Differential diagnosis of hepatitis and cirrhosis. 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.

Inflammatory liver disease of a chronic nature, which is accompanied by the appearance of specific antibodies in the body, an increase in the amount of gamma globulins and a positive response to ongoing immunosuppressive treatment, is called autoimmune hepatitis.

The diagnosis of a pathological condition is confirmed after differential diagnosis with viral inflammation, cholestatic autoimmune liver diseases, Wilson's disease, hemochromatosis, inflammation of alcoholic and drug origin. Experts say that autoimmune hepatitis (AIH) is a diagnosis of exclusion.

Causes and statistics of the disease

According to statistics, 1-1.7 new clinical cases of AIH appear per 100,000 European population per year, with a prevalence of up to 15 cases per the same population. Pathology can occur at any age, it is not tied to gender, but it is known that young women under 35-40 years old meet with liver inflammation of this nature more often than other population groups.

There are also cases of AIH among children. More often the problem occurs during early school age. It happens that the disease initially proceeds in an acute form, and over time becomes chronic. In a child, the disease can have a fulminant (malignant) course, so it is important to conduct an examination and confirm the presence of pathology in the early stages.

The true causes of autoimmune liver disease have not yet been elucidated.

There is an opinion that provocative factors that trigger the process of antibody production can be:

viruses that cause inflammation of the liver (A, B, C);
other viruses (cytomegalovirus, the causative agent of herpes, smallpox, Epstein-Barr);
treatment with interferon preparations against the background of liver damage of viral origin;
yeast fungi;
infectious agents and their toxic substances;
a number of medications.

Important! The latter include anti-tuberculosis drugs, nitrofuran derivatives, Diclofenac, Ketoconazole, etc.

What is autoimmune hepatitis can be explained in a few sentences. In simple terms, the human immune system begins to produce substances that regard its own liver cells as foreign. The process of destruction of hepatocytes by its own protective forces begins.

Classification

There are three main types of the disease, which differ from each other in clinical and laboratory data.

1type

Hepatologists consider this form of the disease a classic. It is typical for young women. In the blood of a patient with type 1, the following antibodies appear:

type 2

This form of pathology is typical for patients of childhood and the elderly. AIH type 2 usually develops at lightning speed and progresses rapidly, often turning into cirrhosis of the liver. The prognosis of survival in patients is worse than in type 1 autoimmune inflammation. Laboratory indicators confirm the presence of LKM-1 antibodies in the patient's blood.

3 type

The form is accompanied by the appearance of SLA and anti-LP antibodies to pancreatic and liver cells. It is similar in its mechanism of development to type 1 pathology. The division into subtypes is of little importance to the patient. Such a classification is interesting only from an academic point of view.

Cryptogenic form

In more than 10% of patients who have signs of autoimmune hepatitis, there are no antibodies in the bloodstream, although all other signs (histology, biochemistry, immunology data) fully indicate the presence of the disease. These patients respond positively to steroid medications. This form is called cryptogenic. Experts say that over time, autoantibodies can still appear.

Symptoms and examination data

Symptoms of autoimmune hepatitis may be mild. In this case, patients are concerned about weakness, decreased performance, fatigue. When contacting a specialist, the following complaints are usually heard:

periodic rise in temperature;
muscle pain;
pain in the joints;
dilated capillaries on the face;
red spots on the hands;
bleeding gums;
yellowness of the skin and sclera;
heaviness and discomfort in the right hypochondrium.

10% of patients, generally speaking, do not know that they have the disease, since asymptomatic AIH occurs.

Diagnosis of autoimmune hepatitis

In the primary diagnosis of autoimmune inflammation of the liver, hepatologists pay attention to the appearance of the patient. The presence of icterus of the sclera and skin, red spots on the hands, the presence of hemorrhagic rashes are specified. The specialist clarifies whether the patient has been taking any medications for a long time, whether he has concomitant diseases, how much alcohol he usually consumes. On palpation and percussion, an increase in the size of the liver and spleen is determined.

Among the laboratory indicators, the level of the following substances is specified:

ALT and AST;
alkaline phosphatase;
albumins;
gamma globulins;
immunoglobulin G;
bilirubin.

To confirm the diagnosis, all subjects undergo a puncture biopsy of the liver with further histological examination. The main signs of AIH are the presence of periportal inflammation, lymphoplasmacytic infiltration, and fibrosis. The infiltrate may contain eosinophilic cells, necrotic areas.

Important! The absence of infiltrates does not rule out the diagnosis of autoimmune inflammation, so a comprehensive diagnosis is required.

Serological examination is an obligatory stage in the differentiation of a pathological condition. The following antibodies are found in the patient's blood, which in a certain combination indicate the presence of a particular type of disease:

ANA (antinuclear antibodies) - substances that negatively affect the nucleus of the cells of the body, that is, in this case, the nuclei of hepatocytes;
anti-LKM-1 (antibodies to type 1 kidney and liver microsomes) are of great importance in determining AIH in children;
SMA (anti-smooth muscle antibodies) - substances that are aimed at combating the smooth muscles of the liver;
anti-LC1 (type 1 antibodies to the cytosolic liver antigen).

Differential Diagnosis

Primary biliary cirrhosis of the liver (PBC), primary sclerosing cholangitis (PSC), and chronic viral hepatitis (CVH) are considered the main pathological conditions with which AIH should be differentiated. This clarification allows you to choose the best recommendations and treatment for autoimmune hepatitis, as well as get the expected prognosis.

AIH with biliary cirrhosis

In patients with PBC, antibodies of the AMA type (substances aimed at combating antigens of the inner surface of mitochondrial membranes) can be detected in 30% of clinical cases, which can be confused with type 1 AIH. To say for sure that the patient does not have autoimmune inflammation will help the following data:

increased levels of alkaline phosphatase;
increase in immunoglobulin M;
the appearance of AMA antibodies in combination with the other two criteria.

AIH with primary sclerosing cholangitis

It has been established that the simultaneous occurrence of both diseases in one clinical case is possible. If the patient complains of itching of the skin, and his level of alkaline phosphatase in the blood is increased, we can talk about PSC. Cholangiography will help confirm or refute the diagnosis.

Important! It should be remembered that the results of cholangiography may be normal in PSC, confirmed by histological examination.

AIH with viral inflammation

Chronic autoimmune hepatitis is not of viral origin, but in 5–8% of patients, clinical tests reveal the presence of markers of viral hepatitis. In this case, the patient's body reacts poorly to the ongoing treatment with steroid drugs. 60% of the examined patients have antibodies to the thyroid gland and rheumatoid factor.

AIH and pregnancy

A woman may already know about her disease or discover it for the first time while carrying a baby. If symptoms occur for the first time, the patient goes to the doctor with the following complaints:

constant weakness;
decrease in working capacity;
pain in the abdomen without a clear localization;
bloating;
loss of appetite;
feeling of discomfort in the right hypochondrium;
spider veins on the skin;
skin itching.

Extrahepatic manifestations of autoimmune inflammation can be a decrease in hemoglobin levels, joint and muscle pain, acne, symptoms of inflammation of the kidneys. During pregnancy, the disease is not characterized by high activity, which allows women to safely bear the child. But there are cases of progression of the disease, against which the frequency of intrauterine death of the fetus and spontaneous interruption of gestation increases several times.

According to statistics, an exacerbation of the pathological condition during pregnancy occurs in every 4th woman, in every 3rd chronic course passes into an acute phase after the birth of babies. Against the background of the progression of the disease, complications from the mother's body are possible in the form of gastrointestinal bleeding, which in 11% of cases leads to death.

Features of treatment

There are absolute and relative indications for the treatment of autoimmune hepatitis.

Absolute

According to statistics, patients whose transaminase levels are increased by 5-10 times in combination with a 2-fold increase in quantitative indicators of gamma globulins have a survival prognosis of only 40% in the absence of adequate treatment over the past six months. If patients do not undergo therapy against the background of histologically confirmed AIH, the disease progresses to cirrhosis in 80% of clinical cases.

Important! In the latter case, a 5-year time interval is associated with 40% of deaths.

The following points are considered absolute indications for the appointment of hormonal therapy:

confirmation of the presence of histological changes;
laboratory data confirming an autoimmune process directed towards the liver;
vivid symptoms and signs of pathology, including extrahepatic manifestations.

relative

This category includes patients who have no symptoms of the disease, the histological picture is not pronounced, there are no signs of cirrhosis. In such cases, survival without immunosuppressive therapy is quite high. There are even cases of prolonged remission, but such moments are considered individually. It should be borne in mind that the transition of a sluggish state into the active phase is possible at any time, therefore, treatment with hormonal agents is justified.

When can treatment not be carried out?

Immunosuppressive treatment is recommended only in the presence of symptoms of the disease or against the background of its histological confirmation. In the absence of indications for therapy, it is not necessary to use hormonal drugs, since they can provoke a number of side effects:

decrease in the amount of albumin in the blood;
portosystemic shunting of blood, against the background of which hepatocellular function worsens.

You should be especially careful when taking hormones against the background of the following diseases and conditions (you can take drugs only if there are clear indications):

diabetes mellitus in the stage of decompensation;
osteopenia - reduced bone density, against which the risk of fractures increases several times;
mental disorders;
low levels of platelets and white blood cells in the bloodstream.

Treatment regimens

The main scheme of therapy is basic. In autoimmune hepatitis, prednisolone and methylprednisolone are considered the initial drugs of choice. To increase the effectiveness of treatment, a derivative of 6-mercaptopurine Azathioprine is added to one of these medicines. According to statistics, the Prednisolone + Azathioprine and Methylprednisolone + Azathioprine regimens can boast a 10-year patient survival rate of at least 90%. But only every third patient can completely get rid of the AIH clinic.

The results of the treatment can be manifested in several ways, the characteristics of which are described in the table.

Immunosuppression options	Peculiarities
Remission	Absolutely all parameters of the patient are normalized (clinical, laboratory, histological). After 2 years of treatment, it is observed in 70% of clinical cases.
Incomplete remission	The progression of the pathological condition stops, but complete remission is not achieved. The doctor reviews the presence of concomitant diseases, the scheme of therapy. As a rule, it is possible to solve the problem in 85% of cases in 3–3.5 years of continuous treatment.
relapse	It usually occurs after discontinuation of treatment: in half of the patients within six months, in 80% of clinical cases after 3 years. It is necessary to return to immunosuppressive therapy with the same doses of drugs or higher.
resistance	The patient's body does not respond to ongoing therapy, the indicators of laboratory and histological studies are deteriorating. Resistance is typical for every tenth patient, it requires a thorough review of the treatment regimen, checking for the presence of concomitant pathologies and their elimination.

Fighting disease in children

Autoimmune hepatitis in children often manifests itself as a fulminant and malignant course, so it is important to make an early diagnosis and choose the optimal treatment. The main drug for a sick child is Prednisolone. It is prescribed at 2 mg per kilogram of the patient's body weight per day. This is the initial dosage, it can gradually reach up to 60 mg of the drug per day.

The treatment regimen for patients may vary. Some experts recommend taking a daily hormonal drug, others are of the opinion that the medicine should be taken every other day. If the baby has acute liver failure, therapy will be ineffective. Lack of a positive response to ongoing treatment is an indication for liver transplantation.

What to choose during pregnancy?

When choosing a treatment regimen for a pregnant woman, it is important to take into account the risk of complications from the mother's body and the fetus. Prednisolone can be used by patients, since its effect on the child is considered harmless. If a woman took Prednisolone + Azathioprine before pregnancy, the last medication should be discarded, as it can cause disturbances in the baby's body.

But in the second option, it is important to assess the risks not only for the fetus, but also for his mother. With the progression of the disease, Azathioprine is not canceled, since this is fraught with the risk of developing fatal complications for the patient.

Side effects of treatment

Complications can occur both under the influence of Prednisolone and under the influence of Azathioprine. Negative reactions of the body in response to hormone treatment:

pathological weight gain;
the appearance of edema on the legs and in the lumbar region;
rashes on the skin;
white stripes (stretch marks) on the abdomen;
softening of the bone.

Possible complications of Azathioprine therapy:

oppression of hematopoiesis in the bone marrow;
decrease in the number of platelets and red blood cells in the blood;
allergic reactions;
infectious complications.

Alternative Treatment

In about 20% of patients, hormone therapy and Azathioprine may not be effective enough. It is important for such patients to choose another drug.

Budesonide

The drug is prescribed both to those patients who have not previously undergone therapy, and to those who have intolerance to drugs based on prednisolone. Budesonide rarely causes the development of side effects and unforeseen reactions. Used in tablet form.

Mycophenolate mofetil

Therapy with this medication has shown high efficiency. It is prescribed in case of a negative response to ongoing treatment with Azathioprine. The optimal dosage of the drug is 2 g per day.

Cyclosporin A

The mechanism of action of the drug is associated with inhibition of the expression of genes responsible for the production of interleukin-2 substance. The latter takes part in the body's immune response. The widespread use of the drug is limited by possible negative consequences:

increased blood pressure;
kidney damage;
violation of fat metabolism in the body with a subsequent risk of atherosclerosis;
complications of an infectious nature, etc.

Tacrolimus

The mechanism of action of the drug is similar to the previous representative of pharmacy. Clinical studies have shown that patients who do not respond to immunosuppressive treatment with prednisolone can achieve remission with tacrolimus. The data are confirmed by biochemical examination.

Cyclophosphamide

Used in patients with individual hypersensitivity to Azathioprine. The scheme of therapy is represented by a combination of Cyclophosphamide and Prednisolone. Long-term use is not recommended due to an increased risk of developing blood problems.

Liver transplant

Unfortunately, in every tenth patient, an organ transplant is considered the only chance to restore the quality of life, get rid of the disease, or eliminate the threat as much as possible. Indications for placing a patient in the waiting list for a donor are the following conditions:

symptoms and signs of decompensated stage of liver cirrhosis;
bleeding from the veins of the esophagus;
progression of pathology against the background of ongoing therapy;
the appearance of pronounced side effects against the background of ongoing treatment in the form of osteoporosis, malignant hypertension, gastrointestinal ulcers, leukopenia, etc.

Disease prognosis

Official statistics show that 40% of patients with severe pathology without therapy died during the first six months from the date of confirmation of the diagnosis. Those who did survive suffered from cirrhosis and liver failure.

How long do patients who carry out treatment and follow the recommendations of specialists about lifestyle and diet live:

The 10-year milestone is crossed by 20% of patients who are on drug treatment;
75% of patients pass the 20-year milestone on the background of drug therapy;
93% of patients undergo a 5-year milestone after an organ transplant.

It is important to seek advice from specialists immediately after the first signs of a pathological condition appear. Early diagnosis and selection of the correct therapeutic regimen will save the life and health of the patient.

Differential diagnosis of viral hepatitis: its essence, markers, the need for

The term viral hepatitis can describe either the clinical disease or the histological findings associated with this disease. Acute hepatitis virus infection can range from subclinical illness to symptomatic disease to fulminant liver failure. Adults with acute hepatitis A or B are usually symptomatic, while those with acute hepatitis C may be asymptomatic.

The clinical picture of most viral hepatitis is very similar, differing only in the severity of the disease and its results. Viral hepatitis A and E are characterized by a cyclic benign course with complete convalescence. In a complex chronic course of hepatitis B, C and D, deaths are observed, in some cases. The primary action for timely treatment is the differential diagnosis of viral hepatitis.

Symptoms and insidiousness of the disease

Typical symptoms of acute chronic hepatitis are: fatigue, anorexia, nausea and vomiting. Very high aminotransferase values (>1000 U/L) and hyperbilirubinemia are often observed. Severe cases of acute hepatitis can rapidly progress to acute liver failure, characterized by poor hepatic synthetic function. This is often defined as a prothrombin time (PT) of 16 seconds or an international normalized ratio (INR) of 1.5 in the absence of prior liver disease.

Fulminant liver failure (FLI) is defined as acute failure that is complicated by encephalopathy. Unlike encephalopathy associated with liver cirrhosis, FPI is due to an increased permeability of the blood-brain barrier and impaired osmoregulation in the brain, which leads to swelling of the brain cells. The resulting cerebral edema is a potentially fatal complication of fulminant liver failure.

FPI may occur in 1% of cases of acute hepatitis caused by hepatitis A or B. Hepatitis E is a common form in Asia, and hepatitis C remains in question. Although the problem of fulminant liver failure may resolve, more than half of all cases result in death if a liver transplant is not performed on time.

Provided that acute viral hepatitis does not progress to FPI, many cases resolve within days, weeks, or months. Alternatively, acute viral hepatitis may develop into chronic hepatitis. Hepatitis A and hepatitis E never progress to chronic hepatitis, either clinically or histologically.

The histological evolution of chronic hepatitis has been demonstrated in approximately 90-95% of cases of acute hepatitis B in newborns, 5% of cases of acute hepatitis B in adults, and up to 85% of cases of acute hepatitis C. Some patients with chronic hepatitis remain asymptomatic throughout their lives, others may complain of fatigue (mild to severe) and dyspepsia.

Approximately 20% of patients with chronic hepatitis B or hepatitis C eventually develop cirrhosis, as evidenced by histological changes, severe fibrosis, and nodular regeneration. Although some patients with cirrhosis have asymptomatic signs, others develop life-threatening complications. Clinical diseases of chronic hepatitis and cirrhosis can take months, years or decades.

Indications for holding

Differential diagnosis of viral hepatitis is necessary for the treatment of leptospirosis, yersiniosis, mononucleosis, malaria, mechanical and hemolytic jaundice, toxic hepatosis. Some acute viral illnesses trigger an immune system response that causes an increase in several types of white blood cells. Differential diagnosis may provide clues to the specific cause of this immune process. For example, it can help determine if an infection is caused by bacteria or viruses.

In malaria, there is a clear alternation of attacks of fever with chills, replaced by fever and sweat, and periods of apyrexia. An increase in the inflamed spleen in size causes very painful sensations. Hemolytic anemia is observed, the indirect proportion of bilirubin in the blood serum predominates.

During the course of obstructive jaundice, stones in the gallbladder and passages, an increase in the head of the pancreas and other symptomatic signs are detected using ultrasound. With this diagnosis, most patients have a moderate increase in the activity of ALT, AST, leukocytosis, and accelerated ESR. Hemolytic jaundice is characterized by anemia, accelerated ESR, and an increase in the indirect proportion of bilirubin in the blood. Stercobilin is always present in the stool.

Differential diagnosis of VH with hepatoses is complex and requires thoughtful and painstaking work from the doctor. In this case, a properly collected anamnesis is essential. Indications for treatment are based on viral assays (including viral nucleic acid determination), disease activity and staging (including biochemical, pathological and/or non-invasive methods), and exclude contraindications. To avoid unnecessary side effects and for a cost-effective approach, emphasis is placed on the importance of rapid and detailed virological assessments, the applicability of transient elastography as an acceptable alternative to liver biopsy, and the relevance of an appropriate follow-up schedule for viral response during therapy.

Prehepatic jaundice

With suprahepatic jaundice, excessive breakdown of red blood cells occurs, which inhibits the ability of the liver to conjugate with bilirubin. This causes unconjugated hyperbilirubinemia. Any bilirubin that manages to combine will be excreted normally, but unconjugated bilirubin left in the bloodstream causes jaundice.

Hepatic jaundice

Liver diseases of all kinds threaten the organ's ability to keep up with bilirubin processing. Starvation, circulating infections, certain drugs, hepatitis, and cirrhosis can cause hepatic jaundice, as well as some hereditary defects in liver chemistry, including Gilbert's syndrome and Crigler-Najjar syndrome.

With hepatocellular (or intrahepatic) jaundice, dysfunction of the liver itself is present. The liver loses the ability to conjugate bilirubin, but in cases where it can also become cirrhotic, it compresses the intrahepatic portions of the biliary tree to cause some degree of obstruction. This results in both unconjugated and conjugated bilirubin in the blood, referred to as a "mixed" picture.

Subhepatic jaundice

Subhepatic forms of jaundice include jaundices caused by the inability of soluble bilirubin to reach the intestine after it has left the liver. These disorders are called obstructive jaundices. The most common cause is the presence of gallstones in the ducts. Other causes are related to birth defects and infections that damage the bile ducts: drugs, infections, cancer, and physical trauma. Some medications, and pregnancy in rare cases, simply cause the bile to stop in the channels.

Subhepatic jaundice refers to obstruction of the bile drainage. Bilirubin that is not excreted from the body combines with the liver, resulting in conjugated hyperbilirubinemia.

Differential diagnostic markers

Definitive diagnosis of hepatitis B or hepatitis C requires a variety of immunological and molecular diagnostic tests and takes a significant amount of time before starting treatment. Recently there have been tabular reports suggesting a screening marker using CBC with Cell Population Data (CPD) for infectious diseases such as sepsis and tuberculosis. If such screening markers for hepatitis are developed, it would help to reduce time to treatment and medical costs.

192 patients with acute viral hepatitis (AVH) from three different hospitals in the Madras metropolitan area, between November 1985 and January 1986, were tested for serological markers of hepatitis A virus (anti-HAVIgM) and hepatitis B virus (HBsAg, HBeAg , anti-HBcIgM and anti-HBs) using an enzyme-linked immunosorbent assay (ELISA). Hepatitis B was diagnosed as the main type of AVH in the hospital (48.9%). Using the HBV anti-HBcIgM marker and anti-HAVIgM, it was possible to find out that 13.5% of cases currently suffering from hepatitis A were either carriers of HBV (8.3%) or cases recovering from a previous attack on hepatitis B (5.3%). Various combinations of HBV marker positivity have been observed and their diagnostic value has been suggested.

Diagnosis of congenital hepatitis in children

Some chemicals in bile can cause itching when too much of them enters the skin. In newborns, insoluble bilirubin can enter the brain and cause irreparable damage. Long-term jaundice can upset the balance of chemicals in bile and cause stones to form. Aside from these potential complications and discoloration of the skin and eyes, jaundice itself is harmless. Other symptoms are determined by the disease causing jaundice.

Newborns are the only large category of patients in whom jaundice itself requires attention. Since insoluble bilirubin can enter the brain, the amount in the blood must not exceed a certain level. If there is a suspicion of increased hemolysis in a newborn, the level of bilirubin should be measured again during the first few days of life. If the bilirubin level, shortly after birth, is too high, treatment should begin immediately. Transfusing most of a child's blood was the only way to reduce the amount of bilirubin a few decades ago. It was then discovered that bright blue light turns bilirubin harmless. The light chemically changes the bilirubin in the blood as it passes through the baby's skin. In 2003, researchers tested a new drug called Stanat that promised to block the production of bilirubin, but was never approved and widely used.

Differentiation of hepatitis from other diseases

In medicine, to differentiate is to look for differences in different but similar diseases.

Common causes of cirrhosis of the liver: prolonged treatment of viral hepatitis C and excessive alcohol abuse. Often there are cases of obesity, which can be a risk factor alone or in combination with excessive alcohol consumption and hepatitis C.

According to the US National Institutes of Health, differential diagnosis of hepatitis has revealed that hepatitis C is more likely to develop in people who have consumed more than two alcoholic beverages per day (including beer and wine) for several years, especially in women. For men, consuming three a day over the same period could put them at risk for cirrhosis. However, the amount for each person varies, and this does not mean that everyone who has ever drunk more than the average value will necessarily develop cirrhosis. Cirrhosis caused by alcohol consumption is often the result of systematic alcohol consumption in volumes several times higher than this value and for 10-12 years.

Cirrhosis of the liver is a diffuse process characterized by fibrosis and transformation of the normal structure of the liver with the formation of nodes. It serves as the end stage of a number of chronic liver diseases. severity and cirrhosis prognosis depend on the volume of the remaining functioning mass of the liver parenchyma, the severity of portal hypertension and the activity of the underlying disease that led to impaired liver function.

ICD-10 K74 Fibrosis and cirrhosis of the liver K70.3 Alcoholic cirrhosis of the liver K71.7 With toxic liver damage K74.3 Primary biliary cirrhosis K74.4 Secondary biliary cirrhosis K74.5 Biliary cirrhosis, unspecified K74.6 Other and unspecified cirrhosis of the liver K72 Chronic liver failure K76.6 portal hypertension.

Diagnosis example

Epidemiology

Cirrhosis of the liver ranks first among the causes of death from diseases of the digestive system (excluding tumors). The prevalence is 2–3% (based on autopsy data). Cirrhosis of the liver observed 2 times more often in men over 40 compared with the general population.

Etiology

The most common causes of liver cirrhosis are the following diseases and conditions. ■ Viral hepatitis - (B, C, D). ■ Almost always, the development of alcoholic cirrhosis is preceded by continuous drinking for more than 10 years. The risk of liver damage is significantly increased with consumption of more than 40–80 g of pure ethanol per day for at least 5 years. ■ Immune liver diseases: autoimmune hepatitis, graft-versus-host disease. ■ Diseases of the biliary tract: extra- and intrahepatic obstruction of the biliary tract caused by various causes, cholangiopathy in children. ■ Metabolic diseases: hemochromatosis, α1-antitrypsin deficiency, Wilson-Konovalov disease, cystic fibrosis (cystic fibrosis), galactosemia, glycogenosis, hereditary tyrosinemia, hereditary fructose intolerance, abetalipoproteinemia, porphyrias. ■ Violation of the venous outflow from the liver: Budd-Chiari syndrome, veno-occlusive disease, severe right ventricular heart failure. ■ The use of hepatotoxic drugs (methotrexate B, amiodarone C), toxins, chemicals. ■ Other infections: schistosomiasis, brucellosis, syphilis, sarcoidosis. ■ Other causes: non-alcoholic steatohepatitis, hypervitaminosis A. The time required for the development of liver fibrosis, largely depends on the etiological factor. The most commonly observed forms of fibrosis and cirrhosis develop slowly: alcoholic cirrhosis of the liver develops over 10–12 years of alcohol abuse, and viral cirrhosis of the liver develops 20–25 years after infection. The fastest rates of development of liver cirrhosis (several months) were observed in patients with biliary obstruction of tumor etiology and in newborns with bile duct atresia.

Prevention

Prevention of liver cirrhosis includes the timely detection of conditions that can lead to its development, and adequate correction of the detected violations. ■ Hemochromatosis. Several studies have demonstrated the cost-effectiveness of population-based screening for hereditary hemochromatosis. During screening, serum iron, total and free iron-binding capacity of serum are determined. If these indicators are increased, they are determined again and, with a significant increase, the patient is examined for hemochromatosis. ■ Screening for alcohol misuse: limiting alcohol consumption significantly reduces the likelihood of developing liver cirrhosisB. It is possible to use a CAGE test (Cut - cut, Angry - angry, Guilty - guilt, Empty - empty), which includes four questions. 1. Have you ever felt that you should cut down on your drinking? 2. Have you ever felt irritated if someone around you (friends, relatives) told you about the need to cut down on your drinking? 3. Have you ever experienced guilt associated with drinking alcohol? 4. Did you ever feel like drinking alcohol the morning after your drinking episode? Sensitivity and specificity are approximately 70%, the main advantage is the possibility of testing when collecting anamnesis. A positive answer to more than two questions raises the suspicion of alcohol dependence, accompanied by changes in behavior and personality. Of the laboratory signs, markers of alcohol abuse can be a predominant increase in AST activity compared to ALT, an increase in GGTP, Ig A, and an increase in the average volume of erythrocytes. All of these features have high specificity with relatively low sensitivity, with the exception of GGTP activity, an increase in which is considered a highly specific sign of both alcohol abuse and alcohol dependence. ■ Screening for hepatitis B and C viruses: for details, see the article "Viral Hepatitis, Acute and Chronic". Individuals with risk factors for chronic hepatitis should be tested for hepatitis B and C viruses. The survival of patients with chronic hepatitis, both with and without cirrhosis, is significantly higher with timely interferon B therapy. ■ Screening for hepatotoxic drugs, primarily methotrexate B and amiodarone C - ALT and AST activity is determined every 1–3 months. These drugs with prolonged use can lead to cirrhosis of the liver. ■ Screening among relatives of patients with chronic liver disease. Relatives of the first degree of kinship are examined: the degree of transferrin saturation and serum concentration of ferritin are determined (detection of congenital hemochromatosis B), serum concentration of ceruloplasmin (diagnosis of Wilson-Konovalov's disease B), detection of α1-antitrypsin deficiency. ■ Screening for non-alcoholic fatty liver disease. Risk factors - type 2 diabetes mellitus, obesity, hyperlipidemia, AST/ALT activity ratio above 1.0; the risk increases especially significantly in patients over 45 years of age. All patients at risk should undergo liver ultrasound to detect steatosis. Patients should be informed about the possibility of developing cirrhosis of the liver.

Screening

Screening for direct detection of liver cirrhosis is not carried out. Screening activities are carried out to identify diseases and conditions that can lead to cirrhosis of the liver (see the Prevention section above).

Classification

Cirrhosis of the liver is divided by etiology (see above section "Etiology") and severity, for which the Child-Pugh A classification is used (Table 4-10). Table 4-10. Determining the severity of liver cirrhosis according to Child-Pugh

Index
Index
Encephalopathy
		Soft, easy to treat	Tension, difficult to treat
Serum bilirubin concentration, µmol/l (mg%)	Less than 34 (<2,0)	34–51 (2,0–3,0)	Over 51 (>3.0)
Serum albumin level, g
Prothrombin time (s), or prothrombin index (%)			More than 6 (<40)

Each of the indicators is evaluated in points (respectively, 1, 2 or 3 points). The interpretation is carried out according to the following criteria. ■ Class A (compensated) - 5-6 points. ■ Class B (subcompensated) - 7–9 points. ■ Class C (decompensated) - 10-15 points.

Diagnostics

Survey plan

Assume the diagnosis of liver cirrhosis allow clinical and anamnestic data (symptoms are very diverse, see the section "Anamnesis and physical examination"), to confirm - the results of laboratory and instrumental examination. It is necessary to establish the etiology of the disease, since in some cases etiotropic therapy can slow down the progression of the disease and reduce mortality. The most common causes are viral hepatitis and alcohol abuse, less common causes are listed in the Etiology section. In some cases, the cause of cirrhosis cannot be detected, in this case, the diagnosis of cryptogenic cirrhosis of the liver is established. When establishing a diagnosis, it is necessary to additionally evaluate the following parameters. ■ The state of the main functions of the liver: the presence of syndromes of cytolysis, cholestasis, the state of the blood coagulation system (hemorrhagic syndrome is typical for cirrhosis), protein-synthetic function of the liver. ■ Identification of hypersplenism syndrome (primarily by platelet count). ■ Identification and assessment of the degree of portal hypertension (dangerous primarily bleeding from varicose veins of the esophagus and stomach - FEGDS). ■ Detection of possible ascites. ■ Assessment of mental status for timely diagnosis of hepatic encephalopathy. The severity of liver cirrhosis is determined by the Child-Pugh classification of hepatocellular function in cirrhosis of the liver (see the "Classification" section).

History and physical examination The following symptoms and syndromes are characteristic. ■ General symptoms: drowsiness, weakness, fatigue and itching of the skin. With severe drowsiness, as well as with irritability and aggressive behavior, it is necessary to exclude hepatic encephalopathy. ■ Changes in the liver and spleen: the liver is thickened and enlarged, but sometimes it can be small. In most patients, a moderately enlarged spleen is palpated (manifestations of portal hypertension). ■ Jaundice: the initial signs of jaundice are invisible to the patient and are characterized by icterus of the sclera and mucous membranes, frenulum of the tongue, a slight darkening of the urine, which patients usually do not attach due importance to. ■ Difficulties in breathing (shallow, rapid breathing) may be due to: ascites with increased intra-abdominal pressure and limitation of diaphragm mobility, chronic heart failure, hydrothorax against the background of edematous-ascitic syndrome. ■ Hemorrhagic syndrome (due to a violation of the synthesis of blood coagulation factors in the liver): bleeding gums, nosebleeds are characteristic. Patients notice that bruises and bruises are formed even with minor mechanical stress. ■ Portal hypertension: ascites, varicose veins of the esophagus and stomach, dilatation of the veins of the anterior abdominal wall in the form of a "Medusa's head", splenomegaly, hepatic encephalopathy. ■ Ascites (manifestation of portal hypertension): an increase in the volume of the abdomen due to the accumulated fluid (more than 10–15 liters of fluid can accumulate, a “frog belly” is typical), with a large amount of it, a picture of “tense ascites” is created, bulging of the navel, sometimes with its gaps, percussion signs of fluid in the abdominal cavity, a positive symptom of fluctuation. ■ Other signs characteristic of liver cirrhosis: ✧ telangiectasia on the upper half of the trunk and face; ✧ palmar erythema; ✧ gynecomastia; ✧ testicular atrophy/amenorrhea; ✧ swelling of the legs (with ascites); ✧ Cruvelier-Baumgarten murmur - venous murmur over the abdomen associated with the functioning of venous collaterals; ✧ Dupuytren's contracture, more typical for liver cirrhosis of alcoholic etiology; ✧ changes in the terminal phalanges of the fingers according to the type of drumsticks; ✧ skeletal muscle atrophy, lack of hair growth in the armpit; ✧ an increase in the parotid salivary glands (typical for patients suffering from alcoholism); ✧ hepatic odor occurs during decompensation of liver functions, precedes and accompanies the development of hepatic coma; ✧ Flapping tremor is also characteristic of decompensated hepatic functions. Particular attention should be paid to the signs of developed complications: ■ symptoms of gastrointestinal bleeding: hematemesis, melena, systolic blood pressure less than 100 mm Hg. with a decrease of 20 mm Hg. when moving to a vertical position, heart rate over 100 per minute; ■ signs of spontaneous bacterial peritonitis - diffuse pain of varying intensity in the abdominal cavity, fever, vomiting, diarrhea, signs of intestinal paresis; ■ confusion, reflecting the development of hepatic encephalopathy; ■ decrease in daily diuresis - a likely sign of the development of renal failure.

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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 clinic at the place of residence, where, after the examination, she was referred for hospitalization at the Medical Center of the WKSMU in the therapeutic department for examination, where she was diagnosed with cirrhosis of the liver of viral etiology and a II disability group 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 7 cm

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 7 cm.

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 constant, 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 - palpable 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 clinic at the place of residence, where, after the examination, she was referred for hospitalization at the Medical Center of the WKSMU in the therapeutic department for examination, where she was diagnosed with cirrhosis of the liver of viral etiology and a II disability group 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.

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 cooked 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 jelly and gelatin, 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, the degree of activity, the 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 CG, 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 liver dysfunction, severity of extrahepatic (systemic) lesions, severity of portal hypertension and hypersplenism, degree of disability - 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 stage II-III activity, severe liver failure, stage IV portal hypertension, intoxication and encephalopathy.

Cause of disability: the most common is "general illness"; 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 CG, 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 discontinued. 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 chronic hepatitis 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, 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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