The Cirrhosis: symptoms, signs, treatment
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Cirrhosis: symptoms and treatment

Content:

Irreversible changes in the structural organization of the liver as a result of chronic diseases, with persistent impairment of its functions, increased pressure in the portal vein system - is called cirrhosis of the liver.

The disease is widespread and is on the sixth place as the cause of death in the age group from 35 to 60 years, with the incidence of about 30 per 100 thousand people a year. Particularly alarming is the fact that the frequency of the disease over the past 10 years has increased by 12%. Men are sick three times more often. The main peak of the incidence falls on the period after forty years.

The liver is the largest digestive and internal secretion in the body of iron.

The most important liver function:

  1. Neutralization and utilization of harmful substances entering the body from the external environment and formed in the process of vital activity.
  2. The construction of proteins, fats and carbohydrates used to form new tissues and replace the cells that have spent their life.
  3. The formation of bile, involved in the processing and cleavage of food masses.
  4. Regulation of rheological properties of blood by synthesis of a part of coagulation factors in it.
  5. Retention of the balance of protein, carbohydrate and fat metabolism by synthesis of albumins, creation of additional reserves (glycogen).



The structure of the liver

The structural unit of the liver is a lobule (acinus), consisting of several cells (hepatocytes). They combine into a kind of hexagonal cylinder.

In the center of the acinus is the hepatic (central) venule, and at the corners of the putative hexahedron, between the hepatocytes - portal tracts.

Portal tracts consist of:

  1. The hepatic artery. It carries fresh, oxygen-rich blood to ensure the vital activity of the liver from the branches of the aorta.
  2. The hepatic venule. It is a branch of the portal (portal) vein, formed by the fusion of the superior and inferior mesenteric veins that carry blood from the intestine. This blood is saturated with substances digested from food. Part of them, without preliminary treatment in the liver itself, can cause irreparable harm to the body.
  3. Bile capillaries. They collect the hepatocyte-secreted enzymes necessary for digestion, thereby forming bile. The bile capillaries, merging into the major bile ducts, depositing part of the formed secretion in the gallbladder, subsequently, through the common bile duct, go into the lumen of the duodenum, where the bile is mixed with food.
  4. Nerve stems.
  5. Lymphatic vessels.

In accordance with the available data on the blood supply, the generality of branching of the bile ducts and innervation, eight segments are isolated in the liver. This is important when carrying out operations on this body. Segments form the right and left lobes of the liver. The conditional border of the lobes passes through the gates of the liver to the site of the inflow of the hepatic veins into the inferior hollow.

It is with the violation of the structure of the liver lobule, an irreversible chain of structural changes in the liver, leading, in the end, to human death.

The processes that occur with the development of cirrhosis:

  1. Death for various reasons of a certain number of hepatocytes.
  2. Formation in their place of connective tissue, compressing and disrupting the normal flow of blood in the portal tracts, the central vein. The resulting connective tissue also disrupts the formation and outflow of bile through the bile capillaries. As a result, part of the bile necessary for digesting food is absorbed directly into the blood, causing intoxication of the body and manifestations of jaundice.
  3. Restructuring of the vascular system, which fed the deceased liver acinus, with the formation of new communications (anastomoses).
  4. Proliferation of bile ducts.
  5. Division of the remaining hepatocytes with the formation of regeneration sites. However, the functional incapacity of these nodes does not allow the appearance of normal hepatic tissue.
  6. Part of the regeneration nodes, due to their uncontrolled growth, impoverished blood supply and squeezing from the sides formed by connective tissue - perish. This causes stimulation of new scar processes leading to compaction of the liver and a decrease in the already limited number of hepatocytes functioning by that time.

The described processes go diffusely, continuously, throughout the liver, are not limited to one segment or lobe. The time interval can stretch for months and even years. Gradually, there is a violation of the genomic apparatus of hepatocytes. With minimal genetic changes, autoimmune mechanisms are included in the process, which activates the rate of inflammatory-sclerotic changes that occur. With the greatest genetic abnormalities, a malignant neoplasm of the liver, the so-called "cirrhosis-cancer," begins to form.

As the volume of damaged liver tissue increases, a qualitative shift in the violation of liver function also occurs.

Causes of liver cirrhosis

  1. Chronic alcohol intoxication. On average, cirrhosis is formed in 10-15 years from the onset of abuse. And, the daily dose of absolute alcohol required for this is 96% alcohol, for a woman three times less than for a man and is 20 grams per day.
  2. Viral hepatitis B, C and D.
  3. Various autoimmune diseases with the initial development of hepatitis.
  4. Diseases of the biliary tract (secondary biliary cirrhosis).
  5. Mechanical blockage of extrahepatic and intrahepatic biliary tract caused by the formation of gallstones. For the development of cirrhosis, the presence of a violation of the passage of bile from 3 to 18 months is sufficient.
  6. Primary sclerosing cholangitis. Very rare disease, combined, as a rule, with the presence of ulcerative colitis. This is the infection of the bile ducts. The inflammatory process extends to the nearby liver tissue, its damage occurs with the further development of cirrhosis.
  7. Intoxication with hepatotoxic chemicals (carbon tetrachloride, imethylnitrosamine, chloroform, benzene, nitro and amino compounds, mercury, gold and lead) and drugs (anti-tuberculosis and anti-cancer drugs, anabolic steroid agents, etc.).
  8. Vegetable poisons: fungi (phalloidin, phalloin, betta-amanitin) and cereals (aflatoxins) formed in overwintered cereals, corn, rice. These substances cause acute toxic dystrophy of the liver with massive tissue necrosis. Instead, cirrhosis is formed in the future.
  9. Genetically caused metabolic disorders (hepatolenticular degeneration, Wilson-Konovalov's disease, hepatocerebral dystrophy, galactosemia, glycogenosis, cystic fibrosis, hemochromatosis, α1-antitrypsin deficiency).
  10. Reduction of blood flow through the portal vein with phlebothrombosis, compression from the outside (chronic pancreatitis , pancreatic tumors).
  11. Prolonged venous congestion of the liver with chronic cardiovascular diseases (constrictive pericarditis, veno-occlusive disease, heart failure).
  12. Primary biliary cirrhosis for no apparent reason. It occurs mainly in women in the climacteric period.
  13. Cryptogenic cirrhosis. The cause of its appearance remained undetected. Characterized by an extremely aggressive ongoing flow. It is an absolute indication for liver transplantation.
  14. Congenital absence of bile ducts in infants.
  15. Rundu-Osler disease. Otherwise, this disease is known as hereditary hemorrhagic telangiectasia. The disease is rare and is caused by congenital maldevelopment and dysfunction of the intrahepatic vascular system of the liver.
  16. Fatty degeneration of the liver in the presence of metabolic disorders (obesity, diabetes mellitus).
  17. Parasitic and infectious liver diseases (echinococcosis, brucellosis, opisthorchiasis , toxoplasmosis , ascariasis, etc.).
  18. The cause of congenital cirrhosis of the liver in newborns can become and developed in the mother during pregnancy viral infection (cytomegalia, herpetic infection, rubella). The ability of these viruses to penetrate the placental barrier and inflict liver damage, becomes here the main mechanism for the onset of cirrhosis in a baby. Developed serum hepatitis during immunization of a pregnant woman, can also cause this pathology in a child born. There are also lesions of the liver in newborns in the presence of mothers of diseases such as syphilis , toxoplasmosis, listeriosis.
  19. After shunting operations on the gastrointestinal tract.

It should be separately noted that in more than half of those who have cirrhotic liver, there are multifactorial reasons for its occurrence. The most common combination is an immoderate passion for alcohol and the presence of chronic hepatitis.

Symptoms of liver cirrhosis

In cases where cirrhosis develops gradually, outside of a clear connection with any intoxication or exposure to an aggressive factor, the disease can carry a latent clinical symptomatology, manifested for the first time in the stage of complications. The intensity of complaints, the manifestation of symptoms and their combinations depends on many components. But in general, in the initial stages of the disease, we can distinguish the following groups of symptoms, which are combined into syndromes.

  1. Asthenic syndrome (decreased appetite, fatigue, general weakness, weight loss, episodes of short-term small body temperature rises, difficulty in concentrating, daytime sleepiness in sleep disturbances, irritability, tearfulness, touchiness and suspicion, suspicion of others, hysterical reactions).
  2. Dyspeptic syndrome (nausea, vomiting, residual bitterness in the mouth, eructation, a feeling of heaviness in the abdomen with fatty food and alcohol with the onset of pain, flatulence).

Gradually the symptomatology expands. Joints increase in size, movements in them become painful. High body temperature is not corrected by prescribing antibiotics. Unpleasant sensations in the abdomen are localized mainly in the upper floor of the abdominal cavity and right upper quadrant.

There is jaundice of the skin and a sclera of the eyes. Skin color can take a variety of shades from yellow-green to bronze-brown. Urine takes the form of a rich dark beer. In this case, feces becomes the color of white clay or chalk.

Along with jaundice, there is a skin itch, which sometimes assumes an obsessive nature. Sometimes intradermally, on the eyelids you can see small yellow spots - xanthelasm. Fingers begin to resemble the contours of the drumsticks. The nail beds are full-blooded.

Fuzzy pains in the abdomen intensify simultaneously with an increase in its size. It becomes difficult for the patient to breathe. He suffocates in a horizontal position, and the lateral surfaces of the abdomen while sinking. When palpating the abdomen, a balloting fluid is determined, indicating the presence of ascites (effusion in the abdominal cavity of non-inflammatory genesis).

Similarly, when you feel your abdomen, you determine an increase in the normal boundaries of the liver with the bulging of the lower edge from under the edge arch. With coarse-nodular cirrhosis, on the contrary, one can note a decrease in liver size.

The hairline in the genital area and underarms thinning.

Drastically reduced sexual desire. In men, the erection weakens and breast size (gynecomastia) increases in size. In women, there are irregularities in the menstrual cycle of various types.

The patient decreases the total muscle mass with a decrease in the tone and strength of the remaining. Children with developed cirrhosis lag behind in sexual and physical development.

The so-called "hepatic signs" begin to be defined:

  • Redness of palmar surface of hands.
  • The manifestation in the superficial sections of the skin of the upper third of the trunk, the contours of small capillaries of red color. They intertwine and resemble small spiders. They are also called "vascular asterisks". Characteristically, when pressing on them, they disappear and appear again after weaning the finger.
  • The tongue takes on a bright scarlet, crimson color and becomes smooth. It is also called "lacquer" in such cases.

Because of the violation of the coagulating system of blood, there are signs of hemorrhagic syndrome. In the initial stages, it manifests itself in the form of a large number of bruises on the body for no particular reason, with the usual effects before, for example, from the elasticity of panties or from a tight bra. With light cuts, the blood stops later than usual. Then there are prolonged nasal and hemorrhoidal bleedings. When vomiting, in the vomit, you can see blood.

Because of the arising difficulties of the blood flow through the liver, the manifestations of the syndrome of portal hypertension, including:

  1. Presence of free fluid in the abdominal cavity (ascites).
  2. Expansion of the submucosal veins of the rectum with the formation of hemorrhoids in its absence earlier.
  3. Increase of the lumen of submucosal veins in the lower third of the esophagus with the formation of plexuses.
  4. Varicose expansion of the subcutaneous veins of the lower extremities with the growth of edema in the subcutaneous tissue.
  5. A significant increase in the spleen in size, which is manifested by pain in the left hypochondrium. In addition, non-palpable earlier, it begins to feel and sometimes you can see its contours in this area of ​​the abdomen.
  6. The appearance of varicose veins on the anterior surface of the abdomen, mostly in the near-bulbous region. Woven together, the appearance of the expanded contours of the veins may resemble the head of the legendary jellyfish Gorgona. Sometimes you can listen to venous noise, especially around the navel - a symptom of Cruewell - Baumgarten. Most of this is observed when the umbilical vein is not enlarged.

Jaundice, accompanied by an increase in signs of portal hypertension, indicates that cirrhosis in its development has passed into the stage of decompensation and all the resources of the remaining individual able-bodied hepatocytes have been exhausted.

It is at this stage of the disease that complications arise that serve as the direct cause of death.

Complications of liver cirrhosis

1. Spontaneous ascites-peritonitis. The most frequent explanation of its development is the theory of "sweating" of intestinal flora, located in the lumen of the intestine with the fall of general immunity, so characteristic for cirrhosis of the liver. Thus, there is a seeding of sterile until this time ascites and there is a symptomatology of the "acute abdomen", sharply increasing intoxication. Sometimes the symptoms can be erased or even smoothed.

2. Bleeding. Due to general bleeding and increasing pressure in the portal system, spontaneous recurrent internal bleeding can occur in the area of ​​the liver gates.

More often there are bleedings from varicose-dilated veins of the esophagus, taking the character of massive hemorrhage. Clinically, the patient feels a sharp weakness with a fainting condition, a chair of black, tarry-like color appears. At a nausea, in vomit masses it is possible to see blood from scarlet color, to a kind of "coffee grounds" in various variations and large quantities. In the absence of timely assistance, such cases end up lethal.

Less often, massive bleeding occurs from the hemorrhoidal veins of the rectum. In such cases, liquid blood can be seen in the stool and the general appearance of fecal matter will resemble raspberry jelly.

In the presence of chronic gastric and duodenal ulcers, bleeding from them during exacerbation can also lead to death.

Unsteady by the usual methods of nosebleeds, also can occur and become part of the general hemorrhagic syndrome.

3. The hepatic coma. This is the extreme degree of manifestation of hepatic encephalopathy, which develops due to massive intoxication due to liver failure. Early signs of encephalopathy are part of the symptomatology of asthenic syndrome and are manifested by changes in the psyche and behavioral reactions to the surrounding. In the future, with the addition of renal failure (the kidneys also do not cope with the detoxification function), neurological symptoms increase, the patient becomes more "deafened", slower. The poisoning of brain cells with toxins reaches such an extent that they can not perform their functions. Deep and prolonged loss of consciousness, with violation of the main groups of reflexes, becomes a manifestation of the onset of the hepatic coma, which, through edema of the brain with compression of vital centers, causes death.

4. Infectious complications. Along with the previously described ascites-peritonitis, due to a reduced immune response to infectious agents, patients with cirrhosis of the liver are more likely to undergo inflammatory processes. This is manifested pneumonia, urinary tract infections. Moreover, the diseases are protracted, they tend to spread to neighboring organs and throughout the body with the help of blood flow. Often lead to sepsis followed by death.

5. Development of hepatocellular cancer (liver cancer-cirrhosis).

6. Portal vein thrombosis.

Laboratory and instrumental methods of diagnosing the disease

1. General blood test:

  • anemia (reduction of erythrocytes and hemoglobin),
  • лейкопения (при присоединении бактериальной инфекции и при активности заболевания возможно увеличение лейкоцитов),
  • тромбоцитопения (дополнительно может указывать на увеличение в размерах селезёнки),
  • повышение СОЭ.

2. Общий анализ мочи:

  • высокий белок (протеинурия),
  • цилиндрурия,
  • микрогематурия (эритроциты в моче),
  • bilirubin and urobilin are detected.

3. Biochemical blood test:

  • increased activity of ALT and AST, alkaline phosphatase,
  • decrease in the level of total protein and albumin in the blood,
  • high content of copper, iron,
  • decrease in potassium concentration,
  • decrease in urea, cholesterol,
  • high rates of thymol test while reducing the sulemic,
  • increase bilirubin.

4. Coagulogram indicates a decrease in blood clotting (a decrease in the prothrombin index).

5. Additionally, a study is made on the markers of viral and autoimmune hepatitis to determine the cause of cirrhosis.

6. Radiation diagnosis of cirrhosis with ultrasound, X-ray methods (CT and MRI).

7. Radionuclide methods (colloidal sulfur, labeled with technetium 99mTc) is used - scintigraphy. With its help, the degree of decrease in liver function is assessed, and the amount of damage assessed.

8. Puncture biopsy of the liver under the supervision of ultrasound or in laparoscopic surgery. Allows to determine in some cases the cause, however, the main purpose of this is to assess sclerotic changes in the structure of the organ tissue for a possible prognosis of the disease. In addition, biopsy is the main method of differential diagnosis of liver cancer and cirrhosis.

9. Endoscopic research methods serve to assess the severity of portal hypertension in the state of submucosal veins in the lower third of the esophagus.

10. Study of feces for latent blood for the detection of gastrointestinal bleeding.

11. It is also necessary to monitor the blood levels of creatinine, electrolytes for the timely determination of the onset of renal insufficiency.

12. Determination of alpha-fetoprotein in the blood, the presence of which allows you to suspect the transition of liver cirrhosis to cancer.

13. Immunogram in the active phase of liver cirrhosis: a decrease in the activity and amount of T-lymphocytes-suppressors, high levels of immunoglobulins, increased sensitivity of T-lymphocytes to liver specific lipoprotein.

Prognosis of the disease

If there are complications (the phase of decompensation), after three years, only 11-40% of patients remain alive.

In other cases, with strict compliance with the diet and medical treatment, it is possible to reach the sick and elderly.

A large spread in the assessment of the severity of cirrhosis, in this regard, received the Child-Rugh scale.

Indicators Points
1 2 3
Ascites No Soft, easy to treat Tense, poorly treatable
Encephalopathy No Light (I-II) Heavy (III-IV)
Bilirubinmkmol / l (mg%) less than 34 (2.0) 34-51 (2.0-3.0) more than 51 (3.0)
Albumin, g more than 35 28-35 less than 28
Prothrombin time, (sec) or prothrombin index (%) 1-4 (more than 60) 4-6 (40-60) more than 6 (less than 40)

The degree of severity of cirrhosis is set by the sum of the scores of all parameters.

5-6 points corresponds to class A.

7-9 - Class B.

With a score of 10-15, class C is set.

Class A - indicates the presence of compensated cirrhosis.

Class B and C - refer to decompensated cirrhosis.

Seven-year boundary in the detection of cirrhosis in the compensated (A) stage reaches half the patients. The further forecast is individual and depends on various factors.

In addition, in the stage of decompensation, with the development of complications, another evaluation system is used - SAPS (Simplified Acute Physiology Score).

Evaluation criteria in this system are more diverse: patient age, pulse and respiratory movements per minute, systolic blood pressure, body temperature, hematocrit, blood leukocytes, urea, potassium, sodium, and plasma bicarbonate, diuresis, and the stage of the hepatic coma.

Treatment of cirrhosis of the liver

Until recently, the diagnosis of "cirrhosis" implied the imposition of the death penalty on the patient.

However, with the development of transplantology, liver transplant operations have already become routine in some countries. Absolute indications for liver transplantation were cryptogenic cirrhosis and cirrhosis in the early stages. After organ transplant, more than 80% of patients live a five-year period and continue to live on.

Great hopes are placed on the development of genetic engineering and stem cell therapy. Developments in this area are already underway.

The basis of therapeutic treatment lies in the strict observance of diet, the limitation of mental and physical loads, and the use of medicines only on indications. It is necessary to exclude vaccination. It is necessary to limit the effect of extremes of temperature in any direction, staying under direct sunlight. It is unacceptable to starve and use doubtful methods of traditional medicine.

Fundamentals of diet therapy for liver cirrhosis :

  1. Excluded from the diet are alcohol, salt, mineral waters containing sodium, baking soda (cakes, biscuit biscuits, cakes, pastries and plain bread), products containing preservatives (pickles, ham, bacon, corned beef, fish and canned meat, canned sauces), mayonnaise, all kinds of cheeses, oysters, mussels, ice cream, sausage.
  2. Refusal of fried and fatty foods.
  3. When making food, only natural seasonings are allowed.
  4. Used meat and fish should be low-fat varieties and only in boiled or stewed. The daily dose of meat products should not exceed 100 gr. and evenly distributed throughout the day. Excess of meat in a negative way affects the patient's well-being. With the appearance of signs of encephalopathy, the use of protein per day should generally be limited to forty grams.
  5. You can eat eggs (interchangeability: one egg corresponds to 50 grams of meat).
  6. Daily consumption of milk should not exceed more than one glass a day. You can use sour cream.
  7. It is necessary to spend unloading days, during which protein food is not included in the diet. These days, by the predominance of products used, can be called "watermelon" or "cucumber".
  8. You can eat boiled rice. Of course, without salt.
  9. Limit butter, but widely used vegetable.
  10. Vegetables and fruits are used fresh. Additional heat treatment is allowed shortly before meals.
  11. In the presence of edema, fluid intake is limited to 1-1.5 liters per day.

Observance of these principles will help to delay the onset of decompensation in some cases for an indefinitely long time.

The use of drugs should be aimed at preventing possible complications.

In addition, drug treatment of major diseases that lead to cirrhosis, leads to a significant decrease in the activity of the process. For example - interferon therapy in the presence of viral hepatitis or the use of glucocorticoids in autoimmune hepatitis.

Widespread use is found in surgical treatment aimed at restoring choleretic output in secondary biliary cirrhosis. Therefore, the search for the cause of cirrhosis is so important.

It is necessary to avoid, especially with decompensation, the use of non-steroidal anti-inflammatory drugs (aspirin, ibuprofen), as a possible cause of bleeding and kidney failure.

Treatment of pathological manifestations and complications in cirrhosis means by itself :

  1. Decrease in ascites conservative (diuretic drugs according to the scheme) and surgical (drainage through drains) by methods.
  2. Removing manifestations of portal hypertension - from the use of non-selective beta-blockers (propranolol, nadolol) to the ligation of the dilated veins during surgery.
  3. Treatment of encephalopathy (nootropics, sorbents).
  4. Treatment of dyspepsia with the help of nutrition correction and the use of enzyme preparations without bile acids (pancreatin). Perhaps in such cases and the use of eubiotics - baktisubtil, enterol, bifidumbacterin and lactobacterin.
  5. Preventive antibiotic therapy for the prevention of infectious complications with planned visits to the dentist, before instrumental manipulation.
  6. The use of preparations containing zinc for the prevention of convulsions in the usual muscular load and in the complex treatment of hepatic insufficiency is shown to reduce hyperammonemia.
  7. To remove itching, antihistamines are used, as well as preparations containing ursodeoxycholic acid.
  8. The appointment of androgens to men with severe manifestations of hypogonadism and the correction of the hormonal background of women for the prevention of dysfunctional uterine bleeding - under the control of the endocrinologist.
  9. Prevention of osteoporosis in patients with chronic cholestasis and primary biliary cirrhosis, in the presence of autoimmune hepatitis with the intake of corticosteroids. For this, calcium is added in addition to vitamin D.
  10. In the presence of single foci of degeneration in the hepatocellular carcinoma and the severity of the disease of class A, the patients are shown surgical removal of the affected segments of the liver. In the clinical class of disease B and C and massive lesion, in anticipation of transplantation, antitumor treatment is prescribed to prevent progression. For this purpose, both the effects of currents and temperatures (percutaneous radiofrequency thermal ablation) and chemotherapy are used by targeting oily solutions of cytostatics to vessels feeding the corresponding segments of the liver (chemoembolization).
  11. Surgical correction of portal hypertension for the prevention of gastrointestinal bleeding, includes the imposition of vascular anastomoses (mesenteric and splenorenal) as well as sclerotherapy of the existing dilated veins.

The treatment for such a severe and severe fatal complication as acute massive bleeding from the esophagus veins includes:

  1. The local application of the Blackmore probe, by means of which an air cuff that swells in the lumen of the esophagus, squeezes the dilated bleeding veins.
  2. Aiming the esophageal wall with sclerosing substances.
  3. Blood substitution therapy.

Unfortunately, this condition and becomes the main cause of death of patients with cirrhosis of the liver.

Prevention of liver cirrhosis is the timely detection and full treatment of diseases that lead to cirrhosis. In addition, it is necessary to eliminate the effects of harmful factors that have a negative effect on liver cells.


| 18 March 2014 | | 5 839 | Uncategorized
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