Surgical treatment of liver cirrhosis presentation. Presentation of liver cirrhosis and its complications. Syndrome of small liver failure

slide 2

Cirrhosis of the liver is a chronic progressive process in the liver, characterized by a significant decrease in the number of functioning hepatocytes, an increase in fibrosis, a restructuring of the normal structure of the liver, and the development of liver failure and portal hypertension.

slide 3

With cirrhosis, the lobular structure is always disturbed.

slide 4

Etiology.

The causes of development correspond to the causes of chronic hepatitis.

Also, cirrhosis of the liver can form against the background of:

1. Obstruction of the biliary tract, both intra- and extrahepatic. (Congenital malformations of the biliary tract).

2. Against the background of prolonged venous congestion in the liver in chronic heart failure (cardiac cirrhosis of the liver).

slide 5

Pathogenesis.

The main factor is the death of liver cells. In place of dead cells, scars form and blood flow to the lobules is disrupted.

Cell breakdown products stimulate the inflammatory response. As a result, all functions of the liver and blood supply to the liver cells are disrupted, since dense connective tissue mechanically compresses the vessels of the liver, as a result, portal hypertension syndrome begins to develop.

slide 6

Initially, venous blood flow in the liver itself becomes difficult, then venous congestion and varicose veins of the esophagus, intestines, rectum and anterior abdominal wall occur. Subsequently, ascites begins to develop and, as a complication, bleeding from varicose veins.

Slide 7

Classification of cirrhosis:

1. by etiology:

Viral

Alcoholic

autoimmune

Toxic

Genetic

Cardiac

cholestatic

Slide 8

2. stages of portal hypertension:

Stage of compensation

Initial decompensation

Severe decompensation

3. stages of liver failure:

Compensated

Subcompensated

Decompensated (up to the development of hepatic coma).

Slide 9

4. Process activity:

active phase

Remission

5. process flow:

slowly progressive

rapidly progressive

stable

Slide 10

Clinic.

It depends on the etiology, the degree of liver dysfunction and the severity of portal hypertension and liver failure syndromes.

Complaints: pain in the right hypochondrium and epigastric region, aggravated after eating (fatty, spicy) and exercise.

Nausea, periodic vomiting, feeling of dryness and bitterness in the mouth, general weakness, fatigue, irritability, skin itching, weight loss. In women, menstrual irregularities. In men - a violation of potency.

slide 11

Objectively: emaciation, up to exhaustion, muscle atrophy, the skin is icteric-pale, dry.

There may be an expansion of the veins of the anterior abdominal wall, an increase in the abdomen, protrusion of the navel, swelling of the lower extremities. Palpitations, deafness of heart tones, arrhythmia, shortness of breath, increased blood pressure.

Against the background of cirrhosis of the liver, chronic gastritis, peptic ulcer, diabetes mellitus develop, the function of the sex glands, adrenal glands is impaired, and toxic encephalopathy develops. It is manifested by sleep disturbance, headaches, memory loss, trembling fingers, apathy.

The liver on palpation is dense, enlarged, with a sharp edge. In the later stages of cirrhosis may be reduced in size.

slide 12

Complications often develop with cirrhosis:

• bleeding from dilated veins of the esophagus, or hemorrhoids.
• development of liver failure with outcome in hepatic coma.
• secondary bacterial infection (severe pneumonia, sepsis, peritonitis).
• transition from liver cirrhosis to cancer.

slide 13

Diagnosis of cirrhosis of the liver:

• KLA - anemia, thrombocytopenia, leukopenia, increased ESR.
• OAM - proteinuria, microhematuria, bilirubin in the urine.

Immunological analysis.

Slide 14

4. Markers of viral infection.

5. Biochemical blood test - hyperbilirubinemia, dysproteinemia, due to an increase in the amount of globulins. An increase in the level of sedimentary samples - sublimate, thymol. Increased levels of transaminases - Al-At, As-At, and alkaline phosphatase.

slide 15

Instrumental research:

• Ultrasound of the liver and gallbladder (unevenness of the liver tissue, an increase in size is detected).
• Computed tomography of the abdominal organs.
• Gastroscopy.
• Colonoscopy.

slide 16

Needle biopsy of the liver, followed by histological examination, can be performed during laparoscopy or percutaneously. Allows you to judge the activity of the process and is an important differential criterion for distinguishing chronic hepatitis from cirrhosis of the liver.

Slide 17

Therapeutic mode. Work with physical and psycho-emotional stress is excluded. Shown short-term rest during the day. Hepatotoxic drugs, physiotherapy and balneotherapy are excluded. In the period of exacerbation - bed rest.

Slide 18

2. Medical nutrition - diet number 5.

Excluded: fatty meats and fish, fried foods, smoked meats, salty and spicy snacks, legumes, sorrel, spinach, fresh fruits, strong coffee, alcohol, carbonated drinks.

Slide 19

3. Antiviral treatment: carried out for hepatitis in the phase of virus reproduction and prevents the development of cirrhosis and liver cancer. Interferons for 6 months (Interferon A, Velferon, Roferon).

Cirrhosis of the liver is a chronic polyetiological progressive liver disease, a chronic polyetiological progressive liver disease, characterized by a significant decrease in the number of functioning hepatocytes, increasing fibrosis, restructuring of the normal structure of the parenchyma and characterized by a significant decrease in the number of functioning hepatocytes, increasing fibrosis, restructuring of the normal structure of the parenchyma and subsequent development of liver failure and portal hypertension with subsequent development of liver failure and portal hypertension

Classification of liver cirrhosis By etiology: By etiology: alcoholic - ranks 1st in the Republic of Belarus alcoholic - ranks 1st in the Republic of Belarus viral - as an outcome of CVH B, C, D viral - as an outcome of CVH B, C, D autoimmune (lupoid ) autoimmune (lupoid) drug (toxic) drug (toxic) primary and secondary biliary primary and secondary biliary congestive - occurs with venous congestion in the liver congestive - occurs with venous congestion in the liver metabolic (hemochromatosis, Wilson-Konovalov's disease, alpha-1 deficiency -antitrypsin) metabolic (hemochromatosis, Wilson-Konovalov's disease, alpha-1-antitrypsin deficiency) cryptogenic - unknown or unidentified etiology cryptogenic - unknown or unidentified etiology

Classification of liver cirrhosis According to morphology: According to morphology: a) macronodular (large-nodular) - irregularly located large nodes up to 5 cm in diameter, separated by connective tissue strands of various widths; more often of viral origin b) micronodular (small-nodular) - regularly located small nodes 1-3 mm in diameter, separated by a network of scar tissue; more often of alcoholic origin c) micro-macronodular (mixed)

Morphopathogenesis of liver cirrhosis Hepatocyte necrosis Hepatocyte necrosis Activation of regeneration, hyperformation of collagen fibers Activation of regeneration, hyperformation of collagen fibers Pericellular fibrosis, fibrous compression of venous vessels, formation of connective tissue septa connecting the central veins with portal fields and containing vascular anastomoses Pericellular fibrosis, fibrous compression of venous vessels , the formation of connective tissue septa connecting the central veins with the portal fields and containing vascular anastomoses; discharge of blood into the hepatic vein system, bypassing the parenchyma of the lobules; (ischemia), development of portal hypertension impaired blood supply to hepatocytes (ischemia), development of portal hypertension necrosis of hepatocytes (pathological circle) necrosis of hepatocytes c (pathological circle)

Clinic of cirrhosis of the liver Complaints: Complaints: pain in the right hypochondrium, epigastrium, aggravated after eating and exercise pain in the right hypochondrium, epigastrium, aggravated after eating and exercise feeling of bitterness and dryness in the mouth feeling of bitterness and dryness in the mouth nausea, sometimes vomiting nausea , sometimes vomiting skin itching (cholestasis) skin itching (cholestasis) fatigue, irritability fatigue, irritability flatulence, loose stools flatulence, loose stools weight loss weight loss impotence in men, menstrual irregularities in women impotence in men, menstrual irregularities in women

Liver cirrhosis clinic Examination: Examination: weight loss up to cachexia, muscle atrophy weight loss up to cachexia, muscle atrophy dry, scaly icteric-pale skin dry, scaly icteric-pale skin jellyfish head) telangiectasias on the upper half of the body telangiectasias on the upper half of the body palmar erythema ("beer drinker's hands") palmar erythema ("beer drinker's hands") Dupuytren's contracture Dupuytren's contracture lacquered, edematous tongue lacquered, edematous tongue gynecomastia, atrophy of the genital organs in men gynecomastia, atrophy of the genital organs in men decrease in the severity of secondary sexual characteristics decrease in the severity of secondary sexual characteristics ascites ascites

The main clinical and laboratory syndromes are mesenchymal-inflammatory (usually mild): mesenchymal-inflammatory (usually mild): ESR, CRP, fibrinogen, α 2 - and γ-globulins, thymol ESR, CRP, fibrinogen, α 2 - and γ-globulins , thymol test hyperthermia, lymphadenopathy, splenomegaly hyperthermia, lymphadenopathy, splenomegaly cytolysis (usually mild, no functioning hepatocytes and no enzymes): cytolysis (usually mild, no functioning hepatocytes and no enzymes): ALT, AST, LDH ALT, AST, LDH hyperthermia , hyperthermia intoxication, cholestasis intoxication: cholestasis: direct bilirubin, alkaline phosphatase, GGTP, direct bilirubin cholesterol, alkaline phosphatase, GGTP, cholesterol jaundice, pruritus, bradycardia, dark urine, light feces insufficiency: synthetic insufficiency: albumin, fibrinogen, prothrombin albumin, fibrinogen, prothrombin hemorrhagic and edematous-ascitic syndrome g hemorrhagic and edematous-ascitic syndrome of detoxification insufficiency: detoxification insufficiency: increase in ammonium ions, a number of hormones increase in ammonium ions, a number of hormones hepatic encephalopathy, hypernatremia, palmar erythema, etc. hepatic encephalopathy, hypernatremia, palmar erythema, etc.

Portal hypertension is an increase in pressure in the portal vein basin caused by impaired blood flow of various origins and localizations (in the portal vessels, hepatic veins, inferior vena cava) Clinically: 1. Varicose veins of the anterior abdominal wall, esophagus, less often the stomach and anorectal zone 2. Ascites 3 Splenomegaly, hypersplenism with cytopenias 4. Portal hypertensive gastropathy

Portosystemic encephalopathy is a syndrome complex of potentially REVERSIBLE mental and neurological manifestations against the background of an existing liver disease due to the effect of nitrogenous metabolic products on the central nervous system 2 main development mechanisms: 2 main development mechanisms: hepatic cell failure hepatic cell failure violation of the neuropsychic status violation of the neuropsychic status deviations in the performance of psychometric tests deviations in the performance of psychometric tests

PSE gradation Degree Level of consciousness Personality and intelligence Neurological symptoms Subclinical Normal Normal Deviations only psychometric tests 1 Sleep and wakefulness rhythm disturbance Memory impairment, decreased attention, agitation, anxiety Asterixis, tremor, apraxia, impaired coordination, handwriting change 2 Lethargy, slow responses Disorientation in time, amnesia , inappropriate behavior Asterixis, dysarthria, reduced reflexes 3 Somnolence up to stupor Disorientation in place, aggressive behavior Asterixis, reduced reflexes, pathological reflexes, muscle rigidity 4 Coma Absent Decerebration

Complications of liver cirrhosis bleeding from varicose veins of the esophagus and stomach bleeding from varicose veins of the esophagus and stomach hepatic encephalopathy and coma hepatic encephalopathy and coma erosive and ulcerative lesions of the stomach and 12PC erosive and ulcerative lesions of the stomach and 12PC hepatocellular carcinoma (cirrhosis cancer) hepatocellular carcinoma (cirrhosis-cancer) spontaneous bacterial peritonitis spontaneous bacterial peritonitis hepatorenal syndrome (a functional form of renal failure that occurs against the background of decompensated liver disease) hepatorenal syndrome (a functional form of renal failure that occurs against the background of decompensation of liver disease) hepato-pulmonary syndrome (impaired arterial oxygenation on due to intrapulmonary vascular dilatation in liver disease) hepatopulmonary syndrome (impaired arterial oxygenation due to intrapulmonary vascular dilatation in liver disease)

Diagnosis of cirrhosis of the liver KLA, OAM, qualitative reactions for the content of bilirubin and urobilin in the urine, PTI KLA, OAM, qualitative reactions for the content of bilirubin and urobilin in the urine, PTI BAC: bilirubin and its fractions, total protein and its fractions, urea, creatinine, AST and ALT activity, alkaline phosphatase, GGTP, cholesterol, TG, LP fractions, uric acid, glucose, thymol and sublimate tests, BAC coagulogram: bilirubin and its fractions, total protein and its fractions, urea, creatinine, AST and ALT activity, alkaline phosphatase , GGTP, cholesterol, TG, LP fractions, uric acid, glucose, thymol and sublimate tests, coagulogram laparoscopy with biopsy (if indicated)

3528-35 51 PTI> 0.70.4-0.7" title="(!LANG: Child-Pugh Cirrhosis Severity Scale Signs 1 point 2 points 3 points Ascites /l) > 3528-35 51 PTI > 0.70.4-0.7" class="link_thumb"> 21 !} Child-Pugh liver cirrhosis severity scale Signs 1 point 2 points 3 points Ascites No Mild Severe Encephalopathy No I and II st. Serum albumin (g/l) > 51 PTI > 0.70.4-0.7 3528-35 51 PTI>0.70.4-0.7"> 3528-35 51 PTI>0.70.4-0.7"> 3528-35 51 PTI>0.70.4-0.7" title="(!LANG: Childe-Pugh Liver Cirrhosis Severity Scale Signs 1 point 2 points 3 points Ascites No Mild Severe Encephalopathy No Stages I and II, III and IV. Serum albumin (g/l) > 3528-35 51 PTI> 0.70.4- 0.7"> title="Child-Pugh liver cirrhosis severity scale Signs 1 point 2 points 3 points Ascites No Mild Severe Encephalopathy No I and II st. Serum albumin (g/l) > 3528-35 51 PTI > 0.70.4-0.7"> !}

Treatment of liver cirrhosis treatment tactics is determined by the prevalence of certain pathological manifestations of the disease treatment tactics is determined by the prevalence of certain pathological manifestations of the disease in the case of liver cirrhosis of viral origin, sometimes antiviral therapy is indicated (slows down the progression of the disease) progression of the disease) in all cases: in all cases: limitation of physical and mental stress limitation of physical and mental stress exclusion of hepatotoxic drugs and alcohol exclusion of hepatotoxic drugs and alcohol diet P (previously - table 5) diet P (previously - table 5) if there are signs cholestasis - UDCA drugs (Ursofalk, Ursosan, Ursor, Choludexan mg / kg / day) in the presence of signs of cholestasis - UDCA drugs (Ursofalk, Ursosan, Ursor, Choludexan mg / kg / day)

PSE restriction of protein in food to 1 g / kg / day restriction of protein in food to 1 g / kg / day lactulose (Duphalac, Portolac) under stool control (soft stools up to 3 times / day) stool control (soft stools up to 3 times / day) ornithine (Hepa-merz g / day in / in 2 injections, then orally 1 sachet of granulate per 200 ml of liquid 2-3 times a day) ornithine (Hepa-merz g / day in / in 2 injections, then orally 1 sachet of granulate per 200 ml of liquid 2-3 times a day) intestinal decontamination: rifaximin, metronidazole, kanamycin intestinal decontamination: rifaximin, metronidazole, kanamycin N-hepa 5%, 8% 500 ml) IV branched amino acids (aminosteryl N-hepa 5%, 8% 500 ml) ademetionine (Heptral) mg/day IV, then mg/day per os ademetionine (Heptral) mg/day IV, then mg/day per os

Cirrhosis of the liver - chronic
diffuse liver disease
characterized by dystrophy and
hepatic necrosis
tissue (parenchyma), overgrowth
connective tissue and
restructuring of the lobular structure
organ.

With cirrhosis is always violated
lobular structure.

Etiology.

Viral hepatitis.
autoimmune hepatitis.
Chronic alcohol abuse.
Genetically determined metabolic disorders
substances.
Toxic substances.
Obstruction of extrahepatic and intrahepatic
bile ducts.
Prolonged venous congestion in the liver

Pathogenesis.

Death is the main factor.
hepatic cells. In place of dead cells
scars form and blood flow to the
slices.
Cell breakdown products stimulate
inflammatory response. As a result
all liver functions are impaired and
blood supply to liver cells
dense connective tissue
compresses the blood vessels of the liver
portal syndrome begins to develop
hypertension.

Initially, venous blood flow is obstructed in
the liver itself, then venous
congestion and varicose veins of the esophagus,
intestines, rectum and anterior abdominal
walls. Subsequently, it begins to develop
ascites and as a complication - bleeding from
varicose veins.

Risk factors

alcohol abuse;
Hepatitis;
The use of drugs that are toxic to
liver;
Overweight or rapid weight gain;
Lack of treatment for diabetes;
The use of large doses of iron.

Morphological classification of liver cirrhosis

Proposed by the World Association of Hepatologists
(Acapulco, 1974) and WHO (1978).
small-nodular, or small-nodular cirrhosis of the liver (diameter
nodes from 1 to 3 mm)
macronodular or macronodular cirrhosis of the liver (diameter
knots over 3 mm)
incomplete septal form of liver cirrhosis
mixed (in which there are different sizes
knots) shape

Etiological classification of liver cirrhosis

There are the following forms of cirrhosis of the liver:
viral
alcoholic
drug
secondary biliary cirrhosis
congenital cirrhosis of the liver, with the following diseases:
a) hepatolenticular degeneration
b) hemochromatosis
c) α1-antitrypsin deficiency
d) tyrosinosis
e) galactosemia
e) glycogenosis
congestive (circulatory failure) cirrhosis of the liver
Budd-Chiari disease and syndrome
exchange-alimentary, under the following conditions:
a) the imposition of a bypass small bowel anastomosis
b) obesity
c) severe forms of diabetes
cirrhosis of the liver of unknown etiology
cryptogenic
primary biliary cirrhosis
indian child

Clinic

Depends on the etiology, on the degree of violation
liver function and severity of syndromes
portal hypertension and hepatic
insufficiency.
Complaints: pain in the right hypochondrium and
epigastric region, intensifying after
food (fatty, spicy) and physical activity.
Nausea, occasional vomiting, dry feeling
and bitterness in the mouth, general weakness,
fatigue, irritability, skin
itching, weight loss. Women have a violation
menstrual cycle. Men have a violation
potency.

Objectively: emaciation, up to exhaustion,
muscle atrophy, icteric-pale skin,
dry.
There may be an enlargement of the veins of the anterior abdominal
walls, enlargement of the abdomen, protrusion of the navel,
edema of the lower extremities. Palpitations, deafness
heart sounds, arrhythmia, shortness of breath, increased
blood pressure.
Against the background of cirrhosis of the liver, chronic
gastritis, peptic ulcer, diabetes,
impaired function of the gonads, adrenal glands and
toxic encephalopathy develops. She is
manifested by sleep disturbance, headaches,
memory loss, trembling fingers, apathy.
The liver is dense on palpation, enlarged in
sizes, with a sharp edge. In the later stages
cirrhosis can be reduced in size.

Inspection

weight loss up to cachexia, muscle atrophy
dry, scaly, yellowish-pale skin
dilatation of the veins of the anterior abdominal wall
(jellyfish head)
telangiectasia on the upper half of the body
palmar erythema ("hands of beer drinkers")
Dupuytren's contracture
varnished, swollen tongue
gynecomastia, atrophy of the genital organs in men
reduction in the severity of secondary sexual
signs
ascites

Telangiectasias

Dupuytren's contracture - proliferation of connective tissue in the palmar fascia along the tendons of the IV-V fingers of the hand

Palmar erythema

Gynecomastia

Ascites, "jellyfish head", umbilical hernia

Often with cirrhosis develop
complications:
- bleeding from enlarged
veins of the esophagus, or
hemorrhoids.
- development of the liver
insufficiency with outcome in
hepatic coma.
- secondary bacterial
infection (severe pneumonia,
sepsis, peritonitis).
- the transition of liver cirrhosis to cancer.

Diagnosis of cirrhosis of the liver:

KLA - anemia, thrombocytopenia,
leukopenia, increased ESR.
2. OAM - proteinuria, microhematuria,
bilirubin in the urine.
3. Immunological analysis.
4. Markers of viral infection.
5. Biochemical blood test -
hyperbilirubinemia, dysproteinemia,
by increasing the number
globulins. Level up
sedimentary samples - sublimate, thymol.
Increasing the level of transaminases - Al-At,
Ac-At, and alkaline phosphatase.
1.

Instrumental research:

1. Ultrasound of the liver and gallbladder
bubble (revealed
fabric irregularity
liver, enlargement).
2. Computed tomography
abdominal organs.
3. Gastroscopy.
4. Colonoscopy.

Needle biopsy of the liver followed by
histological examination,
performed during laparoscopy or through
skin. Allows you to judge the activity
process and is important
differential criterion for distinguishing
chronic hepatitis from cirrhosis of the liver.

Treatment

1. Treatment regimen. Work with
physical and psycho-emotional
loads. Shown short rest in
during the day. Excluded hepatotoxic
drugs, physiotherapy and balneotherapy. AT
period of exacerbation - bed rest.

2.
Medical nutrition - diet number 5.
Excluded: fatty meats and fish,
fried foods, smoked meats, salty and spicy
starters, legumes, sorrel, spinach, fresh
fruits, strong coffee, alcohol, carbonated
beverages.
3.
Antiviral treatment: carried out with
hepatitis in the phase of virus reproduction and
prevents the development of cirrhosis and liver cancer.
Interferons for 6 months (Interferon
A, Velferon, Roferon).

4. Pathogenetic treatment: corticosteroids,
cytostatics.
5. Immunomodulatory therapy has
stimulating and normalizing effect on
immune system: Timalin,
Dpenicillin, Thymogen, T-activin.
6. Metabolic and coenzyme therapy
is aimed at improving the exchange processes in
hepatic cells. Multivitamin complexes:
Decamevit, Undevit, Duovit, vitamin E, Riboxin,
Essentiale.

7.
Detoxification therapy: Hemodez
intravenous drip, 5% glucose.
Enterosorbents - Laktofiltrum, Filtrum,
Enterosgel.
8.
Hepatoprotectors: Corsil, Legalon, Katergen.
9. Treatment of bleeding from dilated veins.
10. Treatment of edematous-ascitic syndrome with
cirrhosis, at first - Veroshpiron, Aldicton, and
then in combination with Uregit, Hypothiazid,
Furosemide.

Prevention

Primary: prevention of viral hepatitis,
effective treatment of acute viral hepatitis,
rational nutrition, control over intake
drugs, alcoholism,
addiction.
Secondary: prevention of exacerbations of the disease.
Restriction of physical activity, correct
employment. Medical nutrition, treatment
associated diseases of the gastrointestinal tract.

Often, even the most severe diseases can be cured much faster if proven folk remedies are used in therapy. So, soda for hepatitis C is one of the most affordable, safe and effective non-traditional medicines. At least, that's what folk healers say. Can Baking Soda Cure Hepatitis C?

Fact or myth: how sodium bicarbonate affects the liver

Baking soda, also known as sodium bicarbonate and sodium bicarbonate, is one of the most popular folk remedies. It has been used for many years in the treatment of various diseases. Carry out with the help of soda and treatment of hepatitis C at home. What is the reason for the positive effect of sodium bicarbonate on liver cells affected by a dangerous virus?

Hepatitis C is the most severe type of viral infection that causes inflammation of a vital organ. A diseased liver is subjected to a heavy load, hepatocytes cannot cope with their work and die, the organ is increasingly polluted with toxins and toxins, which can eventually lead to the development of cirrhosis and a cancerous tumor.

In such a situation, mandatory complex treatment is necessary, which involves not only taking various antiviral and anti-inflammatory drugs, but also the use of agents that normalize the liver, cleanse and restore its cells.

One such remedy is baking soda. It has the following properties:

• accelerates the removal of harmful substances from the diseased organ;
• improves the outflow of bile;
• prevents the death of hepatocytes;
• reduces the risk of developing complications of hepatitis C.

In addition, the tool has an immunomodulatory effect, which is very important for such a serious disease.

However, you need to keep in mind that you can drink soda only after consulting a doctor. Hepatitis C is a dangerous disease that requires adequate therapy. Sodium bicarbonate is allowed to be used in the treatment of this disease only as an auxiliary medicine, since the remedy cannot fight infectious agents.

How to use the remedy

There are many ways to use soda to eliminate the manifestations of viral liver disease. The following recipes are considered the most effective:

1. Treatment of hepatitis C with soda with lemon. You will need 1 medium lemon and 1 tsp. sodium bicarbonate powder. You need to squeeze the juice from citrus and combine the resulting liquid with soda. Mix thoroughly and drink immediately. Take this medicine once a day - 30 minutes before breakfast. You need to drink soda with lemon for 3 days, then you need to take a three-day break and repeat the course.
2. Treatment of hepatitis C with an aqueous solution of soda powder. In 1 cup of warm boiled water, stir 1 tsp. sodium bicarbonate. The drink is taken 2 times a day for 10 days.

It is important to consider that even such a harmless, at first glance, remedy, like baking soda, also has its contraindications. The powder should not be used for diseases of the gastrointestinal tract, pregnancy and lactation, as well as children under 12 years of age.

According to reviews, treatment of the liver with soda shows good results. Nevertheless, we must not forget that hepatitis C therapy should be carried out under the strict supervision of a specialist. The same applies to the use of soda: it is permissible to resort to folk recipes using sodium bicarbonate powder only if the doctor is not against such methods.

What can and cannot be eaten with hepatitis, diet menu table number 5

For various diseases in treatment and prevention centers, patients are usually prescribed diets. There are only 15 diet options, and among them there is a diet number 5, which was specially developed by nutritionist M. Pevzner for patients suffering from diseases of the liver and biliary tract.

• Features of the health-improving diet No. 5
• Prohibited list of products

sample menu

• Option 1
• Option 2

Conclusion

The dietary technique is based on a sparing diet. Adhering to such a diet menu in patients suffering from hepatitis, there is an alleviation of the painful condition. This is achieved in conjunction with drugs, this approach helps to get rid of the unpleasant symptoms and pain that often torment patients suffering from a disease such as hepatitis.

Features of the health-improving diet No. 5

Any of the dietary nutrition systems is aimed at treating certain diseases, so each of them has its own number, which is assigned to it. Diet number 5 is no exception, it is indicated for people who suffer from diseases such as:

1. Hepatitis and cholecystitis in chronic but not acute forms and when the patient is at the stage of recovery.
2. Cirrhosis of the liver.
3. Cholelithiasis.

It provides nutrition with the necessary calorie intake, but only with the restriction of foods that contain fats and cholesterol. Fried foods are excluded from the diet, and a lot of vegetables and fruits are prescribed. The goal of the diet is sparing nutrition, with the help of which the liver is not loaded, even with good nutrition, and the biliary system functions normally.

This diet is characterized by the optimal content of carbohydrates and proteins in the menu with fat restriction. Be sure to recommend products that contain a lot of lipotropic substances, pectins, fiber and drink more fluids. Do not eat foods containing in large numbers nitrogenous extractives, oxalic acid, purines, cholesterol and fat oxidation, all appear during the frying process.

Almost the entire menu consists of boiled, baked, occasionally stewed dishes, cold and very hot dishes are excluded. It is recommended to wipe only sinewy meat and vegetables containing a lot of fiber, vegetables and flour are not sautéed. It is necessary to eat 5-6 times a day and follow such a diet for 1.5-2 years in the future, this will help get rid of health problems and make your figure slimmer.

General principles of diet table number 5 and its purpose

This technique allows you to improve the separation of bile and give the liver a rest, if you strictly adhere to the prescribed diet, then the disease recedes. It is important not only to stick to the menu, but also to eat small and equal portions constantly. It is advisable to chop food every time before eating, drink as much liquid as possible on an empty stomach, cook food without a crust and do not fry.

Self-medication is always dangerous, therefore, before switching to diet table number 5, you should consult a doctor so as not to harm your health, since the symptoms of hepatitis often coincide with the course of other diseases, and the chosen diet may not be suitable for them. It is best to establish an accurate diagnosis of the disease, and then follow the diet that will be prescribed by the doctors.

The principles of the diet are as follows.

1. This diet is low in fat and protein.
2. Be sure to limit yourself in salt.
3. Exclude from the menu products containing oxalic acid and purines.
4. Fish and meat should be consumed only in boiled form.

The daily ration for diet No. 5 should be energy and chemical composition such:

• Proteins - up to 80 grams, of which 50 grams are animal products.
• No more than 90 grams of fat, and 30% should be vegetable fats.
• Carbohydrates no more than 400 gr.
• Liquid at least 1.5-2 liters.
• The energy value for 1 day is approximately 2400-2800 kcal, they can be calculated on a calorie calculator.
• Salt - a maximum of 10 grams per day.

Prohibited list of products

• Vegetables - white cabbage, green onion, radish, radish, spinach, garlic, parsley, pickled mushrooms and vegetables.
• Cereals - legumes, millet, corn, barley and barley.
• All sour fruits that cause flatulence.
• Broths and soups from meat, fish, mushrooms.
• All fatty fish and meats.
• Fatty dairy products - cream, milk, sour cream, fermented baked milk, etc.
• Hot pepper, horseradish, mustard.
• Fresh pastries, puff pastry, muffin.
• Strong tea and coffee, carbonated drinks, cocoa and alcohol.
• Sweets and chocolate.

sample menu

Option 1

Option 2

• First breakfast - oatmeal porridge with milk or water, low-fat cottage cheese with sour cream and a little honey, tea.
• The second breakfast is a baked apple and a little honey.
• Lunch - vegetable soup with olive or sunflower oil, boiled chicken in milk sauce, boiled rice as a side dish, dried fruit compote.
• Snack - rosehip broth.
• Dinner - boiled fish with white sauce from vegetable broth, mashed potatoes, tea, cheesecake with cottage cheese.
• Before going to bed, you can drink kefir.

Conclusion

The trial period of the diet can last for 5 days, if the body responds normally, then you need to continue up to 5 weeks or until complete recovery occurs. Diet table number 5 cannot be called rigid, it is very similar to the approximate diet of people leading healthy lifestyle life.

This diet for hepatitis will be very tasty if you know how to cook. The diet is easily tolerated, since the menu contains only healthy and tasty products, the main thing is to combine products correctly and not be lazy to cook. Diet table number 5 gives high performance and leads to a speedy recovery. In addition, weight is normalized, general condition, mood and appearance patients who adhere to such a diet for a long time.

Cirrhosis of the liver and its complications Lyudmila Yuryevna Ilchenko November 27, 2015 Pirogov Russian National Research Medical University Department of Hospital Therapy No. 2 of the Faculty of Medicine Institute of Poliomyelitis and Viral Encephalitis named after N.I. M. P. Chumakova Department of Viral Hepatitis

EASL facts and figures. http://www. easl. eu/assets/application/files/19d 80b 59a 26a 03c_file. pdf. The prevalence of liver cirrhosis in the EU countries (n= 507.4 million) Early portal hypertension is typical. Early hepatocellular insufficiency is typical. Micronodular CPU Macronodular CPU

Rating of countries in the world in terms of alcohol consumption (n=188) World Health Organization. Global Status Report on Alcohol and Health, 2014 № COUNTRY CONSUMPTION, L 1 Moldova 18.22 2 Czech Republic 16.45 3 Hungary 16.27 4 Russia 15.76 …… …… UK 13.5 France 13.5 Germany 13.5 …… …… Data 2011 URL: http: //www. who. int

Worldwide 14-40 cases of cirrhosis per 100,000 population In Russia 26, 2 cases of cirrhosis per 100,000 population 8th among the most common causes of death in the United States, 9th in the EU countries, 6th in the Russian Federation

Cirrhosis of the liver (LC) - kirros (amber, red) R. Laennec, 1819 chronic diffuse disease characterized by fibrosis (IV) and transformation of the normal structure of the liver with the formation of nodes (WHO)

Criteria for the diagnosis of chronic liver disease (CKD) Etiological factor Degree of activity Stage of the hepatic process IWP. CG – 1994 J. G. Desmet, M. Gerber, J. H. Hoofnagele et al. hepat; 1994; 14:1513-1520 Spectrum of extrahepatic manifestations

Etiology of liver cirrhosis (I) Viral hepatitis (B, C, D) Alcohol (and its surrogates) Non-alcoholic fatty liver disease Genetic diseases - hereditary hemochromatosis - Wilson's disease - α 1-antitrypsin deficiency - cystic fibrosis - galactosemia - glycogenosis - hereditary tyrosinemia - disease Gaucher - hereditary fructose intolerance - hereditary hemorrhagic telangiectasia - abetalipoproteinemia - porphyrias - childhood Indian cirrhosis Diseases of the biliary tract - extrahepatic obstruction of the biliary tract - intrahepatic obstruction of the biliary tract (primary biliary cirrhosis, primary sclerosing cholangitis - cholangiopathy in children (Byler's disease, Alagille's syndrome ...)

Hereditary diseases occurring with liver damage (II) Disease Prevalence Genetically determined defect Wilson-Konovalov disease 1: 30,000 ATP 78 Violation of intracellular copper transport Hereditary hemochromatosis 1: 250 HFE, HJV, TIR 2, HAMP, FPN Violation of iron metabolism Deficiency of alpha- 1 antitrypsin 1: 2,000 A-1AT Accumulation of a mutant glycoprotein in the liver Cystic fibrosis 1: 3,000 CFTR Impaired transport of chloride ions across the apical membrane of epithelial cells Glycogenoses 0, I (a, b), III (a, b), VI, IX 1 : 25,000 Several genes Disorder of glycogen metabolism Gaucher disease I, II 1: 60,000 Type 1 - 1: 90,000 PIF Disorder of glucocerebroside metabolism Gilbert's syndrome 1: 10 - 1: 30 UGT 1 A 1 Disorder of bilirubin metabolism Familial progressive intrahepatic cholestasis I, III (Byler syndrome I, III) 1:100,000 orphan disease ATP 88 1 (FIC 1) ABCB 11 (BCEP) ABCB 4 (MD 3) Insertion of aminophospholipids into the membrane? Bile acid secretion disorder Phospholipid secretion disorder Benign recurrent cholestasis I, II (Summerskil-Walsh syndrome) 1:100,000 orphan disease ATP 88 1 (FIC 1) ABCB 11 (BCEP) Bile acid malabsorption in the terminal ileum

Etiology of liver cirrhosis (III) Viral hepatitis (B, C, D) Alcohol Metabolic disorders - hereditary hemochromatosis - Wilson's disease - childhood Indian cirrhosis - α 1-antitrypsin deficiency - cystic fibrosis - galactosemia - glycogenoses - hereditary tyrosinemia - Gaucher's disease - hereditary fructose intolerance - hereditary hemorrhagic telangiectasia - abetalipoproteinemia - porphyrias Diseases of the biliary tract - intrahepatic obstruction of the biliary tract (primary biliary cirrhosis, primary sclerosing cholangitis - extrahepatic obstruction of the biliary tract - cholangiopathy in children (Byler's disease, Alagille's syndrome ...)

Congenital pathology of the biliary system in newborns and young children (IV) 1 Atresia of the extrahepatic bile ducts (ICD: Q 44. 2) - in a limited area - throughout with the development of a fibrous process Trigger mechanism - perinatal infection (HSV, CMV, rubella virus , toxoplasmosis, etc.) with the subsequent development of a destructive-inflammatory process leading to obliteration of the ducts Symptoms: jaundice, hepato- and splenomegaly Outcomes: mortality by two years - 98%, development of secondary biliary cirrhosis Intrahepatic biliary hypoplasia (ICD: Q 44. 3 ) Congenital stenosis and stricture of the bile ducts (a sharp decrease in their number and size) Etiology is unknown Symptoms: jaundice, pruritus Outcomes: development of secondary biliary cirrhosis by 6-18 months.

Congenital pathology of the biliary system in newborns and young children (V) Cyst of the common bile duct (ICD: Q 44. 4) Etiology unknown Symptoms: pain in the right hypochondrium, jaundice, fever, pruritus, weakness Outcomes: pancreatitis, cholelithiasis, carcinoma , secondary biliary cirrhosis Caroli disease (ICD: Q 44. 7) Etiology unknown Symptoms: right hypochondrium pain, jaundice, fever, pruritus, weakness, malabsorption symptom Outcomes: cholangitis, cholelithiasis, septicemia, secondary biliary cirrhosis General symptoms jaundice , stool acholia high level of GGTP activity no visualization of the gallbladder on ultrasound Caroli's disease

Etiology of liver cirrhosis (VI) Impaired venous outflow from the liver - Budd-Chiari syndrome - veno-occlusive disease - severe right ventricular heart failure - constrictive pericarditis Drugs, toxins, chemicals (methyldopa, methotrexate, amiodarone isoniazid, perhexylene maleate, oxyphenisatin, arsenic compounds, pyrrolidizine alkaloids , oral contraceptives) Immune disorders - autoimmune hepatitis - Diseases associated with immunoglobulin G type 4 (Ig. G 4) - graft-versus-host disease Various causes - other infections (syphilis, schistosomiasis, cytomegalovirus, toxoplasmosis, echinococcosis, brucellosis) - sarcoidosis - non-alcoholic fatty liver disease - jejunoileal shunting for obesity - hypervitaminosis A - cryptogenic cirrhosis

CLASSIFICATION OF CKD (IWP. CG – 1994) II. The degree of activity of the pathological process is minimal (1-3 points) mild (4-8 points) moderately pronounced (9-12 points) pronounced (13-18 points) Histological activity index (HIA), R. G. Knodell et al. , 1981 ALT - 1-5 N - minimal activity ALT - from 5 N to 10 N - moderate activity ALT > 10 N - high activity A 1 A 2 A 3 METAVIR

CLASSIFICATION OF CKD (IWP. CG – 1994) III. Morphological stages of the pathological process 0 - no fibrosis I - mild (portal) fibrosis II - moderate fibrosis (portal-portal septa) III - severe fibrosis (portal-central septa) IV - liver cirrhosis

Stages of fibrosis F 1 F 2 F 3 F 4portal fibrosis porto-portal septa portocentral septa

Morphological signs of CP Micronodular CP nodules less than 3 mm in size, they include one lobule Macronodular CP nodules larger than 3 mm, include elements of two or more pseudolobes Mixed - micro-, macronodular CP

CLASSIFICATION OF CP (IWP. CG - 1994) V. The course of the pathological process is latent, slowly progressing, rapidly progressing, continuously progressing VI. Clinical stages of cirrhosis initial (compensated) or group A (according to Child-Pugh) developed (decompensated) or group B terminal or group C (C+) VII. Impaired liver function without impairment slight moderate significant

Jaundice Icteric staining of tissues (skin, sclera) and tissue fluid (plasma) due to elevated bilirubin levels Bilirubin > 2 N Bilirubin > 3 N Normal bilirubin levels 5.1-17.0 µmol/L (SI) direct bilirubin< 15% (до 1, 7-5, 1 мкмоль/л)

Clinical manifestations of LC (I) General manifestations (weakness, loss of appetite, weight loss, fever) Cutaneous (jaundice, telangiectasia, palmar erythema, nail changes, Dupuytren's contracture) Musculoskeletal (decrease in muscle mass, hypertrophic osteoarthropathy - synovitis, " drum sticks, periostitis; hepatic osteodystrophy, convulsions, umbilical hernia N eurological (hepatic encephalopathy, peripheral polyneuropathy)

Clinical manifestations of LC (II) Gastrointestinal (enlarged parotid salivary glands, diarrhea, cholelithiasis, gastrointestinal bleeding, portal gastro-, entero- and colopathy, peptic ulcer and erosion, gastritis) Hematological (cytopenia, hemolytic anemia, impaired coagulation syndrome, disseminated intravascular coagulation, hemosiderosis) Pulmonary (hypoxemia, hyperventilation, pulmonary hypertension, decreased lung capacity, hydrothorax, hepatopulmonary syndrome) Cardiac (hyperkinetic type of circulation)

Clinical manifestations of LC (III) Renal secondary hyperaldosteronism (glomerulosclerosis, hepatic tubular acidosis) hepatorenal syndrome Endocrine hypogonadism — in men (decreased libido, testicular atrophy, impotence) — in women (dysmenorrhea, infertility, disappearance of secondary sexual characteristics) — feminization — estrogen-related signs (telangiectasias, palmar erythema, gynecomastia, hair loss) diabetes hypovitaminosis D secondary hyperparathyroidism

Clinical analysis of blood and urine Biochemical studies markers of cytolysis (ALT, AST, LDH) markers of cholestasis (bilirubin, alkaline phosphatase, GGTP, 5'HT, lipids) markers of protein-synthetic function (albumin, PI) Serological studies markers of viral hepatitis (IFA, PCR ) autoantibodies (AMA, ANA, SMA, LKM, etc.) immunoglobulins (Ig. M, Ig. G, Ig. A) tumor markers Markers of inflammation (CRP, LAL ...) Iron and copper metabolism (genetic studies) Instrumental studies of ultrasound of organs abdominal cavity, fibroelastometry Dopplerography Computed tomography Magnetic resonance imaging (or MRCT) Liver and spleen scintigraphy X-ray examination of the esophagus Esophagogastroduodenoscopy, entero- and colonoscopy Morphological examination of the liver tissue Methods for diagnosing cirrhosis

Child-Tucotte-Pugh prognostic scale (classification of hepatocellular function in cirrhosis) 1 point (A) Criteria 2 points (B) 3 points (C) Class Bilirubin, N up to 21 µmol/l Albumin, N — 35-40 g/l Prothrombin index, 80-110% INR, 0.7-1.2 Ascites Encephalopathy Up to 2 norms More than 35 80-110 1.7 No 2-3 norms 30-35 60-79 1.7-2.3 Slight transient Occurs periodically Above 3 norms Less than 30 Less than 60 > 2, 3 Large torpid Coma. A (5-6) B (7-9) C (10) Pugh R. N. et al. , Br. J. Durg. 1973; 60:646-

Ultrasound examination First diagnostic examination in CKD Determination of liver size, detection of ascites Indications for biopsy Evaluation of fibrosis, steatosis Determination of portal hypertension Early diagnosis of HCC

Fibro. Scan ® No need to starve Study duration 5 min 10 successful readings Median value = true value Result expressed in kPa Difficulties in interpretation: ascites, obesity Transient elastometry

Transient elastometry in liver cirrhosis Elasticity 16 kPa F 4 according to Metavir Ductopenia, replacement of the bile ducts with fibrous tissue

Fibro. Max TM is a non-invasive method for diagnosing the condition of the liver tissue. Parameters studied: α 2- macroglobulin protease inhibitor apolipoprotein A 1 key protein for collagenase haptoglobin key protein that binds free hemoglobin oxidants AST ALT GGTP Total bilirubin Total cholesterol glucose Lipids Gender, age Height, weight www. biopredictive. com

Liver biopsy Ultrasound-guided To obtain reliable histological results, a sample of liver tissue must be at least 10 mm long and contain at least 6 portal tracts. Percutaneous puncture liver biopsy

Evolution of chronic liver diseases Chronization 25-50 years Stabilization Progression Decompensated LC exitus 5-23% from 2 to 10 years Compensated LC adapt. after Feitelson, Lab Invest, 1994 GCKGCKKHGHG Exitus. Viruses Alcohol Immune Drugs Metabolic Carcinogens Genetic… AI cure 1-7%

Gotye S.V., Konstantinov B.A., Tsirulnikova O.M. Liver transplantation. Guide for doctors. - M. : MIA, 2008. - 248 p. Loginov A. S., Blok Yu. E. Chronic hepatitis and cirrhosis of the liver. - M. : Medicine, 1987. - 272 p. Podymova S. D. Diseases of the liver. - 3rd ed. , revised and additional - M. : Medicine, 1998. - 704 p. Sherlock S., Dooley D. Diseases of the liver and biliary tract: Prakt. hand-in - Per. from English. / Ed. A. N. Mukhina, Z. G. Aprosina. – M. : Geotar Med. , 1999. - 864 p. Schiff Y.R., Sorrel M.F., Maddrey W.S. Cirrhosis of the liver and its complications. Liver transplantation / Per. from English. V. Yu. Khalatova; ed. V. T. Ivashkina, S. V. Gotye, Ya. G. Mosyuk, M. V. Maevskoy - M. : GEOTAR-Media, 2012. - 592 p. Kuntz E. , Kuntz H-D. hepatology. principles and practices. - Springer Medizin Verlag Heidelberg, 2006. - 825 p. Sherlok's Diseases of the Liver and Biliary System - 12th edition / Ed. By J. S. Dooley, A. S. F. Look, A. K. Burroughs, E. J. Heathcote, WILEY-DLACKWELL, 2011. - 771 p. Hepatic Encephalopathy in Chronic Liver Disease: 2014 Practice Guideline by the EASL and AAS LD. Hepatology, 2014. - 61(3): 642-59.

B. A. Runyon. AASLD PRACTICE GUIDELINES. Management of Adult Patients with Ascites Due to Cirrhosis: An Update. Nepatol. 2009; 49:2087-2107. K. F. Murray, R. L. Carithers. AASLD practice guideline: Evaluation of the Patient for Liver Transplantation. Nepatol. 2005; 41:1-26. G. Garcia-Tsao, A. J. Sanyal, N. D. Grace, W. Carey and the Practice Guidelines Committee of the AASLD, the Practice Parameters Committee of the American College of Gastroenterology AASLD. Practice guidelines Prevention and Management of Gastroesophageal Varices and Variceal Hemorrhage in Cirrhosis. Nepatol. 2007; 46:922-938. T. D. Boyer 1, Z. J. Haskal. AASLD practice guideline update. The Role of Transjugular Intrahepatic Portosystemic Shunt (TIPS) in the Management of Portal Hypertension: Update 2009. Nepatol. 2010; 51:1-16. L.D.De. Leve, D.-Ch. Valla, G. Garcia-Tsao. AASLD practice guidelines. Vascular Disorders of the Liver. Nepatol. 2009; 49: 1729-1764. L. G. de Macêdo 1, E. P. de Almeida Lopes. Hepatopulmonary syndrome: an update Syndrome hepatopulmonar: atualização Universidade Federal de Pernambuco (UFPE), Recife, Pernambuco, Brazil Sao Paulo Med J. 2009; 127:223-230. R. de Franchis. Revising consensus in portal hypertension: Report of the Baveno V consensus workshop on methodology of diagnosis and therapy in portal hypertension. Hepatol. 2010; 53:762-768. EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. Hepatol. 2010; 53:397-417.

Ascites Hepatic encephalopathy. COMPLICATIONS OF LIVER CIRRHOSIS PORTAL HYPERTENSION Infectious complications. Splenomegaly Hypersplenism. Hepatorenal syndrome Hepatocellular carcinoma. hepatopulmonary syndrome. Bleeding from varicose veins

Portal hypertension (PH) - increased pressure in the portal vein basin (portal gradient - more than 10-12 mm Hg) caused by impaired blood flow of various origins and localization in the portal vessels, hepatic veins and inferior vena cava Portal hypertension is a phenomenon , which developed as a result of blocking the outflow of blood through the portal vein system in patients with cirrhosis of the liver A. Mc. jndoe,

Blood flow and pressure in the hepatic artery, portal and hepatic veins in PH Inferior vena cava Hepatic vein Blood flow 300 ml / min (N - 1500 ml / min) Pressure 4 mm Hg. Art. LIVER Hepatic artery Blood flow 500 ml/min Pressure 100 mm Hg Art. Portal vein Blood flow 1200 ml/min and above (N - 1000 ml/min) Pressure 12-40 mmHg Art. (N - 4-6 mm Hg) NO, CO, glucagon, RAAS, endothelin, vasoconstrictors, endotoxins, cytokines ... The state of the cardiovascular system, increased resistance of portal and hepatic vessels

PH pathogenesis in liver cirrhosis Liver cirrhosis Increased resistance to portal blood flow Mechanical Fibrosis Nodules Collagenization of the Disse space Dynamic Endothelial dysfunction Portal collaterals Increased pressure in the portal vein Increased blood flow in the portal vein Development of portosystemic collaterals Angiogenesis activation Hyperkinetic type of blood circulation RAAS, endothelin, endocannabinoids, endotoxins, IL, NO, CO, glucagon, prostaglandin E 2 ... Splanchnic vasodilation norm cirrhosis

Hemodynamic parameters assessing the state of portal blood flow Liverv. hepatica v. portae Spleen. Wedged hepatic venous pressure (ZPVD, N - 5.5 cm of water. Art.) Portal pressure of 16-25 cm of water. Art. 10 mmHg Art.

Algorithm for diagnosing PH Anamnesis Presence of chronic liver disease Ultrasound of the abdominal organs (determination of the diameter of the portal and splenic veins) Ultrasound examination - assessment of portal blood flow indices EGDS - characteristics of the veins of the esophagus and stomach Puncture liver biopsy - clarification of the stage of CKD RVVP by means of a low pressure measuring apparatus Angiographic methods…

Ultrasound signs of portal hypertension An increase in the caliber of the vessels of the portal vein system (more than 12.5 cm) and the splenic vein (more than 8 mm) Identification of portosystemic collaterals Splenomegaly Ascites The area of ​​the spleen is 183 square meters. cm

Diagnosis of portal hypertension Doppler ultrasound EGDS catheterization of the hepatic vein selective arteriography spleno-, hepato-, portomanometry CT scan or MRI of the abdominal organs De Franchis R. ECPHR of the Baveno IV J. Hepatol. 2005; 43:167-176 I st. veins 2-3 mm II st. veins 3-5 mm III st. veins > 5 mm according to A. K. Eramishantsev,

Venous collaterals First group In the area of ​​transition of the protective epithelium into the absorbent A) gastroesophageal junction B) rectum Second group - Recanalized fetal circulation system A) in the falciform ligament B) umbilical and paraumbilical veins Third group Retroperitoneal collaterals connecting the portal system with the left renal vein Fourth group In the area of ​​transition of the peritoneum from the abdominal organs to the retroperitoneal tissues A) duodenum B) ascending and descending colon, sigmoid colon C) spleen D) liver The development of collaterals to the pulmonary veins is described

1. Varicose veins of the esophagus (EVV) Frequency of detection in patients with cirrhosis of the liver 25-80% Bleeding from EVV develop in 50% of cases 2. Varicose veins of the stomach Frequency of detection in patients with cirrhosis of the liver 6-78% Bleeding from varicose veins stomach is 20-30% of all bleeding 3. Portal hypertensive gastropathy (PHG) The incidence in patients with cirrhosis of the liver 50-60% In the 2nd tbsp. PHG bleeding frequency develops in almost 100% of cases. Main sources of bleeding De Franchis R. ECPHR of the Baveno IV J. Hepatol. 2005; 43:167-

Endoscopic classification of portal gastropathy - PGP (NIEC, 1997) I st. - mosaic pattern of pink mucosa II st. - the presence of red spots (submucosal vascular formations of red color) III st. - the presence of cherry spots (submucosal vascular formations with the presence of hemorrhages) IV st. - the presence of black spots PGP - changes in the gastric mucosa in patients with cirrhosis, manifested by excessive formation of anastomoses between the vessels of the gastric mucosa and the muscle layer in the absence of macroscopic manifestations of inflammation of the gastric mucosa

I. O. Kovyazina, TsNIIG, 2010 Grade IV HPP - black-brown spots of irregular shape flat spots of black or brown color that do not straighten out when the stomach is insufflated with air, caused by intramucosal hemorrhages

The pathogenesis of portal hypertensive gastropathy is a violation of blood flow in the portal system with the formation of arteriovenous connections, the occurrence of hypoxia of the mucous membrane of the gastroduodenal zone, an increased content of histamine and gastrin in the blood, a decrease in the inactivation of histamine and gastrin in the liver, disorders of gastric mucus formation, a decrease in the secretion of bicarbonates by the pancreas, the presence of H. pylori

Capsule endoscopy CE is a procedure for examining a patient using an endoscopic video capsule, i.e. a video camera built into the capsule, combined with a video signal transmitter. In the process of passing through the gastrointestinal tract, the capsule takes several tens of thousands of images within several hours, which are transmitted to antennas placed on the patient's body, and recorded in the memory of the receiving device. Power can be supplied either from the built-in battery or wirelessly from an external source.

Vascular changes in the small intestine Patient I. Clinical diagnosis: liver cirrhosis of alcoholic etiology, moderate activity. Class A (5 points) Child-Tucotte-Pugh. Portal hypertension: VRVP III st. , expansion of the portal and splenic veins. Held bleeding from RVV (January 2009). I. O. Kovyazina, TsNIIG,

Goals of PH treatment 1. Elimination of the cause of portal hypertension 2. Reduction of pressure in the portal vein system 3. Prevention of bleeding from VRV

I st. veins 2-3 mm II st. veins 3-5 mm III st. veins > 5 mm. Ways to reduce portal pressure (primary and secondary prevention, per os)) non-selective b-blockers propranolol (20 mg, max 320 mg / day) nadolol (40 mg, max 160 mg / day) non-selective b- and a 1-blockers carvedilol ( 6, 25 mg, max 50 mg/day) isosorbide mononitrate (10-20 mg, max 20-40 mg) Bosch J. et al. Hepatol. 2008; 1: 68-92 HR - 55-60 bpm EGD every 2-3 years Prophylactically by mouth: norfloxacin 400 mg ciprofloxacin 500 mg

Ways to reduce portal pressure (with active bleeding for 2-5 days, i.v.) vasopressin (0.4 U/min s.c.) + nitroglycerin 20 mg i.v.) terlipressin 2 mg/4 h for the first 24-48 h , then - 1 mg/4 h; min. - 0.5 mg / 4 hours in the Russian Federation - Remestip (Terlipressin), Ferning-Leciva, Czech Republic: 1 mg every 4-6 hours for 3-5 days, then within 1-2 days after stopping. bleeding) midodrine 2.5-7.5 mg (max. 12.5 mg) (α-adrenergic agonist) somatostatin 250/day, then 250-500 mg/day Bosch J. et al. J. Hepatol 2008; 1: 68-92 PROPHYLACTIC ANTIBIOTICS (7 days) ceftriaxone 1 g/day ciprofloxacin 500 mg/12 hours

Remestip (Terlipressin), Ferning-Leciva, Czech Republic: 1 mg every 4-6 hours for 3-5 days, then for 1-2 days after bleeding stops. Conservative therapy for esophageal bleeding

obturator probe Modern ways hemostasis in bleeding from esophagus and stomach VRV Drug therapy Endoscopic ligation Sclerotherapy? T I P S, bypass Liver transplantation Esophageal cuff Gastric cuff

Mortality from bleeding from varicose veins in cirrhosis of the liver is about 40%; mortality within 2 years - 60% Prognosis is determined by the severity of hepatocellular insufficiency Triad of adverse signs jaundice ascites encephalopathy is accompanied by 80% mortality

Splenomegaly is observed in all liver diseases accompanied by portal hypertension. arterial splenic blood flow increase in the number of arterio-portals. shunts stagnation and plethora of the spleen proliferation of connections. tissue hyperplasia of the reticulohistiocytic system increased pressure over 30 cm aq. Art. (N - 16-25) Splenomegaly in portal hypertension is accompanied by pancytopenia in the peripheral blood (secondary "hypersplenism") deposition sequestration of blood cells

Hypersplenism - strengthening and perversion of the function of the spleen to remove destroyed blood cells - Increased phagocytosis in the splenic pulp - Increased production of antibodies to formed elements by the spleen 1 - thrombocytopenia 2 - leukopenia with neutropenia and lymphopenia 33 - anemia

Evaluation of the degree of hepatocellular insufficiency according to the traditional (Child-Tucotte-Pugh) and improved scales 1 point (A) Criteria 2 points (B) 3 points (C) 2 mm (1 point) 6-7 7-9 3-4 mm (2 points) 8-11 10 From 5 mm (3 points) From 12 А В С Khazanov A. I., Nekrasova N. N. ,

CP stages and mortality forecast within 1 year 1 tbsp. - compensated CP, no RVVP (1%) 2 tbsp. - compensated CP with the presence of RVVP (4%) 3 tbsp. - decompensated cirrhosis with the presence of ascites (20%) 4 tbsp. - decompensated cirrhosis with bleeding from RVVP (57%) 5 tbsp. - cirrhosis with the presence of infectious complications and the development of renal failure (67%) Fede G. et al. J Hepatol. 2012; 56(4): 810-818.

Valetudo mala corpus, non animum tenet Disease tears the body, not the soul Seneca L. A. (3-65) Mens sana in corpore sano In a healthy body - a healthy mind Juvenal D. Yu. (61-127)

1. Ability to serve 2. Ability to move 3. Ability to orientate 4. Ability to communicate 5. Control over one's behavior 6. Ability to learn 7. Ability to work. The quality of life of patients with chronic liver diseases is determined not only by the degree of liver damage, but also by the neuropsychic and somatic components.

Hepatic encephalopathy (HE) is a spectrum of potentially reversible changes in the psychomotor, intellectual, emotional and behavioral function of the brain due to metabolic disorders that develop with hepatocellular insufficiency and / or portosystemic shunting of blood

Classification of PE Stages A, B, C A - - PE associated with acute liver failure B - PE associated with portosystemic shunting of blood in the absence of liver disease C - PE associated with cirrhosis of the liver, portal hypertension and portosystemic shunting of blood K category (according to duration and characteristics of clinical manifestations) episodic persistent (chronic) minimal (latent, subclinical) Subcategories spontaneous, progressive, recurrent mild, severe, treatment-dependent Ferenci P. et al. Consensus: 11th WCG, Vienna, 1998 Hepatol. 2002; 35:716-721.

Liver Deamination of amino acids. Exchange of nitrogen and ammonia Ornithine cycle: liver. Protein and other nitrogen-containing food substrates Ammonia formation Kidneys. Large intestine Small intestine Muscles Hypokalemia, alkalosis Excretion in the form of NH 4 + with urine and stool. Excretion in the gaseous state through the lungs. The breakdown of glutamine. Hydrolysis of protein and urea by ureazo (+) bacteria. Ammonia Formation of glutamine: liver, muscles, astrocytes. Ammonia neutralization 20-30% 10% 5% 5-10% 20% 80%50-60%

µmol/h·g Activity of enzymes involved in the neutralization of ammonia Hassinger D. et al. Klin. Wochenschr. 1990; 68: 175-182 Kaiser S., Gerok W., Hassinger D. Eur. J.Clin. Invest. , 1988; 18:535-

Ammonia content in venous blood in patients with chronic liver diseases (TsNIIG, 2006)) * p<0, 01 N 17- 80 мкмоль/л *

Amino acid imbalance in chronic liver diseases CF = CF - Fisher coefficient (N 3, 0 - 4, 5) phenylalanine + tyrosine + tryptophan valine + leucine + isoleucine Aromatic amino acids. Branched chain amino acids

The most frequent infectious complications (%) of liver cirrhosis (n=248) Mat. Department of hospital therapy No. 2 l / f RNIMU them. N. I. Pirogova, 2010-2013 peritonitis

Additional endogenous factors PE Products of bacterial hydrolysis in the colon M ercaptans (methanethiol, dimethyl sulfide, dimethyl disulfide) - sulfur-containing amino acids - methionine, cysteine, cystine ("fetor hepaticus") Phenols (derivatives of tyrosine, phenylalanine) Aromatic amino acids and their metabolites Short and medium chain fatty acids - dietary fats Gamma-aminobutyric acid (GABA) Serotonin, glutamate/glutamine, endogenous benzodiazepines Micronutrients (high manganese, zinc deficiency…)

Zinc deficiency (colorimetric method) in patients with alcoholic liver cirrhosis Zinc deficiency (1.8-9.0 mmol/l) 60% 20% Zinc level unchanged 10-16 mmol/l Shaposhnikova N. A. et al.,

T. H. Tranah et al. Clinical Liver Disease, Vol 5, No 3, March 2015Pathophysiological mechanisms of PE astroglia

Cerebral energy metabolism disorders Amino acid imbalance Neurotransmission disorders SIBO, infections, systemic inflammatory response, cytokines, oxidative stress, hyponatremia, etc. Hepatic encephalopathy pathogenesis Astroglia dysfunction and edema Liver disease Hepatic cell failure/porto-systemic shunting AMMONIA

Clinical manifestations of PE Decreased social adaptation Decreased visual perception Decreased memory, attention Decreased performance of professional skills Decreased reaction speed Loss of interest in previously important personal values ​​Changes in mood (irritability) Sleep disturbance Neuromuscular disorders sleep period frequent awakenings during the night nightmares daytime sleepiness (sleep inversion)

Stages of hepatic encephalopathy (ad. according to Conn H. O., 2002) Stage PE State of consciousness Intelligence Behavior Neuromuscular disorders 0 (MPE) No change Clinically not detected I (mild) Sleep rhythm disturbance: daytime sleepiness, insomnia at night Decreased attention, concentration, reaction time Accentuation personality. Neurasthenia, euphoria, depression, talkativeness, irritability Violation of fine motor skills, change in handwriting. Small-scale tremor II (medium) Lethargy Lack of sense of time, amnesia, impaired counting Personality changes. Fear, apathy, lack of inhibition Asterixis. Blurred speech. Hyporeflexia, numbness, ataxia III (severe) Somnolence, disorientation in space and time Inability to count Inappropriate behavior, rage, paranoia Hyperreflexia, nystagmus, abnormal reflexes, spasticity IV (coma) Loss of consciousness and pain response No function Loss of function Areflexia, loss tone

State of Consciousness Criteria (West Haven) Grade 0 No detectable change Grade 1 Trivial loss of attention Euphoria or anxiety Decreased attention Loss of counting (addition) Grade 2 Lethargy or apathy Minimal disorientation in time or space Subtle personality changes Inappropriate behavior Counting disturbance (subtraction) Grade 3 Somnolence to a semi-stupor with a preserved response to verbal stimuli Confusion of consciousness Significant disorientation in time or space Grade 4 Coma 1-IV (according to Glasgow - eye opening, speech, movement)

Spectrum of clinical forms of PE in patients with cirrhosis Clinically pronounced PE of I-IV stages 25-35% Minimal manifestations 40-60% Signs of PE and MPE are absent 15-25% Minor impairments in the cognitive sphere Decrease in the speed of psychomotor reactions Decrease in the speed of visual reactions Decreased ability to concentrate attention and short-term memory MPEU 75% of patients with cirrhosis with MPE have a predisposition to the development of manifest forms, the worst indicators of quality of life and survival. MPE affects the ability to drive a car. Has predictive value

The likelihood of developing P E I-IVst. , %102030405060708090100 0 Years of follow-up 1 2 30 5% 10% Baseline MPE -15% 20% 58% Baseline MPE + Forecast in the presence of minimal hepatic encephalopathy

Number connection test Execution time, sec. Stage of encephalopathy 150 IV PE III st. (chronic, caused by provoking factors - infection, severe st.) Assessment of visual-spatial activity

Test number - symbol Line test Evaluation of visual-spatial activity Evaluation of speed and accuracy of motor skills

Electroencephalography in patients with hepatic encephalopathy: slowing -, appearance -, - rhythm

60% 25% 15% Psychometric testing (including EEG) for driving ability Not suitable. Unrestricted Restricted Schomerus H. , Hamster W. , Blunck H. et al. Latent Portosystemic Encephalopathy. I: Nature of Cerebral Functional Defects and their Effect on Fitness to Drive. Dig. Dis. sci. , 1981. CPU alc. – 15 CPU non-alc. – 15 HP – 15 Min. rev. EEG - 10 Violation of the coordination of visual, auditory and vestibular stimuli Violation of attention, psychomotor functions and working memory

profile of disease impact on daily activity 25 20 15 10 5С average values ​​of the index Anxiety Emotions Communication Motor activity Mobility Self-care Sleep and rest Work Housework Entertainment Nutrition Social adaptation Control Patients with cirrhosis without MPE Patients with cirrhosis with MPE encephalopathy - MPE: adapt. according to M. Groeneweg et al. , 1998,

Probability of death in case of manifestation of PE 102030405060708090100

Repeatable Battery for the Assesment of Neuropsychological Status (RBANS) Battery of multiple tests to determine the neuropsychological status 1. Vision test 2. Memorization of different words from the list 3. Memorization of the text (story) 4. The amount of memorized numbers 5. Associativity test 6. Copying a figure 7. Sign-number test 8. Counting backwards 9. Counting with an interval of 3 10. Anxiety scale assessment 11. Depression scale assessment 12. Sleep disturbance assessment 13. Training models…

Flicker frequency 50 - 25 Hz Registration of visual evoked potentials using a HEPAtononorm analyzer (TM)

Magnetic resonance spectroscopy (1H-MRS) A — healthy individuals B — MPE C — moderate PE Ino — myo-inositol peak Gl — glutamine/glutamate peak Häussinger D. et al. Gastroenterol. 1994; 107:1475-1480.

SOURCE: Modified from Lockwood et al. 1991. Positron emission tomography (PET) Healthy individual and patient with moderate hepatic encephalopathy secondary to alcoholic cirrhosis. Cerebral blood flow differs only minimally in the subjects. The brain ammonia metabolic rate (CMRA) and permeability area (PS) - a measure of the extent to which ammonia crosses the blood-brain barrier - is significantly increased in a patient with alcoholic cirrhosis, as indicated by a greater prevalence of brighter areas.

Differential diagnosis intracranial damage (subdural hematoma, intracranial bleeding, stroke, tumor) infections (meningitis, encephalitis, abscess, etc.) metabolic encephalopathy (hypoglycemia, electrolyte imbalance, hypercapnia, hypoxia, uremia) toxic encephalopathy (acute alcohol intoxication) Wilson's disease- Konovalova dyscirculatory encephalopathy secondary hyperammonemia (imposition of urethrosigmostoma) hereditary disorders of the urea cycle encephalopathy due to the use of narcotic drugs, drugs (sedatives, antidepressants, etc.)

Factors provoking the development of PEPE ((I) Gastrointestinal bleeding EVV Erosions and ulcers Portal hypertensive gastropathy, portal enteropathy, colonopathy Mallory-Weiss syndrome Increased protein breakdown in the intestine Increased ammonia production

Mat. Department of hospital therapy No. 2 l / f RNIMU them. N. I. Pirogova, 2010-2013 peritonitis11 12 Infectious complications (AI) Increased protein catabolism Increased ammonia production. Factors provoking the development of PE (II) Infections - Systemic Inflammatory Reaction

LC + urinary infection / pyelonephritis (n = 58/144; 40.3%) Secondary nosocomial infections in patients with alcoholic LC (n = 21/58; 36.2%) Survivors (n=102) Deceased (n=42) Mat. Department of hospital therapy No. 2 l / f RNIMU them. N. I. Pirogova, 2010-2013

Increased protein breakdown in the gut Excessive protein intake / protein tolerance Constipation Increased ammonia production Factors provoking the development of PE ((III)

Anastomosis surgery Proximal anastomoses - 50-60% Distal splenorenal anastomosis - 35% TIPS - 20-25% (Transjugular intrahepatic portosystemic shunting) Increased ammonia shunting from the colon

Transjugular Intrahepatic Portosystemic Shunt - TIPS

Massive diuretic therapy or laparocentesis with removal of a large amount of ascitic fluid Hypokalemia, hyponatremia, alkalosis Vomiting, diarrhea Taking sedatives and tranquilizers Taking alcohol Exo- and endotoxins Decompensation of liver disease Factors provoking the development of PE ((V)

For episodic PE Diet Pharmacotherapy Identify and eliminate the precipitating factor For all forms of PE Treatment of hepatic encephalopathy

Protein deficiency is found in 20-60% of patients with liver cirrhosis Diet in patients with chronic liver disease Anorexia Nausea Malabsorption Hypermetabolic conditions Widely prescribed low protein diets Causes Italian multicentre cooperative project on nutrition in liver cirrhosis. Nutritional status in cirrhosis. J. Hepatol. 1994; 21:

Diet in hepatic encephalopathy Identification and elimination of resolving factors Diet - temporary restriction of protein content in latent PE up to 50 g / day (vegetable protein), with improvement - 1.0-1.5 g / day / kg for I-II st. - up to 40-30 g / day for III-IV st. tube and parenteral nutrition with a protein content of up to 20 g / day, fat - 70-140 g / day, carbohydrates - 280-325 g / day, caloric content - 1800-2500 kcal / day side chain) ESPEN, 1997 - recommendations of the European Society for Parenteral and Enteral Nutrition 1.0-1.5 g / kg (N) 0.5 g / kg PE Morgan T. R. , Moritz T. E. , Mendenhall C. L. , Haas R. and VA Cooperative Study Group #275 Protein consumption and hepatic enencephlopathe in alcoholic hepatitis J. Am. Coll. Nutr. 1995; 14:152-

For episodic PE Diet Pharmacotherapy Identify and eliminate the precipitating factor For all forms of PE Treatment of hepatic encephalopathy

Reducing the formation of NHNH 33 in the colon - suppression of the growth of proteolytic intestinal microflora and the production of ammonia Aminoglycosides Neomycin - per os from 1-2 g / day. up to 3.0 - 6.0 g / day. 7-14 days Rifamycins Rifaximin - per os 1200 mg / day. 7-14 days (long-term, up to 24 weeks) Glycopeptides Vancomycin- per os 2.0 g/day. 7 days Semi-synthetic penicillins Amoxicillin - per os 2.0 g / day. 7-14 days Fluoroquinolones Ciprofloxacin - per os 750-1500 mg / day. 7-10 days Nitroimidazoles Metronidazole - per os 1000 mg / day. 5-7 days

Decreased formation of NHNH 33 in the large intestine NH 3 → NH 4 + Decreased absorption of ammonia in the form of NH 4 +, loss of N with feces increases 4-6 times Lactulose and lactitol (exportal) - 15-45 g / day and more Mechanism of action Production lactic and acetic acids under the influence of intestinal microflora r. H to 5-6 → inhibition of the microflora that produces ammonia, the growth of Lactobacillus Bleeding from EVV Infections Constipation. Enemas with lactulose 20% - 1-3 l

Binding of ammonia in the blood Introduction: per os — 10 g/day Binds ammonia in the blood with the formation of hippuric acid, activates the synthesis of glutamine in perivenous hepatocytes. Congenital hyperammonemia Sodium benzoate The effectiveness of treatment of PE with benzoate was evaluated in one RCT, lactulose was used as a comparison: the improvement in the clinical condition and the frequency of side effects is the same in both groups, the use is limited to side effects: acidosis, electrolyte disorders, cerebral edema, dyspepsia ...

Antagonist of benzodiazepine receptors Introduction: intravenous bolus 0.2-0.3 mg, then intravenous drip 5 mg/hour, with improvement 50 mg/day orally Reduces inhibitory processes in the central nervous system Short duration of effect Means of choice for PE due to intake sedatives and benzodiazepines Flumazenil (Anexat)

Neutralization of ammonia in the ornithine cycle Carbamoylphosphate synthetase 1 Argininosuccinate. Arginine. Ornithine Citrulline Urea CO 2 NH 3 Carbamoyl Phosphate ++ Aspartate. Ornithine

Neutralization of ammonia in the liver - cc regimen for the appointment of L-L- ornithine-L-L- aspartate (LOLA, hepa-merz)) Acute hepatitis (severe course) Cirrhosis of the liver The first 5-7 days - intravenously, 20-40 g per 500-1000 ml of saline , 5 g/hour subsequent 4-12 weeks orally 3-6 g (granulate) 3 times a day Acute hepatitis (moderate and mild course), chronic hepatitis, hepatic steatosis 4-8 weeks orally 3-6 g (granulate) 3 times a day

Clinical and laboratory syndromes in which efferent methods of therapy are effective Parenchymal jaundice (high bilirubin level) Cholestasis syndrome (skin itch, high activity of alkaline phosphatase and GGTP) Cytolytic syndrome (high activity of ALT, AST) Hypercholesterolemia, hypertriglyceridemia

Promising drugs for the treatment of hepatic encephalopathy Zinc salts - stimulating the formation of urea - improving neurotransmission L-carnitine - improving the energy supply of cells Prebiotics, dietary fiber (mucofalk, galactomannan ...) - increasing the content of lactobacilli - reducing endotoxemia - reducing ammonia levels - increasing the content of SCFA RF Butterworth, 2002; Q Liu et al. , 2004; M Iwasa et al. , 2012; NA Shaposhnikova et al. , 2006.

Classification of ascites (askos - bag, bag) 1 tbsp. - ascites, detected only by ultrasound of the abdominal organs 2 tbsp. - moderate ascites, determined during the examination of the patient 3 tbsp. - intense ascites Refractory - ascites resistant to diuretic therapy Wong F. et al. Sepsis in cirrhosis: report on the 7th meeting of the International Ascites Club Gut 2005; 54(5): 718-25 EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. Hepatol. 2010; 53:397–417.

The main causes of ascites development Cirrhosis of the liver 85% Tumors 10% Heart failure 3% Tuberculosis 2% Exacerbation of chronic pancreatitis Budd-Chiari syndrome Veno-occlusive disease Portal vein thrombosis Nephrotic syndrome Diabetic nephropathy Myxedema Meigs syndrome (tumor of the ovary or uterus) Acute alcoholic hepatitis ... Others causes of ascites

Liver cirrhosis C sinusoidal intrahepatic portal hypertension Hyperproduction of NO in splanchnic vessels Splanchnic arterial vasodilation Decrease in effective circulating blood volume Activation of the angiotensin-renin, sympathetic and aldosterone systems Sodium and water retention Increase in circulating blood volume Increase in portal pressure Ascites - abnormal accumulation of fluid in the abdominal cavity Hypoalbuminemia (blood hypoonkia) Edema-ascitic syndrome. Pathogenesis of edematous-ascitic syndrome Coagulopathy - an increase in the permeability of the vascular wall. Metabolic disorders of hormones and biologically active substances Gines P. , et al. NEJM 2004; 350: 1646-1654.

Clinical manifestations of edematous-ascitic syndrome - Increase in body weight - Increase in the volume of the abdomen - Venous subcutaneous collaterals on the abdominal wall of the abdomen - S. Cruveil-Baumgarten - "head of a jellyfish" - "devilish noise" - Appearance of peripheral edema Expansion of the umbilical vein

Diagnosis of ascites in a patient with cirrhosis 1. Physical examination 2. Abdominal ultrasonography - concomitant obesity - multiple postoperative scars on the anterior abdominal wall - elevated AFP level 3. Diagnostic paracentesis (30-40 ml) - cytosis in the AF - histological examination - biochemical analysis of the AF - bacteriological analysis of AF 4. Laparoscopy and biopsy of the peritoneum (tuberculous peritonitis) 5. Assessment of systemic inflammatory response - systemic inflammatory response

Diagnostic paracentesis Indications for the first time identified and clinically verified ascites in patients with cirrhosis with ascites with progressive deterioration of the general condition Contraindications Clinically confirmed fibrinolysis DIC The need for prophylactic infusions of fresh frozen plasma or platelet mass is controversial AF, when removing more than 5 liters of ascitic fluid

Serum-ascitic albumin gradient (SAAG) SAAG = serum albumin - ascitic fluid albumin If SAAG ≥ 1.1 g/dL, portal hypertension is confirmed If SAAG ≤ 1.1 g/dL, portal hypertension is absent (~~97% confidence)

Cause Appearance Protein g/dl Gra-d intg/dl Erythrocytes Leukocytes Other Cirrhosis Straw yellow 1, 1 low 2, 5 varies often high >1000 (>50% lymphocytes + cytology Purulent peritonitis Cloudy or purulent >2 , 5 10000/mm 3 gram (-) pathogens Spontaneous bacterial peritonitis Turbid or purulent 1, 1 low >250/mm 3 gram (-) pathogens Tuberculous peritonitis Clear, hemorrhagic or chylous >2.5 1000 (>70% lymphocytic) / mm 3 seeding of acid-fast bacilli Differential diagnosis of ascitic fluid

Ascites: treatment 1) Bed rest, severe restriction table salt(2 g sodium per day - 88 mmol / day) 1) Fluid restriction to 1-1.2 l / day 3) Diuretics (dose increase in 2-4 days) per os: - spironolactone 100 - 200 mg / day orally ( max - 400 mg / day) - furosemide 40-80 mg / day orally or intravenously (max - 160 mg / day) with IV Lasix - acute decrease in glomerular filtration Weight loss in 4 days by 0.8 kg no yes 4) Paracentesis (albumin transfusion), TIPS, liver transplant n/a Runyon B. A. , AASLD Practice Guidelines Committee. Hepatol. 2009; 49:2087-2107Def. daily urinary sodium excretion

Diuretic therapy of ascites in patients with cirrhosis Potassium-sparing diuretics - spironolactones (veroshpiron, aldactone) - amiloride - thiamterene Loop diuretics - furosemide - ethacrynic acid (uregit) - bumetanide - torasemide free liquid) - vaptans (satavaptan ...)

A patient with ascites and edema should lose no more than 1 kg / day, with ascites without edema - no more than 500 g per day! Complications of diuretic therapy Hyponatremia (< 125 ммоль/л) Гипокалиемия (ммоль/л) Азотемия (креатинин >2 mg / dl) Hepatic encephalopathy Requires constant monitoring of body weight, electrolytes and creatinine and sodium in serum and daily urine, measurement of abdominal volume

Indications for discontinuation of diuretic therapy Hepatic encephalopathy Hyponatremia less than 125 mmol/l with fluid restriction Serum creatinine more than 2 mg/dl

Diuretic-refractory ascites Refractory ascites - failure to respond to sodium restriction in food and high-dose diuretic therapy: verospirone 400 mg / day and furosemide 160 mg / day or rapidly increasing ascites after therapeutic paracentesis physical activity, bacterial infection, NSAID use

IV furosemide 80 mg Urinary sodium excretion in 8 hours: 50 mmol - diuretic-responsive ascites Furosemide test for diuretic-resistant ascites

Complications of ascites Mechanical complications - hydrothorax, atelectasis, shortness of breath - increased pressure in the portal vein - vascular compression - inferior vena cava syndrome, compression of the renal veins - hernia formation - rupture of an umbilical hernia displacement of organs (intraperitoneally, heart rotation) Metabolic complications - impaired electrolyte metabolism - increased uric acid - violation of protein metabolism (catabolism) - changes in pharmacokinetics - hepatic encephalopathy - diuretic-resistant ascites - dilution hyponatremia - hepatorenal syndrome Gynecomastia Convulsions Impotence

Prognosis of patients with cirrhosis with ascites > 50% of patients with cirrhosis develop ascites during the 10-year follow-up 50% of patients with cirrhosis with ascites die within 2 years 50% of patients with refractory ascites die within 6 months and 75% within 1 year Hyponatremia Hypotension Serum creatinine more than 1.2 mg/dL Urinary sodium excretion< 10 ммоль/сут. Неблагоприятные факторы

Spontaneous bacterial peritonitis — SBP (translocation, hematogenous microbial contamination) Risk factors for the development of liver cirrhosis (Child-Pugh C) Bleeding from the gastrointestinal tract History of SBP episode Protein (ascites) 2.5 N Creatinine > 200 mg/ml Clinical manifestations Abdominal pain 76 -82% Fever 69-82% Vomiting 10-14% Diarrhea 10-11% Intestinal paresis 6-8% Septic shock 3-10% Hepatic encephalopathy. SPB - inflammation of the visceral and parietal peritoneum in a patient with cirrhosis with ascites without breaking the integrity internal organs followed by infection

Spontaneous bacterial peritonitis Wong F. et al. Sepsis in cirrhosis: report on the 7th meeting of the International Ascites Club Gut 2005; 54(5): 718-725. Terg R. et al. J. Hepatol. 2008; 48:774-779. Fernandez J. et al. Gastroenterol. 2007; 133:818-824. EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. Hepatol. 2010; 53: 397–417. Escherichia coli, Klebsiella pneumoniae, Pseudomonas, Enterobacter, Citrobacter 70%; Staphylococcus, Streptococcus, Pneumococcus 10-30%: Candida albicans, Aspergillus sp. 30% PMN > 250 cells/mm

Fibrin filaments in the AF of a patient with peritoneal tuberculosis Fibrin filaments in the AF of a patient with cirrhosis with ascites and destructive appendicitis. Spontaneous bacterial peritonitis: suspension, fibrin threads in the AF, PNL >400 /mm 3 Secondary bacterial peritonitis Ultrasound diagnostics

Patient P., 43 years old (C/B No. 5054/2006) LC (Alc. + HBs. Ag+, HBV DNA-) Child-Pugh C (11 points) 11. 06. 25. 08. 06. *eleven. 08. *02. 08.*23. 06. * Edematous-ascitic syndrome, SBP Suspension, fibrin threads in ascitic fluid PMN >400 /mm 3 Hepatic encephalopathy * — coma III DST - 90 sec. ——-96 sec. VZP - 35 Hz Ammonia - 72-128-77 mcg / dl LOLA, Hepa-merz 20-40 g / day IV (5 days) Cefotaxime 6 g / day

Drugs of choice Third generation cephalosporins Drug Dosing regimen Efficacy Cefotaxime 1-3 g every 8 hours 100% Ceftriaxone 1-3 g per day 100% Cefonicide 2 g 2 times a day 90% Alternative drugs: Amoxicillin 1 g + clavulanic acid 0, 2 g every 6 hours - effect. 85% Fluoroquinolones (ofloxacin 400 mg/2 r daily for 7-14 days) Change of antibiotic in the absence of a decrease in the content of PMN in ascitic fluid by 25% after 2 days from the start of therapy EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. Hepatol. 2010; 53: 397–417. Wong F. et al. Sepsis in cirrhosis: report on the 7th meeting of the International Ascites Club Gut 2005; 54(5): 718-775. Prevention of SBP - ciprofloxacin 750 mg/day

The choice of antibiotics for bacterial infections in patients with LC III generation cephalosporins (ceftriaxone / cefatoxime 1-2 g x 2 times a day) up to 14 days Amoxicillin + clavulanic acid 1-2 g / day. up to 14 days Tableted fluoroquinolones (ciprofloxacin/norfloxacin) 1 g/day 7-14 days Rifaximin - non-absorbable (intestinal) ABP 1200 mg/day 10-14 days

Microorganisms in patients Alk. cirrhosis with urinary infection Microorganisms in patients Alc. CPU with SBP Mat. Department of hospital therapy No. 2 l / f RNIMU them. N. I. Pirogova, 2010-2013

Sensitivity to antibacterial drugs Microorganisms Ampicil. Tsefatok. Cefa zolin Ciprof. Amikacin Gentamic Ceftazi dim Imipinem Meronem Vancomicin Levofloc Resistance 83% 91, 2% 56, 3% 94% 76, 2% 88, 4% 90% 8% 12% 10% 11% E. coli — — + + + 0 0 Enteroc. sp. — — + — + + + 0 0 Kl. pneum. — — — + + + Enter. faecfal. + _ _ — + — 0 0 + + — St. e piderm. _ _ _ + + 0 Proteus mirabilis + + + Pseud. aerugin _ _ _ — _ _ + + + 0 + Acinetobacter spp. _ _ _ + + + _ Staph. aureus _ _ _ + + + 0 0 0 Mat. Department of hospital therapy No. 2 l / f RNIMU them. N. I. Pirogova, 2010-2013

30-day mortality in 23.6% of patients with: C. difficile infection - 40% LRTI - 37, 5% spontaneous bacteremia - 37, 0% ICMT - 22, 0% SBP - 17, 0% UTI - 15, 0%The addition of a secondary infection is the most important predictor of death!

Dilutional hyponatremia (dilutional hyponatremia) Occurs in 30-35% of patients with cirrhosis Hypersecretion of antidiuretic hormone under the influence of the periphery. vasodilation, acting on the renal tubules, contributes to fluid retention (when it moves from the extracellular space to the intracellular space) and sodium. With a normal sodium content in the body, its decrease in the blood is noted: - 125-135 mmol / l - mild hyponatremia - less than 125 mmol / l – chronic hyponatremia – Clinical manifestations are nonspecific: – muscle weakness, tremor, hoarseness, acute psychosis, hemiplegia, less often – coma – Therapy – fluid restriction to 800-1000 ml – cancellation of diuretics – aquaretics – vaptans (satavaptan, lixivaptan, tolvaptan…)

hepatorenal syndrome

Liver cirrhosis C sinusoidal intrahepatic portal hypertension Hyperproduction of NO in splanchnic vessels Splanchnic arterial vasodilation Decrease in effective circulating blood volume Activation of the angiotensin-renin, sympathetic and aldosterone systems Renal vasoconstriction Sodium and water retention Increase in circulating blood volume Increase in portal pressure Ascites Hypoalbuminemia as a manifestation of hepatocellular insufficiency (blood hypoonkia) Hepatorenal syndrome Edema-ascitic syndrome. The pathogenesis of hepatorenal syndrome

Hepatorenal syndrome Presence of cirrhosis with ascites Serum creatinine more than 133 µmol/l (1.5 mg/dl) or its increase by 50% No normalization of serum creatinine (up to 133 µmol/l) after 48 hours. after the abolition of diuretics and the introduction of albumin (1 g / kg, max. - 100 g / day) no shock. CVP - 50-120 mm of water. Art. lack of data on the use of nephrotoxic medicines the absence of kidney disease, manifested by proteinuria (more than 500 mg / day), microhematuria (up to 50 er. in p / sp) and / or changes in the kidneys on ultrasound Salerno F. , Gerbes A. , Gines P. et al. Gut 2007; 56: 1310-1318 Salerno F, et al. gut. 2007; 56:1310-

Parameters Type I (acute HRS) Type II (hr. HRS) Course dynamics Blood creatinine/sodium Na excretion Diuresis Liver diseases Risk factors for HRS development Forecast 1-14 days 2 times in 2 weeks , > 221 mmol/l/< 130 ммоль/л Олигоурия (400), анурия (200) алк. гепатит, ФПН инфекции, кровотечения, парацентез, бесконтрольное применение диуретиков летальность до 80% в течение 2 недели, месяцы более 133 ммоль/л / < 130 ммоль/л олигоурия ХЗП (ВЦП, ПБЦ) менее неблагоприятный резистентный асцит. Клиренс креатинина снижение более чем 50%, < 20 мл/мин в течение 2 нед. снижение менее чем 50%Характеристика типов ГРС (эволюция ГРС) < 30 ммоль/л; Fe. Na < 1%

Type I hepatorenal syndrome An increase in serum creatinine by 26.4 mmol/L within 48 hours significantly reduces the survival of ILC EASL,

Hepatorenal syndrome - treatment 1. Cancellation of diuretics and correction of circulating blood volume, water-electrolyte balance and acid-base balance 2. Improvement of glomerular filtration and sodium excretion (dopamine - 2-4 mcg / kg / min; max. dureza increase - 250 mcg/min) Transfusion of albumin solution 1 g/kg (1-3 days), then up to 40 g/day (max. day -100 g) Terlipressin 1 mg (vasoconstrictor) every 4-6 hours, increasing the dose by 30% every 3 days (max. 12 mg / day) - GRS I (Remestip, Ferring-Leciva, Czech Republic), 1 mg, 10-14 days. (in the absence of a decrease in creatinine by 25% - the dose is increased to 2 mg) Norepinephrine 0.5-3 mg / h, octreatide 100-200 mg / 3 s / c, midodrine 2. 5-12. 5 mg 3. Exclusion of nephrotoxic drugs (NSAIDs, aminoglycosides, etc.) 4. Hemodialysis, arteriovenous hemofiltration 5. Surgical treatment (TIPS, etc.) 6. Liver transplantation Salerno F. et al. Gut 2007; 56: 1310-1318 Angeli P. et al. J. Hepatol. 2008; 48(suppl 1): 93-

Hepatopulmonary syndrome - HPS respiratory failure in cirrhosis Liver cirrhosis + HPS - 4-47% Liver cirrhosis Child-Pugh C > 60% Portal hypertension Arterial hypoxemia (at rest, supine RA. O 2< 70 мм рт. ст.) Дилятация легочных артерий (до 500 мкм, N – 6-8 мкм) платипное цианоз по смешанному типу «барабанные пальцы» «часовые стекла» венозное полнокровие в малом круге кровообращения косвенные признаки гиповентиляции дистелектазов в базальных сегментах Портопульмональная гипертензия (ППГ) – повышение легочного артериального давления, артериолярной вазоконстрикцией и локальной гиперпродукцией вазоконстрикторных субстанций. ППГ — у 2-8% больных ЦП

Liver cirrhosis C sinusoidal intrahepatic portal hypertension Hyperproduction of NO in splanchnic vessels Splanchnic arterial vasodilation Opening of pulmonary arteriovenous shunts. Decreased effective volume of circulating blood Activation of the angiotensin-renin, sympathetic and aldosterone systems Renal vasoconstriction. Sodium and water retention An increase in circulating blood volume An increase in portal pressure Ascites Hypoalbuminemia as a manifestation of hepatocellular insufficiency (blood hypotension) Hepatopulmonary syndrome - HPS Hepatorenal syndrome Edema-ascitic syndrome. The pathogenesis of hepatopulmonary syndrome

Types of HPS Type I HPS is formed with diffuse dilatation of the precapillary bed of the lungs. At the same time, respiratory support by inhaling pure oxygen significantly improves oxygenation processes. Type II HPS is due to the presence of locally dilated arterioles and the formation of single intrapulmonary arteriovenous shunts. This variant of HPS is characterized by a lack of response to oxygen inhalation.

2D transthoracic contrast echo. CG for HPS Preparations Levovist®, Ehovist® (microbubbles d > 15 μm; 10 ml IV) Visualization of the right chambers of the heart Microbubbles are “captured” by the pulmonary capillary network and do not normally reach the left parts of the heart (d capillaries - 8-15 μm) va b a - chambers of the heart before DTC Echo. CG, b - microbubbles in the right parts of the heart c - microbubbles in all cavities of the heart (after 4-6 contractions)

Radioisotope scanning of the lungs with HPS Albumin labeled with 99m Tc Size - from 10 to 90 microns (on average - 20-50 microns) Normally, 95% A-99m Tc is "captured" by the lungs With intrapulmonary vasodilation - less than 40% a - front view, b - rear view Visualization of the lungs, liver, spleen, kidneys, bladder, brain, thyroid gland

Hepatopulmonary syndrome - treatment 1. In HPS I - respiratory support: inhalation of humidified oxygen 4-6 l / min for 10-20 minutes with breaks of 10-30 minutes 2. Surgical treatment (TIPS, etc.) - before liver transplantation 3 Type II HPS - selective embolization of individual arteriovenous shunts 4. In severe respiratory failure - drainage of the pleural cavity 5. Liver transplantation, either liver/lung or liver/lung/heart

NATURAL COURSE OF CHRONIC VIRAL HEPATITIS B and C Chronic hepatitis B Cirrhosis of the liver 10-40% Chronic hepatitis C Cirrhosis of the liver 30-50% 10-20 years 10-15 years HCV ALCOHOL HCC (4-6%) integration into the hepatocyte genome involvement of virus regions in the processes of cis- and transactivation under the influence of X-antigen mutation of suppression genes increased level of TGF-a destruction and regeneration of liver tissue apoptosis heredity. Mutations in Pre-SS C 1653T T 1753V A 1762T/G 1764A)

Probability of developing HCC in patients with cirrhosis of various etiologies. Probability Age. Alcohol+HCV Alcohol | 20 | 30 | 50| 40 | 70| 60 | 800, 5 -1, 0 - Takada A., 1993 Alcohol consumption in doses: 41-80 g / day - 2 times the risk of HCC > 80 g / day - 4 times the risk of HCC Donato,

Terms of formation of HCC Rapid progression - 6-20 years Medium - 21-35 years Slow - 35-50 years In 40% of patients with HCC, multiple foci of MRI are detected at the first ultrasound 4-5% Diagnosis of HCC ultrasound AFP tumor markers (L 3 - fraction) Oncogenes DCP - des-gamma-carboxy-prothrombin

HCC treatment tactics Surgical methods (resection, transplantation) Percutaneous tumor destruction (ethanol, cryotherapy, radiofrequency ablation) Transarterial embolization Chemoembolization (doxorubicin, mitomycin, cisplatin, lipiodol) Pharmacotherapy — angiogenesis inhibitors — tyrosine kinase (growth factor signaling) inhibitors — telamerase inhibitors … …. Nexavar (sorafenib) 200 mg (800 mg/day) Five-year survival in 40% of patients from baseline. HCC Improves the three-month survival of patients with late art. HCC

AASLD: Monitoring Patients at Risk for HCC Hepatitis B Asian men (40 years and older) and women (50 years and older) Cirrhosis Relatives with HCC Patients of African descent 20 years and older Patients without cirrhosis with HBe. Ag, high HBV DNA and ALT and/or inflammation on liver biopsy Hepatitis C with fibrosis or cirrhosis of the liver Alcoholic cirrhosis of the liver Hereditary hemochromatosis or cirrhosis Primary biliary cirrhosis (stage cirrhosis) Patients with cirrhosis with the following pathology Alpha-1 antitrypsin deficiency Non-alcoholic steatohepatitis Autoimmune hepatitis Guy J, Kelley RK, Roberts J, Multidisciplinary Management of Hepatocellular Carcinoma. Clin Gastroenterol Hepatol. 2011 Nov 11.

Discriminant function (DF) DF) according to Maddrey, 1978 DF = 4. 6 x (PV patient - PV control) + serum bilirubin level (mg%) With DF > 32, the probability of death is 50%. Maddrey W. C. , Boitnott J. K. , Bedine M. S. et al. Corticosteroid therapy of alcoholic hepatitis. Gastroenterol. , 1978; 75:193-

R = 3.19 - 0.101 (age, years) + 0.147 (albumin on the day of admission, g / l) + 0.0165 (serum bilirubin, μmol) + 0.206 (presence of renal failure - 0 or 1 *) + 0.0065 (serum bilirubin on the day of admission, µmol) + 0.0096 (prothrombin time, s) Louvet A. , Naveau S. , Abdelnour M. et al. The Lille model: a new tool for therapeutic strategy in patients with severe alcoholic hepatitis treated with steroids. Hepatol. 2007; 45(6): 1348-54. At R > 0.45 survival within 6 months. is 25± 3.8%, at R< 0, 45 выживаемость составляет 85± 2. 5% (р<0. 0001) Шкала Лилль

MELD (Model for End-Stage Liver Disease) Model for End-Stage Liver Disease 10 x (0.957 x loge[creatinine mg/dl] + 0.378 x loge[prothrombin time] + 0.643 x etiology of cirrhosis (0 - alcohol , cholestasis; 1 - other etiology) Sheth M, Riggs M, Patel T. BMC Gastroenterol. , 2002, 2, 2. With a score of more than 18 - a high risk of death (50%)

Estimation of survival of patients with cirrhosis based on the MELD model Scores Classification Prognosis of survival 6-10 mild > 10 years 11-18 moderate ~ 3-5 years 19-24 severe< 1 года 25-39 критическая < 3 мес. 40+ терминальная < 2 нед. Freeman R. B. et al. Liver Transpl. 2002; 8(9): 851-858.