Edema with cirrhosis treatment
Most patients with clinical signsactive cirrhosis of the liver, significant changes in functional tests were observed: hyperbilirubinemia, hypoalbuminemia, hypocholesterolemia, decreased prothrombin, increased indices of thymol and γ-globulin. However, only hyperbilirubinemia, an increase in thymol test and hypergammaglobulinemia were statistically significant. These functional tests can serve as biochemical indicators of liver cirrhosis activity, and an increase in the indices of thymol test to 8 units. and γ-globulins up to 30% is regarded as a moderate activity, and above these boundaries - as a pronounced activity.
Statistically significant difference in contenttotal protein of blood serum, albumins, prothrombin, cholesterol with active and inactive liver cirrhosis was not observed. There was a deviation of immunological parameters: an increase in all classes of immunoglobulins, the detection of antibodies to various components of the hepatic cell, a decrease in complementary activity, suppression of blastic transformation of lymphocytes, inhibition of the inhibition of migration of leukocytes. A significant increase in alanine and aspartate aminotransferase is important for assessing the activity in the initial and expanded stages of liver cirrhosis. However, in the terminal stage of liver cirrhosis, these enzymes can not be used as indicators of the activity of the process, since their activity in most patients was within normal limits. This is due to a violation (reduction) of the synthesis of these enzymes in the dystrophic stage of liver cirrhosis.
Morphological signs of liver cirrhosis activity
Morphological signs of cirrhosis activityliver are expressed in the predominance of destructive processes - the emergence of a large number of step necrosis, large areas of necrosis, pronounced hydropic dystrophy, rosette figures, a large number of focal congestions of histiolymphoid infiltrates in various sites of regenerate nodes. Other signs of activity of the process are also noted: thickening of trabeculae due to regeneration of hepatic cells, proliferation of connective tissue between nodes and within them, as well as an inflammatory cellular reaction with violation of the integrity of the border plate.
When studying liver punctures in patients with liver cirrhosis, it was found that in some cases, with a minimum of signs of activity, a known stabilization of the cirrhotic process is possible.
Decompensation of cirrhosis is determined on the basis ofsigns of hepatic cell failure and portal hypertension. The comparative frequency of the main symptoms with compensated and decompensated liver cirrhosis is presented in Table. 2.
Table 2. The incidence of major symptoms with compensated and decompensated hepatic cirrhosis
Decompensation of chronic liver diseases inMost cases are associated with an active process in the liver. This explains the coincidence of a number of clinical symptoms and biochemical indicators characterizing the activity and decompensation of liver diseases. For clinical practice, it is important that the activation of the process causes an increase in hepatic cell failure and portal hypertension.
Prognosis for cirrhosis of the liver
Cirrhosis has the following most severecomplications: hepatic coma, bleeding from varicose veins of the esophagus or less often the stomach, intestines, portal vein thrombosis, the formation of liver cancer. They can only be called conditionally complications, since in fact they are manifestations of the terminal stage of this liver disease.
Gastrointestinal bleeding with cirrhosis of the liver
Gastrointestinal bleeding along withhepatic coma is the most common complication of liver cirrhosis. Bleeding comes from varicose veins of the esophagus or stomach, less likely to result from erosive gastritis and esophagitis, stomach or duodenal ulcers. Important violations are the coagulation system and sudden pressure rises in the portal vein system.
When analyzing the case histories of patients who died fromcirrhosis of the liver in the clinic I Molmi them. IM Sechenov found that the clinical symptomatology of liver cirrhosis (hemorrhagic, edematous-ascitic syndrome, features of development of hepatic cell insufficiency) and lethality from gastrointestinal bleeding, hepatic coma, extrahepatic complications in the terminal stage of cirrhosis did not differ with its viral and alcoholic forms. 45% of patients had bleeding from the enlarged veins of the esophagus and stomach. The majority (34.5%) died immediately after the first bleeding, and 7.8% had repeated bleeding in the period from one year to two years. Only 3,6% of patients had a bleeding in the anamnesis, and death came from other causes. The frequency of bleeding did not depend on the type of cirrhosis of the liver.
When morphological examination of the liver in casesdeath from bleeding destructive processes are usually represented by hydropic dystrophy, necrosis of individual hepatocytes. Stepwise necrosis was rare, mainly near connective tissue layers. Regeneration processes were sufficiently expressed - many binuclear hepatocytes and cells with large nuclei were observed. In the layers of connective tissue, vasoconstriction, histiolymphocytic infiltration, proliferation of the bile ducts were noted.
Encephalopathy with cirrhosis of the liver
Encephalopathy was detected in 67.2% of patients with cirrhosisliver. The majority of them developed terminal liver-cell failure, which served as the direct cause of death, and only a few patients from the time of encephalopathy until death passed from several months to a year. In 1/3 of patients who died during the phenomena of hepatic coma, it was triggered by bleeding from the enlarged veins of the esophagus and stomach.
Morphological examination revealed in thesecases with all forms of cirrhosis of the liver, significant hydropic dystrophy of hepatocytes, a number of step necrosis and large areas of necrosis in the regenerate nodes, as well as focal histophilic infiltration in their various parts. Signs of regenerative processes in the form of binuclear hepatocytes, cells with large nuclei, were weakly expressed. In the layers of connective tissue, abundant diffuse histophiloid infiltration, as well as proliferation of bile ducts, have been found.
Ascites are an excessive accumulation of fluid in the abdominal cavity.
Pathogenesis of ascites in liver cirrhosis
Figure 3. Pathogenesis of ascites. According to existing hypotheses, the leading role may play a delay in sodium, a decrease in effective BCC or the expansion of arterioles.
Ascites were detected in 83.6% of patients in terminalstage of cirrhosis of the liver, while 22% of patients it developed no earlier than a month before death. The lifespan from the time of diagnosis of ascites in the remaining observations was 5 months to 3 years. Only a few patients lived from 5 to 8 years after the appearance of "persistent" ascites against the background of taking diuretic drugs.
A clear dependence of the ascites frequency on the formcirrhosis of the liver was not detected, ascites was observed in the far-gone stage equally often with all cirrhosis. Currently, a relatively rare complication of the terminal stage is ascites-peritonitis due to coccal infection, staphylococcal sepsis, and colibacillosis.
In recent years, the development of liver cancer has increasedagainst cirrhosis of the liver. Viral hepatitis is detected in anamnesis in 28.6% of patients, alcoholism in 14.4%, drug-induced hepatitis in 2, 8 %%, gallbladder and bile duct disease - in 5.6%, etiological factors remained unknown in 48% patients with cirrhosis-cancer. In no case has there been a development of cancer on the background of biliary cirrhosis of the liver. In 75% of cases, liver cancer was hepatocellular and in 25% - cholangiocellular.
Cirrhosis can occur with prolongedclinical remissions, it is possible to stabilize the process. Formed active cirrhosis of the liver is incurable, it leads to death due to hepatic cell failure, bleeding from the dilated veins, intercurrent infections.
Prevention of cirrhosis of the liver consists in eliminatingor restriction of the effect of etiological factors, timely recognition and treatment of chronic hepatitis and fatty hepatosis. When cirrhosis of the liver is important to delay the progression of the disease and ensure the prevention of complications.
The incapacity of patients with cirrhosis of the liver at an early stage is limited, at the stage of the formed cirrhosis in most cases is lost.