Clinic, diagnosis and treatment of hepatic coma. Comatose state of the liver: types and stages, first aid rules Symptoms of hepatic coma

About 3% of all visits to intensive care occur due to hepatic coma, which is always the result of a lack of timely treatment for damaged hepatocytes. 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.

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.

Mental disorders are especially severe 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-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 mental symptoms appear first. 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:

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 pre-comatose states is made using the West Haven scale, which combines general symptoms, EEG readings, ammonia levels, the presence of a flapping tremor, and the time the patient completed a 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.

Just as in acute pancreatitis against the background of diabetes the patient’s breath smells of acetone, in 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:

1. viral or bacterial infection - 60% of infectious lesions of hepatocytes are hepatitis;
2. 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);
3. 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;
4. inhibition of urea synthesis - most often occurs with a low level of Zn (zinc) and taking diuretics;
5. 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;
6. a decrease in the detoxification function of the liver is explained by 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 the consumption of 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:

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. You can also detect a trend in the pathological process using the following studies.

1. Blood biochemistry will show significant electrolyte changes, decreased levels of protein and clotting factors (3-4 times), increased cholesterol and nitrogen metabolism products.
2. 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%.
3. MRS is a highly sensitive method (90–100%) for detecting encephalopathy even in a latent state. It is based on studying changes in the molecular composition of white and gray matter through video imaging under magnetic influence. The advantages of this method: painlessness and effectiveness, however, it is used only in severe cases due to the high cost of the examination.

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 of necrotic liver conditions.

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 can only 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 of the intestinal microflora), while 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.

Symptoms of the last stage of liver cirrhosis are pronounced. At this stage, the disease is characterized by:

• intestinal disorders;
• weakness;
• frequent vomiting;
• loss of body weight;
• exhaustion of the body;
• atrophy of the muscles of the shoulder girdle and intercostal region;
• a strong increase (in certain cases, a decrease) in body temperature.

The last stage of cirrhosis may be accompanied by other, more severe symptoms: speech impairment, uncharacteristic movements of body parts, short periods of agitation, which are replaced by drowsiness.

All therapeutic measures are carried out with the aim of maintaining the vital functions of the patient’s body.

Consequences of the disease

Liver cirrhosis at the last stage is accompanied by the development of the following dangerous complications:

• bleeding of the digestive tract;
• ascitic syndrome;
• hepatic coma;
• bacterial peritonitis;
• cancer.

Consequences such as hepatic coma and bleeding of the digestive tract develop quite often.

Let's consider these violations in more detail.

The development of coma and encephalopathy is extremely dangerous. In this case, various neuromuscular disorders are observed, and thought processes are disrupted. Patients associate such manifestations with a depressive state, in which attention decreases, memory deteriorates, and there is a lack of interest in what is happening around them.

A comatose state develops against the background of liver failure; in this situation, the detoxification function of the organ is disrupted. A diseased liver is not able to neutralize toxic substances formed during metabolism. The most dangerous substance for the nervous system is ammonia, which is synthesized in the large intestine during the breakdown of proteins.

A healthy liver forms urea from ammonia, thereby neutralizing it and removing it from the body naturally. When hepatic coma occurs, a significant amount of ammonia and toxic substances accumulate in the liver. Ammonia has a negative effect on the respiratory center, resulting in hyperventilation. In the bloodstream and brain, the content of aromatic acids increases, while the amount of amino acids, on the contrary, decreases. Against this background, the nervous system cannot function normally.

Liver failure, in addition to signs of damage to the nervous system, is accompanied by a characteristic sweetish odor from the mouth. This symptom occurs at the initial stage of the pathology and becomes more pronounced with the development of encephalopathy.

The development of hepatic coma occurs gradually - appetite decreases, nausea, headaches, and pain in the area of ​​the right hypochondrium and epigastrium occur. Dizziness, fainting, insomnia, and itchy skin may also develop.

To diagnose liver dysfunction, a biochemical blood test is performed. In addition to clinical manifestations, uncharacteristic changes in electroencephalography (ECG) are observed - high-amplitude slow triphasic waves appear.

Carrying out intensive detoxification therapy in certain cases gives positive results. Therefore, immediate hospitalization of a patient with rapidly increasing liver failure is extremely necessary. During treatment, laxatives and cleansing enemas are used. A synthetic disaccharide is also used, after decomposition of which lactic, formic, and acetic acids are formed. In addition, it is important to adhere to a strict diet with the complete exclusion of proteins (meat and fish products, cottage cheese, eggs).

Internal bleeding and portal thrombosis

Varicose veins of the digestive tract are a dangerous complication of the last stage of liver cirrhosis; this disorder occurs quite often - in 40% of cases. There are no manifestations of this condition for a long time; the development of bleeding indicates advanced disease.

Such complications arise due to pressure drop in the portal vein and disruption of the blood clotting process. In addition, in such a situation, the capillaries and venous vessels of the digestive tract are dilated, which also disrupts blood flow.

Against the background of irreversible changes in the liver, portal thrombosis occurs - blood clots form in the portal vein, resulting in the development of portal hypertension. This disorder occurs in 25% of patients. Adequate therapeutic measures can prevent the occurrence of ascitic syndrome and hypersplenism.

Acute thrombosis is observed in very rare cases.

To diagnose this disorder, Doppler ultrasound is used, which reveals a slowdown or complete absence of venous blood flow.

In this case, bleeding is treated with clipping (endoscopic vein ligation). A synthetic analogue of somatostatin, octreotide, is also administered intravenously.

Forecast

It is quite difficult to say for sure how long people live with liver cirrhosis at the last stage. Life expectancy depends on the patient’s behavior and complications that develop. If ascites occurs, the life expectancy of 25% of patients is no more than 3 years. In the case of the development of hepatic encephalopathy, the prognosis is extremely unfavorable - the life expectancy of most patients does not exceed 12 months. With late-stage alcoholic cirrhosis, 40% of patients live 3 years.

The duration and quality of life with liver cirrhosis directly depends on how accurately the patient complies with all the instructions of the attending physician. First of all, it is necessary to completely stop drinking alcohol and other hepatotoxic substances. Compliance with this condition is especially important in alcoholic cirrhosis. Eliminating alcohol allows 60% of patients to live more than 5 years. It is equally important to adhere to a strict diet - avoiding fatty, fried, spicy foods.

It is necessary to conduct full therapeutic courses in a hospital setting, undergo regular examinations in medical institutions and promptly respond to any changes in the body.

The development of severe pathologies of other organs, in particular cancer, significantly worsens the prognosis.

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.

• Stages
• Symptoms and causes
• Causes
• First aid
• Treatment
• Forecast and conclusions

Kinds

There are several types of hepatic coma, namely:

Stages

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

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:

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 liver cirrhosis.

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, first of all you need to call an ambulance and note how much time has passed in order to inform the doctors.

Immediate first aid is to place the person on his side and ensure 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 taken. Further emergency care is 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:

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 in death.

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.

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

Symptoms of liver cirrhosis at the last stage, complications and prognosis for life

Liver cirrhosis develops in several stages, each of which has characteristic symptoms. The last stage of liver cirrhosis is the final phase of the disease and is accompanied by many complications. In the absence of emergency medical care, the terminal stage leads to death.

a brief description of

Cirrhosis is a liver disease that is characterized as a fatal pathology. It consists of irreversible changes in the parenchyma and gradual loss of functionality. As a result of exposure to pathogens, liver cells mutate. Their genome changes, so new hepatocytes are reproduced in a pathologically altered form.

The immune system mistakes mutated liver cells for foreign viral agents and begins to destroy them. A chronic inflammatory process occurs, which leads to the proliferation of fibrous adipose tissue.

The following pathological manifestations are characteristic of cirrhosis:

• healthy parenchyma tissue is almost completely replaced by fibrous stroma;
• the liver changes shape and structure;
• the body ceases to perform its functions.

The development of the disease is chronic, since the destructive process lasts several years and has 4 stages.

A characteristic feature of cirrhosis is the formation of additional false lobules, which consist of fatty connective tissue and do not have their own blood vessels.

Causes of pathology

Cirrhotic changes in the parenchyma are a consequence of liver diseases caused by viral or toxic agents.

There are several types of cirrhosis:

Regardless of the pathogen that provoked the development of cirrhosis, the disease develops in 4 stages. The course of each stage can take from several months to several years, depending on the individual characteristics of the organism.

The exception is the last stage, which is accompanied by severe destructive processes and proceeds quite rapidly.

Symptoms of the last stage

The last phase of cirrhosis is called the end stage. It is characterized by an exacerbation of all negative processes and is accompanied by serious complications.

At this stage, the following symptoms of the disease clearly appear:

Patients have severe liver deformation and splenomegaly. There are also secondary symptoms inherent in this phase of cirrhosis. These include gynecomastia (in men), varicose veins on the abdomen, spider veins, hyperpigmentation and dry skin, redness of the palms. Swelling of the lower extremities appears, the hair on the body thins.

In a quarter of patients in the terminal phase of cirrhosis, a decrease in liver size is observed.

Complications

In addition to the main clinical symptoms, complications appear at the last stage of cirrhosis, which often lead to death. The terminal phase occurs in every patient, regardless of compliance with the prescribed treatment or lifestyle.

Factors that provoke the rapid development of complications are:

Alcohol-dependent patients are more likely than others to ignore their doctor’s instructions. Among this category of patients, the most rapid onset of complications inherent in the terminal stage is observed.

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Ascites

A characteristic complication that occurs as a result of impaired functionality of the portal and inferior hepatic vena cava. Fatty degeneration of the parenchyma causes portal hypertension. This pathology is accompanied by obstruction of blood flow and decreased nutrition of abdominal tissues.

As a result of hypoxic fasting, there is an increased secretion of lymphatic fluid, which accumulates in the abdominal cavity, with a volume of up to 20 liters. A large accumulation of water causes bloating and dilation of the abdominal veins (capita jellyfish).

Ascites in liver cirrhosis

The danger of ascites is that it provokes the following processes:

• respiratory and heart failure;
• sepsis;
• protein deficiency;
• impaired blood flow and bleeding.

Spontaneous peritonitis, which often accompanies ascites, increases the risk of death. Abdominal hydrops can be treated conservatively in the early stages and surgically in acute cases.

Repeated occurrence of ascites is possible, since cirrhosis, which provokes the accumulation of water, is an irreversible disease.

Bleeding

Portal hypertension, which develops as a result of degenerative processes in the liver, often causes internal bleeding. Stagnation and disruption of blood flow provoke expansion and blockage of blood lines. Damage is observed not only in the liver, but also in the gastrointestinal tract, as well as throughout the abdominal cavity.

Since the walls of veins and blood vessels are subject to fibrotic degeneration, they become fragile and brittle. As a result, the wall ruptures and blood is released into the abdominal cavity. Due to the fragility of blood vessels, nosebleeds in cirrhosis are a frequently observed symptom in the terminal stage of the disease.

Internal bleeding is a dangerous condition and requires emergency medical attention. Extensive blood loss quickly leads to the death of the patient.

A condition such as hepatic coma is the final stage in the development of cirrhosis and cannot be treated. This concept is used to define the complete failure of all liver functions and the occurrence of hepatocerebral failure. Hepatic encephalopathy is a consequence of toxic and hypoxic damage to the central nervous system.

It is caused by the following reasons:

• metabolites and toxins that accumulate in the body as a result of impaired liver function;
• deficiency of nutrients in the bloodstream, which leads to insufficient nutrition of the brain and causes disturbances in brain activity.

Neurological disorders and functional liver failure cause confusion, motor and speech disturbances, drowsiness and extensive necrosis of parenchymal tissues. Hepatic coma develops rapidly and ends in the death of the patient.

End-stage treatment

How to cure the last stage of cirrhosis? Unfortunately, the terminal phase of the disease cannot be cured. Conservative treatment carried out at this stage cannot reverse the process of parenchyma destruction and compensate for the loss of liver functionality. Basically, medical methods are designed to alleviate the patient's suffering and maintain vital functions.

The only solution in the last stage of the pathology is organ transplantation.

Forecast for life

The terminal phase of cirrhosis is accompanied by a disappointing prognosis. How long do patients live if the last stage of the disease has occurred? Life expectancy depends on the accompanying complications and individual characteristics of the body.

The table shows the average time, depending on the existing complications:

Hepatic coma is fatal within a few days. The end stage can develop over 2-5 years until complete liver failure and death of the patient.

The last stage of cirrhosis is the most difficult for the patient, as it is accompanied by painful processes and the constant need for medical care. The final phase can be delayed by 15-20 years if timely and adequate treatment is carried out, diet is followed and bad habits are given up.

Today, about three percent of patients are admitted to the intensive care unit. Every patient who comes to the clinic with a hepatic coma is sick with something. Thirty percent of such people have not yet reached the age of forty, and only one in five people survives after treatment for hepatic coma. Most deaths were recorded among patients under ten years of age and over forty years of age.

Hepatic coma and its symptoms

Hepatic coma is the most severe stage of hepatic encephalopathy. The reason for its development is diffuse liver damage and a sharp disruption of the vital functions of the organ. Typically, this condition is caused by symptoms of acute and chronic diseases such as viral hepatitis, cirrhosis of the liver, severe obstructive jaundice, malignant tumors, poisoning with poisons and alcohol. The anatomical and physiological characteristics of the liver change noticeably. Hepatocytes die, the gland itself changes in size

Liver cirrhosis leads to metabolic disorders, although this is not dangerous. But if pathological changes intensify, the organs cease to cope with the task assigned to them, and coma develops. The first symptoms of hepatic coma are manifested by changes in the person’s psycho-emotional sphere. The patient's mood changes sharply, excessive, unreasonable joy appears, during the day the patient increasingly tends to sleep, and at night he is overcome by insomnia.

It is important to know: Before the patient develops coma, signs of precoma appear. This state lasts for a certain period of time and gradually leads the body to a comatose state.

Precoma of hepatic pathology is manifested by the following symptoms:

• pain;
• nausea, vomiting, bloating;
• change in skin tone;
• the patient's face takes on a reddish color;
• the tongue turns crimson.

Hemorrhages appear in different places on the patient’s body. There is bleeding from the nose, uterus and organs.

Precoma turns into coma. This is manifested by the following symptoms:

• a person ceases to navigate, cannot understand where he is and what time it is;
• the patient's mouth smells of liver;
• urination decreases;
• the face becomes sharper;
• breathing uses muscles;
• the temperature drops;
• the tone of the eyeballs decreases;
• blood pressure decreases;
• the pulse is difficult to palpate;
• the patient loses consciousness.

Causes of hepatic coma

The main reason why hepatic coma develops in liver cirrhosis is toxin poisoning. Liver disorders occur because a person:

• drank alcohol for a long time;
• took medications for a long time;
• performed operations;
• suffered from viral and infectious pathologies;
• suffered shock, abortion, stress.

A comatose state negatively affects brain function. The metabolic rate decreases during hepatic coma, toxins enter directly into the blood, move directly to the brain, and provoke the occurrence of cerebral edema. As a result, the prognosis may be sad.

Hepatic coma - treatment

Liver pathology is usually treated in the intensive care unit, regardless of the stage of the disease; it is treated in the intensive care unit; this is not affected by the stage of development of the disease. Every two hours, doctors monitor the level of substances in the blood. If symptoms of a precomatose state appear, the patient must be laid down and his head raised. Special solutions are injected intravenously to replenish blood volume, equalize electrolytes, and blood pH.

Important: The patient is not able to feed himself, so amino acids, glucose, and fat emulsions are infused intravenously.

In addition, through enemas, the patient’s body is cleansed of toxins. If the level of oxygen in the blood is low, additional oxygen therapy is prescribed. To help the liver start working again, doctors prescribe a course of glucocorticosteroids.

– a neurophysiological syndrome that develops in patients with liver failure, which is accompanied by severe depression of the central nervous system. The main signs are the absence of consciousness, the presence of pathological reflexes, decerebrate rigidity of the limbs, and in the terminal stage - the absence of pupillary and corneal reflexes. The diagnosis is established based on the clinic, EEG data, biochemical tests, CT, MRI. Priority areas of treatment are correction of cerebral edema, intracranial hypertension, detoxification, hepatoprotective therapy. The most effective method is liver transplantation.

General information

Diagnostics

Verification of the diagnosis of hepatic coma is based on data from the clinical picture of the disease, laboratory and instrumental research methods. If possible, consultation with a gastroenterologist and resuscitator should be carried out with the participation of the patient’s relatives, since it is important to evaluate the anamnestic data: when the first symptoms appeared, the rate of their progression, possible etiological factors. When examining the patient, attention is drawn to the yellowness of the skin and a liver odor. There is no consciousness. Depending on the stage of coma, reflexes to strong stimuli and pupillary reflexes are preserved or absent.

Characteristic changes in the results of laboratory tests in hepatic coma are signs of hepatocellular failure: hyperbilirubinemia, a significant increase in the activity of serum transaminases, a decrease in the prothrombin index and the number of platelets in the blood, anemia, hypoalbuminemia. When analyzing the cerebrospinal fluid, an increase in protein levels is determined. A toxicological study and blood test for markers of viral hepatitis are required.

Treatment of hepatic coma

Patients in a state of hepatic coma are hospitalized in the intensive care unit. Treatment begins with the fastest possible determination of the cause of the pathology (infectious disease, bleeding from the gastrointestinal tract, mushroom poisoning, etc.) and elimination of the etiological factor. Constant ECG monitoring, pulse oximetry, and intracranial pressure monitoring are mandatory. Hepatic coma is characterized by progressive respiratory failure, so tracheal intubation and artificial ventilation are performed. The drugs of choice for deep sedation are fentanyl and propofol. In order to correct glucose deficiency and oxygen starvation of brain cells, a glucose solution is administered intravenously. If bleeding and coagulopathy occur, fresh frozen plasma is used. A decrease in hemoglobin level below 70 g/l is an indication for blood transfusion. Correction of hypoproteinemia is carried out using albumin.

A rapid (within several hours) deterioration of neurological symptoms indicates intracranial hypertension, therapy for which is indicated even in the absence of invasive methods of controlling intracranial pressure. More than 85% of patients develop cerebral edema. Basic treatment of intracranial hypertension and cerebral edema includes mechanical ventilation and sedation, normalization of body temperature, electrolyte and blood gas composition. If these methods are ineffective, hyperosmolar therapy (intravenous drip administration of mannitol, hypertonic sodium chloride solution), hyperventilation (ventilation in hyperventilation mode makes it possible to reduce ICP for 1-2 hours and gain time for other measures), administration of sodium thiopental, moderate hypothermia, in extreme cases, decompressive craniotomy.

To prevent infectious complications, including during mechanical ventilation, antibiotic therapy (cephalosporins, vancomycin) is carried out. Hepatic coma, like any critical condition, is characterized by stress damage to the gastrointestinal mucosa; To prevent gastrointestinal bleeding, proton pump inhibitors and Vicasol are prescribed. To reduce the absorption of ammonia in the intestines and toxic damage to brain cells, lactulose preparations are used. Ciprofloxacin and metronidazole effectively suppress ammoniogenic flora. L-ornithine-L-aspartate preparations are also prescribed, which stimulate enzyme activity in hepatocytes, muscle and brain cells. To speed up bowel movements, enemas with a solution of magnesium sulfate are given.

Nutrition of a patient with hepatic coma is parenteral, maintaining calorie content and limiting the amount of protein. Hepatoprotective therapy is prescribed to increase the resistance of hepatocytes to damaging factors and accelerate regeneration processes (arginine glutamate, milk thistle preparations, thiotriazoline and other drugs). Extracorporeal detoxification methods (hemodialysis, hemosorption and others) are mandatory.

Prognosis and prevention

Hepatic coma is a prognostically extremely unfavorable condition. The survival rate of patients is no more than 20%; only a small part of patients can wait for a liver transplant. The highest mortality rate is when patients are under 10 and over 40 years of age, the duration of jaundice is less than seven days before the development of severe encephalopathy, the bilirubin level is more than 300 µmol/l, a rapidly progressive decrease in liver size, and severe respiratory failure.

Prevention of hepatic coma consists of timely adequate treatment of liver diseases, competent prescription of medications, exclusion of self-medication by patients, avoidance of poisoning by toxic substances, mushrooms, prevention of viral hepatitis, and abstinence from alcohol.

Liver pathologies today are one of the first places in terms of prevalence among residents of our country. The greatest danger is posed by such a complication of many pathologies as hepatic coma. To understand what it is and how dangerous the pathology is, it is necessary to understand the causes of its occurrence, the mechanism of development, find out whether the disease can be cured and how to increase the life expectancy of patients with this diagnosis

Coma is the last stage of liver failure. In essence, coma is a pathological comatose state associated with complete inhibition of liver function. It is characterized by deterioration of the condition, fainting, impaired breathing, blood circulation, and decreased human vital activity. In most cases, the final result of the pathology is death.

Hepatic coma is not an independent disease, but becomes a consequence of the progression of an existing disease. Toxic damage to the body can also trigger the disease.

The cause of coma can be:

Main factors of pathogenesis:

Factors in the development of pathology:

• liver failure;
• breakdown of protein products that come with food (ammonia poses a particular threat);
• anastomosis (bypassing the filtration through the liver of toxic, harmful components, which subsequently penetrate into the bloodstream).

Symptoms may vary depending on the cause that influenced the occurrence of liver coma. The pathology is also characterized by general symptoms:

Coma with cirrhosis

Hepatic coma is a common consequence of progression of cirrhosis. It occurs at a severe stage of the pathology, which is characterized by a critical disruption of the liver (in particular, the inability to synthesize protein and neutralize toxic substances that penetrate the human body).

The first signals of the initial stage of pathology against the background of cirrhosis:

Gradually the patient's condition worsens. This can be facilitated not only by natural negative processes occurring in the body, but by unfavorable third-party factors (excessive consumption of protein foods, alcohol consumption, the appearance of an infectious disease). New symptoms appear:

• fainting;
• lack of reaction to external stimuli, in particular to bright light;
• muscle atrophy, so the face resembles a mask;
• respiratory arrest and death.

Types and stages of development

There are two types of coma:

Coma has several stages of development:

Often, the first 2 stages of pathology are mistakenly mistaken for mental disorders. This significantly complicates the correct diagnosis. Sometimes the patient’s relatives, noticing characteristic symptoms, begin self-medication - they give antidepressants, psychostimulants. Such pseudo-treatment only worsens the patient's condition.

Choice of therapy method

Coma is determined using a blood biochemistry test. The main signs of pathology:

• critical excess of bilirubin levels;
• significant increase in nitrogen content;
• low lipid levels;
• decreased levels of glucose and prothrombin.

Urine and stool tests are also performed. Increased levels of urobilin and bile acids are observed in the disease.

If an emergency occurs at home, emergency assistance consists of the following measures:

1. Turn the victim onto his left side to make breathing easier.
2. Call an ambulance as soon as possible. Until the doctors arrive, do not touch the patient or change his position.
3. Doctors hospitalize the patient in a hospital.
4. Glucose and Panangin are administered intravenously, which helps to activate the brain and restore blood circulation.
5. Administration of a physical solution with Insulin to eliminate the catatonic state of the patient.
6. During the first 24 hours, the patient is actively administered Prednisolone to neutralize ammonia and remove toxins from the body.
7. To restore liver function, Riboflavin, Pyridoxine, Thiamine and Nicotinic acid are administered.

Further treatment is carried out in a hospital with the help of drug therapy:

Hepatic coma is a pathology with serious consequences. In fact, coma has no complications, but all vital functions of the body are disrupted. Pathology provokes irreversible disorders and significantly worsens the patient’s condition. The risk of death is extremely high.

As for survival, it directly depends on timely diagnosis and competently prescribed treatment. Complete recovery after an illness is extremely doubtful and practically never occurs in medical practice.

The probability of a patient’s recovery at the precoma stage is about 20%, at the second stage – no more than 10%.

Patients in a deep coma rarely come out of it. This succeeds in only 1% of all registered clinical cases. The chances of survival increase with a donor liver transplant.

There are no preventative measures for the disease. You can only try to prevent the occurrence of liver diseases by quitting smoking, drinking alcoholic beverages and fatty, fried foods.

Reviews from experts

Hepatic coma is a frequently discussed topic among doctors. Several reviews from specialists about pathology are presented below:

Egorov B.V., doctor:“The pathology is one of the most severe. It progresses quickly and spontaneously, causing a large number of deaths. It is catastrophically difficult to fight it even at the initial stage. The most favorable course of the disease is possible in the case of a healthy organ transplant. However, based on my practice, many patients do not live to see this point.”

Martynov A.K., doctor:“The disease is skillfully disguised; quite often its first symptoms are perceived as a disruption of the nervous system, a failure of a person’s psycho-emotional state. This is, first of all, indicated by disorientation, and the patient loses not only a sense of the reality of place and time, but also experiences difficulties in determining his own personality.

Apathy, depression, aggression, mood swings - all these are characteristic symptoms of a nervous system disorder. When such signs appear, the patient’s relatives refer him for treatment to a neurologist, psychologist, or psychotherapist.

And at this time, the body continues to destroy the real cause of this condition - liver coma. It is not always possible to determine the correct diagnosis. Moreover, when a pathology is identified, in 15% of cases it is not possible to identify the cause of its occurrence.”

Filatova E.N., doctor:“Liver coma is a global danger that can affect a person at any age. According to statistics and clinical data, adults over 40 years of age are at particular risk. But the worst thing is that in the same group there are children under 10 years old.

An effective method of saving human life in case of pathology is donor organ transplantation. But such an operation is extremely dangerous for the child, and in this case it is difficult to find a suitable donor. As a result, the child’s body cannot cope with such a load. Unfortunately, at the moment, the most gentle and reliable, effective method of treating the pathology does not yet exist.”

Hepatic coma is a terrible threat to the liver. It is very difficult to protect against it, since it is one of the few diseases that is difficult to prevent through preventive measures.

The best option is to always be attentive to your health, monitor the quality of your diet, get rid of bad habits, and devote time to at least minimal physical activity and walks in the air, which will help strengthen the body. Perhaps these simple tips will help avoid death due to this disease.