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Eline Paediatric Medicine: Clinical Nutrition in Kittens
Eline Paediatric Medicine: Clinical Nutrition in Kittens
Eline Paediatric Medicine: Clinical Nutrition in Kittens
S U M M A R Y
This article aims to look at three important areas of kitten medicine; nutrition, investigation of the stunted
kitten and managing the collapsed kitten. The latter two scenarios are common reasons for presenting a kitten
for further veterinary advice and investigation.
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Figures in italics are per 100kcal of metabolisable energy; figures in brackets are % lactulose;
* - values are as fed according to manufacturers recommendations
Recipe 1 Recipe 2
Skimmed milk 70g One whole fresh egg 15g
Low fat curd (not cottage cheese) 15g Protein supplement* 25g
Lean minced beef 8g Milk, sweetened, condensed 17ml
Egg yolk 3g Corn oil 7ml
Vegetable oil 3g Water 250ml
Lactulose 0.8g
Vitamin/mineral mix 0.2g
Total 100g Total 310g
* Protein supplement used was ProBalance Feline (available via www.calvetsupply.com ) – analysis - 47% crude protein,
1% crude fibre and 17% crude fat. The supplement has essential vitamins and minerals, additional nutrients and digestive enzymes.
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Physiological state Energy requirements Weight of food required g/kg body weight*
(kcal / kg bodyweight) Canned diet Dry diet
< 3 months (growth) 250 * 190 60
3 - 6 months (growth) 130 * 100 30
6 - 12 months 80 (neutered) -100 (entire) ** 70-90 20-25
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Figure 3- Radiograph showing a marked reduction in bone density in a kitten with nutritional secondary hyperparathyroidism associated
with feeding an exclusive lean chicken diet.
Liver
Liver contains excessively high levels of vitamin A leading to
painful bone deformities which do not resolve even if the diet
is corrected (Figure 4).
Milk products
Cats generally do love milk but they may lack the enzymes to
digest it resulting in large quantities of fermentable sugars
reaching the colon leading to osmotic diarrhoea.
N.B. Milk is a balanced diet; calcium is NOT in excess hence milk
can not be used to balance diets which have excessive
phosphorus such as an all meat diet.
Fish
Raw fish can contain thiaminase which destroys vitamin B1
(thiamine) as well as potentially containing parasites.
Excessive amounts of fish can cause a relative deficiency of
vitamin E especially if the fish is packed in oil.
Fish that has been improperly preserved or inadequately
refrigerated, particularly the tuna and mackerel family, can
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KIT STURGESS EJCAP - Vol. 16 - Issue 1 - April 2006
INVESTIGATION OF THE
STUNTED KITTEN
Kittens are frequently presented to veterinary surgeons because
they are poorly grown (Figure 5). Based on the DAMNIT-V
system, the most likely causes of stunted growth are highlighted.
D Degenerative; developmental, demented (psychological)
A Anomaly (congenital); allergic, autoimmune
M Metabolic
N Neoplastic, nutritional
I Infectious; inflammatory; idiopathic; immune mediated;
iatrogenic
T Traumatic, toxicity
V Vascular Figure 6 – An under grown kitten with an abscess on its head
secondary to feline infectious peritonitis.
Causes
Abnormality of bone growth
– Chondrodystrophy
Deficient nutrient intake
– Inadequate or inappropriate diet
– Gastrointestinal parasitism
– Persistent vomiting or regurgitation e.g. vascular ring anomaly
– Maldigestion / malabsorption
Increased caloric demand
– Fever
– Chronic infectious or inflammatory disease (Figure 6)
– Major trauma
– Increased caloric loss
– Protein losing enteropathy
– Protein losing nephropathy Figure 7 – Six month old male, Havana kitten weighing less
– Urine nutrient loss e.g. juvenile onset diabetes mellitus, renal 1.7kg and showing neurological signs associated with a
glycosuria portosystemic shunt.
Major organ defect
– Hepatic - portosystemic shunt, glycogen storage disease
(Figure 7)
– Renal - dysplasia, pyelonephritis
– Congenital cardiac anomaly
– Lysosomal storage disease
– Endocrinopathy
– Hypothyroidism (Figure 8)
– Hyposomatotrophism
Key history
– Did the queen have a normal, pregnancy and parturition?
– When was the problem first noticed?
– Has the kitten been slow and poorly grown since birth? Figure 8 – Hypothyroidism causing severe reduction in growth
Suggests a congenital defect. rate and skeletal malformation.
– Was the kitten showing normal development (i.e.
indistinguishable from the other members of the litter) and Physical examination
then suddenly stopped? Suggests an acquired disease. Examination of kittens can be difficult as they rarely stay still and
– Are any other members of the litter similarly affected? can be aggressive if from a feral background. Neonates tend to
– Have kittens in previous litters shown similar signs? show limited responses to disease, initially becoming agitated
– What is the kitten’s diet, appetite and food intake? and crying, progressing to inactivity, hypothermia and loss of the
– Are there signs, other than failure to grow, that indicates suckling reflex. As with all young animals, changes in their status
major organ disease? can be very rapid. Weight gain can be a sensitive indicator of
– Is the kitten’s body proportionate or disproportionate? developing problems and can be easily measured by the owner
– Is the kitten’s body condition good or poor? (Figure 9). Failure to gain weight over any 24 hour period is
worthy of further investigation.
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FCK
Weight (grams)
Age (days)
Figure 9 – Growth curves for a litter of kittens, one kitten’s growth rate began to slow.
A few days later this kitten developed a flat chest (Figure 12).
Thorax
– Shape of thorax - flat chest (Figure 12), pectus excavatum
– Heart rate around 200-220 beats per minute.
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Figure 11 – Cleft palate. Figure 12 – Flat-chested kitten – this condition develops shortly after birth and particularly
affects Burmese kittens.
Table 5 – Characteristics of innocent cardiac murmurs and murmurs associated with congenital heart disease
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Feline paediatric medicine
Parameter
Kitten age (weeks) 2 4 7-12
Total protein (g/l) 40-52 46-52 51-57
Albumin (g/l) 20-24 22-24 24-32
Sodium (mmol/l) - 149-153 147-152
Potassium (mmol/l) - 4.0-4.8 5.0-6.2
Chloride (mmol/l) - 120-124 113-128
Inorganic phosphate (mmol/l) - 2.0-2.4 2.5-3.1
Calcium (mmol/l) - 2.4-3.2 2.2-2.8
Urea (mmol/l) <5 <5 4.2-6.3
Creatinine (µmol/l) - 36-54 36-91
Cholesterol (mmol/l) 4.3-11.6 4.6-11.4 -
ALK-P (U/l) 68-269 90-135 -
ALT(U/l) 11-24 14-26 -
Glucose (mmol/l) 6.08-10.32 7.92-8.96 -
Bilirubin (µmol/l) 1.7-16.9 1.7-3.4 -
Bile acids (µmol/l) <10 <10 -
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Figure 13 – An under grown kitten with skeletal abnormalities Figure 14 – Jugular venipuncture in a week old kitten.
associated with a lysosomal storage disease.
– Many infectious diseases develop too rapidly to obtain results a lengthening of the interval between doses.
quickly enough (especially bacterial culture and sensitivity or – Great care should be taken when administering broad-
paired serum samples) to be of value to that individual but spectrum antimicrobials orally because of their potentially
a knowledge of cause may be beneficial to the rest of the litter adverse effects on the developing gut microflora.
or subsequent litters. – Subcutaneous and intramuscular absorption of drugs is slower
– To minimise the amount of blood required, glucose can be and less reliable than in adults particularly if the kitten is
estimated on a glucometer and 0.5ml EDTA tubes used dehydrated.
making a total bleed of 1.5ml in the smallest of kittens – Antimicrobials administered to the dam do not reach
sufficient for most tests to be carried out. therapeutic concentrations in the milk.
– Ensuring adequate nutritional support either by naso-
Blood volume in cats is estimated at 75ml/kg. A week-old oesophageal or gastric intubation is a vital part of therapy
kitten will weigh around 200g and have 15ml of blood particularly in the face of sepsis.
Drugs
– Absorption, distribution, metabolism and excretion of drugs
can be significantly different from adults.
– Few drugs have had dose rates calculated for use in young
kittens.
– Generally, an increase in the initial dose (/kg) is required with
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CONCLUSIONS
Kitten medicine is a truly challenging but very rewarding area
for the veterinarian. The small size of the patient, speed with
which they deteriorate and lack of localising clinical signs makes
investigation and treatment difficult. The value of success,
however, is great in the hope that your patient will survive and
enjoy the next 15 year or so of life.
ACKNOWLEDGMENTS
Professor T.J. Gruffydd-Jones for Figures 8 and 11
Dr D. Gunn-Moore for Figures 6 and 13
Mrs R. Giles for Figure 1
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