Alcoholic liver cirrhosis differential diagnosis. Liver cirrhosis diagnosis, diagnostic signs. Clinical manifestations of chronic hepatitis

By the word "hepatitis" an ordinary educated person living in a large city means inflammation of the liver caused by viruses. Most often, the cause is drug addiction, sexual contact, blood manipulation and other possible ways of infection. Sometimes they recall alcoholic liver disease, cirrhosis and other conditions that are united by common symptoms and principles of treatment.

General information

But it turns out that sometimes you don’t need to be at risk, use drugs, visit dubious nail salons and use alcohol substitutes to develop hepatitis. Sometimes it occurs without any connection with alcohol intake or with a viral infection. This disease is called autoimmune hepatitis.

For the first time, cases of incomprehensible liver damage began to be recorded since the early 1950s, mainly in young women. They suffered from chronic hepatitis, but at the same time, the level of gamma globulins in their blood was increased. A characteristic feature of this condition was a good response to the use of hormones.

Then, with the improvement of laboratory methods, it became clear that it often occurs in patients with SLE, or systemic lupus erythematosus, which occurs almost exclusively in women. Therefore, in the middle of our century, this disease was called "lupus hepatitis". Then came the era of intensive research on this disease. In the following decades, diagnostic criteria were developed and many drugs were tested. The greatest success was achieved in the treatment of this disease with corticosteroid hormones, as well as cytostatics - immunosuppressants. It can be considered that it is in the treatment of autoimmune hepatitis that hepatology has achieved significant success - it is with this pathology that the right treatment for the first time has led to a significant increase in life expectancy in patients.

Currently, this disease, despite careful study, remains largely mysterious.

But we can recall diseases such as diabetes mellitus and NUC (ulcerative colitis). Despite complete information and understanding of the mechanisms of pathogenesis, the world situation (especially in relation to the first one) is very far from favorable. What is this pathology from modern positions?

Definition

Currently, there is no single generally accepted definition of the disease. Therefore, the most correct, “combined” definition can be formulated as follows: autoimmune hepatitis is a chronic process of inflammation and necrosis in the liver that occurs for unknown reasons, with the circulation of a significant amount of autoantibodies to tissues in the blood, an increase in the level of gamma globulins, which responds well to treatment with immunosuppressants.

Etiology and epidemiology

This disease is simply “lost” against the background of a huge number of chronic viral hepatitis B and C, against the background of alcoholic liver damage. Even in the countries of the European Union, with a perfect level of diagnosis, the prevalence does not exceed two cases per 10 thousand people. Women are three times more likely to develop autoimmune hepatitis than men.

Perhaps this is due to the fact that women are generally more prone to the development of autoimmune pathology than men. Such "big" diseases as systemic scleroderma, systemic lupus erythematosus, rheumatoid arthritis are more common in women. After all, the childbearing function involves the bearing of an organism that is genetically different from the mother. This requires both a great intensity of the immune background, and its tolerance to someone else's (paternal) genetic material.

The chances of getting sick with autoimmune hepatitis are high in two periods of life: both in young (25 years) and in old (60 years) age, although recently these peaks have “flattened out”, and there is a tendency to increase the incidence, both in men and women. and in women at all stages of life.

Etiologically, there is no clear cause of the disease. Many researchers associate the appearance of autoimmune hepatitis with the environmental situation, stress, a chronic decrease in the body's immune defenses, and intoxication (alcohol and drugs). All this adversely affects the function of the immune system and liver.

About classification

Two variants of the development of hepatitis have been identified:

in the first type (occurs in 85% of all cases), patients have antinuclear antibodies and (or) antibodies to smooth muscles. Also, with this type of hepatitis, antibodies to neutrophils are found - this is typical for such a disease as primary sclerosing cholangitis (it is also referred to as connective tissue diseases). The antigen in this situation is a liver-specific protein;
the second type of hepatitis is characterized by the presence of antibodies to microsomes of the liver and kidneys. It is detected mainly in childhood, and in adults it manifests itself in only 20% of cases. A specific antigen for this form of the disease is one of the well-known liver cytochromes - the P 450 - 2 D enzyme. Often this type of disease, in addition to liver damage, is accompanied by the development of type 1 diabetes mellitus, or autoimmune thyroiditis.

How does the disease develop, and how does the autoimmune process lead to liver damage?

Pathogenesis

The basis for the development of a pathological immune response, which ultimately leads to the emergence of autoimmune hepatitis, is the so-called cross-antigenic reactivation, or molecular mimicry. This means that if at the time of "study" of T-lymphocytes in the thymus, some proteins of the body are not studied and recognized by them, then in the future they may encounter a foreign antigen similar to them. And in the future, having met the proteins of their body that fell on the surface of the membrane, similar to enemies, T-lymphocytes successfully organize an attack on them without recognizing their own.

In short, the scheme for the development of autoimmune hepatitis looks something like this:

Genetic predetermination (with hepatitis of the first type).

Associated with certain alleles of the HLA system, or major histocompatibility system. It is these genes that are responsible for a powerful immune response when antigens from the outside world enter.

As we said above, in this case we are talking about “deception” of the “friend or foe” system;

Launching a trigger mechanism (viral hepatitis, drug aggression, herpes infection);
Expression of "false" antigens on the surface of hepatocytes;
Activated lymphocytes (T and B), which respond to these decoys;
There is a production of gamma-globulins, or autoantibodies, a pool of inflammatory mediators (cytokines, metabolites of arachidonic acid) is formed;
Development of alteration (damage) of liver tissues;
The emergence of the clinic of autoimmune hepatitis.

Here is an extremely generalized scheme of the pathogenesis of autoimmune hepatitis. But in fact, as in other systemic diseases, the “key” to the development of the disease is the false acceptance of one’s own structures as foreign and the development of an immune response.

Clinical manifestations

How does autoimmune hepatitis manifest itself? Are there any differences in the course of this hepatitis, according to which it is possible to suspect the presence of immune inflammation of the liver?

Debut

In the initial period of the disease, there are two options for the development:

there are no differences from acute viral hepatitis with a typical picture of the disease.

There are typical clinical manifestations: jaundice, intoxication, laboratory symptom complexes of cytolysis and necrosis of liver tissues. There is weakness, loss of appetite, dark urine, discoloration of feces. ALT and AST (liver aminotransferases) increase tenfold or more. Then intense jaundice develops, skin itching appears (with cholestasis), and patients are usually hospitalized in an infectious diseases hospital with a diagnosis of acute viral hepatitis.

But, unlike viral hepatitis, there is no improvement, and the disease is progressive, and after 1-6 months, antibodies characteristic of the autoimmune process appear in the blood;

autoimmune hepatitis can begin in a different way: symptoms appear that are not associated with liver damage, but resemble various rheumatic diseases: lupus, myocarditis, rheumatism, rheumatoid arthritis.

Often, autoimmune hepatitis manifests with a pronounced articular syndrome: polyarthritis, vascular disorders occur, and a hemorrhagic rash may appear. These patients unsuccessfully go to the doctors: the treatment does not help them, and only after 4-6 months do symptoms such as icterus of the sclera appear, the liver and spleen increase in size.

Sometimes patients are observed for several months with a fever of unknown origin, with an increase in ESR, with diagnoses of thyrotoxicosis, suspected tuberculosis, and with a host of other diagnoses. Naturally, no treatment is carried out, or, on the contrary, they treat “everything” and “from everything”.

Expanded stage

At its height, autoimmune hepatitis is manifested by a variety of symptoms of liver damage:

fever (from 37 ° to 39 ° C), with an increase in ESR even up to 60 mmh and above;
arthralgia - pain in the joints (large in the arms and legs);
hemorrhagic hemorrhages in the skin, or recurrent purpura;
sometimes - psoriasis, symptoms of focal scleroderma;
endocrinopathy - amenorrhea, striae on the thighs and abdomen, hirsutism occurs;
jaundice interspersed, easing during remission and rising during exacerbation;
the liver enlarges and hardens.

Surprisingly, many patients with hepatitis, despite the pronounced manifestations, feel good.

In conclusion, the description of the symptoms must be said that autoimmune hepatitis "lays" the foundation for heart damage, the occurrence of glomerulonephritis, iridocyclitis, amenorrhea, lymphadenopathy, anemia, and many other syndromes.

Most patients with this liver disease have a continuous form of autoimmune hepatitis. Less often there is an alternation of exacerbations and remissions. With a continuously relapsing course, the prognosis is much worse.

Diagnostics

Given the similarity of autoimmune hepatitis and the multifaceted clinical picture, the absence of pathognomonic symptoms, it was decided by an international group to study this disease in 1999 to compile diagnostic criteria and a scoring table that helps to make a diagnosis.

The most characteristic for autoimmune hepatitis were the following criteria:

female;
high levels of gamma globulins;
titers of type-specific antibodies above 1:80;
negative blood test for viral hepatitis (PCR, ELISA);
a liver biopsy showed lobular hepatitis and bridging necrosis, a very characteristic finding.

In summary, it should be said that if the patient has:

the above clinic;
he was not given a blood transfusion;
he did not take drugs with a hepatotoxic effect;
did not abuse alcohol;
did not suffer from acute and chronic hepatitis of viral etiology;

and if at the same time he has a high level of gamma globulins, specific antibodies, and his ALT and AST significantly predominate over the level of alkaline phosphatase - this is “certain autoimmune hepatitis”.

Principles of treatment

Unlike viral liver diseases, in autoimmune hepatitis, the main tactics of treatment is the appointment of corticosteroid hormones. In this case, the main drug is prednisolone. It acts on T - lymphocytes, causing their suppression, and inhibits the cycle of their reactions. As a result, the process of inflammation and necrosis in the liver tissues slows down.

Despite the side effects of hormones, their effect is not to improve well-being (as mentioned above, patients feel good), but to actually prolong life. Therefore, with autoimmune hepatitis, you often have to put up with some of them.

Cytostatic drugs, such as azathioprine, are also used in the treatment. But there are cases when you can not prescribe these drugs, but observe the patient. This is possible with an asymptomatic course, with low rates of transaminases. On the other hand, in case of deep dysfunctions of the organ, in the presence of decompensated cirrhosis, anemia, ascites, portal hypertension, treatment is already too late.

Therefore, the absolute indications for the appointment of hormones and immunosuppressive therapy are a vivid clinical picture, the progression of symptoms, and the picture of bridging and (or) multilobular necrosis proven by a histological examination of a liver biopsy.

In the treatment, hormones are used both separately and in combination with azathioprine. Hormone intake should be long - sometimes from 6 months to six months, and some patients are shown lifelong therapy. The diagnosis we are talking about is so serious that there are no absolute contraindications to the appointment of hormones.

Even diabetes, gastric ulcer, and osteoporosis, which are considered absolute contraindications to corticosteroids in other cases, are relative here.

As for azathioprine, there are still absolute contraindications: a pronounced aplastic effect with inhibition of hematopoietic function, pregnancy, severe leukopenia or malignant neoplasms.

Usually, a noticeable improvement occurs already in the first weeks after prescribing the drugs, and the normalization of laboratory parameters by the end of the year in 75% of patients with correctly selected therapy. But this is true under the condition of a decrease in the level of transferases - ALT and AST in the peripheral blood. If they are not reduced, then there is no need to wait for remission. In general, treatment failures occur in every fifth case.

Forecast

Despite all the successes in the treatment of autoimmune hepatitis, the greatest number of deaths occurs in the early period of the disease, as the most active. If the patient is not diagnosed for a long time, and he does not receive treatment, then there is a chance to live the next five years in only 50% of patients.

Under favorable circumstances, with modern immunosuppressant treatment, there is an 85% chance that the patient will live 10 years.

But the total life expectancy of a patient with the occurrence of such a process in the liver does not exceed 15 years, in extreme cases - 20 years. Therefore, when a type 2 disease occurs in children, this diagnosis still sounds like a sentence. But times are changing. Now cirrhosis of the liver (the outcome of the process) is not a "ticket to the cemetery" without any alternative. Patients with autoimmune liver disease can be on the waiting list for a liver transplant for several years, and after transplantation, life expectancy is significantly extended.

In conclusion, we should express the hope that, due to the progress of nanotechnologies and cellular techniques, in the near future it will be possible to control the development of autoimmune reactions at the cellular level, and autoimmune damage to the liver, as well as other organs and systems, will not take us by surprise.

Ascites (otherwise dropsy of the abdomen) is the accumulation of an excessive amount of fluid in the abdominal cavity. This is not a disease, but an alarming symptom of many diseases. Ascites increases the risk of serious complications, including thrombosis, so this symptom should not be underestimated. The causes of ascites include diseases such as cirrhosis of the liver, kidney failure, tumors of the abdominal cavity, and others. The main symptoms of ascites are abdominal pain, an increase in abdominal circumference, and weight gain. Therapy consists in treating the underlying disease that is causing this symptom (in many cases, cirrhosis of the liver).

1Mechanism of ascites formation
2Etiology of the disease
3Degrees of disease
4Symptoms and diagnosis of pathology
5Therapeutic measures

1Mechanism of ascites formation

Ascites is an excess accumulation of fluid in the peritoneal cavity (physiologically, there is about 150 ml of fluid there). Ascites is observed if the patient has more than 500 ml of fluid in the abdominal cavity. As a rule, it is a serous fluid. It contains more than 3 g/dl of protein (mainly albumin), as well as sodium, potassium and glucose in the same concentrations as in serum. The presence of neutrophils in the fluid may indicate an existing infection. And the presence of red blood cells suggests the distribution of the tumor process in the abdominal cavity.

2Etiology of the disease

The main causes of ascites include:

increase in venous pressure in the vena cava;
obstructed outflow of blood from the liver (for example, cirrhosis of the liver);
obstructed outflow of lymph;
an increase in the permeability of the vessels of the peritoneum (for example, inflammatory processes of various origins);
decrease in plasma oncotic pressure (eg, nephrotic syndrome).

The most common diseases that cause dropsy of the abdomen:

cirrhosis of the liver;
tuberculosis;
congestive circulatory failure;
inflammation of the pancreas;
portal vein thrombosis;
kidney failure;
malignant tumors located in the abdominal cavity and in the pelvic cavity.

Ascites is characterized by the following symptoms: an increase in the circumference of the abdomen, an increase in body weight, abdominal pain, a feeling of discomfort and expulsion outward in the abdominal cavity. Later symptoms are problems with sitting and walking, disorders of the gastrointestinal tract, swelling of the legs and vulva.

3Degrees of disease

Due to the volume of fluid collected in the peritoneal cavity, ascites can be divided into:

soft (I degree);
moderate (II degree);
severe (III degree).

With mild ascites, diagnosis is possible only with the help of ultrasound.

The diagnosis of "moderate ascites" is made when the volume of fluid collected in the peritoneal cavity exceeds 500 ml. The belly looks like the belly of a frog. You can feel the moving fluid in the abdominal cavity. To recognize ascites, the doctor may tap on the patient's abdomen when he lies on one side, then on the other side. Then you can observe the moving fluid in the peritoneum of the patient when changing his position.

Severe ascites gives the characteristic appearance of a standing patient: a large belly and thin limbs. The patient's abdomen is greatly enlarged and dense. The navel is flattened, but an umbilical hernia may occur (more clearly visible during coughing). Blood vessels can show through the skin on the abdomen. These vessels diverge from the navel to the sides. The skin on the abdomen is thin and shiny.

4Symptoms and diagnosis of pathology

As a rule, the first symptom that is observed in patients is the tightness of habitual clothing and the need to loosen the belt. In addition, there is often a feeling of fullness, bloating, or discomfort, nausea, and (less commonly) pain.

If the volume of the collected fluid exceeds 1.5 liters (in very advanced cases), it can reach a feeling of suffocation. Long-lasting dropsy of the abdomen can lead to the development of pleural exudate (hydrothorax), i.e. collection of water in the pleural cavity, which surrounds the lungs. More often it has a right-hand drive than a left-hand drive. Pleural exudate is caused by the flow of fluid from the abdominal cavity into the pleural cavity by lymphatic vessels that pass through the diaphragm.

Ascites is difficult to recognize in an obese patient. The disease must always be differentiated from pregnancy, bladder enlargement, ovarian cancer, which can produce similar symptoms.

To diagnose ascites, the doctor prescribes a blood test, a study of liver enzymes. As a rule, samples of fluid accumulated behind the peritoneum are used to study its composition. An ultrasound is often done before a fluid sample is taken to help assess the size and shape of organs in the abdomen. An alternative to ultrasound is computed tomography. Imaging is of particular importance, especially if the patient is obese or the amount of fluid collected in the peritoneal cavity is small.

Sometimes additional studies are needed, for example, cytopathology. To distinguish ascites caused by hypertension from ascites due to other causes, a diagnosis of fluid taken by means of a puncture of the abdominal cavity (paracentesis) is carried out. Removal of fluid is also carried out for medicinal purposes. It is used at the beginning of the treatment of advanced stage ascites or in the case of ascites resistant to diuretic treatment.

Indications for paracentesis:

recently diagnosed;
in order to differentiate ascites from inflammation of the peritoneum.

The course of the procedure:

during the procedure, the patient is in a reclining position (the body is raised);
the doctor performs the puncture with a needle, the length of which depends on the thickness of the patient's adipose tissue;
the puncture is carried out in a place where the presence of fluid is noted (as a rule, this is a place in the navel area);
for the first time, a fluid volume of 50-100 ml is taken, which is then analyzed.

A sample of the liquid is tested for protein concentration, for the presence of possible bacteria. The appearance of the fluid may suggest the cause of the ascites. Straw-colored fluid occurs with cirrhosis of the liver (although it may be bilious or clear), also with heart failure or nephrotic syndrome (although in this case it may be milky). Purulent and turbid liquid occurs with purulent inflammation of the peritoneum. And with neoplasms, diseases of the pancreas and tuberculosis, the appearance of the liquid is varied (it can be a hemorrhagic, milky liquid, and in the case of tuberculosis, even transparent).

5Therapeutic measures

Ascites is a symptom of various diseases. In 80% of cases, it accompanies cirrhosis of the liver. In about 10% of cases, it is a sign of malignancy. May also occur with heart failure, tuberculosis, nephrotic syndrome, or AIDS. Approximately 5% of patients have at least two causes of ascites.

Treatment of ascites is mainly in the treatment of the underlying disease, which caused it.

Diuretics (spironolactone, furosemide) are used to reduce the fluid content in the peritoneal cavity. Patients should reduce fluid and sodium intake in their diet.

If treatment with diuretics does not bring the desired results, other methods are used to remove excess fluid from the body, including the previously mentioned drainage with a special needle. This type of treatment is used in patients with an acute form of the disease. If the disease is associated with a serious liver condition, liver transplantation is considered.

In a small number of patients who experience relapses, valves are a treatment option. There are several types of them, but none of them prolong the lives of patients and, in general, they are the first step towards a liver transplant.

Bleeding from the esophagus is a serious problem requiring urgent medical attention. help. Severe bleeding if left untreated can be fatal. Small and moderate develops chronic blood loss, leading to a breakdown and complication of the underlying disease.

Causes of the disease

The causes of esophageal bleeding can be many factors, the most common include:

stomach ulcer;
cirrhosis of the liver;
gastritis;
pathology of the esophagus;
varicose veins of the stomach;
tumors;
burn;
cardiovascular diseases;
long-term use of drugs;
alcohol poisoning;
prolonged negative emotions;
hemophilia.

In medicine, there are cases that such a condition is caused by taking medications such as Nise, Aspirin, children are especially susceptible to this. Also, due to severe vomiting, which alcohol poisoning often provokes, the longitudinal membrane of the esophagus is torn and a dangerous condition develops.

Whatever the cause of esophageal bleeding, it must be treated as a critical condition.

Symptoms of the disease

Such a condition is a rather rare disease, which sometimes not only patients, but also doctors cannot determine in a timely manner. This is due to the fact that with unexpressed bleeding, there is a gradual flow of blood into the stomach, which is digested there, while not showing clear signs. Even if this pathology is accompanied by pain, experts often attribute it to gastritis. Excessive bleeding makes it difficult to identify the source of this condition. However, there are specific symptoms of the disease, as a rule, these are:

Hematemesis. When the pathology is caused by trauma, a rush of an ulcer, then a scarlet color of blood is released. This means that she did not have time to undergo digestion, this phenomenon occurs with heavy bleeding. Slight bleeding causes coffee grounds to vomit as the fluid has been processed by gastric juices. If cherry color is released during vomiting, then varicose veins of the stomach take place.
The patient's feces are changing, it has a rich black color. This condition occurs when blood passes through the digestive tract.
A sharp decrease in blood pressure, manifested by dizziness, nausea, malaise, weakness.
Tachycardia, palpitations.
Increased need for water.
Skin change.

The intensity of the signs depends on the degree of hemorrhage, with a slight lesion, the symptoms are sometimes not striking. If a person has at least one of the symptoms, then it is urgent to contact a specialist for diagnosis.

Diagnosis of the disease

For an accurate diagnosis, the following examination is necessary:

how to get rid of esophageal varicose veins

a general blood test establishes the fact of bleeding, which will show a decrease in hemoglobin and red blood cells;
fecal analysis will help determine hidden hemorrhage;
FGDS is an accurate method that will not only help determine the site of bleeding, but also administer a hemostatic injection and suture a burst vessel;
Ultrasound will not help to accurately determine the location of the pathology, but will determine the condition of the internal organs;
MRI, CT will determine the cause of the hemorrhage;
x-ray with the introduction of a dye will detect the localization of the pathology.

First aid

When bleeding, it is important to call for medical help as soon as possible and provide competent pre-medical intervention. Since the imposition of tourniquets is not advisable here, many do not know what to do in this situation.

First of all, you need to calm down yourself. Provide the patient with complete rest. He should be in a horizontal position, which will not only limit physical activity, but help control how much blood he has lost. Since the horizontal position limits its entry into the digestive tract.

It is necessary to create comfort for the patient, you should remove unnecessary clothes from him and cover him with a blanket. An important condition is the control of blood pressure and pulse rate, which should be carried out every 10 minutes. A lower pressure increases the heart rate and indicates that a large amount of blood has been lost. If the blood pressure drops below 80 mm Hg, and the heart rate increases to 130 beats, then this is an indicator of the possibility of a shock state.

In such patients, fainting may occur, indicating extensive blood loss and requiring immediate action. In order to bring a person into consciousness, you can sprinkle him with water or let ammonia be inhaled. Ice, taken orally in small pieces, will help alleviate the condition. The patient should be transported exclusively on a stretcher in a supine position.

Treatment of pathology

Treatment of hemorrhage from the esophagus must be done in a hospital. First of all, measures are taken to stop bleeding, which include:

the introduction of the Blackmore probe, which is located in the esophagus. Then the probe is inflated with air, due to which the cuff is inflated, pressing the vessels. In this cuff there is also a tube that does not increase the vascular lumen, through which nutrition and drugs are supplied. This device can be in the patient's body for several days, until a blood clot forms on the damaged vessel;
with the help of an operative intervention performed by laparoscopy, sutures are applied to the damaged vessel or cauterization is performed using electricity or a laser;
together with surgery, drug therapy is used, which involves the introduction of hemostatic drugs, for example, Vikasol, Calcium Chloride. Sometimes it is required to replenish the blood loss with erythromass;
if the erosive area suggests infection, then a course of antibiotic therapy may be required, for example, Macrolide or Cephalosporin preparations.

Patients for a long time should be on the strictest bed rest. They are forbidden to eat on their own, they receive food by intravenous administration. After they have been allowed to feed on their own, they should eat their food warm and pureed.

Esophageal bleeding is a serious disease, at the first symptoms of which it is necessary to urgently consult a doctor in order to avoid the development of complications and death.

Cirrhosis of the liver is nothing more than a chronic disease with a tendency to progression, characterized by pronounced signs of functional organ failure and the development of portal hypertension.

When making a diagnosis, the doctor indicates the morphological and etiological type of the disease. In addition, the degree of portal hypertension and liver failure, the activity of the process, must be indicated.

But in order to determine the final diagnosis, it is necessary to conduct a differential diagnosis of liver cirrhosis. After all, the symptoms of cirrhosis can be observed in other diseases.

First of all, it is necessary to carry out a differential diagnosis with cancer. Cirrhosis-cancer can develop both against the background of previously transferred viral hepatitis, and against the background of alcoholic cirrhosis. Symptoms such as the rapid progression of the disease, anorexia, severe emaciation, fever, and abdominal pain can suggest the idea of a malignant process.

On palpation, the doctor determines the stony density, tuberous liver, its uneven increase. In cancer, ascites is very pronounced, which practically cannot be corrected with the help of medications. It is important to note that in cancer, unlike cirrhosis, spleen enlargement and endocrine disorders are rare.

To make a diagnosis, the following methods are used:

CT scan;

Liver biopsy;

Angiography;

Determination of alpha-fetoprotein.

Before making a definitive diagnosis of cirrhosis of the liver, differential diagnosis should be carried out, including with polycystic liver disease. Polycystic liver disease is a congenital disease. Patients with polycystic complain of pain in the right hypochondrium, dyspeptic disorders (in the form of flatulence, diarrhea, constipation), as well as weight loss.

On palpation, the liver is dense, bumpy, which can also lead the doctor to think about cirrhosis. In the later stages, jaundice and portal hypertension may develop, which can be treated. The results of computed tomography and ultrasound will help confirm the diagnosis of polycystic disease. The images show multiple round formations with thin walls.

It should also be differentiated from constrictive pericarditis. This pathology is manifested by heaviness in the right hypochondrium, an increase in the size of the liver itself. But the disease is also characterized by symptoms of circulatory decompensation. Therefore, to make a definitive diagnosis, echocardiography is necessary to determine the damage to the heart.

When making a diagnosis, it is often possible to suspect cirrhosis of the liver on the basis of anamnesis - alcohol abuse, past viral hepatitis B, C and D, the presence of characteristic complaints (nosebleeds, dyspeptic disorders, weakness, abdominal pain, etc.) The results of a physical examination are taken into account: telangiectasias in the face and shoulder girdle, erythema of the palmar and digital eminences, blanching of the nails (a sign of low serum albumin), hemorrhagic diathesis (bleeding of the nasal mucosa and gums, subcutaneous petechiae and hemorrhages, localized or generalized purpura), nutritional decline and atrophy of skeletal muscles, grayish-pale skin tone or moderate icterus of the sclera, thickened liver with a sharp lower edge, splenomegaly with a tendency to leukothrombocytopenia, endocrine disorders (hair disorders, acne, gynecomastia, infertility, etc.). The diagnosis is supported by the detection of characteristic biochemical changes: hyperuglobulinemia, hypoalbuminemia, increased activity of aminotransferases, hyperbilirubinemia due to the conjugated pigment fraction, etc.

Ultrasound provides information about the state of the vessels of the portal system. With the help of computed tomography, a change in the size of the liver, a small amount of ascitic fluid, and a decrease in portal blood flow are determined. Esophagoscopy and X-ray examination of the esophagus can detect varicose veins of the esophagus, which is of paramount importance for the diagnosis. Using a morphological study of a liver biopsy, diffusely distributed pseudolobules surrounded by connective tissue septa are revealed. In addition, the morphological type of cirrhosis and the degree of activity of the process are established.

Recognition of the etiological forms of cirrhosis is based on history data (alcoholism, viral hepatitis, etc.), clinical features, identification of specific markers of the etiological factor (detection of antibodies to hepatitis B, C and D viruses in viral cirrhosis, alcoholic hyaline in alcoholic cirrhosis). In the diagnosis of etiological types of cirrhosis, the greatest difficulty is the distinction between primary and secondary biliary cirrhosis of the liver. Distinctive features of the first one are the gradual onset of the disease with itching without pain and temperature, late development of jaundice, early high activity of alkaline phosphatase, which does not correspond to the degree of hyperbilirubinemia, antibodies to the mitochondroid fraction and an increase in the content of IgM. In secondary biliary cirrhosis, along with the symptoms of cirrhosis, signs of the disease that caused it are found. Less often than in primary biliary cirrhosis, melasma, xanthoma and xanthelasma, osteoporosis are observed.

The diagnosis of liver cirrhosis in a-antitrypsin deficiency is made by determining the Pi phenotype using immunoelectrophoresis. Congestive cirrhosis, which forms in the terminal stage, proceeds with persistent ascites, hepatosplenomegaly, but unlike other forms of cirrhosis, it is accompanied by severe shortness of breath, swelling of the jugular veins, cyanosis, and high venous pressure.

Differential diagnosis of liver cirrhosis

Liver cirrhosis must be distinguished from chronic active hepatitis, liver fibrosis, liver cancer, liver echinococcosis, constrictive pericarditis, liver amyloidosis. Due to the fact that cirrhosis develops gradually, a clear distinction from chronic active hepatitis in some cases is impossible. The presence of signs of portal hypertension (varicose veins of the lower third of the esophagus) indicates the transition of hepatitis to cirrhosis. Liver fibrosis as an independent disease is usually not accompanied by clinical symptoms and functional disorders. In some cases, with congenital and alcoholic liver fibrosis, portal hypertension develops, which leads to diagnostic difficulties. Morphologically, with fibrosis, the lobular architectonics of the liver is preserved. Liver cancer is characterized by a more acute development of the disease, a pronounced progressive course, exhaustion, fever, pain, leukocytosis, anemia, and a sharply increased ESR. A pathognomonic sign of liver cancer is a positive Abelev-Tatarinov reaction - the detection of a-fetoproteins (embryonic serum globulins).

The diagnosis is confirmed by targeted biopsy data. In alveolar echinococcosis, the diagnosis is made on the basis of a hemagglutination reaction and latex agglutination with an echinococcal antigen, in which specific antibodies are determined, in some cases laparoscopy is used. With constrictive pericarditis, the first signs of heart compression are characterized by a feeling of heaviness in the right hypochondrium, an increase and thickening of the liver, mainly the left lobe. Shortness of breath occurs during physical exertion, the pulse is soft, small filling. The results of echocardiography serve as a criterion for reliable diagnosis. Liver amyloidosis is reliably diagnosed by needle biopsy data.

Ed. prof. I.N. Bronovets

"Diagnosis of cirrhosis of the liver, diagnostic signs" article from the section

For cirrhosis of the liver, similar in many clinical manifestations to chronic hepatitis, are characterized by:

signs of portal hypertension

Expansion of the veins of the esophagus, hemorrhoidal, hepatic and splenic veins,

Pronounced and persistent ascites.

Signs of hepatocellular insufficiency (decrease in total serum proteins, albumin, transferrin, cholesterol, ChE, alpha-LP, II, V, VII factors of the coagulation system; increased bilirubin (indirect);

· data of a puncture biopsy of a liver sometimes have decisive value for differential diagnostics.

cardiac asthma
Hypertensive crisis
Cardiogenic shock
angina pectoris
Pulmonary edema
myocardial infarction
Paroxysmal ventricular tachycardia
Anaphylactic shock
Complete transverse block with Morgagni-Adems-Stokes syndrome
Acute respiratory failure
Asthma attack
Pulmonary bleeding
Spontaneous pneumothorax
Gastrointestinal bleeding
hepatic colic
hepatic coma
Acute renal failure
Renal eclampsia
Renal colic
Hemolytic crisis
Hemorrhagic vasculitis
diabetic coma
Hypoglycemic coma
Thyrotoxic crisis
Acute adrenal insufficiency

Cardiac asthma: evacuation to hospital lying down, raised headboard accompanied by a physician (emergency staff). Acute left ventricular failure.

2. Type I hypertensive crisis: 6-8 ml of dibazol 0.5% with 2-4 ml of papaverine 0.5%; 40 mg lasix iv (m); 5-10 ml 25% MgSO4 (convulsive syndrome).

20 mg of anaprilin p / i (tachycardia); seduxun, relanium (psychomotor); you can 10 mg of nifedepine (0.075 mg of clonidine) - every 30 minutes until normalization (if nothing). Crisis without complications - treated on the spot, with complications - hospitalization, for the first time - in the hospital.

Acute macrofocal myocardial infarction in the anterior, apical, lateral sections complicated by cardiogenic shock (true, not arrhythmic). Lying with a raised lower end: intramuscularly 0.5-1 ml of mezaton-0.5 ml (to increase blood pressure); 2 ml cordiamine; 1 ml of promedol 2% (BP control); neuroleptanalgesia - 2 ml fentanyl, 1 ml droperidone, mezaton - 0.5 ml IV (slow); 5-10ml 4% DOPA in saline solution or 1-2ml 0.2% NA; 90-180mg prednisolone; KI. Evacuation to the hospital, accompanied by a doctor IV 10,000 heparin.

Hospitalization: the same + rheopolyglucin, thrombolysis (up to 4 hours) - i.v. .

Angina pectoris nitroglycerin p / i every 5 min correction of blood pressure heating pads to the legs 2-4 ml 50% analgin / m 1 ml 2% promedol. Evacuation to the hospital with a paramedic.

Hospital: IV nitroglycerin, oxygen with N oxide.

5. Pulmonary edema complicating the course of concomitant heart disease (mitral stenosis and insufficiency predominate - combined): evacuation to the hospital lying down, an elevated headboard accompanied by a doctor (emergency staff). Acute left ventricular failure.

Help: orthotopic position, nitroglycerin under the tongue (10 min) - until the condition improves (under the control of blood pressure) to blood pressure 90/60; oxygen inhalation through alcohol (KI-40); dropper with physical solution; in / in 1 ml of promedol-2% (slowly) - inhibition of re-irritation of the respiratory center (to stop); in / in 20-60 mg of furosemide (1-3 amps) - the fight against stagnation in the pulmonary circulation, prevention of pulmonary edema; venous tourniquets on the lower limbs for 30-40 minutes; intravenous slow 0.5-1 ml corglicon 0.06%, strophanthin 0.05% - with inefficiency (per 10 ml of saline solution);

In the hospital: if necessary, drugs and diuretics; IV nitroglycerin 8-10 ml 1% in 200 ml saline solution (with increased blood pressure) - 5-10 drops / min, with alcohol n.g. - 4ml per 400ml of saline solution, Na nitroprusside - cap; DOPA (with lowering blood pressure) - 5-10 ml 4% (200 ml saline solution) 60-90 mg prednisolone; IVL with increased pressure on exhalation, inhalation.

6. IHD acute macrofocal myocardial infarction in the region of the lateral section of the left ventricle, the most acute stage.

PMP: nitroglycerin; promedol IR, rest i.v. 0.005% - 2 ml fentanyl, 2 ml - 0.25% droperidol i.v. 10,000 heparin.

Hospital: IV nitroglyceran 1000 IV heparin, thrombolysis. Complications: edema, cardiac asthma, ventricular extrasystole 60-80 mg of lidocaine.

Paroxysmal ventricular tachycardia of the heart PMP: lidocaine or 5-10 ml novocainamide 10% + 0.3-0.5 mezaton - 1 ml / min; 1ml 5% phenazepam (excitation).

Hospital: 4-8ml 2% lidocaine, electrical impulse therapy (external)

Anaphylactic shock: lying down, fixed tongue, cold to the injection site, s / c 0.1% adrenaline (0.5-1 ml of adrenaline - chop the injection site);

i / m (i / v) 100-150 hydrocortisol (60-120 prednisolone) + 2 ml diphenhydramine. Repeatedly s / c 0.5 ml of adrenaline, cordiamine 2 ml; CI 10ml 2.4% - eufilin. Evacuation to the hospital. Hospital + reopoliglyukin, prednisone IVL.

Chronic diffuse liver diseases pose the following main diagnostic tasks for the doctor: 1) timely recognition of chronic hepatitis and cirrhosis of the liver; 2) assessment of the main characteristics of the disease: a) the activity of the pathological process, b) the stage of the disease, c) the degree of dysfunction of the liver parenchyma, d) the nature of the violation of portal blood flow and the degree of compensation of the portal block.

Formed cirrhosis of the liver with severe clinical manifestations usually does not cause diagnostic difficulties. Recognition of chronic hepatitis and clinically latent developing cirrhosis of the liver, especially in the inactive phase, is not so easy. The most common early manifestations of these diseases are pain in the right hypochondrium, weakness, hepatomegaly, and sometimes jaundice. The presence of this symptom complex, especially in patients who have had Botkin's disease, should encourage the doctor to conduct a comprehensive clinical and biochemical (using a set of functional liver tests) examination of the patient. In some cases, it is possible to clarify the diagnosis only with the help of intravital morphological examination of the liver.

To assess the activity of the pathological process, changes in the patient's state of health and violations of functional liver tests may be of some importance. The most significant in this respect is the increase in the activity of transaminases, alkaline phosphatase, the 5th isoenzyme of LDH and organ-specific enzymes for the liver, a decrease in the activity of cholinesterase, and changes in simple and complex proteins. These indicators do not always reflect the presence of an active pathological process in the liver. The most reliable judgment can be made by histological, histochemical changes in the liver biopsy.

A full judgment about the stage of the disease can only be made on the basis of a comprehensive study, including the use of clinical and biochemical methods in combination with laparoscopy and intravital histological examination of the liver. Criteria for judging the stage of the disease are set out in the "Classification" section and in the discussion of individual forms of liver cirrhosis. A particular issue of determining the stage of the disease is the differentiation of chronic hepatitis and cirrhosis of the liver. Late stages of liver cirrhosis can be distinguished from chronic hepatitis by clinical signs. The differentiation of the borderline states of a single pathological process can be made only on the basis of an intravital morphological study of the liver. A laparoscopic sign of the transition of chronic hepatitis to cirrhosis of the liver is the picture described by Kalk (1954) of the "variegated nodular liver". The latter is microscopically characterized by disorganization of the structure of the hepatic lobule with bands of connective tissue. However, the morphological study does not allow to accurately determine the moment of the onset of the formation of cirrhosis of the liver, since this process occurs gradually and the morphological reorganization of the tissue is heterogeneous in different parts of the liver. This makes unreasonable the desire at all costs to delimit the precirrhotic stage of chronic hepatitis from the initial stage of cirrhosis of the liver. X. X. Mansurov (1965) believes that the polarographic analysis of serum proteins allows the most accurate differentiation of chronic hepatitis from cirrhosis of the liver. For cirrhosis, a gentle catalytic wave of the subprogram is characteristic, which is not observed in patients with chronic hepatitis.

The degree of functional disorders does not always correspond to the degree and prevalence of morphological changes in the liver. In addition, in patients with cirrhosis of the liver, a violation of the parameters of some biochemical tests may be due not to changes in hepatocytes, but to the presence of venous collaterals, through which the blood of the portal vein enters the general circulation, bypassing the liver parenchyma.

Criteria for evaluating portal blood flow conditions are outlined in the Portal Hypertension section.

In the differential diagnosis, one must remember the need to distinguish between chronic hepatitis and cirrhosis of the liver from other diseases accompanied by hepatomegaly (fatty and other liver dystrophies, liver granulomatosis, benign liver fibrosis, liver cysts and echinococcus, etc.). A reliable difference between chronic hepatitis and liver dystrophies is possible only with the help of a liver biopsy with its histochemical study.

Hepatomegaly in benign fibrosis is characterized by the absence of any biochemical signs of an active process during long-term follow-up. However, here too, reliable data can only be obtained with the help of a liver biopsy performed under laparoscopic control. Differential diagnosis between chronic hepatitis (liver cirrhosis) and liver granulomatosis can be established on the basis of anamnesis, existing extrahepatic manifestations of syphilis, brucellosis, tuberculosis, sarcoidosis, positive serological and biological samples corresponding to these diseases. Even with significant and prolonged hepatomegaly caused by granulomatosis, usually no changes in functional tests are detected. The liver biopsy has the greatest differential diagnostic value in these cases. Sometimes, according to clinical signs, it is difficult to differentiate focal changes in the liver (cysts, echinococcus, tumors, hemangiomas, etc.) from chronic hepatitis and cirrhosis of the liver. In these cases, X-ray diagnostics, the use of laparoscopy and the method of radioisotope scanning, as well as operational revision can help to correctly recognize the disease.

The morphological type of liver cirrhosis can be most accurately established by comparing the results of laparoscopy and liver biopsy. From this, however, it does not follow that the recognition of the morphological type of cirrhosis becomes impossible without the use of these methods. The peculiarity of some clinical manifestations makes a real attempt to determine the type of cirrhosis based on the clinical picture of the disease. According to our data, the idea of the type of liver cirrhosis, compiled on the basis of clinical signs, does not coincide with the results of a morphological study in 20% of cases. The main clinical signs of various types of liver cirrhosis are shown in Table 10.

TABLE 10. Signs for differentiating liver cirrhosis by morphological type

	Cirrhosis of the liver
	portal	postnecrotic	biliary
The main pathological picture	Pseudolobules are small, of the same type, thin connective tissue strands	Large pseudolobules of various sizes, sometimes containing unchanged lobules or their fragments. Wide bands of connective tissue. Convergence of three or more portal triads	The lobular structure is broken only in the later phases. Inflammatory infiltration and fibrosis around the bile ducts. Signs of bilestasis
picture at laparoscopy	The surface of the liver is fine-grained, the edge is sharp thin	The surface of the liver is coarse, the liver is deformed, sometimes resembling a bunch of grapes	The liver is enlarged, the surface is smooth or granular, greenish in color
Jaundice	Present in the late stages, in the early stages - sometimes with exacerbations	It is detected early, periodically increases with exacerbation	Detects early and stays strong
Hepatocellular insufficiency	Occurs in late stages	Occurs early, increases during exacerbations	Occurs in late stages
portal hypertension	Ahead of functional insufficiency	Available along with functional insufficiency	Develops late or absent altogether
Skin changes		"Spider veins", palmar erythema	xanthomas
Bone changes	Not	Sometimes arthralgia without anatomical changes	"Drum sticks", osteoporosis, enlarged epiphyses, synovitis
Changes in secondary sexual characteristics	frequent	rare	Missing
Liver changes	Enlarged in the early stages, later reduced, palpation smooth surface, sharp edge	In the early stages it is increased, later it is reduced. The edge of the liver is uneven, the surface is tuberous	Large, smooth, painful

Recognition of the morphological type of cirrhosis in the terminal stage is impossible.

The inaccessibility of some research methods to a wide range of doctors determines a kind of staging in establishing a diagnosis of chronic liver diseases.

In the outpatient setting, it is possible to recognize clinically significant cases and identify individuals who may be suspected of clinically latent active chronic hepatitis or liver cirrhosis. Further clarification of the diagnosis can be carried out in general hospitals.

The need to use special research methods requires hospitalization in hospitals, sufficiently equipped with modern equipment.