Liver Diseases
There are a large number of diseases
that affect the liver. This should not be surprising when you consider
how important and metabolically active the liver is. We will discuss a
few of the more common diseases we encounter.
There are many different treatments for
liver disease as you will learn about in this page. Some are surgical,
most are medical. In a siginficant number of cases we encounter a
diseased liver that is chronic in nature, and our treatment goal is to
control the symptoms by helping the liver help itself. Several natural
compounds might be used:
- S-Adenosylmethionine (SAMe, Denosyl)
This is a
precursor to a major antioxidant produced by a normal liver called
glutathione.
- Milk Thistle (Silymarin) (Denamarin).
This compound
has a long history of use in human medicine. We usually use Denamarin
because it contains both SAMe and milk thistle in one product.
VItamin E
prevents damage to the cell membrane of the liver cells
Zinc is a
trace mineral that helps increase glutathione levels. It is also used
in Copper Storage diseases you will learn about in this page. Zinc is
combined with milk thistle and Vitamin E in a product called Marin
Hepatic Lipidosis Pathogenesis
A small amount of fat is normally
present in hepatocytes. The original source of this fat is from the
diet. From the intestines (remember, bile needs to be present for this
to occur) fat is absorbed into bloodstream, binds to albumin and is
presented to hepatocytes. This fat is in several forms, the main ones
being cholesterol, triglycerides, and fatty acids.
Fat is used for energy, the production
of sex and steroid hormones, in cell wall integrity, and as storage for
future energy needs. In a normal liver the rate at which the fat from
the bloodstream enters the liver and the rate at which the liver
utilizes this fat is roughly equal. When there is an imbalance between
the rate of deposition of fat in hepatocytes, and the rate of
utilization of this fat, the amount of triglycerides builds up and
lipidosis results. In many species this excess of fat in the
hepatocytes causes no serious problem. In cats it can become a serious
problem.
The exact mechanism that causes this
imbalance in cats is unknown. It is speculated that excess fat stores
in obese cats overwhelm the liver when these fat stores are needed for
energy (a cat that is not eating or is starving). This sets off a
cascading series of events that involve insulin, glucose, and the
enzyme lipase, leading to excess accumulation of triglycerides in
hepatocytes.
Primary
This disease, seen more often in cats
than in other animals, occurs when excess fat (called triglycerides)
accumulates in liver cells (hepatocytes) and bile accumulates in
hepatocytes (cholestasis). It is technically called Idiopathic Hepatic
Lipidosis (IHL). The idiopathic part means that the specific cause is
unknown. This form of lipidosis causes liver failure, and can lead to
death if left untreated.
Secondary
In this form of hepatic lipidosis the
fat accumulation occurs secondary to some other problem. This is more
common than primary hepatic lipidosis. Secondary hepatic lipidosis does
not cause liver failure. When the primary disease is treated the liver
problem tends to resolve. A large percentage of cats have hepatic
lipidosis secondary to these diseases:
Signalment
IHL can occur in any age or breed of
cat, although it is not commonly seen in young cats. It is the most
common liver disease found in cats.
Toy breed dogs can get a lipidotic liver
after fasting or not eating for a period of time. They become
hypoglycemic (low blood sugar), and can even die.
History
Cats with IHL consistently have anorexia
(not eating), leading to weight loss. They are usually (or were) obese,
and sometimes there is a history of a recent stressful episode that
caused them to stop eating. Many owners will notice jaundice (icterus)
and vomiting. Other symptoms could include diarrhea, constipation,
salivation, and depression.
Physical exam
Cats with IHL have lost weight (although
they could still be obese when examined) and may have yellowish
discoloration (icterus) on the ears, the whites of the eyes, and the
oral mucous membranes (gums). an enlarged liver (hepatomegaly) might
even be palpated. Some of the other common signs of liver disease as described previously might be present on
occasion.
This cat has
icterus (jaundice) of its oral cavity from hepatic lipidosis, although
a severe enough anemia could also cause this appearance.
This is the way the blood looks just after it was obtained
on this cat and spun down in our centrifuge. The serum, which is the
top layer, has the same yellowish-orange appearance as this cat's gums.
Diagnostic Tests
A blood panel will commonly show highly
elevated levels of ALT and Alk Phos, and mild elevations in GGT. In
addition there are commonly high levels of bilirubin in the bloodstream
and the presence of bilirubin in the urine. A bile acids test is
frequently elevated, and the blood ammonia level might also be elevated
on occasion.
Other findings could include anemia, low
albumin (hypoalbuminemia), high cholesterol (hypercholesterolemia), low
BUN, low potassium (hypokalemia), and high glucose (hyperglycemia).
Diseases that can mimic IHL in cats
include FIP, cholangiohepatitis, and
liver cancer. a biopsy of the liver (usually performed when the
ultrasound is done) is needed to verify the diagnosis. IHL usually
involves many hepatocytes, so a general sample of any liver tissue
usually yields diagnostic results. This is not the case with all liver
diseases though. Some are focal and involve only a small portion of the
liver. Fortunately, the ultrasound can pick up these focal areas and a
biopsy needle can be directed to the diseased area by the ultrasound.
Radiography
Radiography might show hepatomegaly or a
normal sized liver. Weight loss might be apparent on the radiograph,
yet abdominal fat stores might be normal.
Ultrasound
Ultrasound reveals hepatomegaly with
telltale changes of the liver parenchyma (internal anatomy of the
liver). Ultrasound might also show inflammation of the pancreas
(pancreatitis).
Exploratory Surgery
If an exploratory surgery is performed
the liver might appear tan or yellowish in color, enlarged, and with
swollen borders. It is greasy to the touch and easily injured.
Exploratory surgery allows us to take a large section of the liver for
biopsy. It also allows visualization of other abdominal organs,
particularly ones that might be implicated in this disease like the
pancreas.
This liver and gallbladder are typical
of a cat with IHL.
Histopathology
A pathologist needs to analyze the liver
microscopically to make a definitive diagnosis.
Treatment
Supportive care is crucial, and may have
to be instituted for a prolonged period of time. Cats with IHL should
be kept in the hospital until they are taking all medications well and
their blood parameters are improving.
Fluids and Electrolytes
This corrects the dehydration that
occurs with a poor appetite and supplies needed sodium, potassium, and
chloride. This fluid is usually given intravenously
(IV) at first. It can be given subcutaneously
(SQ) at home after the initial dehydration is corrected. B-Complex
vitamins are routinely added to the fluid bag to correct a deficiency
that can occur with IHL. Vitamin K might be needed in cats with
clotting problems. This deficiency might be due to anorexia and reduced
synthesis by the atrophied intestines. Simultaneous with fluid therapy
we will begin caloric support.
Caloric Support
This is the most important part of
treatment for IHL, and usually involves the use of a feeding tube. It
is so important that we have devoted a full
page to it.
Cats need at least 60 Kcal/kg/day of
caloric dense high protein diet. The lining of the small intestines
(called villi) will atrophy due to a lack of use, so a short adaptive
period is needed to get them functioning properly again. This is done
by feeding small amounts of food for the first few days, even though
full caloric requirements are not being met.
The protein level of the diet should not
be restricted unless they are showing obvious signs of hepatic
encephalopathy (HE).
Appetite stimulating drugs (Valium,
periactin) have no place in hepatic lipidosis due to their
ineffectiveness, and some of them might even predispose cats to hepatic
encephalopathy (HE).
Human enteral diets do not have adequate
protein, arginine, or taurine for cats.
Antibiotics
A weakened immune system, the stress of
diagnostic tests, hospitalization and treatment, predisposes these cats
to infections. Antibiotics will help in this situation, especially if
mental depression is present from hepatic encephalopathy (excess
ammonia in the bloodstream). Antibiotics minimize the bacteria count in
the colon, thus reducing the amount of ammonia that is absorbed from
the intestines into the bloodstream.
Tetracycline antibiotics should be
avoided if possible because they could be an initiating cause of
hepatic lipidosis.
Lactulose
This drugs helps minimize the ammonia
buildup that leads to vomiting, salivation, and mental depression.
Anti-vomiting medication
Drugs like Reglan can control vomiting
and minimize gastric bleeding due to ulcers. As a general rule we want
to minimize the use of Valium and cortisone in cats with IHL.
Ulcer Medication
Medications like Tagamet and sucralfate
will help protect the stomach lining and make pets feel much better.
These pets are more inclined to eat.
Supplemental Treatment
Some cats might benefit from other
treatment modalities, although this is not the case in all cats. The
mechanisms of action of these supplements are postulated but not proven.
L-Carnitine- This essential amino acid
is required for proper fat utilization by the liver. Even though low
levels are not found in cats with IHL, supplementation might be
beneficial.
Arginine- This is another amino acid. It
comes from muscle protein when cats are fasted. After a prolonged fast
the muscle is depleted of protein and a deficiency of arginine might
occur. A deficiency might lead to high levels of ammonia and eventually
hepatic encephalopathy (HE). It is an essential amino acid in the cat.
Taurine- This is also an amino acid that
could be involved with IHL. It is an essential amino acid, so
supplementation might be helpful.
Ursodiol- This drug has an affect on how
the liver metabolizes cholesterol and decreases the toxic effects of
bile.
When the appetite starts to return we
will slowly decrease the volume of food given via tube feeding. When
your cat is eating well on its own, and the liver tests have improved
on the blood panel, we will remove the feeding tube. This can be
anywhere from several days to several months.
Prognosis
This disease is reversible in most cases
when treated medically. Cure rates range from 65% to 75% when treatment
is started early enough.
Cats that have pancreatitis, remain
persistently hypokalemic (low potassium), or whose elevated bilirubin
does not decrease significantly within 10 days have a guarded to poor
prognosis.
Monitoring
Changes can occur rapidly during the
early phases of treatment, so blood parameters need to be routinely
monitored, especially electrolytes like potassium and phosphorous.
Phosphorous, potassium, and red blood cell levels should be monitored
for the first 72 hours after initiating caloric support. Serum enzymes
and bilirubin should be monitored weekly until appetite returns.
Prevention
Even though the specific cause of IHL is
unknown, obesity is a known predisposition. Since obesity is
controllable you can dramatically reduce the chance of your cat getting
IHL by keeping it at a proper weight.
Overweight cats should be fed Hills
Prescription diet R/D® until they decrease to their
optimum weight. At that time they should be fed Hills Prescription diet
W/D® to maintain their normal weight.
Early treatment dramatically increases
the chance of recovery, so if your cat does not eat for 24 hours it
should be brought to our clinic for an exam and blood testing.
Porto-systemic Shunt (PSS)
Pathophysiology
Ammonia comes from bacteria in the
intestines and when muscles utilize protein as a energy source. In a
normal animal this ammonia gets delivered through the portal vein
directly into the liver. The liver cells metabolize the ammonia to
urea, which is excreted by the kidneys. The liver also detoxifies
bacteria and drugs that are also absorbed from the intestines before
they get into the general circulation and go to the rest of the body.
Shunts occur when the blood supply
through the liver is abnormal. The abnormal blood vessel shunts blood
around the liver instead of through the liver. By bypassing the liver
the toxins that are normally metabolized by the liver (especially
ammonia) are allowed to enter the general circulation before the liver
has a chance to detoxify them. It is this ammonia buildup that causes
most of the symptoms observed with PSS. It is also know as hepatic
encephalopathy (HE) because of its toxic effects on the brain.
Also, important "hepatotrophic"
substances from the pancreas and intestines are prevented from going to
the liver, causing the liver to atrophy.
Several factors can add to HE. A diet
high in protein will add to blood ammonia levels, along with infection,
cancer, and excess use of cortisone. Kidney disease along with
constipation will also add to the problem. Some drugs, notably
barbiturates, Valium, and anesthetics can also be factors.
Shunts can be multiple or single. The
shunt can occur within the liver (intrahepatic) or in the blood supply
before it enters the liver (extrahepatic). Larger breed dogs are more
prone to intrahepatic shunts, extrahepatic shunts are more common in
small breed dogs and cats. It is important to differentiate them for
therapeutic purposes.
There are other diseases that can mimic
PSS. They include liver toxins, liver infection, liver cancer, and
hepatic lipidosis (see previous description). An organ as complex as
the liver necessitates the need for a precise diagnosis before
treatment can be instituted. Also, a pet with chronic liver disease
leading to cirrhosis will sometimes get acquired shunts.
Causes
Congenital
The congenital version of PSS occurs more commonly in
dogs than in cats. Most of these shunts are extrahepatic, meaning the
shunting vessels are located outside of the liver.
Acquired.
Seen mostly in dogs, they occur when there is increased
resistance to blood flow through a fibrotic liver. These shunts occur
inside the liver and are not easily corrected.
Signalment
Congenital shunts tend to be found in
younger dogs and cats (usually less than a year), while acquired shunts
tend to occur in older animals.
Small breed dogs tend to have more
extrahepatic shunts while large breed dogs tend to have intrahepatic
shunts.
In some situations the symptoms of this
disease are so subtle that a diagnosis of congenital shunt is not made
until a pet is much older. We tend to see it more often in male cats as
opposed to female cats.
Several dog breeds are predisposed:
Cat breeds might include:
History
Some of the symptoms of PSS can be
subtle, and easily interpreted as a quiet puppy or kitten. Symptoms can
wax and wane, thus they are easily missed. Some pets seem to have a
preference for fruits and vegetables.
Behavior changes, particularly right
after eating. These changes include depression, head pressing, pica
(eating abnormal things) blindness, lethargy, coma, seizures, and
personality changes. Anorexia, vomiting, diarrhea, and excess
salivation (more so in cats) might be present. Excess urinating and
drinking (PU/PD), blood in the urine (hematuria), urinary tract
infection, and an increased incidence of ammonium urate bladder stones might
also be present. These stones might even cause an obstruction and
prevent normal urination. Other symptoms might include inhibited
growth, fever, and abnormally long recovery periods from anesthesia
(ex.-when a spay or neuter is performed).
Physical Exam
Pets with PSS will commonly be stunted
in growth, but usually exhibit no abnormalities on their neurologic
exams. A small liver might be palpated on smaller animals. Hair coat
might be unkempt and there might be ascites on abdominal palpation.
Other occasional findings include cryptorchidism.
Diagnostic Tests
Several diseases mimic PSS. They include
Distemper, FIP, toxoplasmosis, FeLV related diseases, toxicities,
idiopathic epilepsy, and hypoglycemia. This emphasizes the importance
of proper testing to come to an accurate diagnosis.
Blood Panel
In dogs, a blood panel might show anemia
along with elevated levels of ALT and Alk Phos. The BUN might be low,
cholesterol might be low, the protein level might be low
(hypoproteinemia), and the blood sugar might be low (hypoglycemia) in
the smaller breed dogs. A bile acids tests will show an elevation,
particularly after we feed a meal. If we suspect PSS as the cause to
your pets problem we will run a blood ammonia level, which will come
back elevated if PSS is present. An ammonia tolerance test might be
needed for verification.
In cats the albumin, BUN, and
cholesterol might be low or at the low end of the normal range.
Urinalysis
A urinalysis might show symptoms of
urinary tract infection or abnormal crystals, particularly ammonium
biurate.
Radiography
A radiograph of the liver might show a
small liver (microhepatica), particularly in the dog. The liver might
be hard to evaluate because a lack of abdominal
fat, due to emaciation or a young animal.
Kidney changes and bladder stones might be visible,
although ascites might obscure vision of internal organs. ammonium
urate bladder stones might not show up on a radiograph even though they
are present.
Ultrasound
Ultrasound can give further information
on the liver and its blood supply, and even detect ammonium biurate
bladder stones which normally don't appear on a radiograph. Ultrasound
is better at differentiated intrahepatic shunts as opposed to
extrahepatic shunts.
Positive Contrast Portography
Some consider this test the gold
standard for diagnosis. In this test a special dye is injected directly
into one of the veins of the small intestines while a pet is under anesthesia. A radiograph is taken and the flow of
the dye is followed. If a shunt is present this will show up on the
radiograph.
Biopsy
A biopsy of the liver (usually performed
when the ultrasound is done) will show microscopic abnormalities
consistent with PSS. This usually includes small hepatocytes and a
decrease in the blood vessels within the liver.
Laparotomy
Exploratory surgery to visualize the
vessels directly, or to inject dye into the portal vessels, is also
used to verify the diagnosis. After the dye is injected a radiograph is
taken to assess absorption. Surgical repair can immediately be
initiated.
Scintigraphy
A transcolonic nuclear scan can give a
definitive diagnosis. In this test a small amount of radioactive (99technetium
pertechnetate) material is put into the colon and its absorption is
monitored. In pets with PSS this radioactive material will appear in
the heart before it appears in the liver, the opposite of what should
normally happen. This test does not require anesthesia like the
Positive Contrast Portography test.
Treatment- Medical
Fluids and Electrolytes
This corrects the dehydration that
occurs with a poor appetite and supplies needed sodium, potassium, and
chloride. This fluid is usually given intravenously
(IV) at first. Pets that are severely ill from PSS should not be given
anything orally initially.
Cleansing Enemas
Enema's will decrease the bacterial
count of the intestines, leading to less ammonia absorption.
Lactulose
Lactulose works in the large intestine
to minimize the production of ammonia by bacteria. It does this by
changing the pH and converting ammonia to a form that is not readily
absorbed into the bloodstream. It also stimulates normal colon bacteria
to absorb ammonia, which is then passed in the feces. Finally, it
stimulates the intestines so that ammonia passes through faster, which
means there is less time for absorption.
Antibiotics
These drugs are also administered,
especially if mental depression is present. They minimize the bacteria
count in the colon, thus reducing the amount of ammonia that is
absorbed from the intestines into the bloodstream. They work well with
lactulose to decrease the ammonia level.
Antiparaciticides
Internal
parasites can cause gastrointestinal bleeding and also make the
symptoms of PSS worse.
Dietary Modification
A diet that is restricted in protein may
be beneficial because less ammonia is produced as a by-product of
metabolism. This protein needs to be of high biological value, such as
eggs and dairy products. Meat based proteins should be avoided since
they can increase the chance of HE. Most of the caloric needs of a pet
with PSS should be supplied with carbohydrates like rice and pasta.
Higher fiber diets might also be helpful, as long as the dog or cat is
not undernourished. They can act to minimize ammonia production and
absorption in a manner that is similar to lactulose.
Hill Prescription Diet L/D®
is very helpful in liver disease. It contains added amounts of
nutrients that a diseased liver needs. It also has restricted amounts
of nutrients that can make the condition worse. For example, sodium
(Na) is limited to minimize fluid buildup in the abdomen (ascites).
Instituting these medical treatments is
necessary even if surgery is planned because they will aid in recovery
and make for a better anesthetic risk.
Treatment- Surgical
For many PSS cases surgery is the
treatment of choice. The abnormal vessel that is shunting blood around
the liver is identified and closed (ligated) to minimize blood flowing
through it. When the abnormal blood vessel is ligated blood will now
flow through the liver instead of around it. Several techniques are
used, depending on the particulars of the case and the training and
experience of the surgeon:
- Cellophane Banding
- Ameroid Ring Constrictor
- Suture Ligation
- Thrombogenic Intravascular Coil
- Hydraulic Occluder
This surgery is readily accomplished for solitary extrahepatic shunts.
Intrahepatic shunts can be more difficult to identify and ligate. Post
surgical monitoring is important. If the pressure within the liver
becomes too high due to the increased blood flow through the liver then
the ligation on the shunting vessel(s) must be reduced or removed.
In some cases medical management must
also be utilized to affect a cure. The final outcome of treatment
depends on what age the PSS started, how long it has been present, and
whether it is intrahepatic (worse prognosis) or extrahepatic in nature.
Long Term Monitoring
Pets on long term medical care need to
be monitored carefully. Body weight, albumin, and total protein are
watched to ensure adequate protein in the diet. Initially, these tests
should be performed monthly, then every 3 months. In addition to the
above tests, bile acids are monitored monthly, then every three months
to assess the vitality of the liver. Blood ammonia levels are monitored
monthly to assess effectiveness of treatment. When stable, ammonia
levels can be monitored every 3 months.
Prognosis
Many pets with isolated extrahepatic
shunts return to a normal life after surgery. There is no guarantee
that surgery will correct the problem, especially those pets that
develop the disease very early in life. Some of them will need medical
management simultaneously. The prognosis for pets that are treated only
medically varies. Cats do not do as well as dogs when surgery is
attempted.
Chronic active Hepatitis
This disease is also known as Chronic
canine Inflammatory Hepatic Disease (CCHID). It is a series of
different liver diseases with similar characteristics when analyzed
under the microscope (histopathology). It has similarities to cirrhosis
found in humanoids.
Cause
Usually unknown. In some cases an
infection caused by a bacteria called Leptospirosis or a virus called
adenovirus is the cause. We protect dogs from this adenovirus when we
give a DHLPP vaccine. The "H" stands for hepatitis caused by the
adenovirus. This same vaccine can also protect dogs from Leptospirosis.
Some dogs can get a vaccine reaction to Leptospirosis, and since the
disease is not prevalent, it is not commonly given.
Pathophysiology
The immune system makes antibodies that
affect liver cells. Toxic compounds add to the problem. Some of these
compounds include cholesterol, iron, copper, and toxins located within
the blood vessels. All of this leads to inflammation, and the eventual
replacement of normal liver cells (hepatocytes) with fibrous tissue.
Eventually, the blood flow through the liver is compromised, the blood
pressure within the liver is elevated (hypertension), and numerous
extrahepatic PSS's develop (see PSS above). The body then shows signs
of fluid buildup in the abdomen (ascites) and HE (see above). After a
variable period of time liver failure often results.
Signalment
It tends to occur more often in older
animals. Several dog breeds are predisposed:
- Doberman Pinschers
Most common in middle-aged females
with improper copper metabolism.
- Cocker spaniels
Most often in older males. Typical
symptoms include fluid buildup in the abdomen (ascites) and low albumin
(hypoalbuminemia) on a blood sample.
- West Highland white terriers, Bedlington terriers,
and Skye terriers.
It is associated with copper
accumulation in hepatocytes, sometimes seen more often in young dogs.
History
Symptoms are vague, and come and go
until the disease progresses. The typical symptoms of liver disease are
present, and include PU/PD, anorexia, vomiting, diarrhea, ascites,
icterus, and HE. Ulcers of the stomach can occur and lead to vomiting
blood (hematemesis)
Other symptoms can involve the blood
system, and include bleeding disorders and vomiting blood
(hematemesis). This is because the liver is involved with the
production of clotting factors (remember the physiology section
above?). In occasional cases the opposite occurs, and the liver causes
excessive clotting of blood. This predisposes animals to a problem
known as disseminated intravascular coagulation (abbreviated as DIC).
Physical exam
An exam of a pet with this disease can
vary from normal to many abnormalities. Some of the abnormal findings
are described in the liver exam findings above.
Diagnostic Tests
Blood Panel
A blood panel will commonly show anemia
along with elevated levels of ALT and Alk Phos. There might also be an
elevation in cholesterol, a decrease in BUN, glucose, and albumin.
There might also be an increase in bilirubin, ammonia, and bile acids.
Urinalysis
a urinalysis might show symptoms of
urinary tract infection or abnormal crystals, particularly ammonium
biurate.
Radiography
A radiograph of the liver might show an
enlarged liver (hepatomegaly) initially, eventually it might progress
to a small liver (microhepatica).
Ultrasound
Ultrasound is the best way to make this
diagnosis. The internal architecture (parenchyma) can be analyzed and a
biopsy can be obtained with relative ease. In some cases it is
important to know the coagulation status of the blood with a special
blood panel prior to obtaining this biopsy. In many cases ultrasound is
preferable to exploratory surgery since some of these animals are not
good anesthetic risks and the procedure is much less invasive.
Laparotomy
The liver can be thoroughly visualized
and palpated during an exploratory surgery. A biopsy can easily be
obtained, and post biopsy bleeding can be monitored.
Biopsy
Samples of the liver taken with either a
biopsy needle during ultrasound, or during a laparotomy, will be
analyzed microscopically by a pathologist to make a definitive
diagnosis and to look for a cause if possible.
Treatment
Fluids and Electrolytes
This corrects the dehydration that
occurs with a poor appetite and supplies needed sodium, potassium, and
chloride. This fluid is usually given intravenously
(IV) at first. It can be given subcutaneously
(SQ) at home after the initial dehydration is corrected. B-Complex
vitamins are routinely added to the fluid bag. Care must be taken not
to give excessive amounts of fluids, especially if they contain sodium,
in pets with fluid buildup in the abdomen (ascites).
Treating the Cause (when known)
Antibiotics are used to control
bacterial infections and drugs that are suspected of causing this
disease are stopped. We tend to use antibiotics that have minimal need
for liver metabolism in order to minimize their toxic effects.
Rest
The liver has ability to heal itself if
the disease is not too advanced. Rest can be a big aid, along with
proper nutrition.
Ascites Reduction
Sodium restriction helps minimize fluid
buildup (ascites) in the abdomen. This can be accomplished using Hills
K/D Prescription Diet. Diuretics like Lasix are also used to help pull
this fluid out of the abdomen.
Dietary Modification
Use a diet that is restricted in protein
may be beneficial because less ammonia is produced as a by-product of
metabolism. This protein needs to be of high biological value, such as
eggs and dairy products. Hills Prescription Diet L/D® is
the diet of choice. Meat based proteins should be avoided since they
can increase the chance of HE. Higher fiber diets might also be
helpful, as long as the dog or cat is not undernourished. This is the
same basic diets as for pets with PSS (see above).
A diseased liver needs calories, which
sometimes need to be supplied with a feeding
tube.
Ulcer Treatment
This will make pets more comfortable,
more inclined to eat, and prevent bleeding in the stomach.
Liver Specific Drugs
Corticosteroids- Cortisone is used if
there is evidence that the immune system is implicated as a cause of
the liver problem.
Ursodiol- This drug replaces toxic bile
acids with a type of bile that is less toxic.
Zinc- Supplementation might help reduce
the effects of copper toxicity.
Long Term Monitoring
CCHID monitoring is similar to PSS (see
above). In addition, repeating a liver biopsy 6 months after initiating
therapy used.
Infectious Canine Hepatitis (ICH)
Background
The disease is called hepatitis because
liver cells are one of the prime targets. It is caused by an adenovirus
that is found world wide and affects mainly the dog family (canids).
The virus is very resistant to disinfectants and can remain infectious
in the environment. Many dogs get exposed to this virus, develop
antibodies, and show no symptoms of the disease. Spread of this virus
is usually orally and nasally, but can also be spread by utensils and
external parasites. Within 7 days of exposure most dogs develop an
adequate antibody response to protect the liver and other organs.
Symptoms
ICH can occur in unvaccinated dogs of
any age, but usually occurs in dogs under one year. In the more severe
cases vomiting and diarrhea can occur. These dogs can also have fever,
coughing, swelling of the head and neck due to lymph node enlargement,
abdominal tenderness and even central nervous system signs. These
symptoms may last up to one week, and can be prolonged by other
concurrent diseases like Distemper. A syndrome of this disease can
cause rapid death leading people to conclude that the dog was poisoned.
Dogs that show minimal symptoms can show ocular lesions during the
convalescent phase. In uncomplicated cases these eye lesions heal
completely.
Diagnosis
Blood samples give a clue to this
disease but are not diagnostic. White blood cells can be low, liver
enzyme tests may be elevated, and clotting factors can be disrupted.
These findings, along with the previously described history and
physical exam findings, are how the disease is usually diagnosed.
Antibody tests are available but are not routinely used to make a
diagnosis.
Treatment
Like most viral diseases therapy is
directed towards symptoms. When symptoms are severe enough, intravenous
fluids are administered. Since clotting factors can be disrupted
particular attention needs to be paid to bleeding problems. If bleeding
problems are severe enough, a whole blood transfusion must be
administered. Dogs that are comatose may need intravenous glucose.
Prevention
Most pups receive adequate antibodies
from the bitch, which can last up to 4 months. Vaccines are highly
effective and can confer long term protection. Two vaccines need to be
given at 3-4 weeks apart beginning at 8 weeks of age. The DHLPP
(Distemper-Hepatitis-Leptospirosis-Parainfluenza-Parvo) vaccine
contains protection against this adenovirus. The DHLPP vaccine is also
known as the Da2PL. The a2 part stands for
adenovirus.
A picture of our vaccine label
Copper Toxicosis (Copper Storage
Disease)
The level of copper in the body is maintained by the
excretion of bile. In this disease copper accumulates in hepatocytes,
eventually causing inflammation and scarring, ultimately leading to
liver failure (similar to CCIHD above). Excess copper released from the
liver can cause hemolytic anemia.
Signalment
It is common in certain breeds:
Bedlington terriers- They have a genetic
defect in how they metabolize copper and how it is excreted in the
bile. This leads to excess accumulation in hepatocytes.
West Highland white terriers- They have
a similar genetic defect as Bedlington terriers, but the copper
accumulation is not as severe and does not always lead to liver failure.
Some Dobermans and Skye terriers with
chronic liver disease also have elevated levels of copper in their
hepatocytes. The copper accumulation in the liver might be a cause of
the chronic hepatitis that eventually results, or an effect of a
pre-existing hepatitis.
History
Bedlington's with copper toxicity have
minimal symptoms early in the disease. In the acute form, seen in
younger dogs, symptoms include lethargy, anorexia, and vomiting. Death
can occur in 2-3 days. Middle aged or older dogs have a more chronic
course. Eventually symptoms of liver failure appear, including anemia,
depression, lethargy, and anorexia.
Physical exam
Anemia might cause pale mucous
membranes. There might also be icterus due to both anemia and liver
failure. These dogs will also be weak and underweight.
Diagnostic Tests
A blood panel will commonly show
elevated levels of ALT, GGT and Alk Phos, in addition to high levels of
bilirubin in the bloodstream and the presence of bilirubin in the
urine. A bile acids test is elevated and radiography reveals a small
liver. This disease is diagnosed by liver biopsy.
Treatment
Treatment has two goals: Enhance
excretion of excess copper, and minimize further absorption of copper
from the intestines.
Chelating agents Drugs like penicillamine bind with copper to allow
easier excretion.
Zinc
Zinc will help minimize further copper absorption from
the intestines.
Supportive Care
Similar to other liver diseases previously described
Diet
Hill's Prescription Diet L/D® can be
beneficial in treating this disease.
Long Term Monitoring
Serum enzymes and bilirubin should be
monitored at least every 6 months
Prevention
Bedlington terriers should be screened
at 1 year of age. Treatment at this early age leads to a good prognosis.
Cancer (Neoplasia)
A benign tumor of the liver is called
and adenoma, a malignant one is a carcinoma.
Primary- Arising directly from the liver
-
Adenoma
-
Carcinoma
-
Hemangiosarcoma
-
Hemangioma
-
Leimyosarcoma
-
Fibrosarcoma
-
Fibroma
-
Osteosarcoma
They can arise directly from the
hepatocytes where they are called hepatocellular. If they arise from
the biliary system they are called cholangiocellular. Dogs get more
hepatocellular, cats get more cholangiocellular. The cause of these
primary neoplasia's is unknown in most cases.
Secondary- From another organ that has
spread to the liver
-
Lymphosarcoma
-
Mast cell
-
Pancreatic carcinoma
-
Myeloproliferative
The organs that commonly are the source
of these secondary cancers include:
-
Pancreas
-
Lymph nodes
-
Spleen
-
Mammae
-
Adrenal glands
-
Bone and bone marrow
-
Lungs
-
Thyroid
-
Intestines
Secondary, also know as metastatic,
liver cancers are much more common than primary.
Signalment
Cancer is found in most animals and most
breeds. It tends to be found mostly in older animals.
History
Almost any sign of illness can
potentially be attributed to neoplasia. Common ones include anorexia,
lethargy, weight loss, PU/PD and vomiting.
Physical exam
Exam results of animals with liver
neoplasia mimic the results found in other liver diseases.
Diagnostic Tests
A blood panel will commonly show
elevated levels of liver enzymes, in addition to high levels of
bilirubin in the bloodstream and the presence of bilirubin in the
urine. A bile acids test is elevated and ultrasound reveals
hepatomegaly (enlarged liver) with telltale changes of the liver
parenchyma (internal anatomy of the liver). Ultrasound might also show
inflammation of the pancreas (pancreatitis). A liver biopsy is needed
for a definitive diagnosis. There is an ultrasound picture of liver
cancer in the diagnostic section above.
Treatment
Primary hepatic neoplasms are treated by
removal of the affected liver lobe when possible. If multiple lobes are
involved then surgery is usually not performed. Secondary hepatic
neoplasms are treated with chemotherapy. The results vary, and depend
on the duration, location, and degree of malignancy of the neoplasia.
The prognosis is poor for long term survival.
Supportive care that is similar to other
liver diseases is also used in neoplasia
Prevention
Since the cause is usually unknown
prevention is difficult. Good nutrition and lots of TLC are always
important in preventing any disease.
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