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Neonatal Jaundice




                                   Dr. Kalpana Malla
                                       MD Pediatrics
                           Manipal Teaching Hospital

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



Unconjugated                Glucuronyl Transferase




          (Bilirubin
          Diglucuronide)
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
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
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
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 ++
Pathological Jaundice - Hemolytic
      causes (unconjugated)
Coombs' test positive       Coombs' test
 – Rh incompatibility         negative

 – ABO                  – Red blood cell
   incompatibility        membrane defects
                        – Red blood cell
                          enzyme defects
                        – Drugs
                        – Hemoglobinopathies
                        – Sepsis
Pathological Jaundice - Non-
      hemolytic (unconjugated)
Extravascular sources   Increased
 - cephalohematoma        Enterohepatic
                          circulation
 - Polycythemia:
                        – Cystic fibrosis
  - fetal-maternal
    transfusion,        – Ileal atresia
  - delayed cord        – Hirschsprung's
    clamping              disease
                        – Breast milk jaundice
  - twin-twin
    transfusion
Pathological Jaundice –
Defective Conjugation(unconjugated)

 • Crigler-Najjar syndrome types 1 and 2
 • Gilbert syndrome
 • Hypothyroidism
 • Breast milk jaundice
Pathological Jaundice –
        Defective Conjugation
Metabolic disorder:   Chromosomal
• α1 AT deficiency     disorders
                      • Turner's syndrome,
• Cystic fibrosis
                      • trisomy 18 and 21
• Galactosemia
• Gaucher's disease
• Niemann-Pick
  disease
• Hypothyroidism
Pathological Jaundice –
          Defective excretion
Biliary obstruction:       Infection:
• biliary atresia          • Sepsis
• choledochal cyst         • UTI
• Sclerosing cholangitis   • STORCH
• Dubin-Johnson              infections
  syndrome
• Rotor's syndrome
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
24-72 hrs—Physiological Jaundice
        Exaggerated Physiological
               Jaundice
            (MATERNAL FACTORS)
• -Blood type ABO or Rh incompatibility
• -Breastfeeding
• -Drugs: Diazepam, Oxytocin
• -Maternal illness: gestational diabetes
Exaggerated Physiological Jaundice
                   (neonatal factors)
•   Birth trauma: cephalohematoma, cutaneous
    bruising, instrumented delivery
•   Drugs: Erythromycin, Chloramphenicol
•   Immaturity               ▪ Birth asphyxia
   Acidosis                ▪ Cretinism
•   Hypothermia
•   Hypoglycemia
•   Hypothyroidism
•   Polycythemia
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
Diagnosis
1)History—Antenatal
          Drugs
         Trauma
         Family H/O of jaundice
         Liver disease
         H/O delayed feeding
         Sepsis
         Sibling jaundice
        Splenectomy in family
2. General exam
• 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
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
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
Investigations in RH incompatibility

• Antenatal - (mother Rh-ve, previous baby Rh
   + ve, father Rh +ve.
1) H/o of abortion, H/o having taken Anti D
   gammaglobulin
2) USG for baby maturation ,HSM, ascites,
   hydrominos, gen. anasraca
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.
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
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
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
Jaundice chart
                   Flow

>12mg/dl,age <24 hrs                 <12mg/dl,age>24 hrs
     ↓
                                          Negative
    DCT............................. Negative
    ↓                                  ↓
Positive
  Positive                         Direct bilirubin
   ↓                                   >2mg/dl
Rh, ABO ,Others                     Hepatitis, TORCH,
                         Sepsis, Biliary obstruction
Direct bilirubin < 2mg/dl
            Htc →high → polycythemia
       low
               RBC Morpho, Retics
               ↓
Abnormal                   Normal
Hemolytic A       Breast milk J, Sepsis, IEM
H.sperocytosis    Hypothyroidism, asphyxia, ∝-
  thalassemia    physiologic J,
DIC,Drugs ,ABO incom H.Pyloric stenosis
MANAGEMENT


   • Phototherapy
   • Drugs
   • Exchange transfusion
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
PHOTOTHERAPY
Phototherapy -MTH
Phototherapy -MTH
Phototherapy
• Safe and effective method for treatment of
  neonatal jaundice
• Bilirubin absorbs light maximum at 420-460
  nm
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.
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
Indications
• Precautions
  – Cover the eyes and Genitals
  – Supplemental hydration
  – Watch for side effects
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
• 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
Side Effects
• Immediate –
  – Loose stools
  – Dehydration,
  – Hyperthermia,
  – ‘Bronze baby’ syndrome,
  – Rashes,
  – Upsets maternal infant
    interactions (bond)
• Late –
   – Risk of skin malignancies
   – Damage to intracellular
      DNA
   – Retinal damage
   – Disturbance in circadian
     rhythm
   Testicular damage
Home
            phototherapy




Biliblanket or glow-worm ?
DRUGS
• Phenobarbitone – increase y and z ligands
  -induces liver ezymes - ↑↑ conjugation
                phenobarbitone
• Metalloporphyrins (tin and zinc
  porphyrins and meso prophyrins)
         -inhibits heme oxygenase
• IVIG - Inhibit haemolysis
• Oral agar, Cholestyramine-↓ enterohepatic
  circ
• Albumin infusionsInc albumin binding
• Exchange blood transfusion -- changing
  the babies blood with the other blood.
• Usually in hemolytic disease of
  newborn.
• It removes partially hemolysed and
  antibody coated RBCs and also
  billirubin
Methods of exchange


• Single volume exchange- 80ml/kg
• Double volume exchange- 160ml/kg
  (87% of infant blood volume exchanged
  with new blood)
• Triple volume exchange.
Partial exchange transfusion

•   Polycythemia
•   Chronic anemia with heart failure
•   Hydrops fetalis.
•   Observed pcv - desired pcv X 100 /
    observed pcv.
Exchange Transfusion
Indications:
• Rh and ABO incompatibility
• Unconjugated billirubin > 20 -25mg/dl in
  term, >15 -18mg/dl preterm babies. Sick
  neonates exchange at lower level
• Septicemia /DIC/ sclerema
• Neonatal ITP
• Severe anemia due to any cause with HF
Exchange Transfusion
              (Indications)
•   Early Kernicterus
•   Cong H Sperocytosis
•   G-6- PD deficiency
•   Hepatic coma
In Hemolytic disease of the
           newborn (ABO / Rh)
•   H/O previous severely affected infant
•   Cord Hb <10gm% & bilirubin > 5mg/dl
•   Rate of rise of bilirubun > 0.5mg/100ml/hr
•   Jaundice in first 24 hrs of life
•   Signs of hemolysis-clinical or lab
•   Maternal ab titer > 1in 64
•   Positive DCT
•   Preterm LBW with hyperbilirubinemia
•   Reticulocyte >10
Rh incompatibility
• Due to Rh D-Ag
• < 1 mL of Rh-positive fetal blood is sufficient to
  sensitize the mother
• 90% sensitization during delivery/abortion
• So , most first born infants are not affected due
  to the short period of exposure which is
  insufficient to produce a significant maternal Ig G
  antibody response.
Rh incompatibility
• Sensitized mother produces Ab –IgG types—
  crosses placenta
• Once sensitized –small doses of Ag stimulate
  high Ab titer .
• So, risk and severity of sensitization response
  increases with each subsequent pregnancy with
  Rh-positive blood fetus
ABO incompatibility
• Mother is type O and the baby is either type A or
  B.
• O +ve Mothers makes antibodies which are IgM
  & (IgG) types - IgG types crosses the placenta
• No effects if the mother & baby have same blood
  group or baby is grp O, as there is nothing to
  make antibodies against.
ABO incompatibility
• If mother - type A or B Makes antibodies
  (IgM) type so does not cross the placenta
So, even if baby has a different blood type no
  effect
Selection of blood
• Blood group O – no antigen
                Ab –anti -A, anti-B
• Blood group A – antigen A
                Ab - Anti-B
• Blood group B –antigen B
               Ab – anti -A
Blood for exchange transfusion

• Fresh CPD blood
• Rh HDN-
• ABO incompatibility -
Selection of blood
• In Rh incompatibility: (O,A,B,AB-Negative)
  choice -Rh negative –
              - Preferably baby’s ABO
              - O group cross matched against maternal
   serum
• In ABO incompatibility – “O” blood group same as
   baby’s Rh ( +/-) with low titre of Anti A and Anti B
   antibodies OR ABO type specific blood cross
   matched against infant serum

- Septicemia – Same as baby’s ABO and Rh
Investigations


• Pre exchange: Hb%, PCV, billirubin,
  glucose K+, Ca+.

• Post exchange: Hb%, PCV, billirubin,
  glucose, Calcium, K+, culture.
Procedure
• IN NICU OR OT
• Radiant warmer, Monitor HR, BP and other
  vitals, infants arms and legs are restrained.
• Assistant to record volume in & out, to
  check vitals.
• Blood pre warmed to 37 c
• Dried umbilical cord soaked with wet
  gauze.
• Canulation of umbilical vein- 12 o’clock
• Catheter inserted till free flow of blood
  or SHOULDER UMBILICAL LENGTH.
• Small aliquots of blood removed 5
  to10ml -PUSH PULL method.
• Blood in the bag gently mixed.
• Procedure over 1 to 2 hr.
• Tie around the cord for 1 hr, or hold
  tightly at the end of procedure.
Complications
• Hypocalcemia and Hypomagnesemia -
  Citrate in CPD blood.
• Hypoglycemia
• Metabolic alkalosis or acidosis.
• Hyperkelemia.
• CVS: overload and arrythmias
• Infections: HBV HIV
• Hemolysis
• Hypothermia, NEC.
Other roots for exchange


• Umbilical vein cut down- incision
  above umbilicus in midline.
• Femoral vein canulation with radial
  artery canulation.
Guidelines for management of
             hyperbilirubenemia
Gestation   Photother Exchange Photother Exchange
and birth   apy(      (healthy) apy(sick) (sick)
wt.         healthy)
Preterm:
<1000gm.    5-7      11-13     4-7      10-12
1001-1500 7-10       13-15     6-8      11-13
1501-2000 10-12      15-18     8-10     13-15
2001-2500 12-15      18-20     10-12    15-18
Term:
2500        15-18    20-25     12-15    18-20
Breast milk jaundice
• Late onset
• Due to factors in breast milk –Interfere with
  bilirubin conjugation:
        - Pregnanediol
        - Free fatty acids
        - β-glucoronidase
• Instead of ↓by 7 days it continues to rise may
  go upto 20-30mg/dl by 2nd-3rd wks of age &
  return to normal by 4-12 wks
Management
• Stop breast feeding -48 hrs
• Again resume it, bilirubin may rise again but
  not reach previous high level
Breast feeding jaundice
• Decreased intake of milk leads to increased
  enterohepatic circulation
• Higher levels on day 4 compared to
  formula fed babies due decreased
  intake of milk
Prevention
1. Anti D to be given to the mother after delivery of
     the baby-within 48hrs. Also can be given to all
     unsensitized mothers at 28-32 weeks of
     gestation
2. Amniocentesis and IU transfusion to severely
     affected babies
3. Preterm delivery of severely affected babies
4. Cord blood studies-followed by Phototherapy
5. Exchange transfusion
KERNICTERUS
• Entry of unbound bilirubin into brain as
  free or albumin bound bilirubin
• Acidosis affects bilirubin solubility
• Hyperosmolarity, anoxia and hypercarbia
  disrupt BBB
• Yellow staining of brain assc with
  neuronal injury
• Affects basal ganglia, cranial nerve
  nuclei, brain stem nuclei, hippocampus
  and AHC of spinal cord (cortex usually
  spared)
• Necrosis, neuronal loss and gliosis
  …pathological findings
ACUTE BILIRUBIN
           ENCEPHALOPATHY
• STAGE 1: hypotonia, lethargy, high
  pitched cry and poor suck (D1-3)
• STAGE 2: hypertonia, opisthotonus,
  rigidity, oculogyric crisis, retrocollis,
  fever, seizures. (2nd week)
• Those who survive develop chronic
  bilirubin encephalopathy
• STAGE 3: Hypotonia replaces hypertonia
  after 3rd week age
CHRONIC BILIRUBIN
          ENCEPHALOPATHY
• Choreo-Athetosis
• Partial or complete sensorineural hearing
  loss
• Limitation of upward gaze
• Dental dysplasia
• Intellectual deficits
LOW BILIRUBIN KERNICTERUS
•   In LBW babies, preterms
•   Overt changes not seen
•   Other factors: IVH, drugs, benzyl alcohol
•   More likely to suffer from anoxia,
    hypercarbia and sepsis
TREATMENT
•   Phototherapy
•   Exchange transfusion
•   Albumin infusion
•   Anticonvulsants: phenobarbitone
•   BERA at follow up
Neonatal cholestasis

Intrahepatic                          extrahepatic
Hepatocyte injury          bile injury EH –biliary
                                       atresia
metabolic          viral
                            intrahepatic bile
                              duct paucity
       idiopathic neonatal hepatitis
Thank you
Download more documents and slide shows on The
    Medical Post [ www.themedicalpost.net ]

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Neonatal Jaundice

  • 1. Neonatal Jaundice Dr. Kalpana Malla 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 Coombs' test – Rh incompatibility negative – ABO – Red blood cell incompatibility membrane defects – Red blood cell enzyme defects – Drugs – Hemoglobinopathies – Sepsis
  • 11. Pathological Jaundice - Non- hemolytic (unconjugated) Extravascular sources Increased - cephalohematoma Enterohepatic circulation - Polycythemia: – Cystic fibrosis - fetal-maternal transfusion, – Ileal atresia - delayed cord – Hirschsprung's clamping disease – Breast milk jaundice - twin-twin transfusion
  • 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: Chromosomal • α1 AT deficiency disorders • Turner's syndrome, • Cystic fibrosis • trisomy 18 and 21 • Galactosemia • Gaucher's disease • Niemann-Pick disease • Hypothyroidism
  • 14. Pathological Jaundice – Defective excretion Biliary obstruction: Infection: • biliary atresia • Sepsis • choledochal cyst • UTI • Sclerosing cholangitis • STORCH • Dubin-Johnson infections syndrome • Rotor's syndrome
  • 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 Jaundice Exaggerated 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.
  • 20.
  • 21. Diagnosis 1)History—Antenatal Drugs Trauma Family H/O of jaundice Liver disease H/O delayed feeding Sepsis Sibling jaundice Splenectomy in family
  • 22. 2. General exam • 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
  • 23. 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
  • 24. 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
  • 25. Investigations in RH incompatibility • Antenatal - (mother Rh-ve, previous baby Rh + ve, father Rh +ve. 1) H/o of abortion, H/o having taken Anti D gammaglobulin 2) USG for baby maturation ,HSM, ascites, hydrominos, gen. anasraca
  • 26. 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.
  • 27. 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
  • 28. 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
  • 29. 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
  • 30. Jaundice chart Flow >12mg/dl,age <24 hrs <12mg/dl,age>24 hrs ↓ Negative DCT............................. Negative ↓ ↓ Positive Positive Direct bilirubin ↓ >2mg/dl Rh, ABO ,Others Hepatitis, TORCH, Sepsis, Biliary obstruction
  • 31. Direct bilirubin < 2mg/dl Htc →high → polycythemia low RBC Morpho, Retics ↓ Abnormal Normal Hemolytic A Breast milk J, Sepsis, IEM H.sperocytosis Hypothyroidism, asphyxia, ∝- thalassemia physiologic J, DIC,Drugs ,ABO incom H.Pyloric stenosis
  • 32. MANAGEMENT • Phototherapy • Drugs • Exchange transfusion
  • 33. 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
  • 37.
  • 38.
  • 39. Phototherapy • Safe and effective method for treatment of neonatal jaundice • Bilirubin absorbs light maximum at 420-460 nm
  • 40. 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.
  • 41. 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
  • 42. Indications • Precautions – Cover the eyes and Genitals – Supplemental hydration – Watch for side effects
  • 43.
  • 44. 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
  • 45. • 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
  • 46. Side Effects • Immediate – – Loose stools – Dehydration, – Hyperthermia, – ‘Bronze baby’ syndrome, – Rashes, – Upsets maternal infant interactions (bond)
  • 47. • Late – – Risk of skin malignancies – Damage to intracellular DNA – Retinal damage – Disturbance in circadian rhythm Testicular damage
  • 48. Home phototherapy Biliblanket or glow-worm ?
  • 49. DRUGS • Phenobarbitone – increase y and z ligands -induces liver ezymes - ↑↑ conjugation phenobarbitone • Metalloporphyrins (tin and zinc porphyrins and meso prophyrins) -inhibits heme oxygenase
  • 50. • IVIG - Inhibit haemolysis • Oral agar, Cholestyramine-↓ enterohepatic circ • Albumin infusionsInc albumin binding
  • 51. • Exchange blood transfusion -- changing the babies blood with the other blood. • Usually in hemolytic disease of newborn. • It removes partially hemolysed and antibody coated RBCs and also billirubin
  • 52. Methods of exchange • Single volume exchange- 80ml/kg • Double volume exchange- 160ml/kg (87% of infant blood volume exchanged with new blood) • Triple volume exchange.
  • 53. Partial exchange transfusion • Polycythemia • Chronic anemia with heart failure • Hydrops fetalis. • Observed pcv - desired pcv X 100 / observed pcv.
  • 54. Exchange Transfusion Indications: • Rh and ABO incompatibility • Unconjugated billirubin > 20 -25mg/dl in term, >15 -18mg/dl preterm babies. Sick neonates exchange at lower level • Septicemia /DIC/ sclerema • Neonatal ITP • Severe anemia due to any cause with HF
  • 55. Exchange Transfusion (Indications) • Early Kernicterus • Cong H Sperocytosis • G-6- PD deficiency • Hepatic coma
  • 56. In Hemolytic disease of the newborn (ABO / Rh) • H/O previous severely affected infant • Cord Hb <10gm% & bilirubin > 5mg/dl • Rate of rise of bilirubun > 0.5mg/100ml/hr • Jaundice in first 24 hrs of life • Signs of hemolysis-clinical or lab • Maternal ab titer > 1in 64 • Positive DCT • Preterm LBW with hyperbilirubinemia • Reticulocyte >10
  • 57. Rh incompatibility • Due to Rh D-Ag • < 1 mL of Rh-positive fetal blood is sufficient to sensitize the mother • 90% sensitization during delivery/abortion • So , most first born infants are not affected due to the short period of exposure which is insufficient to produce a significant maternal Ig G antibody response.
  • 58. Rh incompatibility • Sensitized mother produces Ab –IgG types— crosses placenta • Once sensitized –small doses of Ag stimulate high Ab titer . • So, risk and severity of sensitization response increases with each subsequent pregnancy with Rh-positive blood fetus
  • 59. ABO incompatibility • Mother is type O and the baby is either type A or B. • O +ve Mothers makes antibodies which are IgM & (IgG) types - IgG types crosses the placenta • No effects if the mother & baby have same blood group or baby is grp O, as there is nothing to make antibodies against.
  • 60. ABO incompatibility • If mother - type A or B Makes antibodies (IgM) type so does not cross the placenta So, even if baby has a different blood type no effect
  • 61. Selection of blood • Blood group O – no antigen Ab –anti -A, anti-B • Blood group A – antigen A Ab - Anti-B • Blood group B –antigen B Ab – anti -A
  • 62. Blood for exchange transfusion • Fresh CPD blood • Rh HDN- • ABO incompatibility -
  • 63. Selection of blood • In Rh incompatibility: (O,A,B,AB-Negative) choice -Rh negative – - Preferably baby’s ABO - O group cross matched against maternal serum • In ABO incompatibility – “O” blood group same as baby’s Rh ( +/-) with low titre of Anti A and Anti B antibodies OR ABO type specific blood cross matched against infant serum - Septicemia – Same as baby’s ABO and Rh
  • 64. Investigations • Pre exchange: Hb%, PCV, billirubin, glucose K+, Ca+. • Post exchange: Hb%, PCV, billirubin, glucose, Calcium, K+, culture.
  • 65. Procedure • IN NICU OR OT • Radiant warmer, Monitor HR, BP and other vitals, infants arms and legs are restrained. • Assistant to record volume in & out, to check vitals. • Blood pre warmed to 37 c • Dried umbilical cord soaked with wet gauze. • Canulation of umbilical vein- 12 o’clock
  • 66. • Catheter inserted till free flow of blood or SHOULDER UMBILICAL LENGTH. • Small aliquots of blood removed 5 to10ml -PUSH PULL method. • Blood in the bag gently mixed. • Procedure over 1 to 2 hr. • Tie around the cord for 1 hr, or hold tightly at the end of procedure.
  • 67. Complications • Hypocalcemia and Hypomagnesemia - Citrate in CPD blood. • Hypoglycemia • Metabolic alkalosis or acidosis. • Hyperkelemia. • CVS: overload and arrythmias • Infections: HBV HIV • Hemolysis • Hypothermia, NEC.
  • 68. Other roots for exchange • Umbilical vein cut down- incision above umbilicus in midline. • Femoral vein canulation with radial artery canulation.
  • 69. Guidelines for management of hyperbilirubenemia Gestation Photother Exchange Photother Exchange and birth apy( (healthy) apy(sick) (sick) wt. healthy) Preterm: <1000gm. 5-7 11-13 4-7 10-12 1001-1500 7-10 13-15 6-8 11-13 1501-2000 10-12 15-18 8-10 13-15 2001-2500 12-15 18-20 10-12 15-18 Term: 2500 15-18 20-25 12-15 18-20
  • 70. Breast milk jaundice • Late onset • Due to factors in breast milk –Interfere with bilirubin conjugation: - Pregnanediol - Free fatty acids - β-glucoronidase • Instead of ↓by 7 days it continues to rise may go upto 20-30mg/dl by 2nd-3rd wks of age & return to normal by 4-12 wks
  • 71. Management • Stop breast feeding -48 hrs • Again resume it, bilirubin may rise again but not reach previous high level
  • 72. Breast feeding jaundice • Decreased intake of milk leads to increased enterohepatic circulation • Higher levels on day 4 compared to formula fed babies due decreased intake of milk
  • 73. Prevention 1. Anti D to be given to the mother after delivery of the baby-within 48hrs. Also can be given to all unsensitized mothers at 28-32 weeks of gestation 2. Amniocentesis and IU transfusion to severely affected babies 3. Preterm delivery of severely affected babies 4. Cord blood studies-followed by Phototherapy 5. Exchange transfusion
  • 74. KERNICTERUS • Entry of unbound bilirubin into brain as free or albumin bound bilirubin • Acidosis affects bilirubin solubility • Hyperosmolarity, anoxia and hypercarbia disrupt BBB
  • 75. • Yellow staining of brain assc with neuronal injury • Affects basal ganglia, cranial nerve nuclei, brain stem nuclei, hippocampus and AHC of spinal cord (cortex usually spared) • Necrosis, neuronal loss and gliosis …pathological findings
  • 76. ACUTE BILIRUBIN ENCEPHALOPATHY • STAGE 1: hypotonia, lethargy, high pitched cry and poor suck (D1-3) • STAGE 2: hypertonia, opisthotonus, rigidity, oculogyric crisis, retrocollis, fever, seizures. (2nd week) • Those who survive develop chronic bilirubin encephalopathy • STAGE 3: Hypotonia replaces hypertonia after 3rd week age
  • 77. CHRONIC BILIRUBIN ENCEPHALOPATHY • Choreo-Athetosis • Partial or complete sensorineural hearing loss • Limitation of upward gaze • Dental dysplasia • Intellectual deficits
  • 78. LOW BILIRUBIN KERNICTERUS • In LBW babies, preterms • Overt changes not seen • Other factors: IVH, drugs, benzyl alcohol • More likely to suffer from anoxia, hypercarbia and sepsis
  • 79. TREATMENT • Phototherapy • Exchange transfusion • Albumin infusion • Anticonvulsants: phenobarbitone • BERA at follow up
  • 80. Neonatal cholestasis Intrahepatic extrahepatic Hepatocyte injury bile injury EH –biliary atresia metabolic viral intrahepatic bile duct paucity idiopathic neonatal hepatitis
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