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Liver failure (chronic and acute). Stages of intensive therapy for acute liver failure. Causes of chronic liver failure

Liver failure– this is a complex clinical symptoms, resulting from a violation of the compensatory capabilities and functions of the organ, as a result of which the liver cannot maintain homeostasis in the body and ensure normal metabolism in it. There are many reasons for the development of liver failure, but regardless of them, the same changes always occur in liver cells (hepatocytes). Hepatocytes are extremely sensitive to a lack of oxygen, so under certain conditions, liver failure can develop very quickly and be fatal.

Causes of liver failure

Chronic hepatitis and liver cirrhosis sooner or later lead to liver failure.

Liver diseases (acute and chronic hepatitis, cirrhosis, echinococcosis, etc.);
diseases associated with obstruction of the bile ducts, leading to hepatic hypertension and the development dystrophic changes in liver cells;
extrahepatic diseases (cardiovascular and endocrine systems, infectious and autoimmune diseases, etc.);
poisoning with drugs, poisonous mushrooms, chemicals;
extreme effects on the human body (extensive burns, injuries, traumatic and septic shock, massive blood loss and blood transfusions and other similar conditions).

Symptoms of liver failure

In the clinical picture of the disease, several main syndromes are distinguished.

Cholestasis syndrome

This syndrome occurs as a result of obstruction of the flow of bile through the biliary tract due to blockage, most often by a stone or tumor. As a consequence of this, one of the most striking manifestations of the disease occurs - jaundice. The severity of this symptom depends on the level of biliary obstruction. The skin, sclera and mucous membranes can take on various shades, from pale yellow to orange and greenish. With a long course of the pathological process, jaundice may not occur.

Cytolysis syndrome

This syndrome develops when hepatocytes are damaged, as a result of which liver cells cannot perform their function or die. As a result, a large amount of toxic substances enter the bloodstream, which the liver was supposed to neutralize. It is the cytolytic syndrome that causes the main symptoms of the disease.

If hepatocytes die, the patient begins to experience fever, weakness, loss and perversion of appetite, nausea, and sometimes vomiting. The liver may increase in size. Patients notice that the stool becomes light or completely discolored. The cardiovascular system suffers, tachycardia appears, and blood pressure may increase.

With a long chronic course of the disease, the symptoms of liver failure increase slowly and are often masked by signs of the underlying disease. Signs of metabolic disorders and endocrine disorders are detected (menstrual cycle disorders in women, gynecomastia in men). With further progression of the process, the nervous system suffers. Patients are lethargic, apathetic, drowsy, but sometimes the opposite reaction can be observed, expressed in the form of increased excitability, tremors of the limbs and convulsions. Impaired liver function leads to impaired kidney function, as a result of which harmful substances that are normally excreted in the urine accumulate in the body, which increases the symptoms of intoxication. As a result of impaired protein synthesis, anemia can develop.

Portal hypertension syndrome

This syndrome occurs with long-term progression of the process and is practically impossible to correct. Pressure increases in the liver venous system, resulting in edema and ascites (fluid accumulation in the abdominal cavity). There is also overflow of the superficial venous plexuses on the patient’s abdomen, this symptom is called “head of the jellyfish”. Varicose veins of the esophagus also occur, which can cause bleeding from them. Spider veins appear on the patient's chest and shoulders, and erythema (redness) of the palms attracts attention.

At acute course Liver failure symptoms increase very quickly, which can lead to the death of the patient. During the chronic process, several stages are distinguished:

The compensated (initial) stage of liver failure is characterized by all the symptoms described above, which can be expressed to varying degrees. This stage of the disease can last for years.
The decompensated (severe) stage is characterized by an increase in the symptoms of the first stage. Symptoms of the disease increase, patients may behave inappropriately, aggressively, disoriented, speech becomes slurred, slow, and tremor (shaking) of the limbs appears.
The terminal stage (dystrophic) stage is characterized by stupor, the patient can hardly be awakened, and apathy is replaced by excitement. Sometimes patients are completely non-communicative, but the reaction to pain is preserved.
The last stage of liver failure is hepatic coma. The patients are in unconscious, there is no reaction to painful stimuli, convulsions and pathological reflexes appear.

Treatment of liver failure

A patient with liver failure will be prescribed a number of medications (antibacterial, hepatoprotectors, vitamins, laxatives and others). It is unlikely that they will help get rid of the disease, but they will certainly improve a person’s quality of life.

Treatment of this serious disease is a very complex process, which depends on the stage and form of liver failure.

Patients need treatment for the underlying disease that led to the development of liver failure.
Patients are strongly recommended to follow a diet limiting protein to 40–60 g/day and table salt up to 5 g per day. If necessary, patients are transferred to tube feeding; fat emulsions can be used to increase the calorie content of the diet.
Antibacterial therapy begins immediately upon admission of the patient to the hospital; before receiving the results of an analysis of the sensitivity of microflora to antibiotics, broad-spectrum drugs (most often from the group of cephalosporins) are used.
Hypoammonemic drugs (Ornithine, Hepa-Merz) help reduce ammonia levels in the body.
Lactulose-based laxatives (Duphalac, Normaze) also help reduce the absorption of ammonia in the intestines and also suppress intestinal flora, which produces it. For constipation, patients are also given enemas with magnesium sulfate.
Patients may need hormonal and infusion therapy. In case of bleeding, vitamin K (Vikasol) is administered; in case of prolonged or massive bleeding, donor plasma is administered intravenously.
Vitamin therapy and replenishment of microelements. B vitamins, ascorbic, folic, nicotinic, glutamic, and lipoic acids are introduced. To maintain mineral metabolism, it is necessary to introduce calcium, magnesium and phosphorus.
When kidney failure occurs, patients may need hemodialysis to remove ammonia and other toxic substances from the patient's blood that are normally neutralized by the liver. At stages 3–4 of the disease, hemodialysis can improve the prognosis for patients.
With severe ascites, paracentesis is performed to evacuate fluid accumulated in the abdominal cavity.

Treatment of liver failure should only be carried out by a qualified specialist. Self-medication and treatment with folk remedies will inevitably lead to disastrous consequences.

Which doctor should I contact?

Treatment of liver failure is carried out by a hepatologist or gastroenterologist. Additionally, a consultation with an infectious disease specialist is prescribed (if viral hepatitis), oncologist (for liver cancer), cardiologist (for cardiac cirrhosis of the liver), neurologist (for the development of hepatic encephalopathy).

The liver works around the clock and tolerates our weaknesses, bad habits, stress, illness and the world around us. The liver has many functions: it neutralizes toxins, digests food, maintains the body's stability and does a lot of other work.

With the deterioration of the environment due to human activity, the spread of viral hepatitis and other infections, alcoholism and drug addiction, deterioration in the quality of food, in a sedentary manner life and with the development of the pharmaceutical industry, the load on our liver has increased significantly. And when all this happens at the same time and in large quantities, the liver may not be able to cope, and then the risk of developing liver failure develops, which, in turn, can lead to irreversible processes in the body and the death of the patient.

So, liver failure- this is a pathological condition, a syndrome characterized by damage to liver cells and disruption of the liver with the loss of its compensatory capabilities and basic functions, manifested by chronic intoxication of the body. Liver failure can lead to hepatic coma, that is, complete failure of the liver and extensive damage to the brain by decay products.

Some statistics!

From 50 to 80% of all cases of the disease die from liver failure.
Globally, an average of two thousand people die every year due to liver failure.
In 15% of cases of liver failure, the cause of its development cannot be explained.
The most common causes of liver failure are liver damage from alcohol, drugs and viral hepatitis.

Interesting Facts!

The liver has about 500 functions, and in one minute more than 20,000,000 chemical reactions occur in it.
When conducting experiments on animals, they found that after removal of the liver, the animals are in in good condition for 4-8 hours, and after 1-2 days they die in a state of hepatic coma.
Cirrhosis of the liver always manifests itself as liver failure.
Botkin's disease, or viral hepatitis A, in people over 40 years of age with a history of liver and gallbladder diseases, leads to liver failure in 40% of cases. Viral hepatitis A is considered to be a disease among the people childhood, which is quite easily tolerated (equated to chickenpox, rubella, scarlet fever, and so on).
Viral hepatitis E in pregnant women, 20% end in liver failure, while in men and non-pregnant women, viral hepatitis E may not manifest itself at all.
Taking such a seemingly ordinary drug as paracetamol, can lead to the development of fulminant liver failure (fulminant liver failure). And in many countries it is customary to take paracetamol in large doses for common colds and acute respiratory viral infections.
It is from liver failure that most people die due to poisoning with poisonous mushrooms (pale toadstools, fly agarics and others).
In most cases of liver failure in adults, in addition to other causes of the syndrome, the fact is revealed alcohol abuse.

Anatomy of the liver

Liver- an unpaired organ that is located in the upper right part of the abdominal cavity, or in the right hypochondrium. The liver is the largest endocrine gland.

Liver characteristics:

weight - about 1.5 kg,
shape - pear-shaped,
normal liver sizes in adults:
- oblique length - up to 15 cm,
- length of the right lobe - 11.0-12.5 cm,
- length of the left lobe - 6-8 cm,
- height - 8-12 cm,
- thickness - 6-8 cm,
the edges of the liver are smooth,
consistency - soft,
structure - homogeneous,
surfaces are shiny and smooth,
color - brown,
covered with peritoneum - a serous membrane that limits the organs of the abdominal cavity.
has the ability to regenerate (restoration).

Distinguish liver surface:

diaphragmatic surface- corresponds to the shape of the diaphragm,
visceral(addressed to the authorities) surface- adjacent to surrounding organs,
bottom edge - at an acute angle,
superior posterior edge - at an obtuse angle, rounded.

With the help of the falciform hepatic ligament, as well as two longitudinal and transverse grooves, the liver is divided into shares:

right lobe,
left lobe,
square for,
caudal lobe.

From the falciform ligament of the liver comes the circular ligament, which is a transformed umbilical vein, which in the womb connected the placenta to the fetus.

Between the quadrate and caudal lobes of the liver, in the right longitudinal groove there are the gates of the liver, which include the structures:

hepatic artery,
portal vein,
bile duct,
nerves and lymphatic vessels.

Liver regeneration

The liver is an organ that can completely restore its structure after damage, that is, it is capable of regenerating. Even if 70% of liver cells are damaged, it can recover to its normal volume. The same regeneration occurs in lizards when they “grow” their tail.

Liver restoration occurs through the proliferation of hepatocytes (growth and increase in their number), although scientists still do not know why this happens.

The rate of liver regeneration directly depends on age. In children, the speed of organ recovery and the volume to which it is restored is greater than in older people. Regeneration occurs slowly: for children this period is 2-4 weeks, and for older people - from 1 month. The speed and volume of regeneration also depends on individual characteristics and the disease that caused its damage.

Restoration of the liver is possible only if the causes of hepatitis are eliminated, the load on it is reduced, and the body receives a normal amount of useful nutrients.

The liver does not recover if there is an active infectious process in it (viral hepatitis).

Structure of the liver

Serosa- peritoneum.
Fibrous membrane- a capsule from which thin branches of connective tissue extend. They divide the parenchyma (the part of the organ that contains special functioning structures or an organ without membranes) of the liver into lobules.
Liver lobules- a structural and functional unit of the liver, its size is about 1 mm; the liver contains about half a million of them.
Kupffer cells- liver stellate macrophages, immune cells, are located in large numbers in the capillaries of the hepatic lobule. Perform a protective function for the liver.

Structure of the hepatic lobule:

Central lobule of the liver- located in the center of the hepatic lobule.
Hepatocytes- liver cells, which perform the secretory function of the liver, produce bile all the time. Liver cells are arranged in hepatic beams - in two layers. The hepatocyte is located between the bile canaliculus and the intralobular capillary.
Bile ducts- located between the hepatic beams, through which bile from hepatocytes enters the bile ducts.
Intralobular capillaries or sinusoids- blood vessels through which chemical compounds enter hepatocytes and processed substances exit them.

Blood vessels of the liver

Portal vein and hepatic artery - through these vessels, blood from the internal organs enters the liver, and the speed of blood flow in the liver slows down significantly, which contributes to the plethora of the organ;
Interlobular vessels, together with interlobular bile ducts, form the interlobular hepatic triad;
Circumlobular vessels;
Intralobular vessels or sinusoids;
Central vein - collects blood from the sinusoids of the hepatic lobule;
Collecting or sublobular vessels
Hepatic vein- carries blood to the inferior vena cava.

Biliary vessels of the liver

Bile ducts - do not have a membrane, are located between hepatocytes, and collect bile from them;
Interlobular bile ducts;
Around the lobular bile ducts;
Collecting bile ducts;
Bile ducts;
The gallbladder, where from all the bile ducts bile enters through the cystic duct, the gallbladder is a temporary reservoir for bile, where it settles and “matures”; gallbladder volume from 50 to 80 ml;
The common bile duct connects the gallbladder and hepatic ducts to the bulb duodenum where bile is needed to digest food.

Composition of bile

The liver secretes a huge amount of bile per day - up to 1 liter, at least half a liter.

Main function of bile- digestion of fats in the intestine, due to emulsification by bile micelles.

Bile micelles are particles of bile components surrounded by ions, part of a colloid.

Bile happens:

Young or liver bile- secreted directly from the liver, bypassing the gallbladder, has a yellowish straw color, transparent.
Mature or cystic bile- secreted from the gallbladder, has a dark olive color, transparent. In the gallbladder, fluid is absorbed from the bile and mucus (mucin) is released, so the bile becomes viscous and concentrated.
Basal bile- a mixture of young and mature bile, which enters the duodenum, golden yellow in color, transparent.

What is in bile?

Water - In bile, part of the water is about 97%; the main components of bile are dissolved in it.

Bile acids:
- cholic chenodeoxycholic acid - primary bile acids,
- glycocholic and taurocholic acids (compounds with amino acids),
- deoxycholic and lithocholic acids (secondary bile acids, formed in the intestines under the influence of intestinal microflora).
Bile acids are formed from cholesterol in hepatocytes. They are found in bile in the form of salts and anions. The role of bile acids is important in the digestion of fats and the absorption of fatty acids and triglycerides in the intestine. Some of the bile acids are absorbed in the intestines back into the blood and again enter the liver.

Bile pigments:
- bilirubin
- biliverdin.
Bile pigments are formed from hemoglobin in the spleen and Kupffer cells. Any red blood cell is formed in the red bone marrow (erythropoiesis) and destroyed in the spleen, and a small part of them in the liver. Red blood cells contain hemoglobin, which carries oxygen atoms and carbon dioxide, that is, it carries out gas exchange in tissues. After the destruction of the red blood cell, the question arises about the utilization of hemoglobin. Bile pigments are intermediate products of the breakdown of hemoglobin; they are excreted from the body with the help of bile.
These pigments color bile yellow, green and brown colors. And also, after binding to oxygen, it slightly stains urine (urobilinogen) and feces (stercobilinogen).

Liver phospholipids (lecithins)- are formed by the synthesis of phospholipids that come from food. It differs from ordinary phospholipids in that they are not affected by pancreatic enzymes, and in an unchanged form, together with bile acids, participate in the digestion of fats and are partially absorbed back into the blood and enter hepatocytes, and then into bile.

Cholesterol- found in bile in free form or in the form of bile acids synthesized from it. Enters the body with food. Participates in the digestion of fats in the intestines.

Ions:
- sodium,
- calcium,
- potassium,
- chlorine,
- bicarbonates
The ions enter the blood and liver along with food. Their main role is to improve the permeability of cell walls, and the ions are part of the micelles in the small intestine. Due to them, water is absorbed from bile in the gallbladder and its concentration, as well as improved absorption of nutrients in the intestinal wall.

Bile also contains immunoglobulins, heavy metals, and foreign chemical compounds that come from the environment.

Schematic representation of a bile micelle.

Basic functions of the liver - the main laboratory of the body

Bile formation- bile promotes the breakdown and absorption of fat in the intestines.
Detoxification of toxins and other foreign substances, coming from the outside, converting them into harmless substances, which, in turn, are excreted by the kidneys in the urine. This occurs through chemical reactions in hepatocytes (biotransformation). Biotransformation is carried out by combining with proteins, ions, acids and other chemicals.
Participation in protein metabolism- the formation of urea from the breakdown products of protein molecules - ammonia. At elevated levels, ammonia becomes poisonous to the body. Urea from the liver enters the blood and is then excreted through the kidneys.
Participation in carbohydrate metabolism- when there is an excess of glucose in the blood, the liver synthesizes glycogen from it - the glycogenesis reaction. The liver, as well as skeletal muscles, are depots for glycogen reserves. When there is a lack of glucose in the body, glycogen is transformed into glucose - the reaction of glucogenolysis. Glycogen is the body's supply of glucose and energy for the functioning of the musculoskeletal system.
Participation in fat metabolism- with a lack of fat in the body, the liver is able to synthesize carbohydrates (namely glycogen) into fats (triglycerides).
Disposal of hemoglobin breakdown products by converting it into bile pigments and excreting them with bile.
Hematopoiesis in the fetus during pregnancy. The liver is also involved in the formation of blood clotting factors.
Destruction and disposal of excess hormones, vitamins and other biologically active substances.
Depot for some vitamins and microelements, such as vitamins B 12, A, D.

Causes and pathogenesis of liver failure

The mechanism of development of liver failure by stages

Impact unfavorable (hepatotoxic) factors on the membrane of liver cells - hepatocytes.
Start from hepatocytes release enzymes, which continue to destroy (digest) liver cells.
The immune system begins to secrete autoimmune antibodies to damaged hepatocytes, which completely destroy them (necrosis of liver tissue).
Spreading this process to other hepatocytes.
When 70-80% of liver cells are affected, liver failure.
Full or partial loss of liver function.
During a long process, they form anastomoses(additional vessels that, bypassing damaged areas, unite intact vessels) between the portal and inferior vena cava (normally they are connected by liver vessels). Through these anastomoses, blood circulates without entering the liver, which reduces the chances for liver regeneration.
Metabolic acidosis- entry into the blood of toxins that are not processed by the liver, damaging all systems and tissues, possibly damaging the brain.
Violation of all metabolic processes in the body, since the liver stops synthesizing and storing glycogen, forming urea and removing ammonia from the body.
Disruption of the biliary system - bile stagnation (or cholestasis) leads to the release of a large amount of bilirubin into the blood, which has a toxic-allergic reaction to all systems, organs and tissues. In this case, the liver may increase in size.
Hepatic encephalopathy- damage by brain decay products.
Hepatic coma- damage to large areas of the central nervous system is often an irreversible process.

Causes of liver failure

A disease that can lead to liver failure syndrome	Reasons for the development of this disease	What happens in the liver?
Cirrhosis of the liver	Alcohol abuse. Chronic viral hepatitis. Working with toxins, poisons, chemicals, heavy metals, paints and so on. Taking many medications (especially long-term): nonsteroidal anti-inflammatory drugs(paracetamol, analgin, nimesulide and others), antibiotics and antiviral drugs(aminoglycosides, tetracyclines, anti-tuberculosis drugs, antiretroviral drugs for the treatment of AIDS and many others), cytostatics(drugs for the treatment of autoimmune diseases and cancer), any other medicines. Drug use precursors (ingredients for the synthesis of drugs) and psychotropic drugs. Diseases of the biliary system: cholecystitis, biliary dyskinesia, cholelithiasis. Frequent use in food dyes, preservatives, flavor enhancers, which are widely used in this moment in the food industry. Abuse fatty, fried, spicy, salty or smoked foods. Eating poisonous mushrooms (pale toadstool, fly agarics and others). Common infectious diseases(sepsis, HIV, influenza and others). Autoimmune diseases - diseases in which the immune system perceives its own as foreign, affecting its own cells. Congenital liver pathologies(congenital viral hepatitis, congenital tuberculosis, atresia (absence) of blood or biliary vessels, etc.) Other liver diseases in the absence of proper treatment, the presence of concomitant diseases and other factors of stress on the liver, especially dietary disorders.	The development of liver cirrhosis is long, sometimes last for years. Under the influence of hepatotoxic factors, partial destruction of hepatocytes constantly occurs, but thanks to the regenerative function of the liver, hepatocytes are partially restored. With prolonged continuous exposure to toxic factors, when autoimmune processes are involved, the gene material of liver cells changes. In this case, the liver tissue gradually begins to be replaced by connective tissue (which does not have specialized functions). The connective tissue deforms and blocks the hepatic vessels, which increases the pressure in the portal vein (portal hypertension), resulting in the appearance of vascular anastomoses between the portal and inferior vena cava, the appearance of fluid in the abdominal cavity - ascites, and an enlarged spleen - splenomegaly. At the same time, the liver decreases in size, shrinks, and liver failure syndrome appears.
Dystrophies liver (hepatosis): Parenchymal fatty liver degeneration	overeating fats and carbohydrates, diseases gastrointestinal tract, poor nutrition, starvation, anorexia, bulimia, eating badger, bear, dog, camel fats and so on.	The entry of excess fat into the liver (also increased content of carbohydrates in the liver, increased glycogen consumption) or difficulty in the exit of fats from the liver (lack of proteins, disruption of liver enzyme function) lead to the deposition of “excess” fat (triglycerides) in the cytoplasm of hepatocytes. Fat accumulates and gradually ruptures the hepatocyte. Adipose tissue gradually replaces liver tissue, leading to liver failure syndrome.
Parenchymal protein degeneration of the liver	protein metabolism disorder, congenital deficiency of liver enzymes for protein processing, diabetes and other endocrine diseases, alcoholism, viral hepatitis, cholestasis (stagnation of bile in the liver), intoxication in infectious diseases, hypo- and avitaminosis, intoxication as a result of taking medications, drugs, poisonous mushrooms, poisons, chemicals, and so on.	There are three types of proteinaceous liver dystrophy: Granular dystrophy liver- deposition of “extra” protein in the cytoplasm of hepatocytes, while the liver increases in size due to an increase in the water content in hepatocytes (protein molecules attract water molecules by osmosis). This process is also reversible and occurs quite often. Hydropic liver dystrophy - due to a lack of protein in the liver, fluid accumulation in the cytoplasm of hepatocytes is observed. Excess fluid is produced in the cytoplasmic vacuole. At the same time, the liver increases in size. With a long process, hepatocytes are destroyed, balloon degeneration of the liver and its necrosis develop, and as a result, liver failure. Hyaline droplet dystrophy develops as a result of alcoholism, the breakdown products of alcohol with excess protein form hyaline bodies (Mallory bodies). This hyaline accumulates in hepatocytes. At the same time, liver cells lose fluid and begin to produce connective tissue. At this stage, liver cirrhosis may develop. Hyaline can also destroy the hepatocyte wall, leading to its necrosis. In any case, sooner or later liver failure develops.
Parenchymal carbohydrate dystrophy of the liver	glycogen metabolism disorder, diabetes, lack of enzymes for reactions with glycogen, hypo- and avitaminosis, alcoholism and other types of liver intoxication.	Glycogen is normally deposited in the cytoplasm of hepatocytes. With the development of carbohydrate dystrophy, glycogen accumulates not in the cytoplasm, but in the nucleus of the hepatocyte. At the same time, hepatocytes increase significantly in size. With a long process, hepatocytes die or develop connective tissue(cirrhosis of the liver). The outcome is liver failure.
Mesenchymal liver dystrophy or liver amyloidosis	chronic infectious diseases (tuberculosis, syphilis, osteomyelitis and others), immune system diseases, genetic predisposition to amyloid formation.	Amyloidosis- a systemic disease associated with disruption of the immune system, characterized by the deposition of amyloid (insoluble protein) in the wall of the hepatic vessels and bile ducts. Amyloid is produced in mutating immune cells: plasma cells, eosinophils, immunoglobulins, and so on. Condensed liver vessels cannot function fully, there is stagnation of bile in the liver, portal hypertension (increased pressure in the portal vein), and then liver failure.
Hepatitis - inflammation of the liver	viral hepatitis A, B, C, D, E, F. alcoholism, effects on the liver of toxic substances and factors.	The pathogenesis of viral hepatitis is quite complex. But the main role in the damage to hepatocytes is played by immunity. If in viral hepatitis A and E the immune system promotes the release of hepatocytes from the virus, then in viral hepatitis B, D, and F the immune system attacks infected hepatocytes along with the virus. And when special immunoglobulins are produced, the immune system still removes viruses from the liver cells and recovery occurs. Recovery from all viral hepatitis is possible only with the elimination of other hepatotoxic factors, otherwise chronic hepatitis, necrosis or cirrhosis of the liver develops, and the outcome is liver failure. With viral hepatitis C (experts call it “ gentle killer"), elimination of the virus does not occur due to its variability. And the outcome of this disease is chronic hepatitis, cirrhosis or liver cancer, and then liver failure. In addition to liver problems with portal hypertension varicose veins develop in the portal system, as well as overload of the lymphatic system, which ceases to completely collect fluid from the abdominal cavity. Complications of portal hypertension develop: ascites or accumulation of fluid in the abdominal cavity, while the abdomen increases in size, and the amount of fluid in the abdomen reaches up to 5-10 liters; bleeding from varicose veins of the esophagus - can lead to the death of the patient; splenomegaly or enlargement of the spleen, accompanied by a violation of its function.

Can also lead to liver failure extrahepatic causes:

hypo- or avitaminosis,
chronic renal failure(CRF),
hormonal diseases,
lack of oxygen in the body, including anemia,
massive blood loss,
transfusion of incompatible blood group,
surgical operations in the abdominal cavity.

Types of liver failure

There are acute and chronic liver failure.

Acute liver failure

- a type of liver failure that develops as a result of rapid liver damage. The clinical picture of this syndrome develops very quickly (from several hours to 8 weeks) and also quickly leads to hepatic encephalopathy and coma.

It is also possible to develop liver failure at lightning speed - fulminant liver failure, which more often occurs when poisoned by poisons, chemicals, drugs, and so on.

Causes that can lead to acute liver failure:

Depending on the reasons for development, they distinguish forms of acute liver failure:

Endogenous or hepatocellular form- occurs when liver cells are damaged as a result of exposure to hepatotoxic factors. Characterized by rapid necrosis (or death) of hepatocytes.
Exogenous form- develops as a result of a violation of the hepatic and/or extrahepatic circulation (in the portal and inferior vena cava systems), most often with cirrhosis of the liver. In this case, blood with toxic substances bypasses the liver, affecting all organs and systems of the body.
Mixed form- when exposed to both hepatocellular and vascular factors affecting liver function.

After the development of acute liver failure, all toxins that come from the environment or are formed as a result of metabolism have a negative effect on the cells of the entire body. When the brain is damaged, hepatic encephalopathy occurs, then coma and death of the patient.

Acute liver failure - extremely serious condition body, requiring immediate detoxification therapy.

Disease prognosis- in most cases, the unfavorable chance of restoring the vital functions of the liver depends on the ability of the liver to regenerate (its compensatory capabilities), the time before the start of treatment, the degree of brain damage and the elimination of hepatotoxic factors. Acute liver failure itself is a reversible process. And they recover from hepatic coma only in 10-15% of cases.

Chronic liver failure

Chronic liver failure is a type of liver failure that develops gradually with prolonged (chronic) exposure to hepatotoxic factors (from 2 months to several years).

It is characterized by the gradual development of symptoms against the background of exacerbation of chronic diseases of the liver and biliary system.

Causes of chronic liver failure:

As with acute liver failure, there are forms:

exogenous form- damage and necrosis of liver cells occurs gradually, some of the cells are regenerated, but with continued exposure to unfavorable factors, the death of hepatocytes continues.
endogenous form- liver circulatory disorders,
mixed form.

In chronic liver failure, the compensatory capabilities of the liver are more developed, that is, the liver has time to restore some of its cells, which partially continue to perform their functions. But toxins that are not utilized in the liver enter the bloodstream and chronically poison the body.

In the presence of additional hepatotoxic factors, decompensation occurs (loss of the ability to regenerate hepatocytes), and hepatic encephalopathy and then coma and death.

Factors that can lead to encephalopathy and coma in chronic liver failure:

alcohol consumption,
self-administration of medications,
violation of diet, eating large amounts of proteins and fats,
nervous stress,
common infectious process (sepsis, influenza, meningococcemia, chicken pox, tuberculosis and others),
pregnancy, childbirth, termination of pregnancy,
abdominal surgeries and so on.

Current - heavy. As liver failure increases, the patient's condition gradually worsens.

The disease requires urgent adequate treatment and detoxification.

Forecast: unfavorable, in 50-80% of cases of hepatic encephalopathy the patient’s death occurs. In case of compensated chronic liver failure, liver restoration is possible only if all hepatotoxic factors are eliminated and adequate therapy is carried out. Often chronic liver failure in its initial stages is asymptomatic and the diagnosis can be made only on the basis of data from targeted examinations. This is the reason for untimely diagnosis and treatment of the disease, which significantly reduces the chances of recovery.

Photo: liver preparation of a patient suffering from cirrhosis of the liver. The liver is wrinkled, reduced in size, and dilation of the hepatic vessels is observed. The liver tissue was completely overgrown with connective tissue.

What is the difference between acute and chronic liver failure (features)?

Criteria	Acute liver failure	Chronic liver failure
Development timeframe	From a few days to 8 weeks.	From 2 months to several years.
Development mechanism	Develops as a result of rapid necrosis of liver tissue or sudden violation liver blood circulation.	Liver necrosis occurs gradually, some of the damaged cells have time to regenerate, and the liver is able to partially compensate for its functions. It can also develop with a gradual disruption of blood circulation.
Degree of liver damage	Rapid damage to more than 80-90% of all liver cells.	Gradual damage to more than 80% of hepatocytes. Chronic liver failure almost always contributes to the development of symptoms of portal hypertension, in contrast to the acute course of liver failure, in which portal hypertension is not an obligatory symptom.
Severity of the current	The course of the disease is extremely severe, more severe than with chronic liver failure.	The course is severe, in the initial stages it is possible asymptomatic.
Forecast	The prognosis is unfavorable, hepatic encephalopathy and then coma often develop. But the process is reversible with timely treatment and elimination of hepatotoxic factors.	The prognosis is unfavorable; in the absence of timely treatment and elimination of provoking factors, sooner or later it leads to hepatic encephalopathy. Chronic liver failure is an irreversible process. Treatment is aimed at preventing the development of hepatic coma.

Symptoms of liver failure

Group of symptoms	Symptom	How it manifests itself	Mechanism of occurrence
Cholestasis syndrome	Jaundice	Coloring skin and visible mucous membranes in yellow shades: from green and lemon to orange. In dark-skinned people, jaundice may be noticeable only on the mucous membranes, especially on the sclera of the eyeballs.	Cholestasis syndrome associated with impaired outflow of bile from the liver. This occurs due to compression of the biliary tract and the inability of damaged hepatocytes to remove bile. In this case, the breakdown product of hemoglobin, bilirubin, is not excreted in bile and feces. There is a large amount of bile pigments in the blood (bilirubin and biliverdin), which ensure that all tissues are colored in the color of bile. But stool loses its staining with stercobilin. The kidneys try to remove excess bilirubin from the blood, and an increased content of bile pigments in the urine is observed, and as a result, its more intense coloring. An increased amount of bilirubin also has a toxic-allergic effect on the skin, which contributes to the development of itching.
	Stool discoloration	The feces become light in color, up to white and beige.
	Darkening of urine	The color of urine becomes darker, it is compared to the shades of dark beer.
	Itchy skin	A patient with cholestasis is accompanied by itching all over the body, although there may not be a rash.
	Pain in the right hypochondrium	Not a necessary symptom for liver failure. The pain may appear after eating and is aching or cramping in nature.	Pain in the right hypochondrium occurs due to obstruction of the biliary vessels. In this case, the bile bursts the bile ducts and compresses the lobular nerves.
Dyspeptic disorders	Nausea, vomiting, stool disturbances, decreased and perverted appetite.	Nausea and vomiting are associated with food intake and are periodic or constant. Stool disorders in the form of diarrhea, more than 3 times a day. Poor appetite, to the point of refusing to eat. Some patients have a desire to try inedible things (soil, chalk, hair, incompatible foods, etc.).	Digestive disorders are associated with the inability of the liver to participate in the digestion of fats. Decreased appetite may also be a sign of damage to the nervous system and intoxication, which develops against the background of liver necrosis.
Intoxication symptoms	Increased body temperature, weakness, malaise, joint pain (arthralgia), loss of appetite.	Body temperature can rise to high numbers or be constant low-grade (up to 38C). Weakness and malaise are mild or leave the patient bedridden. Arthralgia in large or all groups of joints.	Intoxication symptoms develop as a result of liver tissue breakdown products entering the bloodstream. In acute liver failure, these symptoms are more pronounced than in the chronic form. Intoxication can also be caused by viral hepatitis; in this case, not only toxins from the destroyed liver enter the blood, but also toxins released during the life of the virus.
Changes in liver size	Enlarged liver (hepatomegaly)	These changes in the liver can be determined by a doctor by palpation of the abdomen, as well as by conducting additional research methods.	Liver enlargement is a common symptom of liver failure associated with circulatory disorders in the hepatic vessels, cholestasis, the presence of hepatosis, as well as tumors, cysts, abscesses, tuberculosis, and so on.
Changes in liver size	Liver shrinkage		A shrinkage of the liver is observed in liver cirrhosis, when the liver tissue is completely replaced by connective tissue.
Portal hypertension syndrome	Ascites	The abdomen increases significantly in size, reminiscent of pregnancy.	Ascites is the accumulation of fluid in the abdominal cavity. Its development is associated with impaired patency of the lymphatic vessels, which develops as a result of their compression in the liver by dilated hepatic vessels. Lymphatic system promotes fluid drainage in soft tissues.
	Spider veins	Spider veins are dilations of blood vessels and resemble jellyfish in appearance. Appear on the front wall of the abdomen and on the shoulders.	Spider veins are dilated vessels that arise from the portal veins. Against the background of portal hypertension, anastomoses develop - additional (abnormal) vessels that connect larger veins to each other. Thus, the body tries to restore impaired blood circulation.
	Splenomegaly - enlarged spleen	This symptom can be determined using abdominal palpation and instrumental research methods.	Splenomegaly develops due to circulatory disorders in the spleen, which is a blood depot. It is supplied with blood from the portal and inferior vena cava systems. When the pressure in these vessels increases, more blood is deposited in the spleen. The spleen also takes on some of the functions of the liver, in particular the destruction of red blood cells and the utilization of hemoglobin.
	Bleeding from dilated veins of the esophagus	There is vomiting of bloody contents (or “coffee grounds”), sometimes blood remains are detected only in the stool (melena). It can be acute or chronic. The amount of blood loss also differs individually. It is necessary to differentiate from pulmonary hemorrhage, when the secreted blood is bright scarlet in color, with air bubbles. Aspiration of blood is dangerous (blood entering the lungs - suffocation).	The veins of the esophagus dilate due to portal hypertension. Constantly and long-term dilated vessels lose their mobility and permeability, which is why bleeding occurs from them. Bleeding is also promoted by a blood clotting disorder (associated with liver dysfunction, one of which is the synthesis of certain clotting factors).
Hepatic encephalopathy	Nervous system dysfunction	Dizziness, lethargy, sleep disturbance, confusion or loss of consciousness, inattention, memory loss, lethargy, "blurred mind" increased excitability, delirium, impaired coordination of movements, anxiety, apathy, depression and so on.	Metabolic products and toxins are not neutralized in the liver due to its insufficiency, and affect the structures of the brain, encephalopathy develops. Further brain damage can lead to hepatic coma.
Pulmonary symptoms	Shortness of breath, cough	Patients may complain of difficulty breathing, increased breathing (more than 20 per minute at rest for adults). Shortness of breath first appears during physical activity, and then during rest, especially in the supine position. During sleep, there may be attacks of sudden rapid breathing (the patient develops a fear of suffocation). To facilitate breathing, patients take a forced sitting position. There may also be a cough that produces bloody, blistered sputum.	The appearance of pulmonary symptoms is associated with an increase in pulmonary edema. Pulmonary edema - blood filling pulmonary vessels. This occurs due to disturbances in protein metabolism as a result of liver damage. The blood simply begins to sweat through the walls of the vessels into the alveoli. The development of this symptom is life-threatening, since when the alveoli are completely filled with liquid, breathing may stop.
Circulatory disorders	Promotion blood pressure, Heart arythmy .	Increased blood pressure over 140/90 mm Hg. Art. Arterial hypertension will soon be replaced by hypotension, a decrease in pressure below 90/60 mmHg. Art. Cardiac arrhythmia first manifests itself as bradycardia (less than 60 beats per hour), and then as tachycardia (more than 90 beats per hour).	Violations of general circulation are associated with portal hypertension. In the presence of edema and ascites, fluid leaves the bloodstream in large quantities and enters the soft fabrics. This reduces blood pressure. The work of the heart is also associated with these changes in the bloodstream, and arrhythmia appears.
Amyotrophy	Muscle weakness	The muscles decrease in size, become flabby, and weak. It is difficult for the patient to perform even the simplest physical exercises.	Muscle atrophy is associated with a lack of glycogen, the main source of energy for muscle function. The conversion of glucose into glycogen occurs in the liver, and in liver failure, glycogen is practically not synthesized. After using up stored glycogen, skeletal muscle atrophy gradually increases.
Bleeding disorder	Bleeding	Bleeding from dilated veins of the esophagus, from the vessels of the stomach, nosebleeds, hemorrhagic rash (like bruises), and so on.	Blood clotting disorders occur due to the liver’s failure to perform its function - the formation of blood clotting factors. In this case, the blood becomes “liquid”, and it is extremely difficult to stop the bleeding.

Also, with liver failure, anemia, pulmonary heart failure, acute or chronic renal failure, and intestinal paresis may develop. Absolutely all organs and systems of the body suffer.
Liver failure is characterized by a specific liver odor from the mouth.

Photo of a patient with manifestations of jaundice.

Acute liver failure, clinical features

Stages of acute liver failure:

Latent stage of hepatic encephalopathy - at this stage, patients have no complaints and no pronounced symptoms of liver damage. Changes can only be detected through examination.
Stage I of hepatic encephalopathy - precoma. At the same time, symptoms of liver failure increase: syndromes of cholestasis, portal hypertension, intoxication symptoms, and the first symptoms of damage to the nervous system appear in the form of its inhibition.
Stage II of hepatic encephalopathy - precoma. At this stage, the patient’s condition becomes aggravated, the symptoms of hepatic encephalopathy increase, inhibition is replaced by excitation of the nervous system, and a few pathological reflexes appear. Symptoms of blood clotting disorders become more pronounced, intoxication increases, the liver sharply decreases in size, and cannot be detected by palpation (symptom of “empty hypochondrium”). At this stage, a liver odor appears from the mouth.
Coma- loss of consciousness, the patient exhibits reflexes only to stronger stimuli, signs of multiple organ failure appear (simultaneous hepatic, pulmonary, cardiac, renal failure, cerebral edema).
Deep coma- the patient is unconscious, being observed complete absence reflexes to any stimuli as a result of cerebral edema, multiple organ failure develops. In most cases, this is an irreversible process and the patient’s death occurs.

The main feature of acute liver failure is that each stage lasts from several hours to several days, less often weeks.

A favorable fact is the possibility of reversibility of the process in the case of timely detoxification therapy in the early stages.

Chronic liver failure, clinical features

Photo of a patient with liver cirrhosis and chronic liver failure syndrome. There is a significant increase in the abdomen due to ascites; dilated vessels are visible on the anterior wall of the abdomen. The skin is icteric, dry, the muscles are flabby.

Stages of chronic liver failure:

Stage I - The functionality of the liver is still preserved. This stage is characterized by the appearance of dyspeptic disorders and mild intoxication (weakness, drowsiness).
Stage II - an increase in dyspeptic disorders, intoxication, the appearance of symptoms of damage to the nervous system in the form of inhibition, memory loss, and impaired motor coordination. A liver odor appears from the mouth. At this stage, short-term memory loss is possible. At this stage, the liver only partially performs its functions.
Stage III - significant decrease in liver functionality. Previously occurring symptoms become more pronounced. Manifestations of cholestasis and portal hypertension, blood clotting disorders, aggravation of the nervous system (severe weakness, speech impairment) appear.
Stage IV (hepatic coma) - the liver completely dies and does not function at all. There is loss of consciousness, decreased reflexes, then their absence. Brain swelling develops. Multiple organ failure increases. Most often, this is an irreversible process and the patient dies.

Features of clinical manifestations of chronic liver failure:

each stage develops gradually, over weeks, months, years;
obligatory symptoms are manifestations of portal hypertension;
all symptoms are less pronounced than in the acute course of the syndrome.
Chronic liver failure is an irreversible process and will sooner or later lead to hepatic encephalopathy and coma.

Diagnosis of liver failure

Examination of the patient by a general practitioner, hepatologist or gastroenterologist, or in case of coma - by a resuscitator- determining the history of life and illness, identifying the above symptoms, determining the size of the liver, assessing the condition of the skin and visible mucous membranes.

Laboratory methods for studying the condition of the liver

Laboratory diagnostics allows us to evaluate functional state liver, the degree of its damage.

Indicators	Norm of indicators*		Changes in liver failure

Total bilirubin	Total bilirubin: 8 - 20 µmol/l, indirect bilirubin: up to 15 µmol/l, direct bilirubin: up to 5 µmol/l.			A significant increase in bile pigments - 50-100 times or more, up to 1000 µmol/l. Hepatic encephalopathy occurs when the bilirubin level is more than 200 µmol/l.
AlT(alanine aminotransferase)	0.1 - 0.68 µmol/l or up to 40 IU			Transaminases are enzymes that are released from deteriorating liver or heart cells. The more transaminases, the more pronounced the process of necrosis of liver tissue. In liver failure, transaminases increase tenfold. With complete destruction of the liver, a sharp decrease in transaminase levels is observed.
AsT(aspartate aminotransferase)	0.1 - 0.45 µmol/l or up to 40 IU
Thymol test	0 - 5 units - negative test.			Thymol test - determination of the qualitative ratio of protein components of blood serum. A positive test indicates the presence of a protein metabolism disorder; it is almost always positive in liver failure.
De Ritis coefficient	1,3 - 1,4			This ratio reflects the ratio of AST to ALT. In case of liver failure due to chronic liver diseases, this indicator increases to more than 2. And in the acute process of viral hepatitis, on the contrary, it decreases to less than 1.
GGT(gamma glutamate transferase)	6 - 42 U/l for women, 10 - 71 U/l for adults.			GGT is an enzyme involved in protein metabolism. In case of liver failure, this figure can increase several times if the patient has symptoms of bile stagnation. Interestingly, GGT is used by narcologists in diagnosing alcoholism.

Glucose	3.3 - 5.5 mmol/l			There is a decrease in glucose levels or, less commonly, an increase, this is due to a violation of carbohydrate metabolism, in which the liver plays an important role.
Urea	2.5 - 8.3 mmol/l			In liver failure, a decrease in urea levels is observed, this is due to disturbances in protein metabolism, the lack of synthesis of urea in the liver from ammonia - protein breakdown products.
Total protein, globulins, albumins	Total protein: 65 - 85 g/l, globulins: 20 - 36 g/l, albumins: 30 - 65 g/l			Level reduction total protein, albumins and globulins occurs due to a disorder of protein metabolism
Cholesterol	3.4 - 6.5 mmol/l			An increase in cholesterol levels is observed with severe cholestasis syndrome, but with further liver necrosis, a sharp decrease in cholesterol levels occurs.
Iron	10 - 35 µmol/l			An increase in the level of iron in the blood is associated with necrosis of hepatocytes, in which it is deposited as a result of the destruction of hemoglobin.
Alkaline phosphatase	Up to 240 units/l for women and up to 270 units/l for men			In liver failure there is an increase in activity alkaline phosphatase 3 - 10 times due to cholestasis syndrome, inner shells The biliary tract is a source of alkaline phosphatase.
Blood ammonia	11-32 µmol/l			With liver failure, the level of ammonia nitrogen in the blood increases up to 2 times; with the increase of hepatic encephalopathy, the level of ammonia increases.
Fibrinogen	2 - 4 g/l			There is a decrease in fibrinogen levels due to disruption of its formation in the liver. Fibrinogen is a blood clotting factor; its deficiency, together with the deficiency of other factors, leads to the development of hemorrhagic syndrome.

Hemoglobin	120 - 140 g/l			With liver failure, there is always a decrease in hemoglobin of less than 90 g/l. This is due to disturbances in protein and iron metabolism, as well as the presence of blood loss in hemorrhagic syndrome.
Leukocytes	4 - 9*10 9 /l			An increase in the level of leukocytes and ESR accompanies intoxication syndrome due to liver necrosis or the action of viral hepatitis, that is, inflammation.
ESR(erythrocyte sedimentation rate)	2 - 15 mm/h
Platelets	180 - 320*10 9 /l			There is a decrease in the level of platelets due to an increased need for them, as a result of hemorrhagic syndrome.

Color	Straw, light yellow			Darkening of urine, the color of dark beer, is associated with the appearance of bile pigments in it, due to cholestasis.
Urobilin	5 - 10 mg/l			Increased levels of urobilin in urine are associated with cholestasis syndrome and impaired metabolism of bile pigments.
Protein	Normally there is no protein in urine			The appearance of protein in the urine is associated with a disorder of protein metabolism and may indicate the development of renal failure.

Stercobilin	Normally, stercobilin is present in stool and contributes to the yellow-brown color of stool.			The absence of stercobilin in feces is associated with a violation of the outflow of bile.
hidden blood	Fine hidden blood should not be in stool			The appearance of occult blood in the stool indicates the presence of bleeding from dilated veins of the esophagus or stomach.
Blood test for viral hepatitis
Markers viral hepatitis A: Ig M HAV; viral hepatitis B: antibodies to HBs antigen; viral hepatitis C: Anti-HCV		Normally, in a person who does not suffer from viral hepatitis, markers for hepatitis are not detected.		Determination of markers for viral hepatitis indicates an acute or chronic process.

*All indicator standards are indicated for adults only.

Instrumental methods for diagnosing liver diseases

Using special equipment, you can visualize the liver, assess its condition, size, the presence of additional formations in it, the condition of the liver vessels and bile ducts.

Additional research methods for liver failure

Additional examination is necessary to assess the condition of other organs, since liver failure affects the entire body.

radiography of organs chest,
CT or MRI of the brain,
fibrogastroduodenoscopy (probing of the esophagus, stomach, duodenal bulb),
others according to indications.

Treatment of acute liver failure

Basic principles of treatment of acute liver failure:

The most important thing, if possible, is to eliminate possible reason development of liver failure.
Treatment must be started immediately.
Hospitalization is required! Acute liver failure is treated only in a hospital setting, with severe encephalopathy - in the intensive care unit.
Treatment is aimed at maintaining the body’s condition and metabolism.
If we exclude the cause of the development of liver failure and fully support the patient’s life support for 10 days, regeneration of hepatocytes occurs, which allows the patient to survive.

Stages of intensive care for acute liver failure

Treatment of chronic liver failure

Principles of treatment of chronic liver failure:

treatment of diseases that led to the development of liver failure,
symptomatic treatment,
treatment and prevention of complications of liver failure.
Traditional medicine is powerless in treating this syndrome!
Diet is one of the main measures aimed at restoring liver cells and reducing the formation of ammonia in the body. Protein-free diet.
Cleansing the intestines, since pathogenic intestinal microflora promotes the formation of ammonia and its absorption into the blood, and the liver has lost its ability to form urea from ammonia. To do this, cleansing enemas are prescribed 2 times a day.
It is necessary to correct the main metabolic indicators, according to biochemical research blood (electrolytes, lipoproteins, glucose, etc.).
In addition to taking basic medications, if there are complications, it is necessary to treat them.

The main medications used for chronic liver failure

Type of drugs	Representatives	Mechanism of action	How to use
Lactulose	Dufalak, Normaze, Good luck, Portolac	Lactulose changes the acidity of the intestines, thereby inhibiting the pathogenic intestinal microflora that releases nitrogen. Nitrogen is absorbed into the blood and combines with hydrogen atoms in water to form ammonia. A damaged liver is unable to form urea from this ammonia, and ammonia intoxication occurs.	30 - 50 ml 3 times a day with food. Lactulose can be used long-term.
Broad-spectrum antibiotics	Neomycin has proven itself most well in the treatment of liver failure.	Antibiotics are necessary to suppress intestinal microflora that produces ammonia. You can use any antibacterial drugs, with the exception of those that have a hepatotoxic effect.	Tablets 100 mg - 1-2 tablets 2 times a day. The course of treatment is 5-10 days.
Amino acids	Glutamic acid	Amino acids of these groups bind ammonia in the blood and remove it from the body. Prescribed for ammonia intoxication resulting from chronic liver failure. Cannot be used with Vikasol (vitamin K), which is prescribed to stop bleeding, for example from dilated veins of the esophagus.	Orally 1 g 2-3 times a day. The course of treatment lasts from 1 month to 1 year.
	Ornithine (ornicetyl)		Inside, 3 g granules, diluted in a glass of liquid 2-3 times a day. For intravenous drip administration - 20-40 g/day per 500 ml of 5% glucose or saline solution.
Detoxification infusion therapy	Glucose 5%	Glucose helps replenish necessary energy reserves.	Up to 200 - 500 ml per day of each solution intravenously. In total, up to 2 - 3 liters of solutions can be poured per day, only under control of the volume of urine excreted (diuresis).
Detoxification infusion therapy	Sodium chloride solution 0.9% (saline solution), Ringer's solution, Lact	Electrolyte solutions replenish the volume of circulating blood, the electrolyte composition of the blood improves blood supply to the liver.
Potassium preparations	Potassium chloride	Replenishes the lack of potassium, which almost always occurs with liver failure. Only under control of the level of potassium in the blood, since its excess can lead to heart failure.	10 ml of 4% solution diluted in 200 ml of any liquid for infusion.
Vitamins	Vitamin C	Many vitamins are antioxidants, improve the condition of the vascular walls, improve blood circulation, and help improve the regeneration of liver cells.	Up to 5 ml per day intramuscularly or intravenously.
	B vitamins (B1, B6, B12)		1 ml per day intramuscularly or intravenously with infusion solutions
	Vitamin PP ( a nicotinic acid)		1 ml per 10 ml of water for injection intravenously 1 time per day.
Hepatoprotectors	Essentiale forte	Contains phospholipids, vitamins B1, B2, B6, B12, PP, pantothenate - a substance that promotes the elimination of alcohol. Phospholipids are a source for the structure of hepatocytes and improve their regeneration.	Solution for injection - 5 ml 2-4 times a day, diluted with saline. solution or glucose. After 10 days of injections, you can switch to taking tableted Essentiale. For oral administration: 1st month - 600 mg (2 capsules of 300 mg each) 2-3 times a day with food. Next - 300 mg (1 capsule) 2-3 times a day. The course of treatment is from 2-3 months.
Hepatoprotectors	Heptral	Contains amino acids that improve liver regeneration and help neutralize bile acids.	1 tablet for every 20 kg of patient weight in the morning between meals.

Indications for extracorporeal treatment methods

Extracorporeal methods- methods of treatment outside the patient’s body. In recent years, these methods have become promising for the treatment of liver failure.

Hemodialysis- purification and filtration of blood through an artificial kidney apparatus, also possible through a piece of peritoneum (abdominal hemodialysis). In this case, the blood is forced through filters, freeing it from toxins.

Plasmapheresis - purification of blood from toxic substances using special filters, followed by the return of plasma back into the bloodstream. It is plasmapheresis that has proven itself better in the treatment of liver failure.

Indications:

The development of renal and hepatic failure, usually this occurs at the stage of hepatic coma;
Fulminant liver failure, developing against the background of poisoning with poisons and toxins;
Acute and chronic liver failure with severe intoxication with ammonia, bile pigments, bile acids and other toxic substances.

Indications for liver transplantation

Liver transplantation occurs after partial removal of the affected organ. The liver is transplanted from a donor who is suitable in many respects. Only part of the liver is taken from the donor; for him, this procedure in most cases does not pose a threat to life, since the liver is gradually regenerated.

The transplanted part of the liver in the body of the recipient (the one to whom the organ was transplanted) begins to gradually regenerate to the size of a healthy liver. At the same time, hepatocytes begin to perform their main functions.

The danger of this method is possible rejection of the transplanted organ (foreign agent), so the patient will have to take special drugs(cytostatics and hormones).
Another problem in using this method in the treatment of liver failure is its high cost and difficulties in selecting the most suitable donor.

Complications of the condition in the form of hemorrhagic syndrome and pulmonary heart failure make it difficult to prepare such a patient for a difficult and lengthy operation.

Principles of diet therapy for liver failure:

low-protein, or better yet, protein-free diet;
daily calorie content of food should not be less than 1500 kcal;
food should be tasty and look appetizing, as patients experience a sharp decrease in appetite;
you need to eat often, in small portions;
food should contain a sufficient amount of easily digestible carbohydrates (honey, sugar, fruits, vegetables);
food should contain a large amount of vitamins and microelements;
you need to get an increased amount of fiber;
Fat restriction is necessary only if there are symptoms of cholestasis;
after the patient’s condition improves, you can restore your normal diet by introducing protein products gradually (like complementary foods for children), starting with protein of plant origin (buckwheat, cereals, legumes), then dairy products and, if protein is well tolerated, meat;
If a patient develops hepatic encephalopathy with impaired swallowing or hepatic coma, parenteral nutrition is recommended (administration of solutions of amino acids, carbohydrates, lipoproteins, vitamins, microelements through a vein).

Daily regime:

it is necessary to stop taking alcohol and other hepatotoxic substances (especially medications without consulting a doctor),
drink enough fluids,
give up heavy physical activity,
get enough sleep, improve your psychological state,
avoid constipation, it is necessary to carry out cleansing enemas 2 times a day,
if your condition allows, spend more time in the fresh air, while avoiding open sun rays.

Take care of your health!

Liver failure I Liver failure

a pathological condition characterized by a violation of one or more liver functions, leading to disorders of various types of metabolism and intoxication of the body with products of protein metabolism, which is often accompanied by disturbances in the activity of the central nervous system. up to the development of hepatic coma.

Liver failure can be acute or chronic. Acute P. n. typical for acute diseases liver, complicated by extensive destructive changes. It can be observed, for example, in acute viral hepatitis, toxic liver dystrophy, or acute disorder of its blood supply. Most patients have acute P. n. begins with symptoms of hepatic encephalopathy, or hepatargia, the first signs of which are alternating with agitation, progressive weakness, and. There is a deterioration in the general condition, and jaundice increases. In patients, nausea disappears, nausea appears, and often increases. With the progression of P. n. visual and auditory symptoms, dizziness, fainting, characteristic slow speech, stereotypic responses, flapping of fingers (reminiscent of flapping wings). Pain appears in the right hypochondrium, “liver” from the mouth, and the liver decreases in size. The last two symptoms are the most reliable harbingers of hepatic coma. The final period of hepatic encephalopathy is characterized by a disturbance in orientation in place and time, and stereotypic excitation (motor restlessness, repeated monotonous exclamations). It is actually characterized by a lack of consciousness, but at first the pain persists; with deep hepatic coma it disappears. Deep coma develops extremely quickly and is often complicated by life-threatening dysfunction of many organs and systems. Signs terminal state are divergent, decerebrate rigidity, pathological, convulsions.

In acute P. n. Leukocytosis and an increase in ESR are often observed; with hemorrhagic syndrome, it is associated. The level of bilirubin in the blood exceeds the norm by 5 times or more, reaching in some cases 300 µmol/l and higher (with a norm of 8.5-20.5 µmol/l). serum aminotransferases, as a rule, increases several times. The terminal stage is characterized by hypocholesterolemia, decreased enzyme activity, decreased prothrombin index and other blood clotting factors, sometimes glucose. Subsequently, it appears, increases, and disturbances in acid-base balance are noted. Hepatic is characterized by changes - an increase in the amplitude and a decrease in the frequency of waves of rhythmic activity with the disappearance of the latter in the terminal stage.

Chronic liver failure develops gradually in patients with chronic liver diseases (with chronic hepatitis, liver cirrhosis, etc.). It manifests itself mainly with the same symptoms as acute, but neuropsychiatric disorders are transient and do not usually reach the level of deep coma. Patients may experience decreased memory, drowsiness followed by insomnia, or, conversely, anxiety, periodic soporous states with loss of orientation, stupor, and inappropriate behavior. The progression of chronic P. n., which is often associated with gastrointestinal bleeding, infection and the action of other provoking factors, and is also observed in persons with decompensated cirrhosis of the liver, can, like acute P. n., lead to hepatic coma.

The diagnosis is based on the clinical picture, biochemical studies, and EEG. Significant value has an assessment of clinical manifestations and biochemical parameters over time. Hepatic encephalopathy in chronic P. n. sometimes it is difficult to differentiate from neuropsychiatric disorders of a different nature. In this case diagnostic value It has positive result after adequate therapy.

Treatment of patients even with initial manifestations P.n. carried out in a hospital setting. Among the many proposed methods for treating acute P. n. occupies a central place, the purpose of which is to provide parenteral and detoxification of the body, improve microcirculation, normalize electrolyte disturbances, and restore acid-base balance. For this purpose, a 5-10% glucose solution is infused intravenously (up to 1 1/2 -2 l/day), 1% glutamic acid solution (300 ml/day), 5-10% serum albumin solution (up to 200-400 ml/day), hemodez (300-400 ml/day), 15% sorbitol solution (up to 400 ml/day) or 20% mannitol solution (up to 400 ml/day). Of great importance are those administered parenterally (ascorbic acid in a daily dose of up to 1.0 G, thiamine up to 20-50 mg, riboflavin 8-20 mg, pyridoxine hydrochloride 50-100 mg, cyanocobalamin 200 each mcg, nicotinamide 100 each mg), as well as potassium orotate 0.5-1.0 G. Due to the threat of pulmonary and cerebral edema when large amounts of fluid are administered, an additional dose is prescribed (furosemide 40-80 mg and spironolactone 150-300 mg/day). With the development of hemorrhagic syndrome, Vicasol is indicated (30 mg/ day), etamzilate (4-6 ml/day), aminocaproic acid (5% solution up to 300-400 ml/day). Deficiency of coagulation factors, as well as signs of disseminated intravascular coagulation, are indications for large volume transfusions (at least 800 ml/day) fresh frozen plasma. In some cases, plasma exchange is performed - plasma transfusion after preliminary plasmapheresis. With the progression of acute P. n. most specialists use (for example, prednisolone 100-200 mg/day and more), as well as ornitsetil (10-15 G/day), antibacterial agents (aminoglycosides, etc.), glutamic acid (300-400 ml 1% solution intravenously). Apply (see Plasmapheresis, Cytapheresis), Hemodialysis, hemosorption (Hemosorption) and lymphosorption (see Lymphatic drainage), extracorporeal blood perfusion through the allo- or xenopenic liver, antitoxic serums are administered. Oxygen inhalation and hyperbaric oxygenation (Hyperbaric oxygenation) are widely used.

Treatment of chronic P. n. is aimed mainly at reducing the formation of toxic substances and removing them from the body. In mild cases, the protein content in the daily diet is limited to 50 G, with severe P. n. and the threat of developing hepatic coma is completely excluded. In order to remove toxic products from the body, they are regularly washed with high enemas or irrigations, and laxatives are prescribed (preferably saline). To reduce the formation of ammonia in the intestines, which is of particular importance in the exogenous form of chronic P. n., lactulose is used, which is administered orally in 30-50 ml per day for a long time (several months or even years). To suppress intestinal microflora, it is prescribed orally (neomycin 0.25 G 4 times a day, or ampicillin 0.5 G 4 times a day) in short courses of 5-7 days. Wide Application I found Essentiale, which is prescribed orally or intravenously in 10-20 ml/day in a 5-10% glucose solution. Hemodez is administered (200-400 ml), resort to plasmapheresis and hemosorption.

The prognosis with timely intensive therapy can be quite favorable. With the development of deep hepatic coma, changes in the body become irreversible.

Prevention includes timely and adequate diseases leading to P. n. To prevent the progression of P. n. the effect on provoking factors should be excluded. Patients are prescribed a rational (especially in relation to the amount of protein consumed) diet, consisting mainly of milk and dairy products, and the intake of medications that have a pronounced hepatotoxic or cerebrotoxic effect, as well as diuretics, is excluded or regulated. To prevent gastrointestinal bleeding, use ulcerogenic drugs; for constipation, dysbacteriosis is treated, laxatives are prescribed, for metabolic alkalosis - potassium supplements.

Bible. Blyuger A.F. and Novitsky I.N Practical, Riga, 1984; Galperin E.I., Semendyaeva M.I. and Neklyudova E.A. Liver failure, M., 1978; Krylov A.A. and others. Urgent, p. 122, L., 1988; Loginov A.S. and Yu.E. Chronic and cirrhosis of the liver. M., 1987; Podymova S.D. Liver diseases, p. 46, M., 1984; Khazanov A.I. liver diseases, M., 1988; Shuvalova E.P. and Rakhmanov A.G. Liver failure in viral hepatitis, L., 1986.

II Liver failure

a pathological condition characterized by impaired liver function and usually manifested by jaundice, hemorrhagic syndrome and neuropsychiatric disorders.

1. Small medical encyclopedia. - M.: Medical encyclopedia. 1991-96 2. First aid. - M.: Great Russian Encyclopedia. 1994 3. Encyclopedic Dictionary medical terms. - M.: Soviet Encyclopedia. - 1982-1984.

The liver is a multifunctional organ that neutralizes substances harmful to the body, participates in protein and carbohydrate metabolism, produces specific enzymes necessary for digestion, etc. If the functioning of this organ is disrupted, liver failure is diagnosed. The development of this condition adversely affects all body systems.

This disease can occur both chronically and acute form. In most cases, without targeted treatment, this pathology leads to severe complications and death. More often, the development of liver failure is observed in men, but this disorder also occurs in women. This condition more often observed in older and elderly people.

Features of liver failure

The liver is the largest gland in the body. It has high regenerative capabilities. Even if 70% of the cells are damaged, it can recover and function normally. Liver restoration occurs through the process of proliferation, i.e. growth and increase in the number of functional cells - hepatocytes.

Regeneration of the tissues of this organ is extremely slow and, depending on the general condition of the patient, can take from 2 to 4 weeks. Hepatocellular failure syndrome occurs when liver damage is so severe that full, or sometimes partial, recovery is impossible. The development of liver failure can be observed with different types of tissue damage, including massive fibrous and dystrophic degeneration, necrotic changes in the parenchyma of various etiologies, etc.

The mechanism of development of this pathological condition has already been well studied. First, under the influence of unfavorable factors, the structure of hepatocyte membranes is disrupted. At the same time, functional cells increase the production of enzymes, which worsens the situation and leads to more rapid destruction of the cells of this organ. The situation is aggravated by the start of production immune system autoimmune bodies that destroy damaged cells.

With a long-term process, anastomoses begin to form, i.e., additional small vessels that connect the remaining functional bloodstreams between the inferior vena cava and the portal vein.

Since blood circulates through these vessels, bypassing damaged areas of the liver, this reduces the chances of tissue restoration. Due to impaired liver function, more and more toxins enter the bloodstream, leading to damage to all organs and systems of the body.

Causes of the disease

There are a number of conditions that, as they progress, can cause the development of acute or chronic liver failure. Most often, liver dysfunction is observed in cirrhosis. This disease is characterized by necrotic destruction of organ tissue and further replacement of damaged areas with fibrosis.

Subsequently, the degenerated areas of the liver begin to put pressure on the vessels, triggering the formation of anastomoses and the development of portal hypertension. These processes are often accompanied by the appearance of pronounced ascites. The influence of the following unfavorable factors can provoke first cirrhosis, and then failure:

viral hepatitis;
long-term alcohol abuse;
severe poisoning by toxins;
taking certain medications;
drug use;
some pathologies of the biliary tract;
poor nutrition;
eating poisonous mushrooms;
infectious diseases;
autoimmune pathologies;
congenital abnormalities of liver development.

Conditions in which excess fat enters the tissues of the organ predispose to the appearance of such liver damage. In this case, fat begins to accumulate due to a failure in metabolic processes. Adipose tissue gradually replaces dead hepatocytes. Factors contributing to this problem include:

obesity;
anorexia and bulimia;
some gastrointestinal diseases;
taking alcohol substitutes;
diabetes.
Regular consumption of bear and badger fat.

The appearance of liver failure is often a natural result of the progression of parenchymal degeneration of the organ. Factors contributing to this problem include:

congenital deficiency of enzyme production;
protein metabolism disorders;
endocrine disorders;
hepatitis;
stagnation of bile in the liver;
intoxication in certain viral diseases;
hypo- and vitamin deficiencies.

Less commonly diagnosed is the development of liver dysfunction against the background of parenchymal carbohydrate dystrophy. This pathological condition occurs against the background of metabolic disorders involving glycogen. Lack of vitamins in food, alcohol intoxication and diabetes mellitus predispose to such liver damage. A decrease or complete disruption of liver function is often observed against the background of amyloidosis of this organ.

The occurrence of this pathology is often detected in patients with a predisposition to amyloidosis. Insufficient liver function is caused by gradual deposition of amyloid, i.e., insoluble protein, on the walls of the bile ducts and blood vessels. This contributes to the disruption of oxygen saturation of tissues and nutrients, and in addition, the outflow of bile.

Often the development of liver failure is observed against the background of hepatitis. Destructive action tissues have both viral hepatitis and liver inflammation caused by the influence of breakdown products of alcohol or toxic substances. These conditions lead first to inflammation and then death of large areas of the organ.

The development of renal failure may be the result of malignant neoplasms in this organ. The appearance of a similar problem is often observed in people who have a genetic predisposition to liver cancer. The danger is metastasis from tumors located in other organs.

The long-term adverse effects of carcinogenic substances can also contribute to the formation of malignant neoplasms, and then to failure. As malignant tumors grow, they replace functional liver cells and compress healthy areas of the organ tissue. This leads to the development of inflammation, disruption of the outflow of bile and blocking of blood circulation in healthy tissues. In this case, this pathological condition is accompanied by severe intoxication.

Some diseases can also contribute to liver dysfunction. of cardio-vascular system, including aneurysms and atherosclerosis. Chronic renal failure increases the risk of developing liver dysfunction. In addition, some diseases accompanied by severe hormonal imbalances can contribute to the appearance of such a problem.

There are frequent cases of insufficiency developing in people who have experienced massive blood loss. Contributes to the emergence of the problem of blood transfusion, which is incompatible with the recipient group. IN in rare cases the development of pathology is observed after surgical interventions on the gastrointestinal tract.

Classification of liver failure

There are 3 forms of liver failure, each of which has its own characteristics of development and course. Classic hepatic cell failure, i.e. endogenous, develops as a result of poisoning of the body with highly toxic substances. In this case, there is a rapid death of functional liver cells. In such a situation, only an urgent transplant can save the patient’s life.

In the exogenous form of liver dysfunction due to the influence of certain unfavorable factors, a gradual increasing failure of blood circulation in the tissues of the organ is observed. The level of blood purification from toxins decreases, which leads to gradually increasing intoxication of all tissues of the body.

The mixed form of the course is the result of impaired hepatic circulation and damage to the functional tissues of the organ. In this case, both acute and chronic course pathological process.

Acute form

Acute liver failure develops as a result of rapid damage to large areas of the liver. Clinical manifestations increase rapidly. Symptoms can appear within a few hours to 8 weeks after the influence of an adverse factor on liver tissue. Such a rapid increase in symptoms is due to the fact that this form of pathology is always accompanied by the appearance of extensive foci of inflammation and necrotic damage to organ tissue.

At the same time, up to 80–90% of tissues lose the ability to perform their functions. The course of acute liver failure is always unfavorable and is accompanied by a rapidly increasing deterioration in the patient’s general condition. This form of the disease is extremely short term causes the development of hepatic encephalopathy, coma and death.

Chronic form

In the chronic type of liver failure, the clinical manifestations of the pathology increase over a period of 2 months to several years as the cells of the organ die. Critical level the symptoms of this pathological condition occur when the regenerative capabilities of the cells are so depleted that the organ is unable to recover.

The chronic form of the pathology is in most cases combined with portal hypertension. Despite the fact that in the initial stages there may be an asymptomatic course, in the future the patient’s condition can become extremely serious. The terminal degree of liver damage, in which more than 80–90% of functional cells die, leads to the development of severe complications and death.

Symptoms

Signs of liver damage and failure largely depend on the form of the pathology. With an acute type of liver failure, a rapid deterioration in the condition is observed. Patients have complaints about severe pain in the area of the right hypochondrium. Unpleasant sensations so intense that the patient requires urgent hospitalization. Painful attacks may intensify after eating. Further complaints appear:

for nausea and vomiting;
to increase body temperature;
for chills;
for general weakness;
increased fatigue with minimal physical activity;
for increasing skin itching;
yellowing of the sclera of the eyes and skin;
the smell of rotten meat from the mouth;
tremor of the upper extremities;
to lower blood pressure;
to an enlarged spleen;
for shortness of breath;
for cough;
for bleeding from the gastrointestinal tract;
for massive nasal bleeding;
to a rapid decrease in blood glucose levels;
to a critical decrease in blood pressure.

Patients also experience diarrhea. The stool becomes white or light beige in color. In this case, the urine may darken. Against the background of this pathological condition, patients often experience a decrease in appetite. Some patients have a strong desire to try inedible objects.

As the condition worsens, patients experience pain in the joints, both large and small. There is a change in the size of the liver. Patients experience a rapid increase in abdominal volume due to the accumulation of fluid in the abdominal cavity. In acute types of liver failure, patients experience rapid weight loss.

Within a few hours or days after the onset of the attack, signs of hepatic encephalopathy appear, which is the result of damage to the central nervous system due to an increase in the level of toxic compounds in the blood. In many patients, even in the acute course of the pathology, the appearance of spider veins is observed, which are especially pronounced on the anterior wall of the abdomen and on the shoulders.

There are at least 4 stages of development of the chronic form of insufficiency. Each of them has its own symptoms. initial stage the pathological process is considered compensated, since at this time the appearance of pronounced clinical picture due to the fact that the activity of the remaining healthy cells increases. Only when carrying out laboratory research a decrease in organ function can be detected.

During the transition of the disease to the second decompensated stage, the appearance of pronounced signs portal hypertension. Patients develop pronounced spider veins not only on the skin of the abdomen, but also on the face. Hematomas often appear even without any traumatic impact. Massive bleeding from the gastrointestinal tract and nose is possible. These symptoms are the result of decreased blood clotting.

Most patients already at this stage of chronic liver failure experience the appearance of ascites, emotional lability or the development of depressive disorders. Possible sleep disturbances. Dyspeptic disorders become pronounced, including nausea, vomiting and diarrhea. Cachexia appears, i.e. exhaustion.

Muscle tissue rapidly atrophies. The skin becomes very thin and becomes jaundiced. The sclera of the eyes and mucous membranes can acquire a similar color. The palms and feet may have a red tint. The condition of hair and nails worsens. The patient's general health is also rapidly deteriorating. This stage may last from several weeks to a month or more.

When the disease passes into the third, i.e. terminal, stage, all previously present symptoms become pronounced. The liver decreases in size. The blood hardly clots. This causes the development of massive bleeding. Manifestations from the central nervous system are increasing.

The last stage of the chronic course is coma. This condition in most cases ends in death due to cerebral edema and the development of multiple organ failure.

Complications of the disease

Liver failure syndrome is extremely dangerous because organ damage can cause the development of severe complications caused not only by a decrease in the functional activity of hepatocytes, but also by an increase in toxic substances in the blood. There are a number of conditions, the occurrence of which reduces the patient's chances of survival.

The accumulation of fluid in the abdominal cavity increases the risk of secondary infection. In this case, peritonitis develops. Impaired liver function leads to varicose veins veins of the esophagus, which, combined with a decrease in blood clotting, predisposes to massive bleeding from the upper parts of the organ. The development of this complication ends in death in almost 100% of cases.

The accumulation of toxic substances in the blood often causes the development of deficiency. In addition, in patients with critical liver tissue damage, cases of brain tissue hypoxia and edema are common. Severe respiratory failure may occur. In rare cases, extremely dangerous pulmonary hemorrhage, which in most cases lead to death.

Most patients suffering from chronic liver failure experience atrophy of the mammary glands. Hypogonadism in men is possible. Testicular atrophy and infertility are often observed. In addition to these conditions, patients often experience organ dysfunction due to a chronic course. The development of malignant neoplasms may be observed.

Diagnostics

If signs of liver dysfunction appear, the patient requires consultation with a hepatologist and a number of other specialized specialists. After an external examination and assessment of complaints, the patient is prescribed a series of laboratory and instrumental studies. First of all, it is necessary to carry out general analysis, which allows you to identify the presence of leukocytosis and anemia in the patient.

A coagulogram is required to detect thrombocytopenia. A biochemical analysis is performed, which can be used to clarify the level of alkaline phosphatase, transaminases, bilirubin, creatinine, albumin, etc. After this, general and biochemical urine tests are prescribed.

In this case, an ultrasound of the abdominal organs is necessary. This study helps evaluate the condition of the parenchyma and blood vessels. In addition, the size of the liver is assessed. Ultrasound allows us to exclude the presence of tumor processes. An ECG is often prescribed to assess the patient's condition. To detect diffuse liver damage, hepatoscintigraphy is performed.

As an addition to the necessary studies, an MRI is often prescribed to assess the condition of the organ. In some cases, a biopsy is performed to determine the morphological changes in the tissue samples obtained.

Treatment options

The treatment of acute and chronic forms of this pathological condition has some differences. In acute forms of pathology, the patient requires urgent Care. Most often, when eliminating this pathological condition, medications are used in the form of solutions rather than tablets.

If bleeding is present, therapy aimed at eliminating this disorder is first prescribed. Blood and platelet transfusions are often used. To restore the volume of circulating blood, the administration of saline solutions or saline may be prescribed.

In addition, hemostatic drugs are administered and vitamin complexes. In case of urgent need, urgent surgical intervention is performed to restore the integrity of damaged blood vessels.

After this, treatment is carried out for disorders that arise from liver failure. To reduce the severity of intoxication, intestinal cleansing is prescribed. Medications that have a stimulating effect on intestinal motility, including Metoclopramide and Cerucal, can be administered. As part of detoxification therapy, the use of solutions of Rheosorbilact and Neogemadese is often prescribed.

Often, the treatment regimen for acute types of insufficiency includes infusion therapy, which involves the administration of solutions designed to stabilize blood pressure. A solution of sodium chloride or glucose may be prescribed. Formed diuresis is often used with the prescription of diuretics. In addition, lactulose is used to reduce ammonia production.

To reduce the risk of infection, antibacterial therapy is prescribed. Tranquilizers are often used to suppress motor and mental agitation. According to indications, specialists can use sedatives. Pharmaceutical agents can be used to improve cerebral circulation. To improve liver function, the following medications are mainly prescribed:

The patient requires oxygen inhalation. In addition, hemosorption procedures are prescribed. Hyperbaric oxygen therapy may also be required. In the chronic course of the pathology, therapy is aimed at eliminating the primary disease or factor that caused the malfunction of the organ. For fibrous tissue damage, the formation of malignant neoplasms and some other conditions, surgical treatment may be recommended. Patients with this form of pathology must completely stop drinking alcohol.

Any medications should be used only on the recommendation of a doctor. It is imperative to follow a low protein diet. Avoid exposure to direct sunlight and lifting weights over 2 kg. To stabilize the condition, patients are prescribed a number of medications. To eliminate toxic substances dangerous to brain tissue, lactulose preparations are often used, including:

To eliminate ammonia and transport it from the body, the use of Hepa-Merz and Glutargin is prescribed. Antibiotics are often prescribed to suppress the microflora in the intestines necessary for processing proteins from food. To reduce the risk of developing severe edema and ascites, patients are prescribed Veroshpiron. Drugs are used to reduce pressure in the portal vein.

In the chronic form, Propranolol, Nebilet, Moxidomin, etc. are used to reduce pressure. In addition, in the presence of narrowing of the biliary tract, cholespasmolytics are used. Medications may also be required to reduce excessive bleeding.

In severe cases, when palliative surgical interventions and medications fail to achieve significant improvement and the patient experiences an increase in toxic substances in the blood, the only way to save the patient’s life is liver transplantation.

Diet

If the functioning of liver tissue is insufficient, patients are prescribed a protein-free diet. Easily digestible foods high in plant fiber, microelements and vitamins should be included in the diet. The daily calorie content should be 1500 kcal. The diet should include:

vegetables;
fruits;
cereals;
dairy products;
lean varieties of meat and fish.

Dishes high in fat, containing hot spices, simple carbohydrates, etc. should be excluded from the diet. Food should be taken in small portions, 5–6 per day.

Prognosis and prevention

In both acute and chronic forms of liver failure, the prognosis is unfavorable. In the acute course, death in most cases occurs within 2–3 days to 2 months, unless an organ transplant is performed.

The chronic form of the pathology also has an unfavorable prognosis, although this type of disease manifests itself less aggressively. Even with complex treatment and diet, one can only achieve prolongation of life, but without transplantation the patient will face premature death. The prognosis is worsened by the presence of complications.

To reduce the risk of developing critical liver damage, it is necessary to promptly treat diseases of this organ. As part of the prevention of the described pathological condition, it is necessary to stop taking alcohol and drugs. To reduce the risk of developing deficiency, you should adhere to a healthy diet and exercise regularly.

It is imperative to maintain normal weight. You should avoid eating mushrooms collected in the forest. It is imperative to be vaccinated against hepatitis A and B. It is necessary to take any medications and dietary supplements. Major injuries that would require a blood transfusion should be avoided whenever possible, and all medical procedures should be carried out in a sanitary manner. This will reduce the risk of developing organ failure and avoid premature death.

– acute or chronic syndrome that develops when one or more liver functions are impaired, accompanied by metabolic disorders, intoxication, disturbances in the central nervous system and the development of hepatic coma. The disease occurs with symptoms of hepatic cell failure (jaundice, hemorrhagic, dyspeptic, edematous-ascitic syndromes, fever, weight loss) and hepatic encephalopathy (emotional lability, apathy, speech impairment, hand tremors, ataxia). The extreme degree of liver failure is the development of hepatic coma. Liver failure is detected based on biochemical blood parameters, EEG, and hepatoscintigraphy. Treatment of liver failure is aimed at eliminating intoxication, normalizing electrolyte disturbances, and restoring acid-base balance.

General information

Liver failure develops with massive dystrophic, fibrous or necrotic changes in the liver parenchyma of various etiologies. In gastroenterology and hepatology, acute and chronic liver failure is distinguished. The leading pathogenetic link in liver failure is a violation of the detoxification function of the organ, and therefore toxic metabolic products (ammonia, γ -aminobutyric acid, phenols, mercaptan, fatty acids, etc.) cause damage to the central nervous system. The development of electrolyte disturbances (hypokalemia) and metabolic acidosis is characteristic. Mortality in liver failure reaches 50-80%.

Classification of liver failure

By clinical course distinguish between acute and chronic liver failure. The development of acute liver failure occurs no later than 2 months from the moment of liver damage. Most often, the cause of acute failure is fulminant (fulminant) forms of viral hepatitis, alcoholic, drug or other toxic liver damage. Chronic liver failure is caused by the progression of chronic liver diseases (tumors, fibrosis, cirrhosis, etc.).

Liver failure can develop due to endogenous, exogenous or mixed mechanism. Endogenous failure is based on the death of hepatocytes and the exclusion of over 80% of the liver parenchyma from functioning, which is usually observed in acute viral hepatitis and toxic liver damage. The development of exogenous liver failure is associated with disruption of hepatic blood flow, which leads to the flow of blood saturated with toxic substances from the portal vein directly into the general circulation, bypassing the liver. The exogenous mechanism often occurs during shunting procedures for portal hypertension and liver cirrhosis. Mixed liver failure occurs in the presence of both pathogenetic mechanisms - endogenous and exogenous.

There are three stages in the development of liver failure: initial (compensated), severe (decompensated), terminal dystrophic and hepatic coma. In turn, hepatic coma also unfolds sequentially and includes the phases of precoma, threatening coma and clinically pronounced coma.

Causes of liver failure

The next most common etiological factors for liver failure are medications and toxins. Thus, massive damage to the liver parenchyma can be caused by an overdose of paracetamol, analgesics, sedatives, and diuretics. The strongest toxins that cause liver failure are the poison of the toadstool (amanitoxin), mycotoxin of fungi of the genus Aspergillus (aflatoxin), chemical compounds (carbon tetrachloride, yellow phosphorus, etc.).

In some cases, liver failure may be caused by liver hypoperfusion, which occurs due to veno-occlusive disease, chronic heart failure, Budd-Chiari syndrome, and profuse bleeding. Liver failure can develop with massive infiltration of the liver by tumor cells of lymphoma, metastasis of lung cancer, and pancreatic cancer.

Rare causes of liver failure include acute fatty degeneration liver, autoimmune hepatitis, erythropoietic protoporphyria, galactosemia, tyrosinemia, etc. In some cases, the development of liver failure is associated with surgical interventions (portocaval shunting, transjugular intrahepatic portosystemic shunting, liver resection) or blunt liver trauma.

Factors that provoke the breakdown of compensatory mechanisms and the development of liver failure may include electrolyte imbalance (hypokalemia), vomiting, diarrhea, intercurrent infections, alcohol abuse, gastrointestinal bleeding, laparocentesis, excessive consumption of protein foods, etc.

Symptoms of liver failure

The clinical picture of liver failure includes the syndromes of hepatic cell failure, hepatic encephalopathy and hepatic coma. In the stage of hepatic cell failure, jaundice, telangiectasia, edema, ascites, hemorrhagic diathesis, dyspepsia, abdominal pain, fever, weight loss appear and progress. With chronic liver failure, endocrine disorders develop, accompanied by decreased libido, infertility, testicular atrophy, gynecomastia, alopecia, atrophy of the uterus and mammary glands. Disruption of metabolic processes in the liver is characterized by the appearance of liver odor from the mouth. Laboratory tests at this stage of liver failure reveal an increase in the level of bilirubin, ammonia and phenols in the blood serum, and hypocholesterolemia.

For complex therapy For liver failure, hemosorption, hemodialysis, and ultraviolet irradiation of blood are used.

Prognosis and prevention of liver failure

With timely intensive treatment liver failure, liver dysfunction is reversible, the prognosis is favorable. Hepatic encephalopathy in 80-90% progresses to the terminal stage of liver failure - hepatic coma. In deep coma, death most often occurs.

To prevent liver failure, timely treatment of liver diseases is necessary, eliminating hepatotoxic effects, drug overdoses, and alcohol poisoning.