This document provides information about neonatal jaundice and retinopathy of prematurity (ROP). It defines these conditions and discusses their risk factors, etiology, types, diagnostic evaluation, and management. For neonatal jaundice, the document covers bilirubin metabolism, risk factors, types of jaundice, evaluation, complications like kernicterus, and treatment methods like phototherapy and exchange transfusion. For ROP, it describes the abnormal blood vessel growth in the retina that can lead to blindness if left untreated.

3. At the end of the session the student will
be able To:
Define Neonatal jaundice and ROP
State Risk factors,Etiology,Types and
Diagnostic Evaluation of Neonatal
jaundice and ROP
.
Apply the management of Neonatal
jaundice and ROP at their clinical set-up

4. Definition: Hyperbilirubinemia refers to
an excessive level of bilirubin in the blood
and is characterized by a yellowish
discoloration of the skin, sclerae, mucous
membranes and nails.
Bilirubin is the end product of heme
degradation
Heme biliverdin bilirubin
Bilirubin is released and bound to serum
albumin

6. Hb → globin + haem
1g Hb = 34mg bilirubin
Represent about 75%
Non – heme source
25% of bilirubin
Bilirubin

7. BILIRUBIN METABOLISM

11. Normally s. bilirubin level vary between 0.3
- 1.2mg/dl. A bilirubin level of more than 2
mg/dl manifest biochemically where as level
of >5 mg/dL manifests clinically in neonates
UNCONJUGATED B.
Insoluble in water can not be excreted in
urine
Tightly compounded to s. albumin
Toxic
CONJUGATED B.
Water soluble& can be excreted in urine
Loosely bound to albumin.

12. MAJOR RISK FACTORS
Pre discharge TSB or TCB level in the high-
risk zone
Jaundice observed in the first 24 hours
Blood group incompatibility with positive
direct coombs test, other known hemolytic
disease (glucose-6-phosphate dehydrogenase
deficiency).

13. Cephalo-hematoma or significant
bruising
Exclusive breast-feeding, particularly if
nursing is not going well and weight
loss is excessive
East Asian race*

14. MINOR RISK FACTORS
• Pre discharge TSB or TCB level in the
high intermediate risk zone
• Gestational age 37-38 week
• Jaundice observed before discharge
• Previous sibling with jaundice
• Macrosomic infant of a diabetic mother
• Male gender

15. DECREASED RISK (these factors are
associated with decreased risk of
significant jaundice)
TSB or TCB level in the low-risk zone
Gestational age ≥41 weeks
Exclusive bottle-feeding
Black race
Discharge from hospital after 72 hour

17. • Increases the load of bilirubin to be
metabolized by the liver (hemolytic
anemias, polycythemia, bruising or
internal hemorrhage, shortened red blood
cell life as a result of immaturity or
transfusion of cells, increased
enterohepatic circulation, infection)
• Damages or reduces the activity of the
transferase enzyme or other related
enzymes (genetic deficiency, hypoxia,
infection thyroid deficiency)

18. • Absence or decreased amounts of the
enzyme or reduction of bilirubin uptake
by liver cells (genetic defect, and
prematurity).
• Hypo proteinuria
• Displacement of bilirubin from its
binding sites on albumin by competitive
binding of drugs such as Sulfafurazole
and moxalactam, acidosis, and increased
free fatty acid concentration secondary
to hypoglycemia, starvation, or

19. A) PHYSIOLOGICAL
 In new born babies bilirubin metabolism
is immature which results in the
occurrence of hyperbilirubinemia in the
first few days of life.
 Many factors are implicated:
increased destruction of RBC
increase enterohepatic circulation
decreased ability of the liver to conjugate
bilirubin
decreased uptake by the liver due to low

20. • First appears between 24-72hours of age
• Maximum intensity seen on 4-5th day in
term and 7th day in preterm neonates
• Does not exceed 15 mg/dl
• Clinically undetectable after 14 days.
• No treatment is required but baby should
be observed closely for signs of worsening
jaundice
• Does not rise more than 5mg/dl/day

21. B) PATHOLOGICAL
Appears within 24 hours of age
Increase of bilirubin > 5 mg / dl / day
Serum bilirubin > 15 mg / dl
Jaundice persisting after 14 days
Stool clay / white colored and urine
staining clothes yellow
Direct bilirubin> 2 mg / dl

22. Appearing within 24 hours of age
Hemolytic disease of NB : Rh, ABO
Infections: TORCH, malaria, bacterial
G6PD deficiency
Thalassemia
Spherocytosis

23. Appearing between 24-72 hours of life
Physiological
Sepsis
Polycythemia
Intra ventricular hemorrhage
Increased enterohepatic circulation

24. After 72 hours of age
Sepsis
Cephalohaematoma
Neonatal hepatitis
Extra-hepatic biliary atresia
Breast milk jaundice

25. A-unconjugated hyper bilirubinemia
1-Breast feeding jaundice
In exclusively breast feed infants Appears
at 24-48 hours of age
Occur during first week of life
Disappears by 3week
Its related to inadequate B.F
T/t: Proper and adequate B.F

26. 2-Breast milk jaundice
In 2-4 % EBF babies after the 7th day of
life SBR>10mg/dl beyond 3-4week.Due to
prasence of beta-glucuronidase in milk
Should be differentiated from Hemolytic
jaundice, hypothyroidism, G6PDdeficiency
T/t: Some babies may require PT
Continue breast feeding
Usually declines over a period of time

27. 3-Congenital hypothyroidism
4-Spsis
5-Intestinal stasis.
6-Criggler najjar syndrome

28. B-Conjugated hyperbilirubinemia: fraction
>10% of total SBR
Infection
Galactosemia, fructosemia, tyrosinemia
Cystic fibrosis
Dubin johnson syndrome
Rotors syndrome
Idiopathic neonatal hepatitis
Alpha 1 anti-trypsin deficiency
Hypothyroidism, hypopitutarism

29. Kernicterus is a neurologic syndrome
resulting from the deposition of
unconjugated (indirect) bilirubin in the
basal ganglia and brainstem nuclei.
There is neuronal loss ,necrosis & giliosis .
The pathogenesis of kernicterus is
multifactorial and involves an interaction
between unconjugated bilirubin levels,
albumin binding and unbound bilirubin
levels, passage across the blood-brain
barrier, and neuronal susceptibility to

30. Brain damage caused by bilirubin depends
on:
Level of S.bilirubin & albumin
Bilirubin binding by albumin
Status of BBB
Susceptibility of the CNS

31. Asphyxia
Acidosis
Hypoglycemia
Prematurity
Severe hyper bilirubinemia
G6PD deficiency
7-Crigler-Najjar syndrome type I
Gilbert's syndrome

32. ACUTE FORM
Phase 1 (1st 1-2 days): poor suck,
stupor, seizures
Phase 2 (middle of 1st week):
hypertonia of extensor muscles,
opisthotonus, fever, high pitched cry,
retracted neck
Phase 3 (after the 1st week): hypotonia
CHRONIC FORM
1st year: hypertonia, active deep
tendon reflexes, delayed motor skills
After 1st year: movement disorders

33. Early discharge (<48 hr) with no early
follow-up (within 48 hr of discharge); this
problem is particularly important in near-
term infants (35-37 wk of gestation)
Failure to check the bilirubin level in an
infant noted to be jaundiced in the first 24
hr
Failure to recognize the presence of risk
factors for hyperbilirubinemia
Underestimation of the severity of
jaundice by clinical (visual) assessment

34. Lack of concern regarding the presence of
jaundice
Delay in measuring the serum bilirubin
level despite marked jaundice or delay in
initiating phototherapy in the presence of
elevated bilirubin levels
Failure to respond to parental concern
regarding jaundice, poor feeding, or
lethargy

35. Onset/ duration
Pain
Nausea and vomiting
Loss of weight
Itching
Colour of stool
Colour of urine
Past history
Family history

37. Colour of skin
Severity of jaundice
Anemia
Liver
Spleen
Gall bladder
Ascites
Rash or petechiae

38. Clinical Assessment
of
Jaundic
e
(Kramer’s staging)
Area of body bilirubin level mg/dl
1-Face 4-6mg/dl
2-Upper trunk 6-8mg/dl
3-Lower trunk &thigh 8-14mg/dl
4-Arms & lower legs 14-19mg/dl
5-Palms &soles
≥20mg/dl

39. it depend on the suspected cause and
include
S. bilirubin (total, direct ,indirect)
ABO & Rh of baby and mother
Hb ,blood film
Coombs test, G6PD assay
Blood culture
TORCH screen
LFT
Blood sugar

40. Promote & support breastfeeding
Perform a thorough risk assessment for all
infant
Provide parents with written & verbal
information. About newborn jaundice
Provide appropriate follow-up
Identify preterm infant and provide close
monitoring
Interpret all bilirubin levels according to
infant age in hours

41. Establish nursery protocols for identifying
& evaluating hyperbilirubinemia
Recognize that visual assessment of
bilirubin levels is inaccurate
Measure bilirubin levels in all infants with
jaundice in the first 24 hours after
delivery
Treat newborns as indicated with
physiotherapy or exchange transfusion

42. Purposes:
Reduce level of serum bilirubin and
prevent bilirubin toxicity
Prevention of hyperbilirubinemia: early
feeds, adequate hydration
Reduction of bilirubin levels either by
phototherapy or exchange transfusion
Phototherapy: refers to the use of light
to convert bilirubin molecules in the body
into water soluble isomers that can be

43. • Phototherapy reduce bilirubin level about
2-3mg/dl per day .But intensive
phototherapy can reduce level of bilirubin
by 10mg/dl per day
The therapeutic effect of phototherapy
depends on:
the light energy emitted in the effective
range of wavelengths.
the distance between the lights and the
infant.
and the surface area of exposed skin.
the rate of hemolysis.

45. Serum bilirubin levels and hematocrit should
be monitored every 4-8 hr in infants with
hemolytic disease and those with bilirubin
levels near toxic range for the individual
infant. Serum bilirubin monitoring should
continue for at least 24 hr after cessation of
phototherapy.
Complication:
loose stools, erythematous macular rash,
purpuric rash
overheating, dehydration (increased

46. Bronze baby syndrome occurs in the
presence of direct hyperbilirubinemia ,
The term bronze baby syndrome refers
dark, grayish brown skin discoloration
in infants undergoing phototherapy.
Almost all infants observed with this
syndrome have had significant elevation
of direct- reacting bilirubin and other
evidence of obstructive liver disease. The
discoloration may be due to photo-
induced modification of porphyrins

47. Skin damage
Skin rash
Damage to immature retina
Blocked nose
Hypocalcaemia
Decrease LV output which lead to
decrease renal perfusion
Agitation & distress

48. B-Exchange transfusion:
Double-volume exchange transfusion is
performed if intensive phototherapy has
failed to reduce bilirubin levels to a safe
range and if the risk of kernicterus exceeds
the risk of the procedure. ET replace 85% of
infant blood & reduce bilirubin level by 50%.
It should be used for any newborn with a
total serum bilirubin of greater than 428
μ.mol/l ( 25 mg/dL )
Complication:

49. hypoglycemia
hypocalcemia
thrombocytopenia
volume overload
arrhythmias
infection
B-late complication:
late onset anemia
GVH disease
portal hypertension & portal vein
thrombosis

50. Intravenous immunoglobulin: 500mg/kg
especially in coombs +ve test
Metalloporphyrins: The mechanism of
action is competitive enzymatic
inhibition of conversion of heme protein
to biliverdin.
A single intramuscular dose on the 1st day
of life may reduce the need for
subsequent phototherapy.particularly in
patients with ABO incompatibility or G6PD
deficiency.

51. Complications from metalloporphyrins
include transient erythema if the infant is
receiving phototherapy
phenobarbital: promote liver enzymes and
protein synthesis to induce hepatic bilirubin
metabolism
protoporphyrin: inhibit conversion of
biliverdin to bilirubin by heme oxygenase
Early recognition and treatment of
hyperbilirubinemia prevents severe brain
damage. But brain damage due to kernicterus

53. • Retinopathy of
prematurity (ROP)
is an eye disease
that can happen in
premature babies.
It causes abnormal
blood vessels to
grow in the retina,
and can lead to
blindness

54. • Retinopathy (ret-in-AH-puh-thee) of
prematurity makes blood vessels grow
abnormally and randomly in the eye.
These vessels tend to leak or bleed,
leading to scarring of the retina, the
layer of nerve tissue in the eye.
• When the scars shrink, they pull on the
retina, detaching it from the back of the
eye. Because the retina is a vital part of
vision, its detachment will cause
blindness.

56. The onset of ROP progresses in two phases:
Involves an initial insult such as hyperoxia ,
hypoxia or hypotension at a critical point in
retinal vascularization - causes
vasoconstriction and decreased blood supply
to the developing retina with subsequent
arrest in vascular development.

57. Neovascularization occurs(regulated by the
hypoxic avascular retina).
New vessels growing through the retina into
the vitreous.
Are permeable leading to hemorrhage and
edema.
Extensive and severe extra retinal fibro
vascular proliferation leads to retinal
detachment and abnormal retinal function

58. Prematurity / low gestational age < 30
weeks
Retinal immaturity
Low birth weight(1500gm)
Hyperoxia / Hypoxia/hypercarbia

59. ROP has no signs or symptoms when it
first develops in a newborn.
The only way to detect it is through an
eye exam by an ophthalmologist

60. Ophthalmologic examination by an expert
examiner usually confirms the diagnosis.
Binocular indirect ophthalmoscopy (BIO) is
generally used.
Newer digital camera technology
demonstrated 100% sensitivity in detecting
ROP requiring treatment. But it does not
permit adequate assessment of retinal

62.  Some cases of ROP are mild and correct
themselves. But others progress to scarring,
pulling the retina away from the rest of the eye.
These cases need surgery to prevent vision loss or
blindness
 ROP surgery stops the growth of abnormal blood
vessels. Treatment focuses on the peripheral
retina (the sides of the retina) to preserve the
central retina (the most important part of the
retina). ROP surgery involves scarring areas on the
peripheral retina to stop the abnormal growth and
eliminate pulling on the retina.

63. • Because surgery focuses on the peripheral
retina, some amount of peripheral vision
may be lost. However, by preserving the
central retina, the eye can still do vital
functions like seeing straight ahead,
distinguishing colors, reading, etc

64. The most common methods of ROP surgery
are:-
This is done most often for ROP. Small laser
beams scar the peripheral retina. This
procedure (also called laser therapy or
photocoagulation) lasts about 30–45 minutes
for each eye.

65. A medicine is injected into the eye. This
might be done as an alternative to, or along
with, laser surgery. This is a newer
treatment and results are promising, often
allowing the blood vessels to grow more
normally. Research is ongoing to determine
the long-term side effects of the medicine
on premature infants.

66. This involves placing a
flexible band, usually
made of silicone, around
the circumference of the
eye. The band goes
around the sclera, or the
white of the eye, causing
it to push in, or "buckle."
This, in turn, pushes the
torn retina closer to the

67. This complex surgery involves replacing the
vitreous (the clear gel in the center of the
eye) with a saline (salt) solution. This
allows for the removal of scar tissue and
eases tugging on the retina, which stops it
from pulling away. Vitrectomy can take
several hours

69. • Neonatal jaundice is a yellowish
discoloration of the white part of the
eyes and skin in a newborn baby due to
high bilirubin levels. Other symptoms
may include excess sleepiness or poor
feeding. Complications may include
seizures, cerebral palsy or kernicterus.
• Retinopathy of prematurity (ROP) is an
eye disease that can happen in
premature babies. It causes abnormal
blood vessels to grow in the retina, and

71.  Datta parul,’paediatric nursing”,2nd edition,jaypee
brothers medical publishers(p)ltd,new delhi,page
no:36-46
 Marlow dorothy r,”text book of paediatrics nursing”,6th
edition,elsevier publication,noida,page no:647-652.
 Sharma rimple,”essential of paediatrics nursing”,1st
edition,jaypee publication,new delhi,page no:456-
467..
 Park k,”textbook of preventive and social
medicine”22nd edition,m/s bansidhar bharat
publishers,newdelhi,page no:97-108.
 http://www.childrenshospital.org/conditions-and-
treatments/conditions/r/retinopathy-of-prematurity-
rop/testing-and-diagnosis