Hepatic encephalopathy is one of the possible complications of liver diseases such as cirrhosis, viral hepatitis, acute or chronic insufficiency. This pathological condition is a lesion of the brain and nervous system by ammonia and other toxic intestinal products. In most cases, patients experience a decrease in intelligence, mental disorders, emotional and hormonal disorders, as well as neurological symptoms. Hepatic encephalopathy is not curable, the prognosis for patients is rather pessimistic: in eight cases out of ten, patients fall into a coma, which inevitably leads to death.
Why the disease develops
Hepatic encephalopathy refers to a group of inflammatory diseases that occur against the background of a weakening of the filtration functions of the liver. Causes and mechanismThe development of this pathology is not fully understood, which explains the high mortality rate among patients. Taking into account etiological factors, several of its forms are classified:
- Type A: develops against the background of acute liver failure.
- Type B: Occurs in cirrhosis.
- Type C: Caused by intestinal neurotoxins entering the bloodstream.
The causes of liver failure that cause type A encephalopathy include the effects of hepatitis, long-term alcohol dependence and liver cancer. Also, the disease can occur against the background of poisoning with drugs, narcotic and chemical substances. More rare factors that can provoke type A pathology are:
- Budd-Chiari syndrome;
- consequences of surgery;
- fatty degeneration in pregnant women;
- Westphal-Wilson-Konovalov syndrome.
The second type of hepatic encephalopathy is cirrhosis of the organ, which is characterized by the death of hepatocytes, followed by replacement with fibrous tissue. The result of such changes is organ dysfunction. The pathological process may develop against the background of:
- frequent bleeding within the gastrointestinal tract;
- chronic constipation;
- long-term medication;
- infection;
- presence of parasites in the body;
- kidney failure;
- burns, injuries.
Triggers to emergeHepatic encephalopathy type C is not caused by background liver pathologies, but by intestinal pathogens and neurotoxins. With this form of the disease, severe neurological symptoms are observed. The main cause of this type of hepatic encephalopathy is the rapid growth and division of the intestinal microbiota, which is explained by:
- excessive consumption of animal protein foods;
- consequences of portosystemic shunting;
- active course of chronic duodenitis, colitis, gastroduodenitis.
Pathogenesis of disease
To understand what hepatic encephalopathy is in 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 he althy person, this substance, along with the bloodstream, is transported to the liver, where it is converted into urea. This metabolic process prevents the absorption of toxic elements into the bloodstream. With hepatic encephalopathy, metabolism is disturbed and ammonia, entering the bloodstream, affects the central nervous system.
Intoxication is carried out due to the destruction of the blood-brain barrier. Poisonous substances stimulate the production of glutamine, slow down the rate of oxidation of sugars. As a result, edema is formed, energy starvation of the brain cells occurs. In addition, in addition to ammonia, amino acids enter the brain tissues, which are concentrated in its structures, causing inhibition of the enzyme system and depression of the central nervous system functions. As the disease progresses,the ratio of amino acids in the blood and cerebrospinal fluid decreases. Normally, this indicator is within 3.5 units, and with hepatic encephalopathy it barely reaches 1.5.
When a toxic attack also increases the concentration of chlorine, slows down the conduction of nerve impulses. All this leads to acute liver failure and changes in the acid-base composition of the blood (increased amount 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 that neutralizes toxins. As a result, there is a significant increase in the volume of CSF, which leads to an increase in intracranial pressure and swelling of the brain tissue.
It is noteworthy that a disease such as hepatic encephalopathy can be chronic or occur episodically, leading to a spontaneous outcome. Often, the chronic form of the pathology lasts for several years in patients with cirrhosis.
Initial stages and their symptoms
At the beginning of the development of the disease, there are no obvious symptoms. The first degree of subcompensation may be accompanied by periodic psycho-emotional disorders, slight tremor of the extremities, sleep disturbances, barely noticeable yellowness of the skin and mucous membranes. Patients often notice that they become distracted, inattentive, lose the ability to concentrate on something, but do not attach much importance to these symptoms. About first-degree hepatic encephalopathy, many eventhey do not suspect, believing that fatigue, recent illnesses, beriberi and other factors are the cause of intellectual impairment.
The next stage of encephalopathy has a greater clinical severity. Hepatic decompensation of the second degree is manifested by asterixis (inability to maintain a certain posture, tremor of the limbs) and symptoms such as:
- disorders of the day, characterized by stable sleepiness during the day and insomnia at night;
- prolonged fixation of gaze at one point;
- monotonous, slurred speech;
- visual hallucinations;
- forgetfulness;
- gradual loss of writing skills;
- pain in the right hypochondrium;
- increased irritability;
- mood swings: euphoria can suddenly turn into apathy.
In the second stage of hepatic encephalopathy, the patient becomes lethargic, withdrawn, speaks indistinctly and gives concise answers close to “yes”, “no” to any questions. Against the background of the disease, motor coordination suffers, disorientation in space develops.
Another specific manifestation of this disease is sweeping uncontrolled twitches, muscle tics. Unconscious motor activity occurs with a strong tension of the muscles of the body, limbs. To check if the patient has such a symptom, he is asked to stretch his arms in front of him: the test is considered positive if flexion-extensor reflex movements in the joints of the fingers and hands. With the course of the pathology, the patient ceases to recognize the shape of objects, he develops urinary and fecal incontinence.
Irreversible changes in the last stages
Hepatic encephalopathy grade 3 is considered incurable. There is virtually no chance of a successful outcome in such patients. Sopor is characteristic of this stage in the development of pathology - this condition is characterized by deep depression of consciousness with the loss of voluntary activity, but the presence of conditioned and some acquired reflexes.
In the third degree of hepatic encephalopathy, the following clinical manifestations are observed:
- hyperventilation of the lungs (the patient is breathing heavily);
- sluggishness, numbness;
- a sweet smell comes from the mouth;
- convulsive, epileptic seizures often occur against the background of increased muscle tone.
A patient suffering from this pathology often freezes in one position, falls into a stupor. It is possible to bring a person out of stupor only by physical influence, after which weak facial contractions appear in response to pain. In the future, stupor can lead to a coma.
The last stage of progressive hepatic encephalopathy is the patient's coma. A person loses consciousness and reflexes, not responding to stimuli. In isolated cases, muscle clonus is possible, which is characterized by an unconscious manifestation of primitive reflexes (sucking,grasping). The patient's pupils do not react to light, the sphincters become paralyzed, convulsions and respiratory arrest occur. The immediate cause of death in hepatic encephalopathy is cerebral hydrocephalus, pulmonary edema, toxic shock.
Disease classification
Depending on the severity of the symptoms of hepatic encephalopathy, the disease can occur overtly and latently. The hidden nature of the 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 and chronic. The first progresses rapidly, can develop a couple of days before the coma stage. Signs of chronic hepatic encephalopathy are less pronounced, the course of the disease can be long-term.
Coma on the background of encephalopathy can be true (endogenous) or false. In the first case, we are talking about lightning-fast damage to the central nervous system in people suffering from liver failure or cirrhosis of the liver. With hepatic encephalopathy with a chronic course, a false (exogenous) coma occurs more often. This condition is less dangerous for the patient, and with timely intensive therapy, doctors manage to bring the patient back to consciousness. But despite this, the prognosis leaves no hope: in 90% of cases, patients die within the first month.
Examination
To establish a diagnosis, a neurologist must examine the patient, check his reflexes, conduct a survey, listen to complaints, evaluate the adequacy of answers and behavior. Often, patients are sent to see a doctor together with relatives who could complete the description of the course of the disease, help the doctor in compiling an anamnesis about previous diseases, the patient's addiction to bad habits, taking medications, heredity, etc.
Laboratory and instrumental diagnosis of hepatic encephalopathy is a complex of complex research procedures:
- Biochemical blood test for liver tests. The study allows you to assess the degree of activity of aminotransferases, determine the level of gamma-aminobutyric acid, bilirubin, ammonia. With encephalopathy in the blood, there is a decrease in hemoglobin, albumin, prothrombin, cholinesterase.
- CSF analysis. An increased presence of protein is found in the cerebrospinal fluid.
- Ultrasound of the liver, gallbladder and abdominal organs. The study is carried out to determine the causes of liver failure. If the screening turned out to be uninformative, a liver puncture is performed.
- Electroencephalogram of the brain. The procedure will allow you to get a real idea of the functionality of the central nervous system.
- MRI, CT. These research methods give a detailed answer about the localization of the affected areas, intracranial pressure, and the severity of the patient.
In addition to the basic diagnosis, it is important to conduct a differential study with liver encephalopathy in order to exclude stroke, aneurysm rupture, meningitis, alcoholwithdrawal.
Treatment of acute hepatic encephalopathy
Start the fight against the disease as early as possible. Treatment of the disease is built from three main stages:
- search and elimination of the factor provoking liver failure;
- decrease in blood levels of ammonia, chlorine and other toxic substances;
- stabilizing the ratio of brain neurotransmitters.
In acute hepatic encephalopathy syndrome, therapy begins with the use of diuretics. To relieve swelling of the body and internal organs, the brain, Furosemide, Lasix are administered parenterally.
If the patient's mental disorders are too pronounced, sedatives are prescribed. Valerian and motherwort tinctures may not give the expected effect, as an alternative, stronger drugs are recommended (Haloperidol, Eteperazine, Invega, Rispolept).
If a bacterial infection is the cause of liver failure, antibiotics are prescribed to relieve the inflammation. For the treatment of encephalopathy, as a rule, broad-spectrum antibacterial agents are prescribed, which are active in the lumen of the large intestine in relation to various microorganisms:
- Neomycin.
- Vancomycin.
- Metronidazole.
- Rifaximin.
In parallel with antibiotics, detoxification solutions are administered intravenously. As soon as the condition stabilizes, they are replaced with nutrient solutions of glucose, sodium bicarbonate, potassium in order to replenishthe body is deficient in important trace elements.
Hepatic encephalopathy type C is treated with high lactulose cleansing enemas. 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 ("Duphalac", "Normaze", "Goodluck", "Lizolak"). Together with the feces, the poisonous microelement quickly leaves the body.
In order to prevent cerebral edema in the early stages of the disease, hormonal systemic drugs "Dexamethasone", "Prednisolone" are used. If the general condition of the patient worsens, the patient is hospitalized in the intensive care unit.
In case of hepatic encephalopathy against the background of acute liver failure, the patient is urgently referred for liver transplantation. An organ transplant will increase the chances of survival (statistics say about 70% of operated people who have overcome the five-year threshold). However, due to the high risk of complications and death, an early consultation at a specialized medical center is required for the selection of donors and examination of the recipient.
Diet and diet
In acute liver encephalopathy, fasting for 1-2 days is recommended, 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 1 kilogram of body weight per day. In addition to protein products, the consumption of table s alt is not allowed. To stabilize the condition, the patient is prescribed complexes of Omega-3 fatty acids. With positive dynamics, the daily amount of protein graduallyincrease. The volume is increased every five days by 5-10 g, but the maximum patient is allowed to eat no more than 50 g of lean dietary meat (rabbit, chicken, turkey).
It is worth noting that fasting in the early days of acute encephalopathy is not a prerequisite. If the patient's condition and test results are within acceptable limits, it is enough to exclude protein foods from the diet, preferring low-fat homemade food - soups, cereals, salads, pastries. At the same time, you should pay attention to foods and drinks, the use of which is unacceptable in acute and chronic forms of the disease:
- apples, grapes, cabbage and other fermenting vegetables;
- fermented milk products;
- whole milk;
- alcohol;
- sweet carbonated drinks;
- coffee;
- strong tea.
Hepatic encephalopathy in liver cirrhosis is accompanied by destructive changes in the organ. With successful treatment of the disease, despite the ability of the liver parenchyma to recover quickly, you should constantly adhere to a diet to avoid relapse, as liver cells react sharply to exposure to harmful substances.
Chronic liver encephalopathy therapy
In the chronic course of the disease, adhere to the principles of symptomatic therapy. With an exacerbation of the disease, it is immediately necessary to adjust the diet and switch to a low-protein diet.
Same as in acute liver diseaseencephalopathy, treatment involves the removal of toxic elements from the body. Most often, a two-stage bowel cleansing is required with medications that reduce the degree of ammonia concentration in the blood. To provide the patient with energy, a glucose solution is administered intravenously. In combination with the use of drugs, hepatic encephalopathy is treated with plasmapheresis procedures.
What are the chances that patients are predicted
The success of treatment depends largely on the severity of the patient's condition. For example, coma almost inevitably leads to the death of the patient. The prognosis worsens with a high level of total protein, albumin, as well as the development of ascites, jaundice.
Among patients with liver encephalopathy in the last stages, less than 25% survive, with an initial degree of disease - more than 60%. The chances of recovery increase after transplantation. But if the patient has irreversible brain damage, he will not be able to return to a normal full life.
The effectiveness of therapy for this disease is determined by several factors, including the cause of the disease and the age of the patient. For children under 10 and patients over 40, the prognosis is the least optimistic.
