Differential diagnosis of liver cirrhosis table. Chronic hepatitis and cirrhosis of the liver: diagnosis, recommendations for treatment

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 conduct 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.

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PASSPORT PART

Full name: R.A.M.

Date of birth: 57 years old

Gender Female

Home address: XXX

Occupation: housewife

Date of access: 12/15/2014

COMPLAINTS

The patient complained of constant, dull, non-radiating pain in the epigastric region and right hypochondrium, aggravated after eating and intense physical activity. Bleeding gums after eating. Great physical weakness, increased fatigue that occurs towards the end of the day. Also, the patient complained of constant swelling of the lower extremities in the region of the lower 2/3 of the legs that did not subside after a night's rest. The appearance of "spider veins" in the face and neck.

ANAEMNESIS MORBI

According to the patient on June 5, 1986, on the 7th day after the birth of her daughter with a large loss of blood (premature detachment of a normally located placenta, blood loss of 1200 ml; in the KLA: hemoglobin - 50 g / l; erythrocytes - 2.3x 10 12 / l) and blood transfusion, she developed yellow staining of the mucous membranes. The patient was transferred from the maternity hospital to the infectious diseases hospital with suspected hepatitis, where she stayed for 22 days. During this time, the diagnosis was made: "Viral hepatitis B" and antiviral treatment was carried out. Until 2013, the patient's condition did not change. In the summer of 2013, the patient began to notice the appearance of "spider veins", first on the legs, and then all over the body, weakness, loss of appetite appeared (weight loss by July was 6-7 kg.). There was also a slight staining of the sclera in yellow. The patient went to the polyclinic at the place of residence, where, after the examination, she was referred for hospitalization at the Medical Center of WKSMU in the therapeutic department for examination, where she was diagnosed with cirrhosis of the liver of viral etiology and a group II disability was established. When the patient was discharged, recommendations were given to limit oneself in the consumption of fatty foods, and, if possible, to refuse fried foods and alcohol. Until now, the patient annually underwent examination and detoxification therapy in the therapeutic department of the Medical Center of WKSMU. During hospitalization in 2014, the attending physician drew attention to pastosity of the legs, which the patient herself had not noticed before. In the winter of 2014, the patient noticed that, while performing daily, familiar housework and chores, she became very tired: by the end of the day, physical weakness appeared, apathy towards the environment; which has not been observed before.

ANAEMNESIS VITAE

She was born on July 12, 1957 in the city of Aktobe, the second child in the family (out of four children). Body weight at birth 3800.0. She was breastfed for up to 1 year. As a child, she had chicken pox and measles (without complications). I went to school at the age of 7. I attended physical education classes regularly. She graduated from 11 classes, after graduation she entered the ASPI. Menarche from the age of 13, 4 days each, regular, painless. Pregnancies - 3, childbirth - 1 (girl weighing 3520.0; complication - premature detachment of a normally located placenta), honey. abortion - 2 (without complications). HIV infection, tuberculosis, sexually transmitted diseases denies. Bad habits are denied. Allergy anamnesis without features. Operative interventions were not carried out. Hemotransfusion in 1986 due to large blood loss during childbirth (blood loss 1200 ml; in the KLA: hemoglobin - 50 g / l; erythrocytes - 2.3x 10 12 / l). Material and living conditions are satisfactory.

STATUS PRAESENS COMMUNISIS

General condition: moderate

Consciousness: clear

Position: active in bed

facial expression: calm

Normosthenic physique.

Height 162 cm, weight 60 kg.

Skin covers:

At the time of examination: the skin is pale pink in color, hyperpigmented on the anterior surface of the legs. The color of visible mucous membranes is pale. The subectericity of the sclera is noted.

On the face in the area of ​​the right cheekbone, a single, pale "spider vein" is visible. On the front surface of the chest and abdomen, single "ruby droplets" are noted, in the area of ​​\u200b\u200bthe shins the skin is flaky. Moisture and elasticity of the skin is reduced. The hairline is developed according to the female type. Longitudinal striation is noted on the nail plates of the fingers and toes.

Subcutaneous tissue:

Developed moderately and evenly. The thickness of the fold on the anterior abdominal wall is 2-3 cm. The subcutaneous fat layer is evenly developed.

At the time of examination, pastosity is observed in the lower third of the legs.

Lymphatic system:

Occipital, parotid, submandibular, cervical, supraclavicular, axillary, inguinal lymph nodes are not palpable. Pain in the area of ​​palpation is not observed. When examining hyperemia of the skin in the areas of the location of the lymph nodes is not observed.

Muscular system:

Moderately developed, symmetrical, painless on palpation, normal tone. Local hypertrophies and muscle atrophies were not revealed.

Skeletal system and joints:

Pathological changes were not revealed.

The movements in the limbs are free, painless.

Examination of the organs of the respiratory system. At the time of examination, there were no complaints indicating pathology of the respiratory organs. Breathing through the nose is free. The voice is clear and quiet. Pain when talking and swallowing does not occur. There is no cough. The larynx is painless on palpation. The ribs in the lateral sections have a moderately oblique direction, the Ludowig angle is weakly expressed). No chest deformity noted. Thorax: normosthenic type, conical shape, (supraclavicular and subclavian fossae are moderately pronounced, the shoulder blades are tightly adjacent to the chest, the epigastric angle is ~ 90 degrees).

The chest is symmetrical: the shoulder blades and collarbones are located at the same level in relation to each other. When breathing, the movements of the chest are synchronous, auxiliary muscles do not participate in the act of breathing. Mixed breathing with predominance of the chest. NPV 20 in 1 min. Shortness of breath is not observed. The rhythm of breathing is correct.

PERCUSSION OF THE CHEST

COMPARATIVE PERCUSSION:

A clear pulmonary sound is heard above the lung fields.

TOPOGRAPHIC PERCUSSION:

Inferior border of lungs: Right lung: Left lung:

Lin. parasternalis VI intercostal space

Lin. Clavicularis VII intercostal space

Lin. axillaris ant. 8th rib 8th rib

Lin. axillaris med. IX rib IX rib

Lin. axillaris post. X rib X rib

Lin. Scapularis XI rib XI rib

Lin. paravertebralis spinous process XI vert. Thor

The height of the tops of the lungs:

Right lung in front 4.5 cm above the clavicle

Behind proc. stiloideus VII vert. cerv.

Left lung anteriorly 4 cm above clavicle

Behind proc. Stiloidus VII vert. cerv.

Krenig margin width:

Right 7cm

Left 7.5 cm

AUSCULTATION OF THE LUNGS

Vesicular breathing is heard over the lung fields. Bronchial breathing is heard over the larynx, trachea and large bronchi. Bronchovesicular breathing is not heard. No wheezing, no crepitus. Strengthening of bronchophony over the symmetrical areas of the chest was not detected.

Examination of the circulatory system. At the time of examination, the patient complained of persistent swelling of the lower extremities in the area of ​​the legs (pastosity). When examining the vessels of the neck, normal pulsation of the carotid arteries is noted. When examining the region of the heart, the heart hump and usuration of the ribs are not determined. The apex beat is not visible. On palpation, the apex beat is also not determined. The symptom of "cat's purr" is not defined. The pulsation in the epigastric region is due to the pulsation of the aorta (with a deep breath, the pulsation weakens). There is no heartbeat.

LIMITS OF RELATIVE DULT OF THE HEART

Right: 1 cm outward from the right edge of the sternum in the 4th intercostal space.

Left: on the left mid-clavicular line, in the 5th intercostal space.

Upper: located at the level of the middle of the 3rd intercostal space.

The distance from the right border of relative dullness to the anterior midline is 3 cm.

The distance from the left border of relative dullness to the anterior midline is 7cm.

The relative dullness diameter is 10 cm.

The aortic configuration of the heart is determined.

Diameter of the vascular bundle: 8.5 cm.

BORDERS OF ABSOLUTE DULT OF THE HEART

Right: corresponds to the left edge of the sternum.

Left: located 2 cm medially from the left mid-clavicular line.

Upper: corresponds to the level of the middle of the 4th rib.

The diameter of absolute dullness is 6.5 cm.

Auscultation:

The first and second tones of normal sonority.

The rhythm of the quail and the rhythm of the gallop are not heard.

Noise of pericardial friction is not defined.

Vascular examination:

Radial, carotid, femoral arteries are not tortuous. The temporal artery is soft, tortuous. Konchalovsky's symptom and "pinch" symptom are negative.

The same on the right and left radial artery. The rhythm is correct, 72 beats per minute, full filling, moderate tension, normal pitch and speed. Capillary pulse is not determined.

At the time of examination, blood pressure was 130/80 mm. rt. Art.

Examination of the digestive system. At the time of examination, the patient complained of persistent, dull pain in the epigastric region, aggravated after eating. Bleeding gums after eating.

Appetite at the time of examination is satisfactory, there is no thirst. Chewing and swallowing food is not disturbed. No belching, heartburn, nausea, vomiting. Chair daily, not changed. The action of the intestines is independent, but arbitrary. The discharge of gases is free, odorless.

Examination of the digestive organs:

Mouth: normal smell.

Tongue: Red, with a yellow coating on the back. Cracks, ulcers, imprints of teeth are not observed.

The mucous membrane of the inner surface of the lips, cheeks, hard and soft palate without features, pink color.

Gums: pink color, bleeding after eating (according to the patient). There are no purulent discharges, aphthae, pigmentation.

Zev: mucous pink color, puffiness is not observed. Tonsils are not enlarged, plaque is not observed.

Abdominal examination:

The abdomen is rounded, symmetrical, protrusions and retractions are not observed. Subcutaneous vascular anastomoses are not expressed. There are no scars or hernias. Peristalsis is not disturbed. Stomach

freely participates in the act of breathing.

The circumference of the abdomen at the level of the navel is 85 cm.

Percussion:

During percussion, a tympanic sound of varying severity is heard in all departments, in the region of the liver and spleen - a femoral sound. There is no ascites.

PALPATION:

A) superficial:

With superficial, approximate palpation, the abdomen is soft, there is pain on palpation in the epigastric and right hypochondrium regions. Shchetkin-Blumberg's symptom is negative. Tension of the muscles of the anterior abdominal wall was not detected. There is no diastasis of the rectus abdominis muscles. The umbilical ring is not expanded. Superficial tumors and hernias are not palpable.

B) Deep:

Sigmoid colon - palpated in the form of a cylinder with a diameter of 2 cm, painless, displaced; the surface is flat, smooth;

elastic consistency; purring.

The caecum is palpable in the form of a strand with a diameter of 2.5 cm, painless, displaceable; the surface is flat, smooth; elastic consistency; purring.

The ascending and descending sections of the colon are palpable in the form of cylinders with a diameter of 2.5 cm, painless, displaceable; the surface is flat, smooth; elastic consistency; rumbling.

Transverse colon - palpable in the form of a cylinder with a diameter of 3 cm, painless, displaceable; the surface is flat, smooth; elastic consistency; purring.

Large curvature of the stomach - palpable in the form of a roller 3 cm above the navel, painless; the surface is flat, smooth; elastic consistency; feeling of slipping off the sill.

Examination of the liver and gallbladder:

Table. Borders and sizes of the liver

The border of the left lobe does not protrude beyond the left parasternal line

BY KURLOV

I size (straight) II size (straight) III size (oblique)

Dimensions 11 cm. 8 cm. 7 cm.

Palpation:

The lower edge of the liver is rounded, dense, painful, the surface is smooth.

At the point of the gallbladder, pain is not determined. Symptoms of Ortner, Kare, Georgievsky are negative.

Examination of the spleen:

Upper border of the spleen: upper edge of the IX rib

The lower border of the spleen: 3 cm below the lower edge of the XI rib.

Length of the spleen: 14 cm.

Spleen diameter: 6 cm.

Palpation:

The lower pole of the spleen is palpable, dense in consistency, with a smooth surface, moderate pain.

Auscultation of the abdomen:

Normal bowel sounds are heard over the entire surface of the abdomen.

Examination of the organs of the urinary system. At the time of examination, there were no complaints indicating pathology of the urinary organs.

Pain in the lumbar region and bladder are absent. Dysuric disorders were not identified. Hyperemia and swelling in the kidney area is not detected. Pasternatsky's symptom is negative on both sides.

On palpation, the lower pole of the right kidney is lower than the lower pole of the left kidney. Palpation of the kidneys is painless, the kidneys are easily displaced, elastic consistency. On auscultation, the murmur of the renal arteries is not heard.

With percussion, the bladder above the pubic symphysis is not defined.

Study of the organs of the neuroendocrine system. Consciousness is clear, intellect is normal. Memory for real events is reduced. Sleep is shallow, short, there is insomnia. Mood is good. There are no speech disorders. There are no convulsions. The gait is somewhat constrained, the patient makes stops when walking. Reflexes are preserved, there are no paresis or paralysis. He considers himself a sociable person.

Smell, touch, taste are not changed. There is no decrease in visual acuity. The rumor is good.

CLINICAL SYNDROMES:

1. Asthenovegetative syndrome

2. Syndrome of dystrophic changes

3. Syndrome of small hepatic signs

4. Jaundice syndrome

5. Portal hypertension syndrome

6. Dyspepsia syndrome

RATIONALE FOR PRELIMINARY DIAGNOSIS

Based:

- patient complaints: on constant, dull, non-radiating pain in the epigastric region and right hypochondrium, aggravated after eating and intense physical activity. Bleeding gums after eating. Great physical weakness, increased fatigue that occurs towards the end of the day. Also, the patient complained of constant swelling of the lower extremities in the region of the lower 2/3 of the legs that did not subside after a night's rest. The appearance of "spider veins" in the face and neck;

- medical history: according to the patient on June 5, 1986, on the 7th day after the birth of a daughter with a large loss of blood (premature detachment of a normally located placenta, blood loss 1200 ml; in the KLA: hemoglobin - 50 g / l; erythrocytes - 2.3x 10 12 / l) and blood transfusion, she developed yellow staining of the mucous membranes. The patient was transferred from the maternity hospital to the infectious diseases hospital with suspected hepatitis, where she stayed for 22 days. During this time, the diagnosis was made: "Viral hepatitis B" and antiviral treatment was carried out. Until 2013, the patient's condition did not change. In the summer of 2013, the patient began to notice the appearance of "spider veins", first on the legs, and then all over the body, weakness, loss of appetite appeared (weight loss by July was 6-7 kg.). There was also a slight staining of the sclera in yellow. The patient went to the polyclinic at the place of residence, where, after the examination, she was referred for hospitalization at the Medical Center of WKSMU in the therapeutic department for examination, where she was diagnosed with cirrhosis of the liver of viral etiology and a group II disability was established. When the patient was discharged, recommendations were given to limit oneself in the consumption of fatty foods, and, if possible, to refuse fried foods and alcohol. Until now, the patient annually underwent examination and detoxification therapy in the therapeutic department of the Medical Center of WKSMU. During hospitalization in 2014, the attending physician drew attention to pastosity of the legs, which the patient herself had not noticed before. In the winter of 2014, the patient noticed that, while performing daily, familiar housework and chores, she became very tired: by the end of the day, physical weakness appeared, apathy towards the environment; which has not been observed before;

- life history: Hemotransfusion in 1986 due to large blood loss during childbirth (blood loss 1200 ml; in the KLA: hemoglobin - 50 g / l; erythrocytes - 2.3x 10 12 / l);

- objective research data: The subectericity of the sclera is noted.

On the face in the area of ​​the right cheekbone, a single, pale "spider vein" is visible. On the front surface of the chest and abdomen, single "ruby droplets" are noted, in the area of ​​\u200b\u200bthe shins the skin is flaky. Humidity and elasticity of the skin is reduced; red tongue, pink gums, bleeding after eating (according to the patient). With superficial, approximate palpation, the abdomen is soft, there is pain on palpation in the epigastric and right hypochondrium regions. Hepatosplenomegaly

A preliminary diagnosis is made: Liver cirrhosis of viral etiology in the stage of decompensation.

SURVEY PLAN

1. UAC

Hb - 100 g/l (with the norm for women 120-140 g/l)

erythrocytes - 3.3 x 10 12 / l (at the rate for women 3.5-4.7 10 12 / l)

CPU - 0.85 (at a rate of 0.85-1)

platelets - 176 x 10 9 / l (at a rate of 180-320 10 9 / l)

ESR - 20 mm / h (at the rate for women 2-15 mm / h)

leukocytes - 12 x 10 9 / l (at a rate of 4.0-9.0 x 10 9 / l)

p / i - 5% (at a rate of 1-6%)

s / i - 53 (at a rate of 47-72%)

lymphocytes - 29% (at a rate of 19-37%)

monocytes - 8% (at a rate of 3-11%)

eosinophils - 1% (at a rate of 0.5-5%)

basophils - 1% (at a rate of 0-1%)

Conclusion: mild anemia; leukocytosis; increased ESR, thrombocytopenia

2. OAM

quantity - 100 ml

color - straw yellow

specific gravity - 1018

sugar - no

acetone - no

transparency - transparent

reaction is sour

protein - no

leukocytes - no

erythrocytes - no

squamous epithelium - no

salt - no

Conclusion: norm

3. TANK

Total protein - 50 g / l (at a rate of 60-80 g / l)

Albumins - 26 g / l (at a rate of 35-50 g / l)

Alanine aminotransferase - 38 U / l (at a rate for women up to 31 U / l)

Aspartate aminotransferase - 38 U / l (at a rate for women up to 31 U / l)

Glucose - 4.0 mmol / l (at a rate of 3.5-5.5 mmol / l)

Total bilirubin - 60 µmol/l (at a rate of up to 22.2 µmol/l)

Direct bilirubin - 17 µmol / l (at a rate of ¼ of total bilirubin)

Thymol test - 6 units (at a rate of up to 5 units)

Conclusion: dysproteinemia, increased content of AST, ALT, total and direct bilirubin, thymol test

4. Coagulogram

Activated partial thromboplastin time - 50 sec. (at a rate of 30-40 sec.)

Prothrombin index - 46% (at a rate of 78-142%)

Plasma fibrinogen - 1.5 g / l (at a rate of 2-4 g / l)

Conclusion: acceleration of APTT, decrease in PTI, decrease in fibrinogen

5. Detection of viral markers

HbsAg, HbcorAg were detected.

Conclusion: identified markers of viral hepatitis B

6. FGDS

The esophagus is passable, its veins are varicose from the middle third to 5 mm. The mucosa above them is thinned, purple-bluish in color, the cardia closes completely. There is a large amount of mucus in the stomach, the gastric mucosa is of normal color, the angle is not changed, the pylorus is passable, the duodenal bulb is medium in size, the mucosa is not hyperemic.

Conclusion: varicose veins of the esophagus I degree.

7. Ultrasound of the abdominal organs

There is a small amount of free fluid in the abdominal cavity. The liver is moderately enlarged due to the left lobe (66 mm), the contour is scalloped, the structure of the liver is heterogeneous, compacted along the portal tracts with areas of increased echogenicity. The portal vein is 17 mm, its course is convoluted. The gallbladder is medium in size.

Pancreas with blurred contours, the parenchyma is hyperechoic, heterogeneous; splenic vein in the body pancreas 9.1 mm.

Spleen: 135 X 54 mm, the walls of the vessels are sealed, the splenic vein at the gate is 11 mm, its course is tortuous.

DIFFERENTIAL DIAGNOSIS

Liver cancer. Such liver diseases as primary liver cancer and especially cirrhosis-cancer have a similar clinical picture.

Cirrhosis-cancer occurs both in persons who have had acute viral hepatitis in the past, and in patients with alcoholic liver disease. Cancer can develop against the background of long-term cirrhosis of the liver with vivid clinical symptoms or latent cirrhosis of the liver. Recognition of cirrhosis-cancer is based on the rapid progression of liver disease, exhaustion, fever, abdominal pain, leukocytosis, anemia, and a sharp increase in ESR. The correct diagnosis of primary cancer is helped by a short history of the disease, a significant, sometimes stone density of an unevenly enlarged liver. With a "typical" variant of this liver disease, there are constant weakness, weight loss, anorexia, ascites that is not amenable to diuretic therapy. Ascites develops as a result of thrombosis of the portal vein and its branches, metastases to periportal nodes, and peritoneal carcinomatosis. Unlike cirrhosis of the liver - splenomegaly, endocrine-metabolic disorders are rare.

For the diagnosis of cirrhosis-cancer and primary liver cancer, it is advisable to use a liver scan and ultrasound. However, these are only screening tests indicating "focal" or "diffuse" pathology without a specific diagnosis.

The criteria for a reliable diagnosis in primary liver cancer and cirrhosis-cancer are the detection of fetoprotein in the Abelev-Tatarinov reaction, laparoscopy with targeted biopsy, and angiography, which is especially important for cholangioma.

Accession of acute alcoholic hepatitis in patients with alcoholic cirrhosis of the liver causes jaundice with anorexia, nausea, fever, which must be differentiated from acute viral hepatitis. The correct diagnosis of acute alcoholic hepatitis against the background of liver cirrhosis is facilitated by a carefully collected history that reveals the relationship between the severity of alcoholism and clinical symptoms, the absence of a prodromal period, often associated polyneuropathy, myopathy, muscle atrophy and other somatic manifestations of alcoholism, as well as neutrophilic leukocytosis, an increase in ESR.

Fibrosis of the liver. characterized by excessive formation of collagen tissue. As an independent liver disease, it is usually not accompanied by clinical symptoms and functional disorders. In rare cases, with congenital liver fibrosis, schistosomiasis, sarcoidosis, portal hypertension develops.

Criteria for reliable diagnosis are morphological - in contrast to cirrhosis of the liver, with fibrosis, the lobular architectonics of the liver is preserved. Most often in clinical practice, alveolar echinococcosis, constrictive pericarditis, amyloidosis, and storage diseases are mistaken for liver cirrhosis. Sometimes a differential diagnosis is made with subleukemic myelosis and Waldenström's disease.

Alveolar echinococcosis. With alveolar echinococcosis, the first sign of the disease is an increase in the liver with its unusual density. Diaphragm movement is often limited. Enlargement of the spleen and violations of liver function tests detected in some patients lead to diagnostic errors. Diagnosis is aided by careful X-ray examination, especially with the use of pneumoperitoneum, as well as a liver scan. Criteria for a reliable diagnosis of echinococcosis are specific antibodies. liver cirrhosis treatment diagnosis

Constrictive pericarditis. Constrictive pericarditis (with predominant localization in the right ventricle) - one of the adhesive pericarditis, is the result of a slow overgrowth of the pericardial cavity with fibrous tissue, which limits the diastolic filling of the heart and cardiac output. The disease develops as a result of chronic tuberculous lesions of the heart shirt, injuries and wounds of the heart area, purulent pericarditis. The first signs of heart compression occur among more or less long-term well-being and are characterized by a feeling of heaviness in the right hypochondrium, enlargement and compaction of the liver, mainly the left lobe, often painless on palpation. Shortness of breath occurs only during physical exertion, the pulse is soft, small filling. Typically, an increase in venous pressure without enlargement of the heart.

For the correct recognition of the disease, it is important to take into account the anamnesis and remember that in constrictive pericarditis, stagnation in the liver precedes circulatory decompensation. The criterion for a reliable diagnosis is the data of X-ray kymography or echocardiography.

RATIONALE FOR CLINICAL DIAGNOSIS

Based:

- reasonable preliminary diagnosis: Liver cirrhosis of viral etiology in the stage of decompensation;

- data of laboratory and instrumental studies:- in the KLA: Hb - 100 g / l (at the norm for women 120-140 g / l); platelets - 176 x 10 9 /l (at a rate of 180-320 10 9 /l); ESR - 20 mm / h (at the rate for women 2-15 mm / h); leukocytes - 12 x 10 9 /l (at a rate of 4.0-9.0 x 10 9 /l); - in the BAK: Total protein - 50 g/l (at a rate of 60-80 g/l); Albumins - 26 g / l (at a rate of 35-50 g / l); Alanine aminotransferase - 38 U / l (at a rate for women up to 31 U / l); Aspartate aminotransferase - 38 U / l (at a rate for women up to 31 U / l); Total bilirubin - 60 µmol/l (at a rate of up to 22.2 µmol/l); Direct bilirubin - 17 µmol / l (at a rate of ¼ of total bilirubin); Thymol test - 6 units (at a rate of up to 5 units); - in the coagulogram: Activated partial thromboplastin time - 50 sec. (at a rate of 30-40 sec.); Prothrombin index - 46% (at a rate of 78-142%); Plasma fibrinogen - 1.5 g / l (at a rate of 2-4 g / l); - in case of detection of viral markers: markers of viral hepatitis B were detected; - on FGDS: varicose veins of the esophagus I degree; - on ultrasound of OBP: There is a small amount of free fluid in the abdominal cavity. The liver is moderately enlarged due to the left lobe (66 mm), the contour is scalloped, the structure of the liver is heterogeneous, compacted along the portal tracts with areas of increased echogenicity. The portal vein is 17 mm, its course is convoluted. The gallbladder is medium in size. Pancreas with blurred contours, the parenchyma is hyperechoic, heterogeneous; splenic vein in the body pancreas 9.1 mm.

Spleen: 135 X 54 mm, the walls of the vessels are sealed, the splenic vein at the gate is 11 mm, its course is tortuous;

- by excluding such diseasesy, kak: liver cancer, liver fibrosis, alveolar echinococcosis, constrictive pericarditis.

The clinical diagnosis was made: Cirrhosis of the liver against the background of viral hepatitis B(stage of decompensation). Child-Pugh class" AT" (7 points).

TREATMENT PLAN

Limit mental and physical stress. With a general good condition, therapeutic walking and therapeutic exercises are recommended. Women with active cirrhosis of the liver should avoid pregnancy.

Excluded from food:

Mineral waters containing sodium;

Alcohol;

Salt, food must be prepared without adding salt (salt-free bread, crackers, biscuits and crispbreads are used, as well as salt-free butter);

Products containing baking powder and baking soda (cakes, biscuits, cakes, pastries and regular bread);

Pickles, olives, ham, bacon, corned beef, tongues, oysters, mussels, herring, canned fish and meat, fish and meat pate, sausage, mayonnaise, various canned sauces and all kinds of cheeses, ice cream.

100 g of beef or poultry meat, rabbit or fish and one egg per day are allowed (one egg can replace 50 g of meat). Milk is limited to 1 glass per day. You can eat low-fat sour cream. You can eat boiled rice (without salt). Any vegetables and fruits are allowed fresh or in the form of home-cooked dishes.

Sample menu for a day for a patient with cirrhosis of the liver:

Breakfast: cereal porridge (semolina, buckwheat, millet, barley, oatmeal) with cream and sugar or baked fruit. 60 g of salt-free bread, or bread (slices), or salt-free crackers with unsalted butter and marmalade (jelly or honey), 1 egg, tea or coffee with milk.

Lunch: 60 g of beef or poultry or 90 g of white fish, potatoes, greens, fruits (fresh or baked).

Snack: 60 g of salt-free bread or crispbread, unsalted butter, jam or tomato, tea or coffee with milk.

Dinner: soup without salt, beef, poultry or fish (as for lunch), potatoes, greens, fruit or fruit juice and gelatin jelly, sour cream, tea or coffee with milk.

Medical treatment. There is no specific treatment for cirrhosis of the liver. However, a good effect is the impact on the etiological factor of the pathological process. Interferon is indicated for patients with chronic hepatitis B and C, detected by liver biopsy HBeAg, active hepatitis C.

Also, a positive result is given by the use of a number of drugs:

Hepatoprotectors (karsil, heptral, hepa-merz, ornithine, Essentiale, ursodeoxycholic acid, vitamins B and E).

Preparations of this group increase the resistance of liver tissues to various kinds of adverse effects, reduce damage and destruction of hepatocytes, and contribute to the stabilization of the liver cell membrane.

Glucocorticosteroid hormones (triamcinolone, prednisolone).

The indication is an increase in the activity of the process with compensated cirrhosis of the liver.

Contraindications for glucocorticosteroid therapy will be: pronounced esophageal vein dilatation, a combination of liver cirrhosis with peptic ulcers of the stomach and duodenum, reflux esophagitis.

Doses of drugs are selected individually, taking into account individual tolerance and activity of the process.

Detoxification treatment. Enzyme preparations are used (mezim-forte, pancreatin, festal, wobenzym), which accelerate the processes of digestion in the intestine, reduce the absorption of toxic substances from the colon, and as a result, reduce the severity of dyspeptic disorders. For the same purpose, enterosorbents, activated charcoal, and intestinal enema are used to cleanse the intestines.

Transfusion therapy (blood preparations, its components, blood-substituting and electrolyte solutions).

It is carried out with the development of the following conditions: hemorrhagic syndrome, hepatocellular insufficiency, ascites, electrolyte imbalance.

Extracorporeal hemocorrection. For a while, it allows to reduce the functional load on the liver, cleanses the body of toxic metabolites with a significant development of liver failure, protects against the hepatotoxic effect of the drugs taken.

Surgical treatment for cirrhosis of the liver. The indication for surgical intervention is the presence of portal hypertension, pronounced varicose veins of the esophagus and the upper part of the stomach, with sufficiently preserved liver function, no symptoms of encephalopathy, and high activity of the process. Increasing jaundice and advanced age will be contraindications to surgical intervention. Under such circumstances, as a rule, perform palliative surgery.

1) Rp.: Essentiale forte N

D.t.d. N. 30 in capsulis

Signa: 2 capsules 2 times a day with meals with a little water

2) Rp.: Creon 25000

D.t.d. N. 20 in capsulis

Signa: 1 capsule 1 time per day: ½ capsule at the beginning of a meal; S - during meals

MEDICAL AND LABOR EXAMINATION

Patients with chronic hepatitis I, less often II st. with a stable or slowly progressive course with rare (1-2 times a year) and short-lived (2-3 weeks) exacerbations, functionally compensated or with mild liver dysfunction, without systemic manifestations, in the absence of signs of process activity, and CG IV stage . (liver cirrhosis, stage A according to Child-Pugh) of a stable course with the same frequency and duration of exacerbations and the state of liver functions, with portal hypertension of the 1st stage. without manifestations of hypersplenism. The necessary restrictions can be determined by the decision of the CEC of medical institutions. In such cases, patients retain physical independence, mobility, the ability to engage in normal household activities, economic independence and integration into society.

Temporary disability occurs in the active phase of the disease, with the development of complications. The duration depends on the stage, degree of activity, severity of liver dysfunction, portal hypertension, systemic manifestations, and the effectiveness of treatment. On average, with CVH (B, C, D) with moderate activity 15-28 days, high activity 30-45 days. (up to 2-3 months), with an exacerbation in the initial stage of the cirrhosis 35-40 days; deployed - 60 days. and more.

Contraindicated types and working conditions: work associated with severe physical stress, high predetermined pace, forced body position, vibration, driving vehicles, trauma to the epigastric region; exposure to toxic agents - salts of heavy metals, chlorinated hydrocarbons and naphthalenes, benzene and its homologues; high or low temperatures. This takes into account the stage of chronic hepatitis, the nature of the course, the degree of impaired liver function, the stage of portal hypertension, systemic manifestations, etc.

Indications for referral of patients to the ITU Bureau: progressive nature of the course of the disease; pronounced violations of the liver and portal hypertension, causing limitation of life; need of patients in rational employment.

The necessary minimum examination when referring patients to the ITU office.

Clinical blood test, urine test for urobilin and bile pigments; biochemical blood tests: AST, ALT, LDH, bilirubin, alkaline phosphatase, y-GTP, cholesterol, total protein and fractions, fibrinogen, prothrombin index, sugar, creatinine; Ultrasound of the abdominal organs, scanning of the liver and spleen: liver biopsy (if indicated).

Disability criteria: stage, nature of the course, frequency of exacerbations, degree of activity, quality and duration of remissions, degree of impaired liver function, severity of extrahepatic (systemic) lesions, severity of portal hypertension and hypersplenism, degree of disability - the ability to self-care, movement, professional work ; social factors.

III group of disability is determined in connection with the limitation of the ability to self-service, movement, work activity I stage, patients with chronic hepatitis II stage of a slowly progressive course with exacerbations lasting 4-6 weeks, occurring 2-3 times a year, the activity of the process 1 tbsp. , impaired liver function, mild, rarely moderate, and patients with chronic hepatitis IV st. (cirrhosis of the liver, stage A according to Child-Pugh) with the same frequency and duration of exacerbations, the degree of activity and severity of liver dysfunction, with portal hypertension of the II degree, mild hypersplenism syndrome without hemorrhagic manifestations, working in contraindicated types and working conditions, and in this regard, those who need to be transferred to work in another, accessible profession, or a significant reduction in the volume of production activity.

II group of disability is determined in connection with the limitation of the ability to self-care, movement, work activity II stage, patients with chronic hepatitis II and III stages of intermittent recurrent course with frequent (up to 4-5 times a year) long-term (6-8 weeks) exacerbations , activity II st., impaired liver function of moderate or severe degree, severe extrahepatic (systemic) manifestations, as well as patients with chronic hepatitis IV st. (liver cirrhosis stage B according to Child-Pugh) with the same frequency and duration of exacerbations, the degree of activity and severity of liver dysfunction, with stage III portal hypertension, severe manifestations of hypersplenism syndrome (anemia, leukopenia, thrombocytopenia). In some cases, work in specially created conditions (at home) may be recommended.

I group of disability is determined in connection with the limitation of the ability to self-care, movement, labor activity of the III stage, patients with chronic hepatitis III stage of a rapidly progressive, continuously relapsing course, with activity of the III stage, the development of severe liver failure, systemic lesions with severe dysfunction of the pancreas , kidneys, other organs, exhaustion, as well as patients with chronic hepatitis IV Art. (Child-Pugh stage C liver cirrhosis), with II-III stage activity, severe liver failure, stage IV portal hypertension, intoxication and encephalopathy.

Cause of disability: the most common is "general disease"; with appropriate anamnestic data documented, "disability since childhood" can be established. For medical personnel working in hemodialysis centers, preparation of blood products; departments for the treatment of patients with viral hepatitis; persons working in contact with hepatotropic toxic agents, in the presence of relevant conclusions, the ITU Bureau establishes the cause of "occupational disease". In case of infection and subsequent illness with acute viral hepatitis of surgeons, obstetricians-gynecologists, urologists and other specialists who received an accidental injury during the surgical treatment of patients - carriers of the hepatitis virus, which is confirmed by an accident report at work in the form H-1, the cause of temporary disability , and in the event of a transition to chronic hepatitis, which caused disability and other restrictions on life, the cause of disability will be "labor injury". The cause of disability may be "an illness acquired during military service."

PREVENTION

Improving the system of epidemiological surveillance, vaccination, registration of all forms of viral hepatitis, effective phased treatment of patients aimed at stabilizing the process, equalizing impaired liver functions, portal decompression, clinical examination; control over donors, the use of drugs; observance of sanitary and hygienic conditions in industries using hepatotoxic agents, the fight against alcoholism and drug addiction. Preparation of sick and disabled people to expand the possibilities of household activities, work in accessible types and conditions of production, training and retraining is carried out taking into account the rehabilitation potential and prognosis.

FORECAST

HVG I st. - proceeds benignly, the prognosis is favorable. CVG II, III Art. - it is possible to stabilize the process and long-term remission, including spontaneous, in 30% of patients there is a transition to the stage of cirrhosis, in 10-15% against the background of cirrhosis liver cancer develops. Chronic alcoholic hepatitis - when alcohol is given up, clinical stabilization and a decrease in morphological changes in the liver occur. Medicinal and toxic hepatitis stabilize and regress when contact with the corresponding drugs and toxic agents is stopped. However, the addition of autoimmune mechanisms contributes to the progression of alcoholic hepatitis even in conditions of withdrawal, as well as drug and toxic hepatitis after the cessation of exposure to appropriate stimuli. Autoimmune CG is characterized by unstable and short-term remissions, the formation of severe liver failure, and the relatively rapid development of cirrhosis; the life expectancy of patients from the moment of diagnosis is an average of 5 years. In the stage of cirrhosis, the disease in 30% of cases is latent for a long time. With an active course, the cause of death can be a hepatic coma, massive esophageal-gastric bleeding, the development of carcinoma, and infectious and septic complications.

BIBLIOGRAPHY

1. A.N. Okorokov "Diagnosis of diseases of internal organs" volume 1. M., 2008.

2. K.A. Zhamankulov "Internal diseases".

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Chronic hepatitis is considered a liver disease in which clinical, laboratory and morphological changes persist for 6 or more months.

Etiology.

There are several groups of factors leading to the development of chronic hepatitis (CH):

1. infectious factors.

Among them, viruses are of primary importance, and chronization occurs only in hepatitis caused by viruses B (in 10-15% of cases), C (30-60%), D (90-100%).

Infectious factors also include leptospirosis (Weil-Vasiliev disease), infectious mononucleosis, protozoa (giardia, leishmania), chronic infections (syphilis, tuberculosis, brucellosis, malaria).

2. Toxic factors.

These can be industrial toxins: lead, arsenic, dyes, insecticides, organochlorine compounds, etc.

Many drugs have a toxic effect on the liver: long-term use of sulfonamides, NSAIDs, barbiturates, methyluracil, mercazolil, etc.

Alcohol has a toxic effect on the liver.

1. Toxic-allergic factors.

These include diffuse connective tissue diseases: SLE, SJS, UP, dermatomyositis.

4. Exchange and endocrine disorders.

It should be borne in mind vitamin and protein deficiency, both exo- and endogenous nature, as well as endocrine diseases (diabetes mellitus, thyrotoxicosis, hypothyroidism).

1. Obstruction of the bile ducts.

It can be intrahepatic and extrahepatic.

It should be noted that the etiological factors are the same for CG and liver cirrhosis (LC).

Pathogenesis.

In the pathogenesis of CG and cirrhosis, two main points can be distinguished:

1. Persistence of the virus in hepatocytes, which leads to the death of liver cells and the growth of connective tissue in this place.

2. Immune and autoimmune disorders, in which any substance can serve as a trigger. These processes may prevail or fade into the background, which determines the severity of pathological changes in the liver.

clinical picture.

In the clinical picture of CG, 4 main syndromes are distinguished:

1. Painful.

This is the most common syndrome in HCG. The pains are localized in the right hypochondrium or the upper part of the epigium, radiating to the right half of the lumbar region, the right shoulder, the right shoulder blade. The pains are dull, aggravated by fast walking, running, shaking the body, with errors in the diet (alcohol intake, spicy and fatty foods).

P. Dyspeptic.

Patients may experience nausea, a feeling of bitterness in the mouth, belching, bloating, etc.

Sh. Cellular liver failure.

Clinically, this syndrome is manifested by icterus of the skin and sclera, scratching, the appearance of spider veins (telangiectasias) on the upper half of the body, face and upper limbs, subcutaneous deposition of cholesterol (xanthelasma), hepatic palms (thenar and hypothenar hyperemia), liver enlargement.

The liver with chronic hepatitis is enlarged, it is dense on palpation, the edge is pointed or rounded, the edge is even, the surface is smooth, palpation is painful. The spleen is usually not enlarged. Enlargement of the spleen is more common in active hepatitis according to the clinical classification and in active hepatitis according to the new classification.

The degree of liver dysfunction can be fully judged only after a thorough study of additional examination methods. Since the liver is involved in almost all types of metabolism, the list of additional examination methods is large.

It includes:

1. Study of pigment metabolism based on the results of data on the content of blood serum bilirubin (total, direct and indirect), urine urobilin and stercobilin in feces. The complex of these analyzes makes it possible to identify the type of jaundice: parenchymal or mechanical.

2. Study of protein metabolism. With chronic hepatitis in the blood serum, the synthesis of finely dispersed proteins decreases and the synthesis of coarsely dispersed proteins increases - dysproteinemia. Qualitative reactions confirming this are the thymol test and the Veltman reaction, the quantitative test is the analysis of protein fractions (a decrease in the content of albumins and an increase in the level of alpha-2 and gamma globulins).

In the blood serum, the content of prothrombin and fibrinogen, proteins involved in blood clotting, is reduced, therefore, with chronic hepatitis, the blood coagulation system is disturbed, which can lead to dangerous bleeding.

3. Carbohydrate metabolism also suffers. In patients, fasting blood glucose may increase and the sugar curve may change. However, in addition to the liver, the pancreas is also involved in the utilization of glucose, therefore, only on the basis of these analyzes it is difficult to say which of these organs suffers to a greater extent. Therefore, it is preferable to load with carbohydrate, which would be absorbed only by the liver. Such a carbohydrate is galactose. The patient is given a load in the form of 40 gr. Galactose and monitor its excretion in the urine. Normally, no more than 3 grams should stand out.

4. Fat metabolism. With chronic hepatitis, the level of cholesterol and beta-lipoproteins may increase or decrease.

5. Enzyme exchange.

An increase in the level of alanine transaminase (ALT) indicates damage to hepatocytes, and the severity of chronic hepatitis is judged by the degree of its increase. If the ALT level exceeds the normal values ​​by no more than 5 times, they speak of a mild course of the disease, with an increase in the ALT level by 5-10 times - a course of moderate severity, with an increase of more than 10 times the norm - a severe course.

The increase in the level of lactate dehydrogenase (LDH), its fifth fraction, is important, which indicates the death of liver cells, alkaline phosphatase (AP), which increases with cholestasis.

6. To establish the etiology of chronic hepatitis, the determination of serum markers of hepatitis by radioimmunological and enzyme immunoassay methods using test kits is used. Determine antigens and antibodies.

7. The following instrumental diagnostic methods are used: radionuclide diagnostics, cholangiography, ultrasound, computed tomography.

8. To study the morphology of the liver, a percutaneous puncture biopsy of the liver can be prescribed; if it is impossible to perform it in difficult differential diagnostic cases, laparoscopy or laparotomy with a liver biopsy is prescribed.

1U. Damage to other organs and systems.

Patients with chronic hepatitis often develop astheno-neurotic syndrome, the cardiovascular system may be involved in the process (brady- or tachycardia, arrhythmias appear), urinary system (hepatic-renal syndrome), pancreas, intestines, etc.

ClassificationsHG

1. Clinical classification.

1. Chronic persistent hepatitis.

It is characterized by a benign course. It develops several years after acute hepatitis, exacerbations are rare, respond well to treatment. During the period of remission, the working capacity of patients is preserved.

2. Chronic active hepatitis:

A) moderate activity

B) with pronounced activity (lupoid, necrotizing).

It is characterized by active flow. It develops immediately after acute hepatitis, other organs and systems are involved in the process. Liver functions are significantly affected. Patients' ability to work is often reduced even during remission.

3. Chronic cholestatic hepatitis:

A) with intrahepatic cholestasis

B) with extrahepatic cholestasis.

Signs of cholestasis are the appearance of jaundice, accompanied by itching. In the blood serum, the content of cholesterol, bile acids, beta-lipoproteins, and the level of alkaline phosphatase increase.

P. In 1994, at the World Congress of Gastroenterology in Los Angeles, a new classification of chronic hepatitis was adopted, which is based on histological, serological and clinical criteria.

It distinguishes:

1. Autoimmune hepatitis.

2. Chronic hepatitis B, C, D.

3. Chronic hepatitis of unknown type.

4. Chronic hepatitis, which is not classified as viral or autoimmune.

5. Chronic drug-induced hepatitis.

6. Primary biliary cirrhosis of the liver.

7. Primary sclerosing cholangitis.

8. Wilson-Konovalov's disease.

9. Alpha-1-antitrypsin deficiency of the liver.

The diagnosis according to this classification should include 3 components: etiology, degree of activity and stage of the disease.

The etiology is listed above.

The degree of activity is understood as the totality of clinical data, the level of ALT (see above) and the results of histological examination of liver biopsy specimens.

When determining the stage of the disease, the presence of portal hypertension is assessed, and histologically - the severity of fibrosis.

Cirrhosis of the liver.

Cirrhosis of the liver (LC) is a chronic disease characterized by diffuse damage to the parenchyma and stroma of the liver with nodular regeneration of liver cells, diffuse development of connective tissue with a violation of the lobular structure and the vascular system of the liver.

Etiology and pathogenesis.

As stated above, they are common with CG.

Classification by morphological features:

1. Micronodular cirrhosis, in which the size of regeneration nodes does not exceed 1.0 cm in diameter.
2. Macronodular cirrhosis, in which regeneration nodes are larger than 1.0 cm in diameter.
3. Mixed, macromicronodular cirrhosis.
4. Septal cirrhosis, in which the nodes of regeneration are almost invisible.

The disadvantages of this classification is that a puncture biopsy of the liver must be performed, and the necessary part of the parenchyma, which can be used to judge changes in the entire liver, does not always fall into the punctate.

Cuban (Havana) classification (1954)

1. Portal cirrhosis (corresponds to septal or micronodular).
2. Postnecrotic cirrhosis (corresponds to macronodular).
3. Biliary cirrhosis (corresponds to micronodular).
4. Mixed cirrhosis.

clinical picture.

In the clinical picture of cirrhosis, several syndromes can be distinguished:

1. Painful (see in the CG clinic).

2. Dyspeptic (see in the CG clinic).

3. Cellular and hepatic insufficiency (see in the clinic for chronic hepatitis, however, with cirrhosis it is more pronounced). On an objective examination, unlike chronic hepatitis, the liver first increases in size, and then decreases, its consistency is dense, the edge is sharp, palpation is painless. The surface of the liver is smooth, the edge is even in portal and biliary cirrhosis, the surface is bumpy, the edge is uneven in postnecrotic cirrhosis. With all types of cirrhosis, an enlarged spleen is found.

4. Portal hypertension syndrome.

It is manifested by the expansion of the veins of the esophagus, hemorrhoidal veins, saphenous veins on the anterior abdominal wall ("jellyfish head"), the presence of ascites. The causes of ascites are: hypoalbuminemia, increased activity of the pituitary antidiuretic hormone, which is not inactivated in the liver, impaired aldosterone inactivation in the liver.

5. Damage to other organs and systems (see the clinic of chronic hepatitis). In addition, in cirrhosis, the osteoarticular system is affected: the end phalanges of the fingers change in the form of “drumsticks”, there may be “watch glasses”, osteoporosis often develops, which leads to fractures.

The clinic of cirrhosis depends on the type of cirrhosis, and its severity depends on the stage of the disease. Features of the clinical picture depending on the type of cirrhosis - in the textbook.

Complications of cirrhosis:

1. Hepatic coma.

The mechanism of its development is associated with the accumulation of neurotoxic products (ammonia, phenol) in the body. Clinically, intoxication of the nervous system is manifested by the appearance of a headache, sleep disturbances (drowsiness during the day, insomnia at night), inhibition of reactions, apathy. Then there is a tremor of the fingers, pathological reflexes, patients lose consciousness. Death occurs in 80% of cases.

1. Gastrointestinal bleeding.

They rank second in the structure of mortality after hepatic coma. They are dangerous because the expansion of the veins of the esophagus and hemorrhoidal veins is combined with a violation in the blood coagulation system.

1. Thrombosis of the portal vein.
2. The development of various infectious complications.

Treatment of hCG and cirrhosis.

This is a complex and still unsolved problem. Treatment depends on the type of chronic hepatitis or cirrhosis, the activity of the pathological process in the liver, concomitant diseases, and other factors.

However, all patients without exception are initially prescribed basic therapy, which includes:

1. Mode, sparing physically. Hypothermia, overheating, insolation, hydrotherapy, sauna, vaccination are contraindicated for such patients.
2. The appointment of a diet within tables 5a and 5 according to Pevzner.
3. Detoxification measures, which include infusions of 5% glucose solution, physiological saline, other saline solutions (disol, trisol, etc.), reambirin, etc.
4. Normalization of bowel activity. For this purpose, patients are prescribed antibiotics (kanamycin, etc.) or sulfonamides (salazopyridazine, etc.) for 5-7 days, and then, within 3-4 weeks, biologically active drugs such as lactobacterin, bifidumbacterin, bifiform and others
5. The appointment of enzyme preparations that do not contain bile acids.

Treatment of autoimmune hCG and cirrhosis.

The leading role in their treatment is given to immunosuppressive therapy, that is, glucocorticoids and cytostatics. Currently, two treatment regimens are used:

1. Monotherapy with prednisone.

The initial daily dose of prednisolone is 30-40 mg, then monthly the dose of prednisolone is reduced by 5 mg, leading up to a maintenance dose of 10 mg.

1. The combination of prednisolone at an initial daily dose of 15-20 mg and azathioprine at an initial daily dose of 50 mg. The principle of treatment is the same as in the first scheme, the maintenance dose is 10 and 25 mg, respectively.

This scheme is more preferable, since the initial doses for the combination of drugs are smaller, therefore, the course of treatment is less long and there are fewer complications.

Long-term treatment with this kind of drugs requires the appointment of antibiotics due to the possible development of infectious complications.

Treatment of viral hCG and cirrhosis.

The leading role in their treatment belongs to interferons, while alpha-interferon preparations are used. This is a natural drug - wellferon and recombinant forms (obtained using genetic engineering) - roferon, reaferon, intron-A, viferon, etc. All of them have almost the same efficiency, but patients better tolerate natural wellferon.

Interferons are administered intramuscularly, the interval of administration is 3 times a week. Viferon is available in candles.

Doses of interferons depend on the type of virus that caused hCG or cirrhosis.

For HCG caused by virus B, the dose of interferon is 5000000 IU three times a week for 6 months or 10000000 IU 3 times a week for 3 months.

For HCG caused by virus C, the dose of interferon is 3,000,000 IU 3 times a week for 2 months, and then depending on the effectiveness. If the ALT level normalizes or decreases, continue the introduction of interferons at the original or higher dose for another 6 months. If there is no positive dynamics, then further administration of interferons should be abandoned.

In HCG caused by virus D, the dose of interferon is 5,000,000 IU 3 times a week, if there is no effect, the dose is increased to 10,000,000 IU 3 times a week for up to 12 months.

Stable and long-term remission can be achieved with CG B in 30-50% of cases, with CG C - in 25%, and with CG D - only in 3% of patients.

The most common side effect of interferon therapy is influenza-like syndrome (occurs in 75-90% of patients). It is manifested by the appearance of fever, myalgia and arthralgia. These symptoms are reduced if a paracetamol or aspirin tablet is taken before the interferon injection, and the interferons are administered at bedtime.

Less common are other side effects: weight loss, hair loss, depression, leukopenia, thrombocytopenia.

In addition to interferons, interferon inducers can be used, which include roncoleukin, cycloferon, etc., as well as chemotherapy drugs - vidarabine, ribavirin, etc.

Vitamins (fat- and water-soluble), metabolites and coenzyme agents are used in the treatment of chronic hepatitis and cirrhosis.

With alcoholic liver damage and / or the presence of cholestasis, heptral is prescribed at 800-1600 mg per day orally or parenterally.

Symptomatic therapy of chronic hepatitis and cirrhosis:

1. With jaundice - cholagogues and antispastics.
2. With ascites - diuretics and pain medications.
3. With severe pain syndrome - analgesics.
4. With skin itching - desensitizing drugs, ion-exchange resins (cholestyramine).
5. With bleeding - hemostatic therapy.

The diagnostic tasks are to recognize liver cirrhosis, determine the degree of hepatocellular insufficiency and portal hypertension, as well as establish the etiological or pathogenetic type of the disease. The diagnosis is made on the basis of anamnesis, clinical data, biochemical parameters of blood and instrumental examination.

Compensated cirrhosis of the liver is usually detected incidentally in connection with the examination of patients for other diseases (based on the detected hepatomegaly and splenomegaly of unknown origin). Therefore, a number of researchers suggest calling this form of cirrhosis "latent". To confirm the diagnosis in compensated cirrhosis of the liver, it is always necessary to conduct an instrumental examination, since the changes in the indicators of stress tests in these cases are nonspecific.

At the stage of subcompensation of the process, the following symptoms are of primary importance for the diagnosis: hepatomegaly and splenomegaly, "spider veins", palmar erythema, minor nosebleeds, flatulence, as well as laboratory data - accelerated ESR, dysproteinemia, a decrease in the sublimate test, an increase in the level of total bilirubin (mainly due to associated), a moderate increase in the activity of aminotransferases. A reliable diagnostic sign is a decrease in the content of reduced glutathione in the blood below 24 mg% (0.78 mmol / l).

Diagnosis of decompensated liver cirrhosis, in addition to the listed symptoms, is based mainly on the presence of jaundice, ascites and severe hemorrhagic diathesis. In decompensated liver cirrhosis, there is hypoproteinemia, a pronounced decrease in the content of albumin in the blood, a decrease in the sublimate test, a further increase in total (bound) bilirubin, a decrease in the content of blood coagulation factors (change in the coagulogram), a low coefficient of cholesterol esterification, alkalosis - respiratory and (or) metabolic .

In the presence of these symptoms, the identification of signs of portal hypertension, in particular varicose veins of the esophagus, using esophagoscopy and x-ray examination of the esophagus, is of paramount importance for diagnosis. Depending on the magnitude of portal pressure, there are two degrees of portal hypertension:

• I degree - moderately expressed (portal pressure 150-300 mm of water column), manifested by flatulence, dyspeptic disorders, splenomegaly;
• II degree - pronounced (portal pressure above 300 mm of water column), characterized by visible venous collaterals, varicose veins of the esophagus, ascites.

For the diagnosis of cirrhosis of the liver, non-invasive (ultrasound, x-ray, radioisotope) and invasive - morphological (laparoscopy, targeted biopsy) research methods are used. The most informative for cirrhosis of the liver among non-invasive methods are echography and scintigraphy.

With the help of echography in cirrhosis of the liver, an increase in the liver, a change in its contours (rounded, uneven), as well as splenomegaly, ascites, expansion of the portal and splenic veins are detected.

X-ray examination in cirrhosis of the liver can detect violations in the structure of the liver, as well as changes in its hemodynamics. Plain radiography reveals a change in the size (increase or decrease) and shape of the liver, as well as signs of ascites. A pronounced increase in the organ is accompanied by a high position of the right dome of the diaphragm and a deepening of the right costophrenic sinus.

With ascites, there is a restriction of mobility and an upward displacement of the diaphragm, as well as a downward displacement of the right kidney, large intestine, and down and to the left of the stomach. Pneumoperitoneum allows you to get a relief image of the surface of the body. The introduction of gas into the abdominal cavity also makes it possible to detect small amounts of ascitic fluid. With the help of computed tomography, the size of the liver, a small amount of ascitic fluid, and a decrease in portal blood flow are determined.

Significant changes in the liver in cirrhosis are determined using angiographic research methods. So, with cavography, there is a displacement and deformation of the venous trunks, due to the development of false lobules, sometimes a circular narrowing of the inferior vena cava; with celiacography in case of severe portal hypertension, there is an expansion of the celiac trunk, splenic and left gastric arteries and at the same time narrowing of the common hepatic and proper hepatic arteries, the arterial pattern of the liver is depleted, the segmental arteries are narrowed and tortuous, the branches of the splenic artery, on the contrary, are expanded; In the spleen, there is an intensive accumulation of a contrast agent.

According to X-ray cinematography, carried out in combination with celiacography, the volumetric blood flow in the splenic artery in liver cirrhosis increases by 2-2.5 times, and in the proper hepatic artery decreases by 1.5-2 times. The ratio of these indicators is normally 0.7-1.4, and in cirrhosis with portal hypertension, this ratio increases to 3-6. Splenoportography has the greatest diagnostic value. Conducting this study in cirrhosis of the liver allows you to determine the more vertical location of the portal vein, deformation and decrease in the caliber of its branches, impoverishment of the pattern due to the reduction of small veins. The outflow of blood from the portal system is compensated by dilated collaterals. Collateral outflow of blood through anastomoses and varicose veins can be detected indirectly by introducing a contrast agent into the esophagus, stomach, and intestines. In the case of expansion of the submucosal venous plexuses, rounded superficial contrast defects are visible along the folds.

X-ray examination of the biliary tract - cholegraphy, which allows to detect narrowing of the intrahepatic bile ducts, is mainly used for the differential diagnosis of primary and secondary biliary cirrhosis of the liver.

Radioisotope diagnostics of liver cirrhosis is carried out in order to determine the functional and morphological state of the liver, to assess the state of the organ's blood circulation. Radioisotope hepatography, scanning and scintigraphy, radiocirculography, radioisotope cholegraphy and portography are used. Scintigraphy with various hepatotropic preparations has the greatest diagnostic value. On scintigrams of patients with cirrhosis of the liver, a decrease in the inclusion of a radiopharmaceutical and its uneven distribution, changes in the shape and size of the liver are determined.

The study, performed using colloidal radiopharmaceuticals, makes it possible to quantify their redistribution in the reticuloendothelial system and thereby determine the nature and extent of liver damage. Large-nodular cirrhosis on liver scintigrams is characterized by alternating areas of increased inclusion of a radiopharmaceutical (foci of regeneration of the liver tissue) with areas of reduced inclusion or its complete absence (fibrotic changes). With small-nodular cirrhosis of the liver, a relatively uniform decrease in the accumulation of the drug is noted, more pronounced along the periphery of the organ. For a more detailed study of the liver in cirrhosis, emission computed tomography is used, which allows, on the basis of scintigraphic sections in various sections, to obtain volumetric information about cirrhotic changes in the deep structures of the organ.

To assess the state of the absorption-excretory function of hepatocytes in liver cirrhosis, as well as a differential diagnostic test for intrahepatic and extrahepatic cholestasis, the radioisotope chleography technique is used. The radiopharmaceutical preparations based on iminodiacetic acids used for this purpose make it possible to carry out studies in the presence of high levels of blood bilirubin. Radioisotope portography and intrarectal administration of a cooled 133Xe xeno-air mixture with subsequent registration of the passage of the radiopharmaceutical through the system of the inferior vena cava are the most informative for identifying the causes of portal hypertension and determining porto-caval anastomoses.

Morphological methods include peritoneoscopy and targeted biopsy. Characteristic signs of liver cirrhosis are diffuse granularity and (or) tuberosity of the surface of the liver, microscopically - pseudolobular structure of the organ.

Differential Diagnosis

Liver cirrhosis in the initial stage is differentiated from chronic active hepatitis, fatty hepatosis. In chronic active hepatitis, the liver is moderately dense, with a pointed edge, painful on palpation. With fatty hepatosis, the liver is slightly enlarged, dense in consistency, sometimes sensitive to palpation, has a blunt edge and a smooth surface. Due to the fact that the development of cirrhosis of the liver occurs gradually, their clear distinction in some cases is impossible. The presence of signs of portal hypertension indicates the transition of the pathological process to cirrhotic.

In the advanced stage of the disease, cirrhosis of the liver is differentiated from a malignant tumor of the liver, alveococcosis, subleukemic myelosis, liver amyloidosis.

Liver cancer is characterized by a more rapid development of the disease, a pronounced progressive course, exhaustion, fever, pain syndrome, a rapid increase in the liver (the spleen remains of normal size), which has an uneven surface and "stony" density, leukocytosis, anemia, sharply accelerated ESR. The most reliable signs of liver cancer (primary and cirrhosis-cancer) are the positive Abelev-Tatarinov reaction - the detection of embryonic serum globulins (alpha-fetoproteins) using the agar precipitation reaction, as well as targeted biopsy data, angiography (for cholangioma).

With alveococcosis, an increase in the liver occurs gradually, over a long time; the liver becomes bumpy, acquires an "iron" density, is painful on palpation; the diagnosis is made on the basis of the latex agglutination reaction, in which specific antibodies are detected; in some cases resort to a laparoscopy.

In subleukemic myelosis with a benign course, an enlarged spleen precedes hepatomegaly, portal hypertension is not typical; there is a dissociation between pronounced splenomegaly and a slightly changed blood picture (moderate neutrophilic leukocytosis with a predominance of mature forms). Reliable diagnostic criteria are the data obtained during trephine biopsy - pronounced cellular hyperplasia, an abundance of megakaryocytes, and proliferation of connective tissue.

Cirrhosis of the liver is a diffuse pathological process that develops with excessive fibrosis and the formation of structurally abnormal nodes of regeneration.

Cirrhosis of the liver is the end stage of a wide range of liver diseases.

The variability of liver cirrhosis as a nosological form differs in the features of etiological factors, the activity of the pathological process in the liver, the failure of the liver function, and the degree of progression of portal hypertension.

Epidemiology

Cirrhosis of the liver is the cause of death of patients in 90–95% of cases of outcomes of chronic liver diseases and occupies a leading position among the causes of mortality from diseases of the digestive system.

The prevalence of liver cirrhosis in the world ranges from 25 to 400 per 100,000 population.

It has been established that patients with liver cirrhosis drink obviously hepatotoxic volumes of alcohol 2 times more often than ordinary people; also, anti-HCV in the blood serum of patients with liver cirrhosis is detected 11 times more often than in the population.

Approximately 2 million people die every year from viral cirrhosis of the liver (mainly HCV-, HBV-infectious etiology) and virus-associated hepatocellular carcinomas. Data on mortality from alcoholic cirrhosis of the liver in developed countries are approaching those for viral cirrhosis of the liver.

Etiology

The main most common causes of cirrhosis of the liver:

– alcohol abuse (over 50%);

- viral hepatitis (more often - chronic hepatitis C, less often - hepatitis B, D).

Metabolic disorders that can trigger the onset of cirrhosis of the liver:

- iron overload in hereditary hemochromatosis;

- copper overload in Wilson's disease;

- deficiency of α 1 -antitrypsin;

- cystic fibrosis;

- galactosemia and glycogenoses;

- hereditary tyrosinemia and telangiectasia, porphyrias.

Diseases of the biliary tract, in which cirrhosis of the liver can develop:

- extrahepatic obstruction of the biliary tract;

- intrahepatic obstruction of the biliary tract (primary biliary cirrhosis, primary sclerosing cholangitis);

- cholangiopathy in children (progressive childhood cholestasis, arteriohepatic dysplasia, cholestasis with lymphedema, Zellweger's syndrome);

- obstruction of venous outflow from the liver (Budd-Chiari syndrome, veno-occlusive disease, severe right ventricular failure);

- The toxic effects of pharmaceuticals and toxins can also trigger the onset of cirrhosis.

However, cirrhosis can be caused by immune changes (autoimmune hepatitis, graft-versus-host disease), other disease states (sarcoidosis, non-alcoholic steatohepatitis, hypervitaminosis A, cryptogenic cirrhosis).

In a quarter of cases of liver cirrhosis, the etiology remains unclear. According to most researchers, patients with cirrhosis of the liver of unknown etiology are people with unconfirmed viral and alcoholic cirrhosis of the liver due to inadequate examination.

Pathogenesis

Hepatocellular necrosis and disorders of hepatocyte regeneration, inflammation and fibrosis are interrelated processes that underlie the progression of liver cirrhosis.

Initially, hepatocytes are damaged under the direct influence of etiological agents (alcohol, virus, hepatotoxic substances, etc.) or mediated by the damaging effect of agents of autoimmune and immune aggression.

In the future, the products of cell necrosis and inflammation have a damaging effect on hepatocytes. The resulting ischemia in the central zones of the false lobules can also cause the death of hepatocytes.

An important role in the formation of necrosis is played by immunological disorders caused by dysfunction of Kupffer cells synthesizing pro-inflammatory cytokines (tumor necrosis factor-α, interleukins). The lack of bile acids in the intestine is accompanied by increased bacterial growth and, as a result, endotoxemia and additional stimulation of cytokine production. Of no small importance in the process of cytolysis of hepatocytes belongs to the difficulty in excretion and stagnation of bile, which occur due to impaired intestinal metabolism and reabsorption of bile acids, excessive absorption of lithocholic acid and destruction of cholangiocytes by toxic bile acids.

As a result of necroinflammatory processes, active connective tissue septa are formed.

Fibrogenesis is considered the most important mechanism for the formation and progression of liver cirrhosis. Hepatocellular necrosis, cytokines produced by the cellular structures of the liver, acetaldehyde (formed during the conversion of alcohol), cause degradation of the extracellular matrix space of Disse. These processes are accompanied by the activation of Ito cells, which ultimately leads to the stimulation of fibrogenesis.

Iron overload in hemochromatosis is accompanied by increased secretion of tissue inhibitors of metalloproteinases, which is accompanied by the deposition of collagen in the space of Disse with the formation of fibrils and fibronectin.

These processes underlie the "collagenization" of the sinusoids, which impedes the exchange of substances between the liver cell and the blood, which provokes the formation of portal hypertension.

Cirrhotic changes in the hepatic parenchyma and, as a consequence, portal hypertension, in which portosystemic shunting and hepatocellular insufficiency occur, lead to the formation of parenchymal and arterial vasodilation with a progressive decrease in systemic vascular resistance. This predisposes to a drop in effective arterial volume and a decrease in blood pressure, which creates conditions for fluid retention and an increase in plasma volume.

In response to these processes, cardiac output and heart rate increase, which is inevitably accompanied by an increase in parenchymal blood supply and, in addition, further exacerbates portosystemic shunting, portal hypertension, and hepatocellular insufficiency.

Clinical picture

The disease can be asymptomatic for a long time.

Clinical assessment of the stage and severity of liver cirrhosis is based on the severity of portal hypertension and hepatocellular insufficiency. The stage and severity of the disease are semiquantitatively assessed using the Child-Pugh diagnostic criteria scale.

Compensated (class A) course of liver cirrhosis is characterized by the absence of icterus, ascites and bleeding from varicose veins and encephalopathy.

Subcompensated and decompensated (class B and C, respectively) course is characterized by the occurrence of ascites of varying severity, bleeding from varicose veins, spontaneous peritonitis and pleural empyema, hepatorenal syndrome and hepatic encephalopathy.

In patients with cirrhosis of the liver, various symptoms of damage to almost all organs and systems can be detected, which determine the following syndromes:

• Asthenic (fatigue, loss of appetite of varying severity, weight loss).
• Dermal (icteric staining of the skin, "varnished" tongue and lips, telangiectasia, reddening of the palmar surfaces, skin scratching, seizures in the corners of the mouth, changes in the nail plates).
• Musculoskeletal (hypertrophic osteoarthropathy, hepatic osteodystrophy, convulsions, umbilical hernia).
• Pulmonary (hypoxemia, primary pulmonary hypertension, rapid breathing, decreased lung capacity, accumulation of fluid in the pleural sinus, dilation of intrapulmonary vessels, shortness of breath).
• Cardiac (hyperdynamic circulation).
• Gastrointestinal (enlargement of the parotid salivary glands, loosening of the stool, cholelithiasis, portal hypertensive gastro- and colonopathy, symptomatic (cirrhotic) erosive and ulcerative lesions, gastritis, hepatic odor from the mouth).
• Renal (secondary hyperaldosteronism, in which fluid and sodium retention develops, "hepatic" glomerulosclerosis, renal tubular acidosis, hepatorenal syndrome).
• Hematological (folic acid deficiency and hemolytic anemia, enlarged spleen with pancytopenia, coagulation disorder, DIC, hemosiderosis).
• Endocrine (diabetes, increased levels of parathyroid hormones due to hypovitaminosis D and secondary hyperparathyroidism, hypogonadism: in women - infertility, dysmenorrhea, disappearance of secondary sexual characteristics; in men - decreased libido, hypo- and testicular atrophy, impotence, a decrease in testosterone, feminization ).
• Neurological (hepatic encephalopathy, peripheral neuropathy, seizures).
• Portal hypertension syndrome (varicose veins - gastroesophageal, anorectal, retroperitoneal, "jellyfish head"; ascites, enlarged spleen).

Depending on the flow options, there are:

1. Subacute cirrhosis (hepatitis-cirrhosis).

Often occurs against the background of acute hepatitis with symptoms of the initial stage of liver cirrhosis. The disease lasts from 4 months to one year and is characterized by the transformation of acute hepatitis into cirrhosis of the liver, resulting in death.

2. Rapidly progressive (active) cirrhosis.

Differs in specific clinical, biochemical and morphological signs of high activity of the pathological process in the liver. From the onset of the disease, patients live for about 5 years.

3. Slowly progressive (active) cirrhosis.

A mild clinical picture of the disease is accompanied by constant biochemical and morphological activity. Portal hypertension and liver failure progress slowly. The life expectancy of patients is more than 10 years from the onset of the disease.

4. Sluggish cirrhosis.

Clinical symptoms of disease activity are not detected, the manifestation of biochemical activity is sporadic. At the same time, morphological manifestations of activity are moderately expressed. Portal hypertension develops slowly, functional failure of the liver practically does not occur. The life expectancy of such patients exceeds 15 years. The main cause of death is intercurrent diseases.

5. latent cirrhosis.

Clinical symptoms, biochemical and morphological manifestations of disease activity are not determined. As a rule, portal hypertension and hepatic failure are not formed. In the prevailing number of patients, this form of liver cirrhosis does not adversely affect life expectancy.

Complications

• Bleeding from varicose veins of the digestive tract.
• Hepatorenal syndrome (malaise, thirst, dryness and decreased skin turgor, decreased urination, arterial hypotension).
• Ascites.
• Bacterial peritonitis.
• Thrombosis of the portal vein.
• hepatopulmonary syndrome.
• Accession of a secondary infection (most often with the onset of pneumonia).
• Formation of stones in the gallbladder and ducts in primary biliary cirrhosis.
• Transformation to cirrhosis-cancer.
• Liver failure.

Diagnostics

Among the laboratory and clinical indicators for the detection of liver cirrhosis, it is mandatory to conduct the following studies: hemogram, coagulogram, proteinogram, liver function tests, immunogram, as well as the determination of autoantibodies ANA, AMA, SMA, the determination of the level of α 1 -antitrypsin and protease inhibitor, α -fetoprotein serum, HBsAg, anti-HVC, indicators of iron metabolism.

Indicators reflecting changes in liver function are considered to be markers of syndromes of cytolysis, cholestasis, synthetic inferiority of liver function, as well as the occurrence of regeneration syndrome and tumor growth.

Detection of an increased amount of non-carbohydrate transferrin, IgA, γ-glutamine transferase in the blood plasma; an increase in the average volume of erythrocytes indicates subacute and chronic alcohol intoxication.

Liver fibrosis markers are being studied, however, these markers do not reflect excessive deposition of proteins in the extracellular matrix, but tissue metabolism in general, and individually do not have specificity with respect to liver tissue. The presence in the body of other inflammatory foci is accompanied by a change in their level in the blood serum.

All patients with liver cirrhosis, regardless of the factors that caused it, are determined for markers of viral hepatitis B, C, D, which helps in establishing the severity, prognosis of the disease and allows monitoring the effectiveness of treatment and vaccination.

To identify autoimmune liver damage, markers of the autoimmune process are identified; certain combinations of autoantibodies are characteristic of various autoimmune liver diseases.

Instrumental research methods are carried out: ultrasound, computed and magnetic resonance imaging, endoscopic and radionuclide studies, elastography, puncture liver biopsy.

Histomorphological examination of liver biopsy specimens in cirrhosis reveals a violation of the lobular structure of the liver, the formation of regenerate nodes (or false lobules), fibrous layers (or septa) surrounding false lobules, thickening of the hepatic trabeculae, transformation of hepatocytes (enlarged cells of the regenerative type, dysplastic hepatocytes with polymorphic , hyperchromic nuclei).

According to histomorphological criteria, macronodular, micronodular, mixed and biliary cirrhosis of the liver are distinguished.

Differential Diagnosis

In highly active forms of liver cirrhosis, it is necessary to carry out differential diagnosis with chronic active hepatitis, cholangitis, and "stagnant" liver.

As part of the clarification of the etiology of the occurrence of cirrhosis of the liver, differential diagnosis should be carried out between all its possible causes. First of all, markers of viral hepatitis B, C, D are determined and the patient is tested for alcohol abuse.

Liver cirrhosis must be differentiated from other liver diseases in which nodes are formed or fibrosis develops (nodular regenerative hyperplasia, non-cirrhotic liver fibrosis, schistosomiasis, echinococcosis, opisthorchiasis, tuberculosis, syphilis, brucellosis); malignant neoplasms of various organs with liver metastases.

The final diagnosis is established using a histological examination, in which regeneration nodes are identified.

Treatment

Treatment of liver cirrhosis involves the impact on the cause of its formation - the disease that caused cirrhosis ("basic therapy"), and symptomatic intervention, depending on the expression of clinical manifestations and complications of cirrhosis.

The general principles of treatment include strict lifelong abstinence from alcohol in the presence of alcoholic cirrhosis of the liver, the use of antiviral pharmaceuticals (IFN-α and pegylated IFN-α, nucleoside analogues) for viral cirrhosis of the liver. The exception is patients with decompensated liver cirrhosis.

The use of corticosteroids is justified in cirrhosis of the liver as a result of autoimmune hepatitis, primary biliary cirrhosis of the liver.

The leading drugs in the treatment of liver cirrhosis are those that are aimed at reducing the severity of complications of the disease, such as bleeding from varicose veins, hepatic encephalopathy, ascites, spontaneous bacterial peritonitis.

Traditionally, patients with liver cirrhosis are prescribed drugs with hepatoprotective properties - essential phospholipids, preparations of silymarin, ademethionine, ursodeoxycholic acid.

Antifibrotic therapy is aimed at inhibiting the activation of hepatic stellate cells, preventing damage and death of hepatocytes, or slowing down the proliferation of bile duct epithelial cells, which stimulate fibrogenesis through the release of profibrinogenic agents.

The effect of hepatocyte transplantation on liver function and regression of fibrosis is being studied.

Performing orthotopic liver transplantation for cirrhosis of the liver can save the patient's life.

Forecast

The prognosis for all variants of liver cirrhosis is determined by the degree of morphological changes in the liver, the tendency to progression and the lack of effective methods of treatment.

The average life expectancy is 3-5 years, rarely 10 years or more.

Prevention

Prevention measures are aimed at preventing infection with hepatitis B, C, D viruses, timely full treatment of viral hepatitis; refusal to drink alcoholic beverages, minimizing the effect of hepatotoxic substances.