to stop the bleeding. Several human studies
and case reports have shown that diagnosis of haemoabdomen
does not mandate immediate laparotomy [Goan et al., 1998;
Grisoni et al., 1984; Hiatt et al., 1990; Hoff et al., 2002; Nagy
et al., 1995; Smith et al., 1996]. Fluid resuscitation will lead to
a decline in venous PCV, regardless of the presence of active or
previous bleeding. In a retrospective veterinary study, 40% of
the animals that underwent surgical intervention did not show
active bleeding at the time of surgery [Mongil et al., 1995].
The decision to treat a patient medically or surgically is often
difficult. Haemodynamically unstable patients with signs of
continued bleeding should undergo surgical intervention as soon
as possible [Clarke et al., 2002; Goan et al., 1998; McKenney et
al., 1996; Smith et al., 1996], as mortality in patients with severe
49
immediately identified after inspection of spleen and liver,
abdominal packing is recommended [Sharp and Lociero, 1992].
The abdomen is packed with laparotomy sponges or sterile
towels. Once the packing material appears to have controlled
major blood loss, the pads are methodically removed in a
clockwise fashion starting at the caudal aspect of the abdomen
and bleeding vessels identified and ligated. If the bleeding vessel
cannot be identified very rapidly, the towels are left in place; the
abdomen is temporarily closed, with re-exploration performed
in 24-72 hours. This allows potential coagulopathies to be
controlled and a chance for fluid resuscitation to occur.
Non-surgical therapy
Figure 3: Splenic rupture.
This spleen has been traumatically transected leading to a severe
haemoabdomen
In our experience, most traumatic haemoabdomen patients
can be managed non-surgically. This has also been shown in
various human studies [Goan et al., 1998]. Other indications for
surgery, such as uroabdomen or peritonitis should be ruled out.
Non-surgical management includes maintaining perfusion and
analgesia as described under stabilization. Animals are routinely
monitored for perfusion deficits and PCV changes.
et al., 1985]. Crowe (1993) recommends that increasing PCV
values over time in DPL fluid is diagnostic for active abdominal
haemorrhage.
Monitoring
Concurrent and serial measurements of the venous and
abdominal PCV value were used in the case presented above.
Initially, both values were similar. The venous PCV was lower
at presentation due to fluid shifts from the interstitial to the
intravascular space and initiation of fluid therapy. The stable
abdominal PCV values over time despite declining venous PCV
values are suggestive of an inactive haemoabdomen. Continued
active haemorrhage would dilute the abdominal PCV. This
method is only useful as long as the venous PCV decreases due
to fluid therapy dilution and provided no blood products are
transfused and is only applicable with a pure haemoabdomen
without other fluid contamination.
Both post-operative and non-surgically treated patients need
intensive monitoring. Initially, monitoring of respiration,
perfusion parameters such as heart rate, MM color and
CRT, blood pressure and pulse quality may be necessary
every 30 minutes. Subsequent monitoring depends on the
haemodynamic changes. Tachycardia, pale mucous membranes
and prolonged CRT are signs of hypovolaemic shock and need
to be addressed immediately [de Laforcade 2008]. Anaemia
leading to tachycardia and pale MM can be differentiated from
hypovolaemia by a normal CRT.
Regular serial measurement of abdominal and venous PCV values
(every 1-4 hours) is helpful in deciding if a surgical approach,
blood products or colloids are indicated. Following aggressive
fluid therapy, monitoring of coagulation parameters may be
indicated to decrease the risk of ongoing or new bleeding.
Surgical Therapy
Patients that cannot be stabilized with fluid therapy are clearly
candidates for a surgical approach. Rapid surgical exposure
and a systematic approach are mandatory in order to localize
and ligate the cause of haemorrhage [Herold 2008]. Hepatic
or splenic ruptures are the most common causes of traumatic
haemoabdomen; therefore these organs are primarily inspected
(Figure 3). A modified Pringle maneuver has been described
[Crowe and Devey, 1994] but has not been shown to be useful
in the clinical setting.
Using the modified rule of 20 by Dr. Kirby allows identification
and early correction of potential complications [Sigrist and
Spreng, 2004].
Prognosis
One veterinary study showed that survival for animals with
severe haemoabdomen is 67% for surgically treated patients
and 75% for non-surgically managed patients [Mongil et al.,
1995]. Overall mortality in this study was 27 % [Mongil et al.,
1995]. Other veterinary studies are lacking and other traumarelated factors are important regarding prognosis of patients
with traumatic haemoabdomen.
If a large supply of blood products is available the surgical
exploration can be performed more slowly. If at least 50% of
the blood volume is available as blood products, the following
approach may be used: rapid surgical exposure of the abdomen
is followed by inspection of the spleen and control of potential
splenic ruptures. Following splenic inspection, the abdominal
fluid is suctioned in order to identify other bleeding sources
such as a ruptured renal or hepatic vein [Feliciano and Moore,
2004]. This approach needs time and appropriate transfusion
therapy. If unlimited transfusion therapy is not available or if
large-volume haemorrhage is ongoing and the source is not
50
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52
- N. Sigrist, D. Spreng
CRITICAL CARE
The FECAVA Symposium 2009*
Pain in Companion Animals
INTRODUCTION
FECAVA was proud to present the Pain Symposium at the FECAVA Eurocongress in Lille.It is the most recent in
the series of important Symposia held at FECAVA Eurocongresses each designed to target key area of interest for
practicing veterinarians.
The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or described in terms of such damage” www.iasp-pain.org
In our own experience Pain is the unpleasant and uncomfortable feeling common to such experiences as stubbing a
toe, burning a finger, putting iodine on a cut and bumping the “funny bone”.
Pain is signal which alerts the body to harmful intrusions and acts as a selfprotective reflex. A survey in North
America revealed it was the most common reasons for Veterinary advice to be sought. On some occasions however
pain is an unavoidable part of treatment. For example neccessary procedures such as injections, administering
infusions, routine surgery (sterilisation, castration etc) all result in some pain as do traumatic events such as car
accidents or bite wounds.
It is important for us as veterinary surgeons to control all pain in animals, whatever its origin and to avoid suffering.
It is our duty to treat animals to ensure that they live in the most pain free conditions possible. As pain is very
uncomfortable it usually results in stress and this delays a normal healing processes. Relief of pain therefore has a
double benefit to our patients.
As a veterinary surgeon dealing freequently with surgery ( orthopaedics and neurosurgery) I have found it very
necessary to set up the best possible comfortable situation for my patients. Pain management has always been my
first priority for two reasons. First of all because it is my duty to my patient but secondly because it enables me to
work more effectively ensuring the best postoperative results.
Pain must of course also be controlled in situations where chronic pain is present as part of the daily life of an
animal sometimes for short periods but often for many weeks.
The FECVA Pain Symposium lectures in Lille attracted a large nummer of delegates the speakers keeping their
lectures very practical as FECAVA had asked. I am pleased that we are able to publish papers based on the lectures
here in EJCAP. This will enable those not lucky enough to be inLille to benefit from the Symposium.
Three of the papers are included in this issue, and we hope to publish the remaining three EJCAP 20(2) October. All
the papers will be posted on the FECAVAWebsite as soon as available.
Johan van Tilburg FECAVA President
* Held during the 15th FECAVA Eurocongress /AFVAC/SAVAB/LAK Congress Lille November 2009
To follow in our October issue:
Acute pain scoring - M Gogny, Pain and Hyperalgesia in dogs and cats - M Gogny, Management of Chronic pain- advances - D Holopherne
54
CRITICAL CARE
Diagnosis of chronic pain in small animals
Alessandra Bergadano DVM, Dr.Med.Vet., Dip.ECVAA, PhD. Anaesthesiology Division, Department of Clinical
Veterinary Medicine, Vetsuisse Faculty- University of Berne, Längassstrasse 124, PB 8466 CH-3001 Bern
INTRODUCTION
Understanding and treating pain in animals is one of the most challenging tasks in veterinary medicine. In the
last decade there has been growing interest and research investigating the mechanisms underlying animal pain,
its diagnosis and improving therapeutic options [1]. Dogs and cats can experience physiological or pathological
pain. Many diseases, medical and surgical procedures cause pain in small animals, mainly of short duration (<7
days) [2]. Pathological or “chronic” pain of inflammatory (somatic or visceral), neuropathic or mixed origin is
generally recognised as pain that persists beyond the normal healing process or longer than 1 month [2, 3]. Pathological
pain has no protective action to the body, but on the contrary has a “destructive” action. The most common
causes of inflammatory chronic pain in small animals are musculoskeletal disorders e.g. hip dysplasia, cruciate
ligament rupture, osteoarthritis [4]. Also otitis, lower urinary tract disease in cats and endometritis are possible
non-orthopaedic causes. Diseases or lesions of the nervous system lead to neuropathic pain; the most common
causes are traumatic or surgical lesions to the nervous system e.g. limb amputation leading to phantom pain [5],
polyradiculoneuropathy, fractures, neuromas, tumours (compression) and diabetes. Chronic pain due to cancer [6] is
classified as “of mixed origin”.
To date the most important gap in our knowledge of animal pain is related to its assessment [7] and there is
currently no gold standard to assess nociception in animals and no unit for pain. Subjective assessment of abnormal
demeanour or behaviour is extensively used and multiple scales and scoring systems have been developed in
an attempt to better diagnose and quantify pain, the focus being mainly on acute pain associated with surgery
or trauma. However, there are remarkably few measurement instruments available to the veterinary surgeon to
diagnose and quantify chronic pain. Chronic pain conditions in small animals are so far under-recognised and thus
under-treated.
Chronic pain characteristics
(down-regulation). These molecular changes contribute to the
persistence of pain [8].
In humans the development of chronic pain depends also on
psychosocial factors [10]. How and if cognitive and emotive
factors influence the development of chronic pain in animals is
unknown [11].
Chronic pain is associated with hyperexcitability of the central
nervous system [8]: prolonged afferent nociceptive input induces
an increase in the excitability of central sensory neurons, so
called “winding-up and central sensitisation”. Within the spinal
cord, the hyperexcitable neurons amplify the nociceptive signal,
thereby producing an exaggerated pain signal sent to the brain
[8]. The area of pain can also increase through these central
mechanisms. Furthermore, there are circuits from brain to spinal
cord that can excite the sensory systems [9]. Therefore, central
sensitisation very likely contributes to pain and disability even in
the presence of limited tissue damage.
This aberrant hyperactivity also leads to changes in the RNA
transcription with expression of more and/or new receptors
(up-regulation) to the detriment of the physiological receptors
To summarise, chronic pain is characterised by:
-
-
55
Tissue damage (present, past)
Neuroplasticity (at peripheral, spinal and supraspinal
level)
- Wind-up and central sensitisation,
- Up/down-regulation and modification of receptors,
- Decreased descending inhibition
Psychological influences (in veterinary medicine?)
Diagnosis of chronic pain in small animals - Alessandra Bergadano
Diagnosis of chronic pain
1. History, presenting signs
Diagnosis is “the recognition of a disease or condition by its
outward signs and symptoms”. Indeed pathological pain is a
disease and the rationales for its diagnosis are:
- Neuroplasticity changes are likely determinants of chronic
pain and we need to look for its clinical signs
- Allodynia, hyperalgesia and dysestesia (Figure 1).
- Pain refractory to conventional analgesic therapy
- Some nociceptive alterations can be measured (clinical
exam, imaging techniques, quantitative sensory testing)
- The magnitude of the pathological changes varies among
individuals
2. Behavioural changes,
chronic pain scores
Chronic pain
3. Examination - clinical,
QST, RX, MRI..
Figure 2- Triangulation technique to “encircle” pain as a disease
(adapted from Lindely S. [12]) RX = Radiography
best able to perceive the subtle changes in exercise/activity,
performance, mood, appetite and behaviour that may reflect
chronic pain.
The purpose is to establish a high suspicion of pain: reduced
exercise tolerance in a dog, for example, might be related to
pain due to osteoarthrosis but equally may not (e.g. progressing
heart disease). Some diseases or surgeries (e.g. diabetes in cats,
limb amputation) have a high probability of inducing chronic
pain.
As there is no unique and peculiar outward sign or symptom
of chronic pain (so called “gold standard”), and animals cannot
directly communicate their suffering, a pragmatic approach to
diagnosing chronic pain in small animals is the pain assessment
triangle [12, 13]. This approach relies on the presence of at
least 3 indicative signs allowing to “encircling” the diagnostic
challenge, i.e. the presence of chronic pain (Figure 2). It can/
should be complemented by Quantitative Sensory Testing (QST)
and an analgesic trial.
It is likely that dogs and cats share a common pathophysiology
but present with different clinical signs and behavioural changes
when in pain.
How to proceed practically with the pain assessment triangle:
• Plan enough time and be patient, especially with cats
• Work in a quiet environment with a relaxed animal. [12, 13]
2) Behavioural changes
Thereafter the behavioural assessment looks at changes in the
animal’s behaviour and checks any environmental reason for
these. Behavioural changes are often the only signs of pain in
small animals but may arise for different reasons. Behavioural
changes without environmental or social changes to explain
them should indicate a suspicion of pain as a clinical disease.
Aggressive behaviour towards people when parts of the body
are touched can indicate allodynia and hyperalgesia.
Sudden spontaneous jumps or attempts to bite the tail/limbs,
shaking of (phantom) limb, might evoke dysestesia (altered
sensation), and suggest pain of neural origin. Neuropathic pain
in humans is described as burning, stabbing, like an electric
shock… [15, 16].
In cats, alopecia due to compulsive grooming can be linked to
stress e.g. a new baby arriving in the home or changes in the
living environment of the cat. If no environmental cause can be
identified, back pain could be the reason for this.
Other behavioural changes in dogs and cats that might be
indicative of chronic pain are presented in Table 1.
For a structured and systematic evaluation the best approach
is to ask the owners to fill in a behavioural chart [17, 18] and a
composite chronic pain scale. To date two scales, the Helsinki
chronic pain Index and the Canine Brief Pain Inventory of
Pennsylvania University, have been validated for evaluating
chronic pain in dogs affected by osteoarthritis [19-22] or limb
neoplasia [22]. They quantify two dimensions of chronic pain,
‘severity’ and ‘interference’ and also address the dog’s overall
quality of life.
Other types of chronic pain are actually not addressed and no
validated item for cats is available. For pain of different origin,
its assessment can be done by subjectively describing abnormal
behaviour patterns and demeanour or by using a Visual
Analogue Scale after direct or video-assisted (1) observation of
the animal. This method is simple but is biased by the observer’s
“subjectivity,” meaning that the observer introduces some
personal bias when recording pain assessments and its validity
1) History, presenting signs
The pain assessment should start with the presenting signs and
the complaint of the owner. It is very important to take time
to record a detailed history of the patient (14): the owners are
Figure 1. Stimulus response (SR) relationship of the nociceptive
system. By increasing the intensity of the stimulus there is an
increase in the magnitude of pain, in normal conditions. In case
of central sensitisation the SR curve becomes steeper, as the same
stimulus intensity elicits a stronger pain response “hyperalgesia”,
or the response is shifted to the left, so that stimuli of low intensity
(which do not elicit a pain response in the normal animal) elicit a
pain response “allodynia”.
56
Behavioural signs
Changes in life style
Depression
Reduced/absent jumping
Tendency to get isolated
Reduced interest in playing
(hunting in cats)
Reduced interaction with
owner/other animals
Augmented sleeping times
3) Clinical investigation
- Physical examination:
An accurate physical examination, palpation of muscles and
joints or scars can help in recognising pain. The goal is to
spot some of the clinical features of central neuroplasticity as
hyperalgesia and allodynia: simple stroking can elicit aggressive
reactions and vocalisation. Some locations may be extremely
sensitive to palpation “tender points” and elicit avoidance
behaviours, flight/ aggressive reactions/vocalisation (Figure 3).
Palpation may be difficult or non-specific in the cat.
In dogs affected by osteoarthritis reduction of the range of
movement can be diagnostic.
Aggressive behaviour
Reduced appetite
(towards people and/or other
animals) especially
with manipulation
Changes in sleeping habits
Less grooming (cats)
Altered toileting
Less scratching (cats)
- Observation of gait:
Watching the animal move, run and jump may add useful
information (24, 25). As a rule of thumb, dogs with osteoarthritis
will limp while cats are mainly asymptomatic.
Lameness can be evaluated by a scoring system or with force
plates.
In osteoathritic cats, decreased mobility –as assessed by owners
or with a digital monitor- is indicative of pain [24, 25].
Reduced use of cat door
(cats)
Table 1. Behaviours that might be indicative of chronic pain in
dogs and cats.
in non verbal patients is controversial.
Another approach is to use a simple descriptive scale with 4
categories of pain intensity: 0= no pain, 1= mild pain; 2= moderate
pain; 3= severe pain [23]. The validity and reproducibility of the
scale is observer dependent, and has moderate sensitivity.
- Diagnostic imaging – Radiography (RX), ultra sonography
(US), MRI, CT and arthroscopy are valuable diagnostic aids
and can close the triangulation procedure to diagnose chronic,
pain. They will require deep sedation with a neuroleptanalgesic
mixture or a short general anaesthesia to ensure welfare of the
painful patient (Figure 4).
These findings are extremely important as they represent the
“baseline” values allowing evaluation of the evolution of the
pain syndrome and the efficacy of the analgesic treatment.
- Quantitative sensory testing (QST)
Quantitative Sensory Testing enables us to test specific
components of the nociceptive system such as Aδ or
unmyelinated C-fibres (Table 2). The goal of these adjunctive tests
is to highlight and quantify the clinical signs of neuroplasticity,
hyperalgesia and allodynia. Obtaining an objective quantitative
measure or “threshold” might be helpful for diagnostic, followup and research purposes.
Figure 3. Palpation of the back to individuate tender points in a
8year old female poodle affected by chronic ostheoarthritc pain
Figure 4. Radiological
appearance of the left
carpus in the same dog.
57
Nerve fibre type
Function
Aα
Motor
X
Aβ
Light touch
X
Vibration
X
Aδ
Cool
X
Warm
X (hairy)
C
X (glabrous)
Pin prick
X
Cool pain
X
X
Heat pain
X
X
Table 2. Nerve fibres classification
Typically, hyperalgesia is detected when sensory stimulation
evokes pain at stimulus intensities that do not induce pain in
normal subjects (lower pain threshold) or when a standardised
painful stimulus evokes stronger pain in patients than in normal
subjects (Figure 1). Noxious stimuli vary widely with respect to
the quality of pain sensations produced, as well as to the specific
nociceptive and non-nociceptive afferents activated (Table
2). Heat hyperalgesia represents sensitisation of peripheral
primary nociceptive afferents. On the contrary, hyperalgesia to
mechanical stimuli (pin-prick) is mediated by Aδ fibres and it
involves spinal cord sensitisation [26].
Pain hypersensitivity after low threshold sensory stimulation of
healthy areas, allodynia, is mediated by Aβ fibres and its cause
must be a hyperexcitability of the central nervous system, an
NMDA receptor mediated phenomenon. Indeed, there is no
evidence that peripheral mechanisms could account for higher
pain sensitivity in healthy tissues (Figure 1).
Thus, it is essential to select a stimulus that is relevant to the
clinical question. The choice of the right test will bring important
information on the underlying pathophysiological mechanism,
serving as guidance for a mechanism based therapeutic
approach [27].
i Mechanical thresholds
• Algometer: can be used to identify tender points in
musculoskeletal pain syndromes [28]. Muscle pain is
mediated by C nociceptors.
• Von Frey filaments: they are simple and non expensive tools
to assess allodynic areas. The pain produced is mediated by
Aβ fibres mechanical.
• Pins: elicit hyperalgesia to mechanical stimuli (pinprick)
which is Aδ mediated (Figure 5). A map of the hyperalgesic
area can be drawn and used to evaluate the efficacy of the
therapy (shrinking of the mapped area)
ii. Thermal thresholds
• Warmth: both thermo-electrical and Peltier thermodes can
be used. Requires clipping; the type of activated fibres can
be selected by slow (< 1°C/s; C fibres) or fast (2-10°C/s; Aδ
fibres) rate of heat ramps [29].
Figure 5. Pin-prick to assess hyperalgesia in the same dog.
technique to confirm the existence of chronic pain in dogs and
cats [15, 16]. Nevertheless it has to be kept in mind that to
date there are no normal values for quantitative sensory tests
nor published evidence on the reproducibility, reliability and
validity of these diagnostic procedures for chronic pain in small
animals.
iii Electrophysiological testing
• Nerve conduction
• EMG
Can help to diagnose neurological deficits and musculoskeletal
pathologies [15]. The reader is referred to more in depth
discussion on neuromuscular physiology [31, 32].
• Nociceptive withdrawal reflex and temporal summation
[33].
• Somatosensory evoked potentials (SSEP) [34]
Nociceptive electrical stimulation is applied to peripheral
sensory nerves to evoke reflex spinal and central responses
which are quantified by neurophysiological techniques as
EMG or EEG. These models are considered surrogates of
nociception and wind-up [35]. In humans there is ongoing
research to implement these technically demanding models
as clinical tools for bed side use [36]. So far they remain in
veterinary medicine, tools for the experimental setting.
4) Other diagnostic procedures
i Systemic lidocaine test
Systematically administered lidocaine has been shown to
be successful in diagnosis prediction of the efficacy of Na
channel blocker therapy and treatment of neuropathic pain
in humans [37, 38]. No veterinary studies have evaluated
lidocaine’s analgesic efficacy when used alone for diagnostic
All these QST methods rely on behavioural responses. For a
systematic approach the test results should be structured on an
inventory as is done with humans [30].
QST has been effectively used as part of the triangulation
58
References
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chronic pain is similar in small animals and humans, we can
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tool” in veterinary medicine.
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The diagnosis of chronic pain in small animals is not
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A practical approach relies on: 1: a thorough history review, 2: a
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60
CRITICAL CARE
Locoregional anaesthesia in small animals
Alessandra Bergadano DVM, Dr. Med.Vet., Dip.ECVAA, PhD. Anaesthesiology Division, Department of Clinical
Veterinary Medicine, Vetsuisse Faculty - University of Berne, Längassstrasse 124, PB 8466 CH-3001 Bern
INTRODUCTION
Local anaesthesia consists of applying local anaesthetics and/or analgesics directly at the desired site of action for
blockade of nerve impulses to abolish sensation.
In veterinary medicine, loco-regional anaesthetic (LRA) techniques are routinely performed in bovines and
horses as a diagnostic aid and for surgery. In small animals LRA techniques are underused, probably due to
the availability of safe and potent sedative and anaesthetic drugs. Still, since 2000 [1, 2], there appears to be an
increased or renewed interest, according to the number of scientific publications. LRA techniques can be used for
diagnostic purposes, be part of a balanced anaesthetic protocol or used for post-operative or long term analgesia.
They are effective, safe and easy techniques which can improve the welfare of the veterinary patient. The purpose
of this article is to highlight the advantages of performing LRA , and provide a more detailed description of some
techniques relevant for the small animal practitioner.
Advantages
Disadvantages
Most commonly LRA in small animals is used as part of a
balanced anaesthesia protocol. Balanced anaesthesia consists
of combining hypnotic, analgesic and myorelaxant drugs to
produce an “ideal” anaesthetic state. Thanks to the synergistic
effect of the different drugs, it allows for the use of decreased
total doses reducing undesired drug-related side effects, with
a comparable or better quality of anaesthesia. Loco-regional
anaesthesia in association with general anaesthesia can block
almost totally the transduction, transmission and modulation
of the afferent nociceptive stimulation, avoiding subsequent
neurohumoral activation and prevent winding up and central
sensitization of the central nervous system (CNS). This results in
intraoperative autonomic stability and reduced cardiovascular,
respiratory or central nervous system depression, which is a
major advantage in geriatric or critically ill patients.
Furthermore, LRA can be performed before the onset of
the surgical noxious stimulus according to the “pre-emptive
analgesia concept” [3], which has been shown effective in
preventing central sensitization and reducing the magnitude of
postoperative pain. This might also prevent the appearance of
chronic pain [4].
Overall LRA reduces perioperative morbidity and mortality,
improving the outcome and wellbeing of small veterinary
patients.
The major draw-back is the potential toxicity owing to the
intrinsic mechanism of blocking action at the Na + channels.
Overdose or inadvertent intravenous administration of local
analgesics can result in central nervous system disturbances
(initially seizures, thereafter CNS depression with respiratory
arrest) and cardiovascular depression, with bradycardia,
atrioventricular (AV) blocks, AV dissociation and hypotension.
Bupivacaine has a higher cardiac toxicity as it can block Na +, K+
and sarcoplasmatic Ca++ channels.
In case of an accident the therapy is symptomatic and supportive.
Intubation and controlled ventilation with 100% oxygen
are extremely important as both respiratory and metabolic
acidosis increase CNS toxicity. IV access should be confirmed or
established and seizures treated with IV diazepam or thiopental
to effect. Seizures are generally not noticed in the anaesthetised
patient, and cardiovascular depression is likely to be the most
relevant symptom. Cardiovascular support with fluids and
inotropic drugs is recommended as is standard treatment of
the arrhythmias, recognising that they may be very refractory
to treatment. If cardiac arrest occurs, standard CPR is started. In
humans [5] and experimental dogs [6] the use of lipid infusion
(Intralipid 20%®) (1.5 ml kg-1 bolus followed by an intravenous
infusion at 0.25 ml kg-1 min-1) has proved effective to reverse
refractory cardiac arrest after bupivacaine overdose. Nevertheless
61
Locoregional anaesthesia in small animals - Alessandra Bergadano
as the potential risks of administering these relatively high doses
are uncertain, and the optimal dose has not been established it
is appropriate to administer lipid emulsion only after advanced
cardiac life support has failed.
Simple but important rules to improve safety are:
- aspirate before injection to check for blood
- calculate the maximal total dose to avoid absolute
overdose.
Drugs
Many local anaesthetics, which have different mechanisms of
actions, durations, toxicities and costs can be used, with or
without adjuvants such as opioids, a2 agonists, and adrenergic
drugs.
The most commonly used local anaesthetics in small animals are
lidocaine and bupivacaine. Bupivacaine has a slower onset of
action (approximately 30 minutes depending on the site of use)
but a longer duration of effect (6-8 hours) than lidocaine (1.5-2
hours). Lidocaine - bupivacaine mixtures can be used to offset
the latency of bupivacaine.
Figure 1. Local anaesthetics for topical anaesthesia. In very small
patients lidocaine can be diluted 1:1 with saline and applied with
the tip of an IV catheter
Techniques
improving both the efficacy and safety of the LRA. The use of
electrostimulation allows precise and selective localisation of the
nerves, increasing therefore the success rate of the block [11].
In humans ultrasound guided LRA resulted in improved sensory
and motor block, faster onset of block, and longer duration
of sensory blockade compared with conventional techniques
[12]. This technique is promising also in veterinary medicine.
Furthermore the risk of inadvertent intravascular and intraneural
injection is reduced.
The choice of the technique depends on the indication, special
conditions (i.e. Cesarean section) and the experience of the
veterinarian.
All the blocks must be performed aseptically (aseptical
preparation of the skin, sterile dressing and gloves).
In small animals LRA is mainly applied while the animal is in deep
sedation or under general anaesthesia for increased safety and
comfort for the patient: the animals are more easily positioned,
Drug properties; Table 1
Name
Concentration %
Dose mg/kg
Toxic dose
Lethal Dose
(seizures) mg/kg mg/kg
Onset (min)
Duration of action
Lidocaine
1%, 2%
5
11
16-28
10 min
Intermediate: 1-2 h
Bupivacaine
0,5% 0,75%
2
4
5-11
20 min
Long: 2.5-6 h
Ropivacaine
0.5%
0.1-2
?
?
2-20 min
Long: 2-6 h
Procaine
1%
6
36
100
10 min
Short: 30 Min
the anatomical landmarks as well as the specific nerves and
blood vessel groups are better identified and the insertion of
the needle is more precise and less traumatic.
Essential for a successful loco-regional technique devoid of
complications, is the capability of the anaesthetist to recreate
a virtual three dimensional representation of the anatomical
landmarks, nerves, vessels and cavities. Many superficial
nerves can be palpated or can be localized by using specific
anatomical landmarks. The classical anatomy books are helpful
illustrated guides on where to perform the local anaesthesia. An
electrical nerve stimulator or ultrasound machine can be used
to precisely locate and visualize the nerves, respectively [7-10],
Some LRA techniques relevant for the private practitioner are
presented and shortly discussed below.
1. Topical anaesthesia (Figure 1)
Lidocaine and other local anaesthetics are rapidly absorbed
from mucous membranes. It can be applied for anaesthesia of
the gingiva and after teeth extraction, nasal mucosa (to place
an O2 catheter), eye (lidocaine gel 2%; preservative free), larynx
and trachea for intubation, urogenital tract to place a urinary
catheter or the ovarian ligament for ovariectomy [13].
62
Lidocaine spray
10% solution:
Indication:
Application:
Duration of action:
Advantage:
Complications:
Tipp:
Continue until the entire length of the
incision has been infiltrated.
Duration of action: 0.5 ml kg-1 of a 1:1 mix of lidocaine 2%
+ bupivacaine 0.5% can be used to have
a fast onset and long duration (5-6H) of
action. Dilute with saline 0.9% if more
volume is needed.
Advantage:
easy, very safe
Complications:
systemic toxicity if overdose.
10 mg/spray dose
desensitization of mucosa (intubation!)
spray 1 sec
after ca 1 Minute for 15-20 min (2 mm
depth)
easy, fast, cheap
toxicity (toxic doses easily reached in cats)
not more than 1 spray (10 mg)/cat
Emla cream/patch® 1:1 mixture of lidocaine and prilocaine
Indication:
simple biopsies, IV or arterial catheter
placement
Application:
apply cream + occlusive bandage,
or apply patch
Duration of action: onset after 30 min
Advantage:
simple, expensive
Complications:
none; limited efficacy with thick skin
This infiltration of the wound at the end of the surgery offers
immediate post-operative comfort. This procedure is very popular
in paediatric surgery [14]. There is experimental evidence that
local anaesthetics do not affect wound healing [15, 16].
2.2. Soaker or diffusion catheters (Figure 2)
A modern and very promising “variation” of the infiltration
technique, is the placement in the surgical field of a soaker
catheter allowing the constant infusion of lidocaine, or the
intermittent administration of ropivacaine or bupivacaine after
the closure of the surgical incision. Combined with low doses
of systemic analgesics it offers an excellent analgesia in the first
24-48h post-operation, especially for major surgeries such as
amputations, removal of fibrosarcomes in cats which require
extensive tissue resection [17], total mastectomies or removal of
neoplasias. Special catheters and sets are available on the market,
which have multiple holes to facilitate the diffusion of the local
anaesthetic [18]. The goal is to achieve adequate analgesia with
the minimal effective volume. The recommendations are priming
the catheter with 2 mg/kg lidocaine and thereafter a continuous
infusion at a dose of 2 mg/kg/hr, or bupivacaine may be given as
an intermittent bolus every six hours at a dose of 0.5 to 2 mg/kg
in dogs [19]. A nice update from Clark and Leece on the state of
the art in veterinary medicine is available on the AVA homepage
http://www.ava.eu.com/page/small-animal-members .
Applied on the shaved skin. To maximize the effect of the cream
an occlusive bandage should be applied for 30 min to 1 hour.
This allows a stress-free intravenous catheter placement in
sensitive animals or for arterial puncture or catheterization in
critical animals.
2. Infiltration anaesthesia
2.1. Single shot
Infiltration for surgery
Indication:
minor diagnostic and surgical procedures,
spermatic cord for castration.
Application:
subcutaneous infiltration of the surgical
field or wound
Duration of action: depending on the LA - see Table 1 Advantage:
easy, very safe
Complications:
systemic toxicity if overdose, necrosis in
distal regions
3. Regional anaesthesia
The LA is injected close to one or more nerves to desensitize the
regional territory they supply.
3.1. Peripheral nerve blocks
• Head:
Mandibular, maxillary, oculomotor,
ophthalmic nerves blocks
Infiltration with LA is used to desensitize skin and subcutis
for minor diagnostic and surgical procedures. After aseptical
preparation of the skin the local anaesthetic drug is injected as a
blob for small intervention (i.e skin biopsy or catheter insertion)
or drawing a square or triangular-shape to desensitize larger
areas. Ideally also the deeper tissues should be infiltrated to
ensure complete analgesia. This technique can be useful for
the removal of small masses in geriatric dogs or to offer better
analgesia as part of a balanced anaesthesia protocol. When
anaesthetizing large areas it is important to back the needle out
so that just the tip remains under the skin before changing the
position of the needle to avoid unnecessary tissue trauma.
Figure 2. Soaker catheter in a cat undergoing fibrosarcoma
surgery to administer ropivacaine or bupivacaine for postoperative
analgesia. (Courtesy of Prof. D. Fonda Dip. ECVAA (17))
Incisional line block
Indication:
pre- or post-op analgesia i.e. after
laparatomy or mastectomy.
Application:
with a 22G needle infiltrate the subcutis
and the abdominal muscles (if after
laparatomy) on both sides of the wound.
Insert the needle, aspirate (no blood) and
then inject while retrieving the needle.
63
• Thorax:
Intercostal nerve block; pleural and
interthoracal blocks
• Forelimb:
Plexus block, “three point block” (Ulnar,
median and Radial nerve), ring block
• Hind limb:
Lumbar plexus block, “bi block” (Sciatic
and femoral nerve block), distal sciatic
nerve block, ring block
• IVRA (intravenous regional anaesthesia)
For improved efficacy and safety it is recommended to use a
nerve stimulator when performing regional blocks. Recently
ultrasound guided techniques have been described in veterinary
medicine.
• Head
Blocks of the cranial nerves offer an excellent perioperative
analgesia both for dentistry [20] and major oncologic surgery.
This is extremely important as the head has extensive trigeminal
innervation causing excruciating pain. Furthermore as most of
the patients presented for dental or oncological surgery have an
increased anaesthetic risk due to age and potentially concomitant
diseases, they benefit from the achieved autonomic stability.
Figure 4. Intraoral maxillary nerve block.
Maxillary Nerve Block
Blocked nerves: Maxillary branches of N. Trigeminus. These
nerves innervate the hard and soft palates,
their mucosa, and the nasopharynx (i.e. all the
hemimaxilla) (Figure 3).
Indications:
Maxillectomies. Rhinoscopies with biopsies,
dental procedures.
Technique :
a. Intraoral: palpate the maxillary bone behind
the last molar tooth. Than insert the 22 G
needle and advance the needle dorsally to just
beyond the root tips of the last maxillary molar
then aspirate and slowly inject (Figure 4)
In cats, the maxillary nerve block is performed
intraorally at the base of the ‘V’ notch or divot
near the soft palate juncture, palpable just
medial to the caudal root tips of the maxillary
fourth premolar (20)
b. Extra oral technique (small dogs, cats) The
needle is inserted perpendicular to the long
axis of the head under the ventral border of the
Figure 5. Extraoral maxillary block. The zigomatic arch is
highlighted by the dotted lines.
rostral zygomatic arch. The needle will need to
be directed slightly dorsal from the horizontal
(Figure 5).
Duration:
depends on drugs
Advantage:
Cheap, very effective technique
Complications: Nerve damage
Figure 3. Territory innervated by the maxillary nerve (Courtesy of
Dr A. De Simoi Dip. ECVD).
• Forelimb
Plexus Brachialis Block
Blocked nerves: NN.axillaris, medianus, ulnaris,
musculocutaneus, radialis
Indications:
surgeries below the elbow
Technique :
a) Medial access via the axilla after aseptical
preparation of the skin (Figure 6)
b) Insertion of the needle at the level of the
scapulo-humeral joint parallel to the shoulder
to avoid accidentally entering the thoracic
cavity (Figure 7)
c) Location of the nerves by electrostimulation
(Figure 8)(9). The PBB can be performed also
64
Figure 6. Plexus brachialis in a dog.
Figure 7. Insertion of the shielded needle for the plexus block in a
dog. The scapulo-humeral joint is elevated and the needle inserted
parallel to the joint
blindly with the A. axillaris as anatomical
reference (21).
d) Aspiration, then injection of the drugs by
retrieving the needle
Duration:
depends on drugs
Advantage:
Cheap, very effective technique
Disadvantage Motor block.
Complications: Difficult technique (learning curve), risk of
pneumothorax, nerve damage and intrarterial
injection.
Characteristics:
3.2. Central blocks:
- Epidural anaesthesia/analgesia (more common)
- Spinal anaesthesia
Nerves:
from T12 to S2
Indications:
surgeries beyond the umbilicus, post-operative
analgesia without motor block “ambulatory
epidural”
Epidural anaesthesia
syn. extradural anaesthesia,
peridural anaesthesia
Spinal anaesthesia [22]
syn. subarachnoidal
anaesthesia
Space between dura mater
and ligament flavum
Contains connective tissue,
fat and vessels
Positioning and specific
weight less relevant
Site of action: dorsal and
ventral nerves roots
Space between arachnoidea
and Pia mater
Contains cerebrospinal fluid
(sp. weight 1003-1009)
Positioning and sp. weight
determinant
Site of action: dorsal and
ventral nerves roots
Position of the patient: Sternal or lateral recumbency with the
hind limbs extended cranially. (Figure 9)
Material:
5 or 10 cm long, 20-22G Spinal needle
(Tuhoy or Quinck)
Syringes with NaCl and drugs
Figure 8. Thereafter the nerves are electrolocated. The LA is
injected while retrieving the needle, to reduce the risk of accidental
intravascular administration.
Figure 9. Sternal positioning of a dog for epidural injection. Notice
the extended hind limbs to widen the lumbo-sacral space.
65
Figure 11. Epidural injection and hanging drop. The spinal needle
has been inserted and the saline drop is hanging. Thereafter the
needle is advanced up to when a change in resistance is felt and
usually the saline drop is “sucked in”. NB: the dog is not draped
for the purpose of this picture only!
Figure 10. Landmarks for the epidural injection. The thumb and
middle finger of the non dominant hand are placed on the higher
point of the ileum wings. Thereafter the index finger is placed
exactly on the mid of this virtual line. There is the localisation of
the lumbo-sacral space (red dot), where to perform the epidural
puncture.
Preparation:
Technique:
Figure 12. Fluoroscopic control of the epidural injection. The
contrast medium is migrating cranially and caudally within the
epidural space.
Aseptical preparation of the skin; sterile gloves
and draping extremely important!
1. Location of the lumbosacral space with the
3 finger technique (Figure 10)
2. Insertion of the needle with an angle of 30°
from the vertical plane
3. Application of a drop of NaCl (Hanging
Drop) (Figure 11)
4. Slowly advance the needle to when the
drop is „sucked-in“
Other techniques to confirm the entrance in
the epidural space are the feeling of a loss
of resistance and use of a loss of resistance
syringe or epidural waves [23].
5. Aspiration: no Liquor or Blood? If liquor is
noticed, ½ of the volume must be injected and
the head elevated to avoid cephalad spread.
If blood is noticed, the needle is retrieved
and a second puncture can be attempted; if
blood appears again an alternative to epidural
anaesthesia is recommended.
6. Slow injection of the drugs (Figure 12)
Doses:
Drug
Volume
Onset (min)
Duration (h)
Lidocaine 2% 0.2 ml/kg
10
1-1.5
Bupivacaine
0.2-0.5%
0.2 ml/kg
20-30
4.5-6
Fentanyl
2mg /kg
4-10
6
Morphine
0.1 mg /kg
20
12
Contraindications: - Skin lesions at the injection site (wounds,
skin infection…)
- Ileo-sacral trauma
- Coagulation disorders
- Sepsis
Complications:
- Cranial migration of the LA at C5-C6
generally if unplanned spinal anaesthesia
-> respiratory depression and paralysis
66
Side effects:
Tip:
Remember!
- Infection due to insufficient asepsis
- Direct
nerve
trauma,
neurological
complications
Depend on the drugs used: mainly
hypotension, motor block and urinary
retention (especially with morphine)
Reduce the volume in 1) old, 2) pregnant 3)
very adipose patients and if accidental spinal
injection to avoid cephalad spread
This technique is the most “modular”. By
choosing a) the type of drug (LA, opioids,
a2 agonists, b) the volume and c) the
concentration of the LA, the anaesthetist can
decide on the quality, type, intensity, level and
duration of epidural anaesthesia/ analgesia,
with or without motor block, sympathetic
block, onset, duration, level, side effects,
strength….
[3] Gottschalk A, Smith DS. New concepts in acute pain therapy:
preemptive analgesia. Am Fam Physician 2001 May 15; 63(10):
1979-84.
[4] Wilder-Smith OH, Arendt Nielsen L. Postoperative hyperalgesia. Its
clinical importance and relevance. Anesthesiology 2006; 104(3):
601-7.
[5] Picard J, Ward SC, Zumpe R, Meek T, Barlow J, Harrop-Griffiths
W. Guidelines and the adoption of ‘lipid rescue’ therapy for local
anaesthetic toxicity. Anaesthesia 2009 Feb; 64(2): 122-5.
[6] Weinberg G, Ripper R, Feinstein DL, Hoffman W. Lipid emulsion
infusion rescues dogs from bupivacaine-induced cardiac toxicity.
Reg Anesth Pain Med 2003 May-Jun; 28(3): 198-202.
[7] Campoy L, Korich J, Bezuidenhout A. Peripheral Nerve Blocks in
the Dog DVD course [DVD]: Cornell University; 2009.
[8] Portela D, Melanie P, Briganti A, Breghi G. Nerve stimulatorguided paravertebral lumbar plexus anaesthesia in dogs. Vet Res
Commun 2008 Sep; 32 Suppl 1: S307-10.
[9] Wenger S, Moens Y, Jaggin N, Schatzmann U. Evaluation of the
analgesic effect of lidocaine and bupivacaine used to provide a
brachial plexus block for forelimb surgery in 10 dogs. Vet Rec
2005 May 14; 156(20): 639-42.
[10] Mahler SP, Adogwa AO. Anatomical and experimental studies
of brachial plexus, sciatic, and femoral nerve-location using
peripheral nerve stimulation in the dog. Vet Anaesth Analg 2008
Jan; 35(1): 80-9.
[11] BBraun_USA. Plexus Anaesthesia Principles. Available from:
http://www.bbraunusa.com/stimuplex/pens2.html.
[12] Oberndorfer U, Marhofer P, Bosenberg A, Willschke H, Felfernig
M, Weintraud M, et al. Ultrasonographic guidance for sciatic and
femoral nerve blocks in children. Br J Anaesth 2007 Jun; 98(6):
797-801.
[13] Zilberstein LF, Moens YP, Leterrier E. The effect of local anaesthesia
on anaesthetic requirements for feline ovariectomy. Vet J 2008
Nov; 178(2): 214-8.
[14]. Matsota P, Papageorgiou-Brousta M, Kostopanagiotou G.
Wound infiltration with levobupivacaine: an alternative method
of postoperative pain relief after inguinal hernia repair in children.
Eur J Pediatr Surg 2007 Aug; 17(4): 270-4.
[15] Drucker M, Cardenas E, Arizti P, Valenzuela A, Gamboa A.
Experimental studies on the effect of lidocaine on wound healing.
World J Surg 1998 Apr; 22(4): 394-7; discussion 7-8.
[16] Vasseur PB, Paul HA, Dybdal N, Crumley L. Effects of local
anesthetics on healing of abdominal wounds in rabbits. Am J Vet
Res 1984 Nov; 45(11): 2385-8.
[17] Carotenuto AM, Ravasio G, Stefanello D, Fonda D, editors.
Wound infiltration with ropivacaine or bupivacaine provide 24h of
analgesia after feline injection site sarcoma surgery: a pilot study.
Association of Veterinary Anaesthesists; 2008; Barcelona, E.
[18] MILA. Diffusion_Catheters.
2009; Available from: http://
milainternational.com/files/Diffusion_Catheter_Protocols.pdf.
[19] Hansen BD, editor. Updated opinions on analgesic techniques. 21
st Annual American College of Internal Medicine Forum; 2003.
[20] Reuss-Lamky H. Administering dental nerve blocks. J Am Anim
Hosp Assoc 2007 Sep-Oct; 43(5): 298-305.
[21] Futema F, Fantoni DT. Brachial plexus block in dogs. A new
techique. Veterinary Anaesthesia and Analgesia 2002; 29(3): 1339.
[22] Novello L, Corletto F. Combined spinal-epidural anesthesia in a
dog. Vet Surg 2006 Feb; 35(2): 191-7.
[23] Iff I, Moens Y, Schatzmann U. Use of pressure waves to confirm
the correct placement of epidural needles in dogs. Vet Rec 2007
Jul 7; 161(1): 22-5.
[24] Webb ST, Ghosh S. Intra-articular bupivacaine: potentially
chondrotoxic? Br J Anaesth 2009 April 1, 2009; 102(4): 439-41.
3.3.
Intra-articular anaesthesia/analgesia.
The technique is simple and can be used in the perioperative
period for pre-emptive and postoperative analgesia Local
anaesthetics, opioids and adjuvants can be injected before
the opening of the joint and at joint closure for post operative
analgesia. While bupivacaine has been the LA of choice due
to its long duration of action, there is increasing evidence of
its dose-dependent and time-dependent chondrotoxicity in
humans [24]. It might be safer also in the veterinary patients
to use ropivacaine and LA at low concentrations (<0.2%). For
long term pain relief in patients affected by degenerative joint
disease repeated IA injections with morphine and hyaluronic
acid can be performed under deep sedation.
In conclusion
Loco-regional anaesthesia is easy to learn, to perform and
affordable also in practice; they are rewarding techniques!
It provides excellent perioperative analgesia and improves the
comfort, welfare and outcome of the veterinary patient; it is
effective!
Complications and accidents might occur but are seldom; it is
overall a safe technique!
Failure has to be taken into account. Therefore it is important to
check analgesia on a regular basis and have a rescue analgesia
protocol ready.
Just do it!
Acknowledgments
Many thanks to Dres. S Axiak Dip. ACVA and K Veres for the critical
review of the manuscript.
Further reading
[1]
[2]
Nolan AM. In: Flecknell PA, Waterman-Pearson AE, editors. Pain
Management in Animals. London: W.B Saunders; 2000. p. 32-3.
Jones RS. Combining local and general anaesthesia for better pain
relief in dogs and cats. Vet J 2008 Nov; 178(2): 161-2.
67
CRITICAL CARE
Acute pain management in the
peri-operative period
Françoise Roux DVM, PhD, DACVECC Alfort School of Veterinary Medicine 7 av. du General de Gaulle F-94704 MaisonsAlfort, cedex France. E-mail: [email protected]
INTRODUCTION
Acute pain is present in a patient because of pre-existing disease, the surgical procedure (with associated catheters,
drains, tubes, or complications), or a combination of disease-related and procedure-related sources.
Pain management should be a priority for the clinician, in terms of ethics, to ensure the animal welfare and in terms
of global medical management to reduce morbidity and mortality associated with inadequate pain management.
Lack of or inadequate pain management can lead to increased respiratory, cardio-vascular or gastro-intestinal
morbidity; increased length of stay in hospital and increased risk of developing chronic pain. Treating pain will
improve healing, decrease stress and anxiety related to hospitalisation and will provide a peaceful environment for
the animal and the nursing team.
The clinical signs of pain can sometimes be masked by the clinical signs of the underlying condition (shock, stupor,
comatose, etc.). However, the clinician must always consider that undergoing surgery, even a minor procedure, will
be painful. When a patient is hospitalized, the clinician must always consider that the animal might be in pain. Pain
must be assessed and reassessed constantly and treated adequately according to the level of pain.
Non-pharmacological management
of pain
All measures aiming at the welfare and the comfort of the
patient must be set up: cosy blankets and pillows, heating or
ventilation, administration of water by syringe if the animal
cannot reach water easily, allowing time for rest without light
and noise, grooming for cats etc. The owner’s comfort and
cuddles is very important too.
In the case of fractures, it is imperative to provide a proper
immobilisation of the limb with a bandage because the
manipulation of a fractured limb is extremely painful.
It goes without saying that taking X-rays of a broken bone is
not an emergency and must be done once the patient is stable
and can be sedated or even more often placed under general
anesthesia to get proper quality X-rays.
It is almost useless to give large amount of strong pain
medication before verifying that the patient is hospitalized in
good condition and receives tender loving care.
In case of fractures, it is imperative to provide a proper
immobilization of the limb with a bandage (Photo ©F.Roux)
or treat pain. This concept has shown that the administration of
various drugs can decrease the dose and thus the side effects
and sometimes, depending on the combination, the drugs
have a synergistic effect that provides more analgesia than the
expected cumulative effect. Opioids, NSAIDs, local anaesthetics,
ketamine and gabapentin showed a synergistic effect. Some
Pharmacological management of pain
The concept of multimodal analgesia includes the
administration of two or more types of analgesics to prevent
69
Acute pain management in the peri-operative period - Françoise Roux
IM or IV) every 4 hours as its half-life is much longer. Its onset
of action is also several minutes depending of the route of
administration. As morphine may induce vomiting in the preoperative phase, especially if the patient is not in pain before
surgery (e.g. spay), morphine may be associated with a low dose
of acepromazine (0.05 mg/kg) for its anti-emetic properties. Side
effects of pure-agonists are dose dependant and are vomiting,
bradypnea, bradycardia, myosis, dysphoria. The level of sedation
is also dose-dependant and is less marked with morphine than
fentanyl.
If a patient requires analgesia before surgery, it is advisable to
use pure agonists so that those drugs can be continued during
the per- and postoperative phase.
Both are considered as narcotics and must be kept in locked
cabinets.
Provide a peaceful environment for the animal and the nursing
team. (Photo ©F.Roux)
Fentanyl Patches
Fentanyl patches are useful in the withdrawal phase of IV
administered opiods when the patient is considered able to go
home. The patch delivers a continuous dose of fentanyl through
the skin over a 48 to 72 hours period. The onset of action is 8
hours in cats and 12 hours in dogs, but often the concentration
plateau is reached in 12 hours in cats and 24 hours in dogs; it
is very variable from one patient to another. Thus, the Fentanyl
patch should be placed at least 12 hours before other painkillers
are withdrawn. The plasma concentrations and the efficacy are
highly variable from one animal to another. The patch must be
accompanied by a prescribed “rescue” pain medication in case
the animal seems painful at home.
drugs have very low analgesic properties (ketamine, gabapentin)
themselves but have strong synergistic effects. Such products
are called co-analgesics.
The administration of pain medication must be accompanied by
a monitoring of pain and vital signs to ensure the administration
of an appropriate amount, neither too much nor too little.
Ideally, analgesics are administered in a continuous infusion
to avoid peaks and troughs of analgesic drugs delivery and
therefore pain.
The route of administration is also very important to consider;
for example the use of epidural morphine provides analgesia
comparable if not better than the intravenous route with
considerably lower dosages. Local analgesics can be used in
addition to general analgesics to decrease the dose of systemic
analgesics, thus decreasing side effects. The enteral route may
be used to relay the parenteral route as soon as the patient’s
condition allows. Due to first pass hepatic effect, opioids are
much less effective orally than systemically.
To avoid the emotional component of pain, e.g. related to the
fear of the treatment inflicted or stress of hospitalisation, the
use of low doses of tranquilizers (acepromazine, 0.02 - 0.05 mg
/ kg) may be beneficial.
Doses:
Dose range varies from 2 to 4 µg/kg/h
Cat and dogs <5 kg:
A. Analgesic drugs used for perioperative management
12.5µg/h,
Cat and dogs 5-10 kg:
25µg/h,
Dogs 10-20 kg:
50 µg/h,
Dogs 20-30 kg:
75 µg/h,
Dogs 30-40 kg:
100 µg/h,
Dogs > 40kg:
combination of 2 patches
Buprenorphine
Buprenorphine is also an opiod but as it is also a partial µ-agonist
it provides less analgesia but also less side effects. Once
buprenorphine is bounded to µ-receptors it is hard to displace,
thus it is not easy to use morphine after buprenorphine has been
given. Buprenorphine has a relative long half-life (about 6 hours)
but its onset of action is also relatively long (30-45 minutes).
Buprenorphine can be used in the postoperative setting once
the patient is not in as severe pain as during the immediate
postoperative phase. It is commonly used at 0.01 mg/kg IV
Q6h (range 0.005-0.2 mg/kg). It has a ceiling effect so it is not
helpful to increase the dose more than 0.02 mg/kg.
As the perioperative, and especially the per-operative period,
is usually associated with severe pain, “strong” opioids are
recommended.
Fentanyl and Morphine
In countries like France, where oxymorphone and hydromorphone
are not available for pets, two potent opiods are used
intravenously: fentanyl and morphine. Those drugs are used in
human medicine and used off-label in animals.
Both drugs are µ and κ pure agonists.
Fentanyl has a very short half-life and is used preoperatively with
a syringe pump (see CRI in section B). Its onset of action is very
fast (several minutes).
Morphine can be used as single injections (0.1 – 0.5 mg/kg,
NSAID’s
Non-steroidal anti-inflammatory drugs should be used only in
a haemodynamically stable patient who is eating. They can be
part of the multimodal analgesia for surgery once the patient
70
is stable and well hydrated, especially for orthopaedic surgery.
They are excellent pain medications in the late peri-operative
setting once the patient is ready to go home.
of 5 to 10µg/kg. It can also be used at lower doses of about
0.15 µg/kg/min after a bolus of 10 µg/kg, thus sedation will
be reduced but so will analgesia. Fentanyl can be combined
with ketamine to reduce postoperative central and peripheral
sensitization of neurons.
Gabapentin
Gabapentin was originally an anti-epileptic, which has recently
shown its effectiveness in humans in addition to analgesics,
particularly in neuropathic pain. It is associated in humans with
a sharp decrease in consumption of morphine postoperatively.
Its way of analgesic action is still unknown; it acts on GABA
and NMDA receptors. This drug is only available in oral form.
Its bioavailability is 80% orally in dogs and its half-life is
3 hours. The peak plasma level is reached 2 hours after oral
administration. Even if this drug is only available as an oral form, it
can be administered 4 hours before surgery and postoperatively
dissolved in a small amount of liquid even if the animal is not yet
ready to be fed.
Ketamine:
Used for many years as an anaesthetic, ketamine has recently
shown analgesic properties at low doses (0.1 - 1.0 mg/kg IV)
by antagonism of NMDA receptors. It potentiates the antinociceptive effect of opioids and α -2 agonists. As a co-analgesic,
its use reduces the doses of morphine needed for the same level
of analgesia. Although contra-indicated for anaesthesia in head
trauma patients, ketamine has shown anti-convulsive properties
at low doses and can be used as an analgesic in patients with
head trauma. Ketamine is used as constant rate infusion (0.6
mg/kg /h) and the dose must be reduced gradually.
The dose currently used in dogs is 2-5 mg/kg orally 3 to 4 times
per day and 2.5-5.0 mg/kg 2 times per day in cats. It is easy to
open the capsules and to dissolve the powder in a small amount
of water to be given orally with a syringe. Elimination is via urine
so the dose should be reduced in case of renal impairment. The
cost is modest. Withdrawal should be gradual to avoid anxiety,
behaviour change or seizures.
Medetomidine and Dexmedetomidine
Low doses of medetomidine (1-2 mg/kg/h) or dexmedetomidine
(0.5 - 1 µg/kg/h) have showed analgesic properties with very
few cardiovascular effects observed at anaesthetic doses. Their
analgesic effect is maximised by opioids. Some side effects of
the α 2-agonists may remain, as bradycardia, increased left atrial
pressure and reduced oxygen delivery to tissues. Medetomidine
and Dexmedetomidine are not recommended, even at low
doses, in patients haemodynamically unstable or suffering from
heart disease.
B. Constant rate infusion (CRI)
The intravenous constant infusion of a drug is used to maintain
an equal concentration of the drug in blood throughout its
administration. It is performed using infusion pumps or syringepumps.
The intravenous constant infusion of a drug is performed using
infusion pumps or syringe-pump Photo (©F.Roux)
Most often it requires a loading dose. This loading dose can
be for example half the dose used for intermittent injection
depending on the half-life of the drug.
Fentanyl:
Fentanyl is a very potent opioid analgesic that provides significant
analgesia at doses of 0.3 to 0.7 µg/kg/min after a loading dose
Photo (©F.Roux)
71
Acute pain management in the peri-operative period - Françoise Roux
Lidocaine:
Lidocaine administered IV at anti-arrhythmic dosages provides
systemic analgesia, captures free radicals and increases
the gastro-intestinal motility. Administered during general
anaesthesia, doses of 50 µg/kg/min of lidocaine can significantly
reduce the MAC of isoflurane required to abolish nociceptive
stimuli. Lidocaine should be used with caution in the cat
intravenously and doses should be reduced to 0.2-0.5 mg/kg if
needed for anti-arrhythmic properties. Lidocaine CRI’s are not
recommended in cats. The loading dose for analgesia in dogs is
usually 1 mg/kg followed by a 50 µg/kg/min CRI.
For pets that weigh more than 5kg, it is usually convenient to
pick a rate of 10ml/hour/dog regardless the size of the dog, thus
adjustment of 1ml/hour equals a 10% variation.
For example, take the case of a dog of 20kg, its maintenance
requirements are 50 ml/hour. The pain medication CRI can be
run at 10ml/hour on a separate bag and the maintenance fluid
will be run at 40 ml/h on another line. A single intravenous
catheter is sufficient using a 3-way stopcock.
DRUGS
Concentration
Loading Dose
CRI dose
Fentanyl
50 µg/ml
0.3 - 1 µg/kg
2 - 4 µg/kg/min
Morphine
10 mg/ml
0.05 - 0.2 mg/kg
0.02 - 0.1 mg/kg/h
Ketamine
100 mg/ml
0.5 - 1
0.3 - 0.6 mg/kg/h
Lidocaine
20 mg/ml
0.5 - 1 mg/kg
40 - 80 µg/kg/min (DOGS only)
1 mg/ml
1 - 2 µg/kg
1 - 2 µg/kg/h
0.5 - 1 µg/kg
0.5 - 1 µg/kg/h
Medetomidine
Dexmedetomidine
0.5 mg/ml
Attention, some Drugs are listed per minute or per hour, others in µg or mg.
2) Choose a duration of administration
Usually, CRI bags are prepared for a 25 hour-period, which avoids
the preparation of several bags per day, and also saves time for
nurses and avoids waste if the protocol or the dose change the
next day. The reason why 25 hours is chosen is because the
bag volumes are a multiple of 25 (100ml, 250 ml, 500ml and
1000ml) and it gives 1 hour “bonus” time for the nurses to
change the bag before the patient runs out of pain medication.
How to prepare a CRI?
1) Choose an hourly volume
You must first choose the volume administered per hour,
regardless of the substance used.
It is convenient to prepare a bag dedicated to the pain
medication CRI independent of the daily fluid needed. Some
authors suggested adding the pain medications to the daily
fluid needs, it can be convenient but it is harder subsequently to
adjust the fluids based on the clinical status of the patient (e.g.:
hypovolemia, fluid overload, etc.)
So for an administration at 10 ml/h over 25 hours, you need a
250 ml bag of isotonic crystalloids (NaCl 0,9%) (25 h x 10 ml).
3) Choose the dose of drugs to be administered
For Example
Ketamine CRI at 0.6 mg/kg/h.
Lidocaine CRI at 50 µg/kg/min.
Maintenance requirements are about 2 ml/kg/h for a cat and
2.5 ml/kg/h for a dog.
For cats, due to lower volumes needed as a maintenance rate,
it is sometimes worthwhile to prepare the CRI in maintenance
fluids, especially for low requirements (e.g. cardiac cat).
4) Calculate the amount in mg for 25 hours and the volume
in ml based on the weight and the duration of administration
It is convenient to prepare a bag dedicated for pain
medication(Photo ©F.Roux)
Ketamine CRI:
Ketamine at 0.6 mg/kg/h for a 20 kg dog over 25 hours:
Amount in mg: 0.6 mg x 20 kg x 25 h = 300 mg
Concentration of ketamine: 100 mg/ml
Volume in ml: 300/100 = 3 ml
Lidocaine CRI:
Lidocaine at 50 µg/kg/min for a 20 kg dog over 25 hours:
Amount in mg: 0.05 mg x 20 kg x 60 min x 25 h = 1500 mg
Concentration of lidocaine: 20 mg/ml
Volume in ml: 1500/20 = 75 ml
5) Prepare and label the bag
If volumes are small (less than 5 ml), drug is added to the
crystalloid bag.
72
If volumes are substantial regarding the size of the bag, the
equivalent volume to be added must be discarded before adding
the drug (it is always the case for a lidocaine CRI).
pain. 0,1mg/kg/h is considered to be a high dose used in the
immediate postoperative period of very painful surgery.
It is advisable to wean CRI over at least one or two days.
With the 10ml/h rate, each 1ml/h decrease represents a 10%
dose decrease.
Once the CRI weaning process is initiated, make sure that the
pain medication will be continued with other drugs/route of
injection.
The pain medication should not be discarded when an animal
is feeling better and eating, as it is probably doing so because
it is not painful.
Ketamine CRI at 0.6mg/kg/h for a 20 kg dog over 25 hours.
Add 3 ml of ketamine to a 250 ml NaCl 0.9% bag.
Run at 10 ml/h.
Ketamine (3 ml) represents a tiny volume compared to 250 ml
so it can be added to the bag without discarding the equivalent
volume.
Lidocaine CRI at 50 µg/kg/min for a 20 kg dog over 25 hours.
Take a 250 ml bag, discard 75 ml (leaving 175 ml).
Add 75 ml of lidocaine to the remaining 175 ml NaCl 0.9%.
Run at 10 ml/h.
In this case, the amount of lidocaine (75 ml) is significant
compared to 250 ml therefore the equivalent volume to be
added must be discarded from the 250 ml bag first.
Local analgesia
To be multimodal, the clinician should always think of local
analgesia to decrease the amount of parenteral analgesia given
and thus side effects. For example, epidural analgesia may be
useful in cases of fractures of the pelvis or hind limbs. It provides
excellent analgesia with minimal systemic effects. Wound
soaker catheters are also an excellent mean to decrease systemic
analgesic given.
The MLK (Morphine, Lidocaine, Ketamine) CRI The MLK
is an example of a multimodal analgesia commonly used in the
perioperative setting. Any combination of analgesics and coanalgesic is possible. A variation of MLK can be FLK (Fentanyl
Lidocaine Ketamine), MDK (Morphine, Dexmedetomidine,
Ketamine) or any association of an opiod and a co-analgesic.
MLK is a combination of an opioid (morphine), a local
anaesthetic that stimulates peristalsis and is supposedly effective
for reperfusion injuries and ketamine, which is a co-analgesic
that has demonstrated analgesic properties at low doses. As
the use of lidocaine CRI is controversial in cats, it is advisable to
use MLK CRI’s only in dogs. MK (Morphine-Ketamine) or MDK
(Morphine-Dexmedetomidine-Ketamine) can be used instead in
cats. Most often, it is convenient to run the CRI at 5 ml/h for
small dogs (to avoid fluid overload) and 10 ml/h for medium size
to large size dogs, but any option is possible.
Conclusion
The management of pain is a crucial step in the perioperative
management of patients. It helps decrease surgery complications,
promotes healing, decreases length of stay in the hospital and
provides enhanced patient welfare. Everyone is free to devise a
protocol adapted to their own preferences and the equipment
available, but many of the measures described here can be
done cheaply. The clinician should not forget that beside the
administration of medication, the patient must be hospitalised
in adequate conditions of comfort, the owner must be involved
in the recovery process and the nursing team must always think
of providing tender loving care.
MLK
Rate
Drug Concentration
mg/ml
5 kg dog over
25 hours
10 kg dog over
25 hours
20kg dog over
25 hours
Morphine
0.1 mg/kg/h
10
12.5 mg = 1,25 ml
25 mg = 2.5 ml
50 mg = 5 ml
Lidocaine
50 µg/kg/min
20
375 mg = 18.75 ml
750 mg = 37.5 ml
1500 mg = 75 ml
Ketamine
0.6 mg/kg/h
100
75 mg = 0,75 ml
150 mg = 1.5 ml
300 mg = 3 ml
References
For a 5 kg dog:
At a rate of 5 ml/h, the total volume to go over 25 hours is 125
ml.
Take a 100 ml NaCl 0.9% bag, add 1.25 ml of morphine, 18, 75
ml of lidocaine and 0.75 ml ketamine. This volume, 120 ml (100
+ 1.25 + 18.75 + 0.75 ), will be enough to cover 24 hours.
Dyson DH. Perioperative pain management in veterinary patients. Vet
Clin North Am Small Anim Pract. 2008; 38(6): 1309-27
Lamont LA. Multimodal pain management in veterinary medicine: the
physiologic basis of pharmacologic therapies. Vet Clin North Am
Small Anim Pract. 2008; 38(6): 1173-86
Hansen BD. Analgesia and sedation in the critically ill. Journal of
Veterinary Emergency and Critical Care. 2005; 15(4), 285 - 294
Muir WW. 3rd, Wiese AJ. et al. Effects of morphine, lidocaine, ketamine,
and morphine-lidocaine-ketamine drug combination on minimum
alveolar concentration in dogs anesthetized with isoflurane. Am J
Vet Res. 2003; 64(9): 1155-60.
Mathews KA. Neuropathic pain in dogs and cats: if only they could tell
us if they hurt. Vet Clin North Am Small Anim Pract. 2008; 38(6):
1365-414.
For a 10 kg dog:
At a rate of 10 ml/h, the total volume to go over 25 hours is
250 ml.
Take a 250 ml NaCl 0.9% bag, remove (2,5 + 37,5 + 1,5) 41,5
ml and add 2.5 ml of morphine, 37,5 ml lidocaine and 1.5 ml of
ketamine.
CRI weaning:
The rate of morphine should be adjusted based on the level of
73
GASTEROINTESTINAL SYSTEM
REPRINT PAPER (UK)
Modified functional end-to-end
stapled intestinal anastomosis:
technique and clinical results
in 15 dogs
R. N. White(1)
SUMMARY
Objectives: To evaluate the use of a gastrointestinal anastomosis (GIA) stapling device to perform small intestinal
anastomosis in the dog.
Methods: A retrospective study to evaluate the use of a GIA stapling device to perform small intestinal anastomosis
in 15 dogs.
Results: Reasons for intervention included dehiscence of a previous enterotomy (four of 15), intestinal neoplasia
(five of 15), vascular compromise (three of 15), intussusception (two of 15) and foreign body (one of 15). The mean
time taken to perform the anastomosis was 7.7 minutes (range five to 12 minutes). No operative complications were
recorded and all dogs recovered from the surgery. Major (two dogs) and minor (six dogs) short-term complications
of pyrexia and anorexia were recorded in six dogs. In five of these, the cause was considered to be related to a preexisting peritonitis. One dog was euthanased five months postoperatively for a multi-centric recurrence of intestinal
lymphoma. Six month follow-up confirmed an unremarkable and complete recovery in all remaining dogs. No
major or minor long-term complications were recorded in any individual.
Clinical Significance: A modified stapled functional end-to-end intestinal anastomosis holds merit and should be
considered a viable alternative to other stapled and sutured anastomosis techniques.
considered to be the technique of choice [Steichen and Ravitch
1984, Ullman 1994]. In human beings, a number of different
methods have been reported to achieve the side-to-side enteroanastomosis [Ullman 1994]. These include the open lumina
technique [Chassin and others 1984], functional end-to-end
anastomosis [Yamamoto and Keighley 1999], offset method
[Steichen and Ravitch 1984] and one-stage functional end-toend anastomosis and resection [Ravitch and others 1974].
This paper originally appeared in: Journal of Small
Animal Practice *(2008) 49, 274–281
Introduction
Surgical stapling techniques for performing intestinal anastomosis
are well described in human beings for the treatment of a
wide range of conditions affecting the small bowel [Steichen
and Ravitch 1984]. Three stapled anastomosis techniques
have been described: the everting triangulating end-to-end
anastomosis [McGinty and others 1979], the inverting end-toend anastomosis [Nance 1979] and the antiperistaltic side-toside (functional end to end) anastomosis [Ravitch and Steichen
1972]. Of these, the antiperistaltic side-to-side anastomosis is
The clinical application of surgical stapling as a technique for
small intestinal anastomosis is poorly reported in the dog. To the
author’s knowledge, there has only been one previous description
of the clinical application of stapled entero-anastomosis in small
animals [Ullman and others 1991]. In this study, open lumina
entero-anastomoses were performed in 20 dogs and four cats
(1)Surgical Consultancy Services, c/o The Scott Veterinary Clinic, 405 Goldington Road, Bedford, GB-MK41 0DS E-mail: [email protected]
*Presented by BSAVA(UK)
75
Modified functional end-to-end stapled intestinal anastomosis: technique and clinical results in 15 dogs - R. N. White
and the surgical technique required the use of two different
stapling devices to complete the anastomoses.
least 8 cm on either side of the tumour. Contamination of the
surgical site was minimised by the temporary occlusion of the
intestines using either digital pressure or the placement of Doyen
bowel clamps approximately 10 cm both proximal and distal to
the proposed sites of the enterectomy. A single stay suture of
3-0 polypropylene (Surgipro, Tyco Heathcare UK Ltd) was placed
into the adjacent lateral walls of both the proximal and the distal
loops of intestine near the opening of their lumina. In all cases,
the entero-anastomosis was performed with a multi-use GIA
(linear cutter) stapling gun (Multifire GIA 60, Tyco Heathcare
UK Ltd) using single-use reloadable stapling units (Multifire 3.8
mm GIA 60, Tyco Heathcare UK Ltd) (Fig 1). One limb of the
stapler was placed into each bowel lumen. The open ends of the
bowel were aligned evenly on the forks using the stay sutures to
ensure that the antimesenteric surfaces were in apposition (Fig
2). On all occasions, at least 60 to 70 mm of the stapler’s limbs
were inserted into the loops of the bowel to be anastomosed.
The two limbs of the stapler were engaged and locked (Fig
2). The stapler was “fired” resulting in two double-staggered
staple lines joining the two pieces of bowel; simultaneously, the
knife blade created a stoma by dividing the anastomosed bowel
between the two double-staple lines (Fig 3a–c).
This paper describes the surgical findings of 15 dogs in which
open lumina entero-anastomoses were performed using
a gastrointestinal anastomosis (GIA) stapling instrument.
The surgical technique is described and the perioperative
complications and clinical results were discussed.
Materials And Methods
The medical records of 15 dogs that had undergone intestinal
resection and anastomosis using surgical stapling were reviewed.
The dogs varied in age from 1 to 11 years (mean 5.3 years) and
a variety of breeds were represented. There were eight females
(three entire and five neutered) and seven males (two entire and
five neutered). These data are listed in Table 1.
In dogs with either a clinical history or clinical findings consistent
with peritonitis, further investigations including abdominal
radiography and abdominal ultrasonography were performed.
Where necessary confirmation of a bacterial peritonitis was
achieved by performing cytology (in house) of fluid samples
obtained by diagnostic peritoneal lavage (DPL).
FIG 2. Intra-operative view obtained from a cadaver showing
the placement of the forks of the stapler within the open ends
of the bowel that is to be anastomosed. The two laterally
placed polypropylene stay sutures are used to ensure that the
antimesenteric surfaces of the bowel are in apposition when the two
halves of the instrument are locked
Surgical technique
The open lumina entero-anastomosis was performed as follows.
Under general anaesthesia, a midline cœliotomy was performed.
This extended from 4 to 5 cm caudal to the xiphisternum to 4 to
5 cm caudal to the umbilicus. Following a thorough inspection
of the peritoneal contents and the flushing of the cavity with
copious quantities of warmed sterile saline in the six individuals
with peritonitis, the affected portion of small intestine was
exteriorised and packed off with moistened laparotomy swabs.
Mesenteric vessels supplying the portion of intestine that was to be
resected were ligated using ligatures of 2-0 polyglactin (Polysorb,
Tyco Heathcare UK Ltd). In each case, the damaged portion of
bowel was resected leaving grossly healthy proximal and distal
loops of intestine. In individuals with an intestinal neoplasm,
wide local resection was achieved with margins extending to at
FIG 3. (a) Intra-operative view showing the bowel after the initial
‘firing’ of the stapling device. The two portions of bowel are joined
along with their antimesenteric border. (b) Intra-operative view
showing the lumen of the two portions of bowel following the
initial firing of the stapler. The two double-staple lines can be seen
clearly along with the stoma created between them by the action
of the knife. (c) Similar stapling procedure as that depicted in Fig
3a,b, but performed on two lengths of foam tube. The two double
rows of staples and the created stoma can be seen
2
3a
FIG 1. Multifire GIA 60 showing the two halves of the instrument.
One half houses a blue reloadable stapling unit with its integral
knife
1
3b
3c
76
Case
No.
Breed
Age
(years)
Sex
Aetiology
Peritonitis
Site of
intestine
Time for
anastomosis
Complications
Time to
discharge
1
Crossbred
2
F (N)
Dehiscence
of previous
enterotomy
Yes
Proximal
jejunum
7
Postoperative
pyrexia and
anorexia for 36
hours
Four days
2
Labrador
8
F (N)
Leiomyosarcoma
No
Mid-jejunum
9
None detected
One day
3
Springer
spaniel
3
M (E)
Un-reducible
intussusception
No
Distal
jejunum
(jejunal–ileal
junction)
6
None detected
Less than
24 hours
4
Lurcher
5
F (N)
Vascular
compromise
(penetration injury)
Yes
Distal
jejunum
10
Postoperative
pyrexia and
anorexia for 48
hours (48 hours
open peritoneal
drainage)
Three days
5
Beagle
7
F (N)
Adenocarcinoma
No
Distal
jejunum
7
None detected
Less than
24 hours
6
GSD
7
M (N)
Vascular
compromise
Yes
Mid-jejunum
7
None detected
Three days
7
Boxer
9
M (N)
Leiomyosarcoma
No
Mid-jejunum
9
None detected
Less than
24 hours
8
Crosbred
3
F (N)
Foreign body –
enterectomy
No
Proximal
jejunum
6
None detected
One day
9
Golden
retriever
4
F (E)
Dehiscence
of previous
enterotomy
Yes
Proximal
jejunum
9
Postoperative
pyrexia and
anorexia for 48
hours
Three days
10
Schnauzer
2
M (E)
Vascular
compromise
(strangulated
inguinal hernia)
No
Mid-jejunum
5
None detected
Less than
24 hours
11
Crosbred
1
F (E)
Un-reducible
intussusception
No
Distal
jejunum
(jejunal–ileal
junction)
7
None detected
One day
12
Standard
poodle
11
F (E)
Adenocarcinoma
No
Distal
jejunum
6
Postoperative
pyrexia and
anorexia for 48
hours
Three days
13
Labrador
9
F (E)
Lymphoma
No
Distal
jejunum
(jejunal–ileal
junction)
9
None detected
Less than
24 hours
14
Boxer
5
M (N)
Dehiscence
of previous
enterectomy
Yes
Proximal
jejunum
12
Postoperative
pyrexia and
anorexia for 48
hours (48 hours
open peritoneal
drainage)
Five days
15
Crosbred
4
M (E)
Dehiscence
of previous
enterectomy
Yes
Mid-jejunum
7
Postoperative
pyrexia and
anorexia for 48
hours
Four days
Table 1. Details of dogs undergoing stapled modified functional end-to-end anastomosis
77
4a
5
FIG 5. The completed anastomosis before the closure of the
mesenteric defect. Note the single 3-0 polydioxanone suture placed
at the end of the initial staple line to reduce the tension at this site
4b
was apposed using 3-0 polydioxanone in a simple continuous
pattern. The time taken to perform the intestinal anastomosis
(starting from the exteriorisation of the affected portion of
the intestine and finishing with the completion of the repair
of the mesenteric defect) was recorded for each individual. In
the dogs with intestinal neoplasia, regional mesenteric lymph
node biopsies were obtained for histological staging of their
disease. The anastomosis site was lavaged and omentum draped
over it before performing a routine three-layer closure of the
cœliotomy.
FIG 4. (a) The reloaded stapler has been positioned across the bowel
at 90º to its long axis. The stapler is locked so that the two initial
staple lines are offset and not adjacent to each other. The portions
of bowel containing the two-stay sutures are those which will be
sacrificed following the second firing of the stapler. (b) Similar
stapling procedure as that depicted in Fig 4a, but performed on the
foam tubes. The two double rows of staples from the initial firing
have been placed in the forks of the stapler in an offset position (in
this case approximately 1·5 cm offset)
In dogs with confirmed peritonitis, intra-operative findings
including the response of peritoneum and the extent of the
gross inflammatory response were used to define whether the
peritonitis was localised or generalised in nature. Following the
entero-anastomosis, a decision was taken regarding the need
for open peritoneal drainage in the postoperative period. This
decision was based on the surgeon’s judgement with regard to
the gross clinical findings at the time of surgery. Closure of the
abdomen after open peritoneal drainage was conducted when
the patient’s general condition had improved and when repeat
cytology of peritoneal aspirates showed decreasing bacterial
numbers and normal neutrophil (non-degenerative) morphology
[Staatz and others 2002, Fossum 2007].
The stoma was inspected for evidence of haemorrhage. This
was considered negligible in all cases requiring no further
intervention. The spent staple cartridge from the stapling gun
was discarded and replaced with a new unit. The forks of the
stapler were positioned around the anastomosed bowel at 90º
to its long axis and adjacent to its opening (Fig 4a). The two
limbs of the stapler were engaged and locked in such a way
as to ensure that the two previously stapled edges of intestine
were separated or offset by at least 1 cm (Fig 4b) [Ritchey and
others 1993]. The stapler was “fired” resulting in the completed
anastomosis (Fig 5). The staple lines were inspected for evidence
of haemorrhage or deployment failure. A simple interrupted
anchoring suture of 3-0 polydioxanone (PDS II, Ethilon Ltd) was
placed at the end of the first staple line to reduce the tension at
this site (Fig 5). The suture was placed in such a manner that it
included the serosa and muscularis layers of the antimesenteric
walls of the adjacent portions of the two loops of intestine that
were being anastomosed. The suture did not penetrate the full
thickness of the intestinal walls and, therefore, did not enter
the lumen of either loop of intestine. The mesenteric defect
In all cases, the surgery was performed by the same surgeon
(R. N. W.).
Postoperative management
Postoperative management was variable and dependent on
each animal’s physical status, underlying aetiology and whether
bacterial peritonitis was confirmed before surgical intervention.
All cases received a single intravenous administration of
cefuroxime (Zinacef, GlaxoSmithKline) 20 mg/kg in the
perioperative period. Individuals with confirmed peritonitis
received an extended course of antibiosis with the administration
of both cephalosporin-containing products (cefuroxime or
cephalexin (Ceporex, Schering-Plough Animal Health) and the
addition of a fluoroquinolone (Baytril, Bayer HealthCare) and
metronidazole (Metronidazole 0·5 per cent w/v, Maco Pharma
78
Ltd) for between five and 14 days, postoperatively. Postoperative
analgesia was achieved with the use of both opioid methadone
(Physeptone Injection, Martindale Pharmaceuticals) and
buprenorphine (Vetergesic, Alstoe Animal Health) and nonsteroidal anti-inflammatory carprofen (Rimadyl Small Animal
Injection, Pfizer Animal Health) and meloxicam (Metacam,
Boehringer Ingelheim) agents for between five and seven days,
depending on each individual’s requirement.
Open peritoneal drainage was performed in two dogs (cases
4 and 14) with confirmed generalised peritonitis. In both these
dogs, abdominal closure was accomplished after 48 hours of
open drainage.
In the dogs suffering from intestinal neoplasia, leiomyosarcoma
was confirmed in two cases, adenocarcinoma in two cases and
lymphoma in one individual. Histological evidence of neoplastic
involvement of the mesenteric lymph nodes was confirmed
in the dog with lymphoma (case 13); in the four remaining
dogs with intestinal neoplasia, there was no evidence of local
mesenteric lymph node metastasis. The reason for the localised
vascular compromise was known in two of the three cases; it
was associated with a strangulated inguinal hernia in one and
with a penetration injury in the other. In one case, the cause of
the vascular compromise was unknown, although gross findings
at the time of surgery were consistent with a jejunal artery
infarction. In the two dogs with intussusception, the underlying
aetiology remained undiagnosed.
Oral hydration and feeding were reintroduced after surgery
depending on the patient’s health status, whether they could
tolerate oral food and water and their appetite.
Postoperative follow-up data were obtained from each dog’s
medical records and at six months postoperatively the owners
were contacted by telephone to discuss their dog’s progress.
Operative and short- and long-term postoperative complications
were recorded according to the criteria described by Ryan and
others (2006). Short-term postoperative (within two weeks)
complications were determined from the time after surgery to
when first noted in the medical record. Long-term complications
were defined as occurring between two weeks after surgery
and death or follow-up time. Complications were further
categorised as major or minor. Major complications were defined
as those requiring general anaesthesia and surgical intervention
or resulting in euthanasia. Minor complications were defined as
those that responded to medical or conservative therapy.
In all cases, the intestinal lesion was located either within the
jejunum or within a combination of both the jejunum and ileum.
Entero-anastomosis was performed within the proximal jejunum
in four dogs, the mid-jejunum in five dogs, the distal jejunum in
three dogs and between the distal jejunum and ileum in three
dogs.
No intra-operative complications were recorded in any of the dogs
and all cases made an unremarkable recovery from anaesthesia.
In the six dogs with confirmed pre-existing peritonitis (cases 1,
4, 6, 9, 14 and 15), major short-term complications consisting
of open peritoneal drainage and a delayed cœliotomy closure
were seen in two dogs with a pre-existing diffuse peritonitis
(cases 4 and 14). In both instances, the peritoneal drainage
was undertaken as part of the management of the generalised
peritonitis. In neither case was the complication considered to
be related to the surgical anastomosis procedure. As well as the
two dogs (cases 4 and 14) described above, minor short-term
complications were also seen in three dogs with a pre-existing
localised peritonitis (cases 1, 9 and 15). In all five dogs, the
minor complication consisted of periods of pyrexia and anorexia
which were observed in the first 48 hour period following the
surgery. In each case, the recorded rectal temperature never
exceeded 39.8°C and the complications were managed with
antibiotics and analgesics as described previously, and careful
nursing care in the postoperative period. The cause of the
minor complications in these dogs remained unclear, but was
considered to be related to the pre-existing peritonitis rather
than the surgical anastomosis procedure.
Results
The underlying aetiologies, sites of intestinal lesion, times for
anastomosis construction, complications and times to discharge
are presented in Table 1. The mean time taken to perform the
anastomosis in the 15 dogs was 7.7 minutes (range five to 12
minutes).
Reasons for intervention included dehiscence of a previous
enterotomy (four dogs), intestinal neoplasia (five dogs), vascular
compromise of a localised segment of small intestine (three
dogs), intussusception (two dogs) and an intestinal foreign body
(one dog).
In the four dogs with dehiscence of a previous enterotomy
(cases 1, 4, 14 and 15), the original procedure had been
undertaken to obtain full thickness small intestinal biopsies in
two dogs, for the removal of an intestinal foreign body in one
dog and for the management of an intussception in one dog.
In all four dogs, supporting evidence of peritonitis was acquired
by obtaining abdominal radiographs and performing abdominal
ultrasound examinations. Before surgery, a bacterial peritonitis
was confirmed in each case by performing cytology on samples
obtained by DPL. Two other dogs (cases 4 and 6) also had
clinical findings consistent with peritonitis and in both dogs a
bacterial peritonitis was confirmed before surgery in a similar
manner to that described previously. Broad spectrum antibiotic
cover was instituted in all cases with confirmed peritonitis and
the choice of agents utilised was based on their effective activity
against organisms that are commonly isolated from animals with
peritonitis [Fossum 2007].
In dogs with no evidence of peritonitis, oral hydration and feeding
were reintroduced within 12 hours of the intestinal surgery. In
dogs with confirmed peritonitis, the reintroduction times for
oral water and food were more variable and depended on the
individual’s physical status. In all cases, oral intake of both food
and water had been achieved by 72 hours, postoperatively.
In dogs that were not suffering from a pre-existing peritonitis,
there were no major short-term complications recorded. Minor
79
short-term complications of periods of pyrexia and anorexia
observed within the first 48 hours postoperatively were recorded
in one dog (case 12). Management was similar to that described
for the dogs with pre-existing localised peritonitis. The cause for
the complication in this individual remained unknown, although
an association with the entero-anastomosis procedure could not
be ruled out.
for the mechanical integrity of the anastomoses, the lack of
any clinical data related to the development of dehiscence of
the anastomosis in any of the cases supports the view that the
technique was safe and effective in both the short and long
terms. Despite this apparent margin of safety, and as with other
methods of intestinal anastomosis, it is recommended that
the site of anastomosis is wrapped with omentum as a further
safeguard against the effects of an unforeseen leakage of
intestinal contents.
Six month postoperative follow-up information was available for
all cases. There were no major or minor long-term complications
recorded in any of the cases. In the dog with confirmed
lymphoma (case 13) postoperative systemic chemotherapy
was provided by the administration of oral cyclophosphamide
(Endoxana, Asta Medica Ltd) 50 mg/m2 given every 48 hours,
intravenous vincristine (vincristine sulphate, Mayne Pharma plc)
0.5 mg/m2 every seven days, and oral prednisolone (Prednicare,
Animalcare Ltd) 40 mg/m2 daily for seven days, then at 20 mg/
m2 every 48 hours [Vail 2003]. After eight weeks (induction),
the COP protocol was administered as an alternate-week
treatment. Despite the administration of these drugs, the dog
developed a generalised recurrence of the tumour resulting in
its euthanasia five months after the original intestinal resection.
The lack of clinical signs associated with intestinal obstruction
or peritonitis appeared to support the conclusion that despite
the development of metastatic disease in this individual there
was no evidence to suggest the development of complications
associated with the original intestinal anastomosis.
The study did not address directly the difference in time between
the construction of a sutured end-to-end anastomosis and a
stapled repair. In a study comparing the use of skin staples with
sutures for small intestinal anastomosis in 18 dogs, Coolman
and others (2000) reported a mean time of 9.06 minutes to
perform a hand-sewn approximating anastomosis. Although
no directly comparable data were available, the mean time of
7.7 minutes recorded to perform the stapled anastomosis in the
study implies that the time to complete a stapled anastomosis
was unlikely to be longer than that taken to complete a
more conventional anastomosis using sutures. The procedure
was considered not only quick to perform but also relatively
atraumatic. The lack of bowel manipulation required to fashion
the anastomosis was considered a significant advantage of the
procedure over the more conventional sutured anastomosis.
Although the anastomosis was performed with an open bowel,
the speed, lack of bowel manipulation and ease of application
imply that the procedure, when performed correctly, carries a
low risk of complication. As concluded by Ullman and others
(1991), a further significant advantage of the technique over
conventional anastomosis using sutures is that it allows the
anastomosis of two portions of bowel with large differences of
lumen diameter. This issue is commonly encountered in cases of
intestinal obstruction in which the proximal segment has become
greatly dilated. When anastomising such disparate diameter
segments of intestine with sutures, great care must be taken
to ensure that the two ends of intestine to be anastomosed are
of similar luminal diameter. In some instances, this will require
further manipulation and resection of bowel from one of the
segments to be anastomosed. The use of the stapled functional
end-to-end anastomosis in such circumstances does away with
any of these issues and can be used to anastomose segments
of bowel with widely differing luminal diameters without any
such concerns.
Dogs with no evidence of preoperative peritonitis (cases 2, 3, 5,
7, 8, 10, 11, 12 and 13) were all discharged within one day of their
surgery. Dogs with confirmed pre-existing peritonitis remained
hospitalised for between two and five days, postoperatively.
The 14 dogs alive at six month follow-up had all made an
unremarkable long-term recovery from the surgery with owners
confirming normal digestive function and no requirement for
further medication or dietary manipulation.
Discussion
The procedure of stapled intestinal anastomosis appeared to be
both safe and quick to perform when utilised for the management
of various diseases requiring small intestinal resection in the dog.
There were few noted complications even when the procedure
was used to manage cases with confirmed bacterial peritonitis.
This suggests that provided the manufacturer’s recommendation
that the instrument is not used on ischaemic or necrotic tissues
is adhered to, the stapling procedure can be safely used even
in dogs suffering from an ongoing peritonitis. In all cases, the
anastomoses appeared to heal without serious complication.
In human beings, the use of stapled anastomosis in gastrointestinal
surgery has been compared with hand suturing in several
randomised trails [Beart and Kelly 1981, Brennan and others
1982, McGinn and others 1985, Everett and others 1986, West
of Scotland and Highland Anastomosis Study Group 1991, Hori
and others 2004]. Although the results varied, there appears to
be no consistent difference in anastomosis dehiscence between
the two approaches. These studies also concluded that stapled
anastomoses uniformly afforded a significantly quicker surgery
time. There are also a number of studies that have investigated
the use of stapled anastomosis in patients with traumatic lesions
of the gastrointestinal tract [Brundage and others 1999, 2001,
Witzke and others 2000, Kirkpatrick and others 2003]. In the
presence of peritonitis, results were conflicting in terms of
It has been suggested that the intersection of two or more
staple lines may be hazardous to the integrity of the stapled
anastomosis. Zilling and Walther (1992) reported a reduction in
blood flow at the site of anastomosis, but this reduction was
not considered sufficient to represent a concern with regard to
the integrity of the intestinal anastomosis. Although this study
made no attempt to assess changes in blood flow associated
with the stapling procedure and no information was available
80
whether anastomotic leakage was more likely to occur following
stapled bowel repair rather than hand-sewn repair. In two of
these studies [Witzke and others 2000, Kirkpatrick and others
2003], the rate of intra-abdominal complications including
anastomotic leakage did not differ significantly between stapled
or hand-sewn repairs. On the contrary, two studies [Brundage
and others 1999, 2001] concluded that anastomotic leaks and
intra-abdominal abscess development appeared to be more likely
with stapled bowel repairs compared with sutured anastomoses
in the injured patient.
FIG 6. Photograph of the reloading unit showing the bevelled point
of the unit that allows ease of passage into the bowel lumen. The
length from the tip of the unit to the first staple is approximately
23 mm
In one previous description of stapled entero-anastomosis
in small animals [Ullman and others 1991], postoperative
complications were seen in three animals representing 12·5 per
cent of their study group. Leakage at the anastomotic site was
recorded in one cat and one dog, and the development of a
localised abscess at the staple line was observed in a second
dog. In each of these individuals, the authors concluded that
there was a higher risk for complication development because of
severe pre-existing peritonitis, the colonic site of the anastomosis
or a compromised immune system [Ullman and others 1991].
Further investigations into the prevalence and risk factors for
leakage following hand-sewn intestinal anastomosis in dogs
suggested that a variety of factors may be associated with the
development of intestinal anastomotic leakage in dogs [Allen
and others 1992, Wylie and Hosgood 1994, Ralphs and others
2003]. In particular, dogs with preoperative peritonitis, intestinal
foreign body and/or low serum albumin concentrations were
predicted to be at higher risk for leakage development. In the
present study, although there was no evidence of anastomotic
leakage in any of the dogs, including those with confirmed preexisting peritonitis, the small sample size and a lack of objective
data provided insufficient evidence for any firm conclusions to be
drawn with regard to the safety of stapled entero-anastomosis
when used in dogs with a pre-existing peritonitis.
this type of device should be used with care if the proposed
procedure requires multiple firings across a previous staple line.
Although the use of the GIA 50 stapling instrument has been
described for intestinal anastomosis in the cat [Ullman and others
1991], in the experience of the author, in many instances the size
of this instrument, and similarly the GIA 60 instrument used in
this study, makes the passage of the forks into the lumen of toy
breed dog’s small intestine either very difficult or impossible. In
such circumstances, stapled open lumina entero-anastomoses
can be achieved by using a linear cutter stapling device that
has been designed for endoscopic use. Such devices have much
narrower “forks” that fit comfortably within the lumen of the
small intestines of small dogs. The use of a endoscopic linear
cutter stapling device (Multifire Endo GIA 30, Tyco Healthcare
UK Ltd) can be used to create a stapled functional end-toend anastomosis in a similar manner to that described for the
conventional GIA 50 or GIA 60 stapling instrument and it can
be used safely in smaller dogs where the forks of the GIA 50 or
GIA 60 stapler are considered too large (R. N. White, Personal
observation). Further consideration should be given to the
thickness of the tissues that are to be stapled. The Multifire 3.8
mm GIA 60 reloading unit was chosen in this study because the
height (length) of the “unfired” staple was 3.8 mm and height of
the “fired” staple was approximately 1.5 mm. These dimensions
were considered appropriate for the use of such staples in the
small intestine of the dog (Tyco Healthcare UK Ltd).
A potential complication related to the contact of the knife
on second firing with previously placed staples is that each
time the blade of the knife came into contact with the metal
of a staple the edge of the blade would become blunted. This
might adversely affect its ability to cut through any remaining
tissues in an efficient manner. No specific investigations into
this potential complication were performed but the lack of
evidence supporting the development of dehiscence at the site
of anastomosis suggests that the function of the knife was not
significantly compromised during its passage across the row of
staples from the first firing. It should also be noted that each
cartridge of staples contains its own knife so that a brand new
knife is used during each firing of the stapling device. Therefore,
the knife is only used once and then discarded with each used
staple cartridge. This was not the situation with certain older
linear cutter stapling devices where the knife was contained
within the staple gun itself. In such instances, the same knife
would be utilised during the first and any subsequent firings of
the device. Blunting of the knife was an accepted complication
with multiple firings of such devices and its occurrence
limited the number of subsequent firings that could be safely
undertaken with each unit. A number of these older devices are
still available for veterinary use, but experience suggests that
In three dogs, the entero-anastomosis was performed between
the distal jejunum and the ileum. To ensure that the final
anastomosis is created with an adequate stoma, it is imperative
that an adequate length of distal ileum is available for the
placement of one limb of the staple gun. In the case of the GIA
60 cartridges, the first 20 mm of the cartridge is bevelled to a
blunt to allow ease of passage into the bowel lumen. There is,
therefore, a distance of 23 mm from the point of the cartridge
which contains no staples (Fig 6). When this length is added
to the length of the cartridge which contains and fires the
staples (60 mm in the case of the GIA 60 cartridge), then it can
be concluded that the length of distal ileum required for the
successful use of this stapler was at least 60 mm. It is important
that this factor is taken into consideration at the time of bowel
resection and under certain circumstances the required extent
81
of ileal resection may not leave adequate distal bowel for the
safe use of the stapling device.
Fossum TW. Surgery of the Abdominal Cavity. In: T.W. Fossum, edition
Small Animal Surgery. 3rd edn. Mosby, St Louis, MO, USA; 2007.
pp 317-338
Hori S, Ochiai T, Gunji Y, Hayashi H. & Suzuki T. A prospective
randomized trial of handsutured versus mechanically stapled
anastomosis for gastroduodenostomy after distal gastrectomy.
Gastric Cancer. 2004; 7: 24-30
Kirkpatrick AW, Baxter KA, Simons RK, Germann E, Lucas CE. &
Ledgerwood AM. Intra-abdominal complications after surgical
repair of small bowel injuries: an international review. Journal of
Trauma. 2003; 55: 399-406
Mcginn FP, Gartell PC, Clifford PC. & Brunton FJ. Staples or sutures for
low colorectal anastomosis: a prospective randomized trial. British
Journal of Surgery. 1985; 72: 603-605
Mcginty CP, Kasten MC, Kinder JL. & Hunt RS. Update on stapled bowel
anastomosis. Modern Medicine. 1979; 76: 145-150
Nance FC. New techniques of gastrointestinal anastomoses with the
EEA stapler. Annals of Surgery. 1979; 189: 587-600
Ralphs SC, Jessen CR. & Lipowitz AJ. Risk factors for leakage following
intestinal anastomosis in dogs and cats: 115 cases (1991–2000).
Journal of the American Veterinary Medical Association. 2003;
223: 73-77
Ravitch MM, Ong TH. & Gazzola L. A new precise and rapid technique
of intestinal resection and anastomosis with staples. Surgical
Gynecology and Obstetrics. 1974; 139: 6-10
Ravitch MM. & Steichen FM. Technics of staple suturing in the
gastrointestinal tract. Annals of Surgery. 1972; 175: 815-837
Ritchey ML, Lally KP. & Ostericher R. Comparison of different techniques
of stapled bowel anastomoses in a canine model. Archives of
Surgery. 1993; 128: 1365-1367
Ryan S, Seim H, Macphail C, Bright R. & Monnet E. Comparision of
biofragmentable anastomosis ring and sutured anastomosis for
subtotal colectomy in cats with idiopathic megacolon. Veterinary
Surgery. 2006; 35: 740-748
Staatz AJ, Monnet E. & Seim HB. Open peritoneal drainage versus
primary closure for the treatment of septic peritonitis in dogs and
cats: 42 cases (1993–1999). Veterinary Surgery. 2002; 31: 174180
Steichen FM & Ravitch MM. Operations on the small and large bowel.
In: Stapling in Surgery. Chicago, IL, USA, Year Book Medical
Publishers. 1984; pp 270-310
Ullman SL. Surgical stapling of the small intestine. Veterinary Clinics of
North America: Small Animal Practice. 1994; 24: 305-322
Ullman SL, Pavletic MM & Clark GN. Open intestinal anastomosis
with surgical stapling equipment in 24 dogs and cats. Veterinary
Surgery. 1991; 20: 385-391
Vail D. Lymphoproliferative and myeloproliferative disorders.
In: Dobson JM, Lascelles DX, editors. BSAVA Manual of
Canine and Feline Oncology. 2nd edn. British Small Animal
Veterinary Association, Gloucester, UK. pp 276-292.
West of Scotland and Highland Anastomosis Study Group (1991)
Suturing or stapling in gastrointestinal surgery: a prospective
randomized study. British Journal of Surgery. 2003; 78: 337-341
Witzke JD, Kraatz JJ, Morken JM, Ney AL, West MA, van Camp JM,
Zera RT & Rodriguez JL. Stapled versus hand sewn anastomoses in
patients with small bowel injury: a changing perspective. Journal
of Trauma. 2000; 49: 660-665
Wylie KB & Hosgood G. Mortality and morbidity of small and large
intestinal surgery in dogs and cats: 74 cases (1980–1992). Journal
of the American Animal Hospital Association. 1994; 30: 469-474
Yamamoto T & Keighley MR. Stapled functional end-to-end anastomosis
in Crohn’s disease. Surgery Today. 1999; 29: 679-681
Zilling T. & Walther BS. Are intersecting staple lines a hazard in intestinal
anastomosis? Diseases of the Colon and Rectum. 1992; 35: 892896
Potential advantages of using a GIA (linear cutter) stapler to
perform the final closure of the enterectomy as opposed to the
more conventionally used thoraco-abdominal (linear) stapler
were related to simplicity of technique and the requirement
of only one type of stapling device to complete the entire
anastomosis. One surgeon can easily perform the technique
without the need for a scrubbed surgical assistant. The cost of
the stapling equipment might be considered a disadvantage
of the technique over more conventional sutured anastomosis
techniques.
Conclusions
In conclusion, the findings of this study suggest that the use
of a GIA stapling to perform open lumina entero-anastomosis
was without significant complication even in the presence of
confirmed bacterial peritonitis. The technique was simple and
quick to perform requiring minimal manipulation of the bowel
and no requirement for a scrubbed assistant. The use of the
GIA stapler to perform the final closure of the enterectomy
was considered a viable and practical alternative to the more
conventional use of a thoraco-abdominal stapler.
Acknowledgements
Thanks to Amanda Durman and Julian Foster of Tyco Heathcare
UK Ltd for their assistance with the provision of technical
information. Thanks also to Duncan Henderson and Trevor Bolton
of Direct Medical Supplies Ltd for their support of this study.
References
Allen DA, Smeak DD & Schertel ER. Prevalence of small intestinal
dehiscence and associated clinical factors: a retrospective study in
121 dogs. Journal of the American Animal Hospital Association.
1992; 28: 70-76
Beart RW & Kelly KA. Randomized prospective evaluation of the EEA
stapler for colorectal anastomoses. American Journal of Surgery.
1981; 141: 143-147
Brennan SS, Pickford IR, Evans M. & Pollock AV Staples or sutures for
colonic anastomoses – a controlled clinical trial. British Journal of
Surgery. 1982; 69: 722-724
Brundage SI, Jurkovich GJ, Grossman DC, Tong WC, Mack CD & Maier
RV. Stapled versus sutured gastrointestinal anastomoses in the
trauma patient. Journal of Trauma. 1999; 47: 500-507
Brundage SI, Jurkovich GJ, Hoyt DB, Patel NY, Ross SE, Marburger R,
Stoner M, Ivatury RR, Ku J, Rutherford EJ. & Maier RV Stapled
versus sutured gastrointestinal anastomoses in the trauma patient:
a multicenter trial. Journal of Trauma. 2001; 51: 1054-1061
Chassin JL, Rifkind KM. & Turner JW. Errors and pitfalls in stapling
gastrointestinal tract anastomoses. Surgical Clinics of North
America. 1984; 64: 441-459
Coolman BR, Ehrhart N, Pijanowski G, Ehrhart EJ. & Coolman SL.
Comparison of skin staples with sutures for anastomosis of the
small intestine in dogs. Veterinary Surgery. 2000; 29: 293-302
Everett WG, Friend PJ. & Forty J. Comparison of stapling and handsuture for left-sided large bowel anastomosis. British Journal of
Surgery. 1986; 73: 345-348
82
PRACTICE MANAGEMENT
Cyprus and the Pancyprian
Veterinary Association
Cyprus is the third largest island in the Mediterranean following Sicily
and Sardinia, and is located in the Eastern part of the Mediterranean
Sea. The population of Cyprus is in the region of 800,000. Its economy is
largely based on tourism and agriculture.
The modern and well equipped clinic of Yiannis Stylinou is typical of Cypriot small animal clinics. Yiannis is seen here with
Yiota his wife and clinic partner.
Structured and organised veterinary science first started in
Cyprus with the establishment of the Cyprus Republic in 1960.
Initially all veterinary graduates were involved in state activity.
Gradually, the needs of the state decreased resulting in the
appearance of private veterinary clinics, initially dealing mainly
with the food-producing animals and working animals.
The standard of living of Cypriots has gradually improved with the
result that some Veterinarians have now started to concentrate
on small animals, i.e. domestic cats and dogs, resulting in a
need for the establishment of companion animal veterinary
clinics. In 1978 Cypriot veterinarians became organised forming
‘The Pancyprian Veterinary Association’ (PVA). All Cypriot
veterinarians including those in government service, those
working in commerce, private veterinarians, and owners of
veterinary clinics can be members of PVA.
Today in Cyprus there are 80 veterinary clinics. About 15 of these
are engaged in mixed practice (pet and production animals)
whilst the remainder deal exclusively with pet animals.
most problems. A normal veterinary clinic in Cyprus consists of
at least 6 or more separate rooms:
• Reception area (host area room)
• examination room
• operating room
Most of the veterinary clinics are very well-equipped and possess
the necessary facilities enabling a proper scientific approach to
83
Cyprus and the Pancyprian Veterinary Association
improvement of all our skills. The advantages FECAVA members
have enjoyed by sharing new ideas a points of view from all over
Europe are similarly enjoyed in Cyprus because of this diversity
of training and experience.
The relatively small number of Vets in Cyprus, plus the fact that
there is no Veterinary School and that geographically Cyprus is
distant from major European leaning centres, means that there
is little opportunity for case referral. Almost all problems have to
be solved ‘in house’. There is no easy way out when a difficult
case is encountered and vets in Cyprus have learnt to give a high
quality of treatment to all cases within their own clinics
Cypriot vets are very eager to learn, that is why many of them
often go abroad to the various congresses and workshops,
aiming to upgrade of their knowledge and skills.
The Pancyprian Veterinary Association on an annual basis
organises at least one scientific congress and two or three
workshops with guest lecturers and instructors of international
reputation and standing. Thus an opportunity is given for all
the veterinarians to both refresh and upgrade their knowledge
keeping up with new scientific advances
These events are usually subsidised by the Pancyprian Veterinary
Association and for this reason the cost is to members minimal.
Because of the island’s size, the pharmaceutical market of
Cyprus is small and many veterinary medications are therefore
not available. This makes the work of Cypriot vets difficult and
they have no choice but to use off label substitutes or similar
human medical products.
Tourism is an important industry in Cyprus-Paphos Harbour
• recovery room
• storeroom for medical products (pharmacy)
• laboratory
Even though the veterinary services that are offered in Cyprus
are of a very high standard, nevertheless, there is always room
for improvement and that is the aim of the Pancyprian Veterinary
Association. It was with this and other reasons in mind that PVA
was pleased to become a member of FECAVA
They are fully equipped with appropriate equipment, anaesthetic
machines, diathermy units, dentistry equipment, etc. 90% of the
veterinary clinics in addition to the normal diagnostic equipment
have and more specialised equipment such as X-ray machines,
ultrasound and haematology /biochemistry analysers.
Yiannis Stylianou, FECAVA Director for the PVA
The Cyprus veterinary clinics are mostly family businesses having
2 or more persons.
The personnel of the veterinary clinics in Cyprus is very small
and usually consists of 1-2 veterinarians with 1-2 assistants of
veterinarians and one receptionist.
The PVA organised an Ultra-sound workshop (Limassol Oct 2009)
As mentioned tourism is an important industry in Cyprus.
There are many holiday makers and people choosing Cyprus for
holiday and retirement homes. In some clinics the majority of
clients are expatriates, and in addition to possessing a high level
of veterinary knowledge veterinarians have to be fluent in other
languages, especially English
Unfortunately Cyprus does not have a veterinary school and
that is why the Cypriot veterinarians are graduates of veterinary
schools from many countries of Europe, America and Asia.
We have veterinary graduates from Greece, Russia, the Czech
Republic, Romania, Bulgaria, Hungary, America, etc. In my
opinion this results in a very healthy situation, different ideas
and approaches can be shared to the great advantage and
84
BOOK REVIEWS
BSAVA Manual of Canine and
Feline Behavioural Medicine
(Second Edition)
Edited by Debra Horwitz and
Daniel S. Mills
Published by BSAVA
Distributed by Wiley-Blackwell (January 2010) 324 pages plus CD-ROM,
Paperback, ISBN: 978-1-905319-15-2
€85.10/£74.00
Available from www.wiley.com/go/vet
BSAVA members should order from
www.BSAVA.com for member prices
I also appreciated the fact that, although
the different chapters are written by different authors, there is uniformity in the style
and the presentation.
The CD accompanying the manual (handbook) is also a very useful tool and compliments the manual very well.
In conclusion, this second edition is particularly neat and is certainly a “must” for all
veterinarians, not only those specialising in
behaviour problems.
Dr Arlette Blanchy (B)
Canine and Feline Cytology A Color Atlas and Interpretation Guide, 2nd Edition
Edited by Rose E. Raskin and Denny Meyer
Published by Saunders Elsevier, (http://intl.
elsevierhealth.com.vet ) (2010) 472 pages,
Hardback, ISBN: 978-1-4160-4985-2
€116 £80.99
The concept of having a book devoted
solely to the subject of the behaviour and
behavioural problems of the dog and cat
is very worthwhile. The expert contributors
have all information at their disposal and
make valuable comparisons between the
two species.
The presentation, the format, the illustrations and cover pictures are all very pleasing.
The selection of contributors guarantees an
objective and wide-ranging understanding
of the subject.
I particularly appreciate the first chapters,
which put the investigation of behaviour
problems into their true perspective .They
ensure that we do not forget that above
all, as veterinarians, our first task is to make
a somatic assessment before assuming a
purely behavioural problem.
This manual enables the generalist veterinarian to gain a solid base for dealing with
problems of behaviour. It also enables the
veterinarian more specialised in the field of
behaviour to keep up to date with information on relevant advances in general
medicine.
The details of basic requirements showing
how to avoid behavioural problems are very
useful. I particularly appreciated the very
clear tables and the scale of aggression
chart. The diagrams speak for themselves
and make the explanations to the owner
easier.
The separation of the various chapters is
very practical; it enables readers to directly
identify a link with the client’s reason for
seeking a consultation.
This second edition is quite an improvement
when compared to the first edition. Not
only has an extra chapter on faecal cytology been added, but more important the
paperback edition has become a full sized
hardcover edition. This will make the use of
the book alongside the microscope much
more comfortable. The number of pictures
has increased and the pictures have become
larger and sharper. Apart from the editors
20 other persons contributed to this book.
The book consists of 17 chapters. After two
general introductory chapters, discussing
acquisition and management of samples
and an introduction into cytological interpretation, almost all different topics of
cytology are discussed. The book is full of
colour illustrations, more than 1200 in fact,
and is accompanied by a clear text. The
layout of the chapters has been enormously
improved compared to the first edition.
Most chapters have extra photographs, and
the text and references have been updated,
especially in the chapters on the lymphomas, body cavity fluid, liver, muscoskeletal
system, central nervous system, and the
chapter on advanced diagnostic techniques.
Enough reasons for those who have the
First edition to upgrade to this edition.
For those who are not acquainted with
88
the First edition, a very balanced mixture
of descriptive text of experts is given with
many colour pictures. Each chapter is
provided with an extensive reference list,
covering not only American literature but
also articles in European journals. The book
is completed with a 12 page index.
Reading through the book I became very
enthusiastic about its quality. A few minor
remarks can be made, however. In the
introduction the malignancy criteria are
only barely discussed and illustrated. In
the chapter on classification of malignant
lymphomas the authors decided to put
some emphasis on the REAL classification.
Although this classification is the latest classification used by pathologists, its usefulness for the clinics still has to be proven. A
major disadvantage of the REAL system is
that histology is needed for this classification. This in contrast with the Kiel classification which can be done solely on cytology
and has proven its prognostic usefulness in
the clinic. To give credit to the authors they
do translate the REAL classification into the
Kiel classification.
Although the last chapter on several
advanced diagnostic techniques (especially
a lot of information on immunohistochemistry) is very good and interesting for those
working in academia or in a laboratory,
one doubts its usefulness for practitioners.
Perhaps a better decision would have been
to add some chapters on haematology and
bone marrow cytology, which are currently
lacking in this book.
To conclude, this book has been very
much improved from its first edition and
has become one of the better ones in this
field.
Dr.Erik Teske (NL)
Clinical Endocrinology of Dogs
and Cats. An Illustrated Text
(Second edition)
Edited by Ad Rijnberk and
Hans S. Kooistra
Published by Schlütersche Verlagsgesellschaft mbH & Co.,
(www.schluetersche.de) (2010)
352 pages, 446 illustrations , Hardback
ISBN 978-3-89993-058-0 € 119 £ 109
This is the second edition of a book first
published in 1995 and one eagerly awaited
by many working within the field of small
animal endocrinology. The changes for the
new edition include the insertion of newly
recognised disease entities, further elucidation of mechanisms of disease and progress
in diagnosis and treatment. This book
certainly achieves this and much more.
The book is divided into two separate
BOOK REVIEWS
sections
ti
covering
i
clinical
li i l endocrinology
and reproduction and the other, a smaller
section, providing details on protocols for
endocrine tests and disease treatments and
a few algorithms for common presenting
complaints such as alopecia, polyuria and
polydipsia, weight loss and one for breeding
management of the bitch. The first section
has a good introduction to hormones covering basic principles such as chemical nature,
production and action followed by general
guidelines for diagnosing endocrine diseases. The remainder is divided more traditionally into chapters covering the major
endocrine and reproductive organs including the hypothalamus-pituitary system,
thyroids, adrenals, pancreas and gonads.
The parathyroid glands are included in a
chapter on calciotropic hormones allowing for better integration of the numerous
hormones controlling calcium homeostasis. Each chapter provides a review of the
morphology and physiology of the gland
followed by descriptions of the relevant
disorders highlighting clinical manifestations, differential diagnoses, diagnosis,
treatment and prognosis. Two additional
chapters on tissue hormones and humoral
manifestations of cancer and one on obesity complete this section.
This book is a definite mixture of endocrinology in both health and disease. For me a
knowledge of the former underpins understanding of the latter and this book excels
in providing such relevant information in a
readily comprehensible manner. However,
for some busy veterinary practitioners, a
greater bias on clinical information may
be preferred particularly with regard to
difficulties associated with interpretation of
endocrine test results, treatment availability and cost and problems associated with
treatment failures. The authors do attempt
to address some of this by providing information in a more easily accessible manner
in the form of numerous tables and graphs
and in the protocols of the second section
that may prove helpful.
All of the authors are renowned in the field
of small animal endocrinology and reproduction. Largely emanating from Utrecht
University, the content is now more inter-
nationalised with contributors from Switzerland, Germany and the USA. The editors
hope that the book will serve as an up-todate guide in the rapidly developing field
of endocrinology. It achieves this aim in a
book that is exceptionally and beautifully
illustrated. These illustrations alone would
stimulate ones interest in this discipline.
Retailing at over € 100, this book is not
cheap and for those presented with endocrine or reproductive cases infrequently,
this may prove too expensive. But for those
interested in this field and for undergraduate and postgraduate studies, this book
will serve as a welcome edition that will be
frequently studied and very much enjoyed.
Carmel T Mooney MVB MPhil PhD
DECVIM-CA MRCVS
RCVS Specialist in Small Animal
Endocrinology(IRL)
Hair Loss Disorders in
Domestic Animals
Edited by Lars Mecklenburg, Monika
Linek, Desmond J. Tobin
Published by Wiley-Blackwell
(www.wiley.com/go/vet.) ( June 2009)
288 pages, 85 illustrations. Hardcover
ISBN: 978-0-8138-1082-9
€141.70 £85.00
This is the first veterinary book entirely
dedicated to hair loss seen in small and
large domestic animals. It has been written
by two veterinarians (one pathologist and
one clinical dermatologist) and a biologist,
with the help of contributors (three dermatologists, one anatomist, and one pathologist). A great team!
The book is big and good-looking (280
pages, hard cover).
The first part encompasses the biology of
the hair follicle in 3 chapters: ontogeny,
anatomy and physiology and variation
amongst species. There are beautiful
drawings and microphotographs (including scanning electron microscopy). I have
89
particularly liked the colour cartoon of an
anagen hair follicle. The text is detailed and
there are a lot of references. An appropriate
comparison with the human skin is made
(which is rare in the veterinary literature).
The second part comprises an approach of
alopecic diseases, in 2 chapters. The clinical
aspects, which include clinical pathology,
overlap with dermatology handbooks. The
histopathological aspects provide a good
introduction to skin biopsy and the terminology applicable to alopecic diseases. I
liked he clarification between dysplasia and
dystrophy. In fact this part is rather simple
in comparison to part 1. It is more oriented
towards clinicians.
The third part encompasses non-inflammatory alopecias, in 6 chapters: congenital,
trichomalacia (rare abnormalities of hair
shafts), disorders of hair follicle cycling,
dystrophy and atrophy of the hair follicle,
traumatic alopecia and scarring alopecia.
- The congenital alopecias are very
detailed and well illustrated. Many species
are covered, with a judicious clinicopathological approach, including canine dysplasia
of hair follicle pigmentation.
- The hair cycle disorders (mainly seen
in dogs) first give an excellent overview
of endocrine disorders (hypothyroidism,
spontaneous hyperadrenocorticism, iatrogenic corticoid-induced alopecia, and
sexual disorders). Following this the current
knowledge on alopecia X and canine recurrent flank alopecia is well clarified. Other
rarer conditions are presented with fewer
details (telogen effluvium, post-clipping
alopecia, pattern alopecia and some breed
specific canine hair cycle abnormalities).
- The chapter on hair follicle dystrophy and
atrophy is short but gives an exhaustive
review of ischemic dermatopathies, including dermatomyositis.
- The chapter on traumatic alopecia relates
to self-inflicted hair loss, i.e. mainly pruritic
diseases. It is very short, which is justified
with regard to the fact that pruritus is a
major cause of alopecia and that this book
does not intend to be another dermatology handbook. Similarly, a there are a few
words concerning scarring alopecia.
The fourth part deals with inflammatory
alopecias in 8 chapters: folliculitis due to
intraluminal organisms, eosinophilic folliculitis, pustular folliculitis, lymphocytic mural
folliculitis, histiocytic or granulomatous
mural folliculitis, necrotizing mural folliculitis, alopecia areata, and sebaceous adeni-
BOOK REVIEWS
tis. There is a term ambiguity between
luminal (chapter 1) and pustular (chapter 3)
but the authors limit the word pustular to
i) intramural infundibular ii) sterile pustules
i.e. superficial pemphigus, mainly foliaceus,
described briefly in chapter 3.
- The first chapter on bacterial folliculitis
is very clinical and a bit redundant bearing in mind its coverage in other veterinary
dermatology handbooks. In my experience
feline pyoderma is rare and not commonly
secondary to EGC, head and neck pruritus
or symetric self-induced alopecia, contrary
to what is stated. Dermatophytosis and
demodicosis are well detailed (the trichogramme of dermatophytosis is redundant
as a better one is featured in the first chapter of part 2.). The rarer but interesting
rhabditic folliculitis and straelensiosis are
briefly described.
dermatopathologists. Good clinical and
histopathological descriptions are given,
useful for a differential diagnosis, including neoplastic, paraneoplastic and non
neoplastic diseases.
- Histiocytic or granulomatous mural
folliculitis (chapter 5) is a group of very rare
diseases seen in several species and the
current data is well put together.
which is the alteration of the haircoat
leading often to an early consultation just
because it is readily visible. I like the use of
the plural alopecias, as well as dermatoses
as the plural of dermatosis. This overview
on hair loss disorders is remarkably well
written and exhaustive.
- Necrotizing mural folliculitis (briefly
reviewed in chapter 6) refers to viral diseases in the cat (herpes and cowpox).
Many appropriate references are given
although a few are missing, particularly
from European Journals in other languages
than English. The numerous colour pictures
(clinical and histopathological) are indeed
nice and demonstrative.
- Aopecia areata reviewed in chapter 7 is
an enigmatic dermatosis. I particularly like
this chapter because it is exhaustive and
refers to comparative pathology with a nice
description of the disease in man. Also the
discussions on aetiology and pathogenesis
are well worth reading.
This will be a valuable book for both clinicians and histopathologists, “a clinico-pathologic book”. It should definitely be on the
shelf of dermatologists, dermatopathologists, residents in both disciplines, and also
curious general practitioners interested in
the skin and its pathology.
- Eosinophilic folliculitis/furunculosis of the
dog, cat and horse due to arthropod bites
(stinging insects including fleas, mosquitos
and culicoides) are well reviewed in chapter 2.
- Chapter 8 deals with sebaceous adenitis,
also an enigmatic disease, more common
than alopecia areata, but in fewer details.
There is a short index (4 pages).
Didier-Noël Carlotti, DVM, Dip ECVD (F)
- Lymphocytic mural folliculitis (chapter 4)
is a difficult disease for both clinicians and
In conclusion, this book is original although
it deals with a common chief complaint,
90
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.
2010
8-11 April
BSAVA
Birmingham
Annual Congress
English*
10-11 April
SkSAVA
Senec
CE Oncology (WSAVA)
English/Czech
16-18 April
NSAVA
Tromsø
Spring meeting - Lameness-diagnosis and treatment
Swedish First half
English second half
17 April
CSAVA
Hradec Králové
CE Neurology for practicing Veterinarions III
Czech
17-18 April
CSAVS
Varaždin
CSAVS/FECAVA CE Management In Veterinary Practice
Emercency cases in S.A. reproduction
English
22-24 April
NACAM
Amsterdam
Voorjaarsdagen
Dutch/English
24-26 April
RSAVA
Moscow
Annual Congress
Russian/ English
27 April
BSAVA
Gloucester
CE Endocrinology II: Endocrine Collapse and the unstable diabetic
English
28 April
BSAVA
Gloucester
CE Surgery of the alimentary tract
English
28 April
VICAS
Limerick
CE Dermatology Road Show
English
29 April
BSAVA
Leeds
CE Respiratory Medicine
English
11 May
BSAVA
Gloucester
CE From large kidney to small bladder: Urogenital tract surgery
English
13 - 16 May
VICAS
Dublin
CE Ophthalmology
English
14-15 May
EVSSAR
Louvain - La Neuve (B)
7th Biennial congress
English
22-23 May
ESAVA
Taagepera
CE Reproduction
English
19 May
BSAVA
Beaconsfield
What’s new in veterinary oncology Road Show
English
20 May
BSAVA
Gloucester
CE Introduction to Cytology
English
21 May
BSAVA
Bristol
CE What’s new in veterinary oncology Road Show
English
23 May
BSAVA
Fife
English
25 May
BSAVA
Cheshire
English
25 May
BSAVA
Gloucester
CE Clinical Pathology: Interpretation of biochemical data and an
introduction to diagnostic cytology
English
26 May
VICAS
Sligo
Dermatology
English
27 May
BSAVA
Leeds
Logic and common sense in treating the cardiac patient
English
29-30 May
VÖK
Vienna
Clinical updates in vet practice
German
2-5 June
FECAVA /
WSAVA /SVK
Geneva
16th FECAVA/34th WSAVA/SVK-ASMPA Congress
English and others
7 – 11 June
ESAVS
Halmstadt (S)
Dentistry II
English
12 June
VÖK
Ried/Traunkreis
Reproduction-Seminar
German
14 – 18 June
ESAVS
Luxembourg (L)
Behavioural Medicine I
English
15 June
BSAVA
Gloucester
Abdominal Pot Pourri: pancreatic, adrenal biliary tract and liver
surgery
English
17-20 June
ESFM
Amsterdam (NL)
ESFM Feline Congress - Feline Dentistry &
Feline pain management
English
18-20 June
BASAV
Varna
National Congress
English
19-20 June
VÖK
Ried/Traunkreis
Stomach & Intestinal Surgery
German
21 – 25 June
ESAVS
Bern (CH)
Emergency and Critical Care I
English
21 June – 2 July
ESAVS
Luxembourg (L)
Ophthalmology I
English
24 June
BSAVA
Leeds
Emerging and parasitic diseases of small animals in the UK
English
29 June
BSAVA
Gloucester
GIT I: Pancreatic and liver disease: the old and the new
English
1-3 July
ECVS
Helsinki (Fi)
19th Annual Meeting
English
4-5 July
VÖK
Rankweil
Stomach & Intestinal Surgery
German
5 – 9 July
ESAVS
Vienna (A)
Rehabilitation and Physiotherapy of Small Animals 11
English
12 – 16 July
ESAVS
Luxembourg (L)
Oncology I
English
12 – 23 July
ESAVS
Vienna (A)
Dermatology II with Workshops
English
19 – 23 July
ESAVS
Halmstad (S)
Dentistry III, Advanced with Wet lab
English
21 – 24 July
ESAVS
Bern (CH)
Diagnostic Ultrasound I with Wet lab
English
9 – 20 August
ESAVS
Vienna (A)
Dermatology III with Workshops
English
16 – 20 August
ESAVS
Luxembourg (L)
Cardiology I
English
16 – 20 August
ESAVS
Bern (CH)
Emergency and Critical Care II
English
21 – 25 August
ESAVS
Bern (CH)
Neurology II
English
23 – 27 August
ESAVS
Vienna (A)
Soft Tissue Surgery II Advanced Course with Workshops
English
92
27 – 31 August
ESAVS
Giessen (D)
Surgery / Laser Surgery in Vet Medicine
English
30 Aug. – 3 Sept.
ESAVS
Giessen (D)
Endoscopy Intensive Course with Workshops
English
30 Aug. – 3 Sept.
ESAVS
Vienna (A)
Soft Tissue Surgery II Advanced Course with Workshops
English
1 – 5 September
ESAVS
Luxembourg (L)
Cardiology III
English
4 – 5 September
ESAVS
Giessen (D)
Endoscopy Advanced Course
English
6 – 10 Sept.
ESAVS
Luxembourg (L)
Behavioural Medicine II
English
8 September
VICAS
Limerick
Dermatology Road Show
English
9-11 September
ECVIM-CA
Toulouse (E)
20th Annual Congress
English
15 September
BSAVA
Cheshire
English
13 – 17 Sept.
ESAVS
Brno / Czech Republic
Exotic Pets Medicine & Surgery Course with Wet Lab
English
15-18 September
ESVOT /VOS
Bologna(I)
World Veterinary Orthopaedic Congress
English
17 September
BSAVA
Kegworth
English
20 September
BSAVA
Exeter
English
21 September
BSAVA
Basingstoke
English
20-24 September
ESAVS/EVSSAR
Hunenberg (CH)
Small Animal Reproduction II
English
22 September
VICAS
Naas
English
23-25 September
EVDS-EVDC
Nice (F)
19th European Congress of Veterinary Dentistry
English
23-25 September
ESVD-ECVD
Florence (I)
Annual congress
English, Italian
24-26 September
VÖK
Salzburg
25th Annual Meeting
German, English
28 September
BSAVA
Gloucester
GIT II: Oesophagus, stomach and intestines
English
30 September
BSAVA
Leeds
Oncology I
English
30 Sept - 3 Oct.
AVEPA
Barcelona
AVEPA/SEVC Annual Congress
English, Spanish,
French, German,
Polish
4, 6, 8 October
VICAS
Limerick, Sligo, Naas
Internal Medicine Road Show
English
8-10 October
PSAVA
Warsaw
18th PSAVA Congress
English, Polish
9-10 October
VÖK
Kufstein
GI Diseases
German
9-10 October
CSAVA
Hradec Kralove
18th Annual Meeting
English, Czech
13 October
BSAVA
Newcastle
Wound Management Road Show
English
15 October
BSAVA
Cambridge
English
18 October
BSAVA
Southampton
English
19 October
BSAVA
Gloucester
Haematology
English
20 October
BSAVA
Brands Hatch
English
21 October
BSAVA
Leeds
Oncology II
English
23 October
VÖK/VUW
Vienna
Emergency-Seminar
German
27 October
VICAS
Sligo
English
11-12 November
SSAVA
SLU, Uppsala
Annual Meeting
English mainly
11-12 November
NSAVA
Oslo
Annual Meeting
English
6-7 November
VÖK
Ried/Traunkreis
Cardiology-Forum
German
11 November
VICAS
Croke Park, Dublin
CE Orthopaedics
English
12-13 November
DSAVA
Aarhus
Annual Meeting Vectorborne diseases and Orthopaedics
English, Danish
12-14 November
VICAS
Croke Park, Dublin
BVOA
English
13-14 November
VÖK
Steyr
Ultrasound-Basic-Seminar
German
18 November
BSAVA
Kegworth
Neurology for busy practitioners Road Show
English
19 November
BSAVA
Leeds
English
22 November
BSAVA
Cardiff
English
23 November
BSAVA
Woking
English
15 – 26 Nov.
ESAVS
Utrecht ( NL)
Internal Medicine II
English
23 November
BSAVA
Gloucester
Clinical Nutrition: let food be your first medicine
English
25 November
BSAVA
Leeds
Canine and Feline Medical Neurology: the paralysed, collapsed or
wobbly patient
English
22 – 26 Nov.
ESAVS
Halmstadt (S)
Dentistry IV Oral Surgery with Web lab
English
20-21 November
VÖK
Krems
X-Ray-Seminar
German
23 November
BSAVA
Gloucester
Clinical Nutrition: let food be your first medicine
English
25 November
BSAVA
Leeds
Canine and Feline Medical Neurology: the paralysed, collapsed or
wobbly patient
English
27 November
VÖK
Vienna
Patella-Seminar
German
November
ESAVA
Tallinn
CE Behaviour
English
10-12 December
AFVAC
Paris
Annual Congress
French
93
2011
31 March-3 April
BSAVA
Birmingham
Annual Congress
English
28-30 April
NACAM
Amsterdam
Voorjaarsdagen
Dutch, English
18-21 May
SVK/ASMPA
Interlaken
Annual Congress
German, English,
French
7-9 July
ECVS
Ghent (B)
Annual Scientilic meeting
English
7-11 September
FECAVA/
TSAVA
Istanbul
17th FECAVA EuroCongress
English, Turkish
16-18 September
VÖK
Salzburg
26th Annual Congress
German, English
29 Sept - 2 Oct
AVEPA
Barcelona
AVEPA/SEVC Annual Congress
English, Spanish,
French, German,
Polish
2 to 4 December
AFVAC
Lyon
Annual Congress
French
* 60 Veterinary surgeons or 70 Nurse registrations required for simultaneous translation to be provided
Stop press - late caledar entries HVMS CE Courses
29-30.05.2010
Diagnostic hematology and cytology of the dog and cat
Volos
Greek, English
30-31.10.2010
Common medical problems of parrots
Athens
Greek, English
30.01.2011
Management of common medical problems in pet reptile species
Athens
Greek English
30-31.05.2011
Intensive care in the dog and cat
Thessaloniki
Greek English
4-5.11.2011
Management of the acute abdomen in the dog and the cat
Patra
Greek, English
28-29.01.2012
Management of common medical problems in pet rabbits and rodents
Athens
Greek, English
May 2012 (2 days)
Feline medicine ( endocrinology, cardiology, dermatology, behavioural medicine)
Athens
Greek, English
October 2012 (2 days)
Canine and feline osteoarthropathies ( surgery of the Knee, Stifle and Elbow Joints)
Heraklio
Greek, English
ADVANCE NOTICE
2012
FECAVA /WSAVA/BSAVA BirminghamApril 12-15 April
2013
Voorjaarsdagen 25-27 April
Voorjaarsdagen 26-28 April
94
VÖK Salzburg21-23 September
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
AMVAC
President: Dr Valentin Nicolae Lt.Av. Ion Garofeanun, r.8, district 5,
Bucharest. Romania
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. Milǒ s Urban, Secretariat: B. Misurcova, Palackeho 1-3, 612
42 Brno - Kralovo Pole, Czech Republic
Director: Dr. Davorin Lukman, Specijalističa Veterinarska Praksa
Trnovecka 6, 42000 Varazdin, Croatia
Secretariat: Den Danske Dyraegeforening, Emdrupevej 28 A, DK-2100
Østerbro. Att: Johanne Østerbye.
Director: Dr. Janne Orro
Director: Dr. Oili Gylden, Paarijoentie 185, 11710 Riihimäki, Finland
AFVAC
APMVEAC
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: Ferenc 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-4718 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
Tel: +351 218 404 179 – Fax: +351 218 404 180
Tel: (34) 93 2531522 – Fax: (34) 93 4183979
Tel: (359) 888 272529 – Fax: (359) 2 866 44 50
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Tel: (44) 1452 726700 – Fax: (44) 1452 726701
Tel: (420) 602 336 846 Fax: (420) 311 513241
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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
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
VICAS
Director: Dr. Peter A. Murphy, Summerhill Veterinary Hospital, Wexford,
Co. Wexford Ireland
[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.rs
[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;
SSAVA
E-mail/Website
www.afvac.com
[email protected]
[email protected]
www.aivpa.it andrea.vercelli@
ambulatorioveterinario.com or
[email protected]
[email protected]
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 usava
@ukr.net www.usava.org.va
Tel: (353) 5391 43185 – Fax: (353) 5391 43185
[email protected]
by request
[email protected]
www.veterinaryireland.ie
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]
1 8132983 - Fax (43) 1 8791669 - 7033
[email protected] www.voek.at
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
ECVS
Contact: Executive Secretary – ECVS Office Vetsuisse Faculty University
Tel: (41) 44 635 84 08 – Fax: (41) 44 313 03 84
[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
Contact: Dr. Rory Bell, Department of Veterinary Clinical Studies University Tel: (+44) 141 330 5848 - Fax: +44 141 330 3663
[email protected]
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, Glasgow,
www.esvn.org
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
95

Foodstuffs toxic to small animals - a review

Transcription

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