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An irreversible change in the structural organization of the liver as a result of chronic diseases, with a persistent violation of its functions, an increase in pressure in the portal vein system is called liver cirrhosis.
The disease is widespread and ranks sixth as the cause of death in the 35-60 age group, with about 30 cases per 100,000 population per year. Of particular concern is the fact that the incidence of the disease has increased by 12% over the past 10 years. Men get sick three times more often. The main peak of incidence occurs after forty years.
The liver is the largest digestive and endocrine gland in the body.
The most important functions of the liver:
Neutralization and utilization of harmful substances entering the body from the external environment and formed in the process of life.
Construction of proteins, fats and carbohydrates used for the formation of new tissues and replacement of exhausted cells.
The formation of bile involved in the processing and splitting of food masses.
Regulation of the rheological properties of blood by synthesizing some of the coagulation factors in it.
Maintaining the balance of protein, carbohydrate and fat metabolism by synthesizing albumin, creating additional reserves (glycogen).
Liver structure
The structural unit of the liver is a lobule (acinus), consisting of several cells (hepatocytes). They are combined into a kind of hexagonal cylinder.
In the center of the acinus is the hepatic (central) venule, and in the corners of the putative hexahedron, between the hepatocytes, there are portal tracts.
Portal tracts consist of:
Hepatic artery. It carries fresh, oxygen-rich blood for the vital functions of the liver from the branches of the aorta.
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 intestines. This blood is saturated with substances assimilated from food. Some of them, without preliminary processing in the liver itself, can cause irreparable harm to the body.
Bile capillaries. They collect enzymes secreted by hepatocytes necessary for digestion, thereby forming bile. Bile capillaries, merging into large bile ducts, depositing part of the secretion formed in the gallbladder, subsequently, through the common bile duct, exit into the lumen of the duodenum, where bile is mixed with food.
Nerve trunks.
Lymphatic vessels.
In accordance with the available data on blood supply, the generality of branching of the bile ducts and innervation, eight segments are distinguished in the liver. This is important when conducting operations on this body. The segments form the right and left lobes of the liver. The conditional border of the lobes passes through the gate of the liver to the place of confluence of the hepatic veins into the inferior cavity.
It is with a violation of the structure of the hepatic lobule that an irreversible chain of structural changes in the liver begins, leading, in the end, to the death of a person.
Processes occurring during the development of liver cirrhosis:
Death for various reasons of a certain number of hepatocytes.
The formation of connective tissue in their place, squeezing and disrupting the normal blood flow in the portal tracts, the central vein. The formed connective tissue also disrupts the formation and outflow of bile through the bile capillaries. As a result, part of the bile necessary for the digestion of food is absorbed directly into the bloodstream, causing intoxication of the body and manifestations of jaundice.
Reconstruction of the vascular system that fed the dead hepatic acinus, with the formation of new communications (anastomoses).
Proliferation of the bile ducts.
Division of the remaining hepatocytes with the formation of regenerated nodes. However, the functional incapacity of these nodes does not allow normal liver tissue to appear as a result.
Some of the regenerated nodes, due to their unrestrained growth, depleted blood supply and squeezing from the sides by the formed connective tissue, die. This causes stimulation of new cicatricial processes leading to thickening of the liver and a decrease in the already limited number of hepatocytes functioning by that time.
The described processes proceed diffusely, continuously, throughout the liver, not limited to one segment or lobe. The time span can stretch over months or even years. A disruption of the genomic apparatus of hepatocytes also gradually occurs. With minimal genetic changes, autoimmune mechanisms are involved in the process, which activates the rate of inflammatory-sclerotic changes occurring. With the greatest genetic abnormalities, a malignant neoplasm of the liver, the so-called "cirrhosis-cancer", begins to form.
As the volume of the affected liver tissue grows, a qualitative shift occurs in the dysfunction of the liver.
Reasons for the development of liver cirrhosis
Chronic alcohol intoxication. On average, cirrhosis develops 10-15 years after the onset of abuse. Moreover, the required daily dose of absolute alcohol consumption, calculated as 96% alcohol, for a woman is three times less than for a man and is 20 grams per day.
Viral hepatitis B, C and D.
Various autoimmune diseases with the initial development of hepatitis.
Diseases of the biliary tract (secondary biliary cirrhosis of the liver).
Mechanical blockage of the extrahepatic and intrahepatic biliary tract due to the formation of gallstones. For the development of cirrhosis, it is enough to have a violation of the passage of bile from 3 to 18 months.
Primary sclerosing cholangitis. A very rare disease, usually associated with the presence of ulcerative colitis. In this case, infection of the bile ducts occurs. The inflammatory process spreads to the nearby liver tissue, it is damaged with further
the development of cirrhosis.
Intoxication with hepatotoxic chemical (carbon tetrachloride, imethylnitrosamine, chloroform, benzene, nitro- and amino compounds, mercury, gold and lead) and drugs (anti-tuberculosis and anticancer drugs, anabolic steroids, etc.).
Vegetable poisons: mushroom (phalloidin, phalloin, beta-amanitin) and grain (aflatoxins), formed in overwintered cereals, corn, rice. These substances cause acute toxic liver dystrophy with massive tissue necrosis. Instead, cirrhosis is formed in the future.
Genetically determined metabolic disorders (hepatolenticular degeneration, Wilson-Konovalov disease, hepatocerebral dystrophy, galactosemia, glycogenosis, cystic fibrosis, hemochromatosis, α1-antitrypsin deficiency).
Decreased blood flow through the portal vein with phlebothrombosis, external compression (chronic pancreatitis, pancreatic tumors).
Long-term venous congestion of the liver in chronic cardiovascular diseases (constrictive pericarditis, veno-occlusive disease, heart failure).
Primary biliary cirrhosis for no apparent reason. It occurs mainly in women in menopause.
Cryptogenic cirrhosis. The cause of its occurrence remained unidentified. It is characterized by an extremely aggressive continuous flow. It is an absolute indication for liver transplantation.
Congenital absence of bile ducts in infants.
Randu-Osler disease. This disease is otherwise known as hereditary hemorrhagic telangiectasia. The disease is rare and is caused by congenital underdevelopment and dysfunction of the intrahepatic vascular system of the liver.
Fatty degeneration of the liver in the presence of metabolic disorders (obesity, diabetes mellitus).
Parasitic and infectious liver diseases (echinococcosis, brucellosis, opisthorchiasis, toxoplasmosis, ascariasis, etc.).
The cause of congenital cirrhosis of the liver in newborns can also be a viral infection developed in the mother during pregnancy (cytomegaly, herpes infection, rubella). The ability of these viruses to penetrate the placental barrier and damage the liver becomes here the main mechanism for the onset of cirrhosis in an infant. Developed serum hepatitis during immunization of a pregnant woman can also cause this pathology in a newborn child. Liver lesions in newborns were also noted in the presence of such diseases as syphilis, toxoplasmosis, listeriosis in mothers.
After bypass surgery on the gastrointestinal tract.
It should be noted separately that more than half of those with liver cirrhosis have polyfactorial reasons for its occurrence. The most common combination is an excessive passion for alcohol and the presence of chronic hepatitis.
Symptoms of liver cirrhosis
In cases where liver cirrhosis develops gradually, without a clear connection with any intoxication or exposure to an aggressive factor, the disease can carry latent clinical symptoms, manifesting itself for the first time at 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, the following groups of symptoms can be distinguished, which are combined into syndromes.
Asthenic syndrome (decreased appetite, high fatigue, general weakness, weight loss, episodes of short-term small rises in body temperature, difficulty concentrating, daytime sleepiness with disturbed night sleep, irritability, tearfulness, sensitivity and picky, suspiciousness to others, hysterical reactions).
Dyspeptic syndrome (nausea, vomiting, residual bitterness in the mouth, belching, feeling of heaviness in the abdomen when eating fatty foods and alcohol with pain, flatulence).
Gradually, the symptomatology expands. The joints increase in size, movements in them become painful. High body temperature is not corrected by antibiotics. Unpleasant sensations in the abdomen are localized already mainly in the upper floor of the abdominal cavity and the right hypochondrium.
Jaundice of the skin and sclera of the eyes appears. Skin color can take on various shades from yellow-green to bronze-brown. The urine takes on the appearance of a rich, dark beer. At the same time, the feces become the color of white clay or chalk.
Along with jaundice, itching appears, sometimes taking on an obsessive character. Sometimes intradermally, on the eyelids of the eyes, you can see small yellow spots - xanthelasma. The fingers begin to resemble drumsticks along the contours. The nail beds are full-blooded.
Vague pains in the abdomen increase simultaneously with its increase in size. It becomes difficult for the patient to breathe. He suffocates in a horizontal position, and the lateral surfaces of the abdomen sink in at the same time. On palpation of the abdomen, a balancing fluid is determined, indicating the presence of ascites (an effusion in the abdominal cavity of non-inflammatory genesis).
Also, when palpating the abdomen, an increase in the normal borders of the liver with protrusion of the lower edge from under the costal arch is determined. In case of large nodular cirrhosis, on the contrary, a decrease in liver size can be noted.
The hairline in the genital area and armpits is thinning.
Sex drive sharply decreases. In men, erection weakens and the mammary glands increase in size (gynecomastia). In women, menstrual irregularities of various types are observed.
The patient's total muscle mass decreases with a decrease in tone and strength remaining. Children with advanced cirrhosis lag behind in sexual and physical development.
The so-called "liver signs" begin to be determined:
Redness of the palmar surfaces of the hands.
The appearance in the superficial parts of the skin of the upper third of the body, the contours of small red capillaries. They intertwine and resemble small spiders. They are also called "spider veins". It is characteristic that when pressed on them, they disappear and reappear after the finger is removed.
The tongue takes on a bright scarlet, crimson color and becomes smooth. It is also called in such cases "lacquer".
Due to a violation of the blood coagulation system, signs of hemorrhagic syndrome appear. In the initial stages, it manifests itself in the form of a large number of bruises on the body for no specific reason, with previously usual influences, such as from an elastic band of panties or from a tight bra. With minor cuts, the blood stops later than usual. Then there are prolonged nose and hemorrhoidal bleeding. When vomiting, blood can be seen in the vomit.
Due to the arising difficulties in blood flow through the liver, manifestations of portal hypertension syndrome are increasing, including:
Free fluid in the abdomen (ascites).
Expansion of the submucosal veins of the rectum with the formation of hemorrhoids in the absence of it earlier.
An increase in the lumen of the submucosal veins in the lower third of the esophagus with the formation of plexuses.
Varicose expansion of the saphenous veins of the lower extremities with an increase in edema in the subcutaneous tissue.
A significant increase in the size of the spleen, which is manifested by pain in the left hypochondrium. In addition, previously unpalpable, it begins to be felt and sometimes you can see its contours in this area of the abdomen.
The appearance of varicose veins on the anterior surface of the abdomen, mostly in the umbilical region. Intertwining with each other, the appearance of the enlarged contours of the veins can resemble the appearance of the head of the legendary Gorgon Medusa. Sometimes you can listen to a venous murmur, especially near the navel - a symptom of Cruvellier-Baumgarten. For the most part, this is observed when the umbilical vein is not closed.
Jaundice, accompanied by an increase in signs of portal hypertension, indicates that liver cirrhosis in its development has passed into the stage of decompensation and all the resources of the remaining single able-bodied hepatocytes are exhausted.
It is at this stage of the disease that complications appear that serve as the direct cause of death.
Complications of liver cirrhosis
1. Spontaneous ascites-peritonitis. The most frequent explanation for its development is the theory of "sweating" of the intestinal flora, located in the intestinal lumen when the general immunity falls, so characteristic of cirrhosis of the liver. Thus, there is a seeding of ascites, which was sterile until this time, and symptoms of an "acute abdomen" appear, and intoxication sharply increases. Sometimes the symptoms can be erased or even smoothed out.
2. Bleeding. Due to general bleeding and increased pressure in the portal system, spontaneous recurrent internal bleeding may occur in the area of the hepatic hilum.
More often there are bleeding from varicose veins of the esophagus, taking on the character of massive blood loss. Clinically, the patient feels a sharp weakness with a fainting state, a black, tar-like stool appears. With nausea, in the vomit, you can see blood from scarlet color to the type of "coffee grounds" in various variations and large quantities. In the absence of timely assistance, such cases are fatal.
Less commonly, 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 the feces will resemble raspberry jelly.
In the presence of chronic gastric and duodenal ulcers, bleeding from them during exacerbation can also lead to death.
Nosebleeds that do not stop by conventional methods can also occur and become part of the general hemorrhagic syndrome.
3. Hepatic coma. This is an extreme degree of manifestation of hepatic encephalopathy, which develops due to massive intoxication caused by hepatic failure. Early signs of encephalopathy are included in the symptoms of asthenic syndrome and are manifested by changes in the psyche and behavioral reactions to the environment. Later, with the addition of renal failure (the kidneys also can no longer cope with the detoxification function), the neurological symptoms increase, the patient becomes more "stunned", slower. Poisoning of brain cells with toxins reaches such a degree that they cannot perform their functions. Deep and prolonged loss of consciousness, with a violation of the main groups of reflexes - becomes a manifestation of the onset of hepatic coma,
4. Infectious complications. Along with the previously described ascites-peritonitis, due to a reduced immune response to infectious agents, patients with liver cirrhosis are more often prone to inflammatory processes. This is manifested by pneumonia, urinary tract infections. Moreover, the diseases are protracted, tend to spread to neighboring organs and throughout the body with the help of blood flow. Often lead to sepsis with subsequent death.
5. Development of hepatocellular cancer (liver cirrhosis cancer).
6. Portal vein thrombosis.
Laboratory and instrumental methods for diagnosing the disease
1. Complete blood count:
anemia (decrease in red blood cells and hemoglobin),
leukopenia (with the addition of a bacterial infection and with the activity of the disease, an increase in leukocytes is possible),
thrombocytopenia (may additionally indicate an increase in the size of the spleen),
increased ESR.
2. General urine analysis:
high protein (proteinuria),
cylindruria,
microhematuria (red blood cells in the urine),
revealed bilirubin and urobilin.
3. Biochemical blood test:
increased activity of ALT and AST, alkaline phosphatase,
a decrease in the level of total protein and albumin in the blood,
high content of copper, iron,
lowering the concentration of potassium,
lowering urea, cholesterol,
high rates of thymol test with a simultaneous decrease in sublimate,
increased bilirubin.
4. A coagulogram indicates a decrease in blood clotting (a decrease in the prothrombin index).
5. Additionally, a study is made for markers of viral and autoimmune hepatitis to determine the cause of cirrhosis.
6. Radiation diagnosis of cirrhosis using 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, to assess the extent of the lesion.
8. Puncture liver biopsy under ultrasound control or during laparoscopic surgery. Allows you to determine in some cases the cause, however, the main purpose of its implementation is to assess sclerotic changes in the structure of organ tissue for a possible prognosis of the disease. In addition, biopsy is the main method for the differential diagnosis of liver cancer and cirrhosis.
9. Endoscopic research methods are used to assess the severity of portal hypertension by the state of the submucosal veins of the lower third of the esophagus.
10. Study of feces for occult blood to detect gastrointestinal bleeding.
11. It is also necessary to monitor blood levels of creatinine, electrolytes for the timely determination of the onset of renal failure.
12. Determination of alpha-fetoprotein in the blood, the presence of which allows one to suspect the transition of liver cirrhosis to cancer.
13. Immunogram in the active phase of liver cirrhosis: a drop in the activity and number of suppressor T-lymphocytes, high levels of immunoglobulins, increased sensitivity of T-lymphocytes to hepatic specific lipoprotein.
Disease prognosis
When complications appear (decompensation phase), after three years, only 11-40% of patients remain alive.
In other cases, with strict adherence to the diet and drug treatment, it is possible for patients to reach old age.
In this regard, the Child-Pugh scale has become widespread in assessing the severity of cirrhosis.
The severity of cirrhosis is set according to the sum of points of all parameters.
5-6 points corresponds to class A.
7-9 - class B.
With a total of 10-15 points, class C is awarded.
Class A - indicates the presence of compensated cirrhosis.
Class B and C - refer to decompensated cirrhosis.
Half of the patients reach the seven-year milestone in the detection of cirrhosis in the compensated (A) stage. Further prognosis is individual and depends on various factors.
In addition, at the stage of decompensation, with the development of complications, another assessment system is used - SAPS (Simplified Acute Physiology Score).
Evaluation criteria in this system are more diverse: the patient's age, pulse and respiratory rate per minute, systolic blood pressure, body temperature, hematocrit, blood leukocytes, urea, potassium, sodium, and plasma bicarbonates, daily urine output, and the stage of hepatic coma.
Treatment of liver cirrhosis
Until some time, the establishment of the diagnosis of "cirrhosis of the liver" meant the imposition of the death sentence on the patient.
However, with the development of transplantation, liver transplant operations have become routine in some countries. Cryptogenic cirrhosis and early stage cirrhosis have become the absolute indications for liver transplantation. After organ transplant, more than 80% of patients live the five-year mark and continue to live on.
Great hopes are pinned on the development of genetic engineering and stem cell therapy. Development in this area is already underway.
The basis of therapeutic treatment lies in strict adherence to diet, limitation of mental and physical stress, and the use of drugs only when indicated. Vaccination must be excluded. Exposure to extreme temperature extremes in any direction, exposure to direct sunlight should be limited. Fasting and the use of dubious methods of traditional medicine are unacceptable.
The basics of diet therapy for liver cirrhosis :
Alcohol, salt, mineral waters containing sodium, baking soda (cakes, biscuits, cakes, pastries and ordinary bread), foods containing preservatives (pickles, ham, bacon, corned beef, canned fish and meat, can sauces) are excluded from the diet, mayonnaise, all kinds of cheeses, oysters, mussels, ice cream, sausage.
Avoiding fried and fatty foods.
When preparing food, only natural seasonings are allowed.
The meat and fish used should be of low-fat varieties and only boiled or stewed. The daily dose of meat products should not exceed 100 grams. and evenly distributed throughout the day. Excess meat negatively affects the patient's well-being. With the appearance of signs of encephalopathy, protein intake per day should generally be limited to forty grams.
You can eat eggs (interchangeability: one egg corresponds to 50 grams of meat).
Daily milk intake should not exceed more than one glass per day. The use of sour cream is possible.
It is necessary to carry out fasting days, during which protein food is not included in the diet. According to the prevalence of consumed products, these days can be called "watermelon" or "cucumber".
You can eat boiled rice. Without salt, of course.
Butter is limited, but vegetable oil is widely used.
Vegetables and fruits are consumed fresh. Additional heat treatment is allowed shortly before eating.
In the presence of edema, fluid intake is limited to 1-1.5 liters per day.
Compliance with these principles will help to postpone 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 the main diseases that led 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.
Surgical treatment aimed at restoring bile outflow in secondary biliary cirrhosis is widely used. Therefore, it is so important to find the cause of cirrhosis.
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 renal failure.
Treatment of pathological manifestations and complications of cirrhosis means :
Reduction of ascites by conservative (diuretic drugs according to the scheme) and surgical (removal of fluid through drains) methods.
Removal of manifestations of portal hypertension - from the use of non-selective beta-blockers (propranolol, nadolol) to ligation of dilated veins during surgery.
Treatment of encephalopathy (nootropics, sorbents).
Treatment of dyspepsia with nutritional correction and the use of enzyme preparations without bile acids (pancreatin). Perhaps in such cases, and the use of eubiotics - bactisubtil, enterol, bifidumbacterin and lactobacterin.
Preventive antibiotic therapy for the prevention of infectious complications during planned visits to the dentist, before instrumental manipulations.
Shown the use of preparations containing zinc for the prevention of seizures during normal muscle load and in the treatment of liver failure, to reduce hyperammonemia.
To relieve itching, use antihistamines, as well as drugs containing ursodeoxycholic acid.
The appointment of androgens to men with pronounced manifestations of hypogonadism and the correction of the hormonal background of women for the prevention of dysfunctional uterine bleeding - under the control of an endocrinologist.
Prevention of osteoporosis in patients with chronic cholestasis and primary biliary cirrhosis, in the presence of autoimmune hepatitis with the use of corticosteroids. For this, calcium is additionally introduced in combination with vitamin D.
In the presence of single foci of degeneration into hepatocellular carcinoma and the severity of the course of the disease of class A, patients are shown surgical removal of the affected liver segments. With the clinical class of the disease B and C and massive lesions, while awaiting transplantation, antineoplastic treatment is prescribed to prevent progression. For this, both the effect of currents and temperatures (percutaneous radiofrequency thermal ablation) and chemotherapy by targeted injection of oil solutions of cytostatics into the vessels feeding the corresponding segments of the liver (chemoembolization) are used.
Surgical correction of portal hypertension for the prevention of gastrointestinal bleeding, includes the imposition of vascular anastomoses (mesentericocaval and splenorenal) as well as sclerotherapy of existing dilated veins.
Treatment of such a formidable fatal complication that has developed as acute massive bleeding from the veins of the esophagus includes:
Local application of the Blackmore probe, with the help of which the air cuff swelling in the lumen of the esophagus, compresses the dilated bleeding veins.
Targeted chipping of the esophageal wall with sclerosing substances.
Blood replacement therapy.
Unfortunately, this condition becomes the main cause of death in patients with liver cirrhosis.
Prevention of liver cirrhosis consists in the timely detection and full treatment of diseases leading to cirrhosis. In addition, it is necessary to eliminate the impact of harmful factors that have a negative effect on liver cells.
