Clinical symptomatology and for

Cirrhosis of the liver. Clinical symptoms of liver cirrhosis vary widely depending on the degree of dysfunction of parenchyma, portal hypertension, activity and stage of cirrhotic process.
Postnecrotic cirrhosis according to various statistics is 5-37,5% of all cirrhosis (Kleckner, 1960), according to our data - 32%. In most cases (at least 79%) postnecrotic cirrhosis develops as a consequence of the different options Botkin's disease, but mainly heavy and prolonged reaches the last or after a severe relapse of hepatitis. Reports of postnecrotic cirrhosis of the liver another etiology single.
Postnecrotic cirrhosis occurs mostly in individuals, young and Mature age.
The evolution of this type of cirrhosis corresponds fast, clinically expressed the progression of the disease. In one third of cases of postnecrotic cirrhosis were identified before the expiration of six months after acute hepatitis, and only 18% of patients this period exceeding two years. The clinical picture of postnecrotic cirrhosis of the liver from the very beginning at the forefront are the symptoms of liver failure. The periods of exacerbation (activity) of the disease clinical manifestations resemble acute hepatitis. One of the earliest signs of active postnecrotic cirrhosis are a pain in the right hypochondrium, and epigastric region. They usually appear before other signs of exacerbation. Often simultaneously were impaired General health, dyspeptic symptoms, anorexia.
Jaundice different degrees accompanied by an active phase of postnecrotic cirrhosis in 80% of cases. Often when this happens and Cholesky chair, sometimes there comes playframe - allocation of faeces excess of bile pigments. The last is explained by increased hemolysis. In case of exacerbation seen the emergence of new "vascular asterisks", sometimes itchy skin; often bleeding (often nasal). In periods of progression emerge or worsen violations of the liver.
In 89% of cases in active phase is marked hyperbilirubinemia; even at normal bilirubin level in the plasma is determined by the increase conjugated factions. Always marked urobilinemia, decreased prothrombin index, less frequently violated performance testing Quick - Pytel, samples with diabetes load. Usually identified biochemical signs of exacerbation of cirrhotic process.
Exacerbation, especially clinically rapid, accompanied by a fever of the wrong type, which cannot be explained by any intercurrent diseases. With the rapid progression of the disease is observed, as a rule, remitting, and sometimes hectic type fever. Approximately 40% of cases simultaneously with fever noted neutrophilic leucocytosis (from 10 to 18 thousand of 1 mm3).
Clinically initial stage of postnecrotic cirrhosis corresponds increased, heavy liver. For postnecrotic cirrhosis is characterized by uneven, bumpy surface and its uneven edge. In some cases the surface of the liver remains smooth. With the rapid progression of the disease size of the liver from the very beginning can be reduced. In most patients palpable spleen. Usually there are no obvious symptoms of portal hypertension, however, instrumental examination such is detected. Ascites appears infrequently and only in the active phase.
Upon liquidation of the aggravation of the cirrhotic process ascites may disappear or decrease. This is because the emergence of free fluid in the abdominal cavity caused not so much by a mechanical obstacle portal blood flow, how much is connected with violation of a number of physiological mechanisms aimed at maintaining the constancy of the water environment in the body.
Often there is hyperproteinemia. Manifestations of hypersplenism rare (12%). The most characteristic feature of the initial stage of postnecrotic cirrhosis is the dynamics of indices of functional tests. They significantly changed in the active phase and almost completely back to normal with the transition process in inactive phase. Similarly changing and well-being of patients.
Stage formed cirrhosis clinically differs from the initial appearance of the evident signs of portal hypertension (ascites, visible venous collaterals, varicose veins of the esophagus and bleeding from them), the change of hyperproteinemia a tendency to gipoproteinemii, emerging with the advent of ascites. At this stage, as a rule, there are significant violations of the indices of functional tests in the active phase, but their restoration in the inactive phase remains incomplete. Indicators of functional tests remain moderately disturbed and in the absence of signs of disease progression in cirrhotic process. In one fifth of cases observed of hypersplenism: anemia, leukopenia, thrombocytopenia.
In the final stage all patients expressed signs of portal hypertension and first of all ascites. Often detected right hydrothorax. Due to the presence of ascites and reduce the size of the liver last probed rare. Usually percussion hepatic dullness reduced. Characteristic features of the disorder General power supply: exhaustion, hypovitaminosis (heiloz, "landkarten" language, alvimarine, dry skin), hypoproteinemia. Half of the patients detected hypochromic anemia, development of which is caused by bleeding and hypersplenism. The latter is typical for the final stage of postnecrotic cirrhosis.
Unlike the two previous stages, in the final clinical manifestations does not significantly vary depending on the activity of the process. In inactive phase health, liver remain broken in the same way as with the active progression to cirrhosis.
The nature of the flow of postnecrotic cirrhosis is different. Only this type of cirrhosis may develop acute. In this disease, starting severe acute necrotic hepatitis (usually with a suspended development of hepatic coma), directly evolves into cirrhosis of the liver, clinical and morphological characteristics which can be detected by 10-30-day sickness. Further progression of the disease occurs as rapidly and usually ends fatally, without any period of relative remission.
The most typical discussed forms of cirrhosis relapsing course in separate exacerbation periods of activity, alternating with periods of various duration relative inactivity cirrhotic process.
According to E. M. Tareeva (1963, 1964), on the basis of postnecrotic cirrhosis often than with cirrhosis different morphological type, occurs primary liver cancer.
Death can occur at any stage of the disease development. Often fatal outcome observed in the result expressed functional liver failure with coma. The latter often occurs after the esophago-gastric bleeding.