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Similar to Neonatal jaundice
Neonatal jaundice
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- 2. Neonatal Jaundice Jaundice– yellowish discoloration of skin,mucous membrane and conjunctiva due to excess accumulation of bile pigments in the blood. Nearly 60% of term newborn becomes visibly jaundiced in the first week of life. High bilirubin levels may be toxic to the developing CNS. Newborn appears jaundiced when bilirubin is >7mg/dL
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- 4. Etiology based ontime of appearance First 24 hrs of life - Hemolytic disease (Rh, ABO) - G6PD deficiency - RBC membrane defect (Hereditary Spherocytosis, others) - Large amount of medications to mother – Vit.K, Salicylate - Intrauterine infections - Crigler - Najjar Syndrome 24hrs to 72hrs -Physiological jaundice
- 5. After 72 hrsof life - Septicemia - Neonatal hepatitis - Biliary atresia - Metabolic disease (Galactosemia, alpha-1- antitrypsin def.) - Intestinal obstruction - Hypothyroidism - Breast milk Jaundice Jaundice beyond 14 days is persistant jaundice
- 6. Physiological Jaundice Infantsdevelop visible jaundice due to of unconjugated bilirubin. Appears between 24-72hrs. Total serum bilirubin level peaks by 3 days of age then falls in term neonates.
- 7. Physiological Jaundice Lowactivity of enzyme glucuronosyltransferase. Shorter lifespan of fetal RBC ,80-90days. Low conversion of bilirubin to urobilinogen by intestinal flora high absorption of bilirubin back into circulation.
- 8. Pathological Jaundice Elevationof TSB level to an extent where treatment of jaundice is likely to result into benefit than harm. TSB level >5mg/dl on first day >10mg/dl on second day >15mg/dl thereafter in term newborns. Conjugated bilirubin > 2 mg / dl Jaundice persisting >1 wk in term or > 2 wks in preterm baby
- 9. Prolonged jaundice Persistenceof significant jaundice(10 mg/dl) in a term baby beyond 3 weeks . causes inadequate feeding breast milk jaundice cephalohaematoma hemolytic disease G6PD deficiency hypothyroidism
- 10. Approach History Previous siblingwith jaundice , anaemia splenectomy Maternal illness with fever and rash Labour and delivery events Maternal drugs Liver disease in the family Rh/ABO Incompatibility, G6PD deficiency, crigler – Najjar Syndrome Intrauterine infection Asphyxia, trauma, oxytocin, delayed cord clamping Sulfonamide, nitrofurantoin, antimalarials lead to hemolysis. α - 1 antitrypsin deficiency, cystic fibrosis, Galactosemia
- 11. Examination Small fordate Microcephaly Pallor Bruises, cephalhematoma Petechiae Polycythemia Intrauterine infection Intrauterine infection Hemolysis, bleeding bilirubin load I.U. infection, sepsis, Erythroblastosis
- 12. Hepatosplenomegaly Omphalitis Chorioretinitis Urine staining clay stool Hemolytic anemia, I.U. infection, liver disease Sepsis I.U. infection Cholestasis
- 13. Clinical Estimation Describedby Kramer Dermal staining of bilirubin – clinical guide for level of jaundice. Dermal staining progresses in cephalocaudal direction. 1-Face 4-6 mg / dl 2-Chest 6-8mg / dl 3-Lower abd/thigh 8-12mg / dl 4-Legs 12-14 mg / dl 5-Soles / palms > 15 mg / dl Yellow staining of palms and soles is a danger sign.
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- 15. Clinical features ofKernicterus Stage I – Lethargy irritability vomiting poor feeding hypotonia poor Moro’s reflex muscular spasms/opisthotonus
- 16. Stage II– convulsions rigidity(opisthotonus) loss of deep tendon reflexes no spontaneous movements poor feeding bulging fontanel high-pitched shrill cry Most of the infants die during this stage
- 17. Stage III– stage of apparent recovery in infants who survive beyond stage II spasticity and convulsions decrease. a few involuntary movements may occur.
- 18. Stage IV-Stage of established choreoathetoid CP usually apparent after 3-4 years of age. -involuntary movements with intermittent muscular spasms convulsions deafness loss of upward conjugate movements of the eyes Dysarthria Mental retardation dental dysplasia(yellowish-black teeth)
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