What is hepatic coma and emergency care algorithm for it. What is renal coma and causes of liver failure Hepatic coma how many days left

It is impossible to imagine the existence of a person without a liver; indeed, it is utopian. The need for the liver does not require proof. This has been demonstrated in many scientific experiments on animals by scientists from different countries.

But there are situations when the liver stops working and dies, the person falls into a coma. The cause is infections, liver diseases, toxic effects of medications and other factors that kill liver cells.

The variety of root causes of hepatic coma served as the reason for a detailed study. Understanding the causes and basis of the evolution of coma helps in providing assistance.

With cirrhosis of the liver, as the disease progresses, liver failure progresses, which puts the person into a coma. Let's consider the problem of the origin of hepatic coma in detail.

Before the onset of coma, progression of liver failure (chronic or acute) is observed. With liver failure, hepatocytes undergo necrosis, they are destroyed, and the liver ceases to perform its functions.

Metabolic products (endotoxins, amino acids, mercaptans, ammonia, fatty acids, phenols and others) accumulate in the blood and cause encephalopathy. If help is not provided, the person dies. Liver transplantation is considered effective.

Considering the clinical significance, in practice they use the division into:

1. Liver cell failure,
2. Hepatic-portal failure.

Hepatic-cellular failure (synonyms true, endogenous) with a rapid onset and rapid development of coma and death. Presented by:

The main role is a sharp decline in the mass of active cells and the development of hepatocyte necrosis. With a slow course, the previous mechanism is supplemented by a disruption of clotting and the involvement of a bacterial infection.

Hepatic-portal insufficiency

Portal-hepatic failure (synonyms vascular, exogenous coma) is encountered in liver cirrhosis. Characterized by a slow course, this type of coma is better treated.

Variants of the course of liver failure:

Lightning form. There was no prior, chronic illness in its formation. Failure increases quickly, rapidly, in the presence of an acute disease, in a short time from the onset of the disease.

Extensive, powerful liver necrosis occurs and leads to hepatocellular coma. Coma develops to a severe stage, very quickly and can be fatal.

This form occurs when:

• acute drug-induced hepatitis,
• poisoning by poisonous and toxic agents,
• acute viral hepatitis,
• fatty hepatosis in pregnant women and others.

We meet the chronic form:

• For liver tumors,
• with cirrhosis of the liver,
• for chronic hepatitis and other reasons.

Many months or years pass before the onset of liver failure. More often, portal-hepatic failure is detected, less often hepatic-cellular failure, sometimes a combination of both. The decline in the number of active cells does not happen quickly or bypass paths develop (anastomoses, shunts). Coma has a special course with alternating exacerbations and remissions, a gradual increase in symptoms.

Exacerbation of chronic liver failure is noted:

• For chronic alcoholic hepatitis,
• With cirrhosis of the liver,
• For liver tumors and other reasons.

Both types of liver failure are combined. The coma unfolds and grows rapidly. Complications of a chronic disease can be caused by:

• Septic conditions,
• Overdose of medications (diuretics and others),
• Intestinal or stomach bleeding
• Surgical intervention,
• Drinking alcohol in significant quantities,
• Vascular event and others.
• Combined forms of liver failure:
• Traumatic event
• The burns are large,
• Failure "shock liver"
• Myocardial infarction or stroke,
• Failure of the "septic liver"
• Liver failure in combination with renal failure.
• Liver failure in combination with renal and pancreatic failure.
• In combination with electrolyte deficiency.
• Unidentified liver failure.

The leading sign of liver failure is coma. In the process of coma, precoma and 3 stages are defined:

• In precoma, mental abnormalities predominate, consciousness is not lost, reflexes are preserved.
• In coma 1, wave-like depression of consciousness prevails; in episodes of restoration of consciousness, mental disorders predominate, reflexes are preserved.
• In coma 2, the unconscious status is continuous, reflexes are preserved.
• In coma 3, there is a continuous state of unconsciousness and there are no reflexes.

Treatment is effective in precoma and coma 1, ineffective in coma 2 and ineffective in coma 3.

Hepatic coma in liver cirrhosis

An important difference is the slow decrease in active cell mass. The weight of the liver during coma formation is 1100-1200 grams. Further adaptation of the body to changed conditions. The deterioration of liver function progresses.

At the same time, mechanisms of metabolic changes are involved. As long as all these situations are balanced, the result is satisfactory. If metabolic disorder prevails, coma occurs.

The symptoms of precoma can be quite difficult to recognize. It lasts from 1 to 3 days and appears suddenly.

• The metamorphosis of mental disorders is traced. The mood varies from dejection to euphoria. Excitement turns into deafness. Daytime sleepiness transforms into insomnia at night. Objectively, it can be difficult to discern the beginning of encephalopathy.

Test with an “autograph”: you are asked to write your own name, in a stable condition this does not cause any difficulties, but in the presence of primary symptoms of encephalopathy, difficulties arise and changes in the writing of the phrase are noted. This test can be performed even daily for dynamic control; it is simple and inexpensive.

• Dyspeptic disorders: episodes of nausea, periodic vomiting, loss of appetite, up to anorexia, abdominal pain and fever.
• Manifestations of jaundice increase slowly.
• The skin of the face changes color to crimson-red and this phenomenon coincides with the onset of coma, localized around the nose and mouth, the sign is not obligatory. The color of the mucous membrane of the tongue and the surface of the lips changes to a crimson color.
• Hemorrhagic syndrome increases gradually in proportion to disruptions in blood clotting. Hematomas of various sizes appear on the body, from small to large, especially in places after injections.
• The nature of respiratory movements changes, at times breathing becomes noisy and chest excursions become deeper.
• We will feel an unpleasant, sweetish-nauseating “liver smell” from the oral cavity.
• In parallel, the kidneys may be involved and complicated by renal failure; it is necessary to count the amount of fluid administered and excreted from the body in the urine.
• A patient in a coma appears to be in deep sleep.

• First of all, they collect an anamnesis of life and illness, find out the disease with chronic liver diseases (especially cirrhosis of the liver). If the patient is busy. According to relatives and medical documentation. Find out the drugs. What did the person take before illness? When did you notice the problem? Where did you go?
• Skin color, presence of bruises, and spider veins are objectively assessed. Examine the oral mucosa, its color, and tongue. Measuring the volume of the abdomen to determine ascites. Pay attention to the presence of edema. Manifestations of mental and consciousness disorders are assessed.
• Routine blood and urine tests are taken.
• Mandatory blood biochemistry sampling (bilirubin and its parts, glucose, amylase, urea, creatinine, protein and its parts, ALT, AST, alkaline phosphatase, GGT, bicarbonates, potassium, magnesium, calcium, chlorides).
• Coagulogram (fibrinogen, prothrombin time). Detection of hemorrhagic syndrome.
• Blood serology (to clarify or exclude viral hepatitis).
• Detection of autoimmune liver damage (immunoglobulin levels, ANA, SMA).
• Determination of ceruloplasmin (copper-containing protein) to exclude Wilson-Konovalov disease.
• Determination of acitamenophen in the blood to exclude an overdose of paracetamol.
• Determination of lactate and ammonia to establish intoxication.
• Clarification of blood type and Rh, in case of blood loss or surgery.
• Pregnancy test or objective confirmation of pregnancy. To exclude acute fatty hepatosis.
• Blood tests for medications if suicide is suspected.
• MRI, CT, ultrasound.
• Other laboratory tests and investigations may be required on a case-by-case basis.

The diagnosis of hepatic coma can be established or refuted by daily monitoring, over time, of changes in laboratory tests:

• Decrease in prothrombin index, proconvertin and accelerin.
• In biochemistry, a decrease in cholinesterase, cholesterol, fibrinogen, and albumin levels.
• A carbohydrate metabolism disorder occurs in the form of a decrease in blood glucose.
• A rise in blood lactate is detected. Which is a signal of an unfavorable outcome.
• Bilirubinemia in the blood, from obvious to slight, reflects the intensity of jaundice.
• The level of ammonia in the blood increases over time.
• In a comatose patient, there is an increase in the level of amino acids (tyrosine, methionine, tryptophan, phenylalanine) in the blood.
• Other indicators in blood serum have individual significance.

Treatment

Basic postulates in treatment:

• Lymphosorption– passing lymph through sorbents (ion exchange resins, activated carbon), they absorb toxic substances found in the lymphatic system.
• Hemosorption– passage of blood through sorbents to cleanse it of toxic substances.
• Plasmapheresis– the procedure for collecting blood, further separating its liquid part – plasma, purifying it and returning it to the bloodstream.
• Hemodialysis– indicated in combination with renal failure. The procedure for purifying the blood and removing toxic metabolic products.
• Drainage of the thoracic lymphatic duct– a procedure for removing lymph to optimize hepatic blood flow, along with which the pressure in the portal vein decreases, ammonia intoxication and ascites involution decrease. The effect is short-term.
• MARS – therapy is the latest method of extracorporeal detoxification. Using this technique, the following is extracted from the blood: bile acids, mercaptans, bilirubin, phenols, nitric oxide, endogenous toxins, ammonia, tryptophan and others. However, beneficial substances are not removed. Thanks to this method, it is possible to restore the synthetic function of bile secretion, improve the regulation of homeostasis, regress the degree of encephalopathy, eliminate jaundice, and stimulate liver regeneration.

1. Listing for liver transplantation. This is the most effective and efficient treatment method and increases patient survival. Coma has a progressive course, in most situations the patient is doomed. The prognosis after surgery is more favorable.
2. Prevention of dangerous complications.
3. Additional treatment methods are applicable based on the causes of the coma. Treatment is adjusted individually by the attending physician.

Despite the seriousness of the problem, there is a way out. With modern diagnostics and new treatment methods, it is possible to improve the quality of life of patients.

By identifying the underlying cause of coma and treating it appropriately, patients' chances of survival increase. A diagnosis of liver cirrhosis with an episode of coma indicates an unfavorable prognosis, but with timely liver transplantation, there is a good chance of a good outcome.

Hepatic coma is a severe depression of the functions of the central nervous system, which occurs as a result of liver failure.

This is an emergency condition that requires not just medical assistance, but immediate action - otherwise the patient will not survive.

Total information

With (suppression of all liver functions, which develop against the background of many liver diseases), hepatic coma does not occur immediately. It is preceded by hepatic encephalopathy - brain disorders that arise due to severe liver disease and, as a consequence, the formation of toxic products that cause destruction (destruction) of nerve cells.

Hepatic coma is one of the most severe emergency conditions. This is a disease that is difficult to correct and often ends in death even with competent intensive care in conditions of high diagnostic and therapeutic support.

note

Severe brain damage is observed in 30% of all patients with liver failure, transformed into coma.

Causes

The immediate cause of hepatic coma is decompensation of liver diseases, in which many of its functions are disrupted. Often these are chronic liver diseases, although acute destructive disorders can also result in liver failure and coma. Most often, diseases that provoke the development of hepatic coma can be the following pathologies:

In most cases, hepatic coma occurs not simply against the background of such diseases and the worsening of their course - the cause is the so-called failure of compensation, which, in turn, can be provoked by:

Less commonly, hepatic coma occurs against the background of so-called fulminant liver failure - that is, one that, in turn, can develop suddenly, without preceding liver disease. This rather rare pathology mainly occurs with diseases and conditions such as:

• exposure to hepatotoxic (that is, specifically affecting liver cells) poisons - this can be poisoning, alcohol (counterfeit or regular, but in large doses), industrial poisons;
• severe infectious diseases - both nonspecific (,) and specific ();
• intraoperative shock – hemorrhagic (from loss of a large amount of blood), painful.

In 17% of all clinical cases, the causes of hepatic coma remain unknown.

Development of the condition

Hepatic coma is the terminal (final) stage of brain damage (encephalopathy). From the point of view of biochemical processes, its important mechanism is the destruction (damage) of brain cells due to the impact of endogenous toxins on them (that is, produced by the body itself as a result of disruptions in its activity). Most often these are substances with toxic properties such as:

• ammonia;
• fatty acid;
• phenols.

Formed in the large intestine, ammonia enters the portal vein system and enters hepatocytes through the vessels - but, contrary to expectations, it is not included in the normal cycle of its processing and neutralization (this is the so-called ornithine cycle). The rate of physiological transformations of ammonia sharply decreases, and toxic products that are produced at different stages of its processing begin to enter the general bloodstream . Such toxins interact with each other and “strengthen” each other - as a result:

• their penetrating ability through the blood-brain barrier (a physiological barrier that normally protects brain cells from entering here and being exposed to toxic substances accidentally introduced by the bloodstream) is enhanced;
• water-salt regulation inside brain cells is disrupted.

Such factors (especially water-salt failure) lead to the accumulation of fluid in brain cells. Swelling of the brain tissue occurs.

The harmful effect of toxins on brain cells formed due to a malfunction in the liver is also as follows - they:

• disrupt the sequence of energy processes in nerve cells;
• reduce the rate of glucose processing, without which brain tissue cannot absorb it;
• provoke oxygen starvation of neurons.

All three of these processes not only themselves harm brain cells, but also increase brain swelling, thereby each provoking a double blow to neurons.

The most negative consequence of cerebral edema is wedging of its trunk(displacement between other structures or into the foramen magnum, which is fraught with intense compression and critical impairment of its viability).

Brain stem herniation is the main cause of death in 82% of all clinical cases of hepatic coma.

Symptoms of hepatic coma

The clinical picture of hepatic coma is based on:

• psychoneurological symptoms - manifestations from the central as well as peripheral nervous system;
• signs of liver failure itself.

Clinical manifestations of hepatic coma depend on its stage. There are two stages of this condition:

• shallow (or initial);
• deep.

During the shallow stage of hepatic coma, the following psychoneurological signs are determined:

During the deep stage of hepatic coma, the following psychoneurological signs are determined:

• the patient does not have any reaction to any irritants - painful (pinching, injections), temperature (applying a cold or heated object to the skin), olfactory (bringing a cotton swab with ammonia to the nose);
• Absolute areflexia (absence of reflexes) is observed. In particular, the corneal reflex and the reaction of the patient’s pupils to a directed beam of light do not appear;
• due to paralysis (failure) of the sphincters of the bladder and rectum, involuntary urination and defecation occur;
• Generalized (widespread) clonic convulsions (involuntary twitching of muscles and individual muscle fibers due to changes in muscle tone) are often possible.

Signs of liver failure appear at all stages of hepatic coma. The most common are the following:

• the skin, sclera and visible mucous membranes are jaundiced;
• a typical liver taste is felt from the patient’s mouth - cloying and sweetish;
• hemorrhagic syndrome is observed - gastrointestinal, uterine, nosebleeds, pinpoint hemorrhages in the skin and mucous membranes are possible;
• heart rate is increased;
• blood pressure is reduced;
• body temperature is increased.

The apogee of the deep stage of the liver stage is respiratory arrest (in particular, due to damage to the respiratory center).

In addition to cerebral edema, the most common causes of death can be:

Diagnostics

Signs of coma are quite characteristic. The task of doctors is to determine that it is of hepatic origin. Confirmation of the diagnosis is possible based on clinical symptoms and a history of chronic liver diseases. The details of the medical history that are obtained from the patient’s relatives are important:

• against the background of what disease or condition the pathology arose;
• when did the first symptoms appear?
• how quickly the symptoms of the disease developed.

To confirm the diagnosis and assess the degree of liver and brain disorders, additional diagnostic methods are used - physical, instrumental and laboratory.

Physical examination data are quite similar for many types of coma (with the exception of some nuances):

• upon examination, the patient’s lack of consciousness is recorded, the skin, sclera and visible mucous membranes are icteric;
• the patient does not respond to palpation (palpation) of the anterior abdominal wall, tension is not detected;
• percussion is uninformative;
• during auscultation, peristalsis is weakened (due to concomitant toxic damage to the intestines by toxic waste products of the body, which are not neutralized, since the liver is incapacitated).

The instrumental methods used for this pathology are the following:

Laboratory research methods are also used in the diagnosis of hepatic coma:

• – there are signs of anemia (decrease in the amount of hemoglobin) and an increase in the number of platelets;
• – it notes an increase in the amount, a significant increase in the activity of serum transaminases, a decrease in the amount of total protein;
• – there is a decrease in the prothrombin index;
• cerebrospinal fluid analysis– it contains an increased amount of protein;
• toxicological blood test– detection of toxic compounds in the blood;
• blood test for the presence markers of viral hepatitis.

Differential diagnosis

Differential (distinctive) diagnosis of hepatic coma should be carried out with such pathological conditions as:

• acute cerebrovascular accidents (ischemic and hemorrhagic);
• coma due to metabolic disorders - most often observed with hypokalemia (decreased amount of potassium in the blood serum), uremia (excess nitrogenous substances in the blood);
• terminal (final) stage of toxic encephalopathy (brain damage from various poisons).

Treatment and first aid for hepatic coma

Patients with hepatic coma are urgently hospitalized in the intensive care unit and begin permanent:

• ECG monitoring (continuous monitoring of the electrical activity of the heart);
• pulse oximetry - determination of the degree of blood oxygen saturation;
• control of intracranial pressure.

Treatment is intensive conservative therapy. It is based on the following purposes:

note

It should be remembered that with hepatic coma, stress destruction (destruction) of the mucous membrane of the digestive tract is possible, including the risk of bleeding.

• to enhance enzyme activity in the cells of the liver, muscles and brain, L-ornithine-L-aspartate preparations are used;
• to facilitate bowel movements, regular enemas with a solution of magnesium sulfate or siphon enemas are given;
• to enhance the resistance of liver cells to toxic substances, as well as to speed up (accelerate) regeneration (recovery) processes, arginine glutamate, milk thistle preparations, thiotriazoline and others are administered;
• For the purpose of detoxification, estracorporeal detoxification is carried out. It will be performed using hemosorption (taking blood from the bloodstream, purifying it and returning it to the bloodstream) or hemodialysis (purifying the blood using an artificial kidney machine).

If neurological symptoms worsen significantly over the course of several hours, one should suspect. In this case they carry out:

• artificial pulmonary ventilation (ALV);
• sedation;
• normalization of body temperature;
• correction of electrolyte and gas composition of blood.

If, when using these methods, the proper or no effect is observed, carry out:

• hyperosmolar therapy - for this, mannitol and a hypertonic sodium chloride solution are administered intravenously;
• hyperventilation (increased ventilation of the lungs). Forced mechanical ventilation will reduce intracranial pressure for 1-2 hours, during this period of time other measures are taken;
• moderate cooling of the patient's body.

In extreme cases, decompressive craniotomy is performed - a surgical intervention during which the skull is opened to reduce intracranial pressure.

A patient in a hepatic coma is fed using the parenteral method - intravenous drip administration of nutrients, while the calorie content should be maintained, but the amount of protein should be reduced.

The only highly effective method in the case of end-stage liver failure and hepatic coma is liver transplantation.

Prevention

The prevention of hepatic coma is based on the following measures:

• timely detection and treatment of liver diseases - (especially viral), hepatitis, and others;
• prohibition of self-medication by patients with liver symptoms, even mild ones;
• competent selection and prescription of medications;
• measures that will help avoid poisoning by any poisons - industrial toxic substances, mushrooms, household products, and so on;
• refusal to drink alcoholic beverages.

Also, in case of existing liver diseases, special attention should be paid to diseases and conditions that can provoke the rapid onset of hepatic encephalopathy and its consequences - hepatic coma. First of all this:

Forecast

The prognosis for hepatic coma is extremely unfavorable, the risk of death is very high - less than 20% of all patients survive. The highest mortality (mortality) is observed under such conditions as:

• age under 10 and after 40 years;
• the duration of the period of jaundice is less than seven days before the development of signs of severe encephalopathy;
• the amount of bilirubin in the blood is more than 300 µmol/l;
• rapidly increasing changes in the liver, which lead to its reduction;
• addition of an infectious agent;
• severe degree of respiratory failure.

Kovtonyuk Oksana Vladimirovna, medical observer, surgeon, consultant doctor

The number of days given to such patients is influenced by many factors. Some live up to 10 years, while others die in one.

What affects life expectancy with liver cirrhosis?

The length of life with such a complex disease is influenced by several factors:

• stage of organ damage;
• result of complication;
• causes of the disease;
• age, gender of the patient;
• correctness of the prescribed treatment;
• compliance with doctor's recommendations;
• how strong the patient’s immunity is;
• complications.

How long do they live depending on the stage of the disease?

Liver cirrhosis is an acquired disease; it is rarely congenital. Examinations and observations of patients make it possible to understand what percentage of patients can live more than five years after diagnosis. It must be said that, according to statistics, the survival rate is high. 50% of patients live more than 7 springs. True, the outcome of treatment and life expectancy in liver cirrhosis are influenced by the degree of damage to the organ. In medicine, there are 4 degrees of severity of cirrhosis:

• First (compensation). The initial form of the disease - compensated cirrhosis, is characterized by the ability of living cells of the liver parenchyma to take on their functions and the functions of dead cells. Often a person with the first stage does not feel symptoms of the disease. Life expectancy in this situation is influenced by additional circumstances. On average, patients who experience no signs of the disease live for about 7 years. This is a short period of time, but for a complex diagnosis it is a good indicator.

Cirrhosis, which has reached the point of complications and irreversible cell death, does not give hope for survival for more than a couple of years.

• Second (subcompensation). With the onset of the second stage of the disease, the first symptoms begin to appear. This is due to the fact that subcompensated cirrhosis is characterized by depletion of functional cells. Liver parenchyma cells die, disrupting the functional process of the organ. Symptoms of the second stage of the disease: nausea, weight loss. Life expectancy is no more than 5 years.
• Third (decompensation). During the period of decompensation, healthy parenchyma is replaced by fibrous connective tissue. The organ cannot perform its function, complications develop that end in decomposition. Decompensated cirrhosis brings deterioration in the patient’s condition, the person may die after 3 years. In modern medicine, there is a method that allows, at the decompensated stage, not to wait for the liver to fail, but to increase life expectancy by performing an organ transplant.
• Fourth (terminal). The last stage of development of cirrhosis, the prognosis for recovery is poor. The development of all kinds of complications at the last stage, the decomposition of the organ does not give a chance and the person dies within a year.

Prognosis for the development of complications

How long do people with such a complex diagnosis live? Have you found out whether there is a chance of life with the development of complications? Difficulties arising from the disease are associated with increased blood pressure in the venous trunk and possible bleeding. The result of high blood pressure can be various irreversible processes that lead to death. The nature of the complication itself has a great influence on life expectancy:

During the examination, the specialist interviews and examines the patient to determine the need for fluid puncture. A puncture of the dropsy to sample the fluid is performed if infection (complicated by peritonitis) or cancer is suspected. Cirrhosis complicated by abdominal hydrops worsens the prognosis and, without timely treatment, ends in death. A small percentage of patients are able to live with such a complication for some time, the rest do not survive and die much earlier.

• Hepatic encephalopathy. One of the main complications of liver disease, the complexity of which is influenced by the form of the disease. With such indicators, patients manage to live for two springs. And the more complex the disease is, the less chance there is.

The most difficult and dangerous phase is hepatic coma. During a coma, the process of protein synthesis and maturation is disrupted, and the ability to destroy a toxic product, the result of metabolism, is lost. Signs of the onset of hepatic coma:

1. increased body temperature;
2. constantly want to sleep;
3. emotional imbalance;
4. loss of orientation;
5. difficulty coordinating movement.

With the progression of encephalopathy, against the background of liver disease, a coma may occur. A patient in hepatic coma experiences:

1. loss of consciousness;
2. irritation from a direct light source (the patient may automatically turn away from it);
3. at the beginning, a reaction to stimuli is observed, but soon it disappears;
4. stiffness of the limbs and back of the head;
5. manifestation of pathological reflexes of the central nervous system.

With a long stay in a coma, a situation occurs in which death is recorded. The pupils are dilated, there are no reactions, the valves for regulating the transition of substances from one organ to another are paralyzed. The cause of death in a coma is respiratory arrest.

Prognosis of the disorder depending on the etiology

Depending on the etiology, the alcoholic and biliary (autoimmune) types of the disease are considered less complex. What is the life expectancy in such cases? If, with the alcoholic type, the patient stops drinking, the number of days allotted to him increases and reaches more than 5-6 years. With biliary disease, everything is not so optimistic; after the first signs appear, the patient has no more than 5.

There is a viral type of complication (viral hepatitis). This is the most difficult case in the treatment of cirrhosis with complications. The situation gets even worse when two types develop together: alcoholic and viral. There is no talk of a positive result in these cases; the result is quick death.

Life expectancy depending on the gender and age of the patient

Age always plays a role during illness, and doubly so in case of serious illnesses. The chances of recovering from such a disorder in old age are zero. The higher the age, the lower the body’s defenses and often other chronic diseases are added. True, even for young people, such a disease does not always end positively. Very often, alcoholics, drug addicts and patients with viral hepatitis get cirrhosis of the liver.

The peculiarity of the female body is the sensitivity of cells to ethyl alcohol. Therefore, women alcoholics tolerate the disease much worse than men and their life expectancy is shorter.

What happens if you violate doctor's orders?

It is necessary to follow medical prescriptions when treating any disease, not to mention such a complex one. A positive result will come only if the instructions and recommendations are fully followed. A healthy lifestyle is an important aspect of therapy. It is worth excluding the consumption of alcoholic beverages and smoking, they have a toxic effect on the body. Only strict compliance with the instructions will help not only prolong life, but increase the chances of a comfortable future.

Concurrent effects of other disorders

The development of cirrhosis against the background of other diseases of the internal organs worsens the situation. The worst results occur during oncological diseases. It is impossible to answer the question about life expectancy in such a situation; it is necessary to take into account the complexity of associated pathologies and diseases.

Medical statistics

Medical practice is rich in cases of relief from a serious condition and successful recovery. But dry facts speak for themselves better than words. The worst treatment results were for patients who led a chaotic lifestyle associated with alcohol and drugs. Life expectancy with associated complications is short. If you continue to drink alcohol, there is no talk of increasing the days of life. Death occurs suddenly.

The mortality rate for the third, most severe form of cirrhosis ranges from 60 to 90%. If the patient has survived inflammation of the peritoneum and lives, the probability of recurrence of peritonitis in the first six months is 50%. The more time passes, the higher the figure becomes and reaches 74%. The most common causes of death:

Bleeding or dysfunction of other organs of the excretory system can accelerate the death outcome in cirrhosis.

• Bleeding of internal organs. The mortality rate from the first bleeding ranges from 30 to 50%. Having survived, a relapse may occur and the figure reaches 70%.
• Organ functions are impaired (liver, kidney failure). In coma, death occurs in 100%. If the terminal form is complicated by failure of internal organs or the addition of oncology, the chances of recovery immediately decrease.

How to increase life expectancy?

Facts are numbers that can be argued with. It is possible to increase the days of life with such a serious illness. To do this, you need to follow simple recommendations:

• Having suffered from viral hepatitis, you should not wait for the onset of cirrhosis; you should begin treatment immediately. Most importantly, it is important for patients with hepatitis to follow a diet. Avoid spicy, fatty, fried foods, and eliminate alcohol.
• Self-medication is prohibited; you cannot start or stop drug treatment without a doctor’s prescription.
• It is necessary to strengthen the immune system, protecting the body from viruses.
• Take care of your oral cavity.
• We must not forget about the emotional state. It is important to tune in to a positive outcome, enlisting the support of loved ones and friends.

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The last stage of liver cirrhosis: what should you be prepared for?

The liver is a vital and most unprotected organ, subject to daily toxic attack. Abuse of alcohol, fatty and salty foods, coupled with the poor ecology of large cities, can provoke the development of this dangerous pathology. Liver cirrhosis is a progressive chronic disease characterized by a reduction in the number of hepatocytes, a change in the structure of the parenchyma by replacing healthy tissue with fibrous tissue, resulting in the formation of nodes. These nodes compress healthy liver tissue, as well as blood vessels with bile ducts. All this leads to impaired microcirculation of the organ, portal hypertension and other complications that can lead to death.

Child-Pugh stages of liver cirrhosis are determined by the sum of scores for all existing parameters:

I Art. – 5-6 points (referred to as class A) – compensated;

II Art. – 7-9 points (so-called class B) – subcompensated;

III Art. – points (belongs to class C) – decompensated.

Liver cirrhosis differs significantly in clinical and prognostic factors from liver fibrosis and chronic hepatitis.

Toxic cirrhosis of the liver

It develops as a result of food or occupational poisoning with hepatotropic poisons (acute or chronic intoxication). These include alcohol, mushroom poisons, industrial poisons in hazardous industries, and some medications. Inflammation of liver cells leads to necrosis, i.e. their death. The result is liver failure, which develops into toxic hepatitis. And if it acquires a chronic form, then, as a rule, with the development of cirrhosis of the liver.

Symptoms of toxic liver cirrhosis

In case of toxic damage to the liver, the following symptoms are revealed:

Heaviness in the right hypochondrium;

Deterioration of the condition of the entire body.

What should you know?

In toxic cirrhosis, the diseased liver cannot independently neutralize and remove toxins from the body. Once in the blood, they affect the nervous system, causing mental disorders. Factors such as:

An abundance of fatty foods in the daily diet;

Fasting or strict diets;

Penetration of various poisons into the body, for example, drugs;

Already existing acute or chronic diseases.

Decompensation of liver cirrhosis

The main manifestations of decompensation of liver cirrhosis include hepatic cellular failure, ascites, and portal hypertension. When blood vessels in the liver are compressed, the blood flow of the hepatic artery and the microcirculation of the entire organ are disrupted. Blood backs up into the portal vein, causing portal hypertension. In the first stages of cirrhosis, the liver becomes enlarged and its surface becomes lumpy. There is icteric discoloration of the skin, ascites, an increase in the level of bilirubin in the blood, weight loss, and mental disorders appear. Decompensation of liver cirrhosis manifests itself in various life-threatening complications.

Last stage of liver cirrhosis

Whatever the form of the disease, the last stage is characterized by a more pronounced manifestation of signs of liver failure, as well as complications such as:

Stomach and duodenal ulcers;

Hepatic encephalopathy, which may result in hepatic coma;

Cirrhosis of the liver. Forecast

Many people who have been diagnosed with the last stage of liver cirrhosis are concerned about the issue of life expectancy. What will be the doctors' verdict? The last stage of liver cirrhosis differs from the rest in that the liver itself is sharply reduced in size. Gastric hemorrhage with hepatic coma is the leading cause of death. It is difficult to say how long people live with cirrhosis of the liver. This largely depends on strict adherence to the instructions of the attending physician, as well as the patient’s lifestyle and work in hazardous industries. Some people live a couple of years after being diagnosed with the disease, others live into old age.

How to treat liver cirrhosis

If you notice various symptoms of liver failure, you should immediately contact a medical facility for help. Depending on the course of the disease, the doctor will prescribe inpatient or outpatient treatment, and also refer you for the necessary tests. In cases of toxic poisoning, hepatic coma or gastric bleeding, an urgent call for an ambulance is necessary, as this poses a threat to life. In other cases, a trip to the clinic, which should not be postponed. If the last stage of liver cirrhosis occurs as a result of alcohol abuse, this pathological factor should be excluded. Vitamin therapy, a balanced diet (prescribe diet No. 5), and taking prescribed medications are indicated.

How long do people live with cirrhosis of the liver? Recommendations for prolonging life in different forms of the disease

The life of every person is priceless! Solving the problem of life expectancy in liver cirrhosis is very important.

Over the past decade, there has been a breakthrough in the modernization of diagnosis and improvement of therapeutic techniques in working with cirrhosis of the liver, all of which has significantly improved the outcome of the cirrhotic process.

Despite this, much is in the power of the person himself. The greatest part of success depends on establishing a lifestyle and a smaller part on adequate therapy, the percentage varies depending on the type of cirrhosis.

How long do people live with cirrhosis of the liver? The issue is highly controversial. The lower limit is one month or two, the upper limit is ten years, and sometimes years. Let's consider this issue thoroughly.

Doctors can treat known diseases, but the state of health must be created independently. N. Amosov.

Life expectancy with alcoholic cirrhosis of the liver

Cirrhosis of alcoholic etiology occurs in a third of patients suffering from chronic alcoholism and taking alcohol-containing drinks.

How many years does it take before cirrhosis develops? Typically this process takes from 5-20 years. This disease most often affects the male population. The starting point for survival in cirrhotic damage, the stage of clarifying the diagnosis of cirrhosis.

For no reason, a person who drinks alcohol uncontrollably does not go to the doctor and does not follow the recommendations.

Alcoholics go to the doctor when symptoms worsen and change the quality of life: an increase in jaundice, an increase in ascites, the onset of esophageal bleeding, or the presence of mental and neurological abnormalities.

The real type of cirrhotic process can be established based on the history of life and illness, drinking alcohol and plus data from laboratory tests, physical examination indicators and instrumental results.

How long do people live with alcoholic cirrhosis of the liver? The average life expectancy for liver cirrhosis is about 5 years. There is a direct connection between survival over 5 years and non-cessation of drunkenness.

Among those who do not stop drinking alcohol, half of the people survive after four years, and among those who stop, the number of survivors hovers around 75%.

The combination of viral hepatitis C and alcoholic cirrhosis of the liver reduces life expectancy by half. Despite severe dysfunction, by changing lifestyle and stopping drinking alcoholic beverages, it is possible to compensate for lost functions and improve survival.

In the presence of resistant ascites, infection and the formation of spontaneous bacterial peritonitis, recurrent bleeding from varicose veins of the esophagus, rectum and stomach, life expectancy is limited to a couple of months to one year.

The identified indicators and progressive hypoproteinemia, hypoalbuminemia, hyperbilirubinemia indicate a poor outcome. The development of hepatocellular carcinoma is possible, which inevitably indicates impending death.

In cases where there are no contraindications and abstinence from alcohol, liver transplantation is permitted, which improves the prognosis. Improves the quality of life and gives a person a chance to live long.

It is important to follow a diet and categorically refuse to drink alcoholic beverages.

Life expectancy for viral cirrhosis of the liver

Viral cirrhosis of the liver affects predominantly males; the optimal age category for the disease is young and middle-aged.

From infection with viral acute hepatitis to its transformation into cirrhosis of the liver, how long does it take?

On average, this is recorded within the range of 1-2 years for the early type of cirrhosis, and 1-2 years for the late type of cirrhosis.

At the stage of exacerbation of viral cirrhosis of the liver, the picture of manifestations is similar to that of acute viral cirrhosis. Features in its course are noted:

• prevalence of fever at the acute stage;
• presence and increasing intensity of jaundice, unexpressed nature;
• presence of asthenic syndrome;
• presence of dyspeptic complaints;
• bilirubinemia is present despite therapy;
• liver function failure develops early;
• ascites debuts less frequently and progresses in the last stages;
• at the stage of cirrhosis, dilated varicose veins form;
• the addition of hemorrhagic syndrome is noted;
• in laboratory tests, an increase in the level of proteins, especially globulins, is noticeable. A decrease in protein numbers is typical only in the terminal stage.

In the advanced stage, other organ systems are involved in the pathological mechanism, and malfunctions are diagnosed:

• skin - skin rashes and various skin elements;
• serous membranes - serositis;
• menstrual cycle in women - amenorrhea;
• endocrine system - signs of diabetes;
• reproductive organs - hypoplasia of the genital organs;
• hirsutism.

Associated signs: mild abdominal pain, icteric syndrome, the appearance of fever, splenomegaly, hypersplenism, hepatomegaly, telangiectasia.

In the terminal stage, the symptoms of liver cell failure, the progression of ascites, and the addition of a secondary infection increase.

How long do people live with this diagnosis? A person can live with cirrhosis for an average of about 5 years. After 5 years, 55% of people remain alive. With low-active cirrhosis without objective manifestations, this figure increases and is fixed at about 70%.

The circulation of the viral agent in the blood and the release of viral DNA are associated with the progression of cirrhosis and the risk of consequences, which shortens the life span of the cirrhotic process. The prognosis deteriorates sharply when another infection occurs, especially viral hepatitis.

After a successful liver transplant, the patient lives a long time, with sufficient therapy and a regimen drawn up by the attending physician. In the case of multiplication (replication) of viral agents in the blood and the release of viral DNA, after a liver transplant, a re-infection occurs and the disease starts again.

The prognosis in most situations is uncertain and progression is slow.

The cause of death is hepatic coma, in rare situations from the developed consequences of portal hypertension.

Life expectancy in primary biliary cirrhosis

Cirrhosis is based on an autoimmune nature. How long can you live with autoimmune liver cirrhosis?

Life expectancy when diagnosing primary biliary cirrhosis is determined by the stage of the disease. The average lifespan, without complaints, reaches 10 years and can last up to 20 years.

With an increase in clinical signs and an increase in the activity of the cirrhotic process, life expectancy on average decreases to 7-10 years.

More accurately, life expectancy is reflected in the Mayo Clinic model, which takes into account the following values:

1. Presence of signs of ascites.
2. The value of prothrombin time.
3. The value of bilirubin level.
4. The amount of albumin in the blood serum.
5. Patient's age.

Based on the obtained figure, the period for the proposed liver transplant is calculated, subtracting 1–2 years from it.

The final stage 4 of primary biliary cirrhosis has special features of the presence of complications:

• presence of hepatorenal syndrome;
• progression of liver failure;
• appearance and worsening of ascites;
• onset and worsening of hepatic encephalopathy.

Death is often caused by complications:

• the onset of bleeding from varicose veins;
• progress of septic conditions;
• onset of hepatic coma.

How long do people with liver cirrhosis live when ascites develops?

Ascites is a complication of cirrhosis, which is the result of portal hypertension. A distinction is made between tense and non-tense ascites. Refractory ascites is also distinguished. Life expectancy on average varies from three years and does not exceed five years.

With refractory and tense ascites, the effect of drug therapy is low. They are resistant to diuretic drug therapy.

Laparocentesis is recognized as an effective therapy option, which is associated with the appearance and progression of complications, primarily infectious, which limits rehabilitation opportunities and shortens life expectancy.

How long do people live with cirrhosis of the liver, which is complicated by hepatic coma?

The onset of hepatic coma is combined with the last stage of the cirrhotic process and is associated with high mortality.

Stage 4 liver cirrhosis is the stage at which adverse events occur, including hepatic coma (progressive hepatic encephalopathy).

In most situations, people die immediately; if they can be brought out of a coma and stabilized, life is prolonged in intensive care or in a hospital. The recurrence of coma is high, as is the development of fatal complications.

Mortality rates range from 80% to 100%. There is a chance to prolong life if a liver transplant is performed or MARS therapy is used.

1. Determining the root cause of cirrhosis as early as possible.
2. Treatment of the key disease that served as the root cause for the onset of liver cirrhosis.
3. Preventing re-infection with the hepatitis virus.
4. Refusal of alcohol and drugs.
5. Educational work to prevent sexual transmission of infections.
6. Compliance with general hygiene measures.
7. Use of disposable instruments in hospitals, compliance with sanitary and epidemiological regulations. For personal purposes, use of disposable instruments, in public places (hairdressing salons, dentistry, manicures and others) high-quality processing of instruments.
8. Constant and careful screening of donors.
9. Compliance with the rules and timing of blood transfusion and its formed elements.
10. A strict diet, as prescribed by your doctor.
11. High-quality treatment of infections of other organs, especially the liver and bile secretion organs.
12. Adequate and complete treatment, in consultation with the attending physician.
13. Constant supervision by the attending physician
14. Vaccination against viral hepatitis if required.
15. Regular monitoring of liver parameters and study of the liver as indicated.
16. Exclusion of self-medication, refusal to take hepatotoxic medications.
17. Therapy of existing diseases in humans.

In conclusion of this topic, I would like to note the importance of paying attention to your health. There is always a chance to help yourself. Even in the most severe cases, the necessary measures can be taken. Vaccine prevention measures have been developed that help fight the incidence of hepatitis.

Fact: A person is responsible for everything that happens to him.

Graduated from Smolensk State Medical Academy. Works at the State Budgetary Healthcare Institution CDC 4 DZM Branch 4, Moscow, head. therapeutic department. Work experience 8 years.

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Toxic cirrhosis of the liver: manifestation and treatment

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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.

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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:

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:

• 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 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.

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 of bile from the mouth, 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 detoxification solutions, broad-spectrum antibacterial drugs, glucocorticoids, Furosemide and Aldactone. A complex of vitamins was also prescribed. In order to reduce the concentration of ammonia, an enema was performed.

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

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The pathology begins with the fact that hepatocytes (liver cells) die under the influence of a number of reasons. The organ can no longer neutralize toxins. All these products and their metabolites accumulate in the bloodstream and lead to the development of hepatic encephalopathy. Without treatment, death quickly occurs.

• the mood constantly changes, several times throughout the day;
• bouts of euphoria occur, which turn into a state of stunning;
• During the day there is a pathological desire to sleep, and at night the patient is awake.

Important! Handwriting may change, thoughts may become distracted.

Before hepatic coma develops, there is another stage - precoma. During this period, the painful state sharply intensifies, reaching the point of lack of consciousness in the patient. When examining or talking with a patient in a state of precoma, note the following symptoms:

• attacks of nausea and vomiting, abdominal pain, sudden loss of body weight;
• yellowness of the skin, sclera and mucous membranes, which gradually intensifies;
• the color of the skin becomes bright red, and the lips and tongue become crimson;
• development of hemorrhagic syndrome - in the precoma stage, bruises and hematomas occur, internal bleeding appears.

Important! From the moment of loss of consciousness there are several hours to provide qualified assistance.

• toxic agents (chemicals, ethanol and its derivatives, mushrooms);
• the effect of medications (nonsteroidal anti-inflammatory drugs, antibiotics, barbiturates, inhalational anesthetics) is especially pronounced during pregnancy and alcohol abuse;
• viruses (hepatitis, mononucleosis);
• liver pathology, against the background of which there is a sharp decrease in the volume of organ tissue; diseases of the heart and blood vessels;
• stress, burns, septic abortions, shock conditions.

Stages of hepatic coma

• coma 1 – depression of consciousness occurs in waves, all physiological reflexes are preserved;
• coma 2 – the person is in an unconscious state, does not come out of it, all physiological reflexes are normal;
• coma 3 – the patient is unconscious, there are no reflexes.

• glucose with insulin into a vein;
• fat emulsions;
• mixtures of amino acids.