Additional methods of examination

Clinical blood analyses. An active cirrhotic process is characterized by anaemia, leucopenia, thrombocytopenia, and increased ESR. Anaemia can be due to hypersplenism and gastro-intestinal haemorrhage, and often increased haemolysis, which is accompanied by reticulocytosis of the peripheral blood.

Biochemical blood analysis. The blood serum bilirubin content considerable only in the final stage of the disease. At the same time, the affection of the excretory motion of the cirrhotic liver can be assessed by the presence of the conjugated fraction of bilirubin (bound bilirubin). Its content increases in normal and increased total bilirubin. The blood serum bilirubin content varies in biliary cirrhosis of the liver, mostly at the expense of bound bilirubin.

- Affection of liver cells is manifested by characteristic changes in the protein indices: decreased concentration of serum albumins and hypergammaglobulinaemia which in turn decreases the albumin-globulin coefficient.

- The blood level of lipids and cholesterol also increases considerably in the presence of biliary cirrhosis. A sensitive index of liver dysfunction is the decreased activity of cholinesterase.

- Transaminase activity increases in exacerbation of liver cirrhosis. Activity of alkaline phosphatase also increases in biliary cirrhosis.

- The decreased prothrombin content (which is synthesized by the liver cells), increased antithrombin coagulative activity and decreased total coagulative activity of plasma are important in the aetiology of haemorrhagic diathesis in liver cirrhosis.

- Detection of α-phetoprotein is required for screening on malignant transformation of cirrhosis. Research of the ceruloplasmin maintenance - etiologic factor establishment (Konovalov-Wilson's disease).

Ultrasound examination (ultrasonography) - revealing of hepatomegalia, spleenomegalia and infringement of hepatic structure.

Varicose veins of the esophagus are revealed by X-rays or by upper gastrointestinal endoscopy. Rectoromanoscopia – detection of varicous dilated veins of rectal textures.

Instrumental non-obligatory methods (under indications): hepatoscyntigraphia; computed tomography and magnetic resonance imaging.

Syndrome of portal hypertension

Portal hypertension results from destruction and distortion of the hepatic vasculature leading to obstruction of blood flow and increasing backward pressure, resulting in hypertension in portal circulation. Normal pressure is 2-5 mmHg. Patients developing complications usually have portal pressure above 12 mmHg. On ultrasound maximum normal diameter of portal vein is 1 cm, it becomes dilated in portal hypertension.

Classification

Depending on the etiology and mechanism of developing there are the next forms of the portal hypertension syndrome:

I. Suprahepatic block:

- hepatic veins thrombosis;

- hepatic veins compression;

- vena cava inferior compression and/or thrombosis.

II. Intrahepatic block:

- chronic hepatitis;

- liver cirrhosis;

- tumor of the liver;

- metastatic liver damage.

III. Subhepatic block:

- congenital anomaly of vena porta;

- compression of a portal collector by a tumor;

- spasms.

The features of portal hypertension are as follows: splenomegaly, hypersplenism, collateral circulation and ascites.

Splenomegaly. Splenomegaly is a cardinal finding, and a diagnosis of portal hypertension is unlikely when splenomegaly can not be detected clinically or by ultrasonography. Clinical splenomegaly is present in 35-50% of cases.

Hypersplenism. When spleen becomes enlarged its function of removing cells from circulation also increases, this is called hypersplenism. Moderate thrombocytopenia frequently occurs (platelet count around l00x10⁹/lit). Leukopenia occurs occasionally and anemia rarely.

By definition hypersplenism is characterized by: splenomegaly; cytopenia (thrombocytopenia, granulocytopenia or pancytopenia); normal bone marrow.

Collateral circulation. Increased portal vascular resistance leads to gradual reduction in the flow of portal blood to the liver and simultaneously to the development of collateral vessels, allowing the portal blood to bypass the liver and enter the systemic circulation directly. Collateral vessel formation is more prominent in the following areas:

• in the distal esophagus and proximal stomach (esophagogastric varices);

• in the distal rectum and anus(causing hemorrhoids);

• on the anterior abdominal wall which radiate prominently from the umbilicus forming "caput Medusae";

• renal , lumber, ovarian and testicular vessels (rare).

The most important collateral vessels are the esophagogastric varices as they can cause bleeding which is usually severe and acute. Bleeding from rectum and anus is rare.

Ascites. Accumulation of fluid in peritoneal cavity (ascites) in cirrhosis occurs, owing to two factors: portal hypertension and hepatic dysfunction. Portal hypertension causes transudation of fluid in peritoneal cavity from the portal circulation (due to increased hydrostatic pressure), while the hepatic dysfunction causes ascites by three mechanisms:

• salt and water retention occurs as a result of peripheral arterial vasodilatation and consequent reduction in effective blood volume. Nitric oxide is probably the vasodilator although prostaglandins and atrial natriuretic peptide may also be involved. The reduction in effective blood volume due to vasodilatation stimulates reninangiotensin system that promotes salt and water retention through stimulation of aldosterone. Failure of liver to metabolize aldosterone causes salt and water retention;

• liver is not able to synthesize sufficient proteins thus causing hypoalbuminemia, which results in decreased colloid osmotic pressure of the plasma resulting in leakage of fluid and development of edema and ascites;

• normally liver causes aldosterone metabolism, in case of hepatic dysfunction liver is unable to metabolize it, resulting in secondary hyperaldosteronism, and retention of sodium and water.