What Is Hemolytic Jaundice?

Jaundice is a symptom and sign of yellowing of the skin, sclera and mucous membranes due to elevated bilirubin in the serum. The highest normal bilirubin was 17.1 mol / L (1.0 mg / dl), of which bound bilirubin was 3.42 mol / L and unbound bilirubin was 13.68 mol / L. Hemolytic jaundice is due to the destruction of a large number of red blood cells, forming a large amount of unbound bilirubin, which exceeds the ability of liver cells to take up, bind and excrete. On the other hand, the toxic effects of anemia, hypoxia and red blood cell destruction products due to hemolysis It weakens the metabolic function of bilirubin of liver cells, and causes unbound bilirubin to remain in the blood, which causes jaundice that exceeds normal levels.

Basic Information

Visiting department

Internal medicine

Common causes

Diseases that cause hemolysis

Common symptoms

jaundice

Contagious

no

Causes of hemolytic jaundice

Hemolytic jaundice can occur in any disease that can cause hemolysis, including congenital hemolytic anemia and acquired acquired hemolytic anemia. The former includes thalassemia (thalassemia), hereditary spherocytosis, etc .; the latter includes autoimmune hemolytic anemia, neonatal hemolytic disease, hemolysis after transfusion of different blood types and broad bean disease, primary aminoquinoline, snake poison, Toadstool, paroxysmal nocturnal hemoglobinuria, etc.

Clinical manifestations of hemolytic jaundice

General jaundice is mild, light lemon-colored, and fever, chills, headache, vomiting, low back pain may occur during acute hemolysis, and there are varying degrees of anemia and hemoglobinuria (urine is soy or brown), and severe kidney disease may have acute kidney disease. Functional failure. Chronic hemolysis is mostly congenital, with splenomegaly in addition to anemia.

Hemolytic jaundice test

Total serum bilirubin increased, mainly unconjugated bilirubin, and conjugated bilirubin was basically normal. Due to the increase in unconjugated bilirubin in the blood, the formation of conjugated bilirubin is also compensated, and the biliary excretion from the biliary tract to the intestinal tract also increases, resulting in an increase in urobilinogen, an increase in fecal bilirubin, and a deeper stool color. Increased urobilinogen in the intestine and increased reabsorption into the liver. Due to the effects of hypoxia and toxins, the liver's ability to process urinary bileogen more than normal decreases, resulting in an increase in urobilinogen in the blood and excretion from the kidneys. Therefore, urobilinogen increased in urine, but no bilirubin. Hemoglobin was excreted in the urine during acute hemolysis, and the occult blood test was positive. In addition to anemia in blood tests, there are also increased reticulocytes and a series of vigorous proliferation of bone marrow red blood cells.

Diagnosis of hemolytic jaundice

First determine whether there is jaundice. The yellowing of the skin and mucous membranes may not necessarily cause jaundice. It may be caused by intake of a large amount of carotene food or a certain drug. The skin and mucous membranes are not yellow, and not necessarily without jaundice (invisible jaundice). At this time, the serum total bilirubin is> 17.1 mol / L, but L is not easily detectable by the naked eye, and is also called subclinical jaundice. The presence or absence of jaundice is determined by the amount of total bilirubin in the serum, and all patients with serum bilirubin> 17.1 mol / L are considered to have jaundice.

Secondly, to determine what type of jaundice, the classification of jaundice includes hemolytic, hepatocyte, cholestasis, and congenital non-hemolytic jaundice. Hemolytic jaundice is characterized by anemia, increased reticulocytes, increased unconjugated bilirubin, urobilinogen (+), urinary bilirubin (-), and erythroid hyperplasia in the bone marrow. diagnosis.

Hemolytic jaundice treatment

The treatment of hemolytic jaundice is first of all for the hemolytic disease itself: elimination of the cause (such as the destruction of red blood cells caused by malaria needs to be cured by malaria), and removal of incentives (such as G-6-PD deficiency patients should avoid eating broad beans and Drugs with oxidizing properties), symptomatic treatment (such as the use of adrenocortical hormones for autoimmune hemolytic anemia, plasma exchange, patients with hereditary spherocytosis, some types of thalassemia, and autoimmune hemolysis ineffective in drug treatment Spleenectomy, etc.); followed by symptomatic treatment of yellowing, Yin Zhihuang and Simetyl are commonly used in clinical practice, but it must be emphasized that if the hemolysis is not resolved, yellowing is difficult and the effect is temporary.