Over 60% of newborns experience jaundice due to the normal physiological breakdown of red blood cells in the first few days after birth. Unconjugated bilirubin can potentially be deposited in the brain, causing kernicterus. The liver's ability to conjugate and excrete bilirubin is impaired in preterm and ill newborns compared to healthy full term babies. Conditions like sepsis, hemolytic disease, or liver dysfunction can also cause pathological jaundice beyond the first 2 weeks of life. Timely diagnosis and treatments like phototherapy and exchange transfusion are important to prevent bilirubin encephalopathy.

1. Neonatal
jaundice lecture
Clinical medicine
24th 05,2019
julius

2. introduction
 Over 60% of all newborn babies become
jaundiced visibly
a. ? Hemoglobin conconcentration falls rapidly in
the 1st few days from birth due to hemolysis (1g
of Hb yields 640micromols of bilirubin
b. Red cell life span of the new born is shorter about
70days compared to in adults.
c. Hepatic bilirubin metabolism is less efficient in the
first few days of life.

3. Why jaundice important
 It may be a sign of another disorder, eg
infection
 Unconjugated bilirubin can be deposited in
the brain , basal ganglia causing kernicterus

4. Physiology of bilirubin
 1g of hemoglobin from hem produces
600mcmols(35mg) of unconjugated bilirubin
 Normal term baby breaks down about 0.5g of hb every
24hours
 In the plasma unconjugated bilirubin is bound to
albumin and 5nonomol/l of free unconjugated bilirubin
is normally present
 Unconjugated bilirubin is taken up in the liver by
cytoplasmic protein called ligandin
 Conjugation takes place by addition of 2 molecules of
glucuronic acid in the presence of the enzyme
glucuronyltransferase

5. cont
 Then its transported actively out of the liver cells
into bile and then travels into the gut
 Some converted to urobilinogen by bacteria in
colon
 Within the gut if transit time increases conjugated
bilirubin is deconjugated again by the
glucuronidase produced by the bacteria in the gut
lumen and present in breast milk

6. Note!
 All these functions of the liver are impaired in the
preterm or ill term newborn compared to the normal
healthy full term baby
 In particular defective conjugation cannot cope up with
a large postnatal bilirubin load from breakdown of
blood cells.
 In newborns conjugated bilirubin in duodenum meets
with an enzyme called beta gluconidase and convertes
it into unconjugated bilirubin
 It goes back to the cycle again for conjugation in the
liver cells
 The cycle is called enterohepatic circulation

7. Definition of jaundice
 Yellow coloration of the skin and sclera
produced by bilirubin tissue deposition
 Clinical evaluation: babies become clinically
jaundiced when the bilirubin level reaches 80-
120micromol/l(5mg/dl)
 Management varies according to the infants
gestational age. Age at onset , bilirubin level
and rate of rise and the overall clinical
condition

8. Classification of jaundice
 Physiological
 pathological

9. physiological
 Usually appears between 48-72hours of age.
Maximum intensity on days 4 and 5 in term
babies and day 7 in preterm babies and disappear
by day 14
 It does not extend to palms and soles , does not
need treatment
 Babies remain completely well
 Sets in on day 3 after birth
 Disappears within 2weeks
 Common in newborn especially in pre-term

10. pathological
 Jaundice starts on the first 24hours of life
 Jaundice lasts longer than 14days in term
babies, 21 days in preterm infants jaundice
accompanied with fever or other signs of
illness
 Deep jaundice –palms and soles of baby are
deep yellow.
 Look for cause and treat accordingly.

11. Causes of jaundice
 Physiological :
 Due to normal physiological breakdown of large red blood
cells mass
 Pathological:
 Serious bacterial infection
 Hemolytic disease of the newborn-blood group (rhesus
and ABO incompatibility
 Congenital syphillis or other intrauterine infections
 Liver diseases-hepatitis or biliary atresia
 Hypothyroidism
 Asphyxia
 Birth injuries

12. Prolonged jaundice
 Jaundice more than 1week
 Congenital biliary atresia
 Neonatal hepatitis
 Congenital hypothyroidism
 Congenital hemolytic anemia-pyruvate
kinase,(red blod cells membrane become
weak liable for hemolysis), G6PD enzyme
deficiency, spherocytosis

13. Other causes
 Cephalohematoma
 BMJ
 Metaboloc disorders-galactosemia, (Genetic
metabolic disorder inability to metabolise body
sugar), gylcogen storage disease
 Drugs: vitamin K, suphur drugs,m ASA (they
compete with albumin binding sites(displace
bilirubin in binding sites)
 Genetics.. Gilberts syndrome,(liver does not
properly process bilirubin), robin johnson, crigler
najjar syndrome

14. Predisposing factors
 Prematurity
 Infant of diabetic mother
 Respiratory distress syndrome

15. Clinical presentation
 Yellow coloration of skin and mucus membrane, sclera
 Physical examination: ssigns of sepsis, lethargy, fever,
hypothermia, poor feeding, vomitting
 Hemolytic disease: palor, hepatosplenomegally
 Extravascular hemolysis; birth trauma associated with
cephalohematoma or bruising
 Polycythemia: ruddy complexion of the skin
 Cholestatic jaundice: dark urine, light colored stool

16. investigations
 Bilirubin levels: both total and direct bilirubin
 Coombs test
 Septic screen
 Hepatitis b surface antigen
 Blood group and rhesus factor of the mother
 Serological tests
 Abdominal u/s
 Liver function tests
 T3 , T4(triiodothyronine), thyroxin hormone
respectively.

17. management
 Hydration
 Phototherapy
 Treat the cause
 feeding

18. phototherapy
 It reduces the light wave length of
unconjugated bilirubin
 It does by:
 Geometrical isomerization of bilirubin to
produce water soluble isomers which are
slowly excreted

19. indications
 Hemolytic disease of the newborn
 Small sick babies including those with sepsis
 Bilirubin levels more than 340micromols/ in
mature babies
 It should be continued till bilirubin is
continuously falling consistently and is below
the ‘safe’ line for gestation

20. note
 Note phototherapy conjugated bilirubin
baby..cause photodegradation of porphyrins
which are raised in the plasma of babies with
conjugated hyperbilirubinemia…baby will
change to deep brown color

21. Complications of phototherapy
 Diarhea.. Decreases gut transit time due to irritant
effect on the bowel of the photoisomers of bilirubin
 Increases fluid losss through the skin and gut
 Exposes the child to the risk of
hypothernia/hyperthermia, cause artificial burns
 Causes eryhromatous rash
 Corneal detachment if eyes not bandaged due
photosensitization

22. Exchange blood transfusion
 Used when the bilirubin must be lowered
urgently because it has reached toxic level, or
baby starts to show features of kernicterus

23. Effects of EBT
 Replacing 85% of infants blood volume
 Decreasing tissue and serum concentration of
bilirubin by 30%
 It corrects anemia
 It washes out infants antibodies which are
causing hemolysis

24. The procedure
 Use fresh blood of less than 4days old
 Umbilical vein catheter 10cm long inserted
 The whole procedure should take 45-60min
 Aspirate serially and replace same amount of
blood through the umbilical vein. Use small
volume syringes for low birth weight guys
 Closely monitor the child during the whole
procedure

25. cont
 To achieve a 90-95% swap of the baby’s
blood, twice his blood volume (i.e 2x85mls/kg
=170mls)should be exchanged

26. Other uses of EBT
 Severe non hemolytic anemia from any other
cause
 Sepsis
 To remove drugs or accumulated toxic
metabolites in depressed neonates
 In coagulopathies to remove factors that
perpetuate the coagulation disturbances and
coagulation factors

27. complications
 Catheter induced complications- air emboli, aortic or
portal vein thrombosis, hemorrhge
 Hypoglycemia
 Hypocalcemia..caused by citrate in the blood stream
 Hyperkalemia..if blood stayed more than 3says
 Tissue hypoxia
 Acidemia
 Rentrolental fibroplasia- increase oxygen concentration
in blood damages eyes of the neonate
 Ccf due to fluid overload

28. Bilirubin
encephalopathy(kernicterus)
 This is pathological diagnosis
 There is yellow staining of the basal ganglia
 Mechanism is uncertain
 The cells that are prone to this are the
metabolically active and receive the largest
blood flow
 In neonates, basically are the cells of the
basal ganglia and the midbrain

29. The basal ganglia include
 Globus pallidus
 Cutamae
 Caude nucleus
 The damage is caused by free bilirubin in the
extracellular fluid binding to neural cell
membranes with severe and complex
biochemical sequele for cell.

30. Clinical presentations
 History-progressive jaundice
 Refusal to feed
 Lethargic
 Examination:
 Deep jaundice
 Hypotonic
 Floopy
 hyporeflexia

31. opisthotonus
seizure
high pitched cry
AF bulged

32. complications
 If left untreated the condition is fatal, or may
cause severe brain damage in survivors with
the following manifestations
 Athetoid CP
 Deafness
 Upgaze palsy(conjugate, bilateral , limitation
of the eye movements in upgaze and /or
downgaze
 Intellectual retardation

33. Risk factors
 Short gestation
 Rapidly rising level of serum bilirubin
 Low levels of plasma albumin for the bilirubin
to bind to
 The presence of hypoxia , acidemia,
hypoglycemia, sepsis or some serious illness
that might disrupt the BBB

34. prevention
 Immediate treatment when early signs are
present
 But with late or long standing signs,
permanent CNS damage is inevitable.

35. Neonatal sepsis
 Definition
 Etiology/significance
 Risk factors
 Route of infection
 Diagnosis
 Management
 prevention

36. definition
 Invasion by bacteria in the first 28days of life
 Occurs in 0.1% of live born infants
 Significance:
 A major cause of neonatal mortality
 2/3rd of neonatal mortality deaths occur In the
first 2weeks, and are largely preventable.

37. Routes of infection
 Transplancental
 Ascending vaginal infection
 Exogenous-post partum infection,
nosocomical infection, mechanical
equipments used to handle the baby if
contaminated

38. Risk factors
 Sex: male: female 2:1
 Premature rupture of membranes
 Congenital malformation
 Low birth weight
 Interpartum hemorrhage
 Immature immune system

39. Maternal related risk factors
 Prolonged labor
 Difficult delivery
 Maternal fevers
 Infected birth canal
 Genital/vaginal warts

40. Environmental related
 Hands of the attendant
 Apparatus
 Feeds and medication
 Air-borne from birth attendant

41. classification
 Early onset..within 1week of delivery
 Late onset…………after one week
 Etiology”:
Early onset: causes E.coli, GBS others are
fungi, chlamydia, H. influenza and clostridium
species
Early onset has high mortality rate

42. Clinical features of early onset
NNS
 Refusal to feed
 Lethargy
 Hypothermia/hyperthermia
 Jaundice
 Tarchypnea
 Recession, diarhea , vomiting,irritability,
pseudoparalysis(voluntary restriction or inhibition of
movements because of pain, incoordination.
 Poor weight gain
 Petechial/ septic spots

43. Late onset nns
 Occurs after one week of life
 It has low mortality rate
 Acquired from the mother
 Organisms include: staphylococcus aureus,
epidermidis, E.coli, pseudomonas , candida,
enterobacter

44. Clinical features
 r/s: cyanosis, grunting and dyspnoea
 GIT: intestinal obstruction in generalised
sepsis or necrotising enterocolitis
 CNS: high pitched cry, retracted neck, bulging
anterior fontanel, seizures
 Hematological: bleeding from puncture sites
 Sclerema: hardening of the skin…not specific
feature of any disease

45. investigations
 Full hemogram, IT ratio, c reactive protein
 Blood cultures
 Csf analysis
 Chest radiology
 Surface swab for culture
 Urine culture, biochem, microscopy
 Abdominal x ray, ultrasound

46. management
 Specific
 supportive

47. specific
 Benzylpenicillin 50,000 iu/kg 12hourly
 Gentamycin 3-5mg/kg bwt depending on birth weight/
age
 Second line: cephalosporin 3rd gen, gentamycin
changed to amikacin
 If no clinical or laboratory evidence of infection after 3rd
day..kindly stop treatment
 If pseudomonas organism is isolated; give gentamycin
plus ceftazidime
 If no clinical suspicious and culture is negative stop
after 7days and if its positive treat for 7days

48. Supportive treatment
 Feeding
 Fluid management
 Oxygen
 Anticonvulsants If seizures
 Sunction
 Treat anaemia

49. prevention
 Hand washing before handling babies
 Incubation care
 Isolate sick babies
 Clean environment and equipment
 Clean babies
 Keep sick staff away
 Avoid overcrowding
 Treat mothers infection
 Ensure immunization

50. Congenital syphilis
 Caused by treponema pallidum, a bacteria
 Fetus acquires it in utero through
transplancetal
 Hematogeneous from mother circulation
 Direct contact of the chancre during delivery

51. Clinical features
 Snuffles (syphilitic rhinitis) prolonged, severe,
poor feeding (early symptoms)
 Rash maculopapular desquamation rash over
palms and soles, around mouth and anus
 Mucocutaneous lesions
 Hepatosplenomegally
 Frontal bossing
 Severe consolidated pneumonia at birth

52. cont
 Most infants are asymptomatic at the time of
diagnosis
 If untreated, most infants develop symptoms
within the 1st 5weeks of life.
 Severely ill infants may be born hydrops with
profound anemia

53. Hematological changes
 Hemolytic anemia
 Thrombocytopenia

54. Complications/late features
 Osteochondritis
 Interstitial keratitis
 Frontal bossing
 Hutchisons teeth
 Saddle nose
 Eighth cranial nerve palsychatton joints
 The combination of interstitial keratitis, eighth
cranial nerve deafness and hurtchson teeth is
commoly refered as hurtchsons triad

55. investigations
 Csf exam: reveal pleocytosis, elevated
proteins (neurosyphilis)
 Skin scrappings for micrscopy: treponema
organisms
 Non treponemal syphillitic test
 Serological test
 VDRL

56. treatment
 Parenteral penicillin prefered DOC
 Penicillin G for 10-14/7
 Non treponemal antibody titres should be
monitored during treatment period and
thereafter

57. Neonatal meningitis
 Inflammation of the pia and arachnoid mater
which are membranes covering the brain and
spinal cord
 Etiology: E.coli, and group b streptococci.
Others are H. influenza and streptococci

58. Clinical presentation
 Sudden onset as in nns
 Late onset: convulsions, coma, bulged
anterior fontanel, neck stiffness

59. Predisposing factors
 Prematurity
 Maternal genital infection
 Birth trauma
 Prolonged labor
 Umbilical sepsis
 meningomyelocele

60. investigations
 Septic screen
 Hemogram
 Csf exam
 UECs

61. treatment
 Specific: iv benzylpenicillin plus
aminoglycosides
 Late: cephalosporins plus amikacin

62. complications
 Cerebral abscess
 Hydrocephalus
 Epilepsy
 Mental retardation

63. Hemolytic disease of the
newborn
 Used to be common
 Causes hydrops fetalis, anemia and severe
neonatal jaundice
 The red blood cells of the newborn are
attacked by antibodies from the mom.
 The attack begins while the baby is still in the
womb and caused by incompatibility between
the mothers and babys blood.

64. What happens
 Maternal antibodies cross the placenta and
attack fetal red blood cells
 During pregnancy , some of the mothers
antibodies are transported across the
placenta to fetal circulation.
 This is important for the infant to acquire
immune, but also cause HDU as they target
fetal red blood cells.

65. cont
 A major cause of HDU is incompatibility of the RH
blood group between the mom and fetus
 Commonly triggered by: D antigen others C,c E, e
can also cause hemolysis
 Pregnancies at risk are the D negative carrying a
fetus who is D positive acquired from mom.
 The mom immune response to the fetal D antigen
is to form antibodies against it (anti-D)

66. sensitization
 During first pregnancy it takes place if the mom
blood come incontact with D positive from baby
 An immune response is mounted, causing
sensitization
 Once a mom is sensitized to the D antigen the
serum will contain anti-D
 A small amount of blood is needed for
sensitization to occur
 This typically occurs during the first pregnancy

67. cont
 Sensitization occurs during labor, and
increased during prolonged, or complicated
labor..increased risk of sensitization
 It can also occur earlier in pregnancy e,g.
during prenatal bleed or miscarriage, medical
procedure

68. During subsequent pregnancies
 HDU occurs during subsequent pregnancies
 Initially, the maternal anti-D that is formed at the
time of sensitization is of igM , which does not
cross the placenta
 In subsequent pregnancies, a repeat encounter
with the RhD antigen stimulates the rapid
production of type igG anti-D which can be
transported across the placenta and enter fetal
circulation

69. cont
 Once in the fetal circulation anti-D attaches to
the Rh D antigens found on the fetal red blood
cells, marking them to be removed.
 The rate of hemolysis determines whether the
nature of HDU is mild, moderate or severe

70. mild
 Small increase in the rate of hemolysis is
tolerated by the fetus
 Mild anemia, jaundice which resolve without
treatment
 In moderate: severe jaundice with rapid
increase of bilirubin within 24hours of delivery.
This may cause kernicterus

71. In severe destruction
 Severe anemia
 Liver, spleen, and other organs increase their
production of RBCs to compensate for the
loss
 This causes the liver and spleen to enlarge
(hepatospleenomegally) and liver dysfunction
 Immature red blood cells spill into the
circulation thus called hydrops fetalis

72. A complication of severe HDU
 Hydrops fetalis is the complication
 Fetal tissue become swollen (edematous).
 Its fatal in utero or soon after birth.

73. ABO incompatibilty
 It arises when mom has igG antibodies from
previous exposure to A or B antigens
 The antibodies crosses the placenta by active
transport and affect the fetus or newborn
 Sensitization of the mom to fetal antigens may
have occurred by previous transfusions or by
conditions of pregnancy that result in transfer of
fetal erythrocytes into maternal circulation such
as:

74. cont
 1st trimester abortion
 Ectopic pregnancy
 Amniocentesis
 Manual extraction of placenta
 Normal pregnancy

75. Clinical presentation
 Mild anemia compared to RH
isoimmunization.. Few cells have anti-A or
anti-B antibody binding sites compared to RH
antigenic sites

76. prevention
 Mom carrying rhesus positive child is given
anti-D at gestation period above28weeks and
within seventy hours after birth.
 This antibody binds to fetal RH-positive
erythrocytes entering the maternal circulation
during the fetal-to-maternal transfusion at
birth.

77. Perinatal mortality