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:
Porto-systemic shunt (PSS)
Chronic active hepatitis
Infectious canine hepatitis
Copper storage disease
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
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.
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.
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:
- Diabetes Mellitus
- Tetracycline antibiotics
- Inflammatory Bowel Disease (IBD)
- Malnutrition or even starvation
- Kidney disease
- chronic cystitis
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.
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.
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 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.
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 might show hepatomegaly or a normal sized liver. Weight loss might be apparent on the radiograph, yet abdominal fat stores might be normal.
Ultrasound reveals hepatomegaly with telltale changes of the liver parenchyma (internal anatomy of the liver). Ultrasound might also show inflammation of the pancreas (pancreatitis).
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.
A pathologist needs to analyze the liver microscopically to make a definitive diagnosis.
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.
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.
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.
This drugs helps minimize the ammonia buildup that leads to vomiting, salivation, and mental depression.
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.
Medications like Tagamet and sucralfate will help protect the stomach lining and make pets feel much better. These pets are more inclined to eat.
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.
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.
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.
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.
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.
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.
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.
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:
- Irish wolfhounds
- Yorkshire terriers (20X more prevalent than all the other breeds)
- Miniature schnauzers
- Lhasa Apso (also prevalent compared to other breeds)
- Australian cattle dogs
- Cairn terriers
- Old English sheepdogs
Cat breeds might include:
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).
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.
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.
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.
This young cat with this disease shows elevated live enzymes and also a low BUN
A urinalysis might show symptoms of urinary tract infection or abnormal crystals, particularly ammonium biurate.
This a urine sample from the cat above. It shows the ammonium crystals at the bottom.
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 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. It takes an expert at ultrasound to find thisi rpblem in the liver. Ultrasound is better at differentiated intrahepatic shunts as opposed to extrahepatic shunts.
The abnormal shunt vessels are the white area to the right of the word shunt. They are found wiht the doppler that traces the flow of blood in the liver.
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.
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.
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.
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.
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.
Enema’s will decrease the bacterial count of the intestines, leading to less ammonia absorption.
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.
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. Typical ones include metronidazole (Flagyl) and amoxicillin.
Internal parasites can cause gastrointestinal bleeding and also make the symptoms of PSS worse.
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.
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. 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. Complications in a small number of cases can include seizures and death. A medication called Levetiracetam can be helpful to minimize seizures when started prior to surgery.
Intrahepatic shunts can be more difficult to identify and ligate. They are sometimes corrected with interventional radiology using coils to fix the shunt vessels.
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.
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.
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.
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.
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.
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.
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).
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.
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.
a urinalysis might show symptoms of urinary tract infection or abnormal crystals, particularly ammonium biurate.
A radiograph of the liver might show an enlarged liver (hepatomegaly) initially, eventually it might progress to a small liver (microhepatica).
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.
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.
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.
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.
The liver has ability to heal itself if the disease is not too advanced. Rest can be a big aid, along with proper nutrition.
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.
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.
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.
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.
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.
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.
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.
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
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.
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.
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.
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.
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 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- will help minimize further copper absorption from the intestines.
Similar to other liver diseases previously described
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
Bedlington terriers should be screened at 1 year of age. Treatment at this early age leads to a good prognosis.
A benign tumor of the liver is called and adenoma, a malignant one is a carcinoma.
Primary- Arising directly from the liver
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
- Mast cell
- Pancreatic carcinoma
The organs that commonly are the source of these secondary cancers include:
- Lymph nodes
- Adrenal glands
- Bone and bone marrow
Secondary, also know as metastatic, liver cancers are much more common than primary.
Cancer is found in most animals and most breeds. It tends to be found mostly in older animals.
Almost any sign of illness can potentially be attributed to neoplasia. Common ones include anorexia, lethargy, weight loss, PU/PD and vomiting.
Exam results of animals with liver neoplasia mimic the results found in other liver diseases.
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.
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
Since the cause is usually unknown prevention is difficult. Good nutrition and lots of TLC are always important in preventing any disease.