12 Neonatal jaundice detailed review.pptx

All about neonatal jaundice

1. Neonatal jaundice Dr. Eiman Bakri Consultant Pediatrician/Neonatologist

2. objectives Bilirunin formation. What is neonatal jaundice? Unconjugated bilirubin . Conjugated bilirubin .

3. Heme Degradation Bilirubin

4. Jaundice occurs when the bilirubin production & clearance is disturbed by one or more of the following mechanisms: Excessive production of bilirubin . Reduced hepatic uptake. Impaired conjugation. Decreased hepatocellular excretion. Impaired bile flow.

5. What is neonatal jaundice? A serum bilirubin level greater than 5 mg/dl, causing yellowish discoloration of skin, mucus membranes & sclera. 60% of term, and 80% of preterm newborns. Either unconjugated (toxic, pathological or physiological), OR conjugated (nontoxic, pathological).

6. Jaundice is pathological if: Clinically evident at 1 st day. Last > 2 weeks. Unconjugated (indirect) bilirubin > 5 mg/dl. Conjugated (direct) bilirubin >2 mg/dl. total bilirubin > 12 md /dl. Hepatosplenomegaly & anaemia are present.

7. Skin discoloration first becomes visible on face, then gradually on trunk & extremities.

8. Unconjugated Jaundice

9. Physiological jaundice The commonest cause of neonatal jaundice. Term infants: appears in day 3 of life, and peak level of no more than 12 mg/dl. Preterm infants: later on day 5. and no more than 15 mg/dl. Self limiting, but high levels may require phototherapy. Start to disappear at the end of 1 st week, & resolves by day 10.

10. Physiological jaundice - mechanism Short RBCs life span (70 – 90 days Vs. 120 days in adults). Increased RBC mass. G reater rate of bilirubin production (6 – 10 mg/kg/24hr Vs. 3mg/kg/24hr in adults. Hepatic immaturity.

11. Hemolysis Early onset, 1 st day. Hemolytic diseases of newborn ( Rh , ABO incompatibility). Infections (sepsis). Hemolytic anaemias . hemolysis & RBCs destruction due hematoma & excessive brusing .

12. Hemolytic diseases of newborn Rh incompatibility: Mother is Rh – ve & fetus is Rh + ve . Maternal Rh antibodies, cross the placenta, reach fetal circulation & dystroy it’s RBCs. Prevented by Anti-D within 72 hrs from delivery. Late anemia (6-8 weeks after birth) is common.

13. ABO hemolytic disease ABO incompatibility Type O mothers Type A or B fetuses Presence of IgG anti-A or Anti-B antibodies in type O mother Frequently occurring during the first pregnancy without prior sensitization

14. Breast milk jaundice During 1 st & 2 nd week, resolves by 6 th week. Bilirubin level rarely increases to greater than 2o mg/dl. Breast milk contains inhibitors for bilirubin conjugation, OR increases enterohepatic circulation. Inturruption of breast feeding for 1 – 2 days, rapid decrease in bilirubin to normal levels.

15. Other causes of unconjugated jaundice Drugs that can displace bilirubin from albumin (e.g. sulfonamides, salicylates ). Hypothyrodism (thyroxin is important for formation of conjugation enzymes). Gilbert's syndrome. Crigler-Najjar syndrome. (in both there’s deficiency of bilirubin glucuronyltransferase ).

16. Kernicterus ( Bilirubin Encephalopathy) A complication of unconjugated jaundice. > 20 mg/dl Because it is lipid soluble, unconjugated bilirubin can cross the BBB. Toxic to the developing CNS. Kernicterus results when indirect bilirubin is deposited in brain cells and disrupts neuronal metabolism and function.

17. Structures most commonly affected: B asal ganglia. Hippocampus . Geniculate bodies and cranial nerve nuclei, especially the oculomotor , vestibular and cochlear. The cerebellum can also be affected

18. Kernicterus C linical M anifestations Early (noted after day 4): Severe jaundice, hypotonia , poor sucking and feeding, and absent moro reflex. H igh-pitched cry, hypertonia of extensor muscles with arched back and hyperextended neck, upward gaze, bulging fontanelle and seizures.

19. Later neurological features include sensory hearing loss, mental retardation , muscle rigidity, speech difficulties, seizures and movement disorder. Kernicterus C linical M anifestations

20. Investigations Maternal , neonatal blood groups and Coomb`s test (check for antibodies that attack red blood cells), for ABO and rhesus incompatibility. CBC, blood smear. Reticulocyte count. Infection screen.

21. Management The aim of management of unconjugated hyperbilirubinemia is to avoid kernicterus . Phototherapy. Exchange transfusion.

22. Phototherapy Effective and safe method for reducing indirect bilirubin levels. Term infant if the serum bilirubin is between 16-18 mg/dl at a lower level for premature babies.

23. Phototherapy Works through a process of isomerization . Bilirubin is transformed into isomers that are water soluble and easily excreted. Blue lights and white lights are effective in reducing bilirubin levels. Wave length 425-475nm are used from distance of 40-50cm.

24. Phototherapy Contraindications: conjugated jaundice.

25. Phototherapy Side effects: Increased insensible water loss. Dehydration. Diarrhea. Macular- papular red skin rash. Lethargy. Nasal obstruction by eye pads. Potential for retinal damage. Bronze baby syndrome: in infants with conjugated jaundice.

26. Exchange Transfusion For infants with dangerously high indirect bilirubin levels who are at high risk for kernicterus . Through an umbilical venous catheter placed in the inferior vena cava. Small infusions of whole blood. Should remove 85% of the infant's RBCs (the source of bilirubin ), maternal antibodies, and exchangeable tissue indirect bilirubin .

27. Exchange Transfusion Indications : Bilirubin level is 20mg/dl or more with haemolysis , weight > 2 kg. Physiologic or breast milk jaundice with bilirubin level > 25 mg/dl. Bilirubin level is ,less than 20 mg/dl, Baby weight < than 2kg,

28. Exchange Transfusion Complications : Blood related ( tranasfusion reaction , metabolic instability , infection ). Catheter related (vessel perforation ). Procedure related (hypotension). *Routinely administer intravenous calcium during procedure.

29. Conjugated Jaundice

30. Conjugated Jaundice Defined as a direct bilirubin level >2 mg/ dL or >20% of the total bilirubin . Causes: Infections: TORCH, CMV, sepsis, hepatitis. Cholestasis : congenital biliary atrasia , Choledochal cyst. Rare: Inborn errors of metabolism ( galactosemia ), Cystic fibrosis.

31. Clinical manifestations Dark urine. Pale stool. Others, of the cause.

32. Investigations LFT. Bacterial & viral cultures. TORCH screening. Hepatic ultrasound. M etabolic screening tests.

33. Treatment Specific to the underlying cause. Do not respond to phototherapy or exchange transfusion.