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Uremic encephalopathy in cats. Hepatic encephalopathy in cats and dogs

Source: Proceedings of the conference "Veterinary medicine - theory, practice and training", St. Petersburg, 2006.

Hepatic encephalopathy (hepatoencephalopathy) potentially reversible disorder nervous system caused by metabolic disorders resulting from hepatic cellular failure and or portosystemic blood shunting.

To date, the pathogenesis of hepatoencephalopathy is unclear; there is a complex set of disorders, none of which provides a comprehensive explanation.

Hepatic encephalopathy develops in a number of syndromes, with acute liver failure, liver cirrhosis, liver lipidosis in cats, congenital portocaval anastomoses, liver cell (parenchymal) failure plays an important role.

Chronic hepatoencephalopathy is observed in sick animals with portocaval shunting or with portal vein pathology (hepatoportal microvascular dysplasia)

The varying symptoms of hepatic encephalopathy likely reflect the amount and type of metabolites produced. Coma in acute liver failure is often accompanied by psychomotor agitation and cerebral edema, lethargy and drowsiness are characteristic of chronic encephalopathy, sometimes a decrease in body temperature, damage to astrocytes, disruption of the blood-brain barrier, which in turn can lead to complications inflammatory in nature in the central nervous system.

Clinical picture

With hepatic encephalopathy, almost all parts of the brain are affected, so the clinical picture is complex various syndromes including neurological and mental disorders. Diversity clinical symptoms in hepatoencephalopathy is associated with damage to glutamate receptors. Glutamate is synthesized in neurons from its precursor glutamine, accumulates in synaptic vesicles and is eventually released through a calcium-dependent mechanism. Released glutamate can interact with glutamate receptors of any type located in the synaptic cleft. In astrocytes, glutamate is taken up and converted into glutamine by glutamine centitase. This uses ammonia. Disorders that develop with hepatoencephalopathy include an increase in ammonia levels in the brain, damage to astrocytes, and a decrease in the number of glutamate receptors. Hepatoencephalopathy can manifest itself in different ways. Deep tendon reflexes may be increased muscle tone at some stages it is increased. There may be muscle spasms and twitching, and in some patients coordination of movements is impaired. In some patients, the condition worsens after eating. During a coma, reflexes are weakened and disappear. Lethargy, drowsiness, and decreased body temperature are observed.

Study cerebrospinal fluid

No specific changes in the cerebrospinal fluid were detected during hepatoencephalopathy.

Possible increase in glutamine.

Electroencephalography

With hepatocerebral dystrophy, most patients experience changes in the EEG in the form of slow waves; there may be high-amplitude delta waves and epileptic activity. This method helps in diagnosing hepatic encephalopathy and assessing treatment results. Changes in the EEG are detected on early stages before the appearance of clinical symptoms. They are nonspecific and may appear in other pathological conditions, for example with uremia.

Clinical variants of hepatic encephalopathy.

Acute encephalopathy

Acute hepatoencephalopathy can develop spontaneously under the influence of predisposing factors, especially in patients with bilirubinemia and ascites after removal of a large amount of fluid, which is apparently associated with the loss of water and electrolytes, protein-rich foods contribute to the development of coma, inhibition of liver cell function caused by anemia and a decrease in hepatic blood flow. Patients with acute encephalopathy do not tolerate surgery well. Exacerbation of liver dysfunction occurs as a result of blood loss, anesthesia, and shock. Infectious diseases can contribute to the development of hepatic encephalopathy, especially in cases where they are complicated by bacteremia. Coma may occur due to rich in proteins food or prolonged constipation.

Chronic encephalopathy.

The development of chronic hepatoencephalopathy is caused by significant portosystemic shunting. Shunts can be congenital and are most common in Yorkshire Terriers. Shunts can be acquired, they can consist of many small anastomoses developed in patients with cirrhosis of the liver or from a large collateral vessel. The severity of hepatoencephalopathy depends on the protein content of food. In this case, making a diagnosis can be difficult. The diagnosis becomes obvious if the patient's condition improves when switching to a low-protein diet. Encephalography data can help in making a diagnosis.

Hepatocerebral degeneration (myelopathy)

Myelopathy develops after long-term chronic hepatic encephalopathy. Associated with focal brain damage. Epileptic seizures may be observed, as well as impaired motor function, syndrome of damage to the cerebellum and basal ganglia of the brain.

Pathogenesis.

The metabolic theory of the development of hepatoencephalopathy is based on the reversibility of its main disorders in extensive cerebral disorders. There is no single metabolic disorder that causes hepatoencephalopathy; it is based on a decrease in the hepatic clearance of substances formed in the intestine, both as a result of hepatic cell failure and significant shunting, as well as a violation of amino acid metabolism. Both of these mechanisms lead to disturbances in cerebral neurotransmitter systems. Several neurotoxins, especially ammonia, and several neurotransmitter systems interacting with each other are involved in the pathogenesis of hepatoencephalopathy. In every patient in a state of coma or coma, blood can flow from the portal vein into the systemic veins, bypassing the liver and without undergoing detoxification. In patients with impaired hepatocyte function, such as acute hepatitis, the blood is shunted inside the liver. Damaged hepatocytes are not able to fully detoxify the blood of the portal system, so the blood enters the hepatic veins with toxins. In cirrhosis, blood from the portal vein bypasses the liver through large natural collaterals and enters the systemic veins. In addition, in the liver affected by cirrhosis, portohepatic anastomoses (venous anastomoses) are formed around the lobules, which function as intrahepatic shunts.

Ammonia and glutamine.

In the pathogenesis of hepatoencephalopathy, ammonia is the most studied factor. Ammonia is released during the breakdown of proteins, amino acids, purines and pyrimidines. About half of the ammonia coming from the intestines is synthesized by bacteria, and the rest is formed from food proteins and glutamine. Normally, ammonia is converted into urea and glutamine in the liver. Disruption of the urea cycle leads to the development of encephalopathy. A decrease in the amount of urea in the blood can serve as an indicator of developing hepatoencephalopathy. Ammonia levels are elevated in the blood in 90% of patients, and levels in the brain may also be elevated. When receiving ammonium salts orally, some patients may develop hepatoencephalopathy. Hyperammonemia itself is associated with a decrease in the conduction of excitation in the central nervous system. Ammonia intoxication leads to the development of a hyperkinetic preconvulsant state. In hepatoencephalopathy, the main mechanisms of action of ammonia are a direct effect on neuronal membranes or postsynaptic inhibition and indirect disruption of neuronal functions as a result of the effect on the glutamatergic system.

The urea cycle does not function in the brain, so ammonia is removed from it in different ways. In astrocytes, glutamine is synthesized from glutamate and ammonia under the action of glutamine synthetase. Under conditions of excess ammonia, the reserves of glutamate (an important excitatory neurotransmitter) are depleted and glutamine accumulates. The content of glutamine and alpha-ketaglutarate in the cerebrospinal fluid correlates with the degree of hepatoencephalopathy. It is difficult to assess the contribution of ammonia to the development of hepatoencephalopathy, since changes in other neurotransmitter systems are observed in this condition. In 10% of patients, ammonia levels are normal. Methionine derivatives, especially mercaptans, cause hepatoencephalopathy, so the use of methionine as medicinal product unacceptable. There is evidence that in hepatoencephalopathy, some toxins such as ammonia, fatty acids, phenols, mercaptans act as synergists.

False neurotransmitters.

In hepatoencephalopathy, the transmission of impulses in the catecholamine and dopamine synapses of the brain is suppressed by amines formed under the influence of bacteria in the intestine when the metabolism of neurotransmitter precursors in the brain is disrupted. Decorboxylation of certain amino acids in the intestine leads to the formation of betaphenylethylamine, tyramine and octopamine, the false neurotransmitters. They replace true neurotransmitters. Altered availability of neurotransmitter precursors interferes with normal neurotransmission. In patients with liver diseases, the plasma content of aromatic amino acids - tyrazine, phenylalanine, tryptophan - increases, which is due to a violation of their deamination in the liver. At the same time, the content of branched chain amino acids - valine, leucine, isoleucine - decreases, associated with an increase in their metabolism in skeletal muscles and kidneys as a result of hyperinsulinemia, characteristic of chronic liver failure. These two groups of amino acids compete for passage into the brain. Violation of their ratio in plasma allows aromatic amino acids to penetrate the broken blood-brain barrier. High levels of phenylalanine in the brain lead to suppression of dopamine synthesis and the formation of false neurotransmitters phenylethanolamine and octopamine. In liver diseases, the content of tryptophan in the cerebrospinal fluid and brain increases. Tryptophan is a precursor to the neurotransmitter serotonin. Serotonin is involved in regulating the level of arousal of the cerebral cortex and the sleep-wake cycle. With hepatoencephalopathy, other disorders of serotonin metabolism are observed. Whether disruption in this system is a primary defect requires further study. The severity of hepatoencephalopathy correlates with benzodiazepine activity in blood plasma and urine. The activity of benzodiazepine compounds in the stool of patients with liver cirrhosis is five times higher. Increased sensitivity to benzodeazipines confirms the involvement of this neurotransmitter system in the development of hepatoencephalopathy.

Other metabolic disorders.

With hepatoencephalopathy, hypoglycemia may develop. As liver failure worsens, a progressive disturbance of carbohydrate metabolism is observed. The brain with hepatoencephalopathy becomes sensitive to the effects of harmful factors: opiates, electrolyte disturbances, sepsis, arterial hypotension, hypoxia, which is not observed normally. This must be taken into account when performing operations and administering anesthesia to patients with hepatoencephalopathy.

Diagnosis of hepatoencephalopathy

Laboratory diagnosis of hepatoencephalopathy

Biochemical and hematological parameters results obtained from routine tests can only suggest the presence of hepatoencephalopathy; a test for the concentration of ammonia in the blood, a test for ammonia tolerance, and a test for the content of bile acids in the serum would be more useful in this regard. Hematological parameters in animals with hepatoencephalopathy are not specific and may include mild anemia, poikilocytosis, microcytosis. Similarly, changes in serum concentrations of biochemical parameters associated with liver disease (ALT, AST, albumin, bilirubin, glucose and potassium) are usually not specific; the combination of low albumin and low urea may indicate the presence of liver damage causing hepatoencephalopathy; blood urea nitrogen concentrations are usually very low (less than 6 mg/100 ml). Animals with hepatoencephalopathy exhibit respiratory and metabolic alkalosis. Respiratory alkalosis is secondary to hyperventilation, and metabolic alkalosis results from hypokalemia and severe vomiting.

Blood ammonia concentrations are usually assessed in blood samples taken from an artery, and the serum must be separated from the cells within 30 minutes. It should be emphasized that the severity of neurological signs is not always related to the degree of hyperammonization. Some encephalopathic animals have normal blood ammonia concentrations, while other animals with minimal neurological impairment have significantly elevated ammonia concentrations. If an elevated ammonia concentration (more than 120 mcg/100 ml for dogs) is detected at least 6 hours after ingestion, this will have great importance for diagnosis.

To test tolerance to ammonia, measure the difference between the concentration of ammonia per os before administration and 30 minutes after administration of NH 4 Cl at a dose of 100 mg/kg. Because of the risk of causing hepatoencephalopathy, this test should be performed cautiously and only on dogs in which neurological impairment is minimal and ammonia concentrations are normal and stable. For dogs, testing for nitrogen tolerance can also be done by rectal administration of 5% NH 4 Cl.

Blood ammonia concentration is not diagnostic of hepatoencephalopathy in cats because these animals lack the ability to synthesize arginine, which is involved in ammonia detoxification in the hepatic Krebs-Geselstein cycle. Moreover, cats with long-term anorexia sometimes have elevated blood ammonia concentrations. Forced ingestion of ammonia per os, carried out on a cat with a persistently high concentration of ammonia in the blood, can cause hepatoencephalopathy in the animal, coma, and can even lead to the death of the animal.

Serum bile acid concentrations measured in the fasting state and 2 hours after feeding are considered safe and equally reliable verification to assess liver cell function (see Table). In addition, no special processing of the samples is required since they themselves are relatively stable. The concentration of bile acids in the blood is a very useful indicator for diagnosing hepatoencephalopathy in cats.

Table. Total serum bile acids (normal values for dogs and cats in µmol/l)

		2 hours after eating food

Liver diseases cannot be differentiated by the concentration of serum bile acids, however, if their concentration increases greatly after feeding (more than 150 mmol/l), then the presence of cirrhosis or PSS can be assumed. Most laboratories use either an enzyme method to determine the concentration of bile acids in the blood, which measures general content serum 3alpha-hydroxylated bile acids, or a radioimmunoassay (RIA), which measures specific bile acid residues.

Radiography

Abdominal X-rays should be obtained for all cases of hepatoencephalopathy. The liver in cats and dogs with hepatoencephalopathy can be small, enlarged, or even normal. To identify both inside and outside the hepatic shunt and hepatoportal microvascular dysplasia, studies such as splenoportography, jejunal vein portography, and cranial vein portography can be used. mesenteric artery. The most preferred method is portography through the mesenteric vein. After a ventral incision along midline Two ligatures are placed around the loop of the jejunal vein, the catheter is inserted into the vessel and secured; the use of a metal needle is unacceptable. The abdominal incision is temporarily closed. An appropriate contrast agent is injected into the catheter, after which fluoroscopy or radiography is performed in the lateral and ventrodorsal directions. Omnipak 300 or 350 is used as a contrast, ultravist 370, it is possible to use urografin 70%, but it is not advisable due to possible reactions to this drug in animals. The dose of Omnipack to obtain a high-quality image varies from 1 ml per kg of body weight large dogs up to 2.5 ml per kg in small dogs and cats. An X-ray is taken at the moment the contrast agent passes through the liver, which occurs at the end of the drug administration. Portography, in some cases, is decisive diagnostic value helps to deliver correct diagnosis evaluate the possibility of further treatment.

Ultrasound echography

Ultrasound examination is used to identify intrahepatic shunt and to study the liver and gallbladder system, as well as to study the kidneys. In some cases of intrahepatic shunt in dogs, the liver is small, the liver veins are very small or completely indistinguishable, and the renal pelvis is enlarged. At correct implementation From this study, ultrasound diagnostics can provide decisive data in the diagnosis of hepatoencephalopathy.

Nuclear scintigraphy of the liver is non-invasive method, suitable for diagnosis, but is rarely used in everyday practice.

Liver biopsy

Histopathological findings obtained from liver biopsy in cases of hepatoencephalopathy may be indeterminate. In some cases, with a congenital portacaval shunt, there is an absence of a branch of the portal vein in the triad area. A liver biopsy should be obtained to evaluate other manifestations of hepatopathy, such as liver atrophy, diffuse fatty infiltration, cirrhosis or pre-cirrhosis, fibrosis, cholangiohepatitis and idiopathic lipidosis in cats. Sometimes histological or even cytological examination is decisive in the diagnosis and prognosis of the disease, as it provides the most objective data on the morphology of the liver, helps to give the most correct assessment of the possibility of liver restoration and to choose the right treatment.

Urine examination

A urine test if hepatoencephalopathy is suspected is mandatory. The presence of urate in the urine of a young animal highly likely indicates the presence of a portacaval shunt and is an indication for portography. The following indicators are determined in urine: bilirubin, urobilinogen, hemoglobin, calcium, phosphorus, sediment microscopy.

Differential diagnoses

In young animals, symptoms similar to those of hepatoencephalopathy may appear in the case of idiopathic epilepsy and hypocalcemia plague. As for older dogs, diseases such as encephalitis, hypoglycemia, some toxicoses, metabolic and endocrine diseases, and uremia can be confused with hepatoencephalopathy. In order to exclude differential diagnoses and to determine the nature of the disorders causing hepatoencephalopathy, it may be necessary to use a combination of all research methods.

Treatment.

1. Establishment and elimination of factors contributing to the development of hepatoencephalopathy.

2. Measures aimed at reducing both the formation and adsorption of ammonia and other toxins formed in the colon. These include modification of food proteins intestinal microflora and intestinal environment.

The choice of treatment method depends on clinical picture. Acute or chronic hepatoencephalopathy.

Acute hepatoencephalopathy.

1. identify factors contributing to the occurrence of hepatoencephalopathy

2. cleanse the intestines of nitrogen-containing substances (give a laxative and do an enema)

3. prescribe a protein-free diet

4. lactulose is prescribed

5. antibiotics (neomycin, metrogil)

6. Maintain calorie content of food, amount of fluid and electrolyte balance. For this purpose they carry out infusion therapy.(using drugs Gepasol, Ringer's, Hartmann's solutions.)

7. For treatment, drugs solcoseryl are used, nootropic drugs, glucocorticoids (methylprednisolone) improving drugs rheological properties blood stabilizol, reforman,

Chronic encephalopathy

1. Limit the protein content in the feed.

2. Provide bowel movements 2 times a day

3. Acidify the intestinal contents in order to trap ammonia (in the form of NH4+) and speed up its excretion from the intestines. This is achieved by administering lactulose, which can also be used as a protein-free energy source for intestinal microorganisms, thereby reducing further ammonia production. The standard dose is 2.5-5 ml for cats and 2.5-15 ml for dogs 3 times a day. Recently, a lactulose-related substance, lactitol, taken in powder form, has shown promise in controlling hepatoencephalopathy.

4. If the condition worsens, switch to treatment used for acute encephalopathy

Shunt occlusion

Surgical removal of a portacaval shunt may lead to regression of severe portosystemic encephalopathy this method Treatments can be used for congenital and acquired portacaval shunts.

The liver is one of the most important organs in the body of any living creature. Liver pathologies are always associated with great health risks.

Features of the liver in dogs

The organ is distinguished by its amazing regenerative ability.

The liver has the ability to recover.

Even with eighty percent damage, the liver recovers in most cases. However, there is also back side medals. It is precisely due to the fact that the liver quickly regenerates that many diseases go unnoticed and the behavior of animals practically does not change. The pet feels well all the time, and the disease progresses, and treatment is not prescribed in a timely manner.

Liver pathologies

The most common and dangerous pathologies:

infectious hepatitis;
mycosis;
Cushing's syndrome;
cirrhosis;

The dog has ascites.

Despite the fact that some diseases, at first glance, are in no way related to the liver, nevertheless, when these pathologies occur, it is this organ that always suffers.

General symptoms and signs of disease

During illness, the dog loses interest in food.

General signs that are characteristic of most diseases of this type include periodic symptoms of the disorder digestive system.

The dog loses its appetite and often refuses food altogether. Nausea progresses and diarrhea occurs, which may alternate with constipation. The dog is chronically depressed, constantly sleeps, and activity is significantly reduced.

Dropsy

More severe cases are expressed in the form of ascites, which is expressed in the dog’s sagging belly, pain.

The stool is pale gray in color as a result of stercobilin, which is formed from a bile acid salt. The absence of bile in the digestive tract will be indicated by faded, almost white feces.

The dog's urine takes on a bright orange color, which is associated with problems processing bile acid, resulting in a large amount of bilirubin being excreted through the kidneys from the body. Jaundice appears, which is also associated with the production of bile acid. Blood clotting disorders are less common.

The color of urine in a dog with dropsy is bright orange.

Hepatic encephalopathy

If hepatic encephalopathy occurs, it manifests itself atypical animal behavior . The dog exhibits mood swings, which is expressed by alternating aggression and excessive complaisance and affection. Apathy may occur, and the dog may also fall into a coma. The abdomen is painful; upon palpation, the dog whines and tries to escape. There is a gradual weight loss, which accelerates if the disease progresses rapidly. Polydipsia occurs, often together with polyuria.

With hepatic encephalopathy, the dog becomes lethargic.

Classification of pathologies and causes

Liver problems occur due to a number of factors that affect the body both internally and externally, e.g. internal lesions. Main reasons:

violation of the outflow of bile;

decrease in protective properties;

oncological diseases;

helminthic infestation;

poisonous and toxic substances;

pathogenic fungi;

viruses;

low-quality spoiled food;

infectious pathologies.

Spoiled food is one of the causes of liver problems.

It is worth noting that significant harm to the organ is caused by: salmonellosis, colibacillosis, panleukopenia. To make an accurate diagnosis, it is often necessary to resort to a biopsy.

Infectious hepatitis

This disease is usually of viral origin. The route of transmission is nutritional. The pathology is characterized by feverish conditions, catarrh of the respiratory and digestive tract, often expressed by damage to the central nervous system.

Therapy is carried out comprehensively, using hyperimmune serums, micro and macro enemas.

Prescribe decoctions medicinal plants: string, chamomile, sage, yarrow, St. John's wort.

Disinfectants in the form of potassium permanganate, furatsilin, furazolidone, potassium bicarbonate, boric acid.

with saline or glucose.

Use antibacterial therapy: kefzol, claforan, caricef, fortum, penicillin, ampicillin, benzylpenicillin, ampiox.

Antihistamines: fenkarol, tavegil, suprastin, diphenhydramine, pipolfen.

Support with symptomatic treatment and vitamin therapy.

Leptospirosis

Severe infectious pathology. All breeds are affected, regardless of age and gender. The first symptom to appear is sudden hyperthermia, progressive diarrhea, and cessation of urine production.

Leptospirosis is characterized by progressive diarrhea.

Increasing symptoms are expressed in decreased activity - the dog tries to move as little as possible, lies down more, and is reluctant to respond. Then he refuses food and has difficulty breathing. Signs of damage to the digestive system appear: nausea, bloody vomiting. Foul smell from the mouth, the mucous membranes of the throat are jaundiced, the nose becomes covered with spots. Urine darkens to brown.

Treatment

Most treatment is given through intravenous infusions .

Antibody serums and antibiotics are administered.

Saline solutions are used - Ringer's, Ringer-Locke.

Nutrient solutions - glucose, hydrolysine, rheopolyglucin.

Restore damaged blood vessels: rutin, B vitamins, ascorbic acid.

Nourishes the heart muscle: riboxin, thiatriazoline.

Essentiale is used to restore the liver.

Ascorbic acid restores blood vessels.

Mycosis

A group of diseases that are caused pathogenic fungi. Transmitted by contact. All breeds and ages are susceptible, regardless of gender. The disease is difficult to cure, occurs quite often and in advanced cases is severe.

Expressed skin lesion, which can subsequently fester. , the skin thickens, erosions appear. Next come the signs intestinal disorder: nausea, vomiting, diarrhea or constipation. The animal has a staggering gait due to dizziness.

Mycosis in a dog.

Treatment

A single lesion is eliminated by applying nystatin and griceofulvin .

Multiple infections can be treated with enylcanasole, ketoconasole .

It is acceptable to use ointments candid and nizoral .

Can be used anti-trichophytosis vaccines .

The drug Candide is used for treatment.

Cirrhosis

The disease is of two types - hypertrophic and atrophic. With a hypertrophic form, the liver enlarges, and with an atrophic form, it decreases and seems to harden. , most often, develops as a result of complications of other diseases, due to prolonged neglect of the problem.

The initial stage proceeds without visible symptoms. The progression of the pathology is expressed in decreased appetite, weakness, and chronic drowsiness. On skin sporadic hemorrhages can be seen. Severe symptoms occur immediately before the death of the dog: damage to the central nervous system,... Bloody vomiting and coma occur.

With cirrhosis of the liver, the dog is constantly in a state of drowsiness.

Treatment

Help consists of symptomatic treatment, since cirrhosis is an irreversible process and a sick pet will not fully recover.

The owners can only provide the pet with a comfortable existence, and with proper care the dog can live to old age.

By providing the dog with care, it will live to old age.

Prevention of liver diseases

The essence of prevention comes down to caring care.

It is necessary to carefully monitor any changes in the animal's behavior. Vaccinate in a timely manner, regularly disinfect the habitat, treat against insects, and deworm. Do not ignore the planned medical examination and carry out comprehensive examination the whole body. Watch your diet and avoid random food.

Timely vaccination is the prevention of liver disease.

Video about liver diseases in dogs

(hepatoencephalopathy) is metabolic disorder, affecting the central nervous system and developing due to severe liver damage. The triggering mechanism is the accumulation of ammonia in the body, a product of protein breakdown, caused by insufficient detoxification function of the liver due to its damage. Hepatoencephalopathy is a syndrome characterized by a group of symptoms of liver damage, but is not an independent disease.

The causes of hepatic encephalopathy in dogs and cats are:

. congenital anomalies portosystemic circulation

. acquired - for diseases leading to portal hypertension(cirrhosis, fibrosis, arteriovenous fistulas)

. acute - due to medications, toxins, infections

. in cats

There is a breed predisposition - congenital anomalies are more common among dogs (Yorkshire terrier, Maltese, Irish wolfhound), symptoms appear in young animals.

Acquired liver disease can occur at any age in dogs and cats.

Symptoms of hepatic encephalopathy in dogs and cats include growth failure, lethargy, vomiting, anorexia, confusion, drooping of the head, fermentation,, convulsions, coma.

For diagnosis, it is necessary to undergo clinical and biochemical blood tests, as well as a urine test. Visual diagnostics are prescribed -, angiography.

includes the concentration of ammonia and bile acids in the blood. Liver diseases cannot be differentiated by the concentration of serum bile acids, however, if their concentration increases significantly after eating food, then the presence of cirrhosis or portosystemic shunting can be assumed.

A urine test if hepatoencephalopathy is suspected is mandatory. The presence of urates in the urine of a young animal highly likely indicates the presence of a portacaval shunt. Bilirubin, urobilinogen, and hemoglobin are also determined.

Ultrasound examination is used to identify intrahepatic shunt and to study the liver and gallbladder system.

For congenital disorders of the portosystemic circulation, surgical correction is an effective treatment for hepatic encephalopathy in dogs and cats.

Acquired pathologies are treated using supportive therapy, including:

1. low protein diet,

2. lactulose, which reduces the formation and absorption of ammonia, increases the intensity of feces transit,

3. cleansing enemas,

4. antibiotics that suppress intestinal microflora.

When controlling the disease, special vigilance is required due to the risk of sudden onset dangerous conditions and complications. Hospitalization and intensive care are required. Zoe Polizopoulou dvm, PhD Tim Rallis dvm, PhD
Aristotle University, Thessaloniki, Greece

Zoya Polizopoulo, Researcher, and Tim Rallis is Assistant Professor of Internal Medicine, Department of Veterinary Internal Medicine. Faculty of Veterinary Medicine, Aristotle University, Thessaloniki, Greece.

key provisions

Hepatoencephalopathy is a syndrome with a multifactorial etiology.
Hepatoencephalopathy is characterized by an abnormal neurological condition in patients with portosystemic anastomosis or severe liver failure.
Symptoms develop as a result of the effect of intestinal toxins, not inactivated by the liver, on the cerebral cortex
Diagnosis is difficult because some differential diagnoses cannot be excluded.
There is no specific treatment, if the underlying disease is not eliminated surgically or medically.

etiology and pathogenesis

Hepatoencephalopathy (HE) is often caused by the following factors: congenital portosystemic shunt (PSS), chronic severe hepatocellular disease or cirrhosis with acquired intra- and extrahepatic PSS, or acquired liver dysfunction including liver inflammation last stage in dogs and liver lipidosis in cats. Acute liver disease cannot be common cause NOT, because it is not common in either animal species. Other, although less common, causes of HE include congenital enzyme deficiencies in the urea cycle, organic acidoses, urinary tract obstruction, and infection with urea-degrading microorganisms.

Despite extensive clinical and experimental work performed to elucidate the exact mechanism of neurological dysfunction, the pathogenesis of signs of disease in the central nervous system remains completely unclear. It may be explained by the accumulation of encephalotoxins, changes in the composition of amino acids in the plasma, and increased sensitivity of the brain to various damage due to changes in neurotransmitters and corresponding receptors. "Toxic" substances that are involved in this process alone or in combination with other substances include gamma-aminobutyric acid(GABA), GABA-like agents, short-chain fatty acids, mercaptans (methanethiols), decoy neurotransmitters (tyramine, octopamine, tryptophan) and endogenous benzodiazepine receptor ligands.

The dangerous contents of portal blood are usually neutralized by a healthy liver during normal portal circulation. The presence of a direct connection between the portal and systemic circulations, as well as a sharp decrease in liver cell function, allows these harmful substances to penetrate the blood-brain barrier and enter the central nervous system (CNS), which leads to disruption of normal brain metabolism. The concentration of urea in the blood is a significant, but not the only factor in the pathogenesis of HE in small animals. For example, there are a variety of nitrogen-free neurotransmitter inhibitors that cause CNS depression, but the blood urea concentration will remain within normal limits. Possible mechanism toxic effect ammonia involves interaction with the neuronal membrane Na.K-ATPase cascade, alteration of the normal function of the blood-brain barrier, changes in the transmission of amino acids across the blood-brain barrier, disruption of energy metabolism in the brain and, finally, disruption of chloride removal processes from neurons. Short-chain fatty acids and mercaptans can act in concert with ammonia to promote HE. GABA is a neurotransmitter inhibitor in the brain of small animals.

signs and symptoms

Signs as well as symptoms are NOT dependent on primary disease liver. If NOT caused by congenital PSS, then the diagnosis is made in small animals in early age, usually up to 7 months. Acquired PSS resulting from severe liver disease (cirrhosis or, for example, severe inflammatory process) appears in cats and dogs at an older age. Predisposition of animals to HE occurring after liver diseases associated with chronic hepatitis, has nothing to do with breed or age. It sometimes happens that in Doberman Pinschers or Bedlington Terriers, NOT occurs secondary to copper accumulation in hepatocytes and chronic liver failure.

In small animals suffering from HE, the medical history usually includes chronic, intermittent and recurrent neurological symptoms. Clinical syndromes cannot be classified into syndromes representing acute cases and syndromes characterized by chronic or sub-acute clinical signs. The first group is characterized by serious neurological dysfunctions, the second by subtle and nonspecific symptoms. Certain events can trigger the mechanism sudden violation neurological condition in a previously normal animal. Excess nitrogen from feeding or extensive gastric bleeding leads to the production of large amounts of intestinal encephalotoxins. Such effects may be accelerated by medications that cause liver biotransformation, azotemia, and metabolic imbalance. During HE, almost all symptoms of cerebral syndrome can be observed. Acute cases are characterized by features including dementia, generalized motor seizures, coma, and decerebral rigidity. Complications such as brain herniation due to increased intracranial pressure and cerebral edema are rare. Chronic or subclinical forms of hepatic encephalopathy are associated with nonspecific clinical signs such as anorexia, depression, lethargy, stupor, gastrointestinal disorders (ptyalism, vomiting, diarrhea), jaundice, ascites (especially in dogs), behavioral changes (aggression, hysteria) , ataxia, circling in one place, aimless walking, head pressing, generalized motor seizures and visual disturbances(aneurosis). In cats, behavioral changes and ptyalism are the most common. These signs appear episodically, with a long normal behavior animal in between.

diagnosis

The presence of hepatoencephalopathy in young animals should be considered when signs of a symmetrical brain disorder appear, and these abnormalities would be compatible with signs of congenital PSS such as bad condition bodies, dull, poorly growing coat; As for adult animals, a medical history should be taken into account, including signs chronic dysfunction liver cells, such as anorexia, vomiting, diarrhea, jaundice or ascites.

laboratory assessment of he in dogs and cats (Table 1).

Table 1 Laboratory assessment of HE in dogs and cats

	Congenital	Purchased PSS or liver failure
Hematology
Hematocrit	normal or	normal or
White blood cells		normal or
Platelets		normal or
Dry residue
Blood smear
Target-shaped Ets
Microcytosis
Biochemistry
	Normal or	Normal or
	Normal or	normal or
	normal or	Normal or
Total bilirubin (direct)		normal or
Albumen
Blood urea nitrogen



Ammonia tolerance test*
Bile acids during fasting	Normal or
Bile acids 2 hours after feeding**
Analysis of urine
Bilirubin***
Ammonium biurate crystals
Cholerythrin crystals

SALT - serum alanine aminotraispherase
SAST - serum aspartate aminotransferase
SALP - serum alkaline phosphatase

Increase; - moderate increase; - high magnification;

Decrease; - moderate decrease; - strong decrease;

* - high diagnostic value for dogs
** - diagnostic value for dogs and cats
*** - presence in cats is not normal. In dogs it has diagnostic value if the specific gravity of urine is less than 1.015
- absent; + present; ++ is present in large quantities +++ is present in excess

Biochemical and hematological indicators obtained as a result of routine tests make it possible to only assume the presence of HE, but not to diagnose more accurate diagnosis; A blood ammonia test, an ammonia tolerance test, and a serum bile acid test are more useful in this regard.

Hematologic findings in animals with HE are not specific and may include mild anemia, poikilocytosis, microcytosis, and target cells (see Figure 1).

Figure 1. Blood film obtained from a dog with congenital intrahepatic PSS. Note the presence of red blood cells (arrow), schistocytes (double arrow), dacryocytes, and Hovell-Jolly bodies.

Similarly, changes in serum concentrations of biochemical parameters associated with liver disease (ALT, AST, albumin, bilirubin, glucose and potassium) are usually not specific, and blood urea nitrogen concentrations are usually very low (less than 6 mg/100 ml). Animals with HE exhibit respiratory and metabolic alkalosis. Respiratory alkalosis is secondary to hyperventilation, and metabolic alkalosis results from hypokalemia and severe vomiting.

For check ammonia tolerance measure the difference between the concentration of ammonia per os before administration and 30 minutes after administration of NH 4 Cl at a dose of 100 mg/kg. Because of the risk of causing hepatoencephalopathy, this test should be performed cautiously and only on dogs in which neurological impairment is minimal and ammonia concentrations are normal and stable. For dogs, testing for nitrogen tolerance can also be done by rectal administration of 5% NH 4 Cl.

Concentration ammonia in the blood is not diagnostic of HE in cats because these animals lack the ability to synthesize arginine, which is involved in ammonia detoxification in the hepatic Krebs-Geselstein cycle. Moreover, cats with long-term anorexia sometimes have elevated blood ammonia concentrations. Forced ingestion of ammonia per os, carried out on a cat with a persistently high concentration of ammonia in the blood, can cause hepatoencephalopathy in the animal, coma, and can even lead to the death of the animal.

Concentration serum bile acids, measured in the fasting state and 2 hours after feeding, is considered a safe and equally valid test for assessing liver cell function (see Table 2). In addition, no special processing of the samples is required since they themselves are relatively stable. Blood bile acid concentrations are a very useful indicator for diagnosing HE in cats.

Table 2 Total serum bile acids (normal values for dogs and cats in µmol/l)

Liver diseases cannot be differentiated by the concentration of serum bile acids, however, if their concentration increases greatly after feeding (more than 150 mmol/l), then the presence of cirrhosis or PSS can be assumed. Most laboratories use either an enzymatic method, which measures total serum 3alpha-hydroxylated bile acids, or a radioimmunoassay (RIA), which measures specific bile acid residues, to determine the concentration of bile acids in the blood.

radiography

Abdominal x-rays must be obtained for all cases of HE. The liver in cats and dogs with congenital HE is usually small in size, while in the same animals with acquired poisoning or liver failure, the liver can be small, enlarged, or even normal. Tests such as splenoportography, jejunal vein portography, and cranial mesenteric artery portography can be used to identify both within and outside the hepatic PSS. The most preferred method is portography through the mesenteric vein, performed during any operation that is performed under general anesthesia. After a ventral midline incision, two ligatures are placed around the jejunal vein loop and the catheter is inserted into the vessel and secured. The abdominal incision is temporarily closed. An appropriate contrast agent is injected into the catheter, after which fluoroscopy is performed in the lateral and ventrodorsal directions.

ultrasound echography

Ultrasound examination is used to identify intrahepatic PSS and to study the liver and gallbladder system, as well as to study the kidneys (see Figure 2). In some cases of intrahepatic PSS in dogs, the liver is small, the hepatic veins are very small or indistinguishable, and the renal pelvis is enlarged.

Figure 2 Ultrasound echography of the liver in a dog. Intrahepatic anastomosis between the portal vein (P) and the caudal vena cava (C) and the hepatic vein (H).

Nuclear liver scintigraphy is a noninvasive technique useful for diagnosing PSS, but is rarely used in routine practice.

liver biopsy

Histopathological findings obtained from liver biopsy in cases of HE may be indeterminate. In some cases, with congenital PSS, there is an absence of a branch of the portal vein in the triad region.

A liver biopsy should be obtained to evaluate other manifestations of hepatopathy, such as liver atrophy, diffuse fatty infiltration, cirrhosis or pre-cirrhosis, cholangiohepatitis, and idiopathic lipidosis in cats (see Figures 3 and 4).

Figure 3 Hepatomegaly in a 4-year-old mongrel male with symptoms of HE. Liver histopathology revealed obvious fine nodular cirrhosis.

Figure 4 Fine nodular cirrhosis in a dog with symptoms of HE. (Van Gisson Elastica, 2.5X.)

differential diagnoses

In young dogs, symptoms similar to HE may occur in cases of idiopathic epilepsy and distemper. As for older dogs, conditions such as encephalitis, hypoglycemia, some toxicoses, metabolic and endocrine diseases can be confused with poisoning. In order to exclude differential diagnoses and determine the nature of the disorders causing HE, it may be necessary to use a combination of all the research methods described above.

treatment

Purpose drug treatment HE is the complete exclusion of neurological signs, which requires eliminating predisposing factors while avoiding the formation of encephalotoxins. In addition, if possible, supportive therapeutic measures should be taken to restore fluid and electrolyte balance; etiological treatment (ie, surgical correction of the portosystemic anastomosis) must also be used.

acute syndrome

Acute HE, the development of which is facilitated by unresolved chronic hepatopathy or acute liver disease, is considered serious illness. Treatment, which should be aggressive, is based on food restriction, intravenous fluid therapy, and the use of warm water enemas, which helps remove intestinal “toxins” and thereby prevents further absorption of toxins from the central nervous system. More effective are enemas that contain lactulose (3 parts) and water (7 parts) and are administered at a dose of 20 ml/kg. This mixture is introduced into the colon and kept there for at least 20 minutes. This procedure should be repeated every 6 hours. Circumstances limiting the more frequent or less frequent use of lactulose enemas include dehydration and hypernatremia, which can be avoided by using concomitant fluid therapy and monitoring the patient's condition. Fluids are administered intravenously to increase intracellular volume and correct electrolyte and acid-base imbalances; the liquid should not contain lactic acid, which is converted to bicarbonate. The composition of the solution was selected experimentally (0.45% NaCl in a 2.5% dextrose solution; Na can be added to the solution as needed).

Signs of increasing intracranial pressure and cerebral edema should be recognized and treated as quickly as possible. If the animal's condition stops improving or even worsens, it is necessary to take further measures using anti-edematous therapy to avoid the formation of a brain herniation. Such treatment may include the administration of a 20% mannitol solution intravenously at a dose of 1 g/kg over 30 minutes, which should be repeated every 4 hours; in addition, furosemide is administered (1-2 mg/kg intravenously). The use of corticosteroids to control edema has not produced favorable results in these conditions.

chronic case

Drug treatment of chronic HE is intended to solve the same problems that face treatment acute syndrome, however, this treatment does not need to be carried out as actively. The standard approach to treating a chronic case involves restricting dietary protein, administering agents that reduce the absorption of ammonia from intestinal tract, and the administration of per os antimicrobial agents to reduce ammonia-producing microflora.

Treatment should NOT be carried out against the background of a carbohydrate diet (as a source of necessary energy) with the addition of proteins with high biological value that are easily digestible. The diet should include vitamins (A, B, C, D, E and K), minerals (Ca, Zn and K) and, in particular, the amino acids taurine and arginine, the latter essential for cats. In addition, the diet should be low in aromatic amino acids and the concentration of branched chain amino acids should be high. Also recommended average level fiber in feed. It is very important that the food offered is palatable, as animals with liver disease and HE have poor appetite. These criteria may be met by WALTHAM's PEDIGREE Canine Hepatic Support; The owner himself can produce the required food.

Acidification of the intestinal contents aims to trap ammonia (in the form of NH 4+) and speed up its elimination from the intestines. This is achieved by administering lactulose, which can also be used as a protein-free energy source for intestinal microorganisms, thus reducing further ammonia production. The standard dose is 2.5-5 ml for cats and 2.5-15 ml for dogs per os 3 times a day. Recently, a lactulose-related substance, lactitol, taken in powder form, has shown promising results in controlling HE.

In cases where treatment is ineffective with dietary changes and lactulose alone, antimicrobial agents are added to the treatment regimen. They are used to reduce the number of anaerobic and gram-negative microorganisms that break down urea. Commonly used antimicrobial agents include metronidazole (10 mg/kg for cats and 30-50 mg/kg for dogs), ampicillin (22 mg/kg) and neomycin sulfate (20 mg/kg) per os.

WALTHAM FOCUS VOLUME 7 No. 3 1997

FURTHER READING

Bunch, S. E. Treatment of complications of hepatic failure. In: Nelson, R. W., Couto, C. Q. (eds.). Essentials of Small Animal Internal Medicine. St Louis: Mosby Yearbook, 1992: 42731.

Bunch, S. E. (1992). Clinical manifestations of hepatobiliary disease. In: Nelson, R. W., Couto, C. Q. (eds.). Essentials of Small Animal Internal Medicine. St Louis: Mosby Yearbook, 1992: 36978.

Bunch, S. E. Hepatic encephalopathy. Progress in Veterinary Neurology 1993; 2 : 28796.

Center, S. A. Pathophysiology and laboratory diagnosis of hepatobiliary disorders. In: Ettinger, S. J., Feldman, E. C. (eds.). Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat. Philadelphia: W. B. Saunders, 1989: 1261312.

Johnson, S. E. Diseases of the liver. In: Ettinger, S. J., Feldman, E. C. (eds.). Diseases of the Dog and Cat. Philadelphia: W. B. Saunders, 1995: 131357.

Kornegay, J. N., Maylew, I. G. Metabolic, toxic and nutritional diseases of the nervous system. In: Oliver, J. E. Jr, Hoerlein, B. F., Mayhew, I. G. (eds.). Veterinary Neurology. Philadelphia: W. B. Saunders, 1987: 25577.

Marks, S. L., Rogers, Q. R., Strombeck, D. R. Nutritional support in hepatic disease, Part ii. Dietary management of common liver disorders in dogs and cats. Compendium on Continuing Education and the Practicing Veterinarian 1994; 16 : 128795.

Martin, R. Portosystemic shunts. In: August, J. (ed.). Consultations in Feline Internal Medicine, 2nd Edn. Philadelphia: W. B. Saunders, 1994: 1036.

Rothuizen, J., Van den Ingh, T. S. A. Rectal ammonia tolerance test in the evaluation of portal circulation in dogs with liver disease. Research in Veterinary Science 1992; 32 : 225.

Tyler, J. Hepatoencephalopathy. Part I. Clinical signs and diagnosis. 1990; 12 : 106973.

Tyler, J. Hepatoencephalopathy. Part II. Pathophysiology and treatment. Compendium on Continuing Education and the Practicing Veterinarian 1990; 12 : 126076.

Hepatic encephalopathy in dogs occurs when more than 70% of the function of this organ is lost. In dogs, deviations from the norm are rarely diagnosed, because the functionality of the liver is quite high. The consequences of this disease are very dangerous. The disease can lead to swelling and even herniation of the brain.

IN veterinary practice Doctors sometimes have to give dogs a disappointing diagnosis - hepatic encephalopathy. Often, pet owners do not even suspect that the cause of poor health is liver disease.

Dogs have a predisposition to a large number various diseases that need to be treated for a long time. The liver has the ability to regenerate. Your dog's lifespan largely depends on the condition of his liver.

U healthy pet The liver is a kind of filter, the task of which is to neutralize toxic elements of biological origin that are formed in the intestinal lumen and then enter the blood. If you have this disease internal organ, neurotoxins in the blood enter the structures of the nervous system and affect the cerebral cortex. Hepatic coma or portacaval shunt are synonyms for the same disease in dogs.

What is hepatic encephalopathy?

The disease is rare, but its outcome in most cases is sad. Therefore, one should take the health of dogs very seriously. At the slightest suspicion that your pet is not feeling well, you should contact veterinary clinic, where diagnostic measures will be fully carried out.

The scientific definition is as follows - a metabolic disorder that develops due to a disorder in the liver and affects the activity of the nervous system.

Dog body systems that are affected by the disease:

Nervous - there is a general decrease in neuron function, convulsions;
Digestion – vomiting, nausea, diarrhea;
Urinary – formation of ammonium urate.

Genetic factor

Abdominal vascular abnormalities (portosystemic shunts) are usually diagnosed in young dogs. In adults, the disease is recognized if there is side diseases liver. Most often, the following breeds of dogs suffer from this disease: dachshund, Australian shepherd, miniature schnauzer.

Doberman Pinschers are diagnosed with non-cirrhotic portal hypertension.
Chronic hepatitis is common among cocker spaniels and terriers.
Pathologies of copper metabolism in the liver are recorded in Bedlington Terriers.

Causes of disease in dogs

A congenital change in blood circulation is a single extrarenal vessel or one large intrarenal vessel.
Portosystemic shunt of acquired type - this occurs in diseases that result in the development of portal hypertension.
Acute liver failure is caused by infectious diseases, the presence of toxic substances, in case of uncontrolled use of medications.

Clinical manifestations

The disease can be episodic or progressive. Various diseases The liver in dogs is very insidious. This is due to the fact that the malaise, in most cases, manifests itself only in late stages when therapy may be ineffective.

Symptoms of hepatic encephalopathy in dogs:

Depression, sad state;
Eating inedible objects, one's own and other people's excrement;
Increased thirst and frequent urination;
Repeated vomiting;
Incessant diarrhea;
Complete refusal to eat, very poor appetite;

If the disease is severe (in the case of prolonged early clinical manifestations), the symptoms will look like this:

Partial loss of vision (the pupils will react well to light);
Prostration;
Excessive salivation;
There is a deficit of active consciousness. Sometimes the dog may go into a coma;
Severe form of epilepsy.

The disease is characterized by neurological signs. There are changes in the dog's usual behavior - he reacts to everything inadequately, does not want to play, runs away from the owner, wanders aimlessly around the house. Many people note that the dog looks depressed or may even fall into a stupor. Most often these signs are episodic. They are usually observed several hours after consuming food with a high protein content. These characteristics progress gradually over months or years.

Carrying out an examination of the animal

If the doctor suspects the appearance of encephalopathy, he should prescribe an additional minimum of tests. Testing for the presence of bile acid must be performed twice - the first sample is taken before meals, the second two hours after meals (in this case, the test is taken from a vein).

Encephalopathy is characterized by a standard or slightly higher than normal presence of bile acids in a sample taken in the morning before meals and up to 10 times higher than the established measure of their indicator after feeding.

A laboratory diagnostic method, as a result of which conclusions can be drawn about the functioning of the liver, often shows a low albumin level. Using biochemical analysis, a high degree of urea is detected during normal or reduced level creatinine. Occasionally, low potassium and low cholesterol levels in the blood are observed.

In dogs with liver shunts, tissues and organs experience oxygen starvation(microcytic anemia). Ammonium biurate is present in the urine, and large stones may form. Using additional analysis techniques, characteristic changes can be determined:

X-rays of pets with cirrhosis reveal a significant decrease in liver volume;
Application of ultrasound. In this manner, a decrease in the size of an internal organ is detected. In some cases, it is possible to identify vascular pathology. Dopplerography detects another vessel, but this technology is not considered as an expert method;
Thanks to portography, abnormal vessels are identified;
Portosystemic shunts can be detected by MRI of the liver;
Biopsy;
Manifestations characteristic of hepatic encephalopathy are due to various pathologies, what needs to be excluded when making a veterinarian’s report.

Providing medical care

To reduce clinical effects, ammonia levels need to be controlled. The acidic area of the intestinal zone suppresses the work of enzymes that break down urea into carbon dioxide and a compound of nitrogen with hydrogen, disrupts the microflora that produces this enzyme, and reduces the absorption of ammonia: the lion's share of it is transformed into ammonium, then excreted in excrement.

To reduce ammonia synthesis, you need to give your dog dietary food. Medicines must be used in small doses.

Initial therapy

Treatment of the disease is a very difficult task, and you need to start with eliminating the causes of this condition.

Initially, you need to focus on the restoration process of the acid-base balance, and also direct all actions to inhibit the synthesis and absorption of gastric toxins.

At the first stage, drugs are prescribed depending on the source of the pathology.

If the cause of the disease is a portosystemic shunt, you will most likely need surgical intervention. Before surgery, the condition must be stabilized with medication.

If there is an acute crisis, the dog needs to be put on a diet. It is necessary to carefully monitor the amount of calories, it must be adequate. The amount of protein should be limited. Subsequently, the dog should be fed frequently but in small portions. Dairy products are included in the regular diet. For good cleansing intestines, you need to add a lot of fiber to your diet, which easily dissolves in water.

The treatment method uses:

At viral etiology antibiotics are prescribed - they are necessary to destroy harmful microorganisms in the intestines;
Lactulose;
To improve bowel function, the dog is given a cleansing enema with a warm polyionic solution;
To prevent bleeding in the gastrointestinal tract, special medicines. It is necessary to examine the animal's excrement for the presence of worms. If they are, you need to use anthelmintic drugs;
To control vomiting, use metoclopramide or ondansetron;
For localization seizures veterinarians recommend the use of special medications. All drugs must be used under the supervision of a veterinarian;
You cannot do without medications designed to reduce pressure inside the skull.

Drugs that are metabolized by the liver should be avoided.

Supportive therapeutic actions

To support water balance, prescribe infusion therapy. If there is not enough fluid in the animal’s body, this will lead to an increase in the density of urea, and this can cause a deterioration in the dog’s condition.

If albumin levels are low, blood plasma transfusion is recommended. When there are congenital blood abnormalities, only a surgeon can help. Here conservative treatment will not work. Otherwise, therapy will only provide a slight improvement in the dog’s health.

How successful the treatment will be depends on factors, but the prognosis is generally favorable. High survival rate in cases where the disease has progressed against the background of chronic liver failure.

Preventive measures for liver diseases

The primary basis of prevention is caring for your dog.

You need to be extremely attentive to the dog’s health and monitor the slightest changes in behavior.

It is advisable to monitor any changes in the animal's behavior as best as possible. It is necessary to carry out timely vaccinations and regularly sanitize the habitat pet, carry out treatment against insects, carry out preventive measures for deworming.

Planned measures aimed at identifying and preventing the development of various dangerous diseases. You need to watch what your dog eats. Its diet should be balanced, and in no case should the dog eat random food.

It is not allowed to feed the animal with cheap economy-class food. The owner must comply with the conditions of timely and intensive therapy. Late diagnosis will lead to ineffective veterinary care, and then it will most likely not be possible to save the animal.