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Liver failure in children. Liver failure, symptoms in women and men

Acute liver failure in children (ALF) is a rapidly developing disorder of the synthetic function of the liver, characterized by severe coagulopathy and hepatic encephalopathy. The absence of a history of liver disease is a necessary condition for diagnosing acute liver failure. A decrease in PTI or an increase in prothrombin time is noted, as well as a decrease in the concentration of coagulation factor V by more than 50% of normal in combination with any stage of hepatic encephalopathy lasting less than 26 weeks.

The term “fulminant hepatic failure” was first introduced by Trey and Davidson in 1970 to define a clinical syndrome characterized by acute onset, coagulopathy, and hepatic encephalopathy occurring within 8 weeks of disease onset.

The diagnosis of subfulminant liver failure is established when liver failure develops without hepatic encephalopathy within 26 weeks.

In some cases, acute liver failure occurs against the background of previously undiagnosed liver disease. For example, AKI may be the first symptom of Wilson's disease or α1-antitrypsin deficiency. If previous diseases are detected, the term “acute liver failure” is not used (since the duration of the disease exceeds 26 weeks). However, sometimes it is impossible to establish the fact of chronic liver disease. The exception is patients with Wilson's disease, against the background of which infection with the hepatitis B virus occurs or the development of autoimmune hepatitis. These diseases are the direct causes of short-term liver failure (less than 26 weeks).

Concepts used taking into account the time of onset of hepatic encephalopathy after detection of jaundice:

Hyperacute liver failure (less than 7 days).
Acute liver failure (from 8 to 28 days).
Subacute liver failure (from 4 to 12 weeks).

ICD-10 code

K 72 0 Acute and subacute liver failure.

K 72 9 Liver failure, unspecified.

Epidemiology of acute liver failure

The prevalence of acute liver failure is relatively low. Studies have shown that about 2,000 cases are diagnosed annually in the United States. There are no data on the incidence of acute renal failure in Russians in the literature. Mortality from acute liver failure averages 3-4 people per year per 1 million population and depends on many factors, primarily on the etiology and age of the patient. The most prognostically unfavorable causes of acute renal failure are considered to be viral hepatitis B and hepatitis delta, as well as age (younger than 10 and older than 40 years).

What causes acute kidney failure?

Viral and drug-induced hepatitis are the main causes of acute liver failure. According to data obtained in the USA, in more than half of cases, acute renal failure occurs due to drug-induced liver damage. Moreover, in 42% of cases, the development of acute renal failure is caused by an overdose of paracetamol. In Europe, paracetamol overdose also ranks first among the causes of acute renal failure. In developing countries, viral hepatitis B and delta viruses (in the form of coinfection or superinfection) predominate among diseases causing acute renal failure. Other viral hepatitis is less likely to cause the development of acute renal failure. In approximately 15% of patients, the cause of acute liver failure cannot be determined.

Causes of acute liver failure

Hepatitis viruses A, B (+5), C, E, G7	Impaired synthesis of bile acids
Cytomegalovirus	Galactosemia
Herpes simplex virus	Fructosemia
Epstein-Barr virus	Tyrosinemia
Paramyxovirus	Neonatal hemochromatosis
Adenovirus	Wilson's disease
Drugs and toxins	α-1-antitrypsin deficiency
Dose dependent	Neoplastic
Acetaminophen
	Metastases in the liver in breast or lung cancer, melanoma
Poisoning with mushrooms of the genus Amanita	Pregnancy related
Yellow phosphorus	Acute fatty liver of pregnancy
Bacillus cereus toxin	HELLP syndrome (hemolysis, elevated liver function tests, decreased platelet count)
Idiosyncratic	Other reasons
	Budd-Chiari syndrome
Isoniazid	Veno-occlusive disease
Rifampicin	Autoimmune hepatitis
Vapproic acid	Ischemic shock liver
Disulfiram	Heatstroke
Nonsteroidal anti-inflammatory drugs	Rejection reaction after liver transplantation
Nortriptylene	Cryptogenic
Reye's syndrome (salicylic acid)
Herbal medicine

Symptoms of acute liver failure

The main clinical symptoms of acute liver failure are jaundice (not always diagnosed) and pain in the right hypochondrium. The liver was not enlarged upon examination. The development of ascites and its combination in severe cases with peripheral edema and anasarca are characteristic. Hematomas are sometimes found on the surface of the skin. Bleeding from the mucous membranes of the gastrointestinal tract is often noted, and patients experience tarry stools (melena) or vomiting blood. Encephalopathy and increased ICP are determined to varying degrees of severity. When cerebral edema occurs, systemic hypertension, hyperventilation, altered pupillary reflexes, muscle rigidity, and in severe cases, decerebrate coma are noted.

After taking large doses of paracetamol, anorexia develops during the first day, the patient is bothered by nausea and vomiting (later disappearing). Then the symptoms of acute liver failure described above are detected.

In case of mushroom poisoning, severe abdominal pain and watery diarrhea are noted, occurring 6-24 hours after eating mushrooms and lasting for several days (usually from 1 to 4 days). PE occurs after 2-4 days.

Diagnosis of acute liver failure

Laboratory research

Thrombocytopenia.
Changes in indicators reflecting the synthetic function of the liver. Decrease in the concentration of albumin and cholesterol, coagulation factor V and fibrinogen, decrease in AChE activity, decrease in PTI (or prolongation of prothrombin time).
Significant increase in the activity of ALT and AST transaminases. In case of an overdose of paracetamol, AST activity can exceed 10,000 U/l (the norm is up to 40 U/l). An increase in alkaline phosphatase activity is not always recorded.
Increased concentrations of bilirubin and ammonia in the blood serum.
Hypoglycemia.
Increased lactate content in blood serum.
Increased concentrations of creatinine and urea in the blood serum (with the development of hepatorenal syndrome).

Instrumental diagnosis of acute liver failure

Ultrasound and Doppler studies reveal nonspecific changes, depletion of the vascular pattern, disturbances of portal blood flow of varying degrees, and free fluid in the abdominal cavity. The liver is small.

Histological examination of a liver biopsy reveals necrosis of hepatocytes, which in most cases does not allow establishing the cause of the disease. In acute liver failure, a puncture biopsy is not performed due to the high probability of bleeding due to hypocoagulation. This study is carried out only if a liver transplant is necessary or during an autopsy.

Treatment of acute liver failure

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

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

The most common causes of poisoning are fungi of the genus Amatia and Galerina. Mushrooms of the genus Amatia contain a-amanitin, which has a toxic effect by irreversibly inhibiting 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 units/(kg/day)]. The action of silibinin is based on its ability to prevent the uptake of a-amanitin by hepatocytes and increase antioxidant activity. This drug produces its maximum effect within the first 48 hours after poisoning. Penicillin G helps reduce the concentration of a-amanitin in bile by interrupting the hepatic-intestinal circulation of the toxin.

Measures taken when acute liver failure of any etiology is detected:

Ensure adequate oxygenation. Provide additional oxygen and, if necessary, mechanical ventilation.
Correction of metabolic disorders, electrolytes and CBS.
Monitoring of hemodynamic parameters.
ICP control.
Parenteral administration of glucose to correct hypoglycemia.
Administration of mannitol to reduce ICP.
Parenteral administration of proton pump inhibitors or histamine type II 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 prescribing 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 cases of 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 prescription of glucocorticoid drugs is inappropriate (due to the lack of effect).

Hypocoagulation

FFP is administered [intravenous drip at a dose of 10 ml/(kg day)] and Vikasol [intramuscular or intravenous at a dose of 1 mg/(kg day)]. If the drugs are insufficiently effective, blood coagulation factors are used (Feiba TIM-4 Immuno - blood coagulation factors II, VII, IX and X in combination 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 is performed [for example, quamatel 1-2 mgDkgsut] in 2-3 doses, but not more than 300 mg/day].

Hepatorenal syndrome

Therapeutic measures include replenishment of blood volume in case of hypovolemia (infusion of 5% glucose solution), administration of dopamine [at a dose of 2-4 mcg/(kgh)], and if the drugs are ineffective, HD is performed. It is also recommended to use venovenous hemofiltration.

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

If conservative treatment is ineffective and there are no contraindications, liver transplantation is recommended. Determining indications for liver transplantation is an extremely difficult task. Even with severe forms of acute liver failure, there is a possibility 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 appearance of signs of encephalopathy.

What is the prognosis for acute liver failure?

In case of paracetamol overdose, additional criteria for assessing the severity of the patient’s condition are used:

Hypoglycemia (less than 2.5 mmol/l).
Increased creatinine concentration (more than 200 mmol/l).
The presence of metabolic acidosis (pH less than 7.3).
PE III degree.

The presence of these disorders in children indicates an increased likelihood of death and also indicates a worsening prognosis.

Adverse prognostic factors for the development of acute liver failure:

Increased prothrombin time (more than 100 s).
Decrease in the content of blood coagulation factor V (less than 20-30%).
Prolonged jaundice (more than 7 days).
Age (under 11 and over 40 years old).

Acute liver failure due to hepatitis A or after paracetamol poisoning has a good prognosis.

The survival rate of the organ after liver transplantation performed for acute liver failure, as a rule, is not too high (compared to surgery for chronic liver disease). According to the literature, the survival rate of patients after emergency transplantation during the first year is 66%, and within five years - 59%. After operations performed for chronic liver failure, depending on the diagnosis, an increase in survival rate of up to 82-90% in the first year and up to 71-86% within five years is recorded.

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

0main 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 is 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). The liver synthesizes components of the prothrombin complex (II, VII, IX, X), which depend on vitamin K, as well as other coagulation factors (fibrinogen, VI, XI, XII, XIII). The formation of blood clotting inhibitors: antithrombin and antiplasmin occurs here. The liver also carries out protein catabolism with the participation of the enzymes cathepsins, acid carboxypeptidase, collagenase, dipeptidase; specific metabolism of individual amino acids (90% of phenylalanine is converted into tyrosine, tryptamine, serotonin, and quinolinic acid are formed from tryptophan; histamine is formed from histidine; ethanolamine is formed from serine, the initial product of choline synthesis). Liver enzymes directly cleave hydrogen sulfide from cysteine molecules and 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; formation of ketone bodies (acetoacetic acid, -hydroxybutyric acid); synthesis of triglycerides, phospholipids, lipoproteins; cholesterol synthesis; 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 recombined with glycine and taurine and re-excreted into bile.

The liver is also involved in carbohydrate metabolism. It involves 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, glycogen reserves are exchanged four times in the liver.

The importance of the liver's role in pigment metabolism also difficult to overestimate. It is involved in: the formation of bilirubin; its capture, conjugation and excretion; metabolism and re-excretion of urobilinogens. During the day, 1% of circulating red blood cells disintegrate, 7.5 g of hemoglobin is released, and up to 100-300 mg of bilirubin is formed. 70-80% of bilirubin is associated with glucuronic acid, as well as glycine, sulfuric and phosphoric acids. When 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 colon. Normally, the enterohepatic circulation of urobilinogens is minimal. They are absorbed in the proximal small intestine, re-excreted into bile or broken down in the liver. When hepatocytes are damaged, the re-excretion and breakdown of urobilinogens is disrupted, they enter the general bloodstream and urine. Each bilirubin fraction is a mixture of chemically heterogeneous compounds (up to 8-9 fractions from one serum).

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

The role of the liver is also significant 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 and produces biologically active forms of vitamins B1 (pyridoxal phosphate), folic acid (tetrahydrofolic acid), and choline (cytidine monophosphate choline). The liver deposits and excretes vitamins A, D, K, PP, E, Bl, B2, B12, and folic acid.

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

The liver is one of the main components functional systems detoxification. It is here that the biotransformation of xenobiotics and endogenous toxic substances mainly occurs. The liver creates a powerful barrier to the blood flowing from the intestines. In the intestine, under the influence of bacterial enzymes, protein decomposes into toxic products: phenol, indole, skatole, cadaverine, putrescine, etc. The liver neutralizes all of these products through the processes of oxidation, acetylation, methylation, and the formation of paired compounds with sulfuric and glucuronic acids. Ammonia is neutralized by converting it into urea. In addition, the liver along with the spleen is removed from the flowing blood and up to 70-80% of microorganisms are destroyed. Kupffer cells of the liver not only have pronounced phagocytic activity towards microbes, but also ensure cleansing of the blood from endotoxins of intestinal microflora, antigen-antibody complexes, and tissue breakdown 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 condition of the body in which the liver cannot ensure the maintenance of 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, rickettsia, spirochetes and other hepatotropic infections;

2) toxic hepatitis, degenerative liver lesions that develop 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 less than 2 weeks after the onset of jaundice. Subfulminant hepatitis– acute hepatitis, complicated by acute liver failure with encephalopathy with impaired consciousness within a period of 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 a hepatotropic viral infection. Improved diagnosis of liver diseases has led to an expansion of the alphabet of hepatotropic viruses. Currently, 6 pathogenic viruses have been identified (HAV, HBV, HCV, HDV, HEV, SEN), 4 of which (HBV, HCV, HDV, SEN) have an undoubted ability to cause chronic inflammation of the liver (Table 39.1).

Table 39.1

Hepatotropic viruses

Virus name	Pathogenicity	Chronization

Note: - "?" - unknown.

Development of acute and subacute toxic hepatitis associated with the action of hepatotoxic xenobiotics, including medications. The mechanisms of direct hepatotoxic action include damage to hepatocytes, blockade of tissue respiration processes, and 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 (the poison phalloidin contained in toadstool; aflatoxins contained in molds; ethyl alcohol, inorganic compounds of arsenic, phosphorus, beryllium). One of the rare complications that arise after anesthesia is toxic hepatitis caused by fluoride-containing inhalational anesthetics. Most often they occur after the use of fluorothane, less often they are caused by enflurane and isoflurane. It is believed that such damage occurs more often with repeated use of fluorinated volatile anesthetics or even with the first anesthesia while these patients are taking triiodothyronine.

The development of toxic hepatitis with acute liver disease can also be caused by 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, brufens, paracetamol (possible overdose in children), anticonvulsant sodium valproate (especially when taken in combination with phenobarbital).

Common drugs - analgesics, aminophylline, antiarrhythmic drugs (for example, cordarone) are metabolized in the liver. In patients with hepatopathy of various origins, they can cause worsening functional disorders, even hepatic coma. Unlike infectious hepatitis, the damaging effect of a single dose of xenobiotics quickly reaches a maximum and then regresses at varying 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. Liver cirrhosis is usually combined with manifestations of portal hypertension. A dangerous complication of portal hypertension is the development of bleeding from esophageal varices. The progression of ALE in such circumstances may be associated with excessive intake of dietary protein, the administration of barbiturates and opiates, intestinal infection (in particular, salmonellosis), and uncontrolled administration of diuretics (ammoniogenesis in the kidneys is impaired against the background of alkalosis). Medicinal factors may also be important: the use of methionine, the introduction of conventional, non-specialized amino acid mixtures to correct protein deficiency, which is common in these patients. Surgical stress, systemic hypoxia, transfusion of significant amounts of late-storage citrated blood, and endogenous intoxication of any origin are also important for the progression of acute liver disease in such patients. Undoubtedly, gastrointestinal bleeding has a dramatic effect with microbial breakdown of the blood poured into the intestines and massive ammoniagenesis. Therefore, with deep cirrhotic changes in the liver, aggravation of acute liver failure can be expected after even minor surgical interventions.

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

Factors causing hypoxia of the parenchyma liver: shock; blood loss and all types of hypovolemia, cardiac and respiratory failure, renal failure, hemolysis of red blood cells (poisoning with acetic acid, copper sulfate), gastrointestinal bleeding (rotting of the blood 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 artificial circulation.

As a rule, the clinical manifestations of ALI are quite nonspecific and are detected in the later stages of the disease, therefore 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 acute liver disease, 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,

Hepatic encephalopathy syndrome.

Cholestasis syndrome- disruption 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 uptake, binding and excretion of bilirubin. Impaired excretion causes an increase in the level of conjugated bilirubin in the blood and its appearance in the urine, which is caused by changes in the permeability of liver cells, rupture of bile canaliculi due to necrosis of liver cells, blockage of intrahepatic bile canaliculi with thick bile as a result of destruction and inflammation. In this case, bile regurgitates back into the sinusoids. In the liver, the transformation of urobilinogens is disrupted, and urobilin enters the urine. Jaundice discoloration of the skin and mucous membranes appears when bilirubin increases above 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: itching of the skin, scratching, impaired absorption of fat-soluble vitamins (blurred vision in the dark, bleeding, bone pain), jaundice, dark urine, light-colored feces, xanthomas, xanthelasmas.

Laboratory signs: accumulation of bile components in the blood (cholesterol, phospholipids, bile acids, alkaline phosphatase, γ-glutamyl transpeptidase, 5-nucleotidase, copper, conjugated fraction of bilirubin). With complete disruption 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 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 dysfunction of hepatocytes.

Clinical signs of cytolysis: jaundice, hemorrhagic syndrome, bleeding gums, nosebleeds, hemorrhagic skin rashes, dishormonal disorders, liver signs (palmar erythema, “Chistovich’s stars”, bad breath), weight loss, dyspeptic and asthenic syndromes, nervous -mental disorders.

Laboratory signs: increased activity of alanine aminotransferase, aspartate aminotransferase, aldolase, conjugated (direct) bilirubin in the blood, decreased prothrombin index, albumin, cholesterol esters, cholinesterase activity, fibrinogen, blood clotting factors. Among the new indicators of cytolysis, alpha-glutathione-S-transferase, an enzyme of the hepatocyte cytoplasm, attracts attention. 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: increased body temperature, joint pain, enlarged 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 mercuric test, antibodies to the subcellular components of liver tissue appear (determined using an enzyme-linked immunosorbent assay). 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 representative of this class of samples. It is a component of the extracellular matrix. With its help, for the first time, it became possible to evaluate the function of endothelial elements of the liver, which play an important role in health and disease. Hyaluronate is a marker of liver inflammation and fibrogenesis.

Hemorrhagic syndrome. In APE, there is a decrease in the synthesis of blood coagulation factors. First, the synthesis of VII decreases, then II, IX, X, and with severe hepatic cell failure, 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 into the intestine (acholia). Prothrombin synthesis requires vitamin K, which is fat-soluble and is 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 indicated for the administration of vitamin K, although this rarely leads to the elimination of coagulopathy. Increased consumption of blood coagulation 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 aggravates hypoproteinemia. Bleeding is more common in the gastrointestinal tract, which causes microbial fermentation of blood in the intestines, increased ammonia production and worsening intoxication.

Syndrome portal hypertension, hepatolienal the syndrome manifests itself as 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 lymphatic drainage pathways. Both organs form a single reticulohistiocytic apparatus. The development of portal hypertension leads to the formation of esophageal varices (bleeding) and the development of ascites.

The assessment of the functional capacity of the liver is carried out in three directions: metabolic, excretory, detoxification.

To monitor the completeness of the course of metabolic processes, the following tests are used: determination of the concentration of prothrombin, albumin, and cholinesterase activity. A test with an intravenous load of galactose, as well as determining the level of short-lived procoagulants of hepatic origin: proaccelerin and proconvertin, are more informative. Another group of tests is associated with excretory processes. With certain reservations, this also includes indicators of cholestasis - bilirubin, bile salts, gamma-glutamyl transpeptidase (GGTP) of blood serum. It is also important to determine typical indicators of hepatodepression - bromsulfalein and especially indocyanine tests. A significant part of 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 processes of this kind, the transformation of medicinal substances occurs. Antipyrine, caffeine and lidocaine stress tests, as well as the amidopyrine breath test, are based on this principle.

Hepatic encephalopathy(PE) is a complex of potentially reversible neuropsychiatric disorders, including changes in consciousness, intelligence and behavior and neuromuscular disorders. Currently, the most fully unifying accumulated knowledge about the pathogenesis of hepatic encephalopathy is the “glia” hypothesis, according to which endogenous neurotoxins and amino acid imbalances resulting from hepatocellular failure and (or) portosystemic blood shunting 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 manifest themselves as clinical symptoms of hepatic encephalopathy. Among endogenous neurotoxins, the leading place is given to ammonia.

In recent years, some mechanisms of the neurotoxic effect of ammonia have been discovered, in particular: restriction of the function of the malate-aspartate shuttle, as a result of which the transport of hydrogen ions decreases and the synthesis of ATP in the brain decreases. Ammonia affects the permeability of the blood-brain barrier, which stimulates the transport of aromatic acids into the brain and, as a result, enhances the synthesis of false neurotransmitters and serotonin. Ammonia increases the affinity of postsynaptic serotonin receptors, which play a major role in the regulation of sleep and behavior. The possibility of direct modulation of neuronal activity by ammonia is being 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 is of leading importance, amino acid imbalance and changes in the function of neurotransmitters and their receptors.

The severity of neuropsychiatric symptoms of hepatic encephalopathy ranges from “0” (latent or subclinical form – “LET”) to “4” (deep coma). Neuropsychiatric symptoms in PE include changes in consciousness, intelligence, behavior and neuromuscular disorders. The identified four stages of hepatic encephalopathy can transform into one another. Moreover, most of the symptoms that appeared in earlier stages persist in the next stages. The gradation of hepatic encephalopathy by severity is presented in table. 39.2. The main criterion for determining its stage is the state of consciousness. The rest of the symptoms are of secondary importance. Latent hepatic encephalopathy (stage 0) is characterized by the absence of clinical symptoms and is detected only when additional research methods are used - psychometric tests (number connection test, line test), electroencephalography, evoked potentials, etc. The frequency of LET in patients with liver cirrhosis is 30-70 %. In the 1st stage of hepatic encephalopathy, the rhythm of sleep is disrupted: drowsiness during the day and insomnia at night appear. In the 2nd stage, drowsiness increases and a disturbance of consciousness appears. In the 3rd stage, disorientation in time and space joins the listed changes, confusion of consciousness increases, and the 4th stage begins - coma itself. It is characterized by a lack of consciousness and response to painful stimuli.

Table 39.2

Stages of hepatic encephalopathy (according to N.O.Conn, 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 impairment, handwriting changes, small-scale tremors
2. Medium	lethargy	lack of sense of time, counting disorders, amnesia	lack of inhibition, personality changes, fear, apathy	asterixis, slurred speech, hyporeflexia, torpor, ataxia
3. Heavy	disorientation somnolence 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	termination of function	areflexia, loss of tone

The course of endogenous hepatic coma is most often acute. Brain function disorders occur suddenly, and their dynamics progress. Often in the first stages the patient is agitated and restless. The prognosis of endogenous hepatic coma is poor - without transplantation, the mortality rate of 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%), portocaval anastomosis (6 - 8%), excessive consumption of animal proteins (3 - 7%), surgery for other diseases (2 - 6% ), laparacentesis with removal of a large amount of ascitic fluid (2 - 5%).

After their elimination and appropriate treatment, hepatic encephalopathy regresses. At the same time, the likelihood of a new episode developing increases. The chronically progressive course of encephalopathy presents significant difficulties in treatment. It is rare and develops in elderly patients with severe portacaval shunting of blood after portacaval anastomosis. 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. Considering the many reasons leading to the development of liver failure and the diversity of the clinical picture of this pathology, a unified classification of ALI does not currently exist. From our point of view, from a practical point of view, the working classification presented in Table 39.3 is convenient. It identifies excretory (obstructive jaundice, etc.) and cellular-hepatic (liver cirrhosis, toxic hepatitis, etc.) forms of APEC, as well as two degrees. The decompensated degree of acute liver disease is determined by 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 (hepatoprivate syndrome)		Decompensated
Forms of liver failure	excretory	cellular-hepatic	excretory	cellular-hepatic
Hepatic encephalopathy	LPE – stage 1		2-4 stages
Total bilirubin, µmol/l	less than 100.6		more than 100.6
Bleeding from esophageal varices
Albumin, g/l	more than 30.0	more than 21.2	less than 30.0	less than 21.2
Prothrombin index, %		more than 72.6		less than 72.6

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

Table 39.4

Child–Pugh criteria

Criterion
Criterion
Total bilirubin	28 µmol/l 1.26 g/100ml		more than 67.2
Albumen
Prothorombin index
		small, transient	big, torpid
Encephalopathy		periodic
Every sign
Sum of points

Intensive care. Acute liver failure is an indication for placing patients in the ICU. They need to perform central vein catheterization, maintaining approximately “zero” fluid balance. In patients with acute liver failure, it is important to control glucose levels (risk of hypoglycemia, but it is better not to administer a 40% glucose solution; preference is given to 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:

Improving hepatic blood flow (eliminating hypovolemia, anemia, prescribing cardiotonics, eliminating intestinal paresis);

Blood oxygenation (oxygen inhalation, HBOT);

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 glucose solutions with magnesium, insulin, replenishment of protein losses);

A diet with limited protein intake, especially animal protein (better digestible carbohydrates), parenteral nutrition.

Specific therapy.

Etiological treatment is aimed at eliminating the cause of the development of ALE . In case of 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. For viral hepatitis, antiviral therapy is carried out, the use of which in the early stages of the disease often prevents ALI. 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 reducing its production due to intestinal decontamination (non-absorbable antibiotics), its cleansing (enemas), the use of glutamic acid (1% solution 10.0 ml IV or in Table 1, 0 g 2-3 times/day), lactulose (15-200 ml/day, reaching stool frequency up to 2-3 times).

Ammonia utilization is achieved using arginine hydrochloride (0.3 - 0.5 g/kg/day in 2-3 doses), ornitsethyl (hepa-merz, ornithine-aspartate), sodium benzoate, which binds ammonia to form hippuric acid (10 g/ day).

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 simultaneously prescribe several drugs (for example, Heptral + Essentiale + Ornithine). Recommended doses of hepatoprotectors for the treatment of acute liver failure are:

heptral – 10 – 20 ml (800-1600 mg) IV or IM per day;

natrusil – 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 orally;

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 times a day orally;

lipostabil – 10 – 20 ml IV 1 time per day or 2 caps 3 times per day orally;

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

Table 39.5

Mechanism of action of hepatoprotectors

Drugs	Syndromes
		Mesenchymal cellular inflammation	Impaired biosynthetic function	Cholestasis	Hepatocellular failure

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 for hyperbilirubinemia is ineffective, even if special methods of pre-perfusion treatment of the hemosorbent are used. In the presence of obstructive jaundice, an indispensable condition for efferent therapy should be a preliminary reliable reduction of biliary hypertension by external diversion of bile or internal drainage of the biliary tract. Sometimes the first plasmapheresis operation with plasma replacement 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 fairly traumatic surgery is performed in patients with initial severe liver failure. Albumin-mediated hemodiafiltration using a reciprocal molecular adsorption system, as well as the use of sorption techniques on living hepatocytes, have the highest effectiveness in the treatment of acute liver failure.

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

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

1st 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 ward.

2a degree. Chronic liver disease with a life expectancy without liver transplantation of less than 7 days while in the ICU.

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

3rd degree. The need for constant hospital stay.

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Treatment of acute liver failure

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

Measures taken when acute liver failure of any etiology is detected:

Ensure adequate oxygenation. Provide additional oxygen and, if necessary, mechanical ventilation.
Correction of metabolic disorders, electrolytes and CBS.
Monitoring of hemodynamic parameters.
ICP control.
Parenteral administration of glucose to correct hypoglycemia.
Administration of mannitol to reduce ICP.
Parenteral administration of proton pump inhibitors or histamine type II receptor blockers to prevent gastrointestinal bleeding.

Treatment of complications of acute liver failure

Hepatic encephalopathy

Cerebral edema

Hypocoagulation

Hepatorenal syndrome

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

Increased bilirubin concentration more than 299 µmol/l.
Increased prothrombin time (more than 62 s).
Decrease in ALT activity 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.
Under two years of age.

Source: ilive.com.ua

Obert A.S., Morozova O.P., Yakob L.E., Zinovieva L.I., Ivanov I.V., Pershin O.V.

Acute hepatocellular failure is a clinical concept equivalent to the morphological concept of “massive” or “submassive liver necrosis”. Hepatocellular failure is usually characterized by encephalopathy - a disorder of consciousness, a change in the consistency and reduction in the size of the liver, hemorrhagic syndrome, and often progressive jaundice.

In the literature, the terms “hepatodystrophy”, “malignant” or “fulminant” forms are used as synonyms. The main morphological substrate of these conditions is early acute massive necrosis of the liver. In the future, when presenting the material, the terms “acute hepatic cell failure” (ALF) and “acute hepatic encephalopathy” (AHE) are more often used.

The main etiological factors of acute renal failure in children include viral hepatitis B. An important comatogenic factor is superinfection with the D virus. The provoking role of the addition of HAV and HCV has been confirmed. In recent years, much attention has been attracted in the literature by indications of the predominant frequency of detection of mutant HBV strains, in particular the e-minus strain, in patients with fulminant HBV (Nakayama I. et al., 1995; Sato Sh. et al., 1995; Baymert T.F., Liang T.I. , 1996). ARF occurs predominantly in children of the first year of life in 0.7-1% (Drobinsky N.R., Dokuchaeva K.D., 1972; Nisevich N.I., Uchaikin V.F., 1982, 1990). Mortality, according to N.I. Nisevich, V.F. Uchaikin (1982), is 11.6%. AKI in children, in addition to viral hepatitis, can develop due to drug-induced, toxic liver damage.

Pathogenesis

The most important factors causing acute massive liver necrosis in viral hepatitis are: the high immunogenicity of the pathogen, the massiveness of the infecting dose, and a genetically determined strong type of immune cell reaction. Rapid, super-intensive synthesis and secretion of antibodies in excess develops. The forming antigen-antibody complexes cause massive immune cytolysis, and can also contribute to increased fragility of lysosomal membranes of hepatocytes, release of proteolytic enzymes, and massive necrosis of hepatocytes (A.F. Bluger et al., 1988).

Hepatic coma is the most striking manifestation of acute hepatic cellular failure, its final stage and is clinically characterized by impaired mental activity up to complete loss of consciousness. Disorder of consciousness occurs as a result of the accumulation in the blood serum of numerous cerebrotoxic substances formed as a result of progressive functional inferiority of the liver and autolytic breakdown of the hepatic parenchyma. Among direct cerebrotoxic substances, products of free radical oxidation of hepatocyte membranes are important, which can increase the permeability of brain cell membranes and have a direct toxic effect on the central nervous system. Products of protein metabolism (phenylpyruvate, ammonia, etc.), carbohydrates (pyruvic, lactic, alpha-ketoglutaric acids), and fat (low-molecular fatty acids butyric, valeric, caproic) also have a toxic effect. A sharp drop in the detoxification function of the liver also underlies a significant increase in the blood content of intestinal toxins phenol, indole, skatole, indican, mercaptan and a number of others.

As a direct cause of hepatic coma, the decisive importance is given to the inhibition of oxidative phosphorylation processes with a sharp decrease in the synthesis of high-energy bonds of phosphorus compounds and a drop in the bioenergetic potential of cerebral cells. This is accompanied by a violation of oxidative processes, a decrease in glucose and oxygen consumption, and the development of cerebral hypoxia and hypoglycemia. Hypoglycemia associated with inhibition of gluconeogenesis in the liver can aggravate functional disorders of the central nervous system (deficiency of the main substrate for energy production). An increase in the permeability of neuronal membranes leads to the accumulation of Na and Ca in subcellular structures and a decrease in the K content. The accumulation of hydrogen ions, pyruvic, lactic and tricarboxylic acids of the Krebs cycle inside neurons leads to the development of intracellular metabolic acidosis. The result of these processes is edema-swelling of brain cells.

With APE, the coagulation potential of the blood is depleted, the synthesis of coagulation factors decreases, the enzymes of proteolysis and fibrinolysis are activated, and the activity of their inhibitors is catastrophically reduced. The implementation of various forms of hemostasis pathology occurs in the presence of hypocoagulation and depletion of blood coagulation factors, leading to disruption of microcirculation in the liver with the formation of intravascular blood clots and the occurrence of hemorrhagic syndrome. The synergism of toxic substances increases due to the violation of CBS, the redistribution of electrolytes and contributes to the development of hepatic coma.

Clinic

The clinical picture of acute renal failure is far from clear and varies widely depending on the duration of the disease and the rate of progression of the process.

Manifestations of liver failure are fundamentally the same as in severe forms of the disease, but differ in a more significant degree of severity and rapid dynamics of development: severe weakness, headaches, anorexia, constant nausea, repeated vomiting. Hemorrhagic syndrome progresses: skin petechiae, ecchymoses, and sometimes profuse hemorrhagic rash, melena, bloody urine, bleeding from injection sites, vomiting “coffee grounds”. There is a rapid increase in jaundice. Hypotension, muffled heart sounds, decreased diuresis, and slowed ESR are characteristic.

For acute renal failure, the presence of clinical signs of massive liver necrosis is mandatory. They are characterized by a rapidly progressive decrease in the size of the liver (symptom of “melting liver” or “empty hypochondrium”); the consistency of the liver becomes flabby, doughy, and the lower edge can no longer be felt. A distinct liver odor appears from the mouth. Repeated measurements of the liver size according to percussion and palpation, carried out at short intervals, make it possible to assess the rate of progression of the necrotic process. Indirect signs of beginning massive liver necrosis are spontaneous pain and tenderness on palpation in the right hypochondrium due to necrosis and autolytic breakdown of the liver parenchyma. Characterized by tachycardia, pronounced temperature reaction (T 38-39 ° C), neutrophilic leukocytosis, leukemoid reactions.

In parallel with the clinical signs of acute renal failure and massive liver necrosis, the neurological symptoms of hepatic precoma, which is the highest manifestation of hepatic cellular failure, are increasing. The development of precoma-coma characterizes the transformation of “pure” liver failure into hepatocerebral failure. It is the emergence and rapid progression of impaired consciousness that serve as the main criterion for distinguishing severe non-comatose forms of HBV with a cyclic course from the fulminant variant of the disease (early acute massive liver necrosis).

There are 4 successive stages of progressive neuropsychiatric disorders: acute hepatic encephalopathy (AHE) I-II (precoma); OPE III-IV (coma). This division is of great practical interest, since it allows a more objective assessment of the effectiveness of the therapy and to judge the prognosis; there are no pathognomic symptoms indicating a threat of developing hepatic coma. The totality of clinical data is informative, especially when providing dynamic monitoring of patients.

It is customary to distinguish 4 stages of progression of neuropsychiatric disorders. In this case, an integral assessment of the depression of consciousness can be used, based on taking into account the patient’s reaction to verbal commands and painful stimulation. According to this system, in the precoma stage, the reaction to verbal treatment is slowed down, but purposeful, and to painful stimulation it is preserved. In the first stage of coma, there is no reaction to a cry; pain is characterized by a short-term awakening, sometimes with inadequate speech reactions (moaning, incoherent words) and unfocused movements. In stage II coma, there are no targeted verbal and motor reactions; only undifferentiated movements of the body and limbs occur in response to pain. Clinical monitoring is supplemented by repeated EEG registration, which is considered as the most objective criterion for assessing the depth of coma.

OPE I (precoma I) in older children is characterized by a change in the child’s behavior and usually begins gradually: euphoria is often observed, in other cases there is a feeling of anxiety, melancholy, depression or apathy, memory “gaps”, handwriting disorder, deterioration of orientation in time and space . A slowdown in thinking (slow responses to simple questions) is detected quite early. An important symptom is sleep disturbance. The patient may doze during the day and become noisy at night. Handwriting impairment should be considered as an objective, and most importantly, early-onset sign of acute liver failure. Changes in the EEG are inconsistent and weakly expressed.

OPE II (precoma II) is manifested by more pronounced disturbances of consciousness: confusion becomes more distinct, disorientation in time, space, and personality is observed. Speech is slow. Attacks of excitement, sometimes with delirium, are replaced by depression and drowsiness. The reaction to painful stimuli is preserved. Control of the sphincters is also maintained. One of the most characteristic movement disorders is flapping tremor. In precoma II, clinical signs may appear indicating cerebral edema: facial flushing and sweating, hiccups, hallucinations, yawning, increased blood pressure. Patients carry out the simplest commands with difficulty, periodically completely “switching off”, which corresponds to repeated short-term loss of consciousness. The EEG records an increase in amplitude and a slowdown in rhythm.

OPE III (coma I) corresponds to a shallow coma. Consciousness is absent, but the reaction to strong stimuli (pain, cold, heat) is preserved. The neurological status is characterized by wide pupils with an almost complete lack of reaction to light, a symptom of “floating” eyeballs; pronounced pathological reflexes of Babinsky, Gordon, clonus of the foot muscles. The face becomes amicable, the limbs are rigid, and paroxysmal clonic convulsions are observed. Paresis of smooth muscles leads to intestinal atony with progressive bloating and cessation of urination with a full bladder. EEG changes are characterized by a decrease in amplitude with a rare rhythm. Duration of OPE III is 1-2 days.

OPE IV (coma II) - deep coma, differs from the previous stage in complete areflexia, loss of response to any stimuli. Basically the same abnormalities are recorded in the neurological status. The pupils are wide, their reaction to light disappears, corneal reflexes fade, and sphincter paralysis occurs. The appearance of periodic breathing of the Kussmaul or Cheyne-Stokes type is characteristic. The EEG shows a decrease in cerebral activity up to its complete absence. The duration of OPE IV ranges from several hours to a day, on average 17 hours.

Based on the nature of the initial manifestations of liver failure and the rate of development of clinical symptoms of massive liver necrosis, it is customary to distinguish between the acute and subacute course of acute renal failure. Morphologically, this corresponds to acute and subacute massive liver necrosis. In addition, there is also a fulminant variant of the course of acute liver failure - this is the most rare form. A feature of the fulminant course is the development of massive liver necrosis, acute liver failure with a fatal outcome in the prodromal period, even before the appearance of distinct jaundice (usually in the first 3-4 days from the onset of the disease). In the acute course, the clinical manifestations are the same as in the severe form of the disease, but differ in a more significant degree of severity. Signs of massive liver necrosis and hepatic coma usually develop on the 5th-6th day of the icteric period. The subacute course of APE is characterized by a gradual, wave-like progression of clinical symptoms of liver failure and the development of massive liver necrosis and hepatic coma at 3-5 weeks of the disease. When macronodular cirrhosis develops, hepatic coma occurs at a later date (after 3-6 months).

Features of fulminant forms of viral hepatitis in children of the first year of life

APE is more common in children 1 year of life (up to 20%). The development of acute liver failure with a fatal outcome is 6 times higher in them than in children older than one year.

In children of the first year of life in the first stages of disease development, the clinical diagnosis of APE is difficult. Intoxication is often mild for a long time. Appetite is often preserved, regurgitation and vomiting are episodic. Certain information is provided by a change in the child's behavior - unmotivated restlessness, lethargy, change in sleep rhythm. An objective criterion for the severity of the disease is intense jaundice, especially in combination with a small liver. At the same time, one should remember about the possible discrepancy between the degree of skin icterus and bilirubinemia, as well as the initial stages of acute liver failure in some children with low levels of bilirubin in the blood. During this period, children of the 1st year of life, as well as in the older age group, are characterized by an increase in hemorrhagic syndrome in the form of petechial rash, ecchymoses, bleeding from injection sites, and nosebleeds. Tachycardia, muffled heart sounds, decreased diuresis, leukocytosis, and slowed ESR are noted.

Further development of massive liver necrosis, as in older children, is characterized by a rapidly progressive decrease in its size, pain on palpation, doughy consistency, and hepatic odor from the mouth. Intoxication increases, hemorrhagic syndrome intensifies, which together leads to increased vomiting of “coffee grounds”. Along with this, body temperature rises to febrile levels, tachycardia, toxic shortness of breath, oligoanuria and edematous ascitic syndrome often develop. A significant indicator of the severity of the condition is flatulence, followed by intestinal paresis.

It is very difficult to assess the degree of mental disorders in children in the first year of life; they can be distinguished as OPE II (precoma), OPE III (coma I) and OPE IV (coma II). In addition, it is not always possible to note a gradual increase in the severity of the disease and a clear transition from one stage of coma to another.

OPE II (precoma) is a condition with a predominance of symptoms of a disorder of the central nervous system. Attacks of psychomotor agitation are replaced by attacks of adynamia, drowsiness, children cannot fix their gaze on toys, periodically do not recognize their mother, but react to painful stimuli by crying. The reaction of the pupils to light is preserved, abdominal reflexes are usually not evoked. 50% of children experience convulsive twitching in certain muscle groups, sometimes trembling of the upper limbs, and some children have clonic-tonic convulsions. Constant symptoms are the clinical manifestations of massive liver necrosis described above.

OPE III (coma I) is characterized by a persistent lack of consciousness, the child is restless, does not respond to examination, the pupils are constricted, with a sluggish reaction to light, tremor increases, and convulsions become more frequent. However, at this stage the reaction to strong painful stimuli remains, and swallowing is not impaired.

After 1-2 days, OPE III turns into OPE IV (coma II), the hallmarks of which are a complete lack of response to painful stimuli, dilated pupils without reaction to light, disappearance of the corneal reflex, respiratory distress of the Kussmaul or Cheyne-Stokes type, which occurs periodically convulsions.

Complications OPE

The clinical picture of APE changes significantly with the addition of additional pathological processes. These include the development of cerebral edema, renal failure, massive gastrointestinal bleeding, and the addition of a secondary infection. The majority of these pathological conditions can only conditionally be classified as complications. Rather, we are talking about different options for a particularly severe course of hepatitis B. The exception is a generalized secondary infection, which is a true complication of the underlying disease. Their development further complicates the already extremely difficult prognosis. Timely recognition of these conditions is necessary for adequate intensive care.

The most common complication is edema-swelling of the brain. Clinically, this is manifested by symptoms of cerebral hypertension and irritation of the meninges, intense headaches, dizziness, repeated “cerebral” vomiting that does not bring relief; Characterized by hyperemia and sweating of the face, convulsive twitching, the appearance of oculomotor disorders, increased blood pressure, and progressive disturbances in breathing rhythm.

Massive gastrointestinal bleeding, clinically manifested by vomiting “coffee grounds”, blood clots, dark tarry stools, sometimes with the presence of unchanged blood. Anemia is progressively increasing.

Acute renal failure. For early recognition of renal failure and subsequent monitoring of patients, it is important to take into account hourly urine output. Diuresis less than 35-45 ml/h corresponds to oliguria, less than 15-20 ml/h oligoanuria. With such a volume of urine, even at its maximum concentration, complete excretion of metabolic products is not ensured. Despite such a significant decrease in diuresis, the relative density of urine is sharply reduced (1003-1010), which confirms a violation of the concentration function of the kidneys. Characterized by a rapid increase in body weight due to pulmonary and cerebral edema.

Secondary infection. Most often, pneumonia occurs; a septic process may occur, which is facilitated by prolonged catheterization of the venous vessels. In patients with fulminant hepatitis, the body's resistance is sharply reduced, which facilitates the addition of a secondary infection.

Diagnostics

The main clinical criteria for fulminant forms of viral hepatitis are the combined development of two symptom complexes: hepatic coma and massive liver necrosis. The intensity of jaundice is diagnostically uninformative, since with a truly lightning-fast course it does not have time to reach its maximum development. The main diagnostic difficulties arise at an early stage, before the onset of coma and in the absence of classical signs of massive liver necrosis. Below are clinical and laboratory signs that are precursors of early acute massive liver necrosis of fulminant hepatitis (S.N. Sorinson, 1997):

- progressive increase in the severity of the patient’s condition;

- pain and tenderness in the right hypochondrium;

- progressive reduction in liver size; temperature reaction;

- manifestation of hemorrhagic syndrome;

- the appearance of a slight liver odor in the patient’s breathing zone;

Tachycardia;

- increased breathing and increased blood pressure (with the development of cerebral edema);

- neutrophilic leukocytosis;

- changes in neuropsychic status with the sequential development of a phase of excitation and a phase of inhibition;

- during the excitement phase, euphoria, headaches, autonomic disorders, vomiting;

- against the background of drowsiness, lethargy, attacks of psychomotor agitation;

- impaired coordination of small movements (autograph test, handwriting impairment);

- errors when counting out loud;

- change in Romberg's posture, "flapping tremor";

- changes in the EEG with an increase in the amplitude of the waves and a tendency to slow down the rhythm.

In a general blood test in patients with acute renal failure, there are signs of anemia, especially severe in hemorrhagic syndrome, leukocytosis from moderate to severe. ESR is normal or reduced, but acceleration is also noted in some cases.

Biochemical studies occupy an exceptional place in the diagnosis of acute renal failure. Of the numerous tests, the most informative are the so-called bilirubin-protein and bilirubin-enzyme dissociations. Their essence lies in the fact that with a high content of bilirubin in the blood serum, the level of protein complexes and enzyme activity decrease sharply. The level of total bilirubin increases due to the direct fraction in the first days, then, as the process progresses, the proportion of the indirect fraction increases due to impaired uptake and conjugation of bilirubin by liver cells (massive necrosis of hepatocytes).

Very important in the diagnosis of massive liver necrosis is the blood coagulation indicator prothrombin, the content of which is less than 10% indicating a hopeless prognosis of the disease. Particularly valuable is the study of the levels of proaccelerin and proconvertin, the decrease of which precedes the manifestations of massive liver necrosis. As a result of a sharp disruption of the protein-synthetic function of hepatocytes, the content of β-lipoproteins and total protein decreases due to the albumin fraction, and the sublimate titer decreases. The activity of enzymes (ALT, AST) is different at different stages of acute liver failure. In the early periods, there is usually a significant increase in transaminase activity. Subsequently, as hepatic cell failure increases, enzyme activity decreases. When monitoring patients with severe forms of viral hepatitis, dynamic monitoring of acid-base status (ABS) and water-electrolyte balance is necessary. Characterized by a decrease in potassium content and, conversely, an increase in sodium. Regular changes take place in the ratio of CBS. In the stage of precoma and coma, extracellular alkalosis and intracellular acidosis are detected, which increases the content of free ammonia in brain tissue, disrupts the metabolism of neurocytes and contributes to the deepening of coma.

To identify the etiological factor, it is necessary to test the patient’s blood for markers of viral hepatitis (HBsAg, HBeAg, antiHBcor IgM, antiHBs, antiHBe, antiHCV, antiHDV), PCR (polymerase chain reaction) is informative, with which you can detect HBV DNA, HCV RNA. Taking into account clinical data and the dynamics of HBV markers makes it possible to distinguish between hyperimmune (hyperreactive) and immunotolerant (replicative) variants of fulminant hepatitis B. Early (in the first 7-10) appearance of antiHBe, antiHBs is characteristic of the hyperimmune variant, and the continued circulation of HBeAg, HBsAg, antiHBcor IgM ( without the above-mentioned seroconversion at the same time) for replicative.

For early recognition of acute renal failure, it is important to take into account the level of urea and creatinine.

Treatment

In the treatment of acute renal failure, the use of a therapeutic complex as early as possible plays an extremely important role, i.e. at the first signs of liver failure.

The intensive care program includes a set of therapeutic measures aimed at maintaining vital functions, stabilizing blood circulation, adequate oxygenation, and reducing intracranial pressure.

Emergency measures are carried out immediately upon admission of the patient. These include: ensuring airway patency, gastric lavage, catheterization of the subclavian vein, catheterization of the bladder to measure daily urine output. It is important to insert a permanent nasogastric tube, which allows bile to be sucked out repeatedly.

Considering the sharp impairment of the detoxification function of the liver, protein unloading is absolutely mandatory. At an early age, a water-tea break is prescribed for 8-12 hours, followed by dosed feeding, expressed breast milk or fermented milk mixtures of 20.0 ml every 2 hours with a 6-hour night break. Older children are prescribed sugar-fruit fasting days, then kefir 100.0 after 3 hours. The expansion of the diet depends on the dynamics of liver failure; if positive, table No. 5 according to Pevzner is subsequently prescribed.

With progressive disorders of consciousness, natural nutrition becomes impossible. In this case, feeding is carried out with infant formula through a nasogastric tube in combination with parenteral administration of energy solutions. You can introduce fruit juices, jelly, infusions, liquid semolina porridge, mashed potatoes. Feeding through a tube is carried out fractionally, in small portions of 20-30 ml, and for children over 3 years old, 50-100 ml every 2.5-3 hours.

Overloading the body with products of perverted metabolism requires active detoxification therapy, which is carried out by administering fluids enterally and parenterally. The calculation of liquid is carried out according to the generally accepted scheme, taking into account the daily need for water and its possible losses:

Age-related fluid requirement per 1 kg/weight/day;

With body temperature for each degree above 37 0 C for a duration of more than 8 hours, 10 ml/kg;

For every 20 respiratory movements above normal, 15 ml/kg.

60-70% of the total amount of liquid is administered intravenously. Colloidal preparations (reopolyglucin, albumin, fresh frozen plasma) make up 25% of the infusate. The remaining amount of liquid consists of glucose solutions to which medications are added (trental, contrical, GHB, potassium chloride, etc.). Specific recommendations for the dose and route of administration of individual drugs are presented in the table below.

Dosages and route of administration of drugs used in treatment

acute liver failure

Drugs	Doses, route and frequency of administration	Note

Prednisolone	15 mg/kg per day. IV, infusion every 4 hours without an overnight break
Claforan	100 mg/kg per day. IV, stream in 2 doses
Kanamycin	50 mg/kg per day. by mouth in 4 doses
Trichopolum	30 mg/kg per day. by mouth in 4 doses
Normaze	5-10 ml 2 times through the mouth
Reopoliglyukin	10-15 ml/kg per day. IV, drip
Albumen	10 ml/kg per day. IV, drip
Fresh frozen plasma	up to 20 ml/kg per day. IV, drip
GHB, 20%	100 mg/kg per day. IV, drip in 2 doses
Contrikal	3 thousand units/kg per day. IV, drip in 2 doses	administered in 5% glucose solution
KCl, 7.5%	2-3 ml/kg per day. IV, drip	administered as part of a polarizing and hyperinsular mixture
Polarizing mixture	10% glucose, insulin 1 unit per 5 g of glucose, 7.5% KCl in volume, the final concentration of which in glucose is not > 1%, 25% magnesium sulfate 0.2 ml/kg, 10% calcium chloride 0.2 ml/ kg
Hyperinsular mixture	glucose 20% 5 ml/kg; insulin 1.5 units/kg; KCl 7.5% 0.3 ml/kg; everything is administered intravenously
Heparin	100-150 units/kg per day. s/c, after 6 hours	first portion (1/4 of the daily dose) IV drip with fresh frozen plasma, subsequent SC
Trental, 2%	1-3 mg/kg per day. IV, drip	administered in 5% glucose solution
Curantil, 0.5%	0.5-1 mg/kg per day. IV, drip	administered in 5% glucose solution
Complamin 20 %	10-20 mg/kg per day. IV, drip	administered in 5% glucose solution
Droperidol, 0.25%	0.1 ml/kg, IM, 2-3 times
Solcoseryl	1-2 ml per day. IV, drip 2 times	administered in 5% glucose solution
Ascorbic acid, 5%	1-2 ml per day. i/v, stream	administered in 5% glucose solution
Cocarboxylase	50-100 mg per day. i/v, stream	administered in 5% glucose solution
Riboxin, 2%	0.5-2.0 ml per day. IV, stream or drip	administered in 5-10% glucose solution
Lasix	1-2 mg/kg, IV, bolus 1-2 times

Infusion therapy is carried out evenly throughout the day in combination with diuretics (Lasix, Veroshpiron). Drip administration of fluid continues throughout the entire period of acute renal failure. When carrying out infusion therapy, it is necessary to carry out constant monitoring: temperature, pulse, respiration, diuresis are measured hourly, the child is weighed 2 times a day. An increase in weight indicates fluid retention in the body, which requires additional correction, both the volume of fluid administered and the dose, or a change in prescribed diuretics. Maintaining energy balance is one of the main directions of intensive care for patients with acute renal failure. The most frequently used amino acid mixtures in recent years are aminosteril, aminoped, hepatamin, hepasteril. In children, aminoped is more often used, which contains 18 essential and non-essential amino acids. Available in the form of 5% and 10% solutions. The energy value is 200 and 400 kcal/l. The daily dose of 5% solution for newborns is 20-30 ml/kg, for children over 1 year old - insert table 6 10-20 ml/kg. The infusion rate should not exceed 2 ml/kg/hour. When using a 10% solution, appropriate adjustments are made.

In case of acute renal failure, it is necessary to use large doses of corticosteroids (glucocorticoids prednisolone), which, by suppressing the transformation of lymphocytes and antibody formation, reduce the destruction of liver cells caused by cytotoxic and autoimmune mechanisms, stabilize the membranes of lysosomes and, by blocking the release of histamine, serotonin, and kinins, reduce inflammatory and allergic reactions. The need for early use of hormonal drugs in children with massive liver necrosis is emphasized by all researchers. It is preferable to prescribe prednisolone in a short course of up to 7-10 days, since the clinical effect, regardless of the duration of the course of treatment, appears in the first 3-10 days. Longer administration of prednisolone increases adverse reactions, in 60% drug intolerance develops (hemodeza, albumin, etc.), possibly due to the competitive interaction of drugs for binding sites on serum proteins and disruption of their pharmacokinetics (D.K. Bashirova, G. F. Muklisova, A.P. Zvereva, 1988).

The loss of potassium by hepatocytes, as well as increased hypokalemia due to the use of large doses of glucocorticoids, require the use of its drugs. Potassium is prescribed in the form of a 7.5% KCl solution and is administered as part of a polarizing and hyperinsular mixture. The latter also contributes to the rehabilitation of neuroglia and the reduction of cell edema. It should be borne in mind that in case of anuria, potassium supplements are contraindicated.

According to the results of our research (L.E. Yakob, N.A. Dolgova, 1989), as well as according to literature data, with acute renal failure in young children, the coagulation potential of the blood is depleted, the synthesis of coagulation factors decreases, and the enzymes of proteolysis and fibrinolysis are activated. All this served as the basis for the use of heparin in combination with fresh frozen plasma and contrical as a pathogenetic agent in the treatment of acute renal failure. The main methods for monitoring heparin therapy are the Lee and White clotting time, ethanol and autocoagulation tests.

Impaired microcirculation in the liver and the manifestation of portal vasculitis are the basis for the use of trental, complamin, and chimes in a complex of therapeutic agents.

Removing psychomotor agitation is of great importance in the treatment of patients with APE. The following drugs are used: sodium hydroxybutyrate (GHB), droperidol.

To correct hypoxia, solcoseryl is used, which is a deproteinized extract of calf blood with high RES activity. Solcoseryl contains factors that increase the absorption of oxygen in tissues and accelerate recovery processes. For the same purposes, hyperbaric oxygenation is used (pressure 1.1-1.5 atm., exposure 45-60 minutes, 1-2 times a day, course duration 7-10 days). In the absence of opportunities for HBOT, oxygen therapy is used by the usual inhalation route, i.e., humidified oxygen. Ascorbic acid and cocarboxylase should be a mandatory component of therapy.

To suppress intestinal microflora, patients with APE are recommended to administer orally poorly absorbed antibacterial drugs (kanamycin or trichopolum) and enterosorbents. To suppress putrefactive microflora, it is advisable to use lactulose (normase), an artificial disaccharide consumed by anaerobic lactobacilli, which sharply increases their reproduction and thereby reduces the number of ammonia-forming phenol bacteria. To cleanse the intestines and reduce autointoxication, daily enemas and gastric lavage are indicated.

The use of large doses of glucocorticoids, under conditions of which activation of secondary flora is possible, dictates the need for antibiotic therapy to suppress it. The most effective and frequently used are cephalosporins.

Hemosorption, plasmapheresis, exchange transfusions (20-30% of blood volume), hemoperfusion through a suspension of living hepatocytes should be considered as additional methods of treating acute renal failure.

The most accessible method for children is exchange blood transfusion (EBT), which does not require special equipment and can be performed in any intensive care unit or infectious diseases department. Its principle is to remove cerebrotoxic metabolites from the patient’s blood and deliver essential substances that are not synthesized by the affected liver with the donor’s blood. The indication for APE is the ineffectiveness of intensive therapy for 1-2 days and an increase in symptoms of APE. The multiplicity of OPCs depends on their effectiveness. The volume of replaced blood is determined at the rate of 70 ml per 1 kg of body weight, which approximately corresponds to one volume of bcc. Freshly collected, less often heparinized blood is used, with strict adherence to the instructions for blood transfusions. Stop OPC when you come out of a coma and improve biochemical parameters.

Exit from the specified intensive care complex is carried out as follows. When biochemical tests indicating the severity of hepatic cellular failure (an increase in total bilirubin, a decrease in the level of β-lipoproteins and prothrombin index) stabilize and the first signs of their positive dynamics appear, immediately remove half of the intravenously administered dose of prednisolone, and after 2-3 days another half is removed, which should be completely discontinued after another 2-3 days, and the last 2-3 days the drug can be administered intramuscularly. Contrical and plasma are prescribed until pain and hemorrhagic syndromes are relieved, intoxication is reduced, the liver becomes thickened and the size increases (3-4 days). Infusion therapy is completed when intoxication disappears and the level of total bilirubin decreases to at least 90-100 µmol/l. The duration of the course of antibiotic therapy is 5-7 days.

Treatment of complications of hepatic coma

Edema-swelling of the brain is associated with the cerebrotoxic effect of liver autolysis products and impaired cellular metabolism on the neuron. A paranecrotic process develops in the neuron with swelling of the neuroglia and disruption of its function.

Treatment includes drugs that improve neuroglial function and dehydration therapy. Hormone therapy for acute renal failure continues. The volume of infusion therapy is reduced to 30-40% of the daily physiological (excluding losses) fluid requirement. With good diuresis, up to 30% of the fluid is replenished orally or administered nasogastrically in the form of glucose-saline solutions. Dehydration is carried out with concentrated solutions of plasma, 15% albumin solution, Lasix; Mannitol is used as an osmodiuretic. To improve the function of neuroglia, the following drugs are prescribed: GHB, seduxen, polarizing mixture, hyperinsular mixture. Dopamine administration at a dose of 6-8 mcg/kg/min is effective. Barbiturates are contraindicated in cases of acute renal failure. Oxygen therapy is indicated. When signs of cerebral edema and swelling increase, a lumbar puncture is necessary. With the development of severe external respiratory disorders associated with cerebral edema, patients are transferred to mechanical ventilation.

In acute renal failure, it is advisable to sharply limit or completely eliminate protein to reduce the accumulation of nitrogenous waste; the dose of antibiotics is reduced to 1/5 of the daily dose, administered 2 times a day. For oliganuria, the amount of fluid administered (enterally and parenterally) should correspond to a volume of fluid equal to daily diuresis, loss with perspiration (25 ml/kg). In the absence of vomiting, 60-70% of this volume is administered orally, the rest intravenously. The administration of a hyperinsular mixture and calcium chloride is indicated (do not prescribe additional potassium!). It is necessary to periodically rinse the stomach and intestines. To stimulate diuresis, large doses of furosemide 5-10 mg/kg are indicated; in the absence of a diuretic effect, it can be repeated 2-3 times. Dopmin is important, providing vasodilation of the renal vessels, at a dose of 1-2 mcg/kg/min. In the absence of a therapeutic effect, it is necessary to connect extracorporeal hemodialysis or perform peritoneal hemodialysis.

The main directions of treatment for massive gastrointestinal bleeding are to compensate for the deficiency of coagulation factors (under the control of a coagulogram) and protect the gastric mucosa. For the purpose of replacement therapy, repeated direct blood transfusions, administration of fresh frozen plasma, and hemoconcentrates are indicated. The protection of the gastric mucosa is facilitated by suction of spilled blood, cold on the stomach, ingestion (sucking) of a frozen solution of aminocaproic acid, administration of hemostatics (gelatin, dicinone), Almagel, Maalox, Venter, H2 receptor blockers - cimetidine, ranitidine. In this case, antacids and H2 receptor blockers are taken at intervals of at least 1 hour.

Our body is an incredibly complex mechanism. Thousands of established processes ensure stable functioning of the whole organism. A 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 liver tissue or cholestasis syndrome.

Why does liver failure occur?

There are a lot of reasons for this. The most common ones should be highlighted:

acute and chronic hepatitis;
malignant formations;
diseases of the heart, blood vessels and other organs;
infectious diseases;
poisoning (food products, medications);
past stress (extensive burns, serious injuries, septic shock, major blood loss).

Types and symptoms

Cholestasis syndrome. The disease consists of poor excretion of bile from liver tissue. The symptoms are:

with functional cholestasis. Decreased normal movement of bile, water, bilirubin, acids through the liver tubules;
with morphological cholistasis. Accumulation of bile compounds in the bile ducts;
with clinical cholestasis. Accumulation in the blood of components translated into bile. Itching of the skin, jaundice, and an increase in bilirubin levels in the blood appear.

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:

Jaundice option:

yellow skin tone;
weight loss;
increase in temperature;
skin itching, appearance of vascular networks;
diarrhea, vomiting, pain in the liver;
emotional instability;
the liver and spleen are enlarged.

Holistic option:

skin itching, peeling;
dark urine;
uncharacteristic, light-colored stool;
increased levels of cholesterol and bilirubin in the blood.

Attention! If you experience 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 occurs without visible symptoms and can be detected by special tests;
medium-heavy. Pain in the liver area, colic, yellow discoloration of the skin and mucous membranes;
difficult stage. Can cause serious disruptions in 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 and consciousness.

Symptoms:

nausea, vomiting, diarrhea ;
insomnia, or vice versa drowsiness;
eczema ;
edema, ascites;
infertility.
anorexia;
heart failure;
constant feeling of thirst;
memory impairment.

Liver failure in children

Liver diseases often occur in children. In most cases, they are difficult and require immediate specialist intervention. There are many causes of liver disease in children, here are some of them:

congenital liver pathologies. Sometimes abnormal liver development begins in the womb. This could be a liver cyst, hernia, liver lobulation disorder;
introduction of the hepatitis virus during blood transfusion;
intoxication after poisoning, extensive burns;
excessive protein intake;
heavy blood loss.

Remember! Timely visit to the hospital and appropriate behavior will help preserve the life and health of your child.

Treatment at home

If you decide to be treated at home, the course of medications is still only prescribed by a doctor. The process of treating liver failure directly depends on the type of disease and 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 medications and vitamins aimed at combating the disease gives good results in our time. By following a course of treatment and a special diet, you can get rid of the disease in a certain period of time.

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

Use of drugs

Treatment often follows a certain 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;
Be sure to use B vitamins;
calcium, magnesium;

This is just an approximate, primitive treatment regimen. Do not under any circumstances try to prescribe treatment for yourself. This is extremely dangerous to life and health. The consequences may be irreversible. Only specialists with clear knowledge can prescribe the correct treatment.

Folk remedies for treatment

As with many other diseases, some folk remedies can help with liver-related diseases. Their variety is very great. Of course, there is no certainty that such tools will help you with a 100% guarantee. In addition, the use of some traditional methods can cause complications and irreversible harm to health. Allergies, drop in blood pressure and other phenomena are not excluded when treated with folk remedies. Before using any prescriptions, be sure to consult your physician. Such treatment is only auxiliary to drug treatment. Let's try to figure it out in more detail.

Recipes for cleansing the liver

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

Treatment of cirrhosis

dissolve turmeric (1 tablespoon) in a glass of water. You can add a little honey or sugar for taste. Drink half a glass several times a day;
Chop a clove of garlic and mix with a glass of kefir or yogurt. Drink every morning before meals;
Chop two cloves of garlic, pour boiling water (one glass). Leave to brew for a day. Drink in the morning on an empty stomach before meals;
Boil the oats for an hour, let them 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 half a glass of carrot juice 2 times a day for cirrhosis;
Fresh potato juice can be taken in half a glass for cirrhosis.

Herbs

Since ancient times, our ancestors have noticed and appreciated the extremely beneficial properties of some herbs. Plants can relieve inflammation, normalize blood pressure, energize, rejuvenate, soothe, heal wounds and much more. Nowadays, doctors themselves often prescribe herbal recipes as adjuvant therapy for many diseases.

To help treat liver diseases, there are the following recipes:

St. John's wort, dandelion root, sandy immortelle mixed in a ratio of 2:2:1. Brew 500 grams of boiling water. Take a glass morning and evening;
Mix nettle, rose hips, wheatgrass in a ratio of 1:1:1. Brew a glass of boiling water and leave for 2-3 hours. Take 2-3 doses per day for cirrhosis;
Mix lingonberry leaves, corn silk, dandelion root, linden blossom, and motherwort herb in equal quantities. Pour a liter of boiling water and leave for 5-6 hours. Take half a glass 2 times a day;
Mix yarrow, St. John's wort, juniper fruits in a ratio of 2:2:1. Fill with a liter of water. Boil for 10 minutes, strain, let steep for 12 hours. Take half a glass 2-3 times a day;
mint herb, bearberry, knotweed, St. John's wort, dill seeds, Kuril tea, mix everything in equal proportions, chop well. Boil in a liter of water for 10-15 minutes, strain. Let stand for 10-12 hours. Take a quarter glass 2-3 times a day.

For liver diseases, a special diet is absolutely necessary. There are products that can aggravate the course of the disease, and vice versa, help in healing.

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

Dietary rules for liver diseases:

food should be easily digestible and light;
exclude spicy, salty, sour, smoked, fatty, fried foods;
porridge should be well cooked. It is better to rub large-grain porridges on a sieve;
include foods that have choleretic properties in your food. These are corn, sunflower, peanut oils. Greens: dill, spinach, celery. Fruits include oranges, lemons, grapefruits. Dried apricots, cauliflower, artichokes are useful;
limit protein intake to no more than 20-70 grams per day;
Have a fasting day once a week.

Prohibited products:

mushrooms;
fatty meat;
alcohol;
chocolates;
fatty dairy products;
strong black tea;
radishes, sorrel;
rye breads, fresh pastries.

This is not the entire list of permitted and prohibited products. To create a diet suitable for each type of disease, you should consult a doctor and nutritionist. Your health is in your hands. Stay healthy.