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Note: written for
Beardies, but may be applied to PONS.
Chronic small intestinal
disease is a problem for many beardies. In young dogs
especially, chronic intermittent small bowel diarrhea often
accompanied by weight loss or failure to gain weight may be
the result of bacterial overgrowth. This isn’t the only
presentation, some dogs may not have diarrhea, others may
vomit or have mild colitis, but in general they are young
and not doing well. Bad bacteria can become established for
a variety of reasons, but mostly these can be grouped as due
to defective production of stomach acid, defective gut
motility, defective local immunity, exocrine pancreatic
insufficiency, defective mucus production, unabsorbed
nutrients and malnutrition. Where possible the underlying
cause of the problem should be treated. If this cannot be
determined oral oxytetracycline or tylosin are usually
effective treatments.
Dietary sensitivity
(allergic reaction) and food intolerance can also cause
chronic diarrhea. Usually the two conditions are difficult
to distinguish, and are treated similarly. Exclusion diets
using a protein and carbohydrate source the dog has not
previously experienced. Owners should never feed any treats
during this phase, just the prescribed diet. It can take 6
to 8 weeks for an improvement to be seen. At this point to
confirm diagnosis the dog should be challenged with the
original diet – which should cause problems to reappear
(surprisingly many owners are reluctant to complete this
step). Foods should be reintroduced one item at a time.
Unfortunately, truly allergic dogs develop allergies to the
new ingredients over time. Steroids may help reduce the
allergic response. Raw and home cooked diets may also prove
successful for these dogs, and evidence of allergy to the
grain mites in kibble has recently been reported.
Infiltration of the
lamina propria of the small intestine wall is characteristic
of inflammatory bowel disease (IBD). In the most common form
the invading cells are lymphocytes and plasma cells; less
commonly the invading cells are eosinophils. This condition
may also co-occur with dietary sensitivity, bacterial
overgrowth, giardia, campylobacter and histoplasmosis and
other fungal infections as well as lymphosarcoma.
Co-existing problems should be addressed. Grossly the
intestinal wall may appear normal or thickened, and
definitive diagnosis is made from biopsy samples taken
during endoscopic examination. Treatment is similar to that
for dietary sensitivity. Reducing carbohydrate and/or
replacing other sources with rice can be very helpful, as
can replacing long chain fatty acids with medium chain ones.
Intestinal
lymphangiectasia is a protein losing condition in which flow
of lymph from the intestines is blocked, the lymph ducts can
rupture and release plasma proteins into the intestines. It
may be congenital or acquired, most often subsequent to
congestive heart failure. A diet high in good quality
protein and low in fat, supplemented with fat soluble
vitamins is helpful. Steroids may help relieve clinical
signs. Where possible the underlying cause should be
treated.
Adenocarcinoma is the
most common intestinal tumor, although lymphosarcoma,
leiomyoma, leiomyosarcoma, fibrosarcoma and intestinal
polyps can occur. Signs of these are vague and progress
slowly. Anorexia and weight loss are usually the first
signs. Adenocarcinoma usually occurs in the duodenum or
large intestine, and may spread locally and sometimes to
more distant sites. Mean survival after surgery is about 7
months. Lymphosarcoma usually spreads to the lymph nodes and
response to chemotherapy in dogs is poor. Leiomyoma and
leiomyosarcoma are tumors of the muscle wall, and if you can
resect the tumor this is usually curative as they rarely
metastasize.
The Large
Intestine is between 28 and 90 cms in dogs, and
runs from the end of the ileum to the anus. There are three
sections. The cecum is an 8 to 30 cms. long pouch off the
colon shortly after it leaves the ileum. The colon has two
distinct bends as it passes through the abdomen to the
rectum. The cell layers of the wall are similar to those of
the small intestine; however, there are no villi and fewer
microvilli, but more mucous secreting cells. Cell turnover
here is slower (4 to 7 days). The large intestine’s primary
function is to extract water and electrolytes from the
effluent from the ileum, and to store feces prior to
defecation. A small amount of fermentation of organic
material occurs in the first part of the colon, but this is
of little significance, unlike the same process in
herbivores. Most muscle contractions are actually away from
the rectum, slowing down the passage of the contents while
they are mixed, stored and dehydrated. Towards the anus,
spontaneous giant contractions propel the contents into the
rectum. The large bowel has a limited capacity for removing
water. Normally it removes 90% of the remaining water, but
if excess water comes from the small intestine, it may be
overwhelmed, and the result is diarrhea. Sodium is also
absorbed, and potassium and bicarbonate secreted. The latter
neutralizes acids produced by fermentation. Bacterial
content in the gut is highest in the large intestine, with
10 11 organisms in each gram of feces – nearly 50% of its
dry weight. The bacteria resist bacterial overgrowth with
unfriendly bacteria, while metabolizing any remaining
carbohydrates, proteins and lipids.
Diarrhea is the most
common sign of large bowel disease. It is characterized by a
lot of mucous, and often accompanied by straining. Blood
will be red rather than the black tarry melena seen with
small intestinal bleeding. Frequency of defecation is
increased, but the amount is diminished. Dogs usually remain
bright and normal; weight loss is uncommon. Strictures or
tumors may result in the production of abnormally shaped
feces. Vomiting and weight loss indicate small intestinal
disease is present too. Diarrhea can be the result of
dietary indiscretion or changing diet too quickly for the
enzymes to adapt; whipworm infection; IBD or neoplasia.
Tumors can be benign – adenoma, leiomyoma or malignant –
adenocarcinoma, lymphosarcoma or leiomyosarcoma – although
the latter can usually be surgically removed completely.
Irritable bowel syndrome, also called nervous or spastic
colon, is a vague term for large bowel diarrhea that is
often fiber responsive (psyllium is curative) or caused by
toxins produced by clostridial bacteria. Other causes of
large bowel diarrhea are fungal, bacterial or parasitic.
Constipation may result
from too efficient removal of fluid from the bowel or
insufficient mucous production. Megacolon – enlargement of
the colon leading to poor motility – is rare in dogs, and is
usually acquired secondary to prolonged mechanical or
functional obstruction of defecation.
Function of the rectum
and anus depends on the coordination of conscious and
unconscious muscular movements. The rectum begins as the
colon enters the pelvis. The region is rich in mucous
secreting cells. If these cells become inflamed then mucous
secretion increases, as does straining and the presence of
blood in the feces. Three kinds of glands empty into the
anal region. Anal glands are modified sweat glands that
secrete lipid into the lumen of the anus. The glands of the
paired anal sacs that lie at positions 4 and 8 just below
the skin around the anus secrete a mixture of dead cells,
protein, sebaceous fluid and bacteria into the sacs. The
circumanal glands surround the anus and are non-secretory.
The anus has two sphincters, the internal one is not under
conscious control. The external sphincter surrounds the
internal one, and is under conscious control. The two
sphincters are normally perfectly coordinated, but damage to
the pudendal nerve can result in fecal incontinence.
While the anus is not
involved in digestion, problems can frequently result in
owners deciding to euthanatize the dog. Problems in the area
can include: perineal hernia – rectum, urinary bladder or
prostate gland can herniate into the anal region; rectal
polyps and other tumors; rectal prolapse; proctitis –
inflammation often secondary to colitis; rectal stricture –
usually the result of trauma or surgery; rectal foreign
bodies – these may lodge in the rectum having passed through
the rest of the intestinal tract. Foreign bodies can cause
secondary fistulas and abscesses. Perianal fistulas are
extremely painful and consist of one or multiple tracts
running from the lumen of the anus through the skin in the
region around the anus. Dogs with broad tail bases that
clamp their tails are at increased risk. Low thyroid and
poor immune function may also be inciting factors. Surgery
and/or topical tacrolimus usually is curative.
Anal sac impaction,
inflammation and/or abscessation is common, and owners
notice their dog licking or biting at the area, scooting
their butts, having trouble sitting (or showing reluctance
to do so), pain and straining on defecation. One or both
sacs may be involved, and they can readily be palpated
through the skin. Normal secretions are clear to pale
yellowish brown. Granular material, pus, blood and turbidity
are all abnormal. Normally impacted sacs can be expressed
easily, but sometimes the secretions form a cement-like
block which has to be cleared before you can express them.
Abscesses are extremely painful, and can cause fever. They
can also lead to fistulas forming. In dogs with a chronic
problem, removal of the sacs is recommended. Feeding a high
fiber diet may help express the sacs. Adenocarcinomas may
affect the anal sacs, and usually metastasize to the nearby
lymph nodes.
The Liver
carries out at least 1500 biochemical functions essential to
a dog’s survival. It is involved in the metabolism of
carbohydrates, lipids, protein, vitamins and endocrine
hormones; immune function; storage; making blood clotting
factors, iron regulation and even making blood in utero and
in extreme situations; making, storing and regulating the
secretion of bile; and the detoxifying and excreting of
drugs, hormones and several other substances. Its storage
capacity, functional reserve and regenerative capabilities
are the stuff of legend, but this doesn’t make it easy to
recognize when something is amiss; and often disease is
severe and advanced before a problem is detected.
The liver is composed of
six lobes. About 80% of the volume consists of hepatocytes.
Another important cell type is the Kupffer cell, these line
the blood vessels passing through the liver. These are fixed
macrophages – cells that ingest and detoxify substances.
They are also needed for the metabolism of iron, lipid,
cholesterol and certain hormones. In addition, they have
several important functions in the immune system. Ito cells
are rich in retinoids and store lipids; they also produce
most of the collagen that results in fibrosis of the liver.
The capillaries passing through the liver have fenestrae or
gaps allowing the passage of much larger molecules than most
blood vessels. When blood pressure increases in the liver
though, these close and become less permeable. Blood
sinusoids serve to dissipate the pressure of blood entering
the liver and store blood; the system is usually maintained
at low pressure. Certain bile salts can increase blood flow
and pressure within the liver.
Hepatocytes are arranged
in cords with one side abutting a blood vessel and the other
a bile canaliculus. On both sides surface area is magnified
by the presence of microvilli, greatly increasing the
surface for nutrient, metabolite, drug, toxin and bile
exchange. These cords are supported on a framework of
collagen and reticulin fibers.
Bile is formed in the
hepatocytes and passes into the canaliculi, then to
ductules, ducts and ultimately the gallbladder. Electrolyte
and fluid content is modified during this passage. In the
gall-bladder it is concentrated and stored until it is
expelled into the duodenum to aid in digestion.
Nutrient rich blood from
the stomach, intestines, spleen, pancreas, colon and
gall-bladder flows into the portal circulation and passes
through the liver before entering the rest of the
circulation. Nutrients are removed and further processed
while undesirable substances absorbed from the gut are
removed and/or detoxified. At any one time 10-25% of the
blood is in the liver. Much of it is being stored. The liver
can actually double its blood storage which alone can lead
to liver congestion. During hemorrhage, it can compensate
for loss of 25% of the total blood volume. At rest about 25%
of cardiac output is passing through the liver, this changes
with exercise, posture and at meal times. While two-thirds
of the blood in the liver comes from the portal vein, one
third comes through the hepatic artery, which supplies the
oxygen needed for liver function. Even brief interruption of
blood flow through the hepatic artery can lead to lethal,
septic necrosis.
In newborn puppies most
of the abdominal cavity is occupied by the liver, in the
young dog the ratio of liver to body weight is about 4 to 5:
100, but in older dogs this drops to 2:100. Small livers may
be the result of reduced blood perfusion, chronic fibrosis,
atrophy of the hepatocytes, or loss of their cellular
content. Enlarged liver can result from passive congestion,
infiltrative or inflammatory conditions, blockage of the
bile ducts and cystic liver disease. Drug exposure –
barbiturates etc.; infection or inflammation of the
hepatocytes can result in increased liver mass secondary to
enlargement of the organelles within the cells. If 70% of
the liver is removed, in 6 weeks the remaining liver can
have regrown to pretty much normal size and functional
capacity. During that time, the body must have adequate
glucose and coagulation factors provided, however.
Bile acids are formed
from cholesterol and bound to an amino acid, usually taurine
but sometimes glycine. Bile is secreted in volume into the
intestines when food is consumed, and helps digestion and
absorption of fat. Bile is released in smaller quantities,
sometimes by-passing the gallbladder, at other times. Some
dogs will vomit up bile if they have not been fed –
particularly before the morning feed. Giving a bed-time
cookie is usually enough to prevent this happening.
Early signs of
hepatobiliary disease are usually vague – anorexia,
vomiting, diarrhea/constipation, weight loss, intermittent
fever. A more specific sign would be jaundice – yellowing of
the mucous membranes and non-pigmented skin and eye whites –
this can appear rapidly with major occlusion of the bile
duct or very slowly. Gastrointestinal ulceration and
hemorrhage may occur as disease progresses. Bleeding
tendencies, due to Vitamin K deficiency, usually take a
couple of weeks to appear. Feces may become dark green or
dark-green/orange due to increased blood break down or pale
gray or tan and fatty if bile flow is obstructed.
Significant bleeding into the bowel produces black tarry
feces. Increased drinking and urination and the appearance
of urobilinogen in urine indicate liver disease, although
some animals have problems urinating. Change in liver size
can often be palpated. Neurobehavioral changes – ataxia,
lethargy, stupor, head-pressing, obsessive circling, sudden
unexplained blindness, seizures or coma can indicate severe
acquired liver insufficiency or congenital portosystemic
shunt – where some or all blood from the digestive tract
by-passes the liver and goes directly into the main
circulation. Ascites, the accumulation of fluid in the
abdomen, is often the result of increased blood pressure in
the portal vein usually indicating obstruction.
Diagnosis of liver
disease begins with basic blood testing a complete blood
count and biochemistry profile, in fact in many cases liver
disease can be discovered before any physical signs become
apparent. However, liver enzymes can be elevated by a number
of unrelated conditions – bone disorders or growth;
endocrine disease; gastrointestinal and splenic disease;
hypoxia; drugs; low blood pressure; neoplasia; systemic
infection; trauma; fever; wasp stings or after general
anesthesia! If none of these are apparent follow up with
ultrasound and biopsy are probably the most helpful
procedures for characterizing the cause of the liver
disease. X-rays and nuclear scintigraphy may also be
helpful.
Acute hepatic
failure occurs when a sudden severe insult to the
liver results in compromise of at least 70 to 80% of
functional liver mass, exceeding the liver’s functional
reserve and resulting in signs of liver failure. Diffuse
necrosis of liver tissue is the most obvious and consistent
sign. Causes can include hepatotoxic drugs and anesthetic
agents; chemical and biologic substances (aflatoxin; amanita
mushrooms; blue green algae; pennyroyal oil; heavy metals;
herbicides; fungicides; rodenticides; household cleaners;
industrial chemicals, etc.); infectious or parasitic agents
(viral hepatitis, acute bacterial cholangiohepatitis;
leptospirosis; liver abscess; extrahepatic infections and
sepsis; systemic fungal infection – esp histoplasmosis;
toxoplasmosis; postcaval heartworm infection); systemic or
metabolic disease (acute pancreatitis; acute hemolytic
anemia); trauma; diaphragmatic hernia with liver entrapment;
heat stroke; surgery where blood pressure and oxygen
perfusion is compromised; liver lobe torsion. Treatment
depends on the underlying cause of the liver failure. Given
the liver’s role it is especially vulnerable to a vast array
of substances, and this is something we should consider
before introducing any substance into our dog’s or our
family’s environment. Apart from acetaminophen antidotes
exist for most acute hepatotoxins.
Cholestatic
hepatobiliary disease is the result of impaired
flow or excretion of normal volumes of bile. Substances
normally secreted in the bile build up in circulating blood
serum – bile acids, bilirubin, cholesterol – and there is
increased activity of enzymes associated with the cells of
the biliary tract – alkaline phosphatase (ALP) and
gamma-glutamyltransferase (GGT). Jaundice is the hallmark of
this condition. Cholestasis can result from blockage or
rupture of the bile ducts. This often requires surgical
correction. Common causes are pancreatic disease (edema,
abscesses, cysts or cancer), or gallstones. Retention of
bile in the liver can cause secondary injury to hepatocytes.
Chronic liver disease – hepatic fibrosis and
cirrhosis – can also result from a great many
causes. Repeated exposure to drugs or toxins; infection;
cholestasis; immune injury (chronic idiopathic hepatitis)
and hypoxia often secondary to cardiac failure are all
potential problems. A single episode of massive hepatic
necrosis could cause end stage liver disease. However, the
cause is never determined in most cases. One study showed
that cirrhosis was responsible for 15% of the cases of liver
disease as determined by biopsy.
In cirrhosis fibrous
tissue replaces much of the normal liver and the remaining
cells become disorganized further limiting function. It is
irreversible, and while removing the underlying cause may
slow progression of the disease it can not restore the
liver. Blood flow to the liver is compromised, and blood
pressure increased, so remaining cells are less able to
function.
Nodular
hyperplasia is a common post-mortem finding in dogs
over the age of 8. These nodules are not precursors to
cancerous lesions, and they are not associated with clinical
signs. Unfortunately, they cannot be distinguished from
primary or secondary neoplasia on ultrasound, only by
biopsy.
Liver cancer
may be primary or metastatic and virtually all types of
cancer have been reported. Metastatic cancer from pancreas,
lymph nodes, spleen, mammary glands, adrenal glands, bone,
bone marrow, lungs, thyroid glands and gastrointestinal
tract is more common, and lymphosarcoma and pancreatic
carcinoma are the most common types. Primary tumors are
rare, and they are not associated with viral infection,
exposure to chemical carcinogens, toxins, drugs or prior
liver disease as they are in humans. These tumors can be
benign or malignant.
I am not aware of any
cases of congenital portosystemic shunts being reported in
Beardies. Multiple acquired portosystemic shunts can result
as a compensatory response to prolonged elevated portal
blood pressure. Likewise hepatic arteriovenous fistulas can
form as a result of elevated blood pressure in the hepatic
artery diverting blood into the portal system. Neither
condition is common. Both are more common in younger dogs,
and in certain breeds, but not in beardies.
Hepatic lipidosis
is an excessive accumulation of fat (triglycerides) in the
liver. It is caused by an imbalance between rate of
deposition and dispersal of fat, and can be nutritional,
metabolic, hormonal, toxic or hypoxic in origin. The
clinical significance depends on the severity and underlying
cause. Excess fat does not impair liver function, but
results in a large, pale yellow liver – such as that of the
foie gras goose. Diabetes mellitus is one of the most common
causes. Treating the underlying cause is desirable.
Hypertriglyceridemia – elevated triglyceride (TG)
levels in serum - is the most prevalent lipid disorder in
dogs. It may result in vomiting, diarrhea and non-localized
abdominal pain. Signs frequently resolve with fasting.
Seizures may also be a presenting sign. Reducing dietary fat
is often curative, but feeding gastrointestinal diets (such
as Hill’s i/d) may make the condition worse. Blood
triglycerides must be measured after fasting the dog to
distinguish the condition from normal post feeding elevation
of TG. Other rule-outs include diabetes mellitus, which can
result in marked increase in TG and mild elevation of
cholesterol (CH); protein losing nephropathy due to kidney
disease which increases both TG and CH. The primary cause of
elevated CH is hypothyroidism, although 30% of dogs with
Cushing’s Disease (hyperadrenocorticism) have elevated CH,
too.
The major function of the
exocrine pancreas is to secrete digestive
enzymes and coenzymes. It also secretes bicarbonate to help
neutralize stomach acid, and factors that assist in
absorption of Vitamin B 12, zinc and probably other
nutrients. Pancreatic fluid inhibits bacterial overgrowth in
the duodenum and jejunum, helps with normal degradation of
old brush border cells, and promotes growth of the mucosa
together with biliary secretions. The pancreas protects
itself from digestion by several mechanisms, including
producing an enzyme inhibitor (pancreatic secretory trypsin
inhibitor), which it secretes together with the digestive
enzymes.
The pancreas has left and
right lobes and a small central body where they join
together. Embryonically it grows out from the duodenum to
which it stays connected by two secretory ducts –pancreatic
duct and accessory pancreatic duct. The right lobe lies
alongside the duodenum and the left lobe along the pyloric
region of the stomach.
The acinar cells of the
pancreas secrete enzymes to degrade proteins, lipids and
polysaccharides. Proteolytic and phospholipolytic enzymes
are stored as inactive zymogens, which are normally
activated in the intestines by cleaving a small peptide from
the zymogen, so trypsinogens become trypsins etc. This is
achieved by an enzyme – enteropeptidase – formed in the
enterocytes. The trypsins, chymotrypsins and elastases
cleave polypeptides at specific sites, while
carboxypeptidases lop off terminal carboxyl residues.
At rest the pancreas
secretes about 2% of the bicarbonate and 10% of the enzymes
it does when the animal eats a meal. There are cyclic
increases though in the amounts secreted. After a meal
secretion occurs in two phases, the first, which peaks an
hour or two after eating, is rich in enzymes. The second
phase occurs about 8 to 11 hours after the meal, is more
voluminous and rich in bicarbonate. Low levels of amylase,
lipase and zymogens leak into the blood stream.
Pancreatitis
is inflammation of the exocrine pancreas. Acute pancreatitis
has a sudden onset, may occur repeatedly, but causes little
or no permanent pathologic change. Chronic pancreatitis is a
continuing inflammatory condition resulting in permanent
impairment of function. Pancreatitis seems to result when
the proteolytic enzymes are activated while still in the
pancreas causing autodigestion. This is probably because of
a failure of the normal secretory process. In most cases the
inciting cause is unknown. Some potential causes are:
nutrition/hyperlipoproteinemia – low protein, high fat
diets, and especially prevalent in obese animals; drugs,
toxins, hypercalcemia; duct obstruction – gall stones,
tumors, parasites, trauma, edema, sphincter spasm; duodenal
reflux, pancreatic trauma, loss of circulation/reperfusion
injury; viral, fungal or parasitic infection.
Signs usually include
depression, anorexia, vomiting, sometimes diarrhea and pain
– splinting the stomach (praying). In severe cases the dog
may have collapsed and be in shock. They are usually mildly
to moderately dehydrated and have a fever. In some dogs a
mass at the front of the abdomen can be felt. CT scans are
the most useful for diagnosing pancreatitis, but ultrasound
may be helpful. Fluids and careful electrolyte balance
together with nothing given by mouth is the basis for
treatment. In uncomplicated cases, prognosis is good for
complete recovery, although it is recommended that high fat
foods be avoided in future.
Exocrine
pancreatic insufficiency (EPI) is quite common in
Beardies. Pancreatic acinar cells are progressively lost and
replaced by fibrous tissue so that the body ultimately fails
to produce sufficient digestive enzymes and food is not
absorbed but passes through to the feces largely unchanged.
Signs do not appear until most of the tissue is lost, for
example fat in the feces is usually not observed until
85-90% of the secretory capacity has been lost. Even without
pancreatic enzymes, alternate pathways do exist, and up to
63% of ingested protein and 84% ingested fat will be
absorbed without pancreatic enzymes.
In the majority of dogs
pancreatic acinar atrophy is the primary cause of EPI. The
cause is unknown, although nutritional deficiencies – amino
acid imbalance, copper deficiency, protein-calorie
malnutrition – have been postulated. Malnourishment
secondary to small intestinal mucosal abnormality has also
been suggested as dogs often show g/I disturbance long
before there is significant weight loss. In humans, and
apparently in quite a lot of Beardies, chronic pancreatitis
is the cause of EPI. In some cases diabetes mellitus may
co-exist with EPI. In some dogs congenital EPI has been
reported, as well as EPI secondary to surgical resection of
the duodenum.
In many dogs with EPI,
enzymes malfunction, there are changes in the mucosa of the
small intestine resulting in abnormalities of transport
mechanisms and changes in bacterial presence. Dogs have
often suffered from malabsorption a long time before
diagnosis is made or help sought however, and this may
result in some of the associated changes that have been
reported.
The best test for EPI is
a blood test – serum trypsin-like immunoreactivity (TLI).
This test rules out small intestinal disease (IBD) as the
cause of the malnourishment. Dogs are managed by
supplementing each meal with pancreatic enzymes and most do
quite well. The enzymes – especially lipase – are largely
digested themselves though before they reach the small
intestine. Attempts to maximize enzyme efficacy - such as
predigesting food with enzymes prior to feeding - have not
proven to have any advantage. Highly digestible diets should
be fed, and in most cases dogs require slightly more food
than their healthy counterparts to maintain their ideal
weight. Like all exocrine pancreatic diseases, EPI can be
very painful and dogs may become more aggressive as a result
of the pain as well as hunger. Vitamins B 12 and E may need
to be supplemented in dogs with EPI.
Adenocarcinoma
of the acinar or pancreatic duct cells is relatively
uncommon in dogs. When it does occur, the dogs are older.
These tumors are highly malignant and have usually
metastasized to the duodenal wall, liver and lymph nodes
prior to diagnosis. Signs are usually non-specific -
anorexia, depression, vomiting. If the bile ducts are
involved the dog may develop jaundice, if the pancreatic
duct is blocked there will be signs of EPI, and if the beta
cells are affected signs will be of diabetes mellitus. An
abdominal mass may be palpated, or a tumor visualized via
ultrasound, but diagnosis is usually made via exploratory
surgery. Prognosis is extremely poor |
