Hyperemic (hemolytic) jaundice

Superhepatic jaundice is caused by excessive formation of bilirubin, exceeding the ability of the liver to remove it. The liver is able to metabolize and excrete bile in its bile in an amount 3-4 times greater than its production under normal conditions. When the ability of the liver to metabolize, all bilirubin develops. Superhepatic jaundice. Moreover, in spite of the fact that the liver metabolizes bilirubin more than in norm, all its excess amount from the blood can not be removed, the level of free (unconjugated) bilirubin increases in the blood.

The main features of superhepatic (haemolytic) jaundice:

• icteric sclera and skin, usually mild, has a lemon-yellow hue;
• at the same time there is pallor of the skin (due to anemia);
• pruritus and scratching of the body absent;
• pains in the liver are rare, usually only with calculous gallbladder;
• enlargement of the liver, as a rule, insignificant;
• a significant increase in the spleen in the course of the chronic course of the process;
• anemia of varying severity;
• marked reticulocytosis in peripheral blood;
• decrease in the osmotic resistance of erythrocytes;
• functional tests of the liver (blood levels of ASAT, ALAT, alkaline phosphatase, prothrombin, cholesterol, thymol, sulemic samples) are normal;
• Hyperbilirubinemia rarely exceeds 85.5 μmol / l, indirect (unbound, unconjugated) bilirubin predominates;
• in the urine the content of urobilin is sharply increased, bilirubin is absent;
• observed pleochroism (sharp staining in a dark color) stool due to a large number of stercobilin;
• when chronic hemolysis develops calculous biliary tract, which can manifest as biliary colic. The stones are detected on cholecystograms and ultrasound of the bile ducts;
• puncture biopsy reveals a secondary hemosiderosis of the liver;
• the life span of erythrocytes is shortened (according to studies with 51 Cr).

[1], [2], [3], [4], [5]