1 / 81

Neonatal Jaundice

Neonatal Jaundice. Dr. Kalpana Malla MD Pediatrics Manipal Teaching Hospital. Incidence Term—60% Preterm—80% Bilirubin Source – Hb – 75% Non Hb – 25% ( Myoglobin). Normal Physiology.

Download Presentation

Neonatal Jaundice

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Neonatal Jaundice Dr. KalpanaMalla MD Pediatrics Manipal Teaching Hospital Download more documents and slide shows on The Medical Post [ www.themedicalpost.net ]

  2. Incidence Term—60% Preterm—80% • Bilirubin Source – Hb – 75% Non Hb – 25% (Myoglobin)

  3. Normal Physiology • Bilirubin -breakdown of hemoglobin • Unconjugated bilirubin (insoluble in water) transported to liver- Bound to albumin • Transported into hepatocyte (Ligandin / y- protein ) & conjugated - With glucuronic acid → now water soluble • Secreted into bile

  4. Normal Physiology • Secreted into bile • In ileum & colon, converted to stercobilin • 10-20% (Deconjugated by β glucuronidase)reabsorbed into portal circulation (Enterohepatic circulation )and re-excreted into bile or into urine by kidneys - urobilinogen

  5. Bilirubin Metabolism Unconjugated Glucuronyl Transferase (Bilirubin Diglucuronide)

  6. NEWBORN JAUNDICE(PHYSIOLOGICAL) Etiology 1. Decreased RBC survival 90 days, increased RBC vol /Kg, polycythemia of NB 2. Poor hepatic uptake due to immature liver-decreased ligandin or Y- protein 3. Poor conjugation due to enzyme deficiency-UDPG-T activity

  7. NEWBORN JAUNDICE(PHYSIOLOGICAL) 4. Increased enterohepatic circulation due to - High level of intst beta-glucoronidase - delayed colonization by bacteria - Decreased gut motility 5.Decreased hepatic excretion of bilirubin

  8. PHYSIOLOGICAL JAUNDICE Seen both in term and preterms Self limiting Develops after 24 hours Peaks by day 4- 5 in terms and day 7-8 in preterms Peak levels -12mg/dl in term & 15mg/dl in preterm Gradually subsides by 10-14 days No Treatment necessary

  9. PATHOLOGICAL JAUNDICE Suspect if... Jaundice in first 24 hours Rise of >5mg/24 hours or 0.5 mg/dl/hr Jaundice beyond physiological limits Conjugated bilirubin- >2mg or 20% of total Beyond 2 weeks Signs of underlying illness ++

  10. Pathological Jaundice - Hemolytic causes (unconjugated) Coombs' test positive • Rh incompatibility • ABO incompatibility Coombs' test negative • Red blood cell membrane defects • Red blood cell enzyme defects • Drugs • Hemoglobinopathies • Sepsis

  11. Pathological Jaundice - Non-hemolytic (unconjugated) Extravascular sources - cephalohematoma - Polycythemia: • fetal-maternal transfusion, • delayed cord clamping • twin-twin transfusion Increased Enterohepatic circulation • Cystic fibrosis • Ileal atresia • Hirschsprung's disease • Breast milk jaundice

  12. Pathological Jaundice – Defective Conjugation(unconjugated) Crigler-Najjar syndrome types 1 and 2 Gilbert syndrome Hypothyroidism Breast milk jaundice

  13. Pathological Jaundice – Defective Conjugation Metabolic disorder: • α1 AT deficiency • Cystic fibrosis • Galactosemia • Gaucher's disease • Niemann-Pick disease • Hypothyroidism Chromosomal disorders • Turner's syndrome, • trisomy 18 and 21

  14. Pathological Jaundice – Defective excretion Biliary obstruction: • biliary atresia • choledochal cyst • Sclerosing cholangitis • Dubin-Johnson syndrome • Rotor's syndrome Infection: • Sepsis • UTI • STORCH infections

  15. Causes of Jaundice –as per time of onset Within 24 hrs • HDN—Rh, ABO Incompatibility • IU infections-CMV, HSV, Toxo, Syphilis • RBC Enzyme deficiencies-G-6PD defi, pyruvate kinase deficiency • Drugs—large dose of vit k , syntocin drip, Salicylates, sulphas etc • Hereditary Spherocytosis • Criggler-Najjar syndrome • Alpha thalassemia

  16. 24-72 hrs—Physiological JaundiceExaggerated Physiological Jaundice (MATERNAL FACTORS) • -Blood type ABO or Rh incompatibility • -Breastfeeding • -Drugs: Diazepam, Oxytocin • -Maternal illness: gestational diabetes

  17. Exaggerated Physiological Jaundice (neonatal factors) • Birth trauma: cephalohematoma, cutaneous bruising, instrumented delivery • Drugs: Erythromycin, Chloramphenicol • Immaturity ▪ Birth asphyxia • Acidosis ▪ Cretinism • Hypothermia • Hypoglycemia • Hypothyroidism • Polycythemia

  18. After 72 hrs (within 2 weeks) • Septicemia • Neonatal Hepatitis, other IU infections • Extra hepatic Biliary atresia • Breast milk jaundice • Metabolic diseases—galactosaemia, CF, alpha-1 antitrypsin deficiency, hypothyroidism • Hypertrophic Pyloric stenosis

  19. Diagnosis 1)History—Antenatal Drugs Trauma Family H/O of jaundice Liver disease H/O delayed feeding Sepsis Sibling jaundice Splenectomy in family

  20. Cramer’s Index 1.Face-4-6 mg/dl 2.Chest &Upper trunk – 8-10 mg/dl 3.Lower abdomen,thigh-12 -14mg/dl 4.Forearms &lower legs -15 -18 mg/dl Palms & sloes->15-20 mg/dl 2. General exam

  21. Examine • Gestation age-preterm, IUGR • Cephalhematoma, bruising • Pallor-hemolytic anemia • Patechiea -sepsis, erythroblastosis, cong infections • HSM-hemolytic anemia, cong infections • Evidence of hypothyroidism, cong infections

  22. 3) Lab investigations 1. Hemoglobin, PCV with peripheral smear 2. Total Bilirubin (Total / Direct & Indirect) - >12 mg /<24hr - <12 mg/ >24 hr 3. Bilirubin level –Special tests – • TORCH titres - Thyroid function tests • Metabolic work up - Sepsis screen • USG / X ray abdomen • Blood group and Rh typing • Reticulocyte count

  23. Investigations in RH incompatibility • Antenatal - (mother Rh-ve, previous baby Rh + ve, father Rh +ve. • H/o of abortion, H/o having taken Anti D gammaglobulin • USG for baby maturation ,HSM, ascites, hydrominos, gen. anasraca

  24. Investigations in RH incompatibility • Antenatal - - Blood grp (ABO & Rh) of father ,earlier baby - Indirect Coomb’s test – to detect antibodies in mother’s serum IgG Anti body Titre to D TO be estimated at 12-16,28-32 and 36 weeks. If anti D antibody Titre 1:16 it should be tested serially - Ab titre in mother’s blood ->1:64 dignostic of HDN- TO CONSIDER TERMINATION OF PREGNANCY.

  25. Investigations in RH incompatibility • Anmiocentesis: • Look for lecithin sphingomyelin ratio to suggest maturity. • Shake test for 15 sec. with equal vol etanol 95%-allowed to stand-ring of buble at the disc • Optical density-by spectrophotometer OD.>0.15 denotes maturity of lungs • Alpha feto protein level increased –rh issoimun • Fetal bloob grp prenatally – amniocentesis

  26. POSTNATAL INVESTIGATION BABY Cord blood—all babies of Rh-ve mothers, all Unknown blood groups, all with prior h/o jaundice in earlier babies Blood group-both mother and baby • For evidence of hemolysis – Direct Coombs test Reticulocyte count - >10 suggest hemolysis. Hemoglobin cord Peripheral smear -RBC morphology Bilirubin

  27. Others RBC membrane defects • RBC enzymes –G-6-PD screen Neonatal hepatitis – LFT Metabolic studies – including hypothyroidism Biliary obstruction – USG,HIDA scan • PCV inc  polycythaemia

  28. Jaundice >12mg/dl,age <24 hrs<12mg/dl,age>24 hrs ↓ DCT............................. Negative ↓ ↓ Positive Direct bilirubin ↓ >2mg/dl Rh, ABO ,Others Hepatitis, TORCH, Sepsis, Biliary obstruction Flow chart Negative Positive

  29. Direct bilirubin < 2mg/dl Htc→high → polycythemia RBC Morpho, Retics ↓ Abnormal Normal Hemolytic ABreast milk J, Sepsis, IEM H.sperocytosisHypothyroidism, asphyxia, ∝-thalassemiaphysiologic J, DIC,Drugs ,ABO incom H.Pyloric stenosis low

  30. MANAGEMENT Phototherapy Drugs Exchange transfusion

  31. MANAGEMENT OF JAUNDICE • To Decrease Bilirubin: -↑↑excretion Phototherapy, ET - ↑↑conjugation phenobarbitone - ↓ enterohepatic circ- Agar, Cholestyramine - Inhibit Bili production—metalloporphyrins - Inhibit haemolysis high dose IVIG - Inc albumin binding—Albumin

  32. PHOTOTHERAPY

  33. Phototherapy -MTH

  34. Phototherapy -MTH

  35. Phototherapy • Safe and effective method for treatment of neonatal jaundice • Bilirubin absorbs light maximum at 420-460 nm

  36. Mechanism of Action Conversion of insoluble Bilirubin into soluble bilirubin 1.Photo-isomerization-conversion into soluble form – takes place in extravascular space of skin –conversion to less toxic polar isomer-diffuses into the blood –excreted easily into bile 2.Structural isomerization - conv to lumirubin -rapidly excreted in bile and urine 3. Photo-oxidation- of Bilirubin to water soluble polymers colourless by product.

  37. Indications for Phototherapy TSB > 15 mg % in term TSB > 12 mg% in preterm TSB > 5 mg% within 24 hours Adjuvant to exchange transfusion Prophylactic PT – ELBW, bruised babies, hemolytic disease of NB,VLBW with Perinatal risk factors

  38. Indications • Precautions • Cover the eyes and Genitals • Supplemental hydration • Watch for side effects

  39. Procedure • Best is narrow spectral blue lights (425-475nm) • White lamps (380-700nm) • Distance from skin – 45cm • Intensive PT – 15-20 cm • Shield eyes & genitalia • Space of 5-8cm between phototherapy unit & incubator

  40. Double surface PT – can be given by fiber-optic blankets (biliblankets) Change position once in every 2-4 hrs Skin bleached by PT Level to be checked every 10-20 hrs Frequent temperature monitoring & daily weight check

  41. Side Effects • Immediate – • Loose stools • Dehydration, • Hyperthermia, • ‘Bronze baby’ syndrome, • Rashes, • Upsets maternal infant interactions (bond)

  42. Late – • Risk of skin malignancies • Damage to intracellular DNA • Retinal damage • Disturbance in circadian rhythm Testicular damage

  43. Biliblanket or glow-worm ? Home phototherapy

  44. DRUGS • Phenobarbitone – increase y and z ligands -induces liver ezymes - ↑↑conjugation phenobarbitone • Metalloporphyrins (tin and zinc porphyrins and meso prophyrins) -inhibits heme oxygenase

  45. IVIG - Inhibit haemolysis • Oral agar, Cholestyramine-↓ enterohepatic circ • Albumin infusionsInc albumin binding

More Related