WE can sometimes think that we are
pretty much up to date on a clinical
subject and steer away from CPD in
certain fields, feeling we will gain
more from attending lectures where
we have recognised gaps in our
knowledge.
But taking this approach can mean
that we sometimes miss out on some
real gems of wisdom and thinking and
opinion can change
markedly in even a few
years.
Stressed cats
One such personal
example came from
Professor Danielle
Gunn-Moore’s lecture
at the London Vet
Show: “Feline lower
urinary tract disease in
the 21st century – what
we know now and
didn’t know then”.
Prof. Gunn-
Moore’s whistle-stop
tour through the
condition covered clinical signs, causes,
diagnosis and treatment and highlighted
how much more we have discovered
about the condition in the last 10 years.
The disease is seen most in young-
to middle-aged, neutered, over-weight
cats, with restricted access to outside
and eating a dry diet. The most
common form of FLUTD, feline
idiopathic cystitis (FIC), seems to
directly relate to stress and an alteration
in the affected cat’s nervous system and
inputs to and from the bladder.
As previously recognised, these cats
will often be living in a multi-cat
household and it is interesting to note
that the cat’s stress level may not be
directly proportional to the number of
cats in the house per se, but rather how
many groups of cats there are (a group
being identified by observing its
members sleeping together, grooming
each other and sharing resources such as
food, water, litter trays, resting and
hiding places).
In managing these cases, the owner
will need one set of resources per
group, rather than per cat (unless, of
course, each group consists of just one
cat).
The cat’s individual response to
stress is determined in part by genetics
and part environment. The phrase,
which seems to be increasingly
applicable to many diseases these days,
is that clinical disease results when there
is a combination of a “sensitive
individual in a provocative
environment”.
Cats which develop FIC tend to
respond differently to stress and show exaggerated arousal. Their experiences
in utero and during kittenhood may also
be important. Often they will be living
in a chronically stressful environment
and one to which they have been unable
to adapt – classically living with another
cat they don’t like.
These cats lack cortisol and are
unable to cope in the normal way
(interestingly, black and white cats appear predisposed, but
gingers remain
nonchalant!). Rather
than hiss or show
typical fight or flight
responses, they show
displacement activities
when stressed and
often stereotypical
behaviour, such as
increased eating,
drinking, grooming or
urination. Some may
just freeze. But owners
of susceptible cats may
be able to spot
impending FIC episodes by observing
early stereotypical changes in their cat’s behaviour.
Excessive grooming of their tummy – often attributed to fleas – may in
these cats be an early marker of pain,
becoming evident before haematuria or
dysuria is seen.
Stretched pockets
Looking at a commonly discussed
subject from a different perspective
also allows insights to surface. Anke
Hendrick’s lecture, “The chronically
itchy dog owned by the financially
challenged client – what are the
options?”, hit to the heart of a very
common dilemma in practice.
In this era of financial austerity,
how can we ensure that we don’t
sacrifice good clinical practice? Anke
gave some clear advice to help avoid
costly inappropriate investigations and
highlighted where cost savings could be
made in the treatment of certain
conditions.
She made the point very clearly
early on that to successfully treat the
chronically itchy patient, a diagnosis
should always be sought. This doesn’t
always need to involve lengthy trial
treatment or a myriad of expensive
blood tests or biopsies.
Rather, she recommended stepping
back and carefully prioritising the
differential diagnoses and giving
thought to what is most likely in this
particular case. Take into account the
pattern, change and progression of the
pruritus and response to previous
treatment, along with assessment of
the lesion type and its distribution.
Common things are common; most
pruritic skin disease will be the result
of superficial inflammatory disease,
with ectoparasitic disease, microbial
infections or overgrowth, and
hypersensitivity disorders (namely flea
bite hypersensitivity, atopic dermatitis
and dietary hypersensitivity) seen most
commonly.
Don’t forget, however, that a
combination of causal factors is
frequently seen, and if you find one
factor, don’t stop there. It’s important
to rule out or control any parasitic
disease and/or microbial infection early
on, as these make assessment of any
other underlying disease more difficult.
For parasitic disease, using the very
effective products we have available to
us is a wiser use of the owner’s money
than using cheaper, less effective
products.
For microbial disease, where money
is a concern, there is no evidence to
show that a superficial pyoderma will
respond any better to a
combination of
systemic and topical
treatment than to
systemic treatment
alone.
Once under control,
if there is a risk of
recurrence, following up
systemic treatment
immediately with a
topical on-going
treatment may help to
limit costly flare-ups.
She discussed the hypothesis of
“summation of effects” (where
different pruritogenic stimuli can add
together to give an overall level of
pruritus) and the concept of the
pruritic threshold (where an individual
only starts to show pruritus once its
own threshold has been reached).
Taking one or two factors out of
the equation can mean that an
individual might drop below its pruritic
threshold and you may not have to
treat or address every problem. For
example, a dog with atopic dermatitis
compounded by a staphylococcal or
malassezia overgrowth might not need
any treatment once these secondary
pruritic factors have been brought
under control.
Looking deeper
David Church’s lecture on “The
complicated diabetic – what are the
options?” was a goldmine of useful
information and tips on managing these
often frustrating cases and he
highlighted common factors causing
difficulties with diabetic control.
He categorised these complicated
diabetics into two situations: one where
the insulin appeared not to work, and a
second where the animals were
presenting with inappetance, vomiting
and depression and were severely unwell
as a result of their diabetes (most
commonly ketoacidosis).
A typical scenario of the former
situation was where, despite increasing
insulin doses, there was a minimal
response and persistent hyperglycaemia.
Typically this is the result of insulin
resistance caused by concurrent disease
which he categorised into non-
endocrine (for example, renal failure,
urinary tract infections or heart disease) and endocrine disorders.
If a dog has both diabetes mellitus and
hyperadrenocorticism, the
latter will manifest itself
through lack of response
to insulin (where the
cortisol interferes with
insulin action) long before
typical cushingoid signs
are seen.
Acromegaly in cats is
also now thought to be
much more common than previously thought, with the RVC
diagnosing the condition in about 25-
30% of the diabetic cats tested there.
The classical presentation of the fat-
headed cat with the thick tongue
presents in less than 10% of cases and
most will look like normal cats. Typically
they will be difficult to manage diabetics
who are passionately hungry.
Knowing about any concurrent
disease allows us to suggest treatment,
of course, which may or may not work
in all cases (radiotherapy treatment for
acromegaly improves the diabetic
control in about 80% of cases), but
more importantly it helps us to manage
the client’s expectations, which these
days may be just as important as
anything we do clinically.
