Hepatic encephalopathy: causes, symptoms, treatment, diagnosis, diet
Hepatic encephalopathy is one of the likelycomplications of liver diseases such as cirrhosis, viral hepatitis, acute or chronic insufficiency. This pathological condition is a lesion of the brain and nervous system with ammonia and other toxic products of the intestine. In most cases, patients experience a decrease in intelligence, mental disorders, emotional and hormonal disturbances, and neurological symptoms. Hepatic encephalopathy is not cured, the prognosis for patients is rather pessimistic: in eight cases out of ten, patients fall into a coma that inevitably leads to death.
Why does the disease develop?
Hepatic encephalopathy belongs to the groupinflammatory diseases that occur against the background of a weakening of the filtration functions of the liver. The causes and mechanism of the development of this pathology are not fully understood, which explains the high mortality rate among patients. Given the etiological factors, several of its forms are classified:
- Type A: develops against a background of acute hepatic insufficiency.
- Type B: occurs with cirrhosis.
- Type C: caused by ingestion of intestinal neurotoxins into the bloodstream.
To the causes of hepatic insufficiency, causingencephalopathy type A, include the consequences of hepatitis, long-term alcohol dependence and oncological lesions of the liver. Also, the disease can occur against the background of poisoning with drugs, drugs and chemicals. More rare factors that can cause pathology of type A are:
- Badda-Chiari syndrome;
- consequences of surgery;
- fatty dystrophy in pregnant women;
- the Westphal-Wilson-Konovalov syndrome.
The second type of hepatic encephalopathy isCirrhosis of the organ that is characterized by the death of hepatocytes followed by replacement with fibrous tissue. A consequence of such changes are organ dysfunctions. The pathological process can develop against the background:
- frequent bleeding within the gastrointestinal tract;
- chronic constipation;
- long-term use of medicines;
- presence of parasites in the body;
- renal failure;
- burns, injuries.
Launchers to the development of hepaticType C encephalopathies serve not as background pathologies of the liver, but intestinal pathogens and neurotoxins. With this form of the disease, pronounced neurological symptoms are observed. The main cause of hepatic encephalopathy of this type is the rapid growth and division of the intestinal microbiota, which is explained:
- excessive consumption of protein foods of animal origin;
- consequences of portosystemic shunting;
- active course of chronic duodenitis, colitis, gastroduodenitis.
Pathogenesis of the disease
To understand what is hepatic encephalopathyin humans, one should turn to the physiological characteristics of the human body. As you know, ammonia is produced in our muscles, kidneys, liver and large intestine. In a healthy person, this substance, together with the blood flow, is transported to the liver where it is converted to urea. This metabolic process prevents the absorption of toxic elements into the bloodstream. With hepatic encephalopathy, metabolism is disturbed and ammonia, getting into the blood, affects the central nervous system.
Intoxication is carried out by destructionhemoencephalic barrier. Poisoning substances stimulate the production of glutamine, inhibit the rate of oxidation of sugars. As a result, edema develops, energy starvation of brain cells occurs. In addition to ammonia, amino acids enter the brain tissues, which are concentrated in its structures, causing inhibition of the enzyme system and inhibition of CNS functions. As the disease progresses, the ratio of amino acids in the blood and cerebrospinal fluid decreases significantly. Normally, this figure is within 3.5 units, and with hepatic encephalopathy barely reaches 1.5.
With a toxic attack, thethe concentration of chlorine, the conductivity of nerve impulses slows down. All this leads to acute hepatic insufficiency and changes in the acid-base composition of the blood (increased amounts of ammonia, fatty acids, carbohydrates, cholesterol), electrolyte imbalance. These disorders have a catastrophic effect on the state of astrocyte cells, which are the main protective barrier between the brain and the bloodstream, which neutralizes toxins. As a result, there is a significant increase in the volume of CSF, which leads to increased intracranial pressure and swelling of the brain tissue.
It is noteworthy that such a disease ashepatic encephalopathy, can be chronic or occur sporadically, leading to a spontaneous outcome. Often the chronic form of pathology lasts several years in patients with cirrhosis.
Initial stages and their symptoms
At the onset of the disease, noobvious symptoms. The first degree of subcompensation can be accompanied by periodic psychoemotional disorders, slight tremor of the extremities, sleep disorders, barely noticeable icterus of the skin and mucous membranes. Patients often notice that they become distracted, inattentive, lose the ability to concentrate on anything, but do not attach much importance to these symptoms. About a hepatic encephalopathy of the first degree many do not even suspect, considering that the reason of infringements of intelligence is the fatigue, the diseases transferred in the recent past, beriberi and other factors.
The following is of great clinical severity:stage of encephalopathy. Hepatic decompensation of the second degree is manifested by asterixis (inability to maintain a certain posture, tremor of the extremities) and such symptoms as:
- disorders of the day, characterized by a stable sleepiness during the day and insomnia at night;
- prolonged fixation of a glance at one point;
- monotonous, indistinct speech;
- visual hallucinations;
- gradual loss of written skills;
- pain in the right upper quadrant;
- increased irritability;
- sharp mood swings: the state of euphoria can suddenly be replaced by apathy.
In the second stage of hepatic encephalopathy, the patientbecomes sluggish, withdrawn, indistinctly speaks and gives to any questions laconic answers, close to "yes", "no". On the background of the disease, motor coordination suffers, disorientation in space develops.
Another specific manifestation of thisdiseases are sweeping uncontrollable twitching, muscle tic. Unconscious motor activity happens with a strong strain of the muscles of the body, limbs. To check if the patient has such a symptom, he is asked to extend his hands in front of him: the test is considered positive if there are flexion-extensor reflex movements in the joints of the fingers and hands. With the course of pathology, the patient ceases to recognize the shape of objects, urinary incontinence and feces develop.
Irreversible changes in the last stages
Hepatic encephalopathy of the 3rd degree is consideredincurable. There are practically no chances for a successful outcome in such patients. This stage of development of pathology is characterized by a sopor - this condition is characterized by deep depression of consciousness with loss of voluntary activity, but by the presence of conditioned and some acquired reflexes.
At the third degree of hepatic encephalopathy the following clinical manifestations are observed:
- hyperventilation of the lungs (the patient is breathing heavily);
- retardation, stupor;
- from the mouth cavity comes a sweet smell;
- On a background of the raised muscular tone often there are convulsive, epileptic attacks.
A patient suffering from this pathology, oftenstiffens in one pose, falls into a stupor. To remove a person from a stupor is possible only by physical influence, after which there appear weak mimic contractions in response to pain syndrome. In the future, the sopor can lead to coma.
The last stage of progressive hepaticencephalopathy is a comatose state of the patient. A person loses consciousness and reflexes without reacting to stimuli. In isolated cases, a clone of muscles is possible, which is characterized by an unconscious manifestation of primitive reflexes (sucking, grasping). The pupils of the patient do not react to light, the sphincters are paralyzed, convulsions and respiratory arrest occur. The immediate cause of death in hepatic encephalopathy is hydrocephalus of the brain, pulmonary edema, toxic shock.
Classification of the disease
Depending on the severity of the symptomshepatic encephalopathy, the disease can be open and latent. The hidden nature of pathology is most dangerous for the patient. By the way, according to statistics, asymptomatic liver encephalopathy is diagnosed in 60% of cases of cirrhosis.
There are also acute hepatic encephalopathy andchronic. The first progresses rapidly, can develop a couple of days before the comatose stage. Signs of chronic hepatic encephalopathy are less pronounced, the course of the disease can be long-term.
Coma against encephalopathy is true(endogenous) or false. In the first case it is a question of fulminant lesion of the CNS in persons suffering from hepatic insufficiency or cirrhosis of the liver. With hepatic encephalopathy with a chronic course, a false (exogenous) coma happens more often. This condition is less dangerous for the patient, and with timely intensive therapy, doctors manage to bring the patient to consciousness. But despite this, the forecast leaves no hope: in 90% of cases, patients die within the first month.
To establish a diagnosis, a neurologist shouldexamine the patient, check his reflexes, conduct a survey, listen to complaints, assess the adequacy of responses and behavior. Often, patients are sent to the doctor with relatives, who could supplement the description of the course of the disease, help the doctor in making an anamnesis about the previous illnesses, the patient's addictions to bad habits, taking medications, heredity, etc.
Laboratory and instrumental diagnostics of hepatic encephalopathy is a complex of complex research procedures:
- Biochemical blood test for hepatic assays. The study allows to assess the degree of activity of aminotransferases, to determine the level of gamma-aminobutyric acid, bilirubin, ammonia. With encephalopathy in the blood there is a decrease in the parameters of hemoglobin, albumins, prothrombin, cholinesterase.
- Analysis of cerebrospinal fluid. The composition of the cerebrospinal fluid exhibits an increased presence of protein.
- Ultrasound of the liver, gallbladder and abdominal organs. The study is conducted to determine the causes of liver failure. If the screening turned out to be of little informative, liver puncture is performed.
- Electroencephalogram of the brain. The procedure will give a real idea of the functionality of the central nervous system.
- MRI, CT. These methods of research give a detailed answer about the localization of affected areas, intracranial pressure, the severity of the patient.
In addition to the basic diagnosis, in the encephalopathy of baking it is important to conduct a differential study to exclude stroke, rupture of an aneurysm, meningitis, alcohol abstinence.
Treatment of acute hepatic encephalopathy
Start the fight with the disease as soon as possible. Treatment of the disease is built up with three main stages:
- search and elimination of the factor provoking hepatic insufficiency;
- decrease in the blood level of ammonia, chlorine and other toxic substances;
- stabilization of the ratio of brain neurotransmitters.
In the syndrome of hepatic encephalopathy acuteforms of therapy begin with the use of diuretics. To remove the swelling of the body and internal organs, the brain, parenterally introduce "Furosemide", "Lasix".
If the patient's mental disorders are tooexpressed, prescribe sedatives. Tinctures of valerian and motherwort can not give the expected effect, as an alternative recommend stronger drugs ("Haloperidol", "Etaperazin", "Invega", "Rispolept").
If the cause of liver failurebacterial infection, antibiotics are prescribed to relieve inflammation. For the treatment of encephalopathy, antibacterial agents with a broad spectrum of action are usually prescribed, which manifest activity in the lumen of the large intestine in relation to various microorganisms:
In parallel with antibiotics intravenously leaddetoxifying solutions. Once the condition is stabilized, they are replaced with nutrient solutions of glucose, sodium hydrogen carbonate, potassium in order to replenish the body's deficiency of important trace elements.
When hepatic encephalopathy of type C is usedhigh cleansing enemas with lactulose. To cleanse the intestines, due to which the formation of ammonia is reduced, its absorption is prevented, the patient is prescribed drugs from the group of disaccharides (Dufalac, Normaze, Goodluck, Lizolak). Together with the feces, the poisonous trace element quickly leaves the body.
In order to prevent cerebral edema in the earlystages of the disease use hormonal system drugs "Dexamethasone", "Prednisolone". If the general condition worsens, the patient is hospitalized in the intensive care unit.
With hepatic encephalopathy against a background of acutehepatic insufficiency of the patient is urgently sent for liver transplantation. The organ transplant will increase the chances of survival (statistics speak of 70% of the people who underwent surgery who have overcome the five-year threshold). However, due to the high risk of complications and death, early consultation is required at a specialized medical center for the selection of donors, a survey of the recipient.
Diet and diet
In acute encephalopathy of the liver is recommendedfasting for 1-2 days, after which the patient is prescribed a low-protein diet. With hepatic encephalopathy, the use of vegetable and animal proteins is limited to 0.5 g per kilogram of body weight per day. In addition to protein products, consumption of table salt is not allowed. To stabilize the patient, omega-3 fatty acid complexes are prescribed. With positive dynamics, the daily amount of protein is gradually increased. The volume is increased every five days by 5-10 g, but as much as possible the patient is allowed to eat not more than 50 g of low-fat diet meat (rabbit, chicken, turkey).
It should be noted that fasting in the early days of acuteencephalopathy is not a prerequisite. If the patient's condition and test values are in acceptable values, it is sufficient to exclude protein foods from the diet, preferring low-fat home foods - soups, cereals, salads, baked goods. In this case, it is worth paying attention to food and drinks, the use of which is inadmissible in acute and chronic forms of the disease:
- apples, grapes, cabbage and other vegetables that cause fermentation in the intestines;
- dairy products;
- whole milk;
- sweet fizzy drinks;
- strong tea.
Hepatic encephalopathy in liver cirrhosisis accompanied by destructive changes in the body. With successful treatment of the disease, despite the ability of the liver parenchyma to rapid recovery, one should constantly adhere to a diet in order to avoid relapse, as liver cells react sharply to the influence of harmful substances.
Chronic liver encephalopathy, therapy
In the chronic course of the disease, the principles of symptomatic therapy are followed. When the disease worsens, it is immediately necessary to adjust the diet and switch to a low-protein diet.
As well as with acute form of hepaticencephalopathy, treatment implies the removal of toxic elements from the body. Most often requires two-stage purification of the intestines with the help of medications that reduce the degree of concentration of ammonia in the blood. To provide the patient with energy, a glucose solution is injected intravenously. In combination with the use of drugs, hepatic encephalopathy is treated with plasmapheresis procedures.
What are the chances that patients predict
The success of treatment depends to a large extent on the degreeseverity of the patient's condition. For example, a coma almost inevitably leads to the death of a patient. The prognosis worsens with a high level of total protein, albumin, as well as the development of ascites, jaundice.
Among patients with liver encephalopathythe last stages survive less than 25%, with disease of the initial degree - more than 60%. The chances of recovery are increasing after transplantation. But if the patient has irreversible brain damage, he will not be able to return to normal normal life.
The effectiveness of therapy for this diseaseis determined by several factors, among which the cause of the development of the disease and the age of the patient. For children under 10 years and patients older than 40, the forecast is the least optimistic.