Cat hepatic encephalopathy, also known as hepatic coma, is a mental syndrome caused by acute and chronic diseases or portosystemic shunt. It is also one of the important indicators of acute and chronic liver failure. Cats with hepatic encephalopathy mainly show panic and restlessness to the outside world, and constantly emit hoarse and roar, limb tremor, anorexia, emaciation, vomiting, constipation, iris copper staining and other symptoms.
1¡¢ Pathogenesis of hepatic encephalopathy
The occurrence of hepatic encephalopathy is the result of a variety of factors, mainly related to ammonia, mercaptan and short chain fatty acids, imbalance of branched chain amino acids and aromatic amino acids, formation of pseudoneurotransmitters, etc. Generally speaking, blood ammonia is the most direct nerve factor. Blood ammonia mainly comes from intestinal tract, * *, and skeletal muscle. Most of the ammonia from intestinal tract changes into urea through ornithine metabolic cycle in * * and is discharged by * *. When liver function is abnormal, the clearance of ammonia by * * is reduced, and ammonia production and absorption of intestinal tract increase. Especially when the hepatic portal vein is short circuited, intestinal ammonia directly enters the systemic circulation without liver detoxification, and blood ammonia rises sharply through blood Brain barrier to the brain, causing liver and brain lesions.
Severe liver disease and portal collateral circulation;
¡ñ drowsiness or coma;
There are inducements of hepatic encephalopathy;
Liver function injury;
High blood ammonia level;
The index of bile acid was abnormal.
3¡¢ Treatment and care
During the treatment of cat hepatic encephalopathy, we should pay close attention to and correct the imbalance of water, electrolyte and acid-base balance, reduce the absorption of intestinal bacterial toxins and the interaction between intestinal flora and ammonia substances.
For cats with severe hepatic encephalopathy, warm normal saline was used for enema, followed by lactulose and antibiotics.
Most of the animals with hepatic encephalopathy are in coma state, and are prone to complications. Their condition is changeable. Nursing is very important. Their diet, nutrition and medication are very difficult. Therefore, nasogastric feeding tube, esophageal intubation and gastric intubation can be used to moderately limit the protein content in food.
Steps / METHODS:
Acute hepatic encephalopathy is relatively rapid when it appears, then patients will quickly enter coma state, mainly cause jaundice, will cause patients’ consciousness disorder. And will lead to changes in the patient’s personality, will often go out of depression, but also cause multilingualism.
Hepatic encephalopathy can also cause abnormal behavior of patients, for example, patients will become informal, will scribble, the table and chair in the room are disorderly, disorderly, and will affect the sleep habits of patients, patients will cause excessive excitement of the central nervous system.
Hepatic encephalopathy will also affect the patient’s vision, in clinical patients have a small number of visual impairment. Will also cause some impact on intelligence, will not be able to normal learning, enunciation will not be clear, no ability to calculate, will cause patients often sleepy and coma.
matters needing attention:
Hepatic encephalopathy is a common disease in humans, and it is also very common in animal kingdom, mainly due to liver disease. Patients in peacetime must be paid attention to, suffering from liver disease must be treated as soon as possible.
Related questions and answers
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Cat fatty liver can be divided into primary and secondary, but the mortality rate is higher no matter which.
L-carnitine is a necessary nutrient for cats. When the demand increases or decreases, L-carnitine should be supplemented by diet. L-carnitine is required for fatty acids to enter mitochondria, so the lack of L-carnitine can cause fat to accumulate in * *. However, the detection of L-carnitine concentration in different fatty liver cats did not support this argument.
Primary or idiopathic fatty liver disease (pfld) is common in obese cats, and its pathogenesis is still unclear. However, it may be related to excessive mobilization of peripheral fat. Metabolic disorders of other nutrients usually lead to fat metabolism and transport to * *. Anorexic or obese cats experience excessive metabolism of peripheral fat at the time of stress. Methionine, carnitine, taurine and other nutrients play an important role in fat mobilization and metabolism, so the lack of these nutrients may be related to the pathogenesis of fatty liver. Methionine is an important precursor of the antioxidant glutathione. In addition, the content of glutathione in fatty liver cats also decreased significantly. The relative deficiency of arginine can affect the urea cycle and lead to hepatic encephalopathy. Anorexia caused by disorders of nerves or hormones that affect appetite may cause fatty liver. It has been reported that peripheral insulin resistance does not lead to fatty liver disease.
Secondary fatty liver is more common in cats, and its pathogenesis is similar to that of primary fatty liver. Secondary fatty liver can be seen in any disease that causes anorexia, but it is more common in inflammation, diabetes, cholangitis, other diseases, inflammatory bowel disease, tumor, lymphoma, poison induced liver injury. Secondary fatty liver can be seen in non obese cats or thinner cats. Any anorexia cat is likely to develop fatty liver, so it is necessary to resume diet as soon as possible.
Normal whole blood cell count is often seen in primary fatty liver. Nonspecific abnormalities may include mild to moderate positive cell and positive pigmented anemia. Abnormal red blood cells and Heinz corpuscles were often seen during the initial diagnosis and treatment. But these hematological changes have no diagnostic value.
Common hypertriglyceridemia, sometimes high cholesterol. Fatty liver cats may have hyperglycemia and low serum thyroxine.
Hepatomegaly may be seen in the early stage of the disease, and ascites are not common. Ultrasound can be used to evaluate liver parenchymal disease or biliary disease, and also can be used to screen for potential causes. However, this is not a specific sign of fatty liver, because it can also be seen in a wide range of solid diseases, such as lymphoma or hepatic amyloidosis.
It is important to find out the potential cause of secondary fatty liver disease according to the medical history, physical examination and ultrasound, such as cat specific lipase immunoreactivity assessment.
The purpose of diagnosis is twofold: to confirm the existence of fatty liver and to search for the potential etiology.
The diagnosis of fatty liver should be based on history, symptoms, biochemical, ultrasonic and cytological results, and / or confirmed by pathology.
***Lipid deposition can be easily diagnosed by routine Giemsa staining, diff quick staining or hematoxylin and eosin staining. For rapidly frozen live hepatocytes, it is important to determine whether hepatocyte vacuolization is fat by oil red O staining.
Fine needle aspiration showed that there were no content vacuoles in the hepatocytes. Chromatin gathered at the edge of the vacuoles, making the vacuoles ring like appearance. The size of hepatocytes was significantly different, and inflammatory cells should not appear.
Hepatomegaly was observed by laparoscopy or laparotomy, and the appearance of liver was grayish yellow and red. With the recovery of the disease, pathology can gradually return to normal.
It is not meaningful to measure the concentration of bile acids to evaluate the function of the disease, because it can be increased by the concurrent cholestasis. Fasting cholesterol and blood sugar concentration may be increased, sometimes blood sugar is high enough to make animals produce diabetes. This is usually a metabolic stress response and can be returned to normal after appropriate treatment. But some cats may develop diabetes as a result of underlying disease, or they are already diabetic and have fatty liver disease. High blood sugar, urine sugar and ketone body in urine are highly suggestive of diabetes. Some cats have symptoms of liver failure (low blood level, high blood ammonia level, low urea nitrogen level and low albumin level)
Urine tests often show bilirubinuria (usually abnormal for cats) and fatty urine.
Successful treatment of fatty liver cats requires correction and careful monitoring of fluid and electrolyte disorders (e.g., hypokalemia and hypophosphatemia), but enteral nutrition support is the most important treatment. Nasogastric feeding tube can be inserted in the first few days, and esophagus feeding tube or stomach feeding tube can be inserted after the animal’s condition is stable. In addition, attention should be paid to the treatment of primary disease of fatty liver.
Gastrointestinal feeding tube should be used as soon as possible until fatty liver cats can eat on their own. The most common method is to place nasogastric feeding tube, esophagus feeding tube or stomach feeding tube. The success rate of oral gavage is low for anorexia cats for a long time, and it may cause stress in cats.
The most effective way to reduce the accumulation of protein in the diet is to reduce the accumulation of protein in liver cells. When obese cats were fasted, a small amount of protein could significantly reduce the accumulation of fat and ALP, eliminate the negative nitrogen balance, and reduce the muscle catabolism. Carbohydrate can reduce lipid deposition, but its metabolic abnormality will continue to develop. Concurrent inflammation does not change the diet management policy. Inflammatory cats require that their diet be restored as soon as possible without limiting fat.
Carbohydrates are more intolerant than fats. High carbohydrate in food can cause diarrhea, intestinal spasm, bowel sounds and other symptoms.
The following aspects should be considered in the feeding of fatty liver cats
If severe anemia, it is best to use fresh blood transfusion, because the high ammonia concentration of frozen blood will aggravate hepatic encephalopathy.
Diagnosis and treatment of cat hepatic encephalopathy
Hepatic encephalopathy is the main index of acute and chronic liver failure in cats. The pathological changes of liver and brain in cats are mental syndrome caused by acute and chronic diseases or portal venous shunt. ***It is one of the most important metabolic organs in animals. It is the only organ of albumin (maintaining plasma osmotic pressure) and other plasma proteins (such as coagulation factors) in animals; it is an important organ for maintaining the constant glucose in blood; it is the most important organ for lipid and lipoprotein; it is also responsible for bilirubin metabolism and Biot of various endogenous and exogenous substances (such as ammonia, steroids, drugs, poisons) ransformation£©¡£ In a word, it is a large factory of animal body, metabolism and detoxification. The loss of these functions can cause a variety of clinical manifestations and cause death.
Feline hepatic encephalopathy in cats,
Fhe, formerly known as hepatic coma, is a syndrome caused by severe liver disease, based on metabolic disorders and dysfunction of central nervous system. Its main clinical manifestations are disturbance of consciousness or neuropsychiatric symptoms.
In Chinese veterinary literature, the disease is generally described as “faint”, “faint”, “faint”, “Shenhun”.
Chinese veterinarian’s view on etiology and pathogenesis
Chinese veterinarians do not have the name of hepatic encephalopathy. The main clinical manifestations of this disease are confusion of mind, incoherence of words, trimming of air lines, tremor of limbs, yellow sclera, red tongue and yellow fur, and slippery pulse. Chinese veterinarians believe that the disease is mainly due to exogenous damp heat pestilence toxin, internal resistance of the middle Jiao, cross steaming of liver and gallbladder, liver loss of catharsis, bile overflow; dampness and heat with toxin, depression and fire, heat toxin red hair for acute yellow; if heat toxin entrapped in the pericardium, dizzy delirium, draw empty lines; heat into the camp, forcing blood rash, bleeding. As “Shen’s letter of obedience to life” says, “there are natural diseases and epidemics that cause yellowing, which is commonly known as pestilence Huang (acute yellow). Improper diet, damage to the spleen and stomach, spleen is not healthy movement, phlegm dampness endogenous, abnormal rise and fall, clear does not rise, turbid does not fall, brain conduction loss, turbid Qi mixed with phlegm and dampness, liver odor occurs, blinding the gods leads to delirium, confusion, and abnormal personality. Jaundice, accumulation of diseases such as prolonged, stagnation of Qi and blood, blood stasis, blood stasis, phlegm and blood stasis, water and blood stasis, water and blood stasis, gradually into the drum intestine, water accumulation abdominal cavity, essence and Qi is not distributed, Qi is lost, clear Yang does not rise, turbid Yin does not drop, liver wind moves inward, turbid Yin is mixed with phlegm and blood stasis, and the heart and orifices are covered, causing coma, flutter and tremor. All in all, the disease is caused by excessive heat and toxin, entrapment of pericardium, or abnormal rise and fall of Qi, turbid phlegm with blood stasis, and clear orifices on the upper part. The location of the disease is in the liver and brain, but closely related to the heart. If it is not treated in time, life will be endangered if Yin and yang are separated.
Modern veterinary medicine believes that
Most of the hepatic encephalopathy in cats is caused by various types of liver cirrhosis (most common in posthepatitic cirrhosis), and can also be caused by portosystemic shunt to improve portal hypertension. If subclinical hepatic and cerebral lesions are included, the incidence of hepatic encephalopathy in cirrhosis is significantly increased. A small part of encephalopathy was found in acute phase or fulminant liver failure stage of severe viral hepatitis, toxic hepatitis and drug-induced liver disease. The more rare causes are primary liver cancer, acute fatty liver in pregnancy and severe biliary tract infection.
Cat hepatic encephalopathy, especially portosystemic encephalopathy, often has obvious inducements. The common causes are upper gastrointestinal bleeding, massive excretion of potassium and diuresis, ascites, high protein diet, sedatives, anesthetics, constipation, uremia, surgery, infection, etc.
The pathogenesis of hepatic encephalopathy in cats has not been fully understood. It is generally believed that the pathophysiological basis of hepatic encephalopathy is cell failure and collateral shunt between portal vein and portal vein. The main reason is that many toxic metabolites from the intestinal tract, which are not detoxified and cleared by the liver, enter the circulatory system through collateral branches and reach the brain through the blood-brain barrier, resulting in brain dysfunction. The occurrence of encephalopathy may be the result of multiple factors. However, the metabolic disorder of nitrogen-containing substances including protein, amino acids, mercaptans and the accumulation of inhibitory neurotransmitters may play a major role. Disorders of glucose, water and electrolyte metabolism and hypoxia can interfere with the energy metabolism of the brain and aggravate encephalopathy.
Abnormal lipid metabolism, especially the increase of short chain fatty acids, also plays an important role. In addition, the increase of brain sensitivity in animals with chronic liver disease is also an important factor. There are many theories about the pathogenesis of liver and brain diseases, among which the theory of ammonia poisoning is the most studied and the most reliable.
The clinical symptoms of cat hepatic encephalopathy include personality changes, mental retardation, consciousness disorders and neuromuscular changes. The changes of encephalopathy in acute and chronic liver failure were similar, and the manifestations of liver failure caused by different causes were not found
Personality changes: in chronic liver failure is more significant. Sometimes it becomes childish, euphoria, restless, sometimes
Mental retardation: the general neurological examination may find that the memory of the sick animal is impaired, and clinically, the disease animal will follow
They are sometimes embarrassed by their insight into the deviation.
Disturbance of consciousness: early changes often appear daytime sleepiness. If it gets worse, the movement will be reduced, the eyes will be dull and the face will be expressionless,
Slow response. In the most severe cases, coma occurred. Early coma seems to be general sleep, can wake up. Gradually,
It’s getting harder and harder to wake up. In the rapid confusion or delirium, and
Yell and scream. Neuromuscular changes: liver and brain lesions can cause a kind of involuntary movement, called flutter
(asterixis or flapping tremor). This is a kind of wrist and finger joints constantly bending a straight
Don’t exercise at will. Especially when the sick animal’s elbow is straight, the palm is downward, the fingers are separated, and the wrist is tilted, the hand
If the wrist and finger joints appear once or twice a second, then clap. This kind of flutter is often bilateral
Often in the foot, eyelid, tongue have similar phenomenon. The electrophysiological changes studied by electromyography may occur
There are repetitive electrical lapses in muscles. After the electrical pause, immediately after the muscle
Flapping occurs when the meat loses its tension. Electrical recovery restored to the original position. The origin of this electrical pause phenomenon
It is not clear, but it is obviously related to metabolic disorders of joint muscles. But flutter is not liver failure
Special manifestations, uremia, carbon dioxide poisoning, heart failure, hypoglycemia, hypokalemia may also have this
Performance. However, this phenomenon can only be seen in the early stage of liver and brain lesions,
This phenomenon will disappear.
The course of liver and brain lesions in cats may vary from good to bad, and the following stages are not clearly defined and are only used for clinical evaluation.
The first stage: euphoria or depression, mental retardation, expression retardation and other personality changes, or sleep rhythm changes,
Slight flutter, also known as liver tremor. The two arms of the affected animal were flat, the elbow joint was fixed, and the palm was facing toward
When the fingers are separated from each other, the hand can be seen to deviate laterally, and the metacarpophalangeal joint, wrist joint, and
Even the quick and irregular flutter of the elbow and shoulder joints. Most of EEG were normal.
This period lasts for several days or weeks, sometimes the symptoms are not obvious, easy to be ignored.
In the second stage, there was a slight confusion of consciousness, which was the aggravation of symptoms in the first stage
Sleep disorders and behavioral disorders were the main causes. The ability of orientation and comprehension decreased
The concepts of land and livestock are confused, unclear language and abnormal behavior are common. More sleep
Sleep time is wrong, sleep in the day and wake up at night, even fear, mania and is regarded as a general God
By disease. At this stage, the animals had obvious neurological signs, such as hyperreflexia and muscle tension
In addition, there were characteristic abnormalities in EEG. A sick animal can come out
Now not random movement and dyskinesia.
The third stage (stumpor): in addition to flutter and liver taste. Drowsiness and insanity were the main symptoms, and various neurological signs were persistent
In some cases, the animals were in a state of lethargy, but they could be awakened. But there is often confusion.
The EEG showed abnormal waveform.
Deep coma: loss of consciousness, no response to pain. There is still liver taste, but flutter disappeared, muscle loss
Zhang, the reflex is weak. The pupil often enlarges, can appear paroxysmal convulsion, ankle clonus and breath
Excessive. The EEG was obviously abnormal.
Diagnosis and differential diagnosis
The main diagnostic criteria of cat liver and brain lesions are as follows:
Subclinical liver and brain lesions can be found in the infected animals. Liver and brain lesions with mental symptoms as the only prominent manifestation are easy to be misdiagnosed
For mental illness, therefore, where there are neurotic animals, should be alert to the possibility of liver and brain lesions. Hepatic coma should be associated with
Other diseases that can cause coma, such as diabetes, hypoglycemia, uremia, cerebrovascular accident, brain infection and
Sedative overdose was identified by phase identification. Further ask the history of liver disease, check the size of liver and spleen, liver function, blood ammonia, brain
It is helpful for diagnosis and differential diagnosis.
Modern traditional medical treatment
1¡¢ Clinical syndrome differentiation and treatment of prescriptions and drugs
£¨1£© Refreshing agent
Composition and usage of Herba Artemisiae Scopariae, Herba Lysimachiae, Radix Gardeniae, Radix et Rhizoma Rhei, radix salviae miltiorrhizae, semen persicae, etc
Angelica sinensis, chuanxiong, Chishao, Zhishi, Houpu, Changpu, Dan
Nanxing Sanqian, tianzhuhuang Sanjian and Yujin Siqian. Each dose is fried into 160 Xixi, which can not be taken orally
The animals were fed with 40 cisterns each time, four times a day (for large animals, the oral dose was 40 cisterns)
Function and comment: Resolving Phlegm and resuscitation, calming the nerves. This prescription uses Yinchenhao Decoction and Chengqi Decoction to promote blood circulation and remove blood stasis, clear heat and remove phlegm
It is composed of resuscitation and so on. Fang Zhongyin Chen Qingli liver and gallbladder dampness heat, Gardenia jasminoides in addition to the vexation of heat and diuresis, is the treatment of jaundice
Rhubarb and mirabilite attack and expel intestines, remove heat and eliminate toxic substances; Magnolia officinalis and Fructus aurantii can lower Qi
It is good for reducing jaundice. Artemisia capillaris with Herba Lysimachiae can increase
It has the effect of strengthening gallbladder and reducing jaundice. While Salvia miltiorrhiza can promote blood circulation and remove blood stasis, Angelica sinensis can nourish blood and activate blood circulation
It can relieve pain; peach kernel can break blood circulation and remove blood stasis; red peony can promote blood circulation and detumescence. Tianzhuhuang Qingre
Relieving phlegm and calming constipation. The combination of several drugs can complement each other.
Add and subtract syndrome differentiation heat toxin is exuberant, symptoms see high fever, restlessness, dry mouth, jaundice deepen, add Yinhua, Lian
Forsythia suspensa, Folium Isatidis and Scutellaria baicalensis are used to clear away heat and detoxify, relieve heat and calm nerves. * water retention, symptoms of ascites, limb water
Swelling, water will be unfavorable, add Poria cocos skin, red bean, six one powder to permeate diuresis.
£¨2£© Gannao Jiedu recipe
Composition and usage: rhubarb, Fructus aurantii, Magnolia officinalis, Herba Artemisiae, Radix Ginseng and Fructus Forsythiae
Qian, Huanglian Yiqian, Chishao Sanjian, Danshen Sanjian, Shengdi Sanjian, Yujin Erqian, peony bark Erqian
Water decoction or gastric tube. Each dose is fried into 160 Xixi, 40 Xixi each time, four times a day
Functions and comments
Tongfu Xiehe, cooling blood detoxification. In the prescription, rhubarb can dredge Fu organs and expel heat; Magnolia officinalis and Fructus aurantii can break the knot under the lower Qi, so that the purgative effect is enhanced and the effect of reducing heat is enhanced
In jaundice and ascites subside; mianyinchen Qinggan, cholagogue, damp heat; Yuanshen Yangyin Qingre; red peony, Salvia miltiorrhiza, Shengdi, peony
The skin cools the blood, promotes the blood circulation and relieves the heat. The combination of these herbs can clear the bowels, reduce heat, cool blood and detoxify, so as to open the mind and awaken the mind.
Addition and subtraction of syndrome differentiation
When hot, add honeysuckle, dandelion, Scutellaria, buffalo horn to clear heat toxin. In the case of dampness, Poria cocos, Alisma orientalis and Acorus calamus were added to promote water
Wetness. Abdominal skin and areca nut were increased in patients with obvious ascites.
2¡¢ Other symptomatic treatment
Prevention and nursing
Acute infection of cats is often an important inducement of liver and brain lesions, which should be treated as soon as possible. If the animal has the early manifestation of liver and brain lesions, abdominal puncture and drainage should be avoided. Potassium excretion diuretics should also be stopped. Water and electrolyte disorders and functional changes should be carefully observed and corrected. Most of the animals with hepatic encephalopathy are in coma state, and are prone to complications, and the condition is changeable. Therefore, nursing is very important. The diet, nutrition and medication of comatose patients are very difficult. It is often appropriate to insert gastric tube for feeding, give the medicine on time, and accurately record the amount of water in and out. Generally, the daily water intake should not exceed 40 west per kilogram of livestock. In principle, mild negative water balance should be maintained; for comatose animals, they should turn over frequently to prevent bedsore. Keep the mouth clean and the respiratory tract unobstructed, and observe the changes of pulse and respiration at any time.
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