PEDIATRICS

2ND CASE REPORT

Neonatal Hyperbilirubinemia

Presented by:
Team U1-A
CLINICAL CASE
This is a jaundiced, 4 day old, 3.1 kg, appropriate for gestational age
(AGA) Filipino female infant born at term to a 25-year-old A+
primiparous woman. The pregnancy was otherwise uneventful. Labor
was augmented with oxytocin. The baby was discharged home on day of
life 2 at which time her weight was down 4% from birth weight and she
had mild facial jaundice. In the hospital, she was breast fed every 3 hours
and had 2 wet diapers and one meconium stool over a 24 hour period. In
the office, on day 4, mother reports that she is breastfeeding the baby
every three hours. The urine is described as dark yellow in color and the
stools appear dark green. Physical examination is unremarkable.
SALIENT POINTS OF THE
CASE
 Female
 4day old
 3.1 kg
 Weight loss upto 4% from birth weight
 Breast Feeding
 Mild facial jaundice
 The urine is dark yellow in color
 Presence of dark green stool
 Presence of meconium stool
DIFFERENTIAL
DIAGNOSIS
DDX RULE IN RULE OUT
Breast milk jaundice Yellow skin , yellow Fever ,vomiting
  abdomen , Weight loss
Breast feeding jaundice Yellow skin , yellow Fever ,vomiting
  abdomen, Dehydration ,
weight loss
Neonatal hepatitis Yellow skin , yellow Vomiting ,
  abdomen, fever, enlarge
liver
hypothyroidism Yellow skin , yellow Fever , vomiting
  abdomen, weight loss,
weakness
Biliary atresia Yellow skin , yellow Fever ,vomiting
  abdomen, dark urine
Diabetic mother Weight loss, yellow skin , Fever , vomiting
(gestational) dehydration , weakness
CLINICAL
HISTORY
GENERAL DATA
Patient is an infant, 4-day-old, Female, born on
October 21, 2020 at Tarlac Provincial Hospital,
Filipino, Roman Catholic and was admitted for the
first-time on October 25, 2020 at 8 o’clock in the
morning.
CHIEF COMPLAINT

SKIN YELLOWING
 HISTORY OF PRESENT
ILLNESS
Two days prior to admission, on the day being
discharged after two-day hospital stay, the mother
noticed her infant to lose some weight and had slight
yellowing of the face, it is accompanied by dark
yellow colored urine and dark green colored stools.
PAST MEDICAL HISTORY
The mother confirmed of no history of any kinds
of allergies. She recalled to have childhood history
of illnesses such as chicken pox, and measles. No
history of any blood transfusion. No history of any
surgical procedures.
FAMILY HISTORY
The infant’s father is a 27 years old overseas worker with good physical
and mental health and the mother is a 25-year-old office manager with a
good physical and mental health. There is no history of consanguinity
between the infant’s parents. The infant is the first child of the couple.
The patient has a family history of East Asian Ancestry on the paternal
side. There is no family history of illnesses such as cardiac disease,
hypertension, stroke, diabetes, cancer, galactosemia, G6PD deficiency,
any red blood cell Disorders or any endocrine disorders for both sides of
the family.
MATERNAL HISTORY
The patient was born from a 25-year-old A+ mother
with OB score of G1P1 (1001). There is no exposure
to infection, drugs, chemicals, alcohol and smoke
during pregnancy, labor and delivery. The mother
confirmed that she had regular checkups, pre-natal
screening and took prescribed medications given by
her OB. She also claimed to have healthy and
balance diet. Overall, the mother had a good
maternal health.
 BIRTH HISTORY
The patient is a full-term infant with 38 weeks AOG
delivered via Normal Spontaneous Vaginal Delivery in Tarlac
Provincial Hospital. The labor was noted to be augmented
with oxytocin. The patient’s birthweight is 3,100 grams
which is appropriate for gestational age (AGA). There is a
good APGAR score with 9 at 1 minute and 10 at 5 minutes.
No resuscitation was done. There are no complications or
congenital abnormalities such as cyanosis, jaundice, and
pallor noted and the patient had a good cry after birth.
Newborn screening is also done with no remarkable result.
IMMUNIZATION HISTORY
BCG vaccine and Hepatitis B vaccine (1st dose)
was given in the nursery.
FEEDING HISTORY
The patient was exclusively breastfed by the mother
every 2-3 hours having 8-12 times of feeding
continuously for three days since discharge. No
formula feeding is done. But during feeding time,
there was a poor feeding due to poor latching. The
baby is awake for almost all of the time of feeding
and sometimes cry when hungry. The mother has
not noticed any signs of diarrhea, constipation,
vomiting, hematemesis.
SOCIOECONOMIC AND
ENVIRONMENTAL HISTORY
They live in a 2 story-apartment with 3 rooms and is well-
ventilated. The patient lives with her mother and their stay-in
housemaid. Both of her parents are working but her father is
working overseas. Her parent’s jobs are good paying so they are
financially stable. No one in the home smokes or any
neighborhood near their house. Their house is located near
highway and no near factory in their area. Their water source
for both drinking and washing is from the water district. They
have proper garbage and sewage disposal in their area. They
have 2 dogs in the house and their housemaid is the one who
personally baths their pets.
REVIEW OF SYSTEMS
GENERAL: (-) fever, (+) weight loss, (-) chills, CARDIOVASCULAR: (-) history of heart
(+) poor oral intake, (-) fatigue, (+) irritability murmur, (-) cyanosis
CUTANEOUS: (-) rash, (-) pigmentation, (-) RESPIRATORY: (-) cough, (-) dyspnea
lumps, (-) pruritus, (-) dryness
GASTROINTESTINAL: The mother noticed that
HEAD: (-) headache, (-) dizziness, (-)
her infant defecate once within 24 hours
lightheadedness, (-) syncope with dark green colored stools.
EYES: (-) pain, (-) redness, (-) lacrimation, (-)
diplopia RENAL: She also noticed that her infant only
urinates 2-4 times a day for the past 3 days
EARS: (-) hearing problem, (-) itching, (-)
and a dark yellow colored urine for the last
discharge 24 hours.
NOSE: (-) frequent colds, (-) discharge, (-)
nosebleeds MUSCULOSKELETAL: (-) edema, (-) trauma
MOUTH/THROAT: (-) mouth sores, (-) HEMATOLOGY: (-) ecchymosis, (-) bleeding
dysphagia
NECK: (-) lumps, (-) swollen glands
PHYSICAL EXAMINATION
General Survey  Neonatal jaundice first becomes visible in the
face and forehead. Identification is aided by
The patient is awake, conscious but agitated pressure on the skin, since blanching reveals
the underlying color. Jaundice then gradually
becomes visible on the trunk and extremities.
This cephalocaudal progression is well
described. Jaundice disappears in the opposite
direction.
 The jaundiced neonate requires a full physical
examination with emphasis on the following:
 General: Does the child look well or unwell? 
You may be able to observe the child feeding –
is the baby having difficulty feeding? Is the
baby consolable?
Vitals
· Vitals: If febrile, the newborn will require a
Temp 36.8 full septic work-up. In hemolytic states, there
PR : 118 bpm can be an increase in heart rate and
RR :: 55 breaths/min respiration rate as well as poor perfusion.
· Growth Parameters: Obtain length, weight
Growth parameters and head circumference and compare to
measurements taken at birth. Depending on
Weight : 2.7 the newborn’s age, excessive weight loss or
Height BMI : 50cm insufficient weight gain may point to
dehydration.
HEENT :. · HEENT: Is there pallor? Sclerae and
Head : 34cm circumfrence no cephalohematoma. slightly mucous membranes should be closely
sunken funtanel inspected for jaundice. Look for
Eyes : sclera yellow, conjuctiva yellow cephalohematoma or bruising. Remember
that jaundice first becomes clinically apparent
Ears :unremarkable at the cephalic end of the body, and only
progresses caudally as serum levels
Nose:unremarkable increase.

Throat: . oral mucosa tacky .

 · Cardiovascular: Heart rate, pulse volume,
Cardiovascular: blood pressure, apex location, perfusion.
Severe haemolytic processes can result in
heart failure.
· Respiratory: Respiration rate and rhythm
and oxygen saturation. If the neonate is in
heart failure, there may be respiratory signs.
Respiratory: 55 breath per minutes · Abdomen: Is the abdomen distended? Is
there caput medusa (evidence of portal
hypertension)? Are there any masses?
Check for hepatomegaly and splenomegaly.
Are there any areas of tenderness?,
petechiae, and microcephaly may be
Abdomen: no spleno/hepertomegaly associated with hemolitic anemia , sepsis,
and congenital infections and should trigger
a diagnostic evaluation directed towards
these diagnoses. Neonatal jaundice may be
exacerbated in these situations.
 Neurologic: Level of consciousness.
Cranial nerves, tone, gross motor
movements, quality of the cry, and
Neurologic: primitive reflexes (Moro, grasps,
patient was conscious and awake, agitated and tonic-neck, step).Overt neurologic
had poor sucking findings, such as changes in muscle
tone, seizures, or altered cry
characteristics, in a significantly
jaundiced infant are danger signs
and require immediate attention to
prevent kernicterus.
DIAGNOSTICS
• A complete diagnostic evaluation
• Determination of direct and indirect bilirubin fractions
• Determination of hemoglobin
• Reticulocyte count
• Blood type
• Coombs’ test
• Examination of the peripheral blood smear
DIAGNOSIS

Physiologic Jaundice
NEONATAL
JAUNDICE
Clinical Presentation
Pathogenesis
Workups
ETIOLOGY
Causes of pathologic hyperbilirubinemia can be classified as due to
 increased bilirubin load (i.e., pre-hepatic; either hemolytic or non-hemolytic processes)
 impaired bilirubin conjugation (i.e., hepatic)
 impaired bilirubin excretion (i.e., post-hepatic).
TYPE OF NEONATAL
JAUNDICE
 Risk Factor of Neonatal Jaundice

Ref: https://www.sciencedirect.com/science/article/pii/S1744165X06000199
PRESENTATION
The most notable signs of hyperbilirubinemia
 jaundice
 scleral icterus

 Jaundice refers to yellowing of the skin, which can be seen by blanching the skin with digital
pressure. This should be done centrally, and at multiple levels, since jaundice develops in a
cephalocaudal fashion. Roughly, the following serum levels have been observed to correlate
with clinical findings:
 34-51 umol/L – scleral icterus
 68-86 umol/L – jaundice on face
 258 umol/L – jaundice from face to umbilicus, upper chest 171 umol/L, abdomen 205 umol/L
 340 umol/L – jaundice from head to toe (palms and soles >257umol/L)
PHYSIOLOGY JAUNDICE
 Bilirubin is the product of red blood cell breakdown, specifically heme degradation.
 Bilirubin in this state is not water-soluble, and must become water-soluble to be excreted in bile.
 Bilirubin binds with albumin, and is then conjugated in the liver by the enzyme uridine
diphosphogluconurate (UDP) glucuronyltransferase.
 Several factors specific to the neonate’s physiology contribute to physiologic hyperbilirubinemia:
 Increased production: Fetal erythrocytes have a higher rate of turnover; per kilogram, newborn infants
produce twice the daily adult amount of bilirubin.
 Decreased clearance: Newborns have relatively low UDP-glucuronyltransferase activity (increases until
approximately 14 weeks). They also have slow intestinal motility in the first few days as feeding
becomes established, and this increases small amounts of bilirubin reuptake by the enterohepatic
circulation.
 PATHOLOGICAL JAUNDICE
pathological jaundice following features :
 Clinical jaundice appearing in the first 24 hours or greater than 14 days of life.
 Increases in the level of total bilirubin by more than 8.5 μmol/l (0.5 mg/dL) per hour or (85 μmol/l) 5 mg/dL per 24 hours.
 Total bilirubin more than 331.5 μmol/l (19.5 mg/dL) (hyperbilirubinemia).
 Direct bilirubin more than 34 μmol/l (2.0 mg/dL).

 The signs of pathological jaundice

 the presence of intrauterine growth restriction
 stigma of intrauterine infections (e.g. cataracts, small head, and enlargement of the liver and spleen)
 cephalohematoma,
 bruising
 signs of bleeding in the brain's ventricles
 History of illness is noteworthy.
 Family history of jaundice and anemia,
 family history of neonatal or early infant death due to liver disease,
 maternal illness suggestive of viral infection (fever, rash or lymphadenopathy),
 maternal drugs (e.g. sulphonamides, anti-malarials causing red blood cell destruction in G6PD deficiency) are suggestive of pathological jaundice in
neonates.
RED FLAGS FOR PATHOLOGIC
JAUNDICE
 Jaundice in first 24 hours
 Rapidly rising total bilirubin concentration (>86umol/L/day)
 Younger gestational age
 Previous sibling with jaundice
 Significant bruising
 Jaundice persisting for more than 2-3 weeks
 East Asian ethnicity
Metabolic Pathway of the Degradation of Heme and the Formation of Bilirubin.
• Heme released from the hemoglobin of red cells or from other hemoproteins is degraded by an enzymatic process
involving heme oxygenase, the first and rate-limiting enzyme in a two-step reaction requiring NADPH and oxygen, and
resulting in the release of iron and the formation of carbon monoxide and biliverdin.
• Metalloporphyrins, synthetic heme analogues, can competitively inhibit heme oxygenase activity (indicated by the X).
Biliverdin is further reduced to bilirubin by the enzyme biliverdin reductase.
• Carbon monoxide can activate guanylyl cyclase (GC) and lead to the formation of cyclic guanosine monophosphate
(cGMP). It can also displace oxygen from oxyhemoglobin or be exhaled.
• The bilirubin that is formed is taken up by the liver and conjugated with glucuronides to form bilirubin monoglucuronide
or diglucuronide (BMG and BDG, respectively), in reactions catalyzed by uridine diphosphate and monophosphate
glucuronosyltransferase.
• The bilirubin glucuronides are then excreted into the intestinal lumen but can be deconjugated by bacteria so that the
bilirubin is reabsorbed into the circulation,.
Pathogenesis of BIND in infants.
• BIND=bilirubin-induced neurologic dysfunction
• BBC=bilirubin binding capacity
• CNS=central nervous system
• IVH= intraventricular hemorrhage
• RBC=red blood cell
Ref : https://neoreviews.aappublications.org/content/21/5/e298
Mechanisms of bilirubin-induced neuronal
cell injury.
• ATP=adenosine triphosphate
• Ca=calcium
• CNS=central nervous system

Ref : https://neoreviews.aappublications.org/content/21/5/e298
DIAGNOSIS
 Visual examination help to look for signs of jaundice.
 Neonatal undressed during exam for look a skin under good, preferably natural, light. And check
include :
 the whites of baby's eyes
 baby's gums
 the colour of baby's urine or poo

 If baby has jaundice, checked the level of bilirubin in blood.

 Bilirubin test by :
 a bilirubinometer, shines light on to baby's skin (it calculates the level of bilirubin by analysing how
the light reflects off or is absorbed by the skin)
 a blood test of a sample of blood taken by pricking baby's heel with a needle
Ref : https://journals.physiology.org/doi/abs/10.1152/physrev.00004.2019
Ref: https://www.magonlinelibrary.com/doi/abs/10.12968/bjom.2018.26.6.362?journalCode=bjom
MANAGEMENT
PHOTOTHERAPY
• Uses blue light (wavelength of 430-490 nm)
to convert unconjugated bilirubin into
bilirubin photoproducts (induces
photoisomerization of bilirubin forming
lumirubin that can be excreted in the urine)
• Can be delivered overhead in a closed rib
or via bili blanket
• Fluorescent light
• Spot light
• Fiber optics
• Response is dose dependent
• Maximal skin surface area
• Interruption are minimized
• Major role is to avoid exchange transfusion
FEEDING
• is critical in management
• Baby should be fed every 2-3 hours
• Supplemental formula maybe in
considered (breastmilk jaundice)
• Can help decrease bilirubin levels
• Case to case basis with input from
parents
AAP RECOMMENDATION
• Complicated cases include those
associated with:
• perinatal asphyxia
• acidosis
• hypoxia
• hypothermia
• hypoalbuminemia
• meningitis
• intraventricular hemorrhage
• hemolysis
• hypoglycemia
• signs of kernicterus

Suggested Maximum Indirect Serum Bilirubin

Concentration mg% in PRETERM infants
 AAP RECOMMENDATION
Treatment strategies for indirect hyperbilirubinemia in healthy term infants without hemolysis
BILIRUBIN NOMOGRAM
• For term and near term
newborn w/ negative direct
COOMBS
• TSB
• Above 95th percentile
• > or = to 8mg% at 24 hours
• > or = to 14mg% at 48 hours
• > or = to 16mg% at 72 hours
• > or = to 17mg% at 1st week
of life
• Above 95th percentile group is
at higher risk of bilirubin
induced neurologic
dysfunction including
kernicterus
 PARENT EDUCATION
Jaundice is common,
but in rare instances,
it can lead to severe
morbidity and
mortality which is
largely preventable

Proper feeding practices Check your baby’s Changes in skin and Detect and report worsening
 Feed your baby at least 8 to hydration status behavior Jaundice
12 times every 24 hours  Fewer than six wet  Hard to wake up or will not  Crying inconsolably or with a high
 Ensuring that the baby has a sleep at all pitch.
diapers per day
good "latch"
 Parched, dry mouth  Not breastfeeding or  Is arched like a bow (the head or neck
 Increasing the mother’s milk sucking from a bottle well and heels are bent backward and the
 Sunken soft spot of
supply  Is very fussy body forward)
the head
 Supplementing with formula  Does not have enough wet  Has a stiff, limp, or floppy body
 Decrease bowel
or donor breast milk or dirty diapers  Has strange eye movements
movements
THANK YOU