Overview of Feline Hepatic Encephalopathy
Hepatic encephalopathy (HE) is a degenerative disease of the brain caused by severe hepatic insufficiency in advanced liver disease. It is characterized by abnormal mental status, an altered state of consciousness and impaired neurologic function.
The most common cause is a congenital abnormality present at birth called a portosystemic shunt. This is an anatomical defect that causes blood to be diverted around the liver instead of passing through the liver. The liver cannot detoxify the blood and the toxins reach the brain and cause the clinical syndrome. Patients with liver failure due to toxic or infectious causes can also exhibit signs of HE.
There is no age, sex, or breed predisposition for animals with toxic or infectious liver disease; however, animals with congenital portosystemic shunts are usually brought to the veterinarian within the first year of life.
What to Watch For
The clinical manifestations of HE can range from mild (unusual behavior) to severe (coma).
Unpredictable bouts of aggression
Pressing the head against a wall
Sudden apparent blindness
These unusual behavior changes are often more pronounced a short time after a meal.
Also watch for:
Drinking a lot or urinating a lot
Nausea or hypersalivation (drooling)
Diagnosis of Hepatic Encephalopathy in Cats
Hepatic encephalopathy is a syndrome and not a disease itself. It is diagnosed by a combination of the patient’s history, physical examination findings and laboratory data. These findings can support the presence of significant liver disease in an animal in which no other cause for the neurologic and behavioral signs can be identified. Tests that help make the diagnosis of severe liver disease and resultant HE include:
Complete blood count
Serum chemistry panel
Blood clotting profile
Blood ammonia level or ammonia tolerance test
Bile acid test
Abdominal radiographs or special dye studies
Treatment of Hepatic Encephalopathy in Cats
Remove the predisposing cause, if possible
Home Care and Prevention
When at home, administer proper diet and medications as prescribed. Watch your cat for any of the signs listed above.
One can minimize exacerbations of clinical signs of HE by avoiding some predisposing factors:
Don’t feed high protein meals
Avoid drugs that might induce gastrointestinal bleeding, such as aspirin
Avoid giving tranquilizers or sedatives for travel
Avoid organophosphate insecticides
In-depth Information on Hepatic Encephalopathy in Cats
Hepatic encephalopathy is a neuropsychiatric disorder that occurs in animals and people with advanced liver disease. In cats, it is most often seen when blood is diverted or shunted around the liver, called portosystemic shunting. Blood can be diverted around the liver because of a congenital shunt present at birth or an acquired shunt that occurs secondary to long-term liver disease.
HE is often manifested as a wide range of neurologic abnormalities. The first signs are usually behavioral. At first, the changes are subtle, and they may wax and wane. As the disorder progresses, the signs become more obvious. Signs may be precipitated by a meal. As the syndrome becomes more apparent, cats usually has a few bad days, alternating with days in which the cat is acting fairly normal.
While any severe liver disease can lead to HE, portosystemic shunts are the most likely disorder to produce signs of HE; approximately 95 percent of animals with portosystemic shunts show signs of HE. In decreasing order of frequency, these signs are:
Pacing or circling
Staggering or incoordination
Collapse or weakness
Head or muscle tremors
There are several theories as to what actually causes the neurologic signs that are seen when the liver is not able to function properly. However, ammonia has always been implicated as one of the important toxins that contribute to neurologic signs. The liver converts ammonia into urea. When the liver is too diseased to do this properly, or if blood containing high levels of ammonia bypasses the liver because of a shunt, the ammonia circulates in high levels in the blood stream, and this affects the brain, causing the neurologic signs described.
A grading system has been modified from human medicine, for use in animals. In this system animals with HE are graded on a scale of 1 to 4.
Grade 1. Animal shows listlessness, depression, mental dullness, personality changes, excessive urination.
Grade 2. Animal shows incoordination, disorientation, compulsive pacing or circling, head pressing, apparent blindness, personality changes, salivation and excessive urination.
Grade 3. Stupor, severe salivation and seizures, although uncommon, are present.
Grade 4. Coma
Hepatic encephalopathy is a syndrome that is diagnosed by a combination of history, physical exam findings and laboratory data that shows significant liver disease is present in an animal for which no other cause of the neurological signs can be attributed.
Testing Recommendations for Hepatic Encephalopathy in Cats
Complete blood count (CBC). A CBC is performed to help support a diagnosis of liver disease. A high white blood cell count might be present if an infectious cause of liver disease is present. Changes in the size – usually smaller than normal red blood cells – and shape of red blood cells are often seen in cases of liver disease.
Serum chemistry panel. Depending on the nature of the liver disorder present, various liver parameters will be abnormal on the chemistry panel. Changes in the enzymes ALT, AST, and ALP, may be seen, as well as decreased levels of albumin, and increased levels of bilirubin. Other changes, such as a low urea level and low blood sugar, are sometimes seen.
Urinalysis. Blood and protein may be present in urine secondary to urinary tract inflammation. This inflammation is caused by ammonium urate crystals or stones that tend to form when there is liver disease, especially portosystemic shunts. The crystals or stones form because of high concentrations of ammonia in the urine.
Blood clotting tests. Patients with HE can exhibit clotting problems caused by the diseased liver’s inability to make adequate amounts of clotting factors.
Blood ammonia level or ammonia tolerance test. High ammonia levels in the bloodstream is one factor that contributes to HE. Detection of high levels of ammonia in the bloodstream supports a diagnosis of HE. Alternatively, an ammonia tolerance test can be performed, whereby the animal is given a standard amount of ammonium chloride by stomach tube, and measuring the amount of ammonia in the bloodstream before the test, and then 30 minutes after giving the ammonium chloride. These tests are rarely performed anymore due to the limited clinical availability of the test, the unreliability of the values if the test is not run within 30 minutes of collection, and the fact that some animals with HE have normal blood ammonia concentrations.
Bile acid test. This is a simple blood test that is very sensitive in detecting serious liver dysfunction or portosystemic shunts. Bile acids are very stable in serum, so no extraordinary sample processing is required, as with blood ammonia measurements.
Abdominal radiographs or special dye studies. Abdominal radiographs are important diagnostic tools in evaluating patients with possible HE. Most animals with portosystemic shunts have markedly small livers. An enlarged liver silhouette can be seen in patients with HE secondary to acute hepatitis, liver tumors, or other infiltrative liver diseases. A special radiographic dye study in which dye is injected into an intestinal blood vessel to determine whether the dye flows to the liver in the proper fashion can be performed, however, this is a specialized test that is almost always performed at referral centers or universities.
Abdominal ultrasound. This test is an excellent, non-invasive way to evaluate the liver. Liver tumors and infiltrative liver diseases can often be diagnosed via ultrasound and portosystemic shunts can sometimes be diagnosed by an experienced ultrasonographer. A liver biopsy can also be obtained using ultrasonographic methods.
Liver biopsy. Exploratory surgery and liver biopsy will nearly always diagnose the cause of the liver disorder that has led to the development of HE. Animals with severe liver disease and resultant HE are often not the ideal candidates for anesthesia and surgery, and non-invasive diagnostic methods are preferred.
Transcolonic scintigraphy. This is a specialized, non-invasive test performed only at referral centers or universities. The test is designed to diagnose a portosystemic shunt, the most common condition that leads to HE. Radioactive material is infused into the animal’s colon. In normal animals, the radioactive material enters the intestinal blood supply and arrives at the liver first, and then flows to the heart. If the patient has a portosystemic shunt, the intestinal blood is diverted around the liver, so that the radioactive material arrives at the heart before, or at the same time as, the liver.
The primary goals of therapy of HE are to identify and correct any precipitating factors, reduce the number of toxin-producing bacteria in the intestinal tract, decrease absorption of the intestinal toxins, and promptly recognize and treat any complications of liver dysfunction. Once therapy is initiated, most animals have a dramatic alleviation of the signs of HE.
Remove predisposing cause. There are many factors that can precipitate an episode of HE. Many drugs that require metabolism by the liver can adversely affect the nervous system in animals with liver disorders, most notably anesthetics and sedatives. These drugs should be avoided. Gastrointestinal bleeding can precipitate HE, so potentially ulcer-causing drugs such as aspirin should be discontinued, and gastrointestinal parasites that might cause intestinal bleeding, such as hookworms, should be addressed. Infections can predispose animals to HE, and must be treated promptly.
Antibiotics. Bacteria in the intestinal tract generate ammonia and other toxins that precipitate HE. The primary means of decreasing the number of these detrimental bacteria is with antibiotics. Neomycin, ampicillin and metronidazole are examples antibiotics commonly prescribed to reduce the number of detrimental bacteria in the intestinal tract.
Lactulose. Lactulose is a synthetic sugar. When given orally, it acidifies the contents of the colon. This traps ammonia and other toxins in the colon and prevents it from being absorbed into the bloodstream. These toxins are excreted into the feces instead. Lactulose and antibiotics are best used in combination in patients with moderate-to-severe HE (grades 2, 3 or 4), or if either drug alone fails to eliminate clinical signs.
Diet. Although antibiotic and lactulose therapy is critical in the acute management of HE, dietary therapy has long been considered the backbone of long-term therapy. Animals with liver disease and HE need to have their diet modified, most notably in terms of protein content. A major dilemma in formulating diets for animals with liver disease is the fact that these animals are usually stunted or malnourished, and it is vitally important to maintain body weight and muscle mass while minimizing the signs of HE. Fortunately, there are prescription diets that are designed to provide reduced levels of high quality protein, including a new diet from the Hill’s company specifically designed for animals with liver disease (Hill’s Science Diet Prescription Diet L/D).
Surgery. For portosystemic shunts, surgery can significantly improve your cat’s health. Unfortunately, surgery is not possible for certain types of shunts. Those shunts that are small and occur outside of the liver are the best candidates for surgery. Multiple shunts within the liver are rarely surgical candidates.
Follow-up Care for Cats with Hepatic Encephalopathy
Optimal treatment for your cat requires a combination of home and professional veterinary care. Follow-up can be critical, especially if your cat does not rapidly improve. Administer all prescribed medication as directed. Alert your veterinarian if you are experiencing problems treating your cat and follow all dietary recommendations.
Because HE can be reversible, the prognosis for affected animals with chronic HE is good. Acute exacerbations of HE usually carries a good prognosis if the precipitating factor can be controlled or eliminated, and liver function is stable. If liver function is not stable and is, in fact, deteriorating, the prognosis for controlling HE is guarded.