Hepatic coma is a severe disease that is associated with extensive damage to the functional liver tissue (parenchyma) and severe dysfunction of the central nervous system, blood circulation and metabolism. Develops as a result of acute and chronic liver diseases of any origin. The term hepatic coma is used to describe all stages of the disorder, including precoma, developing coma, stupor, and coma itself.

ICD-10	K72
ICD-9	572.2
MedlinePlus	000302
eMedicine	med/3185
MeSH	D006501

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Often the term is used as a synonym for hepatic encephalopathy, which precedes and is closely associated with hepatic coma, and sometimes it is used to refer to hepatocerebral insufficiency syndrome.

General information

Hepatic coma is the end stage of liver failure.

The study of liver failure began at the end of the 19th century. - in 1877, the Military Medical Journal published a description of the operation performed on dogs by the Russian military doctor N. Eck (he directed the blood coming from the abdominal organs past the liver, into the general bloodstream). Eck's experience with fistula was used in his research in the late 80s by I.P. Pavlov, who noted the picture of meat poisoning up to coma that appeared in operated dogs. However, contemporaries did not appreciate the results of these studies, suggesting that in clinical practice such a picture can be found in very rare cases.

In 1919, Davis et al. experimentally confirmed the conclusions of I. P. Pavlov. Subsequently, based on these findings, a type of hepatic coma was identified (portal-hepatic coma, or portosystemic encephalopathy).

F. Bigler, R. Wilson, N. Kalk, M. Klekner and others studied liver failure and the pathogenesis of hepatic coma.

The prevalence of this disease is about 3% of all admissions to intensive care units.

Forms

Depending on the clinical form of hepatic coma, there are:

• Hepatocellular (“spontaneous”) coma. This endogenous type of disease occurs with necrosis of the parenchyma and is accompanied by the cessation of liver participation in intermediate (intermediary) metabolism, including the neutralization of toxic substances. In this case, as a result of the breakdown of protein in the liver tissue, toxic substances are formed that affect the brain. Some of these toxic substances enter the intestine from the bile duct, are reabsorbed and affect the neutralizing function of the liver. An endogenous type of coma is observed with viral hepatitis and toxic lesions.
• Shunt (portocaval) coma. It is an exogenous type and occurs during true ammonia intoxication. Ammonia comes from the intestines after shunting in cirrhosis, liver diseases that are accompanied by pronounced portocaval anastomoses, excess protein in the diet, as well as bleeding and the presence of blood accumulations in the intestines or stomach.
• Mixed coma, which occurs with necrosis in the liver and is accompanied by the entry of ammonia through the portacaval anastomoses (the anastomosis between the tributaries of the portal vein and the system of the superior and inferior vena cava). Usually observed in cirrhosis.
  Complex (mineral or “false-hepatic”) coma, which develops in patients with chronic liver diseases with severe diarrhea, during massive diuretic therapy or during removal of ascites as a result of electrolyte imbalance ().

Reasons for development

Hepatic coma occurs as a result of the accumulation of toxic substances in the body, which can be endogenous or exogenous in origin.

Causes of hepatic coma include:

• Toxic factors (poisoning with phosphorus, arsenic, chloroform, carbon tetrachloride, dichloroethane, novarsenol, alcohol and mushrooms).
• Hepatotoxic effects of medications (taking atophan, paracetamol, rifadin, aminazine, nitrofuran, sulfonamides, barbiturates and the use of inhalational anesthetics. The toxic effect of these drugs on the liver increases in people who abuse alcohol, with liver pathologies, pregnancy and malnutrition.
• Impact of viruses. Who can be caused by hepatitis B (sometimes hepatitis A), infectious mononucleosis and yellow fever virus.
• Liver diseases that cause a sharp decrease in parenchyma. Such diseases include cirrhosis, alveococcosis, malignant primary neoplasms, cholestasis, which is accompanied by the development of “bile necrosis,” and long-term obstruction of the bile ducts.
• Diseases of organs and systems that are accompanied by involvement of the liver in the pathological process (cardiovascular diseases, etc.)
• Stressful situations that arise in patients with large area burns, septic abortions and various types of shock.

Pathogenesis

The complex mechanism of development of hepatic coma is still not well understood.

Most researchers believe that the structural and functional disorders of astroglia (nervous tissue that forms the supporting apparatus of the brain) observed during hepatic coma occur under the influence of endogenous neurotoxins and amino acid imbalance.

Amino acid imbalance and the production of endogenous neurotoxins develop with liver cell failure or with portosystemic blood shunting.

The main manifestations of hepatic coma are associated with changes resulting from the pathological process:

• permeability of the blood-brain barrier;
• ion channel activity;
• neurotransmission and providing neurons with energy material.

Exogenous hepatic coma is associated with the absorption of intestinal autotoxins, which are formed due to insufficient enzymatic breakdown of food proteins and a disrupted process of their neutralization. Intestinal autotoxins entering the portal blood are normally completely neutralized due to the functioning of the liver.

It is the liver that neutralizes ammonia formed in the intestines. The ammonia content in portal blood is 5-6 times higher than its level in peripheral blood. Ammonia is transformed into urea during the passage of portal blood through the liver.

The liver also metabolizes and detoxifies other intestinal-derived toxins through processes of hydroxylation, deamination, demethylation, acetylation, and pairing. Mercaptans, indican, phenol, indole, valeric, butyric and caproic fatty acids are transformed in the liver into non-toxic substances, which are then excreted from the body.

Impairment or complete loss of the neutralizing function of the liver is accompanied by the entry of toxic substances into the systemic bloodstream, which leads to intoxication of the entire body. Since nervous tissue (neurocytes of the cerebral cortex) is especially sensitive to any toxins, a disturbance of consciousness occurs and coma develops.

This mechanism of coma development explains the origin of shunt hepatic coma, which occurs in decompensated forms of liver cirrhosis. Thanks to the formation of direct portacaval shunts - anastomoses, unpurified blood bypasses the liver and enters directly into the systemic circulation. As a result, progressive hyperammonemia develops, which plays the role of the main comogenic factor.

Massive necrosis of the liver parenchyma plays a decisive role in the development of endogenous coma, but the depth of the coma and the number of dead hepatocytes are not related to each other.

In viral hepatitis B, hepatocytes are affected by the cytolytic action of lymphocytes.

The destruction of liver cells is accompanied by the release and activation of hydrolases and other lysosomal enzymes.

When metabolism in the liver is disrupted, penetration of aromatic amino acids into the brain is observed. The resulting highly toxic derivatives of these amino acids (octopamine and b-phenylethanolamine) are similar in structure to adrenergic mediators, which, when accumulated, disrupt the processes of nerve transmission in synapses, causing a comogenic effect.

Hepatic coma is accompanied by:

• Inhibition of oxidative phosphorylation processes, which leads to disturbances in oxidative processes in the brain, decreased oxygen and glucose consumption and the development of cerebral hypoxia and hypoglycemia.
• An increase in the permeability of biological membranes of cerebral cells, which causes a change in the ratio of electrolytes. As a result, the potassium content in intracellular structures decreases, and the sodium and calcium content increases. Shifts in the acid-base state lead to the accumulation of pyruvic and lactic acids. Since pH changes are multidirectional, intracellular hypokalemic acidosis and associated extracellular alkalosis develop.
• Violation in some cases of water-salt metabolism, which leads to impaired renal function.
• Water retention in the body and its redistribution, which causes a decrease in the volume of circulating blood and an increase in the amount of fluid in the interstitial space.
• Coagulopathy associated with K-hypovitaminosis syndrome, causing a violation of thrombin formation. At the same time, the level of most blood coagulation factors decreases, fibrinogen B appears.

Under the influence of thromboplastic substances released from the damaged liver, intestinal endotoxemia and transfusion of large volumes of blood, disseminated intravascular coagulation (DIC) syndrome occurs, provoking the development of hemorrhages.

Changes in blood rheology can be affected by antithrombin III deficiency and microcirculation disorders.

Symptoms

The clinical picture of hepatic coma is a complex of various symptoms, which includes a variety of mental and motor disorders that appear at different stages of coma development.

Symptoms of stage 1 hepatic coma (precoma) include:

• deterioration of general condition, accompanied by sleep disturbances (drowsiness during the day and insomnia at night);
• slow thinking;
• euphoria or lethargy, unmotivated behavior;
• hiccups and yawning;
• tachycardia;
• sweating

Variable symptoms may occur, including fever and bad breath (bad breath in hepatic coma is characteristically “liver-like”).

Some patients experience moderate jaundice, abdominal pain of varying intensity, hemorrhagic syndrome and disseminated intravascular coagulation syndrome, and may develop oliguria and azotemia, as well as infectious complications.

In most patients, percussion reveals a decrease in liver size.

Signs of stage II hepatic coma (imminent hepatic coma) include:

• severe disturbances of consciousness (loss of orientation in time and space), dizziness and fainting;
• slow speech;
• increasing weakness, adynamia;
• periods of excitement that alternate with deep depression;
• drowsiness, negativism, memory loss;
• the presence of muscle tremors and “flapping” tremor of the hands.

As the pathological processes deepen, pathological reflexes and decerebrate rigidity are added, and convulsions are possible. A divergent strabismus may be observed while the pupillary reflexes are intact.

Stage III or coma stage is accompanied by:

• lack of consciousness and reflexes observed in a normal state;
• muscle rigidity (neck and limb muscles);
• the appearance of pathological reflexes (Zhukovsky, Babinsky, proboscis and grasping);
• periodic stereotypical movements;
• the presence of Kussmaul or Cheyne-Stokes breathing caused by hyperventilation;
• , absence of photoreaction and corneal reflexes;
• convulsions;
• sphincter paralysis;
• stopping breathing.

Diagnostics

Hepatic coma is diagnosed based on:

• Anamnesis data.
• The clinical picture of the disease and data from evaluation studies, during which the processes of higher nervous activity, the patient’s orientation in space and time, his level of consciousness, and vegetative manifestations of the disease are assessed. In the absence of consciousness, neurological examinations are performed to determine the presence of reflexes. The level of circulatory functionality is also assessed.
• The results of a biochemical blood test, which allows you to identify profound disorders that cause coma (coagulation factors are 3-4 times lower than normal, protein levels are reduced and bilirubin levels are increased, there are elevated cholesterol and nitrogen metabolism products, significant electrolyte shifts are detected).
• Electroencephalogram data that reveals a slowing of the alpha rhythm and a decrease in the amplitude of the waves as the coma deepens.

Treatment

Treatment of hepatic coma is aimed at eliminating the factors contributing to the development of coma.
Therapy includes:

• A diet with a sharp restriction of the amount of protein (precoma allows the consumption of up to 50 g of protein per day, and with a threatening coma, protein is completely excluded). The calorie content of food should be 1500-2000 kcal per day (due to easily digestible carbohydrates). Colon cleansing using an enema for the lower intestines, and laxatives for the upper intestines. For enemas, it is recommended to use acidified water, which allows more ammonia to bind.
• Antibiotics that suppress ammonia formation (non-absorbable neomycin and paramonomycin, absorbable ampicillin, etc.).
• Lactulose, which promotes acidification (increased acidity) of intestinal contents.
• Bromocriptine, flumazenil and branched chain amino acids to modify neurotransmitter ratios.

L-ornithine-L_-aspartate is also used to biochemically convert ammonia into less toxic forms.

Basic therapy includes drip infusion treatment, which improves microcirculation, normalizes electrolyte disturbances and CBS, which provides detoxification and parenteral nutrition (a 5-10% solution of glucose or fructose is administered). In this case, it is necessary to control the patient’s body weight, hematocrit indicator and diuresis.

Hepatic coma also requires the use of vitamins in treatment.

Liqmed reminds you: the sooner you seek help from a specialist, the greater your chances of maintaining health and reducing the risk of complications.

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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 develop cirrhosis of the liver.

A 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.
• Watch your mouth.
• 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 becomes chronic, 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. 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 developing 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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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. 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.

Reasons

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, in connection with this, 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 poor 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.

Coma leads to a gradual decrease in the number of viable hepatocytes. If in a healthy person the weight of the gland is from 1600 g to 2000 g, then in a patient it is 1200 g. The liver tries to rearrange its work so as to compensate for the deficiency, but this only worsens the condition. At the same time, metabolism is disrupted. As long as the body maintains a state of balance, the patient feels well, but as metabolic problems intensify, a coma begins. The dangerous condition occurs quickly, with symptoms intensifying within a few days. The first signs are changes in mental reactions:

• 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.

The hepatic coma itself is manifested by a lack of consciousness, a decrease in body temperature, and a decrease in the tone of the eyeballs. The patient's pulse is rapid and barely audible, and his blood pressure is critically low. Breathing is noisy, heavy, and can be clearly heard from a distance. The doctor notes the presence of a sweet odor in the patient’s exhaled air; kidney damage is manifested by a lack of urination (anuria).

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

Hepatic coma occurs as a result of the action on the body of toxic and poisonous substances that accumulate due to the inability of the liver itself. Factors that provoke coma that occurs against the background of liver cirrhosis are:

• 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

The state of hepatic coma does not occur immediately. The disease occurs in several stages. Precoma is the first stage of liver pathology, which lasts from several days to several months. The patient complains of disorientation in space, dizziness, and disturbances in thought processes. The next stage is a threatening coma. As a rule, it develops over 2-3 days, but can reach 10-12 days. Impaired consciousness, psychoemotional disorders, and trembling of the limbs occur. Symptoms gradually increase. Developed hepatic coma is the terminal stage of hepatic encephalopathy against the background of liver cirrhosis. It is characterized by a vivid clinical picture (see symptoms above). The state of hepatic coma develops in three stages:

• 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.

Treatment of liver pathology against the background of liver cirrhosis is carried out in the intensive care unit. Be sure to monitor the body's oxygen saturation, carbon dioxide levels, and blood acidity. Using laboratory diagnostics, the levels of bilirubin, ALT, AST, cholinesterase, sugar and electrolytes are assessed over time. The person is in a lying position with the upper body elevated. Disol, Trisol, Ringer's solutions are infused intravenously to replenish the level of electrolytes, sodium bicarbonate and ascorbic acid to normalize the acid-base balance. Parenteral nutrition is carried out as follows:

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

The intestinal tract is periodically cleansed of toxic substances through a cleansing enema and antibiotics are administered orally. If necessary, oxygen therapy is prescribed. Hormonal drugs are also used to combat liver pathology. Cleansing the body (what the liver should do in the human body) is carried out using the methods described in the table.

Method of cleansing the body	The essence of the procedure
Plasmapheresis	A portion of the patient’s blood is taken and separated into plasma and formed elements in a special apparatus. After the process of cleansing the liquid part, it is returned back to the bloodstream
Lymphosorption	The patient's lymph is passed through special sorption filters that retain toxins, waste, and unnecessary substances
Hemosorption	The procedure is similar to lymphosorption, but the patient’s blood with formed elements is used
Hardware hemodialysis	The patient's blood is passed through a special apparatus, where toxins and their metabolites are removed from it, and then returned to the body
MARS therapy	An extracorporeal detoxification method in which pathological elements are removed from the blood, while useful ones remain

The best treatment option is surgery, during which a gland transplant is performed. Treatment of precoma and 1st degree coma has a favorable prognosis. Deeper stages are usually fatal. With transplantation, the prognosis is more favorable. If specialists bring the patient out of a comatose state, they treat liver cirrhosis and eliminate the factors that led to the development of the pathology.

Diseases of this organ can provoke a serious condition - hepatic coma. It has several stages, can be caused by various reasons and lead to serious consequences, including death. Our article will tell you more about this disease.

Definition and code according to ICD-10

The regulatory document defining the international classification of medical diagnoses ICD-10 regulates the following liver diseases.

ICD code – 10:

• K 72 - , not classified elsewhere.
• By 72.0 - acute and subacute liver failure.
• K 72.1 - chronic liver failure.
• K 72.9 - liver failure unaccounted for.

The disease develops against the background of general intoxication of the body. Phenol, ammonia, sulfur-containing amino acids and low molecular weight fatty acids accumulate in the body. They have a toxic effect on the brain, which increases when the water-electrolyte balance is disturbed.

Forms

Liver dysfunction can be of various types. In total, three variants of hepatic coma have been identified, which can lead to serious consequences.

What types of coma are there:

• Endogenous, in which disorders can be caused by viral forms of hepatitis, dystrophic and destructive processes in the organ during cirrhosis, as well as replacement of healthy liver tissue with a tumor or scars. It is very painful and progresses quickly, with pain felt in the area of ​​the affected organ, hemorrhoidal disorders, jaundice and itching of the skin and a severe “liver” odor from the mouth. Psychosomatic disorders often manifest themselves, periods of increased activity alternate with complete loss of strength, depression and excessive fatigue.
• Exogenous hepatic coma occurs more often with chronic organ dysfunction, cirrhosis and chronic renal failure. This form of disease lacks a characteristic odor and psychosomatic signs. The disease is relatively painless and without pronounced symptoms. The problem can be identified by identifying portal vein hypertension.
• Mixed forms are characterized by symptoms of endogenous and exogenous forms of hepatic coma. At the same time, along with necrotic processes in organ tissue, problems of hematopoietic function are diagnosed, and symptoms may include various manifestations of previous forms of the disease.

Stages of the disease

Depending on the severity of the patient’s condition, there are three stages of this disease. In this case, the central nervous system is affected, brain function is disrupted, and accompanying symptoms are observed.

The disease has the following stages:

1. Precursor or antecedent phase. The patient is emotionally unstable, mood swings are very abrupt and do not depend on external influences. Aggression and sleep disturbances may occur (drowsiness during the day, insomnia at night). It is difficult to concentrate on any issue, consciousness is clouded, mental activity is inhibited. Frequent symptoms: tremors of the limbs, severe headache, nausea, vomiting, hiccups, excessive sweating, dizziness.
2. Excitement phase or threatening coma. Strong emotional upsurge, aggressiveness, anxiety. Mental activity is practically absent, movements are mechanical and without a specific purpose. Disorientation in time and surroundings often occurs. Pain sensations are dull, reactions only to external stimuli.
3. Complete or deep coma. Complete absence of consciousness, emotions and reactions to stimuli. The breathing rate may change (up to a complete stop), blood circulation slows down. The blood pressure level is reduced, sphincter paralysis occurs, and corneal reflexes go out.

Reasons

Hepatic coma develops against the background of existing chronic diseases and pathologies of the liver, as well as due to toxic effects.

The main reasons are:

• Viral hepatitis of groups A, B, C, D, E, G.
• Viral liver diseases, including herpes, infectious mononucleosis, Coxsackie's disease, measles,.
• Vasiliev-Weil disease (icteric leptospirosis).
• Liver damage due to fungal or microplasma infection.
• Severe intoxication with toxic substances.

Threatening factors include the use of alcohol and psychotropic substances, the inclusion in the diet of excessive amounts of protein foods, as well as wild mushrooms.

Pathogenesis

The processes of pathogenesis have not been fully studied. It is known that in this condition the functioning of neurotransmitter systems is disrupted, and an excess of breakdown products (nitrogen compounds, fatty acids and neurotransmitters) negatively affects the functioning of the brain and central nervous system.

Symptoms

Depending on the causes and severity of the disorders, the symptoms of the disease may vary. It is also worth taking into account the individual characteristics of the patient, which also determine the severity of the lesion and the prognosis of treatment.

The main symptoms are:

1. Feelings of anxiety, thinking disorders.
2. Problems sleeping at night, sleepiness during the day.
3. Muscle cramps and increased tone.
4. Yellowing of the skin.
5. Accumulation of fluid in the abdominal cavity (ascites).
6. Bleeding, the appearance of hematomas.
7. Soreness in the liver area.
8. Increased body temperature, chills and fever.
9. Tachycardia, decreased blood pressure.
10. Tremor of the extremities, usually the fingers.

In various stages, there may be increased mental agitation, aggression and sudden mood changes. In addition, evidence of problems in the liver can be a strong bad breath, digestive disorders (prolonged vomiting, constipation or diarrhea), paralysis of the sphincters.

Complications

Progressive liver failure affects the general condition of the patient, threatening his life. This disease has no complications as such, because hepatic coma in itself is a very serious condition, leading to irreversible processes in the body.

Diagnostics

The disease is determined by.

These include bilirubinemia (increased concentration of bile pigment), azotemia (exceeding normal levels of nitrogenous products), decreased levels of prothrombin, cholesterol and glucose.

Urine becomes richly yellow in color, bile acids and urobilin can be found in it, feces become discolored.

Urgent Care

If a sharp deterioration in health occurs outside the walls of a medical institution, the patient must be placed on his side, ensuring normal air flow, and an ambulance must be urgently called.

Before the doctors arrive, you should not change position, shake or move the patient. Such conditions require immediate hospitalization, and already in the hospital an active struggle for the patient’s life begins.

What can be done in the hospital:

• Administer a glucose solution with panangin to improve brain activity.
• A complex of saline and insulin for severe catatonic conditions.
• On the first day, an increased dose of prednisolone is prescribed to relieve the toxic effect on the organ.
• Stimulation of liver activity is carried out using an intravenous or intramuscular solution of nicotinic acid, riboflavin, thiamine chloride and pyridoxine.

First aid consists of reducing symptoms of intoxication, stabilizing respiratory function, water and electrolyte balance and protein metabolism. Until the condition is stabilized and in order to prevent a deep coma, the patient is kept in the intensive care unit.

Treatment

Further treatment measures are agreed upon with the attending physician. The prognosis and chances of recovery depend on many factors, including the presence of concomitant diseases, age and the degree of organ damage.

The following methods are commonly used:

1. Diet and limiting the amount of protein consumed.
2. Taking antibacterial agents that reduce the activity of intestinal flora and the formation of waste products.
3. Maintenance therapy consists of using glucose solution, saline solution, and glucocorticoids.
4. To reduce ammonia levels, you need to take glutamic acid and arginine.
5. Excessive psychosomatic symptoms are corrected with special antipsychotics.
6. In case of dysfunction of the respiratory system, the patient is connected to an oxygen mask.

If a diagnosis of toxic poisoning is made, all measures should be aimed at detoxifying the body. The doctor may suggest a blood transfusion, as well as hemodialysis, if kidney failure is added to the main symptoms.

How long does hepatic coma last?

Even the most highly qualified doctor will not be able to give accurate forecasts. It will be extremely difficult to bring a patient out of a complete coma, so it is best to seek help in the early stages of the disease.

The recovery rate is significantly influenced by accurate diagnosis and elimination of the cause, but in more than 15% of cases it cannot be determined.

Prognosis and prevention

The chances of recovery in patients who have suffered a hepatic coma are extremely low.

Basically, this is no more than 20% of survivors at the precoma stage, less than 10% in the threatening phase and approximately 1% in a deep coma. Even such disappointing forecasts are not always possible, and only with timely and competent treatment.

Irreversible processes that occur in the body under the influence of decay products, as well as suppression of functions or complete failure of an organ, affect the activity of the central nervous system and brain.

It is extremely difficult to bring a person out of a deep coma, and the most successful treatment method at the moment is a donor liver transplant and long-term drug therapy.

There are no preventive measures against this disease. To maintain the health of this organ, it is necessary to follow general recommendations: refuse and take, maintain moderation in diet, and also regularly subject the body to feasible physical activity.

All problems and identified diseases must be treated in time and regularly examined if possible. Hepatic coma, regardless of its forms and stages, causes irreparable harm to health and significantly reduces the quality and life expectancy, so its symptoms should never be ignored.

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The death of hepatocytes significantly disrupts the functioning of this organ and contributes to its complete dysfunction. The inability of the liver to cope with its immediate work leads to complete failure of the organ. Against the background of cirrhosis, the development of hepatic coma often begins, which leads to serious consequences and even death.

What you need to know about hepatic coma

Liver cirrhosis, especially with the development of hepatic coma, carries a disappointing prognosis for the patient. Hepatic coma, as a rule, develops in the last stages of the disease, when therapy is no longer effective. Therefore, it is extremely important to identify the presence of this disease at the initial stages, when it is still possible to prevent its spread and the development of dangerous symptoms. The most serious of which is considered internal bleeding, since in this case blood, in addition to the esophagus, also enters the abdominal cavity.

The primary cause of hepatic coma is the presence of diseases such as viral hepatitis B or C. Toxic damage to the liver also plays a major role in the development of this disease. It also develops as a result of cirrhosis of the liver, poisoning with poisons that directly affect this vital organ, and in the presence of various types of tumors.

Hepatic coma can also develop with jaundice in acute and severe form. The fact is that when the liver malfunctions, dangerous toxins directly penetrate the body, destructively affecting all its internal organs and systems. The most dangerous of which is ammonia, which significantly affects the nervous system. It is formed in the gastrointestinal tract during protein synthesis.

A healthy and normal liver produces urea, which removes with urine all harmful substances and toxins that accumulate in the human body. Accordingly, with hepatic coma, the main filter of the body cannot cope with its work, as a result of which dangerous poisons penetrate into the systemic bloodstream, through which they are carried to various tissues and interfere with the normal functioning of internal organs. Treatment in this case should be emergency.

Clinical picture

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Hyperventilation of the lungs is a common consequence of hepatic coma, as the tissues of the respiratory center are affected. When the liver is unable to cope with the removal of toxins, the cerebral cortex produces amino acids that react with various substances. The result of this is blood saturation and, as a consequence, intoxication of the body. First of all, it is the central nervous system that suffers from this.

With viral hepatitis, only six to ten days are enough for the development of hepatic coma. However, with timely and qualified treatment of this disease, it occurs in quite rare cases.

The same amount of time is needed for the progression of this pathology in liver cirrhosis or. With cirrhosis of the liver, bleeding that occurs in the esophagus is not a rare phenomenon, which significantly increases the intoxication of the body due to the fact that the blood, entering directly into the gastrointestinal tract, disintegrates, and this entails the formation of a large amount of ammonium.

Symptoms of hepatic coma

First of all, in the presence of hepatic coma, symptoms associated with the nervous system appear. If the first signs of damage to the central nervous system appear, therapy should be started immediately, since this disease progresses rapidly and leads to death in a short time.

The dynamics of the development of this severe pathology can be described in several stages:

1. Sudden mood swings in the patient and minor disturbances in motor skills. Common symptoms include insomnia, increased anxiety and severe migraines.
2. Next comes general weakness, lethargy and constant drowsiness. Sometimes the patient becomes disoriented in time and space. There may be manifestations of aggression and inappropriate behavior.
3. At the next stage, disorders and speech defects become obvious, and the patient becomes completely disoriented. This stage is also characterized by severe disturbances in the patient’s consciousness and memory loss.
4. The last stage is the onset of coma.

In addition, along with the symptoms described above, some physical abnormalities also appear. Muscle tone undergoes significant changes, often accompanied by spontaneous muscle contraction, as well as tremors of the limbs.

Many doctors emit a sweetish odor from the mouth, which is characteristic of acute liver failure. Initially, it is barely noticeable, but as the pathology progresses, it becomes more and more obvious and sharp. The appearance of such an aroma is a sure sign of visiting a doctor to undergo a full examination and identify liver pathologies. Therapy in such cases begins immediately, since such a liver odor manifests itself in the early stages of the development of the pathology and timely treatment in such cases can save the patient’s life.

People who already suffer from diseases such as hepatitis or cirrhosis of the liver should be examined first, since they are predisposed to the development of such a serious pathology as hepatic coma.

In the initial stages of the disease, experts identify several symptoms that need to be paid attention to in advance and immediately consult a specialist:

• nausea and vomiting;
• decreased performance;
• abdominal pain;
• progressive pain in the liver area;
• increased irritability and anxiety;
• frequent migraines;
• sudden weight loss.

The last stage, which occurs just before the coma itself, is characterized by complete loss of appetite, aversion to any food and sometimes gastric bleeding. Prolonged and fairly frequent vomiting is also a harbinger of coma. This stage is characterized by the presence of long-term, constantly progressive jaundice with severe complications. Moreover, it is worth noting that all symptoms flow from one to another, and do not appear simultaneously. Therefore, symptomatic treatment will not give any result in this case, but will only aggravate the condition, the result of which will be death.

Diagnosis of hepatic coma

When hepatic coma occurs, the patient experiences the following symptoms:

• lack of response to any external stimuli;
• complete atrophy of the facial muscles;
• specific sweetish odor from the mouth;
• yellowish tint of the skin and mucous membranes;
• dryness and flaking of the skin;
• low or, conversely, very high temperature;
• unconscious vomiting;
• subcutaneous bleeding at the injection site or previously damaged skin.

Also common signs of coma are:

• severe bloating and swelling of the abdomen;
• rapid heartbeat;
• nosebleeds;
• involuntary urination or stool loss;
• touching the liver area causes muscle spasms or unconscious groans;
• the pulse is practically not palpable;
• breathing is noisy and heavy;
• There is practically no reaction of the pupils to light.

This disease is diagnosed in specialized medical institutions, where first of all it will be necessary to take a blood test for biochemistry and an ECG. Since there are quite a large number of diseases in which a person falls into a coma, the examination should be carried out by a qualified and experienced diagnostician.

Therapy for hepatic coma

If the patient is diagnosed with the last stage of hepatic coma, then treatment, as a rule, no longer helps. In most cases, with any therapy, such a patient does not survive. Therefore, identifying the disease in the early stages plays an important role, when treatment can not only have a positive effect, but also save a person from death.

When diagnosing such a disease, urgent hospitalization of the patient in a specialized medical institution is required. During transportation, it is important not to injure the patient, since any physical activity in this condition causes serious complications. The use of sedative medications during hepatic coma is strictly prohibited.

Initially, the patient’s body is detoxified. In this case, it is especially important that the patient is calm both physically and mentally. Often, when treating this disease, lactulose is prescribed to normalize intestinal function. Self-medication in such cases is strictly prohibited, since the result most often is the death of the patient.

A strict diet also plays an important role in the treatment of hepatic coma, which helps prevent increased formation of ammonia and also helps normalize the gastrointestinal tract.

When prescribing any medications, you should make sure that there is no gastric or intestinal bleeding, and also exclude the presence of possible intestinal obstruction. It is necessary to completely remove heavy foods and complex proteins from the diet. To maintain the health and normal functioning of internal organs, special vitamin complexes are prescribed.

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Anyone who wants to stop their family from drinking or wants to give up alcohol themselves, take 5 minutes and read, I’m 100% sure it will help you!

In conclusion

Hepatic coma is a consequence of severe liver damage caused by various factors, including cirrhosis. This pathology in advanced stages inevitably leads to the death of the patient, so it is extremely important to consult a doctor if any symptoms characteristic of this disease appear and undergo a full examination. It must be remembered that the sooner such a disease is diagnosed, the sooner therapy is started, the greater the patient’s chances of avoiding serious consequences and saving himself from death.

Drawing conclusions

If you are reading these lines, we can conclude that you or your loved ones suffer from alcoholism in one way or another.

We conducted an investigation, studied a bunch of materials and, most importantly, tested most of the methods and remedies for alcoholism. The verdict is:

If all drugs were given, it was only a temporary result; as soon as the use was stopped, the craving for alcohol increased sharply.

The only drug that has given significant results is Alcolock.

The main advantage of this drug is that it once and for all eliminates the craving for alcohol without a hangover. Moreover he colorless and odorless, i.e. to cure a patient of alcoholism, it is enough to add a couple of drops of medicine to tea or any other drink or food.

In addition, there is a promotion going on now, every resident of the Russian Federation and the CIS can get Alcolock - FOR FREE!

Attention! Cases of sales of counterfeit drug Alcolock have become more frequent.
By placing an order using the links above, you are guaranteed to receive a quality product from the official manufacturer. In addition, when ordering on the official website, you receive a money-back guarantee (including transportation costs) if the drug does not have a therapeutic effect.