Liver failure - life is at stake! Liver failure, symptoms in women and men Symptoms of acute liver failure

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

With the deterioration of the environment due to human activities, the spread of viral hepatitis and other infections, alcoholism and drug addiction, the deterioration of food quality, a sedentary lifestyle and the development of the pharmaceutical industry, the load on our liver has increased significantly. And when all this falls down 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 to the death of the patient.

So, liver failure- this is a pathological condition, a syndrome characterized by damage to the 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 liver failure 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.
• Worldwide, an average of 2,000 people die every year due to liver failure.
• In 15% of cases of liver failure, it is not possible to explain the cause of its development.
• 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 take place in it.
• When conducting experiments on animals, it was found that after removal of the liver, the animals are in a normal state for 4-8 hours, and after 1-2 days they die in a state of hepatic coma.
• Cirrhosis of the liver always presents with liver failure.
• Botkin's disease, or viral hepatitis A, in people over 40 years of age with a history of liver and gallbladder diseases in 40% of cases leads to liver failure. Viral hepatitis A among the people is considered to be a disease of childhood, which is quite easily tolerated (equate to chicken pox, rubella, scarlet fever, and so on).
• Viral hepatitis E in pregnant women, 20% ends with liver failure, while in men and non-pregnant women, viral hepatitis E may not appear at all.
• Taking such a seemingly ordinary drug as paracetamol, can lead to the development of a fulminant course of liver failure (fulminant liver failure). And in many countries it is customary to take paracetamol in large doses for common colds and SARS.
• It is from liver failure that most people die due to poisonous mushroom poisoning(pale grebes, fly agarics and others).
• In most cases of liver failure in adults, in addition to other causes of the development of the syndrome, the fact is revealed alcohol abuse.

Liver anatomy

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

Characteristics of the liver:

• weight - about 1.5 kg,
• shape - pear-shaped
• normal size of the liver in adults:
  • length along the oblique line - up to 15 cm,
  • the length of the right lobe is 11.0-12.5 cm,
  • the length of the left lobe is 6-8 cm,
  • height - 8-12 cm,
  • thickness - 6-8 cm,
• the edges of the liver are smooth,
• texture is soft
• structure is uniform
• 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 (restore).

Distinguish liver surface:

• diaphragmatic surface- corresponds to the shape of the diaphragm,
• visceral(addressed to authorities) surface- attached to surrounding organs
• bottom edge - at an acute angle
• top 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 share,
• tail share.

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

Between the square and caudal lobes of the liver, in the right longitudinal sulcus, there are gates of the liver, which include the following structures:

• hepatic artery,
• portal vein,
• bile duct,
• nerves and lymphatics.

Liver regeneration

The liver is an organ that can completely restore its structure after damage, that is, it is able to regenerate. Even with the defeat of 70% of the liver cells, it can recover to its normal volume. The same regeneration occurs in lizards when they "grow" their tail.

Recovery of the liver 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 rate of organ recovery and the volume to which it recovers are greater than in the elderly. Regeneration occurs slowly: in children this period is 2-4 weeks, and in the elderly - 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 also when a normal amount of useful nutrients enters the body.

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

The structure of the liver

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

The 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 located in hepatic beams - in two layers. The hepatocyte is located between the bile canaliculi and the intralobular capillary.
• Bile ducts- located between the hepatic beams, along them bile from hepatocytes enters the bile ducts.
• intralobular capillaries or sinusoids- blood vessels through which chemical compounds enter the hepatocytes and processed substances leave them.

Blood vessels of the liver

1. Portal vein and hepatic artery - through these vessels, blood from the internal organs enters the liver, and the rate of blood flow in the liver slows down significantly, which contributes to the plethora of the organ;
2. Interlobular vessels, together with interlobular bile ducts, form the interlobular hepatic triad;
3. Around the lobular vessels;
4. Intralobular vessels or sinusoids;
5. Central vein - collects blood from the sinusoids of the hepatic lobule;
6. Collecting or sublobular vessels,
7. 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, 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 "ripens"; gallbladder volume from 50 to 80 ml;
• The common bile duct connects the gallbladder and hepatic ducts to the duodenal bulb, where bile is needed to digest food.

The composition of bile

A huge amount of bile is secreted per day by the liver - up to 1 liter, at least half a liter.

The 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 hepatic bile- excreted directly from the liver, bypassing the gallbladder, has a yellowish straw color, transparent.
• Mature or gallbladder bile- stands out from the gallbladder, has a dark olive color, transparent. In the gallbladder, fluid is absorbed from the bile and mucus (mucin) is secreted, thus the bile becomes viscous and concentrated.
• Basal bile- a mixture of young and mature bile, which enters the duodenum, golden yellow, transparent.

What is included in bile?

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


2. Bile acids:
   • cholic and chenodeoxycholic acids are the primary bile acids,
   • glycocholic and taurocholic acids (compounds with amino acids),
   • deoxycholic and lithocholic acids (secondary bile acids, formed in the intestine under the action of intestinal microflora).
   Bile acids are formed from cholesterol in hepatocytes. In bile they are in the form of salts and anions. The role of bile acids is great in the digestion of fats and the absorption of fatty acids and triglycerides in the intestine. Part of the bile acids is absorbed in the intestine back into the blood, and again enter the liver.


3. Bile pigments:
   • bilirubin
   • biliverdin.
   Bile pigments are formed from hemoglobin in the spleen and in Kupffer cells. Any erythrocyte is formed in the red bone marrow (erythropoiesis) and destroyed in the spleen, and a small part of them in the liver. Erythrocytes contain hemoglobin, which carries oxygen and carbon dioxide atoms, that is, it carries out gas exchange in tissues. After the destruction of the erythrocyte, there is a question about the utilization of hemoglobin. Bile pigments are intermediate products of the breakdown of hemoglobin, with the help of bile they are excreted from the body.

   These pigments color bile yellow, green, and brown. And also, after binding with oxygen, it slightly stains urine (urobilinogen) and feces (stercobilinogen).



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


5. Cholesterol- in bile is in a 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.


6. Ions:
   • sodium,
   • calcium,
   • potassium,
   • chlorine,
   • bicarbonates
   Ions enter the bloodstream and liver along with food. Their main role is to improve the permeability of cell walls, and 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.

The main 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. With an increased amount of ammonia becomes a poison for the body. Urea from the liver enters the bloodstream, and then excreted with the kidneys.
• Participation in carbohydrate metabolism- with an excess of glucose in the blood, the liver synthesizes glycogen from it - the reaction of glycogenesis. The liver, as well as skeletal muscles, are depots for glycogen storage. With 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 musculoskeletal system to function.
• Participation in fat metabolism- with a lack of fat in the body, the liver is able to synthesize carbohydrates (namely glycogen) into fats (triglycerides).
• Utilization 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 utilization of excess hormones, vitamins and other biologically active substances.
• Depot for some vitamins and trace elements, such as vitamins B 12, A, D.

Causes and pathogenesis of liver failure

The mechanism of development of liver failure in stages

• Impact adverse (hepatotoxic) factors on the membrane of liver cells - hepatocytes.
• Starts from hepatocytes secrete enzymes, which continue to destroy (digest) liver cells.
• The immune system begins to secrete autoimmune antibodies to damaged hepatocytes, which completely destroy them (hepatic tissue necrosis).
• Distribution of this process to other hepatocytes.
• With the defeat of 70-80% of liver cells develops liver failure.
• Full or partial loss of liver function.
• With a long process - are formed anastomoses(additional vessels, which, bypassing the damaged areas, unite intact vessels) between the portal and inferior vena cava (normally, they are connected by the vessels of the liver). Through these anastomoses, the blood circulates without entering the liver, which reduces the chances for liver regeneration.
• metabolic acidosis- the entry of toxins into the blood that are not processed by the liver, they damage all systems and tissues, possibly brain damage.
• Violation of all metabolic processes in the body, as the liver ceases to synthesize and store glycogen, form urea and remove ammonia from the body.
• Violation of the biliary system - bile stasis (or cholestasis) leads to the entry into the blood of a large amount of bilirubin, 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 the decay products of the brain.
• 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	The reasons for the development of this disease	What happens in the liver?
Cirrhosis of the liver	Alcohol abuse. Chronic viral hepatitis. Work with toxins, poisons, chemicals, heavy metals, paints and varnishes and so on. Taking many drugs (especially long-term): non-steroidal anti-inflammatory drugs(paracetamol, analgin, nimesulide and others), antibiotics and antivirals(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 consumption of dyes, preservatives, flavor enhancers, which are widely used in the food industry. Abuse fatty, fried, spicy, salty or smoked foods. Eating poisonous mushrooms(pale grebe, fly agaric and others). Common infectious diseases(sepsis, HIV, influenza and others). Autoimmune diseases - diseases in which the immune system perceives its own as someone else's, affecting its own cells. Congenital pathologies of the liver(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 load factors on the liver, especially dietary disorders.	The process of development of cirrhosis of the liver is long sometimes last for years. Under the influence of hepatotoxic factors, partial destruction of hepatocytes constantly occurs, but due to the regenerative function of the liver, hepatocytes are partially restored. With prolonged, ongoing exposure to toxic factors, when autoimmune processes are connected, the gene material of the 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), as a result - the appearance of vascular anastomoses between the portal and inferior vena cava, the appearance of fluid in the abdominal cavity - ascites, the enlargement of the spleen - splenomegaly. At the same time, the liver decreases in size, shrinks, and a syndrome of liver failure appears.
Dystrophy liver (hepatosis): Parenchymal fatty degeneration of the liver	overeating fats and carbohydrates, diseases of the gastrointestinal tract, malnutrition, starvation, anorexia, bulimia, eating badger, bear, dog, camel fat and so on.	The intake of excess fat into the liver (also an increased content of carbohydrates in the liver, increased glycogen consumption) or difficulty in the exit of fats from the liver (lack of proteins, violation of the enzymatic work of the liver) lead to the deposition of "excess" fat (triglycerides) in the cytoplasm of hepatocytes. Fat accumulates and gradually ruptures the hepatocyte. Adipose tissue gradually replaces the liver tissue, which leads to liver failure syndrome.
Parenchymal proteinaceous dystrophy of the liver	violation of protein metabolism, congenital deficiency of liver enzymes for protein processing, diabetes mellitus 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 dystrophy of the liver: Granular dystrophy liver- deposition of "excess" protein in the cytoplasm of hepatocytes, while the liver increases in size due to an increase in the content of water in hepatocytes (protein molecules attract water molecules by osmosis). This process is still reversible and occurs quite often. Hydropic dystrophy of the liver - due to a lack of protein in the liver, accumulation of fluid in the cytoplasm of hepatocytes is observed. Excess fluid is produced in the cytoplasmic vacuole. In this case, 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 drop 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. In this case, the liver cells lose fluid and begin to produce connective tissue. At this stage, the development of cirrhosis of the liver is possible. Hyaline can also destroy the wall of the hepatocyte, leading to its necrosis. In any case, sooner or later liver failure develops.
Parenchymal carbohydrate degeneration of the liver	violation of glycogen metabolism, 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 degeneration, glycogen accumulates not in the cytoplasm, but in the nucleus of the hepatocyte. At the same time, hepatocytes significantly increase in size. With a long process, the death of hepatocytes occurs or connective tissue develops (liver cirrhosis). Outcome - liver failure.
Liver mesenchymal dystrophy or liver amyloidosis	chronic infectious diseases (tuberculosis, syphilis, osteomyelitis and others), immune system diseases genetic predisposition to the formation of amyloid.	Amyloidosis- a systemic disease associated with a malfunction 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. Sealed vessels of the liver cannot fully function, 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, impact on the liver of toxic substances and factors.	The pathogenesis of viral hepatitis is quite complex. But the main role in the defeat of hepatocytes is played by immunity. If in viral hepatitis A and E immunity promotes the release of hepatocytes from the virus, then in viral hepatitis B, D, and F, immunity affects 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 if other hepatotoxic factors are eliminated, otherwise chronic hepatitis, necrosis or cirrhosis of the liver develops, and the outcome is liver failure. With viral hepatitis C (specialists call it the "gentle killer"), the 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, portal hypertension develops varicose veins in the portal system, as well as an overload of the lymphatic system, which stops completely collecting 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.

It 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 an incompatible blood type,
• surgical operations in the abdominal cavity.

Types of liver failure

Distinguish between acute and chronic liver failure.

Acute liver failure

- a type of liver failure that develops as a result of rapid damage to the liver. 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 the lightning-fast development of liver failure - fulminant liver failure, which often occurs when poisoned by poisons, chemicals, drugs, and so on.

Causes that can lead to acute liver failure:

Depending on the causes of development, there are forms of acute liver failure:

• Endogenous or hepatocellular form- occurs when liver cells are damaged as a result of exposure to hepatotoxic factors. It is 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 systems of the portal and inferior vena cava), most often with cirrhosis of the liver. At the same time, 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 of liver dysfunction.

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 whole organism. With brain damage, hepatic encephalopathy occurs, then coma and death of the patient.

Acute liver failure is an extremely serious condition of the body that requires immediate detoxification therapy.

Disease prognosis- in most cases, unfavorable, the chance to restore the vital functions of the liver depends on the ability of the liver to regenerate (its compensatory capabilities), the time before the start of therapeutic measures, the degree of brain damage and the elimination of hepatotoxic factors. Acute liver failure itself is a reversible process. And from the hepatic coma come out 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 in acute liver failure, there are forms:

• exogenous form- defeat and necrosis of liver cells occurs gradually, some of the cells are regenerated, but with continued exposure to adverse factors, the death of hepatocytes continues.
• endogenous form- violation of the blood circulation of the liver,
• mixed the 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 opportunities for regeneration of hepatocytes), while hepatic encephalopathy and then coma and death may develop.

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

• alcohol consumption,
• self medication,
• violation of the diet, eating a large amount of proteins and fats,
• nervous stress,
• a common infectious process (sepsis, influenza, meningococcemia, chickenpox, tuberculosis, and others),
• pregnancy, childbirth, abortion,
• abdominal surgery and so on.

Current - heavy. With the increase in liver failure, 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 death of the patient occurs. With compensated chronic liver failure, it is possible to restore the liver 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 only be made on the basis of targeted examinations. This is the reason for late diagnosis and treatment of the disease, which significantly reduces the chances of recovery.

A photo: preparation of the liver of a patient with cirrhosis of the liver. The liver is shriveled, reduced in size, there is an expansion of the hepatic vessels. The liver tissue is all overgrown with connective tissue.

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

Criteria	Acute liver failure	Chronic liver failure
Development timeline	From a few days to 8 weeks.	From 2 months to several years.
Development mechanism	It develops as a result of rapid necrosis of the liver tissue or a sharp violation of the blood circulation of the liver.	Liver necrosis occurs gradually, some of the damaged cells have time to regenerate, the liver is able to partially compensate for its functions. It can also develop with a gradual violation of blood circulation.
The degree of liver damage	Rapid damage to more than 80-90% of all liver cells.	Gradual defeat of more than 80% of hepatocytes. Chronic liver failure almost always contributes to the development of symptoms of portal hypertension, in contrast to acute liver failure, in which portal hypertension is not a mandatory symptom.
The severity of the current	The course of the disease is extremely severe, more severe than in chronic liver failure.	The course is severe, in the initial stages an asymptomatic course is possible.
Forecast	The prognosis is unfavorable, hepatic encephalopathy often develops, and then coma. But the process is reversible with timely therapeutic measures and the elimination of hepatotoxic factors.	The prognosis is unfavorable, in the absence of timely treatment and elimination of provoking factors, sooner or later 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 does it manifest	Origin mechanism
cholestasis syndrome	Jaundice	Staining of the skin and visible mucous membranes in yellow shades: from green and lemon to orange. In swarthy people, jaundice can be noticeable only on the mucous membranes, especially on the sclera of the eyeballs.	Cholestasis syndrome associated with a violation of the outflow of bile from the liver. This is due to compression of the biliary tract and the inability of damaged hepatocytes to excrete bile. At the same time, the breakdown product of hemoglobin, bilirubin, is not excreted with bile and feces. In the blood, there is a large amount of bile pigments (bilirubin and biliverdin), which ensure that all tissues are stained in the color of bile. But the feces lose their staining with stercobilin. The kidneys try to remove excess bilirubin from the blood, while there is an increased content of bile pigments in the urine, and as a result, its more intense staining. An increased amount of bilirubin also has a toxic-allergic effect on the skin, which contributes to the development of itching.
	Discoloration of feces	Feces acquire a light color, up to white and beige.
	Darkening of the urine	The color of urine becomes darker, it is compared with shades of dark beer.
	Itching of the skin	A patient with cholestasis is accompanied by itching throughout the body, while there may not be a rash.
	Pain in the right hypochondrium	Not an obligatory symptom in liver failure. Pain can appear after eating, are aching or spasmodic in nature.	Pain in the right hypochondrium occurs due to obstruction of the bile ducts. At the same time, bile bursts the bile ducts and compresses the lobular nerves.
Dyspeptic disorders	Nausea, vomiting, stool disturbance, loss and perversion of appetite.	Nausea and vomiting are associated with food intake, are intermittent or constant. Disorders of the stool in the form of diarrhea, more than 3 times a day. Appetite is poor, up to refusing to eat. Some patients have a desire to try inedible (earth, chalk, hair, incompatible foods, etc.).	Digestive disorders are associated with the inability of the liver to participate in the digestion of fats. A decrease in appetite can also be a sign of damage to the nervous system and intoxication, which develops against the background of liver necrosis.
Intoxication symptoms	Fever, weakness, malaise, joint pain (arthralgia), loss of appetite.	Body temperature can rise to high numbers or be of a permanent subfebrile character (up to 38C). Weakness and malaise are mild or chain the patient to bed. Arthralgia in large or all groups of joints.	Intoxication symptoms develop as a result of the breakdown products of liver tissues 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 which case not only toxins of the destroyed liver enter the blood, but also toxins released during the life of the virus.
Changing the size of the liver	Liver enlargement (hepatomegaly)	These changes in the liver can be determined by the doctor with the help of palpation of the abdomen, as well as during additional research methods.	An enlarged liver 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.
	Liver shrinkage		A decrease in the liver is observed in cirrhosis of the liver, when the liver tissue is completely replaced by connective tissue.
portal hypertension syndrome	Ascites	The abdomen increases significantly in size, resembling pregnancy.	Ascites is the accumulation of fluid in the abdominal cavity. Its development is associated with a violation of the patency of the lymphatic vessels, which develops as a result of their compression in the liver by dilated hepatic vessels. The lymphatic system promotes fluid drainage in soft tissues.
	Vascular asterisks	Vascular asterisks are an expansion of blood vessels, they look like jellyfish. Appear on the front wall of the abdomen and on the shoulders.	Spider veins are dilated vessels that branch off 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 the disturbed blood circulation.
	Splenomegaly - enlargement of the spleen	This symptom can be determined by palpation of the abdomen and instrumental research methods.	Splenomegaly develops due to circulatory disorders in the spleen, which is the blood depot. It is supplied with blood from the system of portal and inferior vena cava. When the pressure in these vessels increases, more blood is deposited in the spleen. Also, the spleen takes over 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 the remains of blood are detected only in the feces (melena). It is either acute or chronic. The amount of blood loss also varies from person to person. 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 against the background of portal hypertension. Constantly and for a long time dilated vessels lose their mobility and permeability, and therefore bleeding occurs from them. Bleeding also contributes to a violation of blood clotting (associated with impaired liver function, one of which is the synthesis of certain clotting factors).
Hepatic encephalopathy	Violation of the nervous system	Dizziness, lethargy, sleep disturbance, confusion or loss of consciousness inattention, memory loss, lethargy, "Blurring the 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 shortness of breath, its increase (more than 20 per minute at rest for adults). Shortness of breath first manifests itself during physical exertion, and then during rest, especially in the supine position. During sleep, there may be attacks of a sharp increase in breathing (the patient develops a fear of suffocation). To facilitate breathing, patients take a forced sitting position. There may also be a cough with bloody sputum with blisters.	The appearance of pulmonary symptoms is associated with an increase in pulmonary edema. Pulmonary edema - blood filling of the pulmonary vessels. This is due to a violation of protein metabolism as a result of liver damage. Blood begins to simply sweat through the walls of blood vessels into the alveoli. The development of this symptom is life-threatening, since when the alveoli are completely filled with liquid, respiratory arrest is possible.
Circulatory disorders	Increased blood pressure, cardiac arrhythmia.	An increase in blood pressure over 140/90 mm Hg. Art. Arterial hypertension will soon be replaced by hypotension, a decrease in pressure below 90/60 mm Hg. Art. Cardiac arrhythmia first manifests itself in the form of bradycardia (less than 60 beats per hour), and then, in the form of tachycardia (more than 90 beats per hour).	Violation of the general circulation is associated with portal hypertension. In the presence of edema and ascites, a large amount of fluid leaves the bloodstream and enters the soft tissues. This lowers blood pressure. With these changes in the bloodstream, the work of the heart is also associated, arrhythmia appears.
Amyotrophy	muscle weakness	Muscles decrease in size, become flabby, 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 work. The conversion of glucose to glycogen occurs in the liver, and with liver failure, glycogen is practically not synthesized. After using the stored glycogen, skeletal muscle atrophy gradually increases.
Blood clotting disorder	Bleeding	Bleeding from dilated veins of the esophagus, from the vessels of the stomach, nosebleeds, hemorrhagic rash (like bruises), and so on.	Violation of blood clotting occurs due to the failure of the liver to function - the formation of blood clotting factors. In this case, the blood becomes "liquid", and the bleeding is extremely difficult to stop.

Also, with liver failure, anemia, pulmonary heart failure, acute or chronic renal failure, intestinal paresis can develop. Absolutely all organs and systems of the body suffer.
In hepatic insufficiency, a specific hepatic odor from the mouth is characteristic.

Photo of a patient with jaundice.

Acute liver failure, features of the clinical course

Stages of acute liver failure:

1. Latent stage of hepatic encephalopathy - at this stage, patients have no complaints, and there are no pronounced symptoms of liver damage. Changes can only be detected by examination.
2. I stage of hepatic encephalopathy - precoma. At the same time, symptoms of liver failure increase: syndromes of cholestasis, portal hypertension, intoxication symptoms, the first symptoms of damage to the nervous system appear in the form of its inhibition.
3. II stage of hepatic encephalopathy - precoma. At this stage, the patient's condition is aggravated, 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, it cannot be detected on palpation (symptom of "empty hypochondrium"). At this stage, a liver smell from the mouth appears.
4. Coma- loss of consciousness, the patient shows reflexes only to stronger stimuli, there are signs of multiple organ failure (simultaneous course of hepatic, pulmonary, cardiac, renal failure, cerebral edema).
5. deep coma- the patient is unconscious, there is a complete absence of reflexes to any stimuli as a result of cerebral edema, multiple organ failure develops. In most cases, this is an irreversible process, the death of the patient 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, features of the clinical course

Photo of a patient with cirrhosis of the liver with 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:

1. I stage - the functionality of the liver is still preserved. This stage is characterized by the appearance of dyspeptic disorders, mild intoxication (weakness, drowsiness).
2. II stage - 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 coordination of movement. There is a liver smell from the mouth. At this stage, short-term memory loss is possible. At this stage, the liver only partially performs its functions.
3. III stage - a significant decrease in the functionality of the liver. Previously appeared symptoms become more pronounced. There are manifestations of cholestasis and portal hypertension, blood clotting disorders, aggravation of the state of the nervous system (severe weakness, impaired speech).
4. IV stage (hepatic coma) - the liver completely dies and does not function at all. There is a loss of consciousness, a decrease in reflexes, then their absence. Brain edema develops. Multiple organ failure is on the rise. Most often, this is an irreversible process, the patient dies.

Features of clinical manifestations of chronic liver failure:

• each stage develops gradually, over weeks, months, years;
• Mandatory 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 sooner or later will lead to hepatic encephalopathy and coma.

Diagnosis of liver failure

Examination of the patient by a general practitioner, hepatologist or gastroenterologist, 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, visible mucous membranes.

Laboratory methods for studying the state of the liver

Laboratory diagnostics allows assessing the functional state of the 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 the indicators of bile pigments - 50-100 times or more, up to 1000 µmol / l. Hepatic encephalopathy occurs when the level of bilirubin 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 transaminase, the more pronounced the process of hepatic tissue necrosis. In liver failure, transaminases increase tenfold. With complete destruction of the liver, there is a sharp decrease in transaminases.
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 violation of protein metabolism, almost always positive in liver failure.
De Ritis coefficient	1,3 – 1,4			This coefficient reflects the ratio of AST to Alt. In liver failure due to chronic liver diseases, this indicator increases by more than 2. And in the acute process of viral hepatitis, on the contrary, it decreases by less than 1.
GGT(gamma-glutamate transferase)	6 - 42 IU / l for women, 10 - 71 IU / l for adults.			GGT is an enzyme involved in protein metabolism. In liver failure, this figure can increase several times if the patient has symptoms of bile stasis. Interestingly, GGT is used by narcologists in the diagnosis of alcoholism.
Glucose	3.3 - 5.5 mmol/l			There is a decrease in glucose levels or, more rarely, its 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			With liver failure, a decrease in the level of urea is observed, this is due to violations of protein metabolism, the lack of synthesis of urea in the liver from ammonia, the products of protein breakdown.
Total protein, globulins, albumins	Total protein: 65 - 85 g / l, globulins: 20 - 36 g / l, albumins: 30 – 65 g/l			A decrease in the level of total protein, albumin and globulins occurs due to a violation 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 U/L for women and up to 270 U/L for men			In liver failure, there is an increase in the activity of alkaline phosphatase by 3-10 times due to cholestasis syndrome, the inner membranes of the biliary tract are a source of alkaline phosphatase.
blood ammonia	11-32 µmol/l			With liver failure, the content of ammonia nitrogen in the blood increases up to 2 times, with an increase in hepatic encephalopathy, the level of ammonia increases.
fibrinogen	2 – 4 g/l			There is a decrease in the level of fibrinogen due to a violation of its formation in the liver. Fibrinogen is a blood coagulation factor, its deficiency in combination with a lack 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 less than 90 g / l. This is due to violations of 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 an intoxication syndrome due to liver necrosis or the action of viral hepatitis, that is, inflammation.
ESR(sedimentation rate of erythrocytes)	2 – 15 mm/h
platelets	180 - 320*10 9 / l			There is a decrease in the level of platelets due to the 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			An increase in the level of urobilin in the urine is associated with cholestasis syndrome and impaired metabolism of bile pigments.
Protein	Normally there is no protein in the urine			The appearance of protein in the urine is associated with a violation of protein metabolism, may indicate the development of renal failure.
Sterkobilin	Normally, stercobilin is present in feces, it contributes to the coloring of feces in yellow-brown colors.			The absence of stercobilin in the feces is associated with a violation of the outflow of bile.
hidden blood	Normally there should be no occult blood in the 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.		The definition of markers for viral hepatitis indicate an acute or chronic process.

*All indicators are indicated for adults only.

Instrumental methods for diagnosing liver diseases

With the help of special equipment, it is possible to visualize the liver, assess its condition, size, the presence of additional formations in it, the state of the vessels of the liver, bile ducts.

Additional research methods for liver failure

An additional examination is necessary to assess the condition of other organs, since the whole body suffers with liver failure.

1. chest x-ray,
2. CT or MRI of the brain
3. fibrogastroduodenoscopy (probing of the esophagus, stomach, duodenal bulb),
4. others as indicated.

Treatment of acute liver failure

Basic principles of therapy for acute liver failure:

• Most importantly, if possible, eliminate the possible cause of liver failure.
• Treatment must begin immediately.
• Hospitalization is required! Acute liver failure is treated only in a hospital, with severe encephalopathy - in the intensive care unit.
• Treatment is aimed at maintaining the state of the body and metabolism.
• If the cause of liver failure is excluded and the life support of the patient is fully maintained for 10 days, hepatocyte regeneration occurs, which makes it possible for the patient to survive.

Stages of intensive care for acute liver failure

1. Stop bleeding in the presence of hemorrhagic syndrome:
   • If necessary, surgical treatment aimed at restoring the integrity of blood vessels
   • The introduction of hemostatic drugs: aminocaproic acid (etamsylate), vitamin K (vikasol), ascorbic acid (vitamin C), vitamin P (rutin), fibrinogen and others.
   • With the ineffectiveness of these measures, it is possible to transfuse donor blood products, namely, platelet mass and other blood coagulation factors.
2. Reducing toxicity:
   • bowel cleansing,
   • protein free diet,
   • the introduction of drugs that stimulate intestinal motility (cerucal, methaclopramide and others),
   • infusion of neogemadez, rheosorbilact for the purpose of detoxification.
3. Restoration of circulating blood volume: intravenous drip injection of physical. solution, other saline solutions under the control of the volume of excreted urine.
4. Improving the blood supply to the liver:
   • Oxygen mask or mechanical ventilation if symptoms of pulmonary edema are present,
   • reduction of swelling of the liver cells: the introduction of osmotic drugs (reopoliglyukin, sorbitol),
   • expansion of intrahepatic vessels: eufillin, droperidol, thiotriazoline,
   • drugs that improve the ability of the liver to perceive oxygen: cocarboxylase, cytochrome C and others.
5. Replenishment of the necessary energy reserves of the body: introduction of glucose, albumin.
6. Decreased intestinal absorption lactulose (dufalac, normase and others), the appointment of antibiotics to disrupt the intestinal microflora.
7. Restoration of liver functions and promotion of its regeneration:
   • Arginine, ornithine, Hepa-Merz - improve the function of the liver, the formation of urea from ammonia,
   • vitamins P, group B,
   • hepatoprotectors with phospholipids and fatty acids: Essentiale, LIV-52, essliver, lipoid C and others,
   • amino acids, except for phenylalanine, tryptophan, methionine, tyrosine.
8. Correction of the brain:
   • sedative (sedative) drugs,
   • improvement of blood circulation of the brain (actovegin, cerebrolysin and others),
   • diuretics (diuretics, for example, lasix, mannitol) to reduce cerebral edema.

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 the treatment of this syndrome!
• Diet is one of the main activities aimed at restoring liver cells and reducing the formation of ammonia in the body. The diet is protein-free.
• Cleansing the intestines, since the pathogenic intestinal microflora contributes to the formation of ammonia and its absorption into the blood, and the liver has lost its ability to form urea from ammonia. For this, cleansing enemas are prescribed 2 times a day.
• It is necessary to correct the main indicators of metabolism, according to biochemical blood tests (electrolytes, lipoproteins, glucose, and so on).
• In addition to taking the main medications, in the presence of complications, it is necessary to carry out their treatment.

The main drugs used in chronic liver failure

Type of drugs	Representatives	Mechanism of action	How it is applied
Lactulose	Dufalac, Normase, Good luck, Portolac	Lactulose changes the acidity of the intestine, thereby inhibiting the pathogenic intestinal microflora that releases nitrogen. Nitrogen is absorbed into the blood and combines with the hydrogen atoms of water to form ammonia. A damaged liver is not able to form urea from this ammonia, ammonia intoxication occurs.	30 - 50 ml 3 times a day with meals. Lactulose can be used for a long time.
Broad spectrum antibiotics	Neomycin most well established in the treatment of liver failure.	Antibiotics are needed to suppress the intestinal microflora that releases 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. It is prescribed for ammonia intoxication, which has developed as a result of chronic liver failure. Do not use with vikasol (vitamin K), which is prescribed to stop bleeding, for example, from dilated veins of the esophagus.	Inside, 1 g 2-3 times a day. The course of treatment is long from 1 month to 1 year.
	Ornithine (ornicetil)		Inside the granules, 3 g, dilute in a glass of liquid 2-3 times a day. For intravenous drip - 20-40g / day per 500 ml of glucose 5% or saline.
Detoxification infusion therapy	Glucose 5%	Glucose contributes to the replenishment of the necessary energy reserves.	Up to 200 - 500 ml per day of each of the solutions intravenously drip. Total solutions per day can be poured up to 2 - 3 liters, only under the control of the volume of excreted urine (diuresis).
	Sodium chloride solution 0.9% (phys. solution), Ringer's solution, Lakt	Electrolyte solutions replenish the volume of circulating blood, the electrolyte composition of the blood improves the blood supply to the liver.
Potassium preparations	Potassium chloride	Compensates for the lack of potassium, which is almost always present in liver failure. Only under the control of the level of potassium in the blood, as its excess can lead to heart failure.	10 ml of a 4% solution diluted in 200 ml of any liquid for infusion.
vitamins	Vitamin C	Many vitamins are antioxidants, improve the condition of the vascular wall, 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 (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, improves their regeneration.	Solution for injection - 5 ml 2-4 times a day, diluted in physical. solution or glucose. After 10 days of injections, you can switch to Essentiale tablets. For oral administration: 1st month - 600 mg (2 capsules of 300 mg) 2-3 times a day with meals. Further - 300 mg (1 capsule) 2-3 times a day. The course of treatment is from 2-3 months.
	Heptral	Contains amino acids that improve liver regeneration, contribute to the neutralization of bile acids.	1 tablet for every 20 kg of the patient's weight in the morning between meals.

Indications for extracorporeal treatments

Extracorporeal methods– methods of treatment outside the body of the patient. 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, it is also possible through a sheet of peritoneum (abdominal hemodialysis). In this case, the blood is driven through the filters, freeing it from toxins.

Plasmapheresis - purification of blood from toxic substances with the help of special filters, followed by the return of the 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 insufficiency, this usually occurs at the stage of hepatic coma;
• Fulminant liver failure, which develops 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 transplant

Liver transplant occurs after partial removal of the affected organ. The liver is transplanted from a donor 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 a possible rejection of the transplanted organ (foreign agent), so the patient will have to take special drugs (cytostatics and hormones) throughout his life.
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, 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, and preferably a 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, fractionally;
• food should contain a sufficient amount of easily digestible carbohydrates (honey, sugar, fruits, vegetables);
• food should contain a large amount of vitamins and minerals;
• need to get more fiber
• fat restriction is necessary only in the presence of symptoms of cholestasis;
• after the patient's condition improves, the usual diet can be restored by introducing protein products gradually (as complementary foods for children), starting with vegetable protein (buckwheat, cereals, legumes), then dairy products and, with good protein tolerance, meat;
• if a patient develops hepatic encephalopathy with a violation of the act of swallowing or hepatic coma, parenteral nutrition is recommended (introduction 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 drugs without consulting a doctor),
• drink enough liquid
• refuse heavy physical exertion,
• get enough sleep, improve your mental state,
• to prevent constipation, it is necessary to carry out cleansing enemas 2 times a day,
• if the condition allows, more to be in the fresh air, while avoiding open sunlight.

Take care of your health!

Acute liver failure (ALF) is a serious complication of many diseases and pathological conditions. In cases of delayed diagnosis and untimely therapy, the lethality with it reaches 60-80%.

The main functions of the liver. The liver plays a very important role in protein exchange. It synthesizes all albumin (12-15 g per day). In addition, transamination and deamination of amino acids are carried out with the participation of the enzymes ALT, AST, glutamate dehydrogenase; formation of urea, glutamine, creatine. 75-90% of -globulins, 50% of -globulins are synthesized in liver cells (-globulins are not synthesized in the liver). In the liver, components of the prothrombin complex (II, VII, IX, X), which depend on vitamin K, are synthesized, as well as other coagulation factors (fibrinogen, VI, XI. XII, XIII). Here, the formation of blood clotting inhibitors: antithrombin and antiplasmin. In the liver, protein catabolism is also carried out with the participation of cathepsin enzymes, acid carboxypeptidase, collagenase, dipeptidase; specific metabolism of individual amino acids (90% of phenylalanine is converted to tyrosine, tryptamine, serotonin, quinoline acid are formed from tryptophan; histamine from histidine, and ethanolamine, the initial product of choline synthesis, from serine). Liver enzymes directly cleave hydrogen sulfide from cysteine ​​molecules, catalyze the oxidation of SH-groups of sulfur-containing amino acids.

The role of the liver in lipid metabolism consists in the oxidation of acylglycerols; the formation of ketone bodies (acetoacetic acid, -hydroxybutyric acid); synthesis of triglycerides, phospholipids, lipoproteins; synthesis of cholesterol; the formation of bile acids (cholic and chenodeoxycholic) up to 0.4 g / day. The liver is involved in the breakdown and absorption of dietary lipids, since the presence of bile is necessary for the hydrolysis and absorption of fats in the intestine. Bile acids are in constant enterohepatic circulation. They pass through the liver and intestines up to 10 times a day (twice with each meal). In hepatocytes, reabsorbed bile acids are rebound to glycine and taurine and re-excreted into bile.

The liver is also involved in carbohydrate metabolism. It includes the inclusion of galactose and fructose in metabolism; gluconeogenesis; synthesis and breakdown of glycogen, the content of which in the liver is 100-300 g; formation of glucuronic acid. During the day, a four-fold exchange of glycogen stores occurs in the liver.

The importance of the liver in pigment metabolism also hard to overestimate. She is involved in: the formation of bilirubin; its capture, conjugation and excretion; metabolism and re-excretion of urobilinogens. During the day, 1% of circulating erythrocytes disintegrates, 7.5 g of hemoglobin is released, up to 100-300 mg of bilirubin is formed. 70-80% of bilirubin is associated with glucuronic acid, as well as with glycine, sulfuric and phosphoric acids. Upon entering the intestine as part of bile, bilirubin is reduced by bacterial dehydrogenases to colorless urobilinogen bodies - d-urobilinogen, i-urobilinogen and 1-urobilinogen (stercobilinogen) in the distal small intestine and in the large intestine. Normally, enterohepatic circulation of urobilinogens is minimal. They are absorbed in the proximal small intestine, re-excreted into the bile or broken down in the liver. With the defeat of hepatocytes, the re-excretion and splitting of urobilinogens is disturbed, they enter the general bloodstream and urine. Each fraction of bilirubin is a mixture of chemically heterogeneous compounds (up to 8-9 fractions from one serum).

The liver is involved in the metabolism of biologically active substances, regulating the content of steroid hormones (glucocorticoids, aldosterone, androgens and estrogens). It forms water-soluble conjugates with glucuronic and sulfuric acids, enzymatic inactivation occurs, and a specific glucocorticoid-binding protein, transcortin, is also formed; non-steroidal hormones are inactivated - insulin, glucagon, thyroid hormones, somatotropic, gonadotropic, antidiuretic hormones. In addition, catecholamines are formed in the liver (tyrosine, a precursor of adrenaline, norepinephrine, dopamine, is formed from phenylalanine in hepatocytes), their inactivation, as well as the formation of serotonin and histamine.

The liver plays an important role in vitamin metabolism. The liver is involved in the absorption of fat-soluble vitamins (A, D, E, K), which requires bile acids. It synthesizes vitamin A from carotene, forms biologically active forms of vitamins B1 (pyridoxal phosphate), folic acid (tetrahydrofolic acid), choline (cytidine monophosphate choline). The liver carries out the deposition and excretion of vitamins A, D, K, PP, E, Bl, B2, B12, folic acid.

The liver is also involved in microelement metabolism. Here is the depot of iron in the body (15 mol/kg of tissue in men and 4 mol/kg in women) in the form of ferritin (23% iron). With an excess, hemosiderin (37% iron) is formed. The liver synthesizes transferrin, which transports iron into the bloodstream. In addition, there is also a copper depot in the liver, and ceruloplasmin is synthesized.

The liver is one of the main components functional systems detoxification. It is in it that the biotransformation of xenobiotics and endogenous toxic substances mainly occurs. The liver creates a powerful barrier to blood flowing from the intestines. In the intestine, under the action of bacterial enzymes, the protein decomposes to toxic products: phenol, indole, skatole, cadaverine, putrescine, etc. The liver neutralizes all these products due to the processes of oxidation, acetylation, methylation, formation of paired compounds with sulfuric and glucuronic acids. Ammonia is neutralized by converting it into urea. In addition, the liver, together with the spleen, is removed from the flowing blood and destroy up to 70-80% of microorganisms. Kupffer cells of the liver not only have a pronounced phagocytic activity against microbes, but also provide blood purification from endotoxins of the intestinal microflora, antigen-antibody complexes, tissue decay products.

There is no unity in understanding the very essence of liver failure, as well as its significance in the thanatogenesis of many pathological conditions.

Liver failure should be understood as a state of the body in which the liver cannot maintain homeostasis and the patient's body's need for metabolism, biotransformation of toxins and biologically active substances.

There are six groups of main causes that determine the development, course and clinical picture of liver failure:

1) fulminant and subfulminant hepatitis caused by viruses, rickettsiae, spirochetes and other hepatotropic infections;

2) toxic hepatitis, degenerative lesions of the liver, developing as a result of toxic or toxic-allergic effects of various chemicals;

3) unfavorable course of chronic hepatitis and liver cirrhosis;

4) prolonged and severe cholestasis;

5) liver necrosis or tumor destruction of the organ;

6) hypoxia of the liver parenchyma.

Fulminant hepatitis- acute hepatitis, complicated by acute liver failure with encephalopathy with impaired consciousness in terms of less than 2 weeks after the onset of jaundice. subfulminant hepatitis- acute hepatitis, complicated by acute liver failure with encephalopathy with impaired consciousness in the period from 2 weeks to 3 months after the onset of jaundice. After the onset of encephalopathy, the acute stage lasts up to 7 days, acute - up to 28 days, subacute - up to 3 months. Mortality in fulminant and subfulminant forms without liver transplantation reaches 80%.

The leading cause of fulminant hepatitis is hepatotropic viral infection. Improving the diagnosis of liver diseases has led to the expansion of the alphabet of hepatotropic viruses. Currently, 6 pathogenic viruses (HAV, HBV, HCV, HDV, HEV, SEN) have been identified, 4 of which (HBV, HCV, HDV, SEN) have the undoubted ability to cause chronic inflammation of the liver (Table 39.1).

Table 39.1

Hepatotropic viruses

Name of the virus	pathogenicity	Chronization

Note: - "?" - unknown.

Development of acute and subacute toxic hepatitis associated with the action of hepatotoxic xenobiotics, including drugs. The mechanisms of direct hepatotoxic action are damage to hepatocytes, blockade of tissue respiration processes, disruption of nucleic acid synthesis. Hepatotoxic poisons are found both in production (carbon tetrachloride, benzene, toluene, FOS, chloroform, nitro dyes, acids, alkalis, lead, etc.) and in everyday life (poison phalloidin contained in pale grebe; aflatoxins contained in mold fungi; ethyl alcohol, inorganic compounds of arsenic, phosphorus, beryllium). One of the rare complications that occur after anesthesia is toxic hepatitis caused by fluorine-containing inhalation anesthetics. Most often they occur after the use of halothane, less often they are caused by enflurane and isoflurane. It is believed that such damage occurs more often with repeated use of fluorine-containing volatile anesthetics or even with the first anesthesia while these patients are receiving triiodothyronine.

The cause of the development of toxic hepatitis with ALF can also be many therapeutic drugs, among which fat-soluble drugs occupy a special place. Hence the high hepatotoxicity of monooxidase inhibitors, tricyclic antidepressants (amitriptyline), erythromycins (not only ethyl succinate and propionate, but also modern esmolate), anti-tuberculosis drugs (isoniazid, rifampicin), sulfosalazine, brufen, paracetamol (possibility of overdose in children), anticonvulsant sodium valproate (especially when taken in combination with phenobarbital).

Habitual drugs - analgesics, aminophylline, antiarrhythmic drugs (for example, cordarone) are metabolized in the liver. In patients with hepatopathy of various origins, they can cause a deepening of functional disorders, up to hepatic coma. In contrast to infectious hepatitis, the damaging effect of a single dose of xenobiotics quickly reaches a maximum and then regresses at different rates. It is necessary to save the patient with intensive treatment and wait for the regeneration of hepatocytes.

unfavorable course chronic hepatitis and cirrhosis of the liver leads to the development of insufficiency of its function. Cirrhosis of the liver, as a rule, is combined with manifestations of portal hypertension. A dangerous complication of portal hypertension is the development of bleeding from varicose veins of the esophagus. The progression of ALF in such circumstances may be associated with excessive intake of dietary protein, the administration of barbiturates and opiates, with intestinal infection (in particular with salmanellosis), uncontrolled administration of diuretics (against the background of alkalosis, ammoniogenesis in the kidneys is disturbed). Drug factors may also be important: the use of methionine, the introduction of conventional, non-specialized amino acid mixtures to correct the protein deficiency that is common in these patients. For the progression of ALF in such patients, surgical stress, systemic hypoxia, transfusion of significant amounts of citrate blood of late storage periods, and endogenous intoxication of any origin are also important. Undoubtedly, gastrointestinal bleeding with microbial decay of the blood that has poured into the intestine and massive ammoniogenesis has a dramatic effect. Therefore, with deep cirrhotic changes in the liver, aggravation of ALF can be expected after even minor surgical interventions.

Prolonged and severe cholestasis with an obstruction to the bile duct at various levels (from the cholangi to the major duodenal papilla) can cause acute renal failure due to high jaundice. Through the stage of intrahepatic cholestasis, the development of ALF in sepsis is possible. Functional decompensation of the liver due to chronic cholestasis occurs, as a rule, with the so-called sclerosing cholangitis.

Causing factors parenchyma hypoxia liver: shock; blood loss and all types of hypovolemia, heart and respiratory failure, renal failure, hemolysis of erythrocytes (poisoning with acetic acid, copper sulphate), gastrointestinal bleeding (blood putrefaction leading to the formation of ammonia, phenol, indole), general hypoxia, extensive injuries and burns , septic conditions, accompanied by massive bacterial invasion and hemolysis, operations using cardiopulmonary bypass.

As a rule, the clinical manifestations of ALF are rather nonspecific and are detected in the late stages of the disease, so the main determinants of its presence and severity are laboratory criteria and the results of stress tests. In the formation of a specific pathological phenomenon leading to the development of ALF, various combinations of the main syndromes that characterize its features are essential:

cholestasis syndrome,

hepatocytolysis syndrome,

inflammatory mesenchymal syndrome,

hemorrhagic syndrome,

Portal hypertension syndrome, hepatolienal syndrome,

Syndrome of hepatic encephalopathy.

cholestasis syndrome- violation of the outflow of bile with the accumulation of its components in the liver and blood. Jaundice is a symptom that develops due to the accumulation of excess bilirubin in the blood. Hepatic jaundice is caused by an isolated or combined violation of the capture, binding and excretion of bilirubin. Excretion disorders cause an increase in the level of conjugated bilirubin in the blood and its appearance in the urine, which is due to a change in the permeability of the liver cells, rupture of the bile ducts due to necrosis of the liver cells, blockage of the intrahepatic bile ducts with thick bile as a result of destruction and inflammation. In this case, bile regurgitation occurs back into the sinusoids. In the liver, the transformation of urobilinogens is disrupted, urobilin enters the urine. Icteric staining of the skin and mucous membranes appears with an increase in bilirubin over 34.2 µmol / l. The liver is capable of metabolizing and secreting bilirubin into bile in an amount 3-4 times higher than its production under physiological conditions.

Clinical signs of cholestasis: skin itching, scratching, malabsorption of fat-soluble vitamins (disordered vision in the dark, bleeding, bone pain), jaundice, dark urine, light feces, xanthomas, xanthelasma.

Laboratory signs: accumulation of bile components in the blood (cholesterol, phospholipids, bile acids, alkaline phosphatase, y-glutamyl transpeptidase, 5-nucleotidase, copper, conjugated fraction of bilirubin). With a complete violation of the outflow of bile, hyperbilirubinemia reaches 257-342 µmol/l, when combined with hemolysis and impaired glomerular filtration in the kidneys, it can reach 684-1026 µmol/l.

Syndrome cytolysis is associated with a violation of the integrity of hepatocytes and membrane permeability, damage to cellular structures and the release of cell components into the intercellular space, as well as into the blood, and impaired function of hepatocytes.

Clinical signs of cytolysis: jaundice, hemorrhagic syndrome, bleeding gums, nosebleeds, hemorrhagic skin rashes, dyshormonal disorders, hepatic signs (palmar erythema, Chistovich's stars, breath odor), weight loss, dyspeptic and asthenic syndromes, nervous -mental disorders.

Laboratory signs: an increase in the activity of alanine aminotransferase, aspartate aminotransferase, aldolase, conjugated (direct) bilirubin in the blood, a decrease in the prothrombin index, albumin, cholesterol esters, cholinesterase activity, fibrinogen, blood coagulation factors. Among the new indicators of cytolysis, attention is drawn to alpha-glutathione-S-transferase, an enzyme of the hepatocyte cytoplasm. As an indicator of cytolysis, it is superior to aminotransferases.

Inflammatory mesenchymal syndrome is an expression of the processes of sensitization of immunocompetent cells and activation of the reticulohistiocytic system in response to antigenic stimulation.

Clinical signs: fever, joint pain, swollen lymph nodes and spleen, skin and kidney damage.

Laboratory signs: an increase in ESR, leukocytes,  2 - and -globulins, immunoglobulins, a positive thymol test, a decrease in the sublimate test, antibodies to subcellular components of the liver tissue appear (determined using enzyme immunoassay). In addition, new markers of mesenchymal inflammatory syndrome and fibrogenesis have been created. Procollagen-3-peptide is one of the new indicators of this class. Hyaluronate is another sample representative of this class. It is a component of the extracellular matrix. With its help, for the first time, it became possible to assess the function of endothelial elements of the liver, which play an important role in normal and pathological conditions. Hyaluronate is a marker of inflammation and liver fibrogenesis.

Hemorrhagic syndrome. With ALF, there is a decrease in the synthesis of blood coagulation factors. Initially, the synthesis of VII decreases, then II, IX, X, and in severe hepatocellular insufficiency, the synthesis of factors I, V, XIII also decreases. With obstructive jaundice, prothrombin synthesis is impaired not as a result of liver damage, but due to the cessation of bile flow to the intestine (acholia). For the synthesis of prothrombin, vitamin K is required, which is fat-soluble and absorbed in the intestine during normal fat digestion. A necessary condition for this is the presence of bile in the small intestine. Therefore, some patients are shown the introduction of vitamin K, although this rarely leads to the elimination of coagulopathy. Increased consumption of blood clotting factors occurs due to the fact that thromboplastic factors are released into the blood from damaged liver cells, platelet thrombi are formed, and the fibrinolytic system is activated. These processes require an increased amount of I, II, V, VII, IX-XI factors, resulting in consumption coagulopathy, i.e. thrombohemorrhagic syndrome occurs. Hemorrhagic syndrome is manifested by bleeding, which in turn leads to the development of hemic hypoxia and deterioration of liver nutrition. Bleeding exacerbates hypoproteinemia. Bleeding is more common in the gastrointestinal tract, which causes microbial fermentation of blood in the intestine, an increase in ammonia production and aggravation of intoxication.

Syndrome portal hypertension, hepatolienal the syndrome manifests itself in the form of a combination of hepato- and splenomegaly, increased spleen function. The combination of damage to the liver and spleen is explained by the close connection of both organs with the portal vein system, the commonality of their innervation and lymph drainage pathways. Both organs form a single reticulohistiocytic apparatus. The development of portal hypertension leads to the formation of varicose veins of the esophagus (bleeding), the development of ascites.

Assessment of the functional capacity of the liver is carried out in three areas: metabolic, excretory, detoxification.

To control the usefulness of the course of metabolic processes, the following tests are used: determination of the concentration of prothrombin, albumin, cholinesterase activity. More informative is the test with an intravenous load of galactose, as well as the determination of the level of short-lived procoagulants of hepatic origin: proaccelerin and proconvertin. Another group of samples is associated with excretory processes. With known reservations, this also includes indicators of cholestasis - bilirubin, bile salts, gamma-glutamyl transpeptidase (GGTP) of blood serum. It is also important to determine the typical indicators of hepatodepression - bromsulfalein and especially indocyanine samples. A significant part of the stress tests is associated with detoxification processes, therefore, with the function of the smooth endoplasmic reticulum and, first of all, with the work of cytochromes P450, P448, etc. In the processes of this kind, the transformation of medicinal substances is carried out. According to this principle, stress tests are built antipyrine, caffeine and lidocaine, as well as amidopyrine breath test.

Hepatic encephalopathy(PE) is a complex of potentially reversible neuropsychiatric disorders, including changes in consciousness, intelligence and behavior, and neuromuscular disorders. Currently, the “glia” hypothesis, which most fully combines the accumulated knowledge about the pathogenesis of hepatic encephalopathy, according to which endogenous neurotoxins and amino acid imbalance resulting from hepatocellular insufficiency and (or) portosystemic shunting of blood, lead to edema and functional disorders of astroglia. The latter change the permeability of the blood-brain barrier, the activity of ion channels, disrupt the process of neurotransmission and the provision of neurons with high-energy compounds. These changes are manifested by clinical symptoms of hepatic encephalopathy. Among endogenous neurotoxins, the leading place is given to ammonia.

In recent years, some mechanisms of the neurotoxic action of ammonia have been revealed, in particular: limitation of the function of the malate-aspartate shuttle, which results in a decrease in the transport of hydrogen ions and a decrease in ATP synthesis in the brain. Ammonia affects the permeability of the blood-brain barrier, which stimulates the transport of aromatic acids to the brain and, as a result, enhances the synthesis of false neurotransmitters and serotonin. Ammonia increases the affinity of postsynaptic serotonin receptors, which play an important role in the regulation of sleep and behavior. Possibility of direct modulation of neuronal activity by ammonia is considered . The group of endogenous neurotoxins also includes mercaptans, short- and medium-chain fatty acids, and phenols. Thus, hepatic encephalopathy is the result of a complex effect and mutual reinforcement of several factors: endogenous neurotoxins, among which ammonia plays a leading role, amino acid imbalance and changes in the function of neurotransmitters and their receptors.

The severity of neuropsychic symptoms of hepatic encephalopathy ranges from "0" (latent or subclinical form - "LPE") to "4" (deep coma). The neuropsychiatric symptoms of PE include changes in consciousness, intelligence, behavior, and neuromuscular disorders. The identified four stages of hepatic encephalopathy can pass one into another. At the same time, most of the symptoms that appeared in the earlier stages persist in the following ones. The gradation of hepatic encephalopathy according to the severity is presented in Table. 39.2. The main criterion for determining its stage is the state of consciousness. The rest of the symptomatology is of subordinate importance. Latent hepatic encephalopathy (stage 0) is characterized by the absence of clinical symptoms and is detected only when using additional research methods - psychometric tests (number connection test, line test), electroencephalography, evoked potentials, etc. The frequency of LPE in patients with liver cirrhosis is 30-70 %. In the 1st stage of hepatic encephalopathy, the rhythm of sleep is disturbed: drowsiness during the day and insomnia at night appear. In the 2nd stage, drowsiness increases and there is a violation of consciousness. In the 3rd stage, disorientation in time and space joins the listed changes, confusion of consciousness increases and the 4th stage begins - the actual coma. It is characterized by a lack of consciousness and reaction to painful stimuli.

Table 39.2

Stages of hepatic encephalopathy (according to H.O. Sonn, 1979)

	State of consciousness	Intelligence	Behavior	Neuromuscular disorders
	not changed	not changed	not changed	not clinically detectable
1. Light	sleep disorders	decreased attention, concentration, reaction speed	personality accentuation, neurasthenia, euphoria, depression, talkativeness, irritability	fine motor disorders, handwriting changes, fine-sweeping tremor
2. Medium	lethargy	lack of sense of time, counting disorders, amnesia	lack of inhibition, personality changes, fear, apathy	asterixis, slurred speech, hyporeflexia, stupor, ataxia
3. Heavy	disorientation doubtfulness stupor	profound amnesia, inability to count	inappropriate behavior, paranoia, rage	hyperreflexia, nystagmus, clonus, pathological reflexes, spasticity
	lack of consciousness and reaction to pain	lack of function	function termination	areflexia, loss of tone

The course of endogenous hepatic coma is most often acute. Brain dysfunction occurs suddenly, and their dynamics progresses. Often in the first stages, there is agitation and anxiety of the patient. The prognosis of endogenous hepatic coma is poor - without transplantation, the mortality rate in patients with fulminant liver diseases reaches 80%.

In most patients, the development of hepatic encephalopathy is associated with provoking factors: gastrointestinal bleeding (19-26%), infection, including peritonitis (9-15%), taking sedatives and tranquilizers (10-14%), massive diuretic therapy (4 - 8%), alcohol intake (5 - 11%), porto-caval anastomosis surgery (6 - 8%), excessive consumption of animal proteins (3 - 7%), surgery for other diseases (2 - 6% ), laparocentesis with the removal of a large amount of ascitic fluid (2 - 5%).

After their elimination and appropriate treatment, hepatic encephalopathy regresses. However, the likelihood of developing a new episode increases. Significant difficulties in the treatment are chronically progressive course of encephalopathy. It is rare and develops in elderly patients with severe porto-caval bypass blood after porto-caval anastomosis surgery. The appearance of encephalopathy in a patient with liver cirrhosis is an unfavorable prognostic sign. Together with other symptoms (ascites, hemorrhagic syndrome, increased jaundice), its appearance indicates decompensation of cirrhosis.

Classification. Given the many causes leading to the development of liver failure, and the diversity of the clinical picture of this pathology, there is currently no single classification of acute liver failure. From our point of view, in practical terms, the working classification presented in Table 39.3 is convenient. It highlights excretory (obstructive jaundice, etc.) and cellular-hepatic (liver cirrhosis, toxic hepatitis, etc.) forms of acute liver failure, as well as two degrees. Decompensated degree of ALF is determined in the presence of two or more signs.

Table 39.3

Classification of liver failure

(Lakhin R.E., 1999)

signs	Degrees and forms of liver failure
	Compensated (hepatoprival syndrome)		Decompensated
Forms of liver failure	excretory	cellular-hepatic	excretory	cellular-hepatic
Hepatic encephalopathy	PPE - 1st stage		2-4 stages
Total bilirubin, µmol/l	less than 100.6		over 100.6
Bleeding from esophageal varices
Albumin, g/l	over 30.0	over 21.2	less than 30.0	less than 21.2
Prothrombin index, %		over 72.6		less than 72.6

For patients with cirrhosis of the liver, it is possible to use the Child-Pugh criteria that have become widespread (Table 39.4). The degree of liver dysfunction on this scale correlates with mortality. So, for example, in patients with cirrhosis of the liver who underwent porto-caval shunting, this figure is 0-10%, 4-31% and 19-76% for classes A, B and C, respectively.

Table 39.4

Childe–Pugh criteria

Criterion
total bilirubin	28 µmol/l 1.26 g/100ml			over 67.2
Albumen
Prothorombin index
			small, transient	big, torpid
Encephalopathy			periodical
Every sign
Sum of points

Intensive therapy. Acute liver failure is an indication for placing patients in the ICU. They need to perform catheterization of the central vein, maintaining approximately “zero” hydrobalance. In patients with ALF, it is important to control glucose levels (the risk of hypoglycemia, however, it is better not to administer a 40% glucose solution, preference is given to the slow administration of a 10% solution, patients are very sensitive to insulin). Given the predisposition of patients to infection, intensive care is of great importance.

Basic therapy:

Improvement of hepatic blood flow (elimination of hypovolemia, anemia, prescription of cardiotonic drugs, elimination of intestinal paresis);

Blood oxygenation (oxygen inhalation, HBO);

Antioxidants (Solcoseryl, Actovegin up to 1000 mg/day IV);

Prevention and treatment of acute respiratory failure;

Prevention and treatment of acute renal failure;

Prevention and treatment of septic complications;

Prevention and treatment of DIC syndrome (+ vitamin K);

Prevention and treatment of mental disorders;

Directed infusion therapy (concentrated solutions of glucose with magnesium, insulin, replenishment of protein losses);

Diet with restriction of protein intake, especially animal (better digestible carbohydrates), parenteral nutrition.

specific therapy.

Etiological treatment is aimed at eliminating the cause of ALF development. . In shock, hypocirculation, for example, urgent normalization of circulating blood volume, cardiac output and microcirculation is required. In case of poisoning with hepatotoxic poisons, special attention is paid to antidote therapy and removal of the poison from the body. In viral hepatitis, antiviral therapy is carried out, the use of which in the early stages of the disease often prevents acute liver failure. The use of combined treatment of autoimmune hepatitis with corticosteroids and azathioprine made it possible to achieve a 20-year survival rate of 80% of patients. However, there remains a significant category of patients resistant to immunosuppression.

Elimination of the negative effects of ammonia, first of all, involves a decrease in its production due to intestinal decontamination (nonabsorbable antibiotics), its cleansing (enemas), the use of glutamic acid (1% solution 10.0 ml IV or in Table 1, 0 g 2-3 r / day), lactulose (15-200 ml / day, reaching an increase in stool up to 2-3 times).

Utilization of ammonia is achieved using arginine hydrochloride (0.3 - 0.5 g / kg / day in 2-3 doses), ornicetil (hepa-merz, ornithine-aspartate), sodium benzoate, which binds ammonia with the formation of hippuric acid (10 g / days).

Of great interest is the use of drugs with a narrowly targeted effect on liver cells - hepatoprotectors. Data on the mechanism of action of these drugs are presented in table. 39.5. Due to the fact that it is different, it is advisable to prescribe several drugs at the same time (for example, heptral + Essentiale + ornithine). The recommended doses of hepatoprotectors in the treatment of ALF are:

heptral - 10 - 20 ml (800-1600 mg) intravenously or intramuscularly per day;

natrosil - 1 teaspoon 3 times a day;

legalon - 1 caps (140 mg) 3 times a day;

Essentiale - 10 - 20 ml per day or 2 caps. 3 times a day inside;

hofitol - 5 ml 1-2 times a day IM or IV;

lipoic acid - 0.5% solution up to 25 mg / kg / day;

lipamide - 0.05 g, 3 r / day inside;

lipostabil - 10 - 20 ml IV 1 time per day or 2 caps 3 times a day inside;

ornitsetil - 1-3 bottles (2-6 g) per day IM or IV.

Table 39.5

The mechanism of action of hepatoprotectors

Preparations	Syndromes
		Mesenchymal cellular inflammation	Impaired biosynthetic function	cholestasis	Hepatocellular insufficiency
Natrusil (milk thistle)
Essentiale
Lipostabil
Sirepar (Vitogepar)
Riboxin
Bemitil (bemactor)

The operation of choice for extracorporeal detoxification has recently been considered to be plasmapheresis in the plasma exchange mode, and to a lesser extent, plasmasorption. Hemosorption on standard sorbents in hyperbilirubinemia is ineffective, even if special methods of preperfusion treatment of hemosorbent are used. In the presence of obstructive jaundice, an indispensable condition for efferent therapy should be considered a preliminary reliable reduction in biliary hypertension by external bile diversion or internal drainage of the biliary tract. Sometimes the first operation of plasmapheresis with plasma exchange mainly with components (native plasma) and blood products (albumin) is performed immediately before surgery, repeating it 1-2 more times with an interval of 1-2 days soon after the operation. A similar approach has to be taken when sufficiently traumatic surgery is performed in patients with initial severe liver failure. Albumin-mediated hemodiafiltration according to the system of return molecular adsorption, as well as the use of sorption techniques on live hepatocytes, have the highest efficiency in the treatment of ALF.

Transplantation is considered a promising direction for severe liver failure. Available data suggest that the one-year survival rate for liver transplantation is 68%; 5-year-old - 62% of the total number of patients operated on.

Indicators of the degree of urgency of transplantation - UNOS criteria.

1 degree. Acute liver failure in adults, acute or chronic failure in a child (less than 18 years old) with an expected life expectancy without liver transplantation of less than 7 days while in the ICU.

2a degree. Chronic liver disease with a liver transplant-free life expectancy of less than 7 days while in the ICU.

2b degree. Stay in the ICU for at least 5 days for acute liver failure.

3 degree. The need for a permanent stay in the hospital.

Violations in the work of these functions indicate liver problems.

What is liver failure

Viral hepatitis and poisoning, combined with uncontrolled medication, greatly harm the human body. The consequence of such phenomena is the syndrome of liver failure. The disease is accompanied by massive necrosis of the cells of the organ and degenerative changes in the parenchyma. EEG, hepatoscintigraphy, biochemical analysis of blood parameters will help to identify the syndrome of hepatocellular insufficiency.

Liver failure - classification

According to the course of the disease, acute and chronic forms are distinguished. Acute liver encephalopathy has its own classification. It is divided into small, acute and heavy. These types of illness manifest themselves in different ways. In acute minor encephalopathy, mild liver cytolysis and cholecystitis are present in combination with signs of the underlying disease. The patient notices:

• drowsiness;
• mild nausea;
• decreased appetite.

If the cause of the disease was a decrease in the number of red blood cells or vasodilation, the patient is diagnosed with sleep disturbance, itching, and a decrease in urine volume. Severe encephalopathy develops due to viral hepatitis and hepatocellular cancer within three days. In 80% of cases, it is fulminant and requires emergency care. Patients have weakness, aversion to food, decreased ability to work. Signs develop in stages.

The classification of liver failure according to the form of the disease includes endogenous and exogenous disease. In the endogenous form, massive cellular liver cytolysis is diagnosed. Exogenous disease is characterized by the entry of toxic substances from the body into the bloodstream. Acute liver failure is characterized by the simultaneous development of these forms with hepatargia.

Stages of liver failure

Clinical manifestations of the disease are formed gradually and depend on the degree of intoxication of the body. Due to the disease, ascites, dyspeptic disorders, varicose / icteric disease occur. At the last stage of the disease, hepatargia develops with hepatic coma. There are 3 stages of liver failure:

The initial stage is characterized by insomnia, weakness, changes in appetite. At a pronounced stage, the patient begins to show pathological reflexes, hypoproteinemic edema. During the terminal stage, the patient is diagnosed with cachexia, dystrophic changes in tissues, loss of consciousness, divergent strabismus, absence of pupillary reactions. The reaction to pain with spontaneous movements disappears.

Liver failure - symptoms

The nature of the disease is determined by two pathological processes: organ tissue necrosis and cholestasis syndrome. With extensive destruction of the liver, the patient begins to fever, pressure rises, tachycardia appears. Cholestasis is accompanied by jaundice. The color of the skin changes from green to orange, set by the degree of biliary dyskinesia. The intensity of manifestations depends on the nature of tissue damage, the rate of development of the disease. Common signs of liver failure:

• lethargy or hyperexcitability;
• drowsiness;
• nausea;
• rigidity;
• cramps / tremors of the limbs.

The filtering ability of the kidneys gradually decreases, the amount of decay products in the body increases. With rapidly developing hepatonecrosis, cellular metabolism is sharply disturbed. Protein fibers are destroyed, which leads to pulmonary edema, hemorrhagic diathesis, cholelithiasis. A person has plantar reflexes, hepatargia.

Symptoms of liver failure in women

The main symptom of the disease is a violation of the menstrual cycle. Also, symptoms of liver failure in women include emotional disorders, sleep disturbance, dystrophic changes in the pelvic organs and abdominal cavity. If the patient is pregnant, then the disease is accompanied by jaundice, cirrhosis, hepatitis E, fatty hepatosis.

Symptoms of liver failure in men

The first manifestation of the disease is a sharp decrease in libido and mental instability. The patient's taste preferences change, there is an aversion to alcohol and nicotine, the face becomes grayish. Lethargy and apathy are replaced by bursts of working capacity, cramps of the limbs. Symptoms of liver failure in men appear faster than in women.

The symptom complex of the disease is the same as in adults. The child becomes inactive, sleeps a lot, there is a perversion of appetite. Liver failure can be diagnosed in children using CT, EEG, and a biochemical blood test. After the discovery of the disease, the child is prescribed lactulose, folic acid, antibiotics, interferon, vitamin D. Diet is mandatory.

Treatment of liver failure

Therapy is carried out in stationary conditions. Patients are regularly taken for analysis of blood and urine. Treatment of liver failure is aimed at eliminating the underlying disease that affected the functionality of the organ, and at eliminating encephalopathy. Patients are given daily antibiotics, anabolic steroids, fresh liver extracts, glucose, insulin, methionine, glucocorticoid hormones. If a sharp decrease in the number of protein fractions in the blood is established, patients are prescribed albumin injections or plasma transfusions.

Liver failure - diet

The patient's menu should contain a lot of carbohydrates. Proteins with fats are completely removed from the diet. The diet for liver failure consists of a large number of vegetables, fruits, and dairy products. Pickled, fried, spicy, smoked dishes are excluded from the menu. If after therapy the condition of the body has improved, 40 grams of protein is added to the diet.

Video: liver failure - what is it

The information presented in the article is for informational purposes only. The materials of the article do not call for self-treatment. Only a qualified doctor can make a diagnosis and give recommendations for treatment based on the individual characteristics of a particular patient.

Liver failure - life is at stake!

Classification

The nature of acute and chronic insufficiency differs.

The acute form develops in the acute form of hepatitis, poisoning or subacute liver dystrophy.

The chronic form is characteristic of cirrhosis of the liver, chronic hepatitis. Both forms of insufficiency can end in hepatic coma.

The stages differ: compensated, decompensated, dystrophic and hepatic coma.

Endogenous - is a complication of the death or degeneration of liver tissue and is characteristic of cirrhosis, hepatitis.

Exogenous is self-poisoning of the body by metabolic products and substances produced by the intestinal microflora. This happens if the above substances enter the blood through the walls of the intestine and do not pass through the liver, for example, if the portal vein is clogged. This form of insufficiency does not cause changes in the quality of liver tissue.

The reasons

Hepatogenic: diseases and phenomena that directly affect the liver tissue.

Extrahepatic: processes that affect liver function indirectly.

• Dystrophy ( use of drugs, sulfonamides, antibiotics, poisoning with toxic substances, alcohol, mushrooms)
• Hepatitis
• Cirrhosis.

Symptoms

• Aversion to food
• Aversion to alcohol in people who drink before)
• Aversion to nicotine in former smokers)
• Lethargy
• Weakness
• mood instability
• The complexion becomes grayish or yellowish
• Night blindness appears
• The menstrual cycle is disturbed in women, libido in men, other hormonal disorders appear
• Has a tendency to bleed
• Puffiness.

The exogenous form is characterized by:

• Mental instability of a temporary nature up to mental disorders
• bad dream
• neurological symptoms.

Acute liver failure

The main symptom of acute liver failure is hepatic encephalopathy.

The condition causes death in 50 to 90% of cases.

1. Viral hepatitis

3. Poisoning with poisons that destroy liver cells ( counterfeit alcohol, mushrooms)

5. Liver dystrophy during pregnancy, passing in an acute form.

• General deterioration in well-being
• Yellowing of the sclera, skin
• Rotten meat smell from the mouth
• Trembling of limbs
• Puffiness.

Urgently go to the hospital.

Diagnostics

5. Blood biochemistry

6. Analysis for alpha-fetoprotein

7. Abdominal ultrasound

9. Radionuclide scanning

In children

In newborn babies under the age of 15 days, liver failure is often caused by the immaturity of the production of certain enzymes.

In addition, in babies, the cause of this condition may be hypoxia and an increased amount of proteins in the body.

If you do not provide urgent help to the baby, he falls into a coma.

Treatment of a baby with liver failure is carried out only in the hospital. In the future, after being discharged home, the child should adhere to a special diet for a long time and take increased doses of vitamins of the group B, A, C, K.

Treatment

It is necessary to maintain the vital activity of the patient's body and at the same time fight the underlying ailment that caused this condition.

If the cause of deficiency is poisoning, toxins are removed from the body with the help of laxatives. To cleanse the body of ammonia, use intravenous injections. glutamic acid twice or thrice a day for 3-4 days.

Use of oxygen installations and oxygen pillows is obligatory.

In the chronic form of insufficiency, drugs are prescribed that alleviate the patient's condition, reduce the proportion of protein in food, enemas are shown to cleanse the intestines, as well as from time to time antibiotics, vitamins of the group AT in the form of injections vitohepat.

Diet

2. The basis of the diet is plant foods ( juices from vegetables and fruits, honey, puree soups, compotes with boiled fruits, rosehip broth, jelly, jelly).

3. Eat food once every 2 hours in a semi-liquid or liquid form.

4. Refuse salt completely.

5. Drink up to 1.5 liters of fluid per day in the absence of edema.

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Liver failure: symptoms and treatment of the disease

Our body is an incredibly complex mechanism. Thousands of established processes ensure the stable operation of the whole organism. Failure in one of the organs can lead to disruption of all vital processes. One of the common diseases is liver failure, its symptoms depend on the type and nature of the disease. Necrosis of the liver tissue or cholestasis syndrome.

Why does liver failure occur?

There are a lot of causes. The most common of them should be highlighted:

• acute and chronic hepatitis;
• malignant formations;
• diseases of the heart, blood vessels and other organs;
• infectious diseases;
• poisoning (food, medicines);
• transferred stresses (extensive burns, serious injuries, septic shock, large blood loss).

Types and symptoms

cholestasis syndrome. The disease consists in poor excretion of bile from the liver tissues. The symptoms are:

• with functional holistasis. Decrease in the normal movement of bile, water, bilirubin, acids through the tubules of the liver;
• with morphological holistasis. Accumulation of bile compounds in the bile ducts;
• with clinical holistasis. Accumulation in the blood of components that are converted into bile. There is itching of the skin, jaundice, an increase in bilirubin in the blood.

necrosis syndrome. This disease destroys the structure of the liver, as a result of various factors. A very dangerous disease. Often leads to complications and death. Symptoms are divided depending on the type:

• yellow skin tone;
• weight loss;
• temperature rise;
• skin itching, the appearance of a vascular network;
• diarrhea, vomiting, pain in the liver;
• emotional unstable state;
• the liver and spleen are enlarged.

• skin itching, peeling;
• dark urine;
• uncharacteristic, light feces;
• increased levels of cholesterol and bilirubin in the blood.

Attention! If you have at least a few of these symptoms, you should immediately consult a doctor.

Acute liver failure

Severe liver disease is divided into three stages of severity:

• light. It proceeds without visible symptoms, it can be detected by passing special tests;
• medium heavy. Pain in the liver, colic, yellow skin and mucous membranes;
• hard stage. It can cause serious malfunctions of the body, leading to hepatic coma.

Chronic form of the disease

In the process of long-term destruction of liver cells due to various influences, a chronic form of liver failure occurs. The consequence may be the onset of encephalopathy, mental disorder of behavior, consciousness.

Symptoms:

• nausea, vomiting, diarrhea;
• insomnia, or vice versa drowsiness;
• eczema;
• edema, ascites;
• infertility.
• anorexia;
• disruptions in the work of the heart;
• constant feeling of thirst;
• memory deterioration.

Liver failure in children

Often, liver disease occurs in children. In most cases, they are difficult and require immediate intervention by a specialist. There are many causes of liver disease in children, here are some of them:

• congenital pathologies of the liver. Sometimes abnormal liver development begins in the womb. It can be a liver cyst, hernia, violation of liver lobulation;
• introduction of the hepatitis virus during blood transfusion;
• intoxication after poisoning, extensive burns;
• excessive protein intake;
• profuse blood loss.

Remember! Timely treatment to the hospital and adequate behavior will help save the life and health of your child.

Treatment at home

If you decide to be treated at home, the course of drugs is still prescribed only by a doctor. The process of treating liver failure directly depends on the type of disease, its complexity.

In particularly difficult cases with a severe and dangerous course of the disease, treatment should only be inpatient. In milder forms, the fight against the disease can be carried out at home, under the close supervision of a doctor. Taking drugs and vitamins aimed at combating the disease gives good results in our time. By following the course of treatment and a special diet, you can get rid of the disease for a certain period of time.

Interesting to know! The human liver has half a thousand functions. In a minute, 20 million chemical reactions take place in this small organ.

Use of drugs

Treatment often follows a specific pattern:

• the patient's intake of protein and table salt is sharply limited;
• antibacterial drugs such as ciprofloxacin are administered;
• drip infusions of drugs such as ornithine, glucose, sodium chloride;
• lactulose injections;
• the use of B vitamins is mandatory;
• calcium, magnesium;

This is just an approximate, primitive scheme of treatment. Never try to self-medicate yourself. This is extremely dangerous for life and health. The consequences may be irreversible. Only specialists with clear knowledge can prescribe the right treatment.

Folk remedies for treatment

As with many other diseases, some folk remedies can help with diseases associated with the liver. Their diversity is very great. Of course, there is no certainty that such funds will help you with a 100% guarantee. In addition, the use of some folk methods can cause complications and irreversible harm to health. Allergies, pressure drop and other phenomena are not excluded in the treatment of folk remedies. Be sure to check with your doctor before using any prescription. Such treatment is only an adjunct to medical treatment. Let's try to understand in more detail.

Liver Cleansing Recipes

1. Pour boiling water over corn stigmas (use only ripe cobs) and cook for 10-15 minutes. Take a decoction in the morning and in the evening, 200 grams.
2. St. John's wort (1 tablespoon) pour milk (200 grams). Boil for 10 minutes, strain, let stand. Take 50 grams 3-4 times a day.
3. Grate the peeled beets, boil in water for 15 minutes. The remedy should be taken in a quarter cup 3-4 times a day.

Treatment of cirrhosis

• turmeric (1 tablespoon) dissolve in a glass of water. For taste, you can add a little honey or sugar. Drink half a glass several times a day;
• mince a clove of garlic, mix with a glass of kefir or yogurt. Drink every morning before meals;
• chop two garlic cloves, pour boiling water (one glass). Leave to infuse for a day. Drink in the morning on an empty stomach before meals;
• Boil oats for an hour, let it brew. Take half a glass 2-3 times a day;
• lemon, honey, garlic. Mix the ingredients in a ratio of 2:2:1. Take a teaspoon 2 times a day;
• take carrot juice in half a glass 2 times a day for cirrhosis;
• fresh potato juice can be taken with cirrhosis in half a glass.

Herbs

Since ancient times, our ancestors have noticed and appreciated the extremely beneficial properties of certain herbs. Plants are able to relieve inflammation, normalize blood pressure, energize, rejuvenate, soothe, heal wounds and much more. These days doctors themselves often prescribe herbal prescriptions as adjuvant therapy for many ailments.

To help in the treatment of liver diseases, there are the following recipes:

• St. John's wort, dandelion root, sandy immortelle mix in a ratio of 2:2:1. Brew 500 grams of boiling water. Take a glass in the morning and evening;
• nettle, wild rose, couch grass mixed in a ratio of 1:1:1. Brew a glass of boiling water, leave for 2-3 hours. Take with cirrhosis for 2-3 doses per day;
• lingonberry leaves, corn stigmas, dandelion root, linden blossom, motherwort herb mixed in equal amounts. Pour a liter of boiling water, leave for 5-6 hours. Take half a glass 2 times a day;
• yarrow, St. John's wort, juniper fruits mixed in a ratio of 2:2:1. Pour in a liter of water. Boil for 10 minutes, strain, let it brew for 12 hours. Take half a glass 2-3 times a day;
• mint grass, bearberry, knotweed, St. John's wort, dill seeds, Kuril tea, mix everything in equal proportions, chop well. Boil in a liter of water for a minute, strain. Let stand for hours. Take a quarter cup 2-3 times a day.

Diet for liver failure

With liver diseases, a special diet is absolutely necessary. There are products that can exacerbate the course of the disease, and vice versa, become assistants in the cure.

Remember! The goal of any diet is to alleviate the condition of the disease and avoid complications.

Rules for nutrition in diseases of the liver:

• food should be easy to digest, be light;
• exclude spicy, salty, sour, smoked, fatty, fried;
• porridge should be well cooked. Coarse-grain cereals are best rubbed on a sieve;
• include foods that have a choleretic property in your food. These are corn, sunflower, peanut oils. From greens dill, spinach, celery. From fruits oranges, lemons, grapefruits. Useful dried apricots, cauliflower, artichokes;
• limit the use of proteins, no more than grams per day;
• once a week arrange a fasting day.

Prohibited Products:

• mushrooms;
• fat meat;
• alcohol;
• chocolate candies;
• fatty dairy products;
• strong black tea;
• radish, sorrel;
• rye breads, fresh pastries.

© 2017 Treatment with folk remedies - the best recipes

The information is provided for informational purposes.

Liver failure: symptoms and treatment

Liver failure - the main symptoms:

• Headache
• Dizziness
• Elevated temperature
• Nausea
• Loss of appetite
• Hair loss
• Pain in the right hypochondrium
• Heaviness in the right hypochondrium
• Bad breath
• Swelling of the legs
• Fever
• Aggressiveness
• An increase in the volume of the abdomen
• Trembling of limbs
• Phlebeurysm
• yellowing of the skin
• swelling of the face
• Redness of the palms
• Bundle of nails
• Atrophy of the mammary glands

A disease that is characterized by a violation of the integrity of the liver tissues due to their acute or chronic damage is called liver failure. This disease is considered complex, due to the fact that after liver damage, metabolic processes are disturbed. If you do not take appropriate measures to cure the disease, then under certain conditions, liver failure can quickly and rapidly develop and lead to death.

Classification

The disease is classified according to two criteria: the nature of the course and stages.

According to the nature of the course, two stages of the disease are distinguished:

Acute liver failure occurs due to the loss of the ability of the liver to perform its functions. The disease manifests itself predominantly within a few days and is characterized by a severe form of the course of symptoms. Often the acute form is fatal, so it is very important to know the symptoms in order to recognize the disease at an early stage.

Acute liver failure is subdivided, in turn, into major and minor. A large one is a classic form of manifestation of the disease, which is quite clearly seen in clinical and laboratory studies. Small acute liver failure occurs more often in children against the background of serious illnesses (poisoning, intestinal infections, pneumonia, etc.). This subspecies is very difficult to diagnose due to the absence of symptoms of the disease. A small species can develop both rapidly and over several years.

Chronic liver failure develops through a slow course of the disease. Due to the gradual dysfunction of the liver with the progressive course of a chronic disease of the parenchyma, a chronic form of the disease is formed. Diseases such as cirrhosis of the liver or chronic hepatitis are the result of chronic liver failure. Both manifestations end in hepatic coma followed by death.

Additionally, there are two types of liver failure:

The endogenous species is characterized by the manifestation of complications during death or dystrophic changes in the liver tissues. This species is characteristic of cirrhosis of the liver and chronic hepatitis.

The exogenous species is formed as a result of self-poisoning of the body, which is caused by metabolic products and substances that are produced by the intestinal microflora. It occurs due to the entry of these substances into the blood through the walls of the intestine, when they stop in the liver. The reason for the stop can be a blockage of the veins, therefore, as a result, self-destruction of the liver is observed.

According to the severity, four stages are distinguished:

1. Initial or compensated, which is characterized by an asymptomatic course of the disease. At the initial stage, the liver begins to actively respond to toxins.
2. Decompensated. The first signs of the disease appear. At this stage, a blood test indicates the development of the disease.
3. Dystrophic or terminal. The pre-final stage, upon the onset of which the patient has serious violations of the functioning of the liver. Against the background of which there is also a violation of the work of the whole organism from the central nervous system to metabolism.
4. Stage of hepatic coma. It is characterized by a deepening of liver damage, which ultimately leads to death. The last stage is characterized by the complexity of treatment, since the liver passes into the stage of death.

Causes of the disease

The disease "liver failure" is diagnosed in both men and women, moreover, it has no age restrictions, so you can get sick both in childhood and in the elderly. The causes of liver failure are varied and unpredictable. It is important to know them in order to be able to determine the diagnosis prematurely and speed up treatment. So, the reasons that can provoke liver failure in humans are as follows:

1. Liver diseases, which include: malignant tumors and other neoplasms, cirrhosis, acute and chronic hepatitis, echinococcus, etc. Any of these signs can serve as an impetus for the development of a fatal disease. Cirrhosis and hepatitis can be both the cause of the disease and its consequences.
2. Blockage of the bile ducts, as a result of which an increase in the pressure of bile hypertension is predicted. Failure of hypertension disrupts blood circulation in the liver, which causes the development of dystrophic abnormalities in the cells of this organ.
3. Diseases of the heart, blood vessels, infectious infections of the body, insufficiency of the endocrine glands, autoimmune diseases. Any violation in the body can cause the development of a serious disease, so it is much easier to eliminate signs of abnormalities at an early stage than to try to cure serious diseases.
4. Taking medications (especially for a long time) can leave its mark on the liver. As you know, any medicine affects the liver, so it is very important to maintain the correct dosages of drugs and not violate the frequency of administration.
5. Poisoning by various organic and inorganic substances: poisonous mushrooms, alcohol, tobacco, chemicals, etc.
6. extreme influences. The cause of a fatal disease can be even a minor burn on the skin, to which appropriate therapeutic measures simply will not be taken. In addition: trauma, blood loss, allergies, septic shock and other factors can be the root cause of liver failure.
7. Deviation in the functioning of the kidneys, tuberculosis, urolithiasis, pyelonephritis, congenital anomalies and much more, are the causes of a disease such as renal and hepatic malaise.

The main cause of renal and hepatic disease is the lack of balance between constriction and expansion of blood vessels. The reason for the lack of balance can serve as a banal cause of alcohol abuse, as well as poisoning, both food and respiratory. The disease of renal-hepatic insufficiency is no less serious than damage to the liver alone, since an increase in mortality from this type of disease is observed every year.

Based on all the causes, a complex of symptoms of the disease manifests itself. What are these symptoms and their main features, we will consider in more detail.

Symptoms of the disease

The symptoms of liver failure are very diverse, but they are the first factors, after the discovery of which it is necessary to hurry to the doctor. The initial stages of the disease are manifested in the form of a general malaise of the body, the appearance of mania and other motor disturbances. During flexion / extension of the fingers, a tremor symptom may be observed, that is, lateral signs or trembling, which often occurs with sudden movements.

Liver failure and its symptoms are always accompanied by the development of jaundice and neuritis. The patient has a rise in temperature to the level of 40 degrees with an exacerbation of the disease, as well as swelling of the legs. An unpleasant but specific odor arises from the mouth, indicating the beginning of the formation of trimethylamine and dimethyl sulfide. There is a disorder of the endocrine system, there is an increase in hair loss, up to baldness, libido decreases, atrophy of the uterus and mammary glands occurs in women, stratification and crumbling of nails. In women, liver failure at an early age can adversely affect fertility, that is, provoke the development of infertility.

In addition, during the entire period of the disease, the patient has an increase in headaches, feverish manifestations, dizziness up to fainting and an aggressive state. Let us consider in more detail what symptoms are inherent in the three stages of the disease.

Stages of chronic liver failure

Often, chronic liver failure is characterized by four stages, which have their own symptoms.

1. The compensated stage is often asymptomatic, but the following negative processes are observed inside the body: an increase in pressure in the hepatic system, overflow of the venous plexuses on the abdomen, varicose veins. At the initial stage, you can notice the indistinct appearance of spider veins on the patient's body and reddening of the palms. The patient refuses to eat food, because of disgust. There is a slight weight loss.
2. The decompensated stage is due to an increase in the symptoms of the disease. The first signs of the disease begin to appear: aggression, disorientation in the area, slurred speech, trembling of the limbs. Relatives can observe a significant change in a person's behavior.
3. The dystrophic stage is caused by the occurrence of stupor. The patient becomes inadequate, it is very difficult to wake him up, and in moments of wakefulness, apathy is periodically replaced by excitement. There are swelling of the face, legs, accumulation of fluid in the abdominal cavity. Also, the patient may appear in the morning or evening periods of bleeding from the nose or gastrointestinal tract.
4. At the final stage, the patient has the appearance of a hepatic coma, as a result of which the patient is unconscious, while there is no reaction to external pain stimuli. The patient's vision is reduced, strabismus develops, cerebral edema and fluid accumulation occur. Chronic liver failure develops in each individual case in different ways, often over decades.

Acute symptoms

Acute liver failure occurs predominantly rapidly with a pronounced picture of symptoms. This species has the following symptoms:

• sudden onset of weakness
• nausea, vomiting and other signs similar to poisoning;
• increase in body temperature;
• an increase in jaundice, while you can observe a change in skin color to yellow. The eyeballs of the patient also become yellow;
• smell from the mouth;
• a decrease in the size of the liver, which manifests itself in the form of pain symptoms;
• lethargy, anxiety and speech impairment.

Acute liver failure is characterized by a change in the composition of the blood: an increase in bilirubin occurs, which indicates the breakdown of hemoglobin and its decrease, as well as a decrease in the prothrombin index.

It is very important to deliver the patient to the clinic on time in order to be able to take medication. Otherwise, acute liver failure can be fatal in the shortest possible time.

Symptoms of kidney disease

The symptoms of renal and hepatic disease are almost identical to the above, only the only difference is the damage to the kidneys, which indicates their pain and the manifestation of the following signs:

1. The presence of pain first in the liver, and then in the kidneys.
2. Temperature rise.
3. Signs of jaundice.
4. In the urine, erythrocytes, protein and bile components are found.
5. Hemorrhagic diathesis is formed, the cause of which is intoxication of the body.

The main danger of a renal-hepatic disease is the involvement of other organs and systems in the process of pathology: the gastrointestinal tract, central nervous system, respiratory organs, etc. In a chronic form, the functioning of the liver tissues stops, as a result of which toxins begin to be excreted through the gastrointestinal tract and lungs. This is an abnormal condition, so the body is under severe stress.

Before starting treatment, it is important to correctly diagnose the disease. See the next section for what you need to diagnose.

Diagnostics

If all of the above symptoms are found, then you should immediately contact the hospital or call an ambulance. The clinic will require diagnostics to be able to make a correct diagnosis. First of all, the diagnosis begins with a survey and examination of the patient. Often this is not enough to make a correct diagnosis, so the doctor will prescribe clinical measures.

Clinical activities include blood donation to identify biochemical data for bilirubin, alkaline photophase, LDH, AST and ALT. According to these indicators, the doctor reveals not only the presence of signs of the disease, but also at what stage the liver disease is. The higher the indicators, the more active the process of decay of liver cells.

Additionally, ultrasound may be required, on the basis of which it is possible to determine the nature of the disease (acute or chronic), to identify the size of the liver and the presence of structural and dystrophic changes.

The following diagnostic measures are not excluded:

These additional analyzes and data will give an idea of ​​how other human organs and systems are involved in the disease process.

Treatment

Treatment of liver failure is a rather complicated and lengthy procedure, which depends primarily on the stage of the disease.

An important place in the treatment process is given to infusion therapy, through which proper nutrition is provided and the body is detoxified. It is also necessary to improve liver microcirculation, normalize or restore the balance of acid-base balance.

The patient is prescribed laxatives and enemas to cleanse the gastrointestinal tract of toxins and get rid of constipation. A dropper with a solution of glucose, vitamins B6, B12, and lipoic acid is administered daily.

If the disease has passed into the stage of hepatic coma, then they resort to intensive drug treatments. The purpose of these measures is to keep the patient alive so that hepatic function can return to normal. A solution of sodium or potassium bicarbonate is introduced, and humidified oxygen is inhaled through a nasal catheter. If the pressure decreases, then albumin is administered intravenously.

The patient must be hospitalized and under the supervision of nurses. In addition to medical procedures, the following conditions are met:

• daily monitoring of a blood test to determine the composition of albumin;
• urinary monitoring;
• pressure ulcer prevention;
• weighing daily.

Preparations of hypoammonemic effects can reduce the level of ammonia in the body.

If the patient has a connection with renal failure, then additional hemodialysis will be required in order to remove ammonia and other toxins from the blood, which are normally neutralized by the liver. With edema or ascites, paracentesis is necessary, which will help remove excess fluid from the body.

In addition to all of the above, to normalize the liver, you will need to maintain proper nutrition, or rather, diet.

Diet

A diet in the treatment of liver disease is a mandatory procedure, since the liver receives a significant blow precisely from malnutrition. The diet includes the following procedures:

1. Reducing the level of protein and fat to 30 grams per day, and carbohydrates to 300.
2. It is preferable to eat plant foods, which include: fruits, vegetables, honey, compotes, jelly.
3. Eat food only in liquid or semi-liquid composition. At the same time, you need to eat little by little, but every 2 hours.
4. Eliminate salt from your diet altogether.
5. If there are no edema, then about 1.5 liters of fluid should be drunk per day.

Diet plays an important role in the treatment of liver failure, so a complex effect will allow you to get rid of the symptoms of the disease and return to your previous healthy life.

If you think that you have liver failure and the symptoms characteristic of this disease, then doctors can help you: a hepatologist, a gastroenterologist, a general practitioner.

We also suggest using our online disease diagnostic service, which, based on the symptoms entered, selects probable diseases.

Jaundice is a pathological process, the formation of which is affected by a high concentration of bilirubin in the blood. The disease can be diagnosed in both adults and children. Any disease can cause such a pathological condition, and they are all completely different.

Viral hepatitis B is an inflammatory viral disease that mainly affects the liver tissue. After a person recovers from this disease, he develops a strong lifelong immunity. But the transition of an acute form of hepatitis B into a chronic progressive one is possible. It is also possible that the carrier of the virus.

Thrombocytopenic purpura or Werlhof's disease is a disease that occurs against the background of a decrease in the number of platelets and their pathological tendency to stick together, and is characterized by the appearance of multiple hemorrhages on the surface of the skin and mucous membranes. The disease belongs to the group of hemorrhagic diathesis, it is quite rare (according to statistics, 10–100 people a year fall ill with it). It was first described in 1735 by the famous German physician Paul Werlhof, after whom it got its name. Most often, everything manifests itself under the age of 10 years, while it affects both sexes with the same frequency, and if we talk about statistics among adults (after 10 years of age), then women get sick twice as often as men.

With the help of exercise and abstinence, most people can do without medicine.

Symptoms and treatment of human diseases

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All information provided is subject to mandatory consultation by the attending physician!

Questions and suggestions:

Very often, despite experience, pediatricians do not take into account certain symptoms on the part of the child's body. Especially if it concerns babies under one year old, who still do not know how to talk and complain about some kind of discomfort. That is why it is not uncommon when parents bring their child to a specialist too late, and conventional therapy can no longer be dispensed with.

Of course, it is very sad when some pediatricians, attributing everything to the insufficient development of the gastrointestinal tract system of the baby, leave aside some symptoms that simply scream about the pathology of the liver. So modern parents are highly recommended to independently pay attention to any changes related to the child.

First of all, a pregnant woman needs to assess the risks. Any chronic disease of one of the parents or relatives (diabetes mellitus, problems with blood clotting or metabolism), taking antibiotics or toxic drugs, "communication" with toxins on duty, living near a chemical plant, eating environmentally polluted products - all this automatically increases the "chance" of the baby to get a congenital disease of the liver and biliary tract.

Also, a child can catch a dangerous virus even after discharge from the hospital.

Thus, mothers and fathers should understand some rules for monitoring the health of the baby and immediately consult a doctor in order to conduct appropriate tests and examinations when:

. the skin and mucous membranes, in particular the eyes, in a child a little older than two weeks become icteric (yes, some doctors will point out the physiological characteristics of infancy, but you still need to check);

The child's stool becomes colorless, that is, acholic (during the normal functioning of the digestive system, bile containing bilirubin must flow from the gallbladder to the intestines to help it digest food, and after this function is completed, it turns into a pigment called stercobilin, which colors the feces masses in brown color);

Visually, an increase in the liver is observed (in the normal state, it protrudes only a centimeter from under the right costal arch; when there is a violation, the tummy becomes asymmetrical and it can be seen that its right side is very swollen, directly hanging over the lower abdomen);

The blood begins to clot poorly (although true wounds in infancy are a rare phenomenon, but sometimes diaper rash with wounds speaks of the degree of blood clotting; if the blood cannot be stopped for a long time when the crust is removed, then most likely the process of disruption of the work and the spleen is started);

The baby's tummy evenly increases (this indicates the appearance of ascites, that is, the accumulation of fluid in the abdominal cavity; as a rule, the next stage is liver failure and cirrhosis, in which the child can live up to a maximum of three years of age).

You should not postpone a visit to a specialist and the start of examinations with such symptoms indefinitely. The sooner the cause of jaundice and bloating is established, the easier it will be to eliminate it.

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Treatment of acute liver failure

The basis of the treatment of acute liver failure are measures aimed at eliminating etiological factors (if they are detected), and post-syndromic therapy, which allows to correct complications.

In case of poisoning with paracetamol, gastric lavage is performed through a wide probe. If a tablet is found in the wash water, enterosorbents (for example, activated charcoal) are prescribed. In the absence of a tablet in the wash water, it is recommended to administer acetylcysteine ​​at a dose of 140 mg/kg (simultaneously through a nasogastric tube), and then appoint 70 mg/kg orally every 4 hours for three days. Acetylcysteine ​​produces the greatest effect when it is used in the first 36 hours after paracetamol poisoning.

Most often, poisoning is caused by fungi of the genus Amatia and Galerina. Fungi of the genus Amatia contain a-amanitin, which has a toxic effect by irreversible inhibition of RNA polymerase. Therapy for this condition includes the use of silibinin [orally at a dose of 20–50 mg/(kg/day)] and penicillin G [intravenously at a dose of 1 mg/(kg/day) or 1,800,000 IU/(kg/day)]. The action of silibinin is based on its ability to prevent the uptake of α-amanitin by hepatocytes and increase antioxidant activity. This drug produces its maximum effect during the first 48 hours after poisoning. Penicillin G helps to reduce the concentration of a-amanitin in bile by interrupting the hepato-intestinal circulation of the toxin.

Measures performed upon detection of acute liver failure of any etiology:

• Ensuring adequate oxygenation. Carry out the supply of additional oxygen, and if necessary - IVL.
• Correction of metabolic disorders, electrolytes and CBS.
• Monitoring of hemodynamic parameters.
• ICP control.
• Parenteral administration of glucose to correct hypoglycemia.
• Introduction of mannitol to reduce ICP.
• Parenteral administration of proton pump inhibitors or type II histamine receptor blockers to prevent gastrointestinal bleeding.

Treatment of complications of acute liver failure

Hepatic encephalopathy

To correct PE, it is necessary to limit the intake of protein from food and prescribe lactulose at a dose of 3-10 g / day orally (children under one year old - 3 g / day, from 1 to 6 years old - 3-7 g / day, 7-14 years old - 7 -10 mg/day).

Cerebral edema

General measures include ensuring rest and a certain position of the head (at an angle of 100 degrees to the horizontal surface), preventing arterial hypotension and hypoxemia. Specific therapy consists of mannitol at a dose of 0.4 g/kg every hour (intravenous bolus) until ICP normalizes. It should be noted that the use of this drug is ineffective in renal failure and hyperosmolarity of blood serum. With the development of hepatic coma, hyperventilation often has a positive effect. In the treatment of cerebral edema caused by acute liver failure, the appointment of glucocorticoid drugs is impractical (due to the lack of effect).

Hypocoagulation

Carry out the introduction of FFP [intravenously drip at a dose of 10 ml/(kgxday)] and vikasol [intramuscularly or intravenously at a dose of 1 mg/(kgxday)]. With insufficient effectiveness of drugs, blood coagulation factors are used (Feiba TIM-4 Immuno - blood coagulation factors II, VII, IX and X in a combination of 75-100 IU / kg). To prevent gastrointestinal bleeding against the background of hypocoagulation, parenteral administration of proton pump inhibitors or type 2 histamine receptor blockers [for example, Kvamatel 1-2 mg Dkghsut) is performed in 2-3 doses, but not more than 300 mg / day].

Hepatorenal syndrome

Therapeutic measures include the replenishment of BCC in case of hypovolemia (infusion of 5% glucose solution), the appointment of dopamine [at a dose of 2-4 μg / (kghh)], and if the drugs are ineffective, HD is performed. It is also recommended to use veno-venous hemofiltration.

The development of sepsis is an indication for the use of antibacterial drugs. Preparations are prescribed, taking into account the sensitivity of the microflora being sown. The use of antibiotics is combined with passive immunization with pentaglobin. Newborns are prescribed 250 mg / kg, infants - 1.7 ml / (kghh) intravenously drip. Older children and adults are recommended to administer 0.4 ml/(kghh) until a total dose of 100 ml is reached, then a continuous infusion of pentaglobin4 [0.2 ml/(kghh)] is carried out over the next 72 hours, increasing the rate of administration to 15 ml /(kghh)].

If conservative treatment fails and there are no contraindications, liver transplantation is recommended. Determining indications for liver transplantation is an extremely difficult task. Even in severe forms of acute liver failure, there is a chance of recovery. On the other hand, irreversible changes in other organs, including the brain, may occur at any time, which are considered a contraindication to liver transplantation.

With the development of acute liver failure, spontaneous recovery rarely occurs in patients with significantly reduced synthetic liver function (low albumin concentration, severe coagulopathy), high bilirubin levels, low ALT activity, and also with a longer period between the onset of the disease and the onset of signs of encephalopathy.

Criteria for determining indications for liver transplantation in the development of acute liver failure (according to various studies):

• Increasing the concentration of bilirubin more than 299 µmol / l.
• Increase in prothrombin time (more than 62 s).
• Decreased activity of ALT less than 1288 U / l.
• Leukocytosis (more than 9 thousand).
• The duration of the disease before the development of PE is more than 10.5 days.
• Age under two years old.

Source: ilive.com.ua