Jaundice child MUCLecture_2022_123116346.pptx

Jaundice child MUCLecture_2022_123116346.pptx

1. Jaundice (Hyperbilirubinemia ) Lecturer Assistant Kareem AL- Khafajy

2. Objectives: At the end of the lecture the student will be able to: Describe the concept of bilirubinemia Recognize the causes of bilirubinemia 3. Evaluate the prognosis of the condition of the infant receiving the different types of therapy for hyperbilirubinemia e.g. phototherapy and exchange blood transfusion 4. Develop awareness for the serious side effects of hyperbilirubinemia

3. Definition of Hyperbilirubinemia Refers to the increased level of accumulated bilirubin in the blood & characterized by jaundice. Normally there is balance between the destruction of RBCs and secretion of it’s products Kareem AL-Khafajy

4. Metabolic of Bilirubin Kareem AL-Khafajy

5. Causes of Hyper bilirubinemia : physiologic ( developmental) factors such as, prematurity. 2. An association with breast-feeding or breast milk. 3. Excess production of bilirubin e.g. hemolytic disease. 4. Disturbed capacity of the liver to secrete conjugated bilirubin, e.g. enzyme deficiency, bile duct obstruction .

6. Physiologic jaundice: ( NON pathologic ) Is the most common cause and is Relatively mild self-limited. It appears on 2nd or 3rd day and peaks on 4 th or 5th and decreases on the 6th day to 7th day

7. Causes Higher concentration of circulating RBCs Immature liver Absence of intestinal flora in the newborn which is responsible for reducing urobilinogen to be excreted by feces. The ↓ intestinal motility if feeding is delayed Kareem AL-Khafajy

8. Complications of hyperbilirubinemia: Unconjugated bilirubin is highly toxic to neurons. sever damage of the brain , which occurs when the serum concentrations reaches toxic levels & crosses the blood-brain barrier in the newborn causing irreversible brain damage.

9. Anemia in this condition is caused by the destruction of the RBCs which stimulate the increase production of +++ RBC leading to more hemolysis. Hyperbilirubinemia in the first 24hrs after birth result of: Erythroblastosis fetalis in which there is an abnormally rapid rate of RBCs destruction. The major cause of erythrocyte destruction is: Rh & ABO incompatibility.

10. Signs of bilirubin encephalopathy : Rigid extension of all limbs Lethargic Poor feeding Irritability Cry Seizures Discoloration of skin and eyes

11. Diagnostic evaluation: Amniocentesis & analysis of bilirubin Levels in the amniotic fluid if it is Increasing then there is progressive hemolysis Rh-antibody tiers in the maternal blood can be evaluated ( indirect coombs test ) can be confirmed by detecting antibodies attached to the circulating RBCs in the infant’s blood ( direct coombs test ).

12. Therapeutic management:- Primary goals are to prevent bilirubin encephalopathy. Early Initiation of br. Or bottle feeding. Phototherapy. Early initiation of feeding (breast feeding) if bilirubin is 17mg /dl stop breast feeding for 24 hours and resume when it decreases.

13. Phototherapy Phototherapy, in which the baby is placed under a fluorescent light are placed 12 to 30 inches , lowers the bilirubin in the neonate's blood. Term newborns are generally scheduled for phototherapy when the total serum bilirubin level rises to 10 to 12 mg/ dL at 24 hours of age .

14. B lood Exchange : this will help to: Remove the sensitized RBCs Decrease the serum bilirubin level to prevent brain damage Correct anemia Prevent cardiac failure