home Audience 1 How long do they live in an induced coma without a liver? Symptoms and causes

How long do they live in an induced coma without a liver? Symptoms and causes

At least 3% of all visits to the inpatient intensive care unit are associated with a severe form of liver tissue dysfunction, when massive death of liver cells—hepatocytes—occurs. One of the most important organs of the human digestive system no longer copes with its functional purpose, the blood is not cleansed of toxins, the breakdown of fatty acids is not carried out, and other vital processes cease to occur. Against this background, acute liver failure develops, intoxication of the body and the patient falls into coma.

In its etiology, this particular type of coma does not differ from other types of human vegetative state. The centers of the cerebral cortex, as well as the central nervous system, are in a depressed state and do not respond to external and internal stimuli. Congenital and acquired reflexes are completely absent.

The only peculiarity of this type of coma is that it occurs after the liver tissue ceases functional activity.

It is important to understand that hepatic coma is not an independent disease. This is a specific state of the body, which already acts as negative consequences and severe complications as a result of an existing liver disease that has not received drug treatment. Patients in this category did not take any therapeutic measures to stabilize their health for a long period of time.

Children under 10 years of age, as well as adults over 40 years of age, are at risk of morbidity. Survival rate in acute phase the development of a comatose state is at an average level and largely depends on what exactly provoked the failure of the liver, how timely the person applied for qualified assistance to a healthcare institution, as well as from the individual qualities and vital resources of the patient. Of 5 patients admitted to intensive care with a diagnosis of hepatic coma, 1 person consistently dies.

Causes of pathology

The onset of a coma is always associated with poisoning of the blood, lymphatic fluid and all body tissues with toxic substances that have accumulated as a result of the absence of signs of liver function, as one of the organs of the digestive system responsible for cleansing the body of toxins. The causative factors that cause hepatic coma are the presence of the following diseases in a person.

Viral or bacterial infection

At least 60% of all cases of mass death of liver hepatocytes are due to the fact that the patient is diagnosed with a concomitant illness such as viral hepatitis. Microorganisms of this strain invade the liver cells, deplete them and lead to the cessation of its vital activity.

It is extremely difficult to bring a patient with hepatitis out of a comatose state, since viral activity does not stop, but only worsens in its manifestation. At the same time, doctors also have to deal with the consequences of intoxication of the body. If the cause of the disease is precisely the presence of this factor, then the likelihood of death is extremely high.

Excess protein

With long-term consumption of dishes containing a large number of protein foods of plant and animal origin, the tissues of all organs, especially the liver, are saturated with toxic products of protein breakdown.

This condition is quite often diagnosed in people who abuse protein diets, or are meat lovers, eating it daily, several times a day and in large quantities.

Oncological process

A person’s hereditary or acquired tendency to develop cancerous tumors in the liver tissue can also cause the gradual degeneration of hepatocytes into a malignant substrate. In such cases, after hospitalization of the patient and a series of diagnostic measures, it is established that he has 1-2, and sometimes even 3 stages of oncology.

Chronic renal failure

The work of the liver and kidneys is closely interconnected, since both perform the function of cleansing the body of poisons and toxic substances. In addition, the kidneys also ensure the removal of urea outside the excretory system. If the activity of this organ is reduced, then the nitrogenous substances that make up urine accumulate in the liver and, after reaching a critical concentration, provoke extensive poisoning of the body.

Impaired circulation of fluids

Maintaining a sedentary and sedentary lifestyle, the presence of diseases such as thrombosis of the great vessels, heart failure, lead to a decrease in the circulatory activity of blood and lymph. In this regard, a stagnation effect occurs and during hematopoiesis, which occurs after eating, the liver receives increased stress, which, with a systematic effect, leads to the development of liver failure.

Chronic intoxication

Constant impact on the human digestive system of such external irritants as poor condition environment in terms of ecology, consumption of large quantities of alcoholic beverages, drugs, food products containing salts heavy metals and toxins, smoking, drinking contaminated water, leads to the gradual accumulation harmful substances in organ tissues, its poisoning and death of hepatocytes.

In such conditions, hepatic coma in liver cirrhosis is quite common. Especially if the patient has been abusing alcohol for a long period of time. Systematic use of medications has an equally destructive effect, so treatment with medications should also be measured and controlled.

Types of hepatic coma

In order to make it easier to identify the cause of the development of the disease and to form a unified therapeutic set of measures aimed at removing the patient from the pathological condition, who are classified into the following types:

It is possible to determine what type of renal coma a particular patient has only through a comprehensive diagnosis of the body and blood tests. After this, a long process of blood detoxification begins, as well as restoration of the functioning of the liver as an independent digestive organ.

Prognosis - how long do people live with hepatic coma and what can be done?

The further fate of the patient largely depends on skillful actions medical personnel, the severity of intoxication of the body, as well as what exactly provoked the occurrence of this pathological condition of the body. Probability of occurrence fatal outcome is extremely high, and on average, every fifth patient who enters a comatose state never comes out of it, and after 1-3 days of drug therapy, doctors diagnose the onset of death.

It is believed that if coma is caused by short-term exposure to heavy metal salts, poisons, chemicals on the liver toxic effect, and before that the person led a completely decent lifestyle and did not influence negative influence on the organs of the digestive system, then in this case it is possible to completely restore the body with a standard life expectancy, but subject to a strict diet. We are talking about gentle nutrition, when the patient completely excludes alcohol, fatty, smoked, salted, pickled and fried foods from his future life.

Hepatic coma, complicated by cirrhosis of the liver with signs of full-fledged foci of necrosis, gives little chance of long life. The probability that such a patient will survive is no more than 25%. After returning to consciousness, patients in this category live no longer than 2-3 years. Then in their abdominal cavity fluid begins to accumulate, and foci of necrosis with bright pronounced signs total decay of organ tissue. Complicated forms of the development of the disease with the initial stage of encephalopathy indicate that the life expectancy of such a patient will not exceed 1 year.

Hepatic coma - the most severe stage of hepatic encephalopathy - develops as a result of diffuse liver damage and sudden violation its vital functions and is observed in acute and chronic diseases, when the pathological process leads to the death of most of the liver tissue. Among the causes of acute liver failure, viral hepatitis ranks first; another common cause is toxic liver damage, including drug-induced hepatitis. In this article we will look at what hepatic coma is, and what needs to be done in case of hepatic coma, and what assistance to provide if the diagnosis is confirmed.

Hepatic coma can also develop when chronic hepatitis, liver cirrhosis, severe obstructive jaundice, malignant neoplasm liver, severe cholangitis, poisoning with poisons acting on the liver: phosphorus, arsenic, mercury, lead, carbon tetrachloride, mushroom poison. Next, you will learn what to do in case of hepatic coma, what are its causes and symptoms.

Reasons for development hepatic coma

The pathogenesis of damage to nerve cells in acute liver failure is associated primarily with parenchymal liver failure and a violation of its antitoxic function, i.e., the ability to neutralize numerous toxic products formed during the metabolic process. In chronic liver diseases, the development of portocaval anastomoses leads to the fact that part of the blood from portal vein enters the hollows, bypassing the liver, which aggravates intoxication.

Particularly toxic to nervous system ammonia, which is formed in the colon as a result of the breakdown of food proteins under the influence of intestinal flora. Ammonia entering through the portal vein system is neutralized by a healthy liver by forming urea from it, which is excreted from the body in the urine. During hepatic coma, a large amount of ammonia and other toxic products of protein breakdown accumulate in the patient’s blood. The irritating effect of ammonia on the respiratory center is the cause of hyperventilation often observed in hepatic encephalopathy.

When the antitoxic function of the liver is turned off, intoxication is enhanced by the breakdown of food proteins by intestinal bacteria. At the same time, in the blood and, apparently, in the brain, the concentration of aromatic amino acids increases (the metabolism of which is normally carried out by the liver) and the concentration of branched-chain amino acids decreases. Aromatic acids (phenylalanine, tyrosine, tryptophan) are precursors of false neurotransmitters. False neurotransmitters compete with normal brain transmitters (dopamine, norepinephrine), disrupt the interaction of neurons in the brain, which leads to depression of the nervous system.

May also play a role increased content in the blood and brain of the inhibitory transmitter formed in the intestines gamma-aminobutyric acid, apparently due to a decrease in its hepatic clearance.

Thus, with hepatic coma, self-poisoning of the body and mainly the nervous system occurs. With hepatitis, toxic liver dystrophy and hepatic encephalopathy often develop in severe cases, serious concomitant diseases, as well as in pregnant women. Coma develops more often in the 1st week of illness, less often in the 2nd, sometimes after the start of recovery. In cirrhosis, the reasons leading to decompensation of liver functions, in particular detoxification, are different. Among them are alcohol overload, infection, hypokalemia, exacerbation of hepatitis, and the use of hepatotoxic drugs. In case of esophageal bleeding, which often complicates the course of liver cirrhosis, the blood poured into the intestinal tract during breakdown becomes an additional source of ammonium, aggravating the existing disorders of nitrogen metabolism.

Symptoms of hepatic coma

The clinical picture of increasing liver failure manifests itself primarily cerebral symptoms caused by toxic damage to the central nervous system. The dynamics of these disorders, which make up a large symptom complex of hepatic encephalopathy, allows us to roughly distinguish the following main stages of hepatic encephalopathy:

1. Minor impairments of consciousness and motor skills; during this period, lethargy, apathy, agitation, anxiety, euphoria, fatigue, persistent headache, drowsiness during the day and insomnia at night, and adynamia predominate.

2. Drowsiness, disorientation, inappropriate behavior.

3. Severe disturbances of consciousness, stupor, severe disorientation in time and space, unclear speech.

4. Deep unconsciousness, coma.

Simultaneously with mental disorders, changes appear muscle tone, tremors of the hands, sometimes twitching of the muscles of the limbs (asterixis), ataxia and rigidity.

In the diagnosis of increasing liver failure, in addition to signs of damage to the nervous system, the characteristic “liver” sweetish odor from the mouth is of certain importance. This symptom appears quite early, and as liver failure and encephalopathy increase, the intensity of bad breath increases.

In patients with viral hepatitis and cirrhosis, hepatic coma most often develops gradually. Early signs of deterioration are loss of appetite, the occurrence or intensification of nausea, headache, pain in the epigastric region or right hypochondrium. It is often possible to note before this that the patient’s performance has decreased, he has become lethargic, taciturn, and indifferent to his surroundings. Sometimes deterioration is accompanied by irritability and general anxiety. These changes in the patient’s behavior and psyche are the result of incipient toxic brain damage. Early symptoms also include dizziness, fainting, insomnia at night with drowsiness during the day, memory loss, and delirium. Sometimes persistent hiccups and yawning are observed. There is often itchy skin.

In the precomatous state of hepatic coma, complete aversion to food and persistent repeated vomiting occur. Pain in the liver area intensifies, its size increases with acute hepatitis decrease, the consistency becomes soft. Patients lose weight. The appearance or increase in intensity of jaundice may also be one of the signs of an impending coma. The progression of liver dysfunction in a precomatous state is manifested, in particular, by hemorrhagic diathesis caused by a decrease in the production of prothrombin and fibrinogen in the liver.

The sequence with which neuro-cerebral phenomena develop during coma is characteristic. Lethargy gradually gives way to drowsiness, which is especially noticeable during the day and turns into prolonged sleep. During this sleep, the patient can be awakened for a short time. He opens his eyes, mutters something in response to a question, sometimes fulfills simple requests (show tongue, open eyes, etc.) and then plunges back into deep dream. Periodically, against the background of long sleep, strong motor agitation, convulsions, and delirium occur. Finally, the excitement stops, and the reaction even to strong stimuli gradually disappears.

Diagnosis of hepatic coma

A patient in a state of hepatic coma is motionless, does not respond to stimuli (handling, touch, injection), which indicates a deep damage to the nervous system. The face is haggard. An unpleasant “liver” odor emanates from the mouth. The intense icteric color of the skin, sclera and oral mucosa is noteworthy. The skin is dry, cold, covered with numerous abrasions from scratching. There are multiple hemorrhages on the skin and conjunctiva, which is especially noticeable at the injection sites. Nasal and uterine bleeding, as well as vomiting in the form coffee grounds. In the terminal period, the temperature rises to 39–40 °C. The abdomen is somewhat swollen. With percussion liver dullness reduced. The liver becomes soft and doughy. Its palpation is sharply painful and causes a reaction from the patient in the form of a groan or short motor excitement. Progressive shrinkage of the liver is characteristic feature hepatic coma in acute hepatitis. The spleen is often enlarged; against the background of severe ascites, it can be difficult to palpate.

Hepatic coma is accompanied by severe arterial hypotension. Instead of the bradycardia characteristic of viral hepatitis, tachycardia and weak pulse appear. Breathing becomes noisy, sometimes arrhythmic in the form of Cheyne-Stokes or Kussmaul breathing. The pupils are dilated and poorly responsive to light. Involuntary defecation and urination are noted, and the amount of urine is significantly reduced. Urine is dark brown in color and contains urobilin and bile pigments, as well as protein, red blood cells, and casts.

Thus, the diagnosis of hepatic encephalopathy may be suspected prehospital stage based on a thorough examination of the medical history and examination data. To correctly assess the condition of a patient with jaundice and cirrhosis of the liver and timely identify the first signs of coma, it is necessary to remember that the severity of the condition is determined not by the severity of jaundice, but by the presence and severity of neuropsychiatric symptoms. Diagnostic value the latter is especially great due to its constancy, a certain sequence of development and early appearance. In this regard, such microsymptoms as persistent, increasing lethargy, drowsiness, headache, loss of appetite, nausea and abdominal pain in patients with jaundice should be regarded as the first symptoms of an impending coma and serve as a signal for taking urgent measures.

In the hospital, liver dysfunction is confirmed by biochemical research blood, however, correlations between the severity of encephalopathy and indicators liver function No. Encephalopathy, in addition to clinical signs, is manifested by nonspecific EEG changes in the form of slow, high-amplitude triphasic waves.

Differential diagnosis hepatic coma

Differential diagnosis is carried out with uremic, diabetic and hypoglycemic coma. The similarity of hepatic coma with uremic coma, which develops in the final stage of some kidney diseases, is due to disorders of the nervous system, the appearance of mild jaundice with uremia, skin hemorrhages and skin itching. However, upon careful examination, a patient with uremia notices a characteristic ammonia odor from the mouth, an earthy skin tone with a coating of urea in the form of small pityriasis scales, and a sharp constriction of the pupils. Uremic coma is characterized by arterial hypertension and hypertrophy of the left ventricle of the heart. Sometimes a pericardial friction rub is heard. With uremia, hypothermia is observed throughout the course of the disease. The character of urine is of particular importance for diagnosis. In hepatic coma, urine is the color of beer and contains urobilin and bile pigments, and in uremia it is light, with a low relative density. Urine rich yellow color, with a high relative density, even in the presence of other changes in it, allows you to completely eliminate uremia. Rapid shrinkage and tenderness of the liver speak in favor of hepatic coma.

Diabetic coma characterized by pink or pale, very dry skin, and an acetone odor from the breath. As a rule, in this case, large Kussmaul breathing, a sharp decrease in muscle tone and hypotonia of the eyeballs are observed.

In some cases, it is necessary to differentiate hepatic coma from hypoglycemic coma. Signs of hypoglycemia: increased tone muscles, rhythmic, calm breathing, convulsions, profuse sweating, suddenness and rapidity of development of these phenomena and rapid improvement in well-being after intravenous administration of 20 - 40 ml of 40% glucose solution.

What to do with hepatic coma: treatment methods

Treatment initiated with severe symptoms of hepatic coma is usually ineffective. Mortality in this case exceeds 80%; the causes of death may be intoxication, gastrointestinal bleeding, cerebral edema, disorders heart rate. Diagnosis of hepatic coma during the period of precursors or during the initial symptoms of precoma should be considered timely. It is during this period that intensive detoxification therapy can be effective, so patients with increasing liver failure in the initial stages of precoma must be immediately hospitalized in a therapeutic or infectious diseases hospital. The doctor is required to ensure transportation of the patient while maintaining maximum physical rest. Application sedatives Even with psychomotor agitation it is not recommended. Symptomatic therapy for hepatic coma at the prehospital stage with severe intoxication and persistent arterial hypotension may include detoxification therapy (isotonic sodium chloride solution, 5% glucose solution, hemodez), polyglucin, mesaton or dopamine.

The hospital also adheres to the principle of maximum physical and mental sparing of patients. For the purpose of detoxification, laxatives and high cleansing enemas are used 1 – 2 times a day. The use of lactulose, a synthetic disaccharide that decomposes in the large intestine into lactic, formic and acetic acid. Acidification of intestinal contents causes osmotic and acid diarrhea, changes bacterial flora in favor of non-nitrogen-producing bacteria and reduces the concentration of free (non-ionized) ammonia in the intestine. Lactulose is prescribed orally at 15–45 ml 2–4 times a day. The drug is contraindicated in cases of suspected intestinal obstruction. Side effects in case of overdose are dehydration, hypernatremia, severe diarrhea. In addition, lactulose can be prescribed in the form of enemas (300 ml of lactulose is added to 700 ml of water, 2 - 4 enemas per day).

An alternative to lactulose in the treatment of hepatic encephalopathy can be the antibiotic neomycin, which suppresses the ammonia-producing intestinal flora. The drug can be administered orally (1 g every 4–6 hours) or in the form of enemas (1–2 g in 100–200 ml of isotonic sodium chloride solution 2–4 times a day). Its side effects are nephrotoxic and ototoxic. If neomycin is intolerant, metronidazole may be indicated - 250 mg 3 times a day. IN severe cases If monotherapy is ineffective, combined treatment with lactulose and neomycin is carried out.

Proteins (meat, fish, cottage cheese, eggs) are limited, and in case of severe encephalopathy, completely excluded from the diet. Sufficient energy supply is achieved by intravenous administration of glucose - up to 3 liters of 10% solution in a precomatose state. For better absorption of glucose during hepatic coma, insulin is simultaneously used at the rate of 10 units per 50 g of pure glucose. Considering the hypokalemia common in these patients, 3–6 g of potassium chloride is added to the solution. Vitamin therapy is indicated (B vitamins, ascorbic acid, to combat bleeding - vitamin K, Vicasol). Feasibility of appointment steroid hormones Not recognized by everyone, their use is possible, apparently, for alcoholic liver damage.

It should be emphasized that only early hospitalization can in many cases save the life of a patient with increasing liver failure.

Therefore, every patient who comes to the clinic with such a diagnosis has a history of some kind of liver disease (usually cirrhosis or hepatitis). About 30% of those admitted are people under 40 years of age, and only 1 out of 5 people survives such a pathology. The highest mortality rate is recorded among patients under 10 years of age and over 40 years of age.

Liver and nerves

About the connection between liver disorders and mental disorders has been known since ancient times. According to the records found, Babylonian doctors (2000 BC) called the liver “mood” and “soul”, and its health was considered the source of extrasensory abilities (prediction, clairvoyance). In ancient Chinese manuscripts, the liver was described as the seat of blood and soul. And the well-known Hippocrates (V-IV centuries BC) told how patients with a diseased liver lost their minds and barked like dogs.

It's especially hard mental disorders manifest themselves in patients with alcoholic cirrhosis, among whom the risk of deep coma and death is even greater than with hepatitis.

Therefore, the presence of neuropsychiatric disorders during long-term cirrhosis or hepatitis, as well as their transition to a coma, is a long time ago known fact. But the pathophysiology of the onset of this condition and the effectiveness of conservative treatment methods are still associated with a number of questions.

Stages of coma

Hepatic coma is the result of prolonged destruction of the liver under the influence of pathogenic influences. It occurs when more than 50% of hepatocytes are destroyed, and the level of toxins in the blood has reached such a level that it has crossed the brain barrier and caused damage to the central nervous system (hepatic encephalopathy). A superficial consideration of the mechanism of development of this condition is as follows: acute liver failure leads to the fact that hepatocytes cannot bind toxic substances and remove them from the body.

Accumulated toxic products enter the extrahepatic vessels and are transported along with the blood to other organs. The central nervous system suffers the most, which is why the first symptoms appear mental symptoms. Only one in five patients hospitalized as a result of hepatic coma survives. The likelihood of death also depends on the stage of the coma:

causeless change of mood from melancholy to euphoria;
confusion with impaired orientation in space;
the patient recognizes those around him, but has difficulty solving even the simplest logical and numerical problems;
There are no changes on the EEG yet

a sharp change in attacks of excitement and drowsiness;
lethargy

yellowness of the skin;
vomiting and nausea;
sweet putrid breath

complete lack of consciousness;
lack of reaction to light with dilated pupils;
depressed breathing;
increased heart rate;
decreased blood pressure;
against the background of extraneous noise, heart sounds are difficult to hear;
hyperthermia;
EEG synchronous delta waves

The percentage of survival if the patient was brought to the clinic with a specific stage of coma is indicated in parentheses. A more precise distinction between comatose and previous states is carried out using the West Haven scale, which combines general symptoms, EEG readings, ammonia levels, presence of flapping tremor, and time the patient completed the numerical test.

At all stages of hepatic coma, doctors record elevated levels of ammonia in the patient’s blood and brain.

Precoma and the threatening stage are shallow comatose states, during which clarity of consciousness periodically occurs. The pupils are constricted, reflexes to painful stimuli are observed, but tendon reactions are absent. When hepatic coma occurs directly, the patient's face changes. The wide palpebral fissure, drooping corner of the mouth, smoothing of the frontal and nasolabial folds are more reminiscent of a lifeless mask than a human face.

Similar to how with acute pancreatitis against the background of diabetes mellitus, the patient’s breath smells of acetone; in case of hepatic coma, the patient smells of mold.

Causes

Poisoning of the body with toxic substances not bound by the liver is a consequence of the following disorders:

viral or bacterial infection - 60% of infectious lesions of hepatocytes are hepatitis;
metabolic disorders - most often they are associated with a sharp change in protein levels. This occurs with a long-term protein diet, amino acid deficiency, bleeding in the gastrointestinal tract, extensive hematomas and surgery. Pathology can also be caused by electrolyte imbalance - reduced Na (sodium), Mg (magnesium), K (potassium) or increased levels of Mn (manganese);
propensity for oncology - the degeneration of hepatocytes into cancer cells occurs extremely rarely (only 0.41% of all cancer cases). However, metastases from other organs suppress intrabiological processes, contributing to liver failure;
inhibition of urea synthesis - most often occurs with a low level of Zn (zinc) and taking diuretics;
disruption of circulatory processes - with thrombosis, heart failure and impaired lymph outflow, unbound substances stagnate. Because of this, the liver receives a large one-time load during hematopoiesis that occurs after eating;
decreased detoxification function of the liver - explained external influences: consumption of alcohol or certain medications, disruption of the intestinal microbiota due to poor nutrition, stress, infections, toxin poisoning, which is also often caused by eating junk food. Hepatic precoma in massive cirrhosis is more commonplace than an individual manifestation.

A favorable prognosis is determined by timely identification of the cause of hepatic coma, but in 8–15% of cases it cannot be determined.

Types of coma

The clinical picture described above is general, since specific symptoms of hepatic coma, characteristic of a condition of a certain etiology, often appear. From this point of view, it is customary to distinguish the following types of coma:

rapid progression;
development of deep coma within a couple of hours;
high mortality

increase in icteric, hemorrhagic, neurological and dyspeptic disorders;
there are periods of psychomotor agitation;
breathing is impaired and there is a “liver odor”

slow flow;
rare transition into deep coma;
no “liver odor”

jaundice and hemorrhage are much less pronounced than with endogenous coma;
There are no attacks of excitement; on the contrary, the patient is withdrawn and silent

For the first time, the mechanism of development (pathogenesis) of hepatic coma was observed at the end of the 19th century by the Russian military scientist N. Eck, who directed blood circulation in the body past the liver. Later, this experience was scientifically described by I. Pavlov. The scientist managed to experimentally reproduce the process of accumulation of phenol, ammonia and other toxins in dogs. In large quantities, unpurified blood soon caused signs of meat poisoning in animals and led to death. At that time, the medical community did not appreciate the significance of this work, since it was believed that the extreme stage of destruction of hepatocytes occurs very rarely. Only 40 years later (1919) the experiment was repeated by European and American scientists and recognized by the international medical community.

I.P. Pavlov provided the first description of the mechanism of development of exogenous hepatic coma, caused by the accumulation of ammonia and other toxins in the blood.

Recent research has relegated the importance of Pavlov's discovery to the background, since in 1976 the scientist Fisher was able to understand the cause of the accumulation of toxins at the micro level, identifying dysbiosis as one of the main stimulating pathogenic factors. It was found that when the intestinal microflora is disrupted, bacterial waste products accumulate, which causes an increase in the level of amino acids - tyramine and, as a result, octopamine. The latter displaces dopamine and norepinephrine (excitatory mediators) from the synapses of the central nervous system. That is why in exogenous coma the patient does not show signs of agitation. Only a depressed state is typical, since depressed dopamine also reduces serotonin (“the hormone of happiness”).

Recent experiments have shown that a false coma occurs when the liver ceases to control the level of hormones responsible for water-salt balance. And endogenous coma is caused by a complex of pathological mechanisms.

Diagnostics

Examination of the liver itself (ultrasound, puncture, etc.) at the coma stage is carried out in those patients whose health has seriously deteriorated. Most often, the most important role in the diagnosis of hepatocellular failure and comatose states is given to microbiological tests. The level of toxins in the blood (ammonia, phenol, bilirubin, etc.) is mainly determined, when elevated, the diagnosis becomes obvious. Also detect a trend pathological process based on the following research.

Blood biochemistry will show significant electrolyte changes, a decrease in protein levels and clotting factors (3-4 times), high cholesterol and products of nitrogen metabolism.
The EEG will show a decrease in the alpha rhythm, however, in latent and first stages of encephalopathy, the sensitivity of this examination method is only 30%. A good alternative is the VP-R-300 method, which determines the electrical response of the brain to an external stimulus or the performance of a cognitive task (the same numerical test). The sensitivity of recognition of evoked brain potentials is 80%.
MRS is a highly sensitive method (90–100%) for detecting encephalopathy even in a latent state. It is based on the study of changes in the molecular composition of white and gray matter by video visualization under magnetic influence. The advantages of this method: painlessness and effectiveness, however, it is used only in severe cases due to high cost examinations.

In 90% of patients with exogenous coma, intestinal dysbiosis is detected, so additional examinations of the gastrointestinal tract may be necessary.

Conservative treatment

Although the liver is an organ that is silent for a long time and patiently, threatening pain signs in the right hypochondrium appear long before the onset of coma. Therefore, timely therapy and periodic observation are good prevention necrotic conditions of the liver.

Signs of hepatic coma appear only with massive liver necrosis, when at least 70% of hepatocytes die.

Conservative treatment of hepatic coma is more likely to delay the moment when an urgent transplant is needed. Drug therapy allows only to stop destructive processes in the liver and is usually carried out according to the following scheme:

The difference between probiotics and prebiotics is that the former consist of living bacteria (natural representatives intestinal microflora), and the latter are synthetic drugs that do not contain living microorganisms, but accelerate their growth in their usual environment.

In deep coma, an urgent liver transplant may be needed. This procedure is not only expensive, but also risky, since the donor organ does not always take root, and even the most powerful immunosuppressants do not stop the production of regenerative antibodies. If liver transplantation is not possible, other types of surgery are performed to correct the liver condition, but their effectiveness is low (maximum plus 1–5 years), and death is inevitable.

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Liver cancer

Liver cancer is malignant disease, characterized by a gradual loss of organ function, which leads to inevitable death. The basis of the pathological process in the liver is the replacement healthy cells– hepatocytes into atypical – cancerous.

The disease occurs throughout the globe. On average, 40–50 people per 100 thousand of the population die from liver cancer per year. Liver cancer distribution and incidence:

the highest incidence rate occurs in the countries of Asia (Kazakhstan, China, India, Nepal, Japan) and Africa (Nigeria, Sudan, Ethiopia, Angola, Zambia, Botswana) and amounts to 98.9 cases per 100 thousand population per year;
15 cases of the disease per 100 thousand people per year occur in African countries (Nigeria, South Africa, Madagascar) and Oceania;
9 cases of incidence per 100 thousand population per year are found in the countries of Asia (eastern part of Russia), Europe (Ukraine, Moldova, Spain, Italy), South America (Brazil, Chile);
5.6 cases of liver cancer incidence per 100 thousand people per year occur in Europe (Norway, Sweden, Finland, Germany, the Netherlands, Belgium), North America (USA, Alaska), South America (Argentina) and Australia;
The lowest incidence rate occurs in the countries of North America (Canada, Mexico) and Europe (Great Britain, Ireland) - 1 case per 100 thousand people per year.

Liver cancer affects any age, but most often occurs in people between 50 and 60 years of age. Men get sick 4–5 times more often than women.

The prognosis for life with liver cancer is unfavorable, patient survival varies from 1.5 years to 1 month depending on the stage of the process, tumor structure, laboratory data and symptomatic manifestations. A table was developed based on the most important data for the forecast.

System for determining the survival of patients with liver cancer using the CLIP system:

Childe-Pugh class

Mononodular, less than 50% of the liver parenchyma is affected

Multinodular, less than 50% of the liver parenchyma is affected

Massive damage to more than 50% of the liver parenchyma

Alpha fetoprotein is a biological marker found in blood serum. When substances become more than 400 units. talk about the appearance of liver cancer

Portal vein thrombosis

Number of points according to the CLIP system

Average patient survival, month

Causes

The occurrence of liver cancer is promoted by many factors that negatively affect the liver and lead to its destruction:

Based on morphological characteristics, liver cancer is divided into microscopic and macroscopic forms:

Tumors from liver epithelial cells:
- hepatocellular cancer (tumor of hepatocytes - liver cells);
- cholangiocarcinoma (tumor of the intrahepatic bile ducts);
- hepatocholangiocellular cancer (mixed tumor);
- cystadenocarcinoma (tumor from the intrahepatic bile ducts, spreading to the extrahepatic ones);
- hepatoblastoma (liver tumor of embryonic origin).
Mixed epithelial cell tumors:
- cholangiocillary liver tumor + mixed epithelial tumors;
- neoplasms from the epithelium of unspecified origin.

Tumors from liver mesenchyme:

neoplastic hemangioendothelioma (tumor of the hepatic arteries);
angiosarcoma (tumor from inner shell liver vessels).

Tumors from other cells:

squamous cell carcinoma of the liver (tumor of squamous epithelium);
leiomyosarcoma (smooth muscle tumor);
malignant non-Hodgkin's lymphoma (a tumor of lymphocytes that are found in the liver);
fibrosarcoma (tumor of the connective tissue of the liver);
malignant mesothelioma (tumor of mesothelioid cells of the liver).

Nodular liver cancer is the most common type tumor process, occurs in 60–85% of cancer cases. The liver increases in size and contains irregularly shaped foci in its structure from several millimeters to several centimeters;
Massive form of liver cancer is less common, occurring in 25% of cancer cases. The tumor usually occupies the right lobe because it is quite large;
The diffuse form of liver cancer is the rarest form, observed in 9–12% of cases of the tumor process. The liver does not enlarge in this form of the disease. The tumor grows into all structures of the liver and gradually replaces healthy cells.

Depending on the growth of the tumor, there are:

infiltrative type - the tumor grows into the surrounding tissues, and it is practically impossible to separate it from the organ;
expansive type - the tumor has the appearance of clearly demarcated healthy tissue liver nodes:
- mononodular type – 1 – 2 nodes in the liver;
- multinodular type - 3 or more nodes in the liver;
mixed type - the tumor includes both characteristics.

Depending on the degree of differentiation of tumor cells, the following are distinguished:

well-differentiated tumor;
moderately differentiated tumor;
poorly differentiated tumor;
undifferentiated tumor.

Determination of the stage of the oncological process according to the TNM system:

T – primary tumor

T X – insufficient data to evaluate the primary tumor;
T 1 – the primary tumor in the liver is not detected;
T 2 – one small liver tumor delimited from the vessels;
T 3 – multiple tumor foci in the liver, not exceeding 5 centimeters in diameter, growing into the vessels;
T 4 – multiple tumor foci in the liver, reaching 5 or more centimeters in diameter, growing into the vessels and spreading to neighboring organs (peritoneum, pancreas, stomach) except the gallbladder.

N – regional (nearby) lymph nodes

N X – there is not enough data to assess regional lymph nodes;
N 0 – no signs of damage to the regional lymph nodes of the liver;
N 1 – the presence of metastases in the regional lymph nodes of the liver.

M – distant metastases

M X – insufficient data to identify distant metastases;
M 0 – distant metastases are not detected;
M 1 – there are distant metastases (distant metastases are usually found in the lungs, mediastinum and breast).

Interpretation of results by stages:

Criteria for determining the stage of liver cancer:

Less than 50% parenchyma

Free legal advice:

More than 50% parenchyma

Ascites (presence of free fluid in the abdominal cavity)

Albumin (a protein substance synthesized in the liver)

Bilirubin (destroyed red blood cells, which, with preserved organ function, are utilized by the liver)

Less than 50 µmol/l

More than 50 µmol/l

Liver cancer stage

Average survival rate of untreated patients

The severity of the oncological process in the liver is assessed using a table developed by Child and Pugh. This table allows you to evaluate liver function:

Ascites (loose fluid in the abdominal cavity)

Small amount, easy to treat

Large amounts of fluid that cannot be treated with medication

Serum bilirubin, µmol/l (mg%) – destroyed red blood cells that are utilized by the liver

Less than 34 (2.0) with a norm of up to 20 (0.5)

Albumin, g – a protein substance that is synthesized in the liver

More than 35 (the norm is 40 and above)

PTI (prothrombin index) is a substance produced in the liver that is involved in blood clotting

More than 60 (norm from)

The sum of points 5 – 6 corresponds to class A (compensation stage) – the liver fully copes with all functions.

The sum of points 7 – 9 corresponds to class B (stage of subcompensation) – persistent liver destruction, requiring constant medical intervention.

A score of 10–15 corresponds to class C (stage of decompensation) – the liver parenchyma is completely replaced by cancer cells or connective tissue. Constant medical care is needed to prolong the patient's existence.

Depending on the route of metastasis of liver cancer, there are:

hematogenous route – tumor cells spread in the body through the bloodstream;
lymphogenous pathway - tumor cells spread throughout the body through the lymphatic ducts;
implantation path - tumor cells directly attach to nearby structures (stomach, peritoneum, etc.).

Liver cancer symptoms

increase in body temperature to 37.5 0 C;
headache;
dizziness;
noise in ears;
visual impairment;
hallucinations;
decreased memory and attention;
drowsiness;
apathy;
general weakness;
dyspnea;
wet cough with a small amount of mucous sputum;
pain in the heart area;
decreased blood pressure;
increased heart rate;
the appearance of edema of the lower extremities;
sudden weight loss;
decreased appetite;
nausea;
vomiting of blood, intestinal contents;
salivation;
heartburn;
hiccups;
ulcerative lesions of the oral mucosa (stomatitis);
pain in the stomach and hypochondrium;
the liver initially increases in volume sharply, and then, as the disease progresses, becomes smaller;
enlarged spleen;
ascites (presence of free fluid in the abdominal cavity) with disease progression can reach up to 15 – 20 liters;
tarry diarrhea, occasionally mixed with blood;
pain in the lumbar region;
urinary disturbance;
erectile disfunction;
impotence;
gynecomastia (increase mammary gland) in men;
yellowing of the skin;
the appearance of spider veins on the body;
varicose veins in the lower extremities;
dryness and flaking of the skin;
brittle nails and hair.

Diagnostics

To diagnose the disease, a complete comprehensive examination is necessary, combining specialist consultations, laboratory, instrumental methods research and mandatory confirmation of liver cancer analysis by taking a biopsy.

Laboratory examination methods

general blood test, which will be characterized by an increase in the number of leukocytes, a shift leukocyte formula to the left, an increase in ESR (erythrocyte sedimentation rate), a decrease in red blood cells, hemoglobin and platelets;
a general urinalysis, in which the appearance of protein, an increase in leukocytes and epithelial cells in the field of view, as well as a decrease in the specific gravity of urine will be observed;
biochemical analysis + liver tests:

Change in liver cancer

3.11 – 6.48 µmol/l

0.565 – 1.695 mmol/l

Remains unchanged or decreases

High density lipoproteins

Remains unchanged or decreases

Low density lipoproteins

Remains unchanged

8.6 – 20.5 µmol/l

0.1 - 0.68 mmol/(h l)

0.1 - 0.45 mmol/(h l)

Remains unchanged or decreases

0.177 mmol/l

serum test for cancer markers (alpha-fetoprotein), which will show a positive response.

Instrumental examination methods

Ultrasound of the liver, which can indicate a possible oncological process. This survey requires clarification;
CT ( CT scan) liver allows you to more accurately diagnose liver cancer, examine the structure of the tumor and undamaged cells, identify foci of the tumor process in neighboring tissues and damage to regional lymph nodes (arrows indicate tumor foci);
MRI (magnetic resonance imaging) of the liver also allows one to suspect cancer, but unlike CT, it takes much longer (about 1 hour), is accompanied by unpleasant knocking sounds that can irritate the patient and the cost of this examination is higher.

Liver biopsy>

Specialist consultations

therapist;
gastroenterologist;
oncologist;
surgeon.

Liver cancer treatment

Drug treatment of the disease is aimed only at improving the quality of life, with the exception of chemotherapy, which is aimed at destroying tumor cells, but such treatment is effective only when combined with surgical treatment.

The most effective method on at this stage development of medicine is surgical removal tumors and regional lymph nodes or liver transplantation with appointment in postoperative period chemotherapy and radiation.

Drug treatment

chemotherapy - drugs such as doxirubomycin, cyclophosvane, leukeran are used to treat liver cancer. Combinations, frequency of administration and dose are decided by the oncologist for each patient individually;
non-steroidal anti-inflammatory drugs - diclofenac 3.0 intramuscularly 1 time per day;
narcotic analgesics, for intense pain syndrome - morphine 1% - 1.0 ml intravenously or omnopon 2% - 2.0 intravenously. Drugs can only be used if the disease is confirmed histologically by taking a biopsy;
sorbents - enterosgel 1 tablespoon 3 times a day before meals;
detoxification therapy - rheosorbilact 200.0 ml intravenous drip;
enzymes - Creon 1 tablet 3 times a day with meals;
diuretics - furosemide 40 – 80 mg 3 times a week;
general strengthening drugs - B vitamins, vitamin A, vitamin C in tablets once a day.

Surgery

liver resection - removal of the tumor with part of the unaffected organ tissue and regional lymph nodes;
liver transplantation;
radiofrequency ablation - a needle-shaped probe is immersed into the liver tumor under the control of an ultrasound machine and begins to produce low-frequency currents with a temperature of 122 - 212 F. The procedure lasts 10 - 15 minutes.

Traditional treatment

Traditional treatment for liver cancer is prohibited.

Diet that eases the course of the disease

What you can eat from food:

Not fatty varieties meat (veal, beef);
Low-fat varieties of poultry and fish (white meat chicken, pike perch);
Soups with vegetable broths;
Boiled vegetables;
Fermented milk products with low fat content;
Porridge – buckwheat, oatmeal, rice;
Boiled eggs or omelettes cooked in the oven;
Baked fruits, compotes, jelly.

What is forbidden to eat from food:

Fatty, fried, spicy, salty foods;
Fatty meats and fish;
Mushrooms in any form;
Legumes;
Wheat cereals;
Fresh vegetables;
Pickles, canned food, marinades;
Sauces, herbs, spices, ketchup, mayonnaise, mustard;
Coffee;
Pastries, cakes, sweets, chocolate;
Alcohol;
Carbonated drinks and juices in tetra packs.

Comatose liver: types and stages, first aid rules

Hepatic coma is a pathological condition that is the final stage of hepatic encephalopathy.

This is a complete depression of the central nervous system, resulting from a severe form of intoxication with liver failure.

Coma develops due to an increase in the concentration in the body of substances such as ammonia, phenols, sulfur-containing and aromatic amino acids, and fatty acids with low molecular weight.

These substances are metabolic products and have a harmful toxic effect on the brain. The pathogenesis of this condition of the body is varied.

The important question is “How long do people with hepatic coma live?”

Unfortunately, all the signs and pathogenesis of the disease indicate irreversible processes in the body. This means that death occurs in almost 90% of cases.

There are several types of hepatic coma, namely:

Hepatocellular coma is also called endogenous. This type of coma develops with the destruction of the liver parenchyma, that is, with necrosis of hepatocytes. This condition occurs in various liver diseases: hepatitis, cirrhosis, poisoning with toxic substances;
Portocaval coma, or exogenous. This type of coma occurs in patients who suffer from cirrhosis complicated by portal hypertension;
Mixed. This is a type of coma that develops, including the factors of endogenous and exogenous coma.
False. This type of coma develops in patients with cirrhosis, namely due to potassium deficiency in the body.

Stages

According to the clinical picture, hepatic coma can manifest itself in 3 stages. These include precoma, threatening coma, frolicking coma.

Prekoma. This is a human condition in which disorientation in space, impaired thinking, and other disorders are manifested. This stage of coma can last for several months.
Threatening coma. This condition is characterized by disorders of consciousness, depression, impaired coordination of movements, tremors of the limbs, speech disturbances, attacks of activity can suddenly change to drowsiness. This stage can last from several hours to 3 days; it rarely happens that this condition lasts 10 days.
Developed coma. This is a state of the body in which a person completely lacks consciousness, while reflexes to strong stimuli remain, and rigidity of the muscles of the neck and limbs develops. And other symptoms that appeared earlier also intensify, for example, jaundice, the smell of bile from the mouth, hemorrhagic diathesis.

In this condition, sepsis often manifests itself, as a result of which there is a high body temperature, leukocytosis and olirugia are intensified. This stage can last a few minutes or several days.

Symptoms and causes

Symptoms can be completely different depending on the stage and type:

Disorders with confusion (anxiety, melancholy, apathy, sleep disorders);
tremor of the extremities, usually the fingers;
muscle changes (rigidity, foot muscle clonus, etc.);
at stages 2 and 3, the pupils are dilated, the person does not react to light, and breathing may stop;
strong bilious odor from the mouth;
yellowness of the skin and mucous membranes;
ascites;
petenchial effusions of blood in the oral cavity;
severe pain in the liver area;
liver size may shrink;
infection is often associated, usually sepsis;
increased body temperature;
convulsions;
decreased blood pressure, dull heartbeats, tachycardia;
sphincter paralysis.

Other symptoms may also appear as there may be different causes and complications of this condition.

Causes

The most common cause of hepatic coma is hepatitis in various forms: alcoholic, viral, acute, toxic.

Coma can also develop with a progressive disorder of the blood supply to the liver. This disorder is provoked by thrombosis of the hepatic vein, and is possible during surgical intervention in case of mistaken ligation of the vein. One of the most common causes is cirrhosis of the liver.

Less common signs are portal vein thrombosis, schistosomiasis, etc.

Pathogenesis. It should be noted that metabolic disturbances significantly accelerate the onset of hepatic coma. The main toxic substance is ammonia, as well as aromatic amino acids, etc. These substances are formed in the large intestine.

The pathogenesis of hepatic coma includes a process in which lipids are oxidized, and this is what leads to the fact that the permeability of cells becomes much greater and, therefore, various autolysis products, etc., accumulate, that is, toxic poisons.

Also, the pathogenesis of this condition includes circulatory disorders, circulatory hypoxia and intravascular hypercoagulation. The following processes aggravate central nervous system disorders in hepatic coma:

Violation of acid-base and water-electrolyte balance;
Hemodynamic processes;
Hypoxia;
Kidney failure.

First aid

If a person shows signs of a hepatic coma, the first thing you need to do is call “ Ambulance"and record how much time has passed to inform the doctors.

Urgent first first aid consists of placing the person on his side and ensuring that there is normal air access.

This condition is characterized by disorders of thinking and behavior, so care must also be taken to ensure that the person does not injure himself. If the patient is vomiting, then the oral cavity should be cleaned of vomit.

Also, emergency first aid is to give the patient drink in large quantities. In order not to aggravate the situation, no further actions are being taken.Next urgent Care provided by doctors in the intensive care unit. Since in this case only drug therapy is needed.

Treatment

Treatment of hepatic coma consists of the following measures:

Colon cleansing. Depending on the patient’s condition, this is done either with an enema or laxatives.
To reduce the formation and concentration of toxic substances, antibacterial drugs are immediately prescribed.
Glucocorticoids and solutions for intravenous administration (glucose, sodium chloride, etc.) are prescribed. How many are needed should only be decided by qualified specialists.
Treatment of coma, the causes of which are toxic poisoning, is carried out with detoxification drugs (drugs are administered into the intestines, using a probe, drugs in the form of infusions, etc.).
If the cause of coma is renal failure, the patient is prescribed hemodialysis.
If there is hypoxia, then additional oxygen is supplied, usually through the nose.
It is imperative that people who have hepatic coma be prescribed a complex of vitamins and coenzymes. This is necessary to maintain energy balance.

Therapeutic therapy is prescribed individually to each patient, based on test results (general, biochemical, liver tests).

Forecast and conclusions

Hepatic coma is the last stage of encephalopathy, which has a very unfavorable prognosis. It is better, of course, to treat encephalopathy in its early stages. Self-medication in this case is strictly prohibited.

According to medical practice, the prognosis is as follows: about 80-90% of cases end fatal.

How long do patients diagnosed with hepatic coma live? As a rule, death occurs after a few days. With subacute liver dystrophy, the prognosis is favorable, since with proper therapy the mortality rate is much lower, but liver cirrhosis may develop as a result.

Patient Victor, 43 years old. The man was admitted with a diagnosis of hepatic coma, his condition is extremely serious. Symptoms of the disease: tremor of the limbs, strong smell bile from the oral cavity, severe pain in the right hypochondrium. Additional studies have shown that ascitic syndrome is also present.

He was urgently hospitalized in the intensive care unit. The patient was prescribed intravenous administration of detoxification solutions and antibacterial drugs wide range actions, glucocorticoids, Furosemide and Aldactone. A complex of vitamins was also prescribed. In order to reduce the concentration of ammonia, an enema was performed.

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Brief information. Furosemide and Aldactone are taken in combination for ascites.

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Hepatic coma is a type of neurophysiological syndrome. It develops against the background of decompensated renal failure with complete dysfunction of the central nervous system due to severe intoxication. Comatose state is last stage encephalopathy. In fact, coma is damage to brain cells by cerebrotoxic components, such as ammonia, that easily penetrate the brain.

Etiology and types of dysfunction

Coma occurs as a result severe forms diffuse intoxication, mechanical damage or destruction of most cells after inflammatory processes. 30% of patients admitted with a similar diagnosis are under the age of 40 years.

Severe lesions of the functional tissue (parenchyma) of the liver are based on the following reasons:

The mechanism of development of tissue destruction is aggravated by disturbances in metabolic processes caused by harmful influence on the permeability of cell membranes by lipid oxidation products. The most common cause of hepatic coma is toxic damage from alcohol, dangerous chemicals, or products of the breakdown and activity of hepatitis viruses. Since the toxic effect on the liver is irreversible, they do not live long after a coma, and 9 out of 10 sick people die.

Doctors classify several types of disorders:

hepatocellular, or true (endogenous);
portocaval, or shunt (exogenous);
mixed;
false, or hypokalemic.

In hepatocellular coma, necrobiosis of hepatocytes occurs, followed by their complete necrosis and disruption of the organ’s architecture. This is evidence of a severe progressive pathological process. Total necrosis is accompanied by wrinkling and thickening of hepatocytes. This type of coma occurs in people who have had Botkin's disease, who use large doses alcohol, drugs.

Exogenous coma develops against the background of cirrhosis, complicated by portal hypertension due to circulatory disorders in the portal venous vessel. The cause of shunt coma cannot be excluded in the form of overuse food containing only proteins. At mixed form a coma is observed, including endogenous and exogenous phases. The appearance of pseudohepatic syndrome is observed in patients with cirrhosis of the liver, in which potassium deficiency is recorded. Mineral coma occurs in people taking diuretic medications.

Liver failure

Stages and signs of coma syndrome

Signs of dysfunction develop over 2 weeks. First, the appetite disappears, the taste buds do not work, and the person quickly gets tired. Then severe headaches appear, unbearable itching.The clinical picture of coma has 3 stages:

1. Precomatose state. A person loses spatial orientation, thinking processes are disrupted, and stupor sets in. Characteristic is either a euphoric state or unmotivated crying. Reflexes are preserved, and the person can still be returned to normal life. The onset of precoma should be the complete destruction of more than 80% of hepatocytes.
2. Coma is threatening. There is no coordination of movements, consciousness and speech function are impaired, symptoms of hand tremors appear, paroxysms of motor excitation alternate with lethargy. Changes are observed when taking an electroencephalogram.
3. The patient is in unconscious, there is a reaction only to a powerful stimulus. The excitation of the skeletal muscles, the back of the head and the resistance to deforming forces are significantly enhanced.

Signs of jaundice and hemorrhagic diathesis develop. The appearance of sepsis is possible, the symptoms of which occur in the form of high temperature, leukocytosis, and a decrease in the amount of urine produced by the kidneys, which are observed from several minutes to several days. Additional indications hepatic coma is accompanied by anxiety, insomnia, dilated pupils, a pronounced odor of bile from the mouth, sphincter spasms, infectious infections, and an increase in heart rate.

Other symptoms are possible, depending on the type and stage of the disease:

impaired blood circulation;
acid-base balance disorder;
lack of air;
changes in hemodynamic characteristics.

It can end in unexpected respiratory arrest and death if emergency assistance is not provided in time. Signs of hepatic encephalopathy are clearly recorded by laboratory tests. Biochemical analysis blood plasma shows a decrease in the amount of proteins, an increase in bilirubin, nitrogen metabolism metabolites, and cholesterol.

Providing first aid and therapeutic measures

If signs of coma appear, you must immediately call an ambulance and record the time of the onset of the attack. Before her arrival, the person is placed on his side. This ensures natural access of air into the lungs. Since in this condition the patient does not control his behavior, it is necessary to prevent accidental spontaneous damage. If vomit has accumulated in the mouth, the cavity should be cleaned. Lack of water in the body aggravates the situation. This is where emergency first aid ends. Next, resuscitation actions are carried out in a hospital setting.

Treatment begins with intestinal lavage. If the patient is conscious, an enema is given or laxatives are administered. To prevent further formation of toxic metabolites and reduce their concentration, the use of antibacterial medications is indicated. It is possible to prescribe glucocorticosteroids, intravenous solutions- sodium chloride, glucose. The prescription is written by a medical expert.

Therapy of hepatic encephalopathy, the cause of which is a toxic lesion, is carried out by the introduction of detoxifying agents. Infusions are administered into the intestinal cavity. In cases where coma is the result of renal failure, the patient is referred to a hemodialysis procedure. In acute oxygen starvation brain cells are supplied with oxygen through the nasal passage. To prevent loss of energy balance, the patient is prescribed the use of a complex of micronutrients and coenzymes. All procedures and medications are prescribed based on individual clinical data.

An optimistic prognosis concerns patients with subacute destruction of liver cells and intercellular substance.

A competent course of treatment will help you survive, but cirrhosis of the liver cannot be avoided. A patient who has fallen into a coma, as the final stage of encephalopathy, has little prospects. The best treatment options are early stages diseases. Medical statistics show that a maximum of 20% of people survive coma attacks. But they also live literally for a few days.

And a little about secrets...

A healthy liver is the key to your longevity. This organ performs a huge number of vital functions. If the first symptoms of the disease were noticed gastrointestinal tract or liver, namely: yellowing of the sclera of the eyes, nausea, rare or frequent bowel movements, you simply must take action.