Geriatric Feline Medicine

After the usual introductions, descriptions of revision related snacks and beverages and what other revision topics they are trying to escape, we cracked on with the cats:

So, let’s start with a biiiig differentials list!

All good suggestions, now let’s try and rationalise these thoughts

So let’s start with inappetance:

And more specifically, CAN’T eat

Followed by WON’T

And excellent point that it is a cat, and they like to be as difficult as possible…

Now we can start to think more specifically about GI causes of inappetance

http://twitter.com/ClaireVRoberts/status/340155065526542336

So a nice long list of GI differentials for the inappetant cat that is losing weight. Now let’s prioritise:

Now Dylan has been nagged to use the #vetfinals he is straight on in with the right answer!

Cats like to do things in style, so why bother getting one disease when you can have a handy package of three? However, they can exist as separate conditions:

Now we’ve covered the GI differentials and had a more thorough think about our causes, let’s go back to our initial list and have a re-think:

What about hyperthyroidism?

The other presenting sign in this case was weight loss – we need some differentials for this as well:

So weight loss occurs because:
1. We are not getting enough in or not absorbing correctly
2. We have an increased energy requirement
3. We are losing too much

So why might energy requirements be increased in a geriatric cat?

Now we have lots of nicely thought through differentials, we can start thinking more about the particular case in question

Let’s take a history!

The results of our questioning…

‘Never any good at this’… Unless they are a proper crazy cat lady who has been weighing her darling kitty daily and trying to tempt it with seventeen types of cat food a week (but then it would have been presented the second it started looking a teensy bit peaky, rather than with a 2mo history…)

Ideas please!

Let’s think about our urine sample then:

And what must always come with a urine sample??

Excellent Y4 Urinary teaching there – we do remember something!!

We have blood… We have urine…

What else can we do with our urine sample?

What will we be looking for on our dipstick?

And what about our bloods?

Time for results…

Proteinuria – why might we have this?

Going back to our history…

Cat’s can’t read… 5 years at vet school have taught us something…

Summary note: bloodwork and complications with CRF

Clinical pathology

Azotemia – increased BUN
Increased creatinine
Increased phosphate
Normal calcium

Non-regenerative
anaemia

+/- hypokalemia
– Due to reduced intake, leads to myopathies and cervical ventroflexion (drooping cats!)

 

Hypertension

Target organs are the kidney, eye, brain and heart – any increase in blood pressure risks end-organ damage!

Measuring in the conscious patient with non-invasive Doppler

Normal: <150mmHg

– Low: 150-160mmHg
– Moderate: 160-180mmHg

– High: >180mmHg

>200mmHg – treat even if
showing no clinical signs!


Renal secondary hyperparathyroidism

Reduced active
vitamin D production in the damaged kidney

Compromised
phosphate excretion

High phosphate binds
calcium

PTH secreted to
maintain levels of calcium

Increased risk of:

– Calcification of soft tissues

– Deterioration of clinical
signs – PTH renotoxic in excess

– Hyperphosphataemia
further inhibits vitamin D

So, we’ve stabilised our cat, what are we going to do with it now?

She’s mentioned staging… Now I could write lots of notes about this, or just give you the website from which the lovely IRIS people have linked a full description, staging posters and quick note flashcards – staging for everyone! Spoilt vet students…
 http://www.iris-kidney.com/guidelines/en/staging_ckd.shtml 

Quick note on benazepril and hypertension, Rach is due in the pub… (how to make the entire of final year VERY jealous…)

Summary note: treatment of chronic renal failure

If a patient definitely has CRF:

You have checked the
azotemia is renal in origin and the history and clinical exam etc fits with CRF

1. Stabilise it
2. Check the creatinine again
3. IRIS stage it
4. Sub-stage it
5. Treatment, management,
prognosis
6. Monitor!

 

Remember, if an animal is presented already in CRF then:

– Disease is advanced

– Disease will
progress (stage II onwards)

– Underlying cause is
often unknown

So, we need to:
– Maximise quality of
life

– Manage owner
expectations

– Majority of care is
at home

 

Treatment aims

Can we stabilise the
animal?

How advanced is the
disease?

Treat the cause
where possible

Slow disease down –
renoprotective

Support the animal –
symptomatic treatment

 

Treat early in the
course of disease

Once stabilised,
stage the disease (IRIS I-IV)

Stage I or II: treat
the underlying cause, rarely possible

Stage II – IV:
renoprotective therapies (slowing down progression of the disease and improving
the prognosis)

Stage IV:
symptomatic therapies

 

Aims

Decrease blood urea
and clinical signs associated with uraemia – azotemia makes the patient feel
ill

Maintain hydration –
maintain flow through kidney

Decrease glomerular
pressure – prevents damage

Control systemic
blood pressure – predisposes to high glomerular pressure

Reduce proteinuria –
poor prognostic indicator

Control phosphate
and PTH levels – cannot be excreted leading to secondary hyperparathyroidism

Maintain PCV – may
be anaemic

Stabilisation
Istin

Drops BP by 40mmHg – 1st choice for hypertension

Correct metabolic disturbances

Hyperphosphataemia – diet

Acid-base – fluids

Electrolytes

Manage renal hyperphosphatemia

Diet – improves survival

Monitor

Phosphate binders if won’t eat diet/or not working

 

Reverse hypokalemia

Hartmann’s if producing urine

Potassium to fluids – maintenance and deficiency

Can be a cause of inappetance

Adjunct therapy

Gastric protectants e.g. sucralfate

– Often have a concurrent GI problem e.g. vomiting, ulceration
– May need only short term as they can resolve the GI problems once the kidneys are sorted

H2 antagonists e.g. ranitidine, famotidine

Proton pump inhibitors e.g. omeprazole

Anti-emetics

Assisted nutrition (NOT hand-feeding or syringe feeding as can develop food aversion)

– Oesophagostomy tubes
– Nasoesophageal tubes
– PEG tubes

 
Management

Diets

Renal diets improve
prognosis

Ensure adequate
fluid intake – usually mildly dehydrated

Ensure adequate
energy intake – skinny

Low
protein/phosphorous/sodium so less for the kidneys to do

– Protein – reduce nitrogenous
wastes

– Phosphorous – prevent
nutritional secondary hyperparathyroidism
– Sodium – BP control

High potassium/B
vitamins/fatty acids

– Potassium not conserved
– B vits soluble and lost in
urine
– FAs – calories and
palatability

Used if proteinuric
in stage I, renoprotective in
stage II-early III, symptomatic therapy
in late III-IV

Change slowly

 

Benazepril (Fortekor)

Prevents conversion
of angiotensin I into angiotensin II (an ACE inhibitor)

Dilute afferent arteriole

-> Decrease glomerular pressure
->  Decrease proteinuria
-> Decreases angiotensin and
aldosterone (may decrease fibrosis)
Limited effects on systemic
BP – second choice drug for hypertension
– Drop by 10mmHg – want 40mmHg
drop
Reduced renal degeneration

Only use when stable or
can go azotemic

Monitor creatinine –
initially decreased GFR so increases creatinine, then return to normal

 

Other considerations

Anaemia

Mild and
non-regenerative, normocytic, normochromic anaemia

If kidneys are
hypoxic then treat with EPO

– Max. 4 doses – good effect on
red cells
– Eventually develop antibodies
– kills off EPO and PCV drops dramatically

 

Hyperthyroidism

Mild high BP may be
supporting the kidneys in a hyperthyroid cat

Kidney problem revealed on
thyroid meds

– Clinical CRF as GFR decreases

 

Prognosis

Depends on:

– Stage of disease
– The animal
– Owner’s finance

And a little photo to cheer you all up and celebrate making it to the end of another #vetfinals session:

Next week is more cows with Wendela, Tuesday 4th June at 8pm – see you then!