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JAVMA, Vol 241, No. 4, August 15, 2012 Scientific Reports 477
SMALL ANIMALS
An 8-month-old sexually intact male Saint Bernard was
evaluated at the surgical service of the Tufts Cummings
School of Veterinary Medicine Foster Hospital for Small
Animals because of bilateral osteochondritis dissecans of
the shoulder joints following a 2-month history of bilateral
forelimb lameness. The dog was acquired from a breeder
at 11 weeks of age, at which time it had diarrhea and was
eating a chicken-based adult dry dog food (3/4 cup, q 8 h).a
The owners were unaware of whether the dog had diarrhea
before they acquired it. The diarrhea continued for 7 days
after arriving at the new owners’ home, at which time the
owners began feeding the dog a homemade cooked ham-
burger and rice diet (diet proportions consisted of 2 lb of
ground hamburger and 1 1/2 cups of white rice, q 8 h).
The dog was also dewormed during the first 7 days of liv-
ing with the owners. The dog’s diarrhea resolved within 3
days after changing the diet, and the owner interpreted this
improvement to mean that the dog had a food allergy (pre-
sumably to chicken) and decided to continue the home-
made diet. After feeding the homemade diet for 7 days,
the owners chose to provide dietary supplementation with
a commercial product for dogs.b In an effort to make the
homemade diet more complete, some human foods and
Seizures and severe nutrient deficiencies
in a puppy fed a homemade diet
Dana Hutchinson, dvm, dacvn; Lisa M. Freeman, dvm, phd, dacvn; Robert McCarthy, dvm, ms, dacvs;
John Anastasio, dvm; Scott P. Shaw, dvm, dacvecc; James Sutherland-Smith, bvsc, dacvr
Case Description—An 8-month-old male Saint Bernard developed tetanic seizures and hyper-
thermia during evaluation of bilateral osteochondritis dissecans of the shoulder joints. Further
investigation revealed that the dog was receiving an unbalanced homemade diet.
Clinical Findings—Preliminary evaluation of the dog revealed bilateral signs of pain and
mild muscle wasting in the shoulder joint areas. Serum biochemical analysis revealed se-
vere hypocalcemia, hyponatremia, hypochloremia, hyperphosphatemia, vitamin D deficien-
cy, and taurine deficiency. Diffuse osteopenia was identified on radiographs of the mandible
and long bones, confirming bone demineralization. Analysis of the homemade diet revealed
that the dog’s diet was severely deficient in a variety of nutrients.
Treatment and Outcome—The dog responded positively to treatment for hypocalcemia,
hyperthermia, and seizures. The dog’s diet was changed to a complete and balanced canine
diet formulated for growth. Body weight and body condition were monitored, and dietary
intake was adjusted to achieve optimal body condition during growth. After initial evaluation,
serial monitoring of serum calcium and taurine concentrations revealed that values were
within reference limits and the dog had no further clinical signs associated with dietary
deficiency.
Clinical Relevance—Findings in this puppy highlight the risks associated with feeding an
unbalanced homemade diet during growth and the importance of obtaining a thorough
dietary history from all patients. For owners who elect to feed a homemade diet, it is
critical to have the homemade diet carefully formulated by a veterinary nutritionist to avoid
severe nutrient imbalances, especially in young, growing dogs. (J Am Vet Med Assoc
2012;241:477–483)
a small amount of the chicken-based adult dry dog food
were added (Table 1). Whenever the owner attempted to
increase the small amount of the chicken-based adult dry
dog food incorporated into the homemade diet, the dog
reportedly had recurrence of diarrhea.
This diet was fed for 5 months prior to the initial
evaluation at the authors’ hospital. During this time, the
dog was seen by the referring veterinarian for vaccina-
tions and deworming and was assessed to be in good body
condition. No further diarrhea occurred following initia-
tion of the homemade diet and deworming. At 7 months
of age, the dog was evaluated by the referring veterinar-
ian because of bilateral forelimb lameness with signs of
pain localized to the shoulder joint region. Findings on
radiographs of the shoulder joints were consistent with
bilateral osteochondritis dissecans of the shoulder joints.
Subchondral bone flattening of the caudal portion of the
humeral head was evident in both shoulder joints. Osteo-
penia was not detected on these radiographs (Figure 1).
The referring veterinarian prescribed oral administration
of an NSAID as needed until the dog could be evaluated at
the authors’ hospital.
From the Department of Clinical Sciences, Cummings School of Veterinar y
Medicine, Tufts University, North Grafton, MA 01536. Dr. Hutchinson’s
present address is Hill’s Pet Nutriton, 41 Hay St, Newbury, MA 01951.
Dr. Hutchinson’s residency program was supported by Nestlé Purina PetCare.
The authors thank Dr. Scott Osgood for providing radiographic images.
Address correspondence to Dr. Freeman (lisa.freeman@tufts.edu).
Abbreviations
AAFCO Association of American Feed Control Officials
BCS Body condition score
iPTH Intact parathyroid hormone
NRC National Research Council
478 Scientific Reports JAVMA, Vol 241, No. 4, August 15, 2012
SMALL ANIMALS
On referral, the dog had bilateral forelimb lame-
ness with signs of shoulder joint pain, a BCS of 4 of 9,1
mild generalized muscle wasting, and a body weight of
44 kg (96.8 lb). No other abnormalities were noted on
physical examination, but following the initial exami-
nation, the dog developed focal tremors that progressed
to focal seizures. The dog became tachycardic (220
beats/min) and hyperthermic (39.4°C [103°F]) and was
taken to the intensive care unit, where diazepam (0.5
mg/kg [0.23 mg/lb], IV, once), oxygen via a face mask,
and lactated Ringer’s solution (22.7 mL/kg [10.3 mL/
lb], IV bolus, once) were administered.
Initial biochemical analysis revealed several elec-
trolyte abnormalities, including respiratory alkalo-
sis without compensation (venous pH, 7.5 [reference
range, 7.33 to 7.47]; bicarbonate concentration, 24.5
mmol/L [reference range, 18 to 24 mmol/L]; and car-
bon dioxide concentration, 26 mEq/L [reference range,
Ingredient Amount consumed/d
Beef, ground, 90% lean meat/10% fat (pan cooked without added fat) 2 lb
White long-grain rice (boiled) 1.5 cups
Raw apple with skin 0.5 medium-sized apple
Broccoli (boiled without added fat) 0.33 cups
Chicken-based adult dry dog fooda 0.33 cups
Whole raw egg (with shell) 0.43 egg (fed 3 times/wk)
Dietary supplementb 0.5 of manufacturer’s scoop
Dry matter, 4,099.3 kcal/kg. Moisture, 64.4%. Proportions of metabolizable energy from protein, 38.78%;
metabolizable energy from carbohydrates, 18.04%; and metabolizable energy from fat, 43.19%.
Table 1—Diet composition of a homemade diet fed to a Saint Bernard puppy from 11 weeks of age
until 8 months of age.
Figure 1—Lateral radiographic views of the left shoulder joint (A) and left elbow joint (B) of a 7-month-old male Saint Bernard. Sub-
chondral bone flattening of the caudal portion of the humeral head is present (white arrow), which is consistent with osteochondritis
dissecans of the shoulder joint. Although diffuse osteopenia was not detected, there is a mild diffuse reduction in cortical opacity and
a double cortical line is present along the cranial border of the radius (white arrows).
JAVMA, Vol 241, No. 4, August 15, 2012 Scientific Reports 479
SMALL ANIMALS
14 to 28 mEq/L]), hypocalcemia (total calcium concen-
tration, 7.7 mg/dL [reference range, 9.4 to 11.8 mg/dL];
ionized calcium concentration, 0.8 mmol/L [reference
range, 1.2 to 1.4 mmol/L]), hyponatremia (137 mEq/L;
reference range, 140 to 150 mEq/L), hypochloremia
(90 mEq/L; reference range, 106 to 116 mEq/L), hyper-
phosphatemia (7.9 mg/dL; reference range, 2.6 to 7.2
mg/dL), hyperalbuminemia (4.4 g/dL; reference range,
2.8 to 4.0 g/dL), hypoglobulinemia (2.0 g/dL; reference
range, 2.3 to 4.2 g/dL), high alkaline phosphatase activ-
ity (181 U/L; reference range, 12 to 127 U/L), and high
creatine kinase activity (453 U/L; reference range, 22
to 422 U/L). Serum magnesium concentration was 1.8
mEq/L (reference range, 1.8 to 2.6 mEq/L), and potassi-
um concentration was 3.8 mEq/L (reference range, 3.7
to 5.4 mEq/L). Findings on CBC were within reference
limits. The dog’s severe hypocalcemia was suspected to
be the cause of the seizures, and a bolus of 10% calcium
gluconate (45.5 mg/kg [20.7 mg/lb], IV) was adminis-
tered over several minutes.
During the initial management of the seizures,
the dog became cyanotic and its body temperature
increased to 42.2°C (108°F). An additional bolus of
calcium gluconate (68.2 mg/kg [31.0 mg/lb], IV) was
administered over several minutes, and the dog was
also treated with propofol (4.6 mg/kg [2.1 mg/lb],
IV). Systolic arterial blood pressure ranged from 75 to
90 mm Hg. The dog was then intubated, and cold water
gastric lavage was performed. Calcium gluconate (18
mg/kg/h [8.2 mg/lb/h], IV), diazepam (0.3 mg/kg/h [0.1
mg/lb/h], IV), and lactated Ringer’s solution (2.5 mL/
kg/h [1.1 mL/lb/h], IV) were also initiated as constant
rate infusions. The dog remained intubated, and anes-
thesia was maintained with 3% isoflurane for an addi-
tional hour as body temperature decreased to 37.8°C
(100°F). Systolic arterial blood pressure returned to
110 mm Hg after intubation. Inhalation anesthesia was
then discontinued and the dog was extubated.
Point-of-care testing was used to measure clinico-
pathologic values at 2 hours and 6 hours after initial
evaluation. By 6 hours after admission, acid-base and
biochemical abnormalities seen at initial evaluation
had been corrected except for hypocalcemia (ionized
calcium concentration, 1.1 mmol/L; reference range,
1.2 to 1.4 mmol/L), hyponatremia (139.6 mmol/L;
reference range, 147 to 154 mmol/L), hypochloremia
(106 mmol/L; reference range, 109 to 120 mmol/L),
and hypokalemia (3.3 mmol/L; reference range, 3.8 to
4.9 mmol/L). For the remainder of the dog’s first day
of hospitalization, administration of calcium gluconate,
diazepam, and lactated Ringer solution was continued
and the dog remained in the intensive care unit.
To determine the cause for the dog’s severe hypocal-
cemia, which was thought to be due to either nutritional
secondary hyperparathyroidism or primary hypopara-
thyroidism, blood was collected for analysis of iPTH,
ionized calcium, and 25-hydroxyvitamin D concentra-
tions. In addition, a detailed dietary history was collected
from the owners and a computer analysis was performed
to compare the nutrients in the homemade diet with di-
etary requirements for growth in dogs.2,3 The diet had
multiple and substantial deficiencies, including calcium,
phosphorus, and vitamin D, all of which were < 50%
below minimum requirements set by the NRC3 as well
as the AAFCO (Table 2).2 Additional dietary deficien-
cies in sodium, chloride, iron, iodine, choline, copper,
folic acid, vitamin A, and linoleic acid were identified.
Although there are no established minimum dietary re-
quirements for taurine in dogs, blood was also collected
for analysis of serum and whole blood taurine concen-
trations because of the low amount of taurine in the
homemade diet and previous studies4–7 of dilated cardio-
myopathy associated with taurine deficiency that have
included Saint Bernards and other giant-breed dogs.
Intravenous administration of calcium gluconate
and lactated Ringer’s solution was continued until day
2 of hospitalization when the hypocalcemia resolved.
Serum ionized calcium concentration was 1.3 mmol/L.
Hyponatremia, hypochloremia, and hypokalemia also
resolved by day 2. Serum sodium, chloride, and potas-
sium concentrations were 142.6 mEq/L, 115 mmol/L,
and 3.8 mmol/L, respectively. Serum ionized calcium
concentrations were monitored to ensure serum cal-
cium concentrations remained stable as the IV admin-
istration of calcium gluconate was gradually reduced.
NRC AAFCO
minimum minimum Homemade
Nutrient/1,000 kcal requirement* requirement diet
Protein (g) 35 62.9 96.94
Arginine (g) 1.33 1.77 6.25
Histidine (g) 0.5 0.63 2.87
Isoleucine (g) 1.0 1.29 4.13
Leucine (g) 1.63 2.06 7.21
Lysine (g) 1.4 2.20 7.43
Methionine-cysteine (g) 1.05 1.51 3.28
Phenylalanine-tyrosine (g) 2.0 2.54 6.52
Threonine (g) 1.25 1.66 3.5
Tryptophan (g) 0.35 0.57 0.42
Valine (g) 1.13 1.37 4.62
Crude fat (g) 21.3 22.9 47.99
Linoleic acid (g) 3.0 2.9 1.78
Calcium (g) 2.0 2.9 0.79
Phosphorus (g) 2.5 2.3 1.13
Potassium (g) 1.1 1.7 1.66
Sodium (mg) 550 860 370
Chloride (mg) 720 1,290 10
Magnesium (mg) 45 110 170
Iron (mg) 18 23 13.22
Copper (mg) 2.7 2.1 0.68
Manganese (mg) 1.4 1.4 0.75
Zinc (mg) 10 34 22.65
Iodine (µg) 220 430 80
Selenium (µg) 52.5 30 90
Vitamin A 303 428.7 34.7
(retinol equivalents)
Vitamin D (µg) 2.75 3.57 0.02
Vitamin E (mg) 6.0 14 10.21
Thiamine (mg) 0.27 0.29 54.25
Riboflavin (mg) 1.05 0.63 3.19
Pantothenic acid (mg) 3.0 2.9 3.58
Niacin (mg) 3.4 3.3 23.98
Pyridoxine (mg) 0.3 0.29 2.35
Folic acid (µg) 54 50 0.17
Vitamin B12 (µg) 7 6 10
Choline (mg) 340 343 327.3
Taurine (g) 0.08† 0.25† 0.35
*Adequate intake reported for nutrients without published NRC
minimum requirements. †No dietary requirement established for
dogs; NRC and AAFCO allowances for feline extruded diets are pro-
vided for a point of reference.
Table 2—Comparison of the nutritional content of a homemade
diet fed to an 8-month-old puppy to the NRC3 and AAFCO2 di-
etary recommendations for growth in dogs.
480 Scientific Reports JAVMA, Vol 241, No. 4, August 15, 2012
SMALL ANIMALS
Oral administration of calcium carbonatec (56.8 mg/
kg [25.8 mg/lb], PO, q 6 h) was initiated as IV admin-
istration of calcium gluconate was being discontin-
ued. While awaiting results of determination of iPTH,
25-hydroxyvitamin D, and taurine concentrations,
administration of calcitriold (5.7 ng/kg [2.6 ng/lb], PO,
q 12 h) and taurinee (11.4 mg/kg [5.2 mg/lb], PO,
q 12 h) was initiated on the second day of hospital-
ization. Also on day 2, feeding with a commercial dietf
designed to meet the dietary requirements for growth
in dogs was initiated to achieve estimated resting en-
ergy requirements (1,196 kcal/d divided into 4 meals
[ie, approx two-thirds of a can {306 kcal}, q 6 h]) until
the most appropriate long-term diet was established.8
Although calorie requirements were likely higher be-
cause of the dog’s age, a conservative calorie estimate
was initially used during hospitalization to account for
the physical inactivity.
To assist in determining the cause for the hypo-
calcemia, radiographs of the forelimbs that had been
obtained by the referring veterinarian were reviewed.
Although osteopenia was not apparent radiographically
in the humerus or scapula, diffuse cortical thinning and
a double cortical line were present along the cranial as-
pect of the radial cortex in the lateral view. This latter
finding has been associated with osteopenia.9 Because
changes on the radiographs of the forelimb were subtle,
radiography of the mandible was performed to further
investigate the possibility of bone loss. The mandible
is known to undergo demineralization in other situa-
tions of altered calcium homeostasis, such as renal hy-
perparathyroidism, which can result in osteomalacia
marked by softening and degenerative changes of the
jaw and facial skeleton (ie, rubber jaw).10 Radiographic
findings of the mandible were consistent with diffuse
osteopenia (Figure 2). Radiographic features included
decreased mandibular corticomedullary distinction, a
partial loss of visualization of the lamina dura around
the tooth roots, and only faint mineralization of the hy-
oid bones.
The dog was discharged from the hospital on day 3.
Because of the owner’s continued concerns that the dog
had a food allergy to chicken, the owner was instructed
to feed a fish-based commercial dietg that met the mini-
mum requirements of the AAFCO for growth in dogs.
Because the dog was in good body condition, the pre-
vious intake of homemade diet was used as a starting
point for calorie requirements (2,080 kcal/d); therefore,
an initial recommendation of 5.25 cups/d of the com-
mercial diet was made (divided into 2 meals). The owner
also was instructed to feed no added human or pet foods,
supplements, or treats other than a controlled number
of specific hydrolyzed dog biscuits.h In addition, only
unflavored heartworm preventative and toothpaste were
recommended because flavored heartworm and tooth-
paste can contain chicken, beef, or pork. While await-
ing results of iPTH, 25-hydroxyvitamin D, and taurine
testing, the administration of calcitriol (5.7 ng/kg, PO,
q 12 h), taurine (11.4 mg/kg, PO, q 12 h), and calcium
carbonate (56.8 mg/kg, PO, q 6 h) was to be continued.
Ionized calcium concentrations were reassessed 3
days after hospital discharge and were within reference
limits (1.4 mmol/L; reference range, 1.2 to 1.4 mmol/L);
therefore, calcium gluconate and calcitriol administra-
tion were discontinued. Results for determination of
iPTH, 25-hydroxyvitamin D, and taurine were available
at this time: iPTH concentration was within reference
range (1.8 pmol/L; reference range, 0.5 to 5.0 pmol/L),
but 25-hydroxyvitamin D concentration was low (18
nmol; reference range, 60 to 215 nmol), supporting a
diagnosis of vitamin D deficiency and nutritional sec-
ondary hyperparathyroidism. In addition, whole blood
(160 nmol/mL; reference range, 200 to 350 nmol/mL)
and plasma (29 nmol/mL; reference range, 60 to 120
nmol/mL) taurine concentrations were low, supporting
a diagnosis of taurine deficiency.
An echocardiogram was performed
2 weeks after hospital discharge; contrac-
tile function and cardiac chamber size
were within reference limits. Although
taurine intake from the recommended
fish-based commercial diet was 1,087
mg taurine/d, dietary supplementation
with taurine (11.4 mg/kg, PO, q 12 h)
was continued until serum taurine con-
centrations could be reassessed 4 weeks
after hospital discharge.
The dog was weighed once weekly
on the same scale and assessed for BCS,
and the amount of food was adjusted to
ensure a lean BCS (ie, 4/9) and optimal
growth. All clinicopathologic values at 2
and 4 weeks following hospital discharge
were within reference limits, including
serum ionized calcium concentrations.
Whole blood taurine concentration was
reassessed 4 weeks after hospital dis-
charge and had increased to 408 nmol/
mL (reference range, 200 to 350 nmol/
mL). As a result, dietary supplementation
with taurine was discontinued. The dog’s
Figure 2—Right lateral radiographic view of the mandible and maxilla of the same
puppy as in Figure 1; images were obtained 4 weeks later than those in Figure 1.
There is decreased mandibular corticomedullary distinction (white arrows), a partial
loss of visualization of the lamina dura around the tooth roots (white arrowheads),
and only faint mineralization of the hyoid bones (black arrow). These changes are
consistent with osteopenia.
JAVMA, Vol 241, No. 4, August 15, 2012 Scientific Reports 481
SMALL ANIMALS
initial mild bilateral forelimb lameness had resolved dur-
ing the weeks following hospital discharge; therefore, no
further diagnostic testing or treatment was pursued by
the owner for this problem.
Discussion
The homemade diet fed to this growing giant-breed
dog resulted in multiple and severe nutrient deficien-
cies. Of initial primary concern was the severe hypocal-
cemia resulting in seizures (with resultant hyperther-
mia and metabolic abnormalities). Calcium plays an
important role in stabilizing sodium channels on axons
of nerves and preventing muscle tetany. This role ex-
plains why the patient developed muscle tremors and
eventual seizures because of severe hypocalcemia.11
Although hypocalcemia was the most likely cause
of the seizures, other causes of seizures were initially
considered, such as idiopathic epilepsy, toxins, or head
trauma. However, the severe hypocalcemia quickly nar-
rowed the differential diagnoses to nutritional second-
ary hyperparathyroidism or primary hypoparathyroid-
ism. In this case, a complete dietary history was key to
aiding the clinicians because a homemade diet of this
composition (ie, meat and rice) is known to have im-
portant nutrient deficiencies. The diagnosis of primary
hypoparathyroidism was later excluded when an iPTH
concentration within reference range was detected. Al-
though the dog had been compensating for very low
blood calcium concentrations for some time at home, a
possible cause for acute seizures at our hospital could
be respiratory alkalosis from panting, which decreased
the dog’s already low blood calcium concentration be-
low the critical threshold, resulting in seizures.12
Many of the physical and clinicopathologic abnor-
malities found at the time of admission were likely the
result of the seizures. The initial acid-base abnormality
was respiratory alkalosis without compensation. How-
ever, as seizure activity progressed and lactic acidosis
developed, the dog’s acid-base status included mixed
respiratory alkalosis and metabolic acidosis. Hyperther-
mia and resulting mild dehydration were the most like-
ly cause of the dog’s high creatinine kinase activity, hy-
perphosphatemia, and hyperalbuminemia. Low serum
globulin concentration and high alkaline phosphatase
activity are likely explained by the dog’s age. The other
clinicopathologic abnormalities can be attributed to
nutrient deficiencies of the homemade diet, including
the determination of hyponatremia, hypochloremia,
and hypocalcemia.
Dogs typically compensate for low amounts of
calcium in the diet through integrated actions of para-
thyroid hormone, vitamin D, and calcitonin. The se-
vere hypocalcemia and radiographically evident bone
changes were likely a result of the low dietary amounts
of calcium, vitamin D, and phosphorus and the calci-
um-to-phosphorus ratio of the diet (0.7). The low di-
etary amount of calcium was particularly deleterious in
this young dog because calcium requirement is highest
during growth. This dog was eating only 27% of the
AAFCO minimum requirements for calcium for growth
in dogs, although results of previous studies2,13,14 sug-
gest that large-breed puppies are even more susceptible
to harmful effects of low-calcium diets during growth
than are puppies of smaller breeds.
Nutritional secondary hyperparathyroidism typi-
cally arises from low dietary amounts of calcium and
low or recommended dietary amounts of phosphorus.
Although serum calcium concentrations are initially
maintained in nutritional secondary hyperparathyroid-
ism, hypocalcemia can develop once calcium is de-
pleted from bone. Parathyroid hormone is released in
response to the low blood ionized calcium concentra-
tions, causing bone resorption and increased produc-
tion of calcitriol from the kidneys. As a result, a high
serum iPTH concentration would be expected in nu-
tritional secondary hyperparathyroidism but was not
seen in this dog, possibly due to IV administration of
calcium gluconate prior to collection of blood samples
for determination of iPTH concentration. The half-life
of parathyroid hormone is < 30 minutes in people and
decreases in response to calcium administration.11 Also
in nutritional secondary hyperparathyroidism, serum
phosphorus concentration is usually low or within ref-
erence limits but was mildly high at initial analysis in
the dog of the present report. Serum phosphorus con-
centration did return to within reference limits on day 3
of hospitalization. Conversely, vitamin D concentration
is typically high in nutritional secondary hyperparathy-
roidism but was low in the dog of the present report,
possibly due to the concurrent severe dietary deficiency
of vitamin D. Another possible cause for the low serum
vitamin D concentration is severe intestinal disease
resulting in malabsorption of nutrients, although this
puppy had no gastrointestinal signs for several months
prior to referral. Because vitamin D is involved in cal-
cium absorption in the gastrointestinal tract, signs of
vitamin D deficiency overlap with those of calcium and
phosphorus deficiency, including slowed growth, de-
fective skeletal mineralization, pathological fractures,
and, rarely, type I vitamin D–dependent rickets.15,16
Typically, severe chronic calcium deficiency results
in diffuse osteopenia that is radiographically evident. In
a recent report,17 diffuse osteopenia involving the ver-
tebral column, mandible, and scapula was described in
a puppy fed a homemade premix and raw beef diet. In
another report18 involving dietary deficiency of calcium
and phosphorus in a growing dog, diffuse osteopenia of
the long bones was described. In the dog of the present
report, long bone demineralization was not detected
on radiographs of the forelimb at initial evaluation but
was apparent on the radiographs of the dog’s mandible.
In most species, bone loss during hypocalcemia occurs
first in the mandible, followed by cranial bones, ribs,
vertebrae, and long bones.19 The alveolar bone of the
mandible is often first affected because this type of bone
has the highest rate of renewal.19
In addition to calcium, vitamin D, and phosphorus
deficiencies, the homemade diet fed to the dog of the
present report also was deficient in a variety of other
nutrients. Nearly all nutrients found to be deficient
in the diet were below the minimum requirements of
both the AAFCO and NRC,2 although 2 (ie, tryptophan
and zinc) were only below the minimum requirements
of the AAFCO. Although the dog did not have obvi-
ous signs of other deficiencies, such as ophthalmic le-
482 Scientific Reports JAVMA, Vol 241, No. 4, August 15, 2012
SMALL ANIMALS
sions from vitamin A deficiency or anemia from iron
deficiency, deficiencies may have been identified in the
dog if more sensitive measures, such as serum vitamin
A concentrations or total iron-binding capacity, were
assessed. However, these additional tests were not fea-
sible because of financial constraints.
An additional nutrient that was of concern on the
basis of the evaluation of the homemade diet was tau-
rine. Taurine is not considered to be an essential nutri-
ent in dogs, but taurine deficiency–associated dilated
cardiomyopathy has been identified in some dogs, es-
pecially of certain breeds.4–7 Many of the breeds con-
sidered at higher risk are large and giant breeds, in-
cluding Saint Bernards.4–7 Therefore, plasma and whole
blood taurine concentrations were assessed because of
the low dietary concentrations (compared with dietary
taurine requirements in cats) in conjunction with the
signalment of the dog. Both plasma and whole blood
taurine concentrations were low at the time of admis-
sion. Dietary supplementation with taurine was initi-
ated, and at the same time, dietary intake of taurine also
was substantially increased. The diet also contained
concentrations of methionine and cysteine that met the
minimum requirements of the AAFCO and NRC, in
which case dogs should be able to endogenously syn-
thesize adequate taurine. Whether dietary supplemen-
tation with taurine was required is unclear, but given
the low blood concentrations and possible deleterious
effects of deficiency (and unlikely adverse effects), di-
etary supplementation with taurine was thought to be
warranted. The taurine supplement was chosen on the
basis of results of a study20 investigating quality con-
trol and disintegration properties of commercial taurine
supplements.
There were a number of nutrients to consider in
selecting the optimal diet for this growing dog with
multiple nutritional deficiencies. These included a diet
that was nutritionally balanced and one with increased
concentrations of calcium. Although serum calcium
concentrations had returned to within reference limits
before hospital discharge, restoring whole body stores
and bone mineral content could take several months.17
The fish-based commercial diet selected contained 4.5 g
of calcium/1,000 kcal (1.92% calcium on a dry-matter
basis). Although some authors recommend lower cal-
cium intake for growing large- and giant-breed dogs to
reduce the risk of developmental orthopedic diseases
(0.7% to 1.2% dry-matter basis),21 the diet was chosen
on the basis of the severity of the dog’s calcium defi-
ciency, results of studies3,14 on normal growth when
feeding medium- to large-breed puppies diets with 3.9
to 5.7 g of calcium/1,000 kcal, and the NRC’s safe upper
limit for calcium of 4.5 g/1,000 kcal. Excess calcium is
only 1 risk factor for developmental orthopedic disease
in large-breed puppies, with rapid growth, excessive
biomechanical forces, and genetics also playing pivotal
roles.22–25 In the dog of the present report, growth was
carefully controlled with frequent assessment of weight
and BCS, with adjustment of calories.
Another reason for the diet selected in the treat-
ment of the dog of the present report was the purported
history of a food allergy. Although it was explained to
the owner that a food allergy was an unlikely cause of
the dog’s diarrhea as a young puppy (other possible
causes included stress of transport, infectious causes,
or other dietary properties such as fat), the owner was
still highly concerned with feeding a diet containing
chicken. The clinicians were concerned that if the pos-
sibility of a food allergy were not considered, the owner
may have returned to an unbalanced homemade diet
again if diarrhea returned on the recommended diet. In
addition, it was possible that the dog had a food allergy
to chicken, considering that up to one-third of food al-
lergies develop in the first year of life, and chicken is
reported to be one of the common allergens in dogs.26,27
If a food allergy did exist in this dog, there were also a
variety of ingredients other than chicken, on the basis
of this dog’s early diet, that could have been allergens,
such as rice, wheat, fish, corn, or egg (although given
that the homemade diet contained rice and egg, these
were considered to be unlikely allergens). Confirma-
tion of an adverse food reaction would have required an
exclusive elimination diet trial for 8 to 10 weeks while
feeding a novel or hydrolyzed protein diet, followed by
reexposure to the allergen with return of signs.27 With
all of these issues to consider and after careful discus-
sion with the owner, the fish-based commercial diet
was selected. Although not a true elimination diet trial
because it contained rice and fish, the diet chosen was
otherwise novel, avoiding chicken, corn, and wheat
that had been present in the chicken-based adult dry
dog food. Although there are a small number of com-
mercial novel protein or hydrolyzed diets that meet the
dietary growth requirements, the fish-based commer-
cial diet was chosen over these diets because it provided
the highest amounts of nutrients of concern for the dog
of the present report (eg, calcium, phosphorus, vitamin
D, and taurine) and it also more closely met AAFCO
requirements for growth.
Cooked meat and rice diets (eg, chicken and rice or
hamburger and rice [other carbohydrate sources such
as potato may be used in place of rice]) are commonly
recommended by veterinarians for the temporary feed-
ing of dogs with gastrointestinal abnormalities. Unless
homemade diets are very carefully formulated (even
when other foods or dietary supplements are added,
as was done in this case), they are typically extremely
nutritionally unbalanced. Feeding these diets for a few
days is unlikely to induce harm. In an adult dog, even
severe deficiencies do not often manifest themselves in
obvious clinical signs unless used long term. However,
in growing puppies, particularly a large-breed puppy as
in this case, the dietary imbalances can induce severe
clinical signs. This highlights the importance of ob-
taining a thorough dietary history and making specific
recommendations to the owner regarding diet for both
healthy animals and animals that require a modified
diet because of gastrointestinal problems or other medi-
cal conditions. When owners insist on feeding a home-
made diet, veterinarians should work with a board-
certified veterinary nutritionist to formulate a balanced
homemade recipe, formulate a plan for monitoring the
animal, and ensure that the owner continues to follow
the recipe. Also, given the unique requirements of grow-
ing animals (ie, all dogs < 12 to 16 months, depending
on size) and their sensitivity to imbalances, homemade
JAVMA, Vol 241, No. 4, August 15, 2012 Scientific Reports 483
SMALL ANIMALS
diets, commercial foods that are not complete and bal-
anced, or commercial foods that do not meet require-
ments for growth should be avoided in this group.
a. Purina Proplan Chicken and Rice Adult Dry, Nestlé Purina Pet-
Care, St Louis, Mo.
b. Nupro All Natural Dog Supplement, Nutri-Pet Research Inc,
Manalapan, NJ.
c. CVS calcium carbonate, 1,250-mg tablets, CVS Pharmacy, Woon-
socket, RI.
d. Calcitriol capsules, TEVA Pharmaceuticals, Sellersville, Pa.
e. Taurine tablets, PetAg Inc, Hampshire, Ill.
f. Purina Proplan Chicken and Rice Puppy Canned, Nestlé Purina
PetCare, St Louis, Mo.
g. Purina Veterinary Diets DRM Canine Dry, Nestlé Purina Pet-
Care, St Louis, Mo.
h. Purina Gentle Snackers, Nestlé Purina PetCare, St Louis, Mo.
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