Summary: Hepatic cerebropathy is a functional syndrome of the central nervous system based on metabolic disorders caused by severe liver disease, which is complex and seriously affects the quality of life and the prognosis of patients. The purpose of this paper is to raise public awareness of the disease, promote early diagnosis, effective treatment and active prevention, and reduce the risks to patients.
Introduction
Hepatitis is common among patients with severe liver diseases, such as cirrhosis and severe hepatitis, which can lead to mental disorders, behavioural disorders and comas, causing great suffering not only to patients but also to families and societies. In-depth knowledge of liver cerebral diseases is of great importance for the early identification of patients, timely treatment and prevention of their deterioration.
II. Epidemiology and morbidity mechanisms
(i) Causes
1. Hepatic cirrhosis: Hepatic cirrhosis due to various causes is the most common cause of hepatic cerebral disease. Hepatic cirrhosis is severely impaired, hepatic cells are significantly reduced and hepatic detoxification and metabolic disorders, among others, contribute to the accumulation of internal toxins and the risk of hepatic cerebral disease. For example, alcohol cirrhosis is associated with chronic alcohol consumption and repeated liver damage, leading to advanced liver cerebral disease.
Hepatitis 2. Hepatitis: In cases of acute hepatitis or sub-acute hepatitis, large areas of the liver have died and the liver function has deteriorated sharply, prompting hepatitis. Virus infections (e.g., hepatitis B virus, hepatitis C virus), drug poisoning (e.g., overdose of acetaminophenol), and self-immuno-hepatitis may lead to severe hepatitis and, consequently, to hepatitis.
3. Other factors: hysteria, haemorrhaging in the upper digestive tract, large quantities of abdominal water, high-protein diet, infections, constipation, use of sedatives and anaesthesia can also induce liver cerebral diseases. A nitrogen-containing substance such as ammonia absorbed in the intestinal tract enters the cycling directly without a full liver detoxification, leading to increased haemocal ammonia and liver encephalitis.
(ii) Incidence mechanisms
1. Aminotoxicity doctrine: ammonia is a key factor in the hepatococcult mechanism. The intestinal tract is the main part of the production of ammonia, and when the liver function is impaired, the intestinal intake of ammonia cannot be excreted from the liver ‘ s active synthetic urea, leading to an increase in blood ammonia. The ammonia can enter the brain tissue through a blood-brain barrier, interfere with brain energy metabolism, alter brain neurotransmitters, e.g. inhibiting the combination of an irritating neurotransmitting avalum acid with a synaptic receptor, while enhancing the effect of inhibitive neurotransmitting gamma-aminobutyric acid, leading to central nervous system functional disorders and cognitive disorders.
2. Hypothetical neurotransmitters: In the case of liver diseases, phenylethylamide and cheeseamine in the intestinal tract (e.g. phenylpropamine, greamine, etc.) resulting from bacterial detached effects cannot be effectively removed from the liver. Once they enter the brain tissue, they produce phenylethanolamine and hydroxyphenolamine, respectively, under the effect of the brain hydroxylase, which are similar to normal neurotransmitters of adrenaline, but have much less physiology than gonaline, which is known as pseudo-neurological neurotransmitanetic. The accumulation of false neurotransmitters in the synapses can replace normal neurotransmitters, causing neurotransmitters to develop disorders, leading to functional inhibitions of the brain and a change of mind.
3. Gamma-aminobutyric acid/benzodiazepine (GABA/BZ) compound doctrine: GABA levels are elevated in the brain of a liver brain patient, and GABA is an inhibiting neurotransmittance that can be combined with a GABA/BZ receptor in a synaptic membrane, opening the chlorine ion channel, increasing the internal flow of chlorine ion, leading to hyperpolarization of neurons and inhibiting the transmission of nervous impulses. At the same time, phenyldiazepines of internal or external origin can enhance GABA ‘ s proxies and receptors and further exacerbate central nervous system inhibition.
4. Other factors: sedimentation of manganese in the neurological section may affect the function of a nervous cell; inflammatory media such as tumour cause of death – alpha, white cell media -1 may also play a role in hepatic cerebropathy, which can affect the permeability of the blood-brain barrier and the metabolism of neurotransmitters within the brain.
III. Clinical performance
(i) One part (pre-dumption)
Patients can experience mild personality changes and behavioural disorders, such as exultment or apathy, discoloration or drowning. There is a piston-like tremor, i.e. when the patient stretches his or her arms and separates his or her fingers, he or she turns his or her hands to the outside side, and he or she moves his or her hands, wrists and even elbows and shoulder joints in an irregular manner. The EEG is so normal that there are generally no visible signs of the nervous system that it can easily be ignored.
(ii) Phase II (pre-mortem)
The main manifestations are unconsciousness, sleep disorders and behavioural disorders. The patient ‘ s orientation, calculus, and the confusion about time, place and character. There’s sleeping addiction, awakening, etc. Lack of clarity, writing barriers and behavioural anomalies are also common. This period of swarms is present, and the EMPs are characterized by an abnormality, with neurologic signs such as gill-reflection, increased muscle tension, ankle larvae and Babinski positive.
(iii) Three (sleeping period)
The patient falls asleep but is awakened and is able to answer when he wakes up, but is often unconscious and hallucinating. Various neurometric signs persist or are aggravated, such as tremors of pistons, increased muscle tension, and Cone beams are often positive. The EEG is clearly abnormal.
(iv) Four (in coma)
Patients are unconscious, can’t be awakened. In shallow comas, there is still a reaction to pain irritation, and cylindrical reflexes and muscle tension continue to swell; in deep comas, reflections disappear, muscle tension is reduced, pupils are dispersed and respiratory function disorders occur. The EEG is clearly abnormal.
Diagnosis
(i) Medical history and clinical performance
The patients are asked in detail whether they have a history of liver diseases such as cirrhosis and severe hepatitis, as well as whether they are induced by door-to-door diversion surgery and haemorrhage in the upper digestive tract. Hepatic cerebral disorders can be initially suspected when combined with typical clinical manifestations, such as cognitive disorders, behavioural disorders and tremors. However, these symptoms are not specific and need to be further examined for diagnosis.
(ii) Laboratory inspection
1. Serumaminometry: Most cases of hepatological cerebral disease have increased, but the increase is not entirely consistent with the severity of the disease, and approximately 10% – 20% of patients are normal, so that hepatococcal disease cannot be determined on an individual basis, but there is some point of reference for the diagnosis of the disease and its effects.
2. Hepatic function examination: Hepatic function can be shown to be severely impaired, e.g. a decrease in pure blood protein, a rise in chlamydia and an increase in the duration of the enzymes, which helps to understand the underlying liver disease.
EEG: EEG can be of some assistance in the diagnosis of liver cerebral diseases, especially in the early stages of diagnosis. Hepatic cerebral brain patients can experience widespread slow waves, and three waves can occur during the pre-circle period, which increases the degree of abnormality as the condition progresses. However, other brain disorders can also be found in the EMPs, which need to be combined with a combination of clinical findings.
(iii) Psychopsychological tests
The cognitive function and mental state of a patient can be tested, such as the digital connection test and the wood plot test, which is of some significance for the early detection of minor cognitive disorders in persons with liver cerebral problems and can be used as a complementary diagnostic tool.
(iv) Visual inspection
Head C.T. or MRI examinations exclude other structural brain pathologies such as cerebrovascular accidents, brain tumours, etc., but there is generally no specific change in the early stages of liver cerebropathy, which can be detected in the later stages of the disease.
Treatment
(i) Removal of incentives
Active treatment of digestive tract haemorrhage, control of infection, correction of hydro-hydrolysis and acid alkali balance disorders, avoidance of high levels of abdominal water, discontinuation of medications that could induce hepatological cerebral disease (e.g. sedatives, etc.), maintenance of excrement (e.g., laxatives such as lactose) etc. are essential for the prevention and treatment of hepatic cerebral disease.
(ii) Reduction in intestinal ammonia generation and absorption
Dietary adjustments: Limiting protein intake, granting protein-free or low-protein diets during the onset of a liver cerebral disease, increasing protein intake as the condition improves, and giving priority to plant proteins, as the plant proteins contain alkyl amino acids that compete with aromatic amino acids to enter the brain and reduce the formation of false neurotransmitters.
Clean intestinal tracts: Permeable laxatives, such as lactating nuts or ractrotol, can be used, followed by oral ingestion in the intestinal tract, which increases intestinal penetration pressure, reduces the absorption of ammonia while promoting intestinal creeping, accelerates excreta discharge and reduces the generation and absorption of intestinal ammonia and other toxins. Intestines can also be used, for example, with physico-saline water or a weak acid solution (e.g., a rare acetic acid solution), but alkaline solutions can be banned because alkaline environments can facilitate ammonia absorption.
3. Inhibition of intestinal bacteria: oral antibiotics such as neocin, nitrazine, lysergium, and so forth, inhibiting intestinal bacteria and reducing the production of ammonia. However, the long-term use of antibiotics can lead to intestinal herbology disorders, among others, and requires careful use.
(iii) Promoting the metabolic removal of ammonia
1. A bird aminomate OT formulation: it promotes the metabolism of internal ammonia, transforms toxic ammonia into non-toxic urea and azinamamine, thereby reducing hemocal levels and improving liver encephalopathy.
2. Presamate: urea synthesis can be facilitated, but in case of severe liver function failure, the reduction of ammonia may be limited due to reduced enzyme activity required for bird amino acid cycling and is acidic and more appropriate for liver brain patients associated with alkaline poisoning.
(iv) Controlling neurotransmitters
Subsistence amino acid formulations: can correct the imbalance in plasma between systolic amino acids and aromatic amino acids, competitive inhibition of aromatic amino acids into brain tissues, reduction of false neurotransmittances, improvement of patients ‘ mental state and neuropsychiatric symptoms.
Fluomasini: Hepatological encephalopathy caused by non-benzodiazepines is not effective for non-benzodiazepines, but is competitively combined with a central nervous system phenylbenzodiazepine receptor and reverses the coma caused by benzodiazepines.
Five Other Treatments
For persons with cerebral edema, dehydration agents such as gesellol can be used to reduce the internal pressure of the skull; for patients with severe liver failure and ineffective internal treatment, treatments such as liver transplants can be considered, but problems such as a shortage of supplies, high surgical risks and post-operative immune exclusion require a comprehensive assessment of the patient ‘ s condition.
Prevention
(i) Active treatment of underlying liver diseases
In cases of hepatitis diseases such as cirrhosis and hepatitis, early diagnosis, treatment and control of the progress of the conditions, such as antiviral treatment of hepatitis B and C and alcohol and alcohol-related hepatitis, are needed to reduce the risk of hepatococcal diseases.
(ii) A reasonable diet
The dietary principles of low proteins, high vitamins and the right amount of calorie should be followed by cirrhosis in the liver to avoid a one-time ingestion of large amounts of protein and to prevent haematoma from rising. At the same time, a balanced and nutritional diet should be ensured, with more vitamin-rich foods such as vegetables and fruits.
(iii) Avoidance of inducement factors
Inducing factors such as haemorrhaging in the upper digestive tract, infection, high levels of abdominal water and the use of sedatives should be avoided as much as possible. In the case of patients with oesophagus diarrhea, hemorrhage prevention measures, such as the use of non-selective beta-receptor retardants, should be taken; in the case of patients requiring sedatives, the choice should be made for medications with low liver effects and the dose should be strictly controlled.
(iv) Regular monitoring
For persons with liver diseases, hepatic functions, blood ammonia, electroencephalograms, etc., as well as neuropsychological tests, early detection of signs of hepatoccal cerebral disease, and timely preventive and curative measures.
Conclusion
Hepatic cerebral disease is a serious complication of serious liver diseases, with complex causes, multi-sectional disease, multi-clinical performance, multi-factorial diagnosis, and treatment with a combination of removal of cause, reduction of intestinal ammonia generation and absorption, promotion of ammonia metabolism, and neurotransmitting. The key to the prevention of liver cerebral disease is active treatment of underlying liver diseases, a reasonable diet, avoidance of induction factors and regular monitoring. Increased awareness of and public attention to hepatitis could effectively reduce the incidence and mortality of hepatitis and improve the quality of life and preparation of patients.
Hepatic cerebral disease
