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Neonatal Jaundice

Neonatal Jaundice. By Dr Swati Prashant,MD Paediatrics www.paediatrics4all.com drprashantw@gmail.com Index Medical college,Indore,MP,India. JAUNDICE. Jaundice is the commonest abnormal finding during the initial wks .of life .

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Neonatal Jaundice

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  1. Neonatal Jaundice By Dr Swati Prashant,MD Paediatrics www.paediatrics4all.com drprashantw@gmail.com Index Medical college,Indore,MP,India www.paediatrics4all.com

  2. JAUNDICE • Jaundice is the commonest abnormal finding during the initial wks .of life . • Over 2/3 rd patients develop clinical jaundice . • Typically there is cephalo-pedal progression of yellowish discoloraion of skin . • Normal adult bilirubin is <2 mg /dl. • In newborn it reaches normally upto12-15 mg /dl . www.paediatrics4all.com

  3. Mechanism Of Jaundice • Hb.→ lysis→ Heme +globin • heme → biliverdin by Heme oxygenase. • Biliverdin → Bilirubin by Biliverdin Reductase enzyme. • This Bilirubin (unconjugated) leaves the RE system and enters Plasma . • In blood it is bound to Albumin. www.paediatrics4all.com

  4. Mechanism contd. • IT is carried to the Liver. • Hepatocytes contains a Y Protein (Ligandin ) site on its cell wall membrane . • Bilirubin gets detached from the Albumin and is bound to Y protein . • From here it is taken up inside the cell. • It goes to the Endoplasmic Reticulum of the cell . www.paediatrics4all.com

  5. Mechanism contd. • In ER CONJUGATION takes place with the help of UDPG –T (uridine diphosphate glucoronyl Transferase enzyme. • This conjugated bilirubin is the Direct Bilirubin. • IT is excreted in Bile . • It enters the GIT. • Sterile intestine contains Glucoronidase enzyme . www.paediatrics4all.com

  6. This enzyme degrades conjugated Bilirubin to unconjugated bilirubin . • This is reabsorbed from the gut , enters blood and goes to Liver again for conjugation . • This is called enterohepatic ciculation . www.paediatrics4all.com

  7. Types of Jaundice • 1) Physiological , normal or exaggerated. • 2) Pathological—a) unconjugated (indirect) • b) cojugated (direct ). www.paediatrics4all.com

  8. Physiological jaundice • Criteria • 1)Direct bili. < 2 mg /dl . • 2)Appearance after 36 hrs. Of age. • 3)Rate of rise of Bili. <5 mg /day . • 4)Usually does not exceed > 15 mg /dl . • 5)Peak by 5 th day and disappears by 2 wks . • 6)healhty newborn . www.paediatrics4all.com

  9. Physiological jaundice co. • Why there is a physiological jaundice? • 1)↑ Bilirubin synthesis (↑ RBC load, • enterohepatic circulation • 3)Defective hepatic uptake (↓ Ligandin ,binding Ligandin by others .) • 4)Defective bilirubin conjugation (↓ UDPG activity . • 5)Defective excretion (meconium plug ,delayed feeds . www.paediatrics4all.com

  10. Exaggerated physiological Jaundice • Levels go slightly higher , or may prolong . • Causes---1) Polycythemia, delayed cord clamping, cephalhematoma , IVH . • 2)↓calories , • 3)↓conjugation due to ↓UDPG activity • Hypothyroidism, Breast milk jaundice , drugs . • 4)↓hepatic perfusion—hypoxia CHD www.paediatrics4all.com

  11. jundice • ↑ enterohepatic circulation . www.paediatrics4all.com

  12. Pathological Jaundice • Unconjugated • Conjugated • Unconjugated Hyperbil --- • It is pathological • Occuring mostly within 24 hrs of life . • Total bilirubin >15 mg /dl • Direct bilirubin >2 mg /dl Indirect is more. • Rate of rise is >5 mg/dl . www.paediatrics4all.com

  13. Unconjugated bil . Co . • Indirect bilirubin is ↑. • Causes---- • 1)↑ Bilirubin production • 2 )Rh ,ABO Incompatibility . • 3 ) Hereditary Spherocytosis (shape defects ) • 4 ) Enzyme defects (G6PD deficiency , PYRUVATE Kinase df . αThal. ,large doses of vit K . www.paediatrics4all.com

  14. CAUSES COntd. • 4) SEPSIS • 5)Pyloric stenosis , bowel obstruction • Due to ↓ clearance • Inborn errors of Metabolism • a) Criggler Najjar syndrome type 1 & 2 . • Type 1---AR-- se bil .>30 mg/dl—complete absence of UDPG ACTIVITY . • Type 2---AD --Sr Bil <20 mg ---partial absence- www.paediatrics4all.com

  15. Causes • ↓ clearance may also be due to Hypothyroidism , breast milk jaundice . www.paediatrics4all.com

  16. Rh and ABO Incompatibility. • During labor fetal blood crosses to mother’s side. • Ag. Present in fetal RBC’s cause stimulation of antibody formation in mother . • Ab . Are of IgG TYPE .They cross the placenta in enough amt . In next pregnancy • If the baby is again Rh positive . www.paediatrics4all.com

  17. Isoimmunisation ctd. • In the fetus they produce hemolysis causing anemia and Jaundice . • It may cause Hydrops fetalis . www.paediatrics4all.com

  18. ABO incompatibility • Mothers who are O group + ,carrying A ,B AB Fetus, this fetus can be isoimmunised . • Disease is milder . • Investigations ---Blood group , Indirect Coomb’s test in mother . • Blood group , Direct Coomb’s test ,Sr. Bil. ,CBC , PS , Reti. Count. ,G6PD deficiency . www.paediatrics4all.com

  19. In Criggler Najjar type ---Phenobarbitone is the drug of choice . • In Hypothyroidism , Thyroxine given alleviates jaundice . • Investigations---CBC ,Blood grp. , Sr . Bil . ,Coombs test ,CRP ,Blood C/S ,PS ,G6PD ,TSH , X –ray chest & abd. www.paediatrics4all.com

  20. High Risk group • Prematurity , LBW , Blood group incompatibility , birth asphyxia ,Infants of DM, Oxytocin use , Cephalhematoma , problems in B/F . www.paediatrics4all.com

  21. Complications • Transient encephalopathy • Kernicterus • KERNICTERUS • It is due to bilirubin toxicity of Brain . • It causes staining ,necrosis & gliosis of the neurons . www.paediatrics4all.com

  22. Kernicterus ctd. • Parts affected are • Basal ganglia , Hippocampal cortex ,subthalamic nucleus , cerebellum . • 3 Phases of Kernicterus • 1)Poor sucking , lethargy ,hypotonia • 2)Fever , Hypertonia , Opisthotonus • 3)High pitched cry , convulsions ,coma death. • Choreoathetosis , CP , MR ,Sensorineural deafness . www.paediatrics4all.com

  23. Treatment of Jaundice • Phototherapy • Phenobarbitone • Exchange trnsfusion • T/t of cause—Thyroxine , stop B/F ,sepsis , etc. www.paediatrics4all.com

  24. Phototherapy • Mechanism---1) geometric isomerization—unconjugatd bil . Is converted to more soluble products (Lumirubin ). • 2)stucturalisomerization---bil is excreted in bile without conjugation . • Bilirubin absorbs max . Light in blue range (420—500nm ) www.paediatrics4all.com

  25. Photo . ctd. • Blue and alternate white light used . • Distance of 45 cm is maintained . • Eyes and srotum covered . • Indications ----Sr BIL . >12—15 MG/DL. • Rising titres www.paediatrics4all.com

  26. Complications of Phototherapy • Hyperthermia (20-30 ml/kg of extra fluids given ) • Retinal damage • Bronze baby syndrome(sr . Urine skin becomes brownish . ) • Electric shock. • Loose stools. www.paediatrics4all.com

  27. Exchange Transfusion • It is the most rapid method of lowering sr. Bil. • It removes hemolysed cells and aantibody coated RBC’S. • Amount of blood taken is 180ml/kg • Rh of mother and group of baby is considered in selecting blood. • Umbilical vein is canulised. www.paediatrics4all.com

  28. ET www.paediatrics4all.com

  29. Complications of ET • Sepsis, thrombocytopenia , Portal vein thrombosis , portal or umbilical vein perforation , Arrythmias , cardiac arrest,metabolic disturbances , HIV , HB. • (ET is indicated when • ---cord blood is >5mg • ----cord Hb <10gms. • ---Bil .>10 within 24hrs. www.paediatrics4all.com

  30. Conjugated hyperbil. • Biliary Atresia • Neonatal hepatitis • TORCH infections • Sepsis • Hypothyroidism • Cyst www.paediatrics4all.com

  31. Conjugated Hyperbil. Contd. • It is rare newborn .But is presence always signifies pathology . • Cord blood is>2 mg/dl ,or >15 % of TSB . • In Biliary Atresia , stools are clay coloured , failure to thrive , anemia , vitamin defi.,along with jaundice .T/t is surgery. • Neonatal Hepatitis ---obstutive jaundice is transient.Causes are variable. www.paediatrics4all.com

  32. THANK YOU • Our group websites for students • Pharmacology4students.com • Psm4students.com • Anatomy4students.com • Microbiology4students.com • Biochemistry4students.com • We invite faculties/students to write on topics of undergraduate levels. by dr swati prashant MD. drprashantw@gmail.com

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