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Introduction:
The Yorkshire Terrier is, by
definition, an "active, independent,
devoted, and hardy" small toy
terrier. They are long-lived dogs,
with a life span averaging 13
- 14 years of age. However, the
Yorkshire Terrier is not without
its problems.
.
Due to advances in canine medicine,
health problems are being
discovered, treated, prevented,
and/or avoided by careful
breeding. The following problems
do occur occasionally in
the Yorkshire Terrier. Conscientious
breeders, however, are
working towards the elimination
of these problems.
.
INTRODUCTION:
The Yorkshire Terrier is, by
definition, an "active, independent, devoted, and hardy" small toy terrier.
They are long-lived dogs, with a life span averaging 13 - 14 years of age.
However, the Yorkshire Terrier is not without its problems.
.
Coat Inheritance: Clarence Little
in "The Inheritance of Coat Colour in Dogs" classifies the Yorkshire Terriers
is:
at B C (or Cch)
D (or dd or ddl) E G m S t
.
BASIC TYPICAL INFORMATION:
BREEDING:
Females - normal delivery
Males - normal and eager
Litter size: 1-4
Birth weight 3-6 oz.
As Mothers: Want owners' presence
and help; 20% of the breed is c-section; most prone to pregnancy complication
of uterine inertia or eclampsia.
AKC Standard: Dewclaws are removed
and tails are docked
Ears: If not standing by 8 weeks
clip hair and may need support training.
Whelp issues: Prone to malocclusions;
retained baby teeth, high survival rate with proper care.
DEVELOPMENTAL STAGES:* Dog Behavior
the Genetic Basis, Scott & Fuller
Pups must be insured to be stimulated
to defecate and urinate, when crying always attempt to insure they have
voided even if it appears dam is cleaning them
Birth - no senses, taste is
developed no other sensory responses
Two to three days - swings head
from side to side to touch dam or other whelps indicating sense of touch
developing. Other sensory capacities begin developing at about 3 days of
age.
EEG studies show full vision
is not present until age of 7 to 8 weeks
Hearing appears first at approximately
20 days but is not fully developed to age 6 to 7 weeks
Motor capacities begin to develop
at age 7 to 8 weeks but are not fully formed to 12-14 weeks of age.
Learning capacity does not begin
until age 1 month for any type of retention
.
Due to advances in canine medicine,
health problems are being discovered, treated, prevented, and/or avoided
by careful breeding. The following problems do occur occasionally in the
Yorkshire Terrier. The YORKSHIRE TERRIER CLUB OF AMERICA FOUNDATION, The
Yorkshire Terrier club of America and conscientious breedersare working
towards the elimination of these problems.
.
ALLERGIES:
Allergies can be broken down
into inhalant, contact, or food allergy origins. Flea allergies, grass
allergies, and environmental toxin induced allergies are the most common
causes of skin conditions in Yorkie. Allergies can be chronic or seasonal.
They can be minor or severe in occurrence. They tend to become worse with
age. Treatment is much better than in bygone days. Environmental controls,
antihistamine treatment, and desensitization injections have made huge
strides in the last few years.
.
Glucocorticoids (steriods) should
be used only as a last resort due to serious side effects. Diagnosis and
treatment of chronic or severe cases by a Board Licensed Veterinary Dermatologist
is recommended.
Inheritance: Unknown
.
ANASARCA: Also called WALRUS
PUPPY; RUBBER PUPPY; WATER PUPPY
Usually lethal lymphedema of
newborns; huge size (often 3 pounds) requires c-section to deliver.
Inheritance: Autosomal Recessive
.
AZOSPERMIA
Spermtogenci arrest; the sudden
onset of sterility in a formerly known fertile male; may be immune-mediated
Inheritance: Unknown
.
ALLERGIES:
Allergies can be broken down
into inhalant, contact, or food
allergy origins. Flea allergies,
grass allergies, and environmental
toxin induced allergies are
the most common causes of skin
conditions in Yorkie. Allergies
can be chronic or seasonal. They
can be minor or severe in occurrence.
They tend to become worse
with age. Treatment is much
better than in bygone days.
Environmental controls, antihistamine
treatment, and desensitization
injections have made huge strides
in the last few years.
.
Glucocorticoids (steriods) should
be used only as a last resort due
to serious side effects. Diagnosis
and treatment of chronic or
severe cases by a Board Licensed
Veterinary Dermatologist is
recommended.
.
BLADDER STONES:
Some of the most common ones
include:
Struvite
This urolith is diagnosed in
almost half the cases of bladder
stones. It is also called MAP
(Magnesium-Ammonium-Phosphate),
or triple phosphate. It is the
predominant stone type in female
dogs of all breeds.
.
Several factors predispose dogs
to getting
struvite uroliths:
* Excess struvite crystals in
the urine that set the stage for
the formation of the urolith.
Some breeds have a genetic
predisposition to forming excess
amounts of these crystals
in the urine.
* Urinary Tract Infection (UTI)-
some bacteria produce a
byproduct called urease. Urease
will increase the pH of the
urine and promote ammonium in
the urine.
* The formation of an alkaline
(pH greater that 7.0) urine
from the diet or urease producing
bacteria will cause the
struvite crystals to precipitate
out of solution and begin
the formation of a urolith.
* Urine that stays in the bladder
longer than usual gives
the struvite crystals further
opportunity to precipitate out
of solution and form a urolith.
* Struvite uroliths come in
many different shapes and sizes,
are radiodense, and form in
an alkaline urine.
.
Calcium Oxalate
This is the second most prevalent
type of urolith after Strive,
making up around 30-50% of the
uroliths, especially in male
dogs of all species. They come
in two versions; the monohydrate
and the dihydrate. Sometimes
the two are found together,
sometimes they are found with
other uroliths like calcium
phosphate, Strive, or ammonia
urate.
This is a problem most commonly
in older male dogs. It is
suspected that there is a correlation
with hormone changes
that occur as a pet ages. The
Yorkshire Terrier is prone to
these along with many other
breeds.
.
Several predisposing factors
work together to increase the
chance of this urolith forming:
* Increased calcium in the bloodstream
(hypercalcemia)
* Increased calcium in the urine
(hypercalciuria) with no
increase in hypercalcemia
* Concurrent Cushing's disease
* Use of cortisone
.
Urate and Ammonium Urate
This is a common urolith found
in some breeds around middle
age, with males affected much
more often than females. This is
because they metabolize protein
differently in the liver, with
the end result being uric acid
buildup in the urine. They are
found in Yorkshire terriers.
There does not seem to be a
connection with a urinary tract
infection, and they tend to
form in an acidic urine.
Urate stones are radiolucent.
If they get large or covered with
other minerals they might become
radiopaque. Urate calculi
tend to be small and occur as
several stones. These stones usually
form in the bladder, and when
passed through the urethra, can
become lodged.
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* Ammonium urate uroliths are
sometimes formed in pets with
liver disease such as PSS (see
liver shunt) due to improper
metabolism of ammonia to urea.
This will cause excess uric
acid levels in the bloodstream.
The kidneys filter out this excess
uric acid in the production
of urine, thus increasing the level
of uric acid in the bladder.
The excess ammonia that is in the
bloodstream from the liver problem
also builds up in the urine
in the bladder. These two compounds
combine to form the
ammonium urate bladder stone.
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Dogs with ammonium urate bladder
stones might have ammonium
urate crystals in their urine
and a low specific gravity (dilute urine).
These stones might not be seen
on a radiograph because they are
radiolucent. This same radiograph
might also show a small liver,
an indication of PSS. This small
liver is due to the diverted blood
flow to the liver. Dogs with
PSS will commonly have abnormalities
in the blood sample to give
us further clues.
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* Compound Uroliths
Most bladder stones are caused
predominantly by one type of
mineral. The more common ones
have been described above. In
a small percent of cases, the
bladder stone is caused by a
combination of minerals in similar
quantities. These stones are
called mixed uroliths. Some
bladder stones consist of a core
mineral surrounded by a lesser
amount of a different mineral
in a different layer. These
are called compound uroliths.
.
Why some minerals form mixed
uroliths and others form
compound uroliths is not understood.
.
Compound uroliths form when
the factors that predispose to
one type of stone formation
have now changed to factors that
favor a different type of stone
formation. If a struvite stone is
treated with antibiotics and
urinary acidifiers the problem
tends to resolve. The change
in urine pH might promote excess
calcium in the urine, resulting
in a shell of calcium oxalate
formation around the core struvite
stone. The opposite can
occur also- a struvite stone
can form over a calcium oxalate
stone.
.
In general, these stones are
removed surgically and an effort
is made to medically prevent
the mineral that is at the core
of the stone.
.
Miscellaneous Uroliths
There are other uroliths that
occur, although they are
relatively uncommon. They include
cystine, silica, calcium
phosphate, and miscellaneous
minerals.
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CATARACTS
The lens of the eye is clear
and is located behind the pupil.
The job of the lens is to focus
light into the retina. When the
lens becomes unhealthy, it turns
white or opaque. Cataracts
are generally considered a common
old age change, but a
juvenile form also occurs. Juvenile
cataracts are inherited
and are not usually present
at birth, although this condition
can present itself at any age-
months to years. Juvenile cataracts
affect different areas of the
lens depending upon the breed of
dog. They do not always result
in the lens becoming completely
opaque. Complete cataracts result
in blindness that can only be
corrected by cataract surgery.
Yearly CERF examinations are an
important tool in diagnosing
this condition. Proper treatment
can be hastened by early diagnosis.
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CAMPYLOBACTERIOSIS
Commonly mistaken for Parvovirus,
but needs different
treatment. It's a BACTERIAL
imbalance in the digestive
tract. It is a disease that
produces acute infectious diarrhea
in puppies and kittens. This
is NOT a new form of Parvo.
Parvo tests will show a LOW
positive & subsequent tests
will continue to show low positives,
will be inconclusive, or
will give erratic results. This
disease is so similar to Parvo,
that some dogs have tested in
the low positive for Parvo. But
they do not have Parvo, and
it has been recommended that
three parvo tests are needed
to exclude Parvo.
.
This disease can be tested for
specifically, so if you have an
affected dog that appears to
have Parvo, but in your mind
know that, that could not be
possible, have them tested for
"Camby". It is important to
note that this disease can be
transferred between humans,
dogs, cats and other livestock.
It starts with fecal mucus sheath
& continues to get progressively
softer until it is watery and
contains blood. It then becomes
explosive. Vomiting may accompany
and may or may not also
contain blood. Feces have a
sweet/flowery aroma along with a
"slaughterhouse on a summer
day" smell (similar to parvo
diarrhea but with a floral hint).
Feces are usually mustard
colored. Dogs dehydrate at an
astounding rate.
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COCCIDIOSIS
A diarrhea disease caused by
a species of coccidia commonly
found in the feces of puppies,
and occasionally, adult dogs.
Coccidia are not worms; they
are microscopic parasites
which live within cells of the
intestinal lining. Because they
live in the intestinal tract
and commonly cause diarrhea,
they are often confused with
worms.
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COLLAPSING TRACHEA
Collapsing Trachea is a problem
common to Toy Breeds. The
trachea is a long tube that
carries air from the neck to the chest.
It is reinforced with rings
of cartilage that help keep it rigid as
air moves in and out of the
tube. When the cartilage weakens,
the trachea may collapse while
the dog is breathing. While many
affected dogs do fine, this
isn't the case in all of the Toy's. The
round cartilage rings may flatten,
forcing the dog to try to
breathe through an extremely
narrow opening.
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The symptoms of the condition---shortness
of breath, coughing,
fatigue---usually appear after
the age of five, although they
can begin as early as birth.
Generally young dogs tolerate
collapsing trachea pretty well
until they get older.
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CUSHING'S SYNDROME
Cushing's Syndromeis also known
as 'Hyperadrenocorticism'
and is a combination of clinical
and chemical abnormalities
resulting from chronic
exposure to excessive amounts of
glucocorticoids. It is a condition
that occurs in most species
but is most commonly encountered
in the dog and the horse.
Cushing's disease is the result
of the overproduction of
cortison, an natural steriod
hormone, by the adrenal glands.
It is rare in dogs under five
years old. In about 80 percent of
the dogs the disease is caused
by a lesion in the pituitary gland
at the base of the brain that
overstimulates the adrenals, while
in about 20 percent of cases
one of the adrenal glands itself will
have a tumor that excretes cortisol
independent of what's
happening in the body. About
half of those tumors are
maliganant and spread, and about
half of them are benign
and generally tend to stay small.
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Glucocorticoids have many functions
and are essential for
life being responsible or indirectly
responsible for a range
of metabolic functions including
blood glucose levels, fat
production and distribution,
protein metabolism, inflammation,
thirst, counteracting shock,
the skin and the immune system.
The list goes on.
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Cushing's Syndrome is a collection
of symptoms caused by
an excess of a hormone called
cortisol. There are three main
causes of Cushing's Syndrome:
a tumor on the pituitary gland;
a tumor on the adrenal gland;
or veterinarians who over-
prescribe corticosteroids to
treat itching skin. It is, as yet,
unknown whether there is an
inherited predisposition to
Cushing's Syndrome in Yorkshire
Terriers.
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In the base of all our brains
is a small grouping of cells which
constitute the pituitary gland.
This gland has many functions
and is the 'director' of much
of the bodies function. It gathers
information about body hormone
levels and then produces its
own regulatory hormones that
through 'feedback' mechanisms
govern their production. One
of its functions is to govern the
level of glucocorticoids in
the blood stream. It does this by
producing a hormone called ACTH
that flows through the blood
stream to the adrenal glands.
The adrenal glands are very small
pockets of specialized cells
sitting behind each kidney that are
responsible for producing the
bodies glucocorticoid. ACTH
stimulates the production of
glucocorticoid in the adrenal gland.
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Excessive production of ACTH
in the pituitary will produce
excessive glucocorticoid production.
Similarly, an abnormality
in one or both adrenals will
cause an overproduction and both
conditions will produce Cushing's
Syndrome. The principal
cause of overproduction is due
to tumours growing in either
the pituitary gland (usually
benign, small and unlikely to cause
other symptoms) or the adrenal
gland (50% benign, 50%
malignant and spreading to other
areas of the body).
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Diagnosis is based on clinical
symptoms and confirmed with
selective blood tests. Symptoms
are varied but includes increased
thirst with subsequently increased
urine output, an excessive
appetite, abdominal distension,
often skin changes, with hair loss
on flanks, dandruff, thickened
and pigmented skin. The dogs
become weak and lethargic with
muscle wastage. Diabetes can
be a secondary symptom. Confirmatory
blood tests are many
and varied but can be used to
produce a diagnosis and then used
to determine where in the body
the problem lies.
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The symptoms of Cushing's disease
can also appear if a dog is
taking steriods for a medical
condition and ends up with too
much in his system. Steroids
are found in a lot of creams, eye
ointments and ear ointments,
and if you get overzealous with
their administration, that can
cause these signs as well. When
you stop using the products,
these symptoms will go away. The
typical signs of Cushing's disease
are increased thirst and urination,
panting, hair loss (usually
on the trunk) and weakness.
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Symptoms:
* He is drinking huge amounts
of water and urinating frequently
* He is losing coat
* His skin is darkening
* His muscles are atrophying
and he develops a pot belly.
* If your vet finds the following
four symptoms, your Yorkie
probably has Cushing's Syndrome:
* The dog is drinking copious
amounts of water and
urinating frequently.
* The dog has an elevated SGPT.
* The dog has an elevated alkaline
phophatase level.
* The dog's ratio of urinary
cortisol to urinary creatinine
is greater than 24
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Cushing's Syndrome is usually
treated successfully with a
drug called Lysodren, newer
drugs are 'Vetoryl' (Trilostane)
and Anapryl. Surgery is rarely
recommended and radiation
therapy, used in humans, is
very expensive and rarely available
for dogs. Adrenal tumours can
be surgically removed in a
percentage of cases but pituitary
surgery would only be
attempted in rare cases at very
specialized centers
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Cryptorchidism
Cryptorchidism is the failure
of one or both of the testicles
to descend into the scrotum.
Normal descent is often
complete by 6 to 8 weeks of
age but may be delayed to as
late as 6 months of age. The
undescended testicle may be
found within the abdominal cavity,
in the inguinal canal or
under the skin next to the penis.
The condition is considered
hereditary in most breeds. There
is not complete agreement
on the mode of inheritance.
Because of the increased incidence
of cancer in retained testicles,
cryptorchid dogs should always
be neutered. A neutered cryptorchid
dog should have no other
expected health risks due to
this condition.
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DRY EYE (ACTUAL NAME: KERATOCONJUNCTIVITIS
SICCA (KCS))
KCS or "dryeye" is an eye disease
caused by abnormal tear
production. The lacrimal glands
produce the watery secretions
that make up the bulk of the
tears. A deficiency in this secretion
causes KCS in small animals.
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Normal tears are essential for
the health and transparency of the
cornea (the surface of the eye).
Tears cleanse and lubricate the
cornea, carry nutrients, and
play a role in the control of infection
and in healing. Deficient tear
production as in KCS causes
chronic irritation of the cornea
and conjunctiva. Corneal
ulcers and eventually corneal
scarring occur, and blindness
can result.
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There is a predisposition to
this condition in some breeds as
listed below. KCS can also occur
in any breed as a result of
viral infection, inflammation,
drug-related toxicity, or
immune-mediated disease. Congenital
KCS (ie. the dog is born
with the condition) is rare.
It may be one-sided and has been
seen in toy breeds such as the
Yorkshire terrier, pug, Pekingese,
and Chihuahua. These dogs have
very small or absent tear-
producing (lacrimal) glands.
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GIARDIASIS
Caused by a protozoan of the
giardia species. Giardia are one-
celled organisms that live in
the small intestines of dogs and
cats. Dogs get the infection
from drinking water from streams
or other sources contaminated
with infective oocysts. Young
dogs can develop diarrhea that
may be acute or chronic,
intermittent or persistent,
and may be accompanied by weight loss.
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HEART DEFECTS
A variety of heart defects can
occur in every breed of pure-
bred dogs. A careful examination
of puppies by a veterinarian
at 6 weeks of age is recommended
since most congenital heart
problems can be detected this
way.
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* Valvular Endocardiosis is
a degenerative change of unknown
cause affecting the subendocardial
valve leaflets and chordae
tendineae in the middle aged
to elderly dog. Smaller breeds are
predisposed. And it is relatively
common in Yorkshire Terriers.
Also known as chronic myxomatous
valvular heart disease, this
disorder is the most important
cause of heart disease in veterinary
practice.
* Cardiomyopathy, is another
heart disease identified with
Yorkies and other small toy
breeds.
* Patent Ductus Arteriosus (PDA)
At birth, mammals must
adapt from living in a fluid
environment (the amniotic fluid)
and acquiring oxygen through
the mother's blood, to breathing
air and acquiring oxygen through
their own lungs. The ductus
arteriosus is very important
in the adaptation process. This is a
small communicating blood vessel
between the pulmonary artery
(which carries blood to the
lungs), and the aorta (which carries
blood to the rest of the body).
Before birth, most of the blood
from the fetal heart bypasses
the fetal lungs via the ductus
arteriosus. The lungs gradually
become functional fairly late in
fetal development. At birth,
the blood supply from the mother is
of course cut off, the dog (or
other mammal) begins breathing on
its own, and blood flow through
the ductus arteriosus decreases
dramatically. Within a few days,
the ductus closes off completely.
Where the ductus does not close,
the dog is left with a patent
ductus arteriosus (PDA). The
extent to which this affects the dog
depends on the degree of patency,
or opening, of the ductus.
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HGE OR HEMORRHAGIC GASTRIC ENTERITIS
Particularly dangerous to the
toy and smaller breed dogs. Any
kind of bacterial diarrhea can
quickly dehydrate a dog, and the
tinies are at greater risk,
as they have little weight to lose before
they are dehydrated and need
IV rehydration. Your dog can get
infected anywhere. Then it can
be from 2-10 days after exposure,
that your dog can come down
with this problem. The symptoms
start with vomiting, lethargy,
refusing to eat, and progressing to
mucous covered stool, loose
stools, severe diarrhea and bloody
diarrhea. It is important to
have a culture done first so that you
know exactly what bacteria you
are treating, and get them started
on antibiotics. DO NOT waste
time, especially with the tiny toy
dogs , as they do not have the
spare fluids to lose thru diarrhea,
especially bloody diarrhea.
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HYPOGLYCEMIA
Hypoglycemia is when the blood
sugar levels (glucose) fall well below
normal. Glucose is what the
body uses as fuel and is necessary for
the brain tissue and muscles
to function. Hypoglycemia is often seen
in toy breeds, and frequently
in young toy puppies. It can cause your
puppy to become confused, disoriented,
drowsy, have the shivers,
stagger about, collapse, fall
into a coma, or have seizures. Typical
signs are listlessness, depression,
staggering gait, muscular weakness,
and tremors -- especially of
the face. Puppies with a severe drop in
the blood sugar develope seizures
or become stuperous and go into
a coma. Some puppies may only
exhibit weakness or a wobbly gait,
and occasionally a puppy that
seemed just fine is found in a coma.
Most of the time the symptoms
can be controlled by eating, or by
giving some glucose such as
honey water to the puppy. If not
treated it can result in death.
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HYDROCEPHALUS
With hydrocephalus there is
an abnormal build-up of
cerebrospinal fluid (CSF) in
cavities ( the ventricles) in the brain.
The resulting increased pressure
on the brain causes the clinical
signs that occur with this condition.
.
Hydrocephalus can be primary
(congenital ) - the animal is born
with the condition, or secondary
- the condition is acquired later
in life due to some disease
process that blocks normal drainage
of the CSF. The primary form,
discussed here, is seen most often
in brachycephalic (dogs with
a shortened head) and toy breeds.
.
Puppies with severe hydrocephalus
often die at a very early age
due to pressure from the increased
fluid in the brain. In other less
severely affected pups, the
signs gradually become apparent over
the first few months of life,
and in some mild cases the condition
is only diagnosed later in life.
.
Symptoms: The types of signs
seen with this condition include
unthriftiness (smaller than
littermates, slow to grow), a domed
skull (which gradually becomes
more pronounced), abnormal
movement behaviours (restlessness,
aimless walking), problems
with vision, and seizures. These
pups are very slow to learn - it
may be extremely difficult to
housetrain them for example.
.
Generally the signs gradually
worsen, although by 2 years of age
they may stabilize. To minimize
brain damage, the condition must
be recognized and appropriate
treatment begun early. However,
affected animals will likely
always be slow and have a limited
ability to learn.
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HYPOTHYROIDISM
Hypothyroidism is an underproduction
of hormones by the thyroid
gland. It is characterized as
an underproduction of hormone by the
thyroid gland. It occurs in
many breeds, including Yorkshire Terriers.
Diagnosis is done by a blood
test for complete thyroid activity.
Symptoms include poor haircoat,
infertility, lethargy, and cold
intolerance. Treatment with
synthetic hormones is very successful
in controlling this condition.
Blood tests to evaluate dosage is
important on a yearly basis.
However Yorkies are in the low
precendence for TGAA testing.
.
Symptoms:
* Abnormal loss of coat (often
bilateral and symmetrical),
poor coat condition, fading
of coat color
* Chronic skin disorders and
infections, skin allergies,
dry or scaling skin
* Weight gain
* Infertility
* Fatigue, lethargy
* Intolerance of cold
.
It is important to determine
the exact cause of your dog's
hypothyroidism before embarking
on a course of treatment.
Your veterinarian must run a
full thyroid panel and have
the blood tested at a laboratory
which uses canine thyroid
values. Do not be tempted to
start thyroid treatment without
proper veterinary supervision.
The balance of the endocrine
system is critical to your dog's
health and you can cause an
otherwise healthy thyroid gland
to atrophy by giving
medication improperly.
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INTUSSUSCEPTION
Intussusception is a problem
with the intestine (bowel),
wherein one portion of the bowel
slides into the next,
much like the pieces of a telescope.
When this occurs, it
creates an obstruction in the
bowel, with the walls of the
intestines pressing against
one another. This in turn can
cause dangerous inflammation,
swelling, and decreased
blood flow to the intestines
involved.
.
Intussusceptions generally occur
as a secondary problem
to some disorder or disease
that causes increased intestinal
mobility or inflammation. Chronic
parasite infestation may
be the most common cause but
anything that causes chronic
intestinal disease can lead
to an intussusception. There are
times when intussuceptions occur
for no apparent reason so
it is likely that primary intussusception
can occur. They have
been reported following ingestion
of foreign bodies, trauma,
ovariohysterectomy surgery,
infiltrative or inflammatory bowel
diseases and other conditions
that cause intestinal irritability.
.
Intussusception can be chronic
sometimes. It can also be a
"come and go" problem -- intussuscpetions
occasionally will
resolve on their own and then
recur. I have removed one
surgically, put the remaining
intestinal ends back together and
watched a new intussusception
form right at the same site.
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LEGG-PERTHES (LEGG-CALVE-PERTHES
DISEASE)
Legg-Perthe's disease is a degeneration
of the hip joint occurring
in young dogs. It is also known
as Legg-Calve-Perthe's Disease,
Perthe's disease, Calve-Perthe's
disease, or in medical terminology,
avascular necrosis of the femoral
head and neck. The former
names recognize the original
researchers in the disease as it
occurs in humans.
.
Most of the time the clinical
signs of this disease occur in 4 to
11 month old dogs and usually
consist of lameness of one leg
only. Pain may be mild to very
severe.
Some dogs have mild
forms of this condition and
do not require medical care. In other
dogs, the condition cause sufficient
pain and deformity of the hip
joint to require surgical intervention.
Atrophy of the muscles of the
affected leg is not uncommon.
If this is severe it can slow the
recovery period considerably
and may make medical therapy less
likely to work.
.
Definitive diagnosis is made
by X-rays. As changes to bone occur
slowly, X-rays taken early in
the course of the disease may appear
normal. Repeating the X-rays
in 3 to 4 weeks will reveal the bony
changes. A dog affected with
LPD suffers a loss of blood supply to
an area of the femur (thigh
bone) known as the neck. Because the
bone loses its blood supply,
it dies. As a result of the loss of bone
tissue, the neck of the femur
collapses. The neck attaches the head
of the femur to the body of
the femur. When the neck collapses, the
head of the femur is moved,
and may also become deformed. These
changes are readily apparent
in X-rays. The head of the femur is
the "ball" which sits in the
"socket" on the pelvis, making up the
hip joint. Therefore, changes
to the head result in disruption of
function of the hip joint which
causes the pain and lameness.The
term "avascular necrosis" means
death of tissue due to lack of
blood supply. In most dogs,
only one hip is affected, and males
and females are equally affected.
.
Treatment of this condition
varies according to the severity of
the signs seen. In mild cases,
enforced rest may be sufficient to
allow healing of the damaged
areas to occur. In some cases,
immobilization of the affected
limb using an Ehmer sling may
be beneficial to recovery. Many
dogs have advanced cases of
this disease by the time they
are examined by a veterinarian and
medical treatment is not likely
to work. In these dogs, excision
of the femoral head (ball portion
of the hip joint) is often
beneficial. Removal of this
section of the bone diminishes painful
bony contact in the hip joint.
Recovery from this surgery can
be slow with recovery periods
of up to one year sometimes
occurring before good use of
the affected leg returns. If muscle
atrophy is not present at the
time of surgery the recovery time is
usually much less. Pain relief
and anti-inflammatory medications
may be beneficial.
.
There is a stronger tendency
to treat this as a medical condition
prior to surgery right now.
A general rule of thumb is to allow
non-surgical therapy a month
to show a beneficial response. If
one is not seen, surgical repair
should be considered more carefully.
.
Treatment of LPD usually consists
of surgery to remove the
damaged femoral head and neck
(femoral head ostectomy).
Mildly affected animals may
recover soundness with only cage
rest. Affected animals will
probably always have some gait
abnormalities, but make satisfactory
pets after recovering
from surgery.
.
Prevention of the disease is
only possible through genetic means.
Affected animals should not
be bred. Breeding stock should
have their hips X-rayed to insure
that they are not affected
with mild LPD, the symptoms
of which went unnoticed during
the dog's adolescence. Extreme
caution should be used when
considering breeding animals
that have produced LPD, or
have LPD affected littermates.
.
LUXATED PATELLAE (SLIPPING PATELLA'S)
This is a problem in many small
breeds of dogs, including
Yorkies . In this disorder,
the knee cap slips out of the trochlear
groove. Diagnosis is by X-ray
and palpation exam. The severity
of the condition is quite variable.
It can occur in one back leg,
or both. Grade 1 cases can be
very mild, with minor gaiting
anomalies. Mild cases will do
such things as: pick up a leg for
a few steps when moving over
irregular ground (gravel or long
grass), lope or gallop rather
than trot. They are often straight in
the stifle and have no "drive"
to their rear movement. Grade 3
and 4 cases, are less common
and do require surgical correction.
This condition does weaken the
integrity of the joint, predisposing
to arthritis and traumatic injury.
.
The patella or kneecap is usually
located directly in the centre of
the knee joint. It is held in
place by ligaments and rests in a groove
on the femur (thigh bone). The
muscle of the thigh or quadriceps
attaches at the top of the kneecap
and on the tibia (calf bone)
directly below the groove or
trochlea of the femur. Its contraction
causes the knee to extend. In
a normal knee, all these structures
are well aligned. The femur
is directly above the tibia and when
the quadriceps contracts, the
patella glides up the groove.
.
Luxation, or dislocation of
the patella, occurs when the tibia is
rotated inward or when the lower
portion of the femur is curved,
causing a misalignment of the
structures of the knee so that the
patella slides out of its groove
and moves in toward the centerline
when the knee extends. In a
small percentage of the cases, the
luxation is said to be lateral
because the patella is dislocated
outwards but this is very uncommon
in small breed dogs. Patellar
luxation occurs mostly in toy
and small breeds of dogs weighing
10 kg or less such as the miniature
poodle, the pomeranian and
the Yorkshire terrier. A study
has shown that females are 1.5 times
more affected than males.
.
Causes: In the majority of cases,
patellar luxation is a congenital
condition because the abnormalities
(weak ligaments, a too-shallow
groove and internal rotation
of the tibia) are present at birth though
the actual luxation may appear
some time later. It is thought to be
inherited although the exact
mode of transmission has not been
determined. In some cases, the
condition is acquired through trauma.
.
Symptoms:
* The symptoms may appear at
weaning or may go undetected at
first.
* There can be an occasional
rear lameness.
* The dog can be seen running
and suddenly yelping in pain,
walking on three legs, unable
to flex the stifle. Sometimes, he
will make a kind of hop and
thus be able to replace the patella
himself.
* In other cases, he will show
much pain and will hold the leg up
for several days.
* In very severe cases, the
animal cannot put weight at all on its
hind legs at all and drags himself.
Even if it is very often bilateral,
the patellar luxation can occur
in one knee or be worse on one side.
.
The diagnosis is made by palpating
and manipulating the knee
joint to see if the patella
can be luxated manually. Depending
on the laxity, the condition
can be classified from Grade 1
(minimal) to Grade 4 (severe).
Radiography is used to document
the condition, evaluate the
extent of the changes to the trochlear
ridges, see if any osteoarthritis
has developed and evaluate the
bone conformation.
.
Treatment consists from confined
rest to replacement of the
patella. Though surgery is not
necessary for every dog, it is
the treatment of choice, especially
if it has persistent lameness.
It should be performed early,
before osteoarthritis has affected
the joint. This is especially
true for luxations graded 2 to 4 as
the joints are easily luxated
and remain so until replaced. Many
techniques are available and
the method chosen depend on the
veterinarian, the severity of
the disorder and the lifestyle of the
dog. Conservative treatments
such as prednisone and/or restricted
activity doesn't give much benefit
and is recommended mostly for
mildly affected or older dogs.
For more severe cases, if the disorder
is not corrected by surgery,
joint pathology increases with age as
repeated dislocations will damage
the cartilage of the patella and
lead to osteoarthritis, making
the joint more and more swollen
and painful with poor mobility.
The additional strain caused by the
misaligned force of the quadriceps
can also increase the rotation of
the tibia, thus the severity
of the problem. The condition also
predisposes to strained and
even torn and cruciate ligaments. The
results after surgery are better
if it is performed before arthritic
changes occur and depend on
the severity of the condition . For
grades 1, 2, or 3, the dog can
usually use its leg in a normal fashion
after 30 days or so.
.
PANCREATITIS
Pancreatitis is inflammation
of the pancreas, an elongated
gland that serves many functions
in the process of digestion
and metabolism. When digestive
enzymes that normally are
excreted into the intestinal
tract are activated in the pancreas
instead, they cause inflammation.
Foods high in fat, or a lot
of greasy table scraps, tend
to trigger pancreatitis.
.
This is a serious, potentially
life-threatening disease.
Mortality is upwards of 20 to
25 percent. Affected animals
will have severe abdominal pain,
loss of appetite, lethargy,
depression, vomiting and diarrhea.
Dehydration is also a danger.
.
The Role of the Pancreas
The pancreas is a glandular
organ located near the liver and
duodenum. It has two different
types of glandular functions.
The first is its endocrine function:
it makes insulin, which is a
very important hormone in the
control of metabolism and
blood sugar levels. The pancreas
also has an exocrine glandular
function: it makes digestive
enzymes that are secreted into the
intestine and are critical for
the normal digestion of food.
.
Pancreatitis is a condition
where the pancreas becomes inflamed.
The time course can be either
chronic (slow and smoldering
over weeks to months) or acute
(rapid in onset). Inflammation
can be particularly severe in
the pancreas because the organ
contains digestive enzymes.
These powerful enzymes are normally
stored in an inactive state
and are only activated when released
into the intestine. This is
necessary or the pancreas might "digest
itself." In cases of severe
inflammation, the digestive enzymes can
be activated within the pancreas,
which only worsens the swelling
and inflammation. Sometimes
the swelling in an inflamed pancreas
can become so severe as to obstruct
the outflow of bile coming via
the bile duct, which passes
near the pancreas on its way from the
liver to the duodenum.
.
In chronic pancreatitis, scar
tissue (fibrosis) develops. This interferes
with the normal function of
the pancreas.
.
The Causes of Pancreatitis
Pancreatitis can occur in dogs,
cats or humans. In humans, it
can be a complication of alcoholism.
Humans are prone to
abscesses — bacterial infections
of the pancreas — while bacteria
are rarely involved in cases
of pancreatitis in cats and dogs. If
you want to learn more about
pancreatitis in humans, several
links are provided at the end
of this article.
.
Very little is known about the
causes of pancreatitis in dogs and
cats. The disease appears to
be more common in dogs. There is
some evidence, at least in dogs,
that certain cases are brought
on by dietary indiscretion,
especially by eating foods that are
very high in fat. Also, dogs
with other serious illnesses such as
diabetes, Cushing's disease
and cancer, or dogs that are recovering
from surgery, are at higher
risk for pancreatitis than are dogs that
are otherwise healthy.
.
Symptoms:
* Dogs with acute pancreatitis
usually have vomiting and often
have abdominal pain. Often dogs
will stop eating and seem quite
sick. Dogs with severe, acute
pancreatitis are at risk for dehydration
and associated complications
(blood clotting abnormalities, kidney
failure, fluid buildup around
the lungs, diabetes). They require
hospitalization for IV fluids
and sometimes intensive care.
* The signs of chronic pancreatitis
are more subtle and may be
difficult to detect. Sometimes
intermittent vomiting, diarrhea or
signs of vague abdominal pain
will be reported. It appears that
many times the disease progresses
without detection. In some
cases, either diabetes (due
to lack of ability to make insulin
because of pancreatic damage)
or pancreatic exocrine insufficiency
(inability to make enough digestive
enzymes)may eventually result.
.
Diagnosis of pancreatitis can
be difficult because no available test
is 100% reliable. Two digestive
enzymes made in the pancreas can
be measured in the blood. Elevations
in these enzymes (lipase and
amylase) can provide supportive
evidence for pancreatitis. The
lipase test appears to the be
better of the two, but it is not always
available on the routine chemistry
panel. Veterinarians may add
it as a special test when dogs
are presented for evaluation of
vomiting. Some dogs with pancreatitis
do not have elevations in
lipase and amylase so when these
blood values are normal, it does
not exclude the diagnosis of
pancreatitis.
.
There is a relatively new test
called TLI (trypsin-like
immunoreactivity) that appears
to show promise in the diagnosis
of acute pancreatitis, at least
in cats. The TLI seems to be more
reliably elevated than is lipase.
The current problem with the test
is turn-around time. It is performed
at only a limited number of
labs and the samples have to
be shipped, often out of state, so it
may take one to two weeks for
results. This hampers its diagnostic
usefulness.
.
Ultrasound can be helpful in
the diagnosis of pancreatitis. However,
ultrasound of pancreas is technically
difficult. Abnormalities are not
always seen, even when acute
pancreatitis is present.
.
There is no specific treatment
for pancreatitis. At present, the
treatment is predominantly supportive
allowing time for the
inflammation to subside while
preventing complications.
.
In dogs, most cases of acute
pancreatitis will resolve in a few days,
with complete rest of the GI
tract. Dogs must be maintained NPO
(this stands for "nothing per
os," which means that no food or
water can be given by mouth).
When nothing is taken by mouth,
the stimulus for pancreatic
secretion abates, which allows the
inflammation to subside. When
the enzymes (lipase and amylase)
have fallen to normal or nearly
normal then water and a very
low fat diet is instituted.
To prevent dehydration during the period
of complete bowel rest, dogs
must be given fluid therapy; usually
fluids are given intravenously.
This is why patients with pancreatitis
are generally hospitalized.
Steroids and other anti-inflammatory a
gents don't seem to aid recovery
in dogs with pancreatitis.
.
In severe cases of pancreatitis
in dogs, pain killers may be needed.
Also, plasma transfusions may
benefit some patients. It is thought
the certain proteins in plasma
can bind the damaging pancreatic
enzymes being released from
the damaged pancreas.
Surgery is generally not indicated
except when abscesses or cysts are
present. Even with treatment,
some cases of pancreatitis may be fatal.
.
Reduced fats are indicated as
assisting in preventing recurrence
during the convalescent phase
of pancreatitis in dogs, and probably
in cats. For dogs it is critical
to avoid invasions of the garbage
can because dietary indiscretion
seems to underly many cases.
There is some anecdotal evidence
that dietary supplementation
with pancreatic enzymes may
help in prevention of recurrence
or treatment of chronic pancreatitis.
Although this seems to be a
harmless therapy, there is no
experimental evidence to support its use.
.
PARVOVIRUS
Canine parvovirus is an acute,
highly contagious disease of dogs
that was first described in
the early 1970's. The disease is transmitted
by oral contact with infected
feces. Parvo affects dogs of all ages,
but most cases occur in pupies
6 to 20 weeks of age. Parvovirus is
characterized by severe, bloody
diarrhea and vomiting, high fever
and lethargy. The diarrhea is
particularly foul smelling and is
sometimes yellow in color. Parvo
can also attack a dog's heart
causing congestive heart failure.
This complication can occur
months or years after an apparent
recovery from the intestinal
form of the disease. Puppies
who survive parvo infection usually
remain somewhat un-healthy and
weak for life.
.
POISON
What To Do For A Poisoned Animal
.
Before You Call the ASPCA Animal
Poison Control Center
If you suspect that your pet
has been exposed to a poison, it is
important not to panic. While
rapid response is important,
panicking generally interferes
with the process of helping your
animal.
.
Take 30 to 60 seconds to safely
collect and have at hand the
material involved. This may
be of great benefit to the Center
professionals as they determine
exactly what poison or poisons
are involved. In the event that
you need to take your animal to
your local veterinarian, be
sure to take with you any product
container. Also bring any material
your pet may have vomited
or chewed, collected in a zip-lock
bag.
.
If your animal is seizuring,
losing consciousness, unconscious or
having difficulty breathing,
you should contact your veterinarian
immediately. Most veterinarians
are familiar with the consulting
services of the Center. Depending
on your particular situation,
your local veterinarian may
want to contact the Center personally
while you bring your pet to
the animal hospital.
Call the ASPCA Animal Poison
Control Center 888-4ANI-HELP
(888-426-4435)
.
There is a $45 consultation
fee for this service. A credit card
number may be required.
When you call the Center, be ready to
provide:
* Your name, address and telephone
number
* Information concerning the
exposure (the amount of agent,
the time since exposure, etc.).
For various reasons, it is
important to know exactly what
poison the animal was
exposed to. [If the agent is
part of the Animal Product Safety
Service, the consultation is
at no cost to the caller.]
* The species, breed, age, sex,
weight and number of animals
involved
* The agent your animal(s) has
been exposed to, if known
* The problems your animal(s)
is experiencing.
Be Prepared
Your animal may become poisoned
in spite of your best efforts
to prevent it. Because of this,
you should be prepared.
Your animal companions regularly
should be seen by a local
veterinarian to maintain overall
health. You should know the
veterinarian's procedures for
emergency situations, especially
ones that occur after usual
business hours. You should keep
the telephone numbers for the
veterinarian, the Animal Poison
Control Center, and a local
emergency veterinary service in a
convenient location.
* You may benefit by keeping
a pet safety kit on hand for
emergencies. Such a kit should
contain:
* A fresh bottle of hydrogen
peroxide 3% (USP)
* Can of soft dog or cat food,
as appropriate
* Turkey baster, bulb syringe
or large medicine syringe
* Saline eye solution to flush
out eye contaminants
* Artificial tear gel to lubricate
eyes after flushing
* Mild grease-cutting dishwashing
liquid in order to bathe
an animal after skin contamination
* Rubber gloves to prevent you
from being exposed while
you bathe the animal
* Forceps to remove stingers
* Muzzle to keep the animal
from hurting you while it is excited
or in pain
* Pet carrier to help carry
the animal to your local veterinarian
PROGRESSIVE RETINAL ATROPHY
While not yet common in Yorkies,
Progressive Retinal Atrophy
(PRA), is an incurable hereditary
eye disease which, as the name
implies, progressively attacks
and destroys the retina of the eye,
causing blindness. The retina
is essential to eyesight, for it is here
that a visual image is formed
before being transmitted via the
optic nerve to the brain. A
defect in an enzyme causes a chemical
compound to form that kills
the cells in the retina.
.
PRA begins with night blindness,
followed by gradual loss of
day vision and, eventually,
total sightlessness. In some affected
breeds, vision loss is observed
in puppies, and the dogs may
become blind before or soon
after maturity. In other breeds,
the disease can go undetected
until the dog is several years old
and has passed the PRA gene
to subsequent generations of
puppies. Like retinitis pigmentosa
in humans, canine PRA is
not one disease but a group
of related ones. All are characterized
by malformation or degeneration
of the retinal visual cells.
.
Most forms of PRA are caused
by different, autosomal recessive
gene defects. This means that
for offspring to be affected, both
parents must carry one copy
of the same mutant gene. Both
parents could have normal eyesight,but
have 1 gene for normal
enzyme production that is dominate
over the 1 recessive gene
for the abnormal enzyme defect.
In this case the parents would
be considered carriers.
When a carrier is bred to another dog
with 1 dominant normal gene
and 1 recessive abnormal enzyme
defect gene (i.e., another carrier),
25% of the offspring will be
afflicted with PRA, 50% will
be carriers like their parents, and
25% will possess the normal
2 dominant correct enzyme genes.
If a dog afflicted with PRA
is bred to another dog who is neither
afflicted nor a carrier, then
all the offspring from that breeding
will be carriers (possessing
1 dominant normal enzyme gene and
1 recessive abnormal enzyme
gene). All of these offspring are then
capable of producing PRA if
they are bred to another carrier or
a PRA afflicted dog.
.
In some cases, breeders have
resorted to producing "test litters"
as a means of identifying and
removing all carriers and affected
dogs from their lines. The disease
afflicts an estimated 80 breeds
of dogs worldwide. While PRA
is not widespread among Yorkshire
Terriers, it can, and does,
occur in Yorkies and should not be
ignored in breeding or selecting
a puppy.
.
Research has achieved some success
in developing a test for the
defective gene in other breeds
such as the Mastiff and Irish Setter.
Carriers of the mutant gene
for one type of PRA in Irish Setters
can be detected with a new blood
test developed at the Cornell
College of Veterinary Medicine.
The unequivocal DNA blood
test for rod-cone dysplasia-1
(rcd-1) in Irish Setters gives researchers
hope that similar tests for
other affected breeds will produce
equally promising results.
.
Meanwhile, the best recourse
available to Yorkie breeders and
buyers alike is regular eye
checks by qualified veterinarians,
and honest disclosure of the
problem when diagnosed. Until
the method of detecting the
defective gene in Yorkies is available,
buyers and breeders alike must
depend upon vigilance and
careful research of pedigrees
to reduce the occurrence of PRA
in the breed.
.
Until development of the first
DNA test, PRA can only be detected
by electro- retinography testing.
Conclusive diagnosis for Yorkie
still requires examination by
a canine ophthalmologist. Using
special equipment the opthamologist
will examine your dog's eyes
for a thinning of the retina,
which causes the dog's eyes to be
hyper-reflective. They may also
observe a paleness of the optic
disk and a reduction of blood
vessels in the eyes. This test, which
is available at regional veterinary
centers, identifies only dogs
affected by PRA - not the clinically
normal animals that carry
one copy of the defective gene.
Thus, a carrier can still be
unknowingly used in breeding.
Responsible breeders will supply
information on the eyes of their
dogs in the form of one or more
of the following: eye examination
reports (preferably from veterinary
ophthalmologists), electroretinogram
(ERGs), and examination
forms for the Canine Eye Registry
Foundation (CERF).
.
Since the various forms of PRA
are progressive it is important
that repetitive checks of a
dog's eye health are obtained as they
age, potentially as old as 6
to 7 years (PRA has been observed in
Yorkies (a long lived breed)
as old as 9 years), or prior to breeding.
Although some Yorkies have been
diagnosed as young as 12 months,
a single eye check at a young
age (e.g., 2 or 3 years old) does not
ensure a dog is not afflicted.
Often, the symptoms of the disease
can go un-noticed by owners
until it has progressed significantly.
Since the disease advances slowly,
an afflicted dog can adapt by
depending more heavily on his
sense of smell and hearing. Often
an afflicted dog can cope very
well until total blindness occurs.
It is not unusual for owners
of afflicted dogs to be unaware of
the problem until an eye examination
is obtained.
.
Not all retinal degeneration
is caused by genetic PRA. non-PRA
retinal degeneration does exist
and can be distinguished in the
early stages of development
from genetic PRA. When either type
of retinal degeneration is found
in an advanced state (e.g., the
retina in nearly totally degenerated)
it is not possible to distinguish
between the two types by eye
examination. This is further reasoning
for routine and periodic eye
examinations. Also, because the
determination of PRA can be
subjective and have significant
consequences, a second opinion
would be a good idea.
.
If the CERF information is obtained
for dogs 6 years old or older
and for 3 generations on both
sides of the pedigree, then that is
even better. However, be aware
that a CERF will not guarantee the
lack of a problem, and likewise,
not having a CERF does not indicate
the presence of PRA. Some breeders
have their dog's eyes checked
and never register the results
with the CERF.
.
PORTAL SHUNT (LIVER SHUNT)
This condition is often referred
to as a "liver shunt" but the current
favored term appears to be portosystemic
shunt. These have also
been referred to by more exact
terms since there are specific types
of shunts that vary slightly.
.
There are three shunt types:
intrahepatic, extrahepatic, or
microvascular. The most common
is Portosystemic shunt (PSS)
occurs in many dog breeds the
Yorkshire Terrier is one. It is
an abnormal flow of blood between
the liver and the body.
Since the liver is responsible
for detoxifying the body,
metabolizing nutrients and eliminating
drugs, the blood
bypassing the liver can cause
indications of a possible PSS
which might include, but are
not limited to, neurobehavioral
abnormalities, anorexia, hypoglycemia,
intermittent
gastrointestinal symptoms, urinary
tract problems, drug
intolerance, unthriftiness and
stunted growth.
.
Signs of PSS usually appear
before two years of age, but later
onset has been recorded. If
an animal has a confirmed PSS,
corrective surgery can be helpful
in the long-term management
of these animals. Dietary manipulation
is also important in
maintaining PSS animals. Mode
of inheritance has not been
established.
.
Symptoms:
Most shunts cause recognizable
by the time a dog is a young
adult but once in a while one
is diagnosed at a later time in
life. Since the severity of
the condition can vary widely depending
on how much blood flow is diverted
past the liver it is possible
for a lot of variation in clinical
signs & time of onset for the
signs to occur. Often, this
condition is recognized after a puppy
fails to grow, making an early
diagnosis pretty common.
.
Signs of portosystemic shunts
include:
* poor weight gain
* sensitivity to sedatives (especially
diazepam)
* depression
* pushing the head against a
solid object
* seizures
* weakness
* salivation
* vomiting
* poor appetite
* increased drinking and urinating
* balance problems
* frequent urinary tract disease
or early onset of bladder stones.
* If these signs increase dramatically
after eating, it is a strong
supportive sign of a portosystemic
shunt.
.
Most dogs will be diagnosed
with port-systemic shunts under
one year of age, but dogs as
old as eight have been diagnosed
with the condition. Animals
are usually stunted, thin, depressed,
have trouble gaining weight,
and are usually characterized by
the owners as chronic "poor
doers". In most affected dogs there
will be some degree of behavioral
signs ranging from listlessness,
apathy, or depression to more
severe signs of circling, head pressing,
stupor, drooling, blindness,
or convulsions, some leading to coma.
.
These behavioral changes are
due to an accumulation of toxins
(especially ammonia) that affect
the brain causing a condition
called Hepatic Encephalopathy.
These toxins are most abundant
in the blood stream following
the dog eating, especially a high
protein meal, and may remain
high for hours afterward. Not all
dogs with the shunt will show
this meal associated behavioral change,
but in 25% of the affected dogs
that do, the diagnosis becomes
clearer. A high percent of affected
animals show an intolerance to
anesthetics or tranquilizers,
and will show increased recovery times
following use of these products.
Even anti-convulsants used to control
seizures may be potentially
dangerous if allowed to concentrate in a
dog with functional shunt.
.
Approximately 75% of affected
individuals will show digestive system
symptoms including poor appetite,
ascites, vomiting, drooling,
diarrhea, or occasionally deranged
appetite (eating paper, etc.).
Urinary system symptoms may
include increased thirst and urination,
& in a majority of porto-systemic
shunt cases, there will be crystals
or stones formed in the urinary
tract. These crystals will be either uric
acid or ammonium urate (ammonium
biurate or thorn-apple crystals.).
There can be bladder stones
formed or crystals may be noted on the
hair around the prepuce or vulva.
.
? In virtually all porto-systemic
shunts there will be a significant
rise in the bile acid levels
over normal. The use of bile acids in
screening clinically normal
dogs for liver shunts is not currently
being advised due to the variation
of normal bile acid levels in
Yorkshire Terriers, and other
breeds as well.
.
? Routine performed serum chemistries
are fairly nonspecific
toward confirming the diagnosis
of porto-systemic shunts, but
there may be a decreased total
protein (primarily albumin),
decreased blood glucose, decreased
cholesterol, and decreased
blood urea nitrogen (BUN). The
uric acid levels may be elevated
in a significant number of affected
individuals. Acid levels are
extremely important in the diagnostic
screening of symptomatic
potential shunts. Fasting and
2-hr. post meal blood samples are
evaluated for bile acid levels.
.
? Liver function testing with
Bromosulfaphthalein (BSP) or </ | | |