Hepatic encephalopathy is a degenerative pathology of the brain caused by severe liver failure in the presence of advanced liver disease. It is characterized by abnormal mental state, impaired state of consciousness and impaired neurological function.
Hepatic encephalopathy recognizes a congenital anomaly, called a portosystemic shunt, as the most common cause. The term portosystemic shunt refers to the presence of abnormal vessels that allow the passage of venous blood from the stomach, spleen, pancreas and intestine directly into the systemic circulation bypassing the liver circulation. The result is the inability of the liver to “detoxify” the blood and metabolize toxins. The latter, therefore, accumulate in the body until they reach the brain, giving rise to the clinical syndrome. Dogs with liver failure due to toxic or infectious causes may also exhibit signs of liver encephalopathy.
Animals suffering from toxic or infectious liver disease do not have any predisposition related to age, gender or race. In general, however, in the case of a congenital portosystemic shunt, the diagnosis occurs within the first year of life.
Hepatic encephalopathy often occurs with a wide range of neurological abnormalities. The first symptoms are typically behavioral in nature. Initially, the changes are imperceptible and intermittent. During its progression, the pathology manifests itself with gradually more evident signs. The signs can be precipitated from a meal.
Although any severe liver disease may result in the onset of hepatic encephalopathy, the portosystemic shunt is the disorder that is most likely to produce signs of hepatic encephalopathy. About 95% of animals with portosystemic shunts exhibit signs of hepatic encephalopathy. In descending order of frequency, these symptoms are:
- Personality changes
- Restlessness, aimless compulsive walking or circling (movements in a circle)
- Staggering or ataxia (lack of coordination of voluntary movements)
- Head pressing (compulsive act that consists in pressing the head against a wall or an object for no apparent reason)
- Head or muscle tremors
The extent of the clinical manifestations of hepatic encephalopathy can vary from mild (unusual behavior) to severe (coma).
There are several theories regarding the actual causes of neurological symptoms observable in the presence of liver dysfunction. However, ammonia has always been implicated as one of the main contributing toxins of neurological symptoms.
The liver converts ammonia into urea. When organ impairment does not allow the liver to perform this function or if the blood, containing high levels of ammonia, bypasses the liver due to a shunt, the high amount of ammonia circulates in the bloodstream causing the neurological signs described above .
In addition, attention should also be paid to the following symptoms:
Staging of canine hepatic encephalopathy
The staging of animal liver encephalopathy is based on the staging system used for the human being, suitably modified. The stages vary from 1 to 4.
Stage 1 – The animal manifests apathy, killing, mental dulling, personality changes, polyuria.
Stage 2 – The animal manifests ataxia, disorientation, compulsive ambulatory walking or circling, head pressing, apparent blindness, personality changes, salivation and polyuria.
Stage 3 – Stupid state, severe salivation and epileptic seizures.
Stage 4 – Coma.
The diagnosis is based on the anamnesis, physical examination results and laboratory data that show the presence of a significant liver disease whose neurological symptoms are not attributable to any other cause.
Recommended diagnostic tests include:
- Complete blood count test. It can help support a diagnosis of liver disease. If the liver disease is due to an infectious cause, the number of white blood cells may be high. In cases of liver disease, changes in the shape and size of red blood cells are often observed (in general the size is smaller than that of normal red blood cells).
- Biochemical profile. Depending on the nature of the liver disorder present, the results will show various abnormal liver parameters. It is possible to observe: enzymatic alterations (ALT, AST and ALP), reduced albumin levels and increased bilirubin levels. Sometimes it is also possible to observe alterations of different types, such as low urea level and low blood sugar levels.
- Urine analysis. Blood and proteins may be present in the urine secondary to inflammation of the urinary tract. This inflammation is caused by ammonium urate crystals or calculations which tend to form in the presence of liver disease, particularly portosystemic shunts. Crystals or stones are formed in consideration of the high concentrations of ammonia in the urine.
- Coagulation test. Dogs with hepatic encephalopathy can exhibit clotting problems due to the inability of the diseased liver to synthesize an adequate level of clotting factors.
- Fasting serum ammonia levels or ammonia tolerance test. High blood levels of ammonia are a contributing factor in liver encephalopathy. The detection of high levels of ammonia in the blood supports a diagnosis of hepatic encephalopathy. Alternatively, an ammonia tolerance test can be performed. However, such a test is contraindicated when its levels are high. It can also exacerbate liver encephalopathy. However, it is little used in consideration of the technical execution attention it requires.
- Bile acid analysis. It is a simple blood test very sensitive in detecting severe liver dysfunction or portosystemic shunts.
- Abdominal radiographs or special contrast studies. Abdominal radiographs are important diagnostic tools for evaluating patients with possible hepatic encephalopathy. Most animals with portosystemic shunts have markedly small livers. One can observe a enlarged liver in patients with liver encephalopathy secondary to acute hepatitis, liver tumors or other infiltrative liver diseases. A special contrast study can be performed in which the contrast medium is injected into an intestinal blood vessel to determine if it flows properly to the liver.
- Abdominal ultrasound. It is an excellent and non-invasive way to evaluate the liver. Liver malignancies and infiltrative liver disease can often be diagnosed by ultrasound. Sometimes, thanks to the expertise of an expert sonographer, it is also possible to diagnose portosystemic shunts. Thanks to the help of the ultrasound-guided mode, it is also possible to proceed with the collection of a biopsy sample of liver tissue.
- Liver biopsy. Exploratory surgery and liver biopsy will almost always diagnose the cause of the liver disorder that led to the development of liver encephalopathy. Animals with severe liver disease resulting in hepatic encephalopathy are often not the ideal candidates for anesthesia and surgery. In these cases, non-invasive diagnostic methods are preferable.
- Liver scan. It represents a non-invasive means of investigation designed for the diagnosis of a portosystemic shunt, the most common condition that leads to the onset of liver encephalopathy. However, it requires specialized equipment and the use of a radioactive tracer.
The primary therapeutic objectives are: to identify and correct any precipitating factors, to reduce the number of bacteria that produce toxins in the intestinal tract, to decrease the absorption of intestinal toxins and to recognize and promptly treat any complications of liver dysfunction. Once therapy is started, most animals experience a dramatic reduction in the signs of hepatic encephalopathy.
- Remove the predisposing cause. There are many factors that can precipitate an episode of hepatic encephalopathy. Many drugs that require liver metabolism can adversely affect the nervous system of animals suffering from liver disorders, especially anesthetics and sedatives. These drugs should be avoided. Gastrointestinal bleeding can precipitate hepatic encephalopathy, therefore the drugs that can potentially cause it ulcers, such as aspirin, should be discontinued and any gastrointestinal parasites (such as hookworms) that could cause gastrointestinal bleeding should be evaluated and resolved. Infections can predispose animals to liver encephalopathy and must be treated promptly.
- Antibiotics. The bacteria present in the intestinal tract generate ammonia and other toxins that precipitate liver encephalopathy. The primary means of reducing the number of these harmful bacteria are antibiotics. Neomycin, ampicillin and metronidazole are examples of commonly prescribed antibiotics to reduce the number of harmful bacteria in the intestinal tract.
- Lactulose. Lactulose is a synthetic sugar. When administered orally, it acidifies the contents of the colon. This acidification traps ammonia and other toxins in the colon and prevents their absorption into the bloodstream by promoting their expulsion in the stool. In patients with moderate to severe hepatic encephalopathy (stages 2, 3 or 4), lactulose and antibiotics are more effective when used in combination. The same applies if the single use of one of the two drugs in question does not contribute to the resolution of clinical signs.
- Diet. Although therapy through the use of antibiotics and lactulose is fundamental in the acute management of hepatic encephalopathy, diet therapy has long been considered the cornerstone of long-term therapy. Animals with liver disease and liver encephalopathy need food changes, particularly in terms of protein content. Since animals affected by the above conditions usually have a poor body condition, it is vitally important to maintain their body weight and muscle mass while minimizing the signs of liver encephalopathy. Fortunately, there are clinically proven therapeutic diets specially formulated to bring reduced levels of high quality proteins (for example, Hill’s Science Diet Prescription Diet L / D, among others).
- Surgical intervention. In the case of portosystemic shunts, surgery can significantly improve dog health. Unfortunately, for some types of shunts the surgical approach is not always possible. Small and extrahepatic shunts are the best candidates for surgery. Multiple intrahepatic shunts are rarely surgical candidates.
What to do at home
Administer an appropriate diet and prescribed medications in the manner recommended by the veterinarian. Promptly notify your veterinarian if you experience any problems following the prescribed therapy and nutritional recommendations.
It is possible to minimize the exacerbations of clinical signs by avoiding some predisposing factors, including:
- Do not give your dog high protein meals
- Avoid the administration of drugs that could induce gastrointestinal bleeding, such as aspirin
- Avoid the administration of tranquilizers or sedatives when traveling
- Avoid using organophosphate insecticides