Approach to Neonatal jaundice

Dr. Ghufran A. Hariri
Senior Family Resident (R4)
Supervised by :
DR. Yazeed A. Khojah
Consultant Family & Palliative Medicine

• Introduction
• Etiology
• Types
• Risk factors
• Approach
• History
• Physical exam
• Investigation
• Treatment
• Follow up
• Complications
• Prognosis
• Screening
• Prevention
• Summery

INTRODUCTION
• Definition :
• It is yellowish discoloration of the skin and sclera of a neonates.
• Neonate refers to baby in the first 28 days of life.
• Can be classified to Physiologic Vs. Pathologic.
• Epidemiology:
• Jaundice is the most common condition in
neonates that requires medical attention.
• 50%-70% term infants.
• 80% of preterm infants.

ETIOLOGY
• Physiological ( Benign neonatal hyperbilirubinemia ):
• increased bilirubin production & decreased excretory
capacity.
• Increased bilirubin load.
• 2ry to increased red blood cell (RBC) volume &
Decreased RBC life span.
• Term neonates (60 – 90 days)
• premature neonates (35 – 50 days)
• Decreased uptake by the liver.
• Decreased conjugation in the liver.
• Decreased excretion into bile.

ETIOLOGY (Cont.)
• Pathological:
• Pathologic neonatal jaundice
occurs when additional factors
accompany the basic mechanisms
described in physiological jaundice.

ETIOLOGY
Physiological
jaundice
Pathological
jaundice
Same as
physiological jaundice
Other factors
Unconjugated
Hyperbilirubinemia
Increased
production
ABO incompatibility
G6PD deficiency
Cephalohematoma or significant bruising
Other hemoglobinopathies or
RBC membrane defects
Decreased
clearance
Glibert syndrome
Crigler Najjar type 1 and 2
Hypothyriodism
Increase enterohepatic
circulation
Breast feeding jaundice
Breast milk jaundice
Intestinal obstruction
Ileus
Conjugated
Hyperbilirubinemia
Intrahepatic
disease
Metabolic /genetic factors :
Alpha 1 antitrypsin deficiency/ Cystic fibrosis/
Dubin Johnson syndrome /Zellweger’s syndrome/
Rotor’s syndrome /Glactosaemia.
Infections : TORCH /UTI ( E.coli)
Neonatal haemochromatosis
Idiopathic neonatal hepatitis
Total parental nutrition
Shock
extrahepatic
obstruction
Biliary atresia
Choledochal cyst
Bile duct stenosis
cholelithiasis

Physiological jaundice
( Benign neonatal
hyperbilirubinemia )
Pathological jaundice
Type of
hyperbilirubinemia
Always unconjugated
hyperbilirubinemia.
Can be either
conjugated or unconjugated
hyperbilirubinemia
Onset
> 24 hours after birth
Can present < 24
hours after birth
Peak total serum
bilirubin
< 15 mg/dl (in the case of
a full term, breastfed infant)
May rise > 15 mg/dl
Daily rise in serum
bilirubin
< 5 mg/dl/day > 5 mg/dl/day
Etiology
Hemolysis of fetal
hemoglobin and an
immature hepatic
metabolism of bilirubin.
See “ETIOLOGY“
TYPES

Breast Milk Vs. Breast Feeding Jaundice
• Breast Feeding Jaundice (Suboptimal Intake Jaundice):
• Onset within 1 week
• Pathophysiology:
• Could be due to insufficient milk production or poor feeding →
lack of calories, hypovolemia and significant weight loss
and inadequate quantities of bowel movements to remove bilirubin
from the body → ↑ enterohepatic circulation → increased
reabsorption of bilirubin from the intestines → unconjugated
hyperbilirubinemia.

• Establishment of successful breastfeeding, one of the mainstays of
preventing hyperbilirubinemia.
• Signs of adequate intake in breasted infants includes:
• 4-6 wet diapers per day
• 3-4 stools per day by the fourth day of life, and a transition to seedy,
mustard-colored stools by the third or fourth day of life.

• Breastfeeding women whose infants have jaundice are at increased
risk of early cessation of breastfeeding.
• Management :
• The American Academy of Pediatrics recommends promoting
breastfeeding for infants with jaundice, assessing for the
adequacy of breastfeeding, and increasing the frequency to eight
to 12 times per day.

• Breast Milk Jaundice (BMJ) :
• Indirect hyperbilirubinemia.
• Usually bilirubin levels peak within 2 weeks after birth, are elevated for 4–
10 days, then return to normal levels at 3–12 weeks.
• Etiology not clearly understood.
• Most of the proposed etiologies involve the factors present in the human
breast milk itself. Other hypotheses suggest potential genetic mutations
present in the affected neonates.

• BMJ is a diagnosis of exclusion
• A detailed history and physical examination showing that the infant is
thriving and that lactation is well established are key elements to
diagnosis.

• Distinguishing between breastfeeding jaundice and breast milk jaundice is
important, because bilirubin-induced encephalopathy occurs more
commonly in breastfeeding jaundice.
• Breast milk jaundice in otherwise healthy full-term infants rarely
causes kernicterus.
• The prognosis is EXCELLENT, although jaundice in breastfed infants may
persist for as long as 12 weeks.

• Management :
• 1-For healthy term infants with breast milk or
breastfeeding jaundice who have bilirubin levels of 12
mg/dL- to 17 mg/dL (170 µmol/L):
• Increase breastfeeding to 8-12 times per day.
• Recheck the serum bilirubin level in 12-24 hours.
• Reassure the mother about the relatively benign
nature of breast milk .
• Continue breastfeeding and supplement with
formula.

• Management (Cont.) :
• 2-For infants with serum bilirubin levels in the range of 17-25 mg/dL
(294-430 µmol/L):
• Add phototherapy to any of the previously stated treatment options.
• Temporary interruption of breastfeeding is rarely needed and is not
recommended unless serum bilirubin levels reach 20 mg/dl.

MCQ
The current recommendation for the treatment of breast milk jaundice (NOT breastfeeding
failure jaundice) is:
A. Continue to breastfeed
B. Stop breastfeeding and change to a cow’s milk formula
C. Stop breastfeeding and change to soy milk formula
D. Stop breastfeeding and treat with rehydration solution (e.g., Pedialyte)

RISK FACTORS :
• Major risk factors :
• Pre-discharge TcB or TSB level in high-risk range.
• Jaundice in first 24 hours after delivery.
• Exclusively breastfeeding particularly if nursing is not going well and weight loss
is excessive.
• ABO incompatibility & positive Coombs’ test and other known hemolytic disease
(eg, G6PD deficiency).
• Cephalohematoma or significant bruising.
• Delivery at 35 to 36 weeks’ gestation.
• Sibling received phototherapy.
• East Asian race.

RISK FACTORS (Cont.) :
• Minor risk factors
• Pre-discharge TcB or TSB level in high-intermediate–risk range
• Macrosomia; mother has diabetes
• Maternal age 25 years or older.
• Delivery at 37 to 38 weeks’ gestation.
• Jaundice before hospital discharge.
• Sibling had jaundice.
• Male sex

RISK FACTORS (Cont.) :
• Decreased risk
• TSB or TcB level in the low-risk zone.
• Gestational age 41 wk or more.
• Exclusive bottle feeding.
• Black race.
• Discharge from hospital after 72 h.
(these factors are associated with decreased risk of significant
jaundice, listed in order of decreasing importance)

CASE APPROACH
• Amy, a 4-day-old infant, is brought to clinic because “she is yellow.” She was
born at term to a 25-year-old woman. Maternal lab results are as follows:
blood type A+, syphilis negative, rubella immune, group B streptococcus
(GBS) negative.
• Amy has been breastfeeding every 3 to 5 hours. She has had one stool and
three wet diapers per day. Her weight is 15% less than her birth weight. On
your examination, you notice jaundice from the head to the thighs. Her total
bilirubin level is 21.6 mg/dL. The conjugated (direct) fraction is 0.4 mg/dL.

APPROACH
1. History
2. Physical Exam
3. Investigation
4. Treatment

1.HISTORY
• Patient profile :
• Asian heritage / American Indian.
• Male gender.
• Decrease gestational age.
• Presenting complain :
• Onset and progression of jaundice ( physiological vs. pathological )
• Yellowish discoloration of skin ( face ) and/or sclera
• Cephalocaudal progression :
• When jaundice appears first in the face then progresses in
cephalocaudal direction ( increase in total bilirubin)

Onset of Jaundice
at <24h of age
Hemolytic Disorders:
Rhesus incompatibility
ABO incompatibility
pyruvate kinase defi
Spherocytosis
G6PD defi.
.
Congenital infections
At 24h to 2w of age
Infection e.g. UTI
Hemolysis e.g. G6PD defi. /ABO
incompatibility
Bruising
Polycythemia
Crigler Najjar syndrome
At > 2w of age
Unconjugated :
Infection e.g. UTI
Hypothyroidism
Hemolysis e.g. G6PD defi.
High GI obstruction e.g. pyloric stenosis
Conjugated:
Bile duct obstruction
Neonatal hepatitis

1.HISTORY (Cont.)
• Associated symptoms :
• Dark urine
• Light-colored stools
• GI symptoms ( vomiting )
• Poor feeding
• loss of weight
• lethargy
• Fever

1.HISTORY (Cont.)
• Birth history :
• Anti-natal history :
• Maternal blood group.
• antenatal screening results.
• Maternal DM.
• Maternal exposure to Sulphonamides or
antimalarials
• Congenital infection e.g TORCH.

1.HISTORY (Cont.)
• Natal history:
• Gestational time : decrease gestational age
• Type of delivery:
• Instrument-assisted delivery with forceps or
vacuum extraction cephalohematoma.
• Complication : perinatal asphyxia
• Delayed cord clamping (> 3 min) can lead to
polycythemia.
• Use of oxytocin during delivery

1.HISTORY (Cont.)
• Post Natal History :
• Birthweight small for gestational
age
• Macrosomia
• ( suggest maternal DM which
is a common risk factor for
neonatal jaundice).
• Birth traumas.

1.HISTORY (Cont.)
• Feeding History:
• Breast feeding.
• Total parental nutrition.
• Family History:
• History of jaundice in siblings specially
if it required treatment.
• History of anemia.
• History of splenectomy.
• History hemolytic disorders.
• History of liver disease.
• Bile stones or gallbladder removal.

2.PHYSICAL EXAM
• In most infants, YELLOW COLOR is the only finding on physical examination.
• Visual inspection is NOT an accurate method to determine bilirubin levels
and often misses severe hyperbilirubinemia.
• Neonatal jaundice FIRST becomes visible in the face and forehead.
Identification is aided by pressure on the skin, since blanching reveals the
underlying color.
• Jaundice then gradually becomes visible on the trunk and extremities.

2.PHYSICAL EXAM (Cont.)
• visible jaundice in the lower extremities strongly suggests the need to check
the bilirubin level.
• If congenital infection/ hemolytic anemia or sepsis present pt. May present
with the following in addition to jaundice :
• Microcephaly
• Hepatosplenomegaly
• Chorioretinitis
• petechiae

3.INVESTIGATIONS
• LABORATORY
• Bilirubin level
• Transcutaneous Bilirubinometer TcB
• ( screening test ) needs confirmation by total serum bilirubin if
transcutaneous value is >205.2 micromol/L ( 12 mg /dl ).
• cannot be used to monitor the progress of phototherapy.
• better than visual assessment.
• Total serum Bilirubin TSB
• To confirm the diagnosis.
• Differentiation of direct (conjugated) and Indirect
(unconjugated )Bilirubin.

3.INVESTIGATIONS (Cont.)
• Nomogram for hour-specific bilirubin values:
• useful tool for predicting, either before or
at the time of hospital discharge, which
infants are likely to develop high serum
bilirubin values. Infants identified in this
manner require close follow-up monitoring
and repeated bilirubin measurements.
• Direct Coombs Test
• To diagnose ABO or RH iso immunization

• Direct bilirubin.
• If High ( > 34.2 micromol/L ) ( 2mg /dl) need focused work up for
conjugated hyperbilirubinemia
• Indirect ( unconjugated ) bilirubin derived by subtracting the direct
bilirubin for TCB.
• In infants who have hepatosplenomegaly, petechiae,
thrombocytopenia, or other findings suggestive of hepatobiliary
disease, metabolic disorder, or congenital infection, early
measurement of bilirubin fractions is suggested.
• Normal range total bilirubin newborn 0.8-12 mg/dl

• CBC
• WBC: high or low > sepsis
• Platelets: low > sepsis
• Htc:
• <45% hemolytic anemia
• >65% polycythemia if capillary sample is
taken should take arterial or venous sample
to confirm polycythemia.
• Reticulocyte count:
• high > hemolysis

• Blood type and Rh determination in mother &
infant
• Peripheral blood film for erythrocyte
morphology
• Liver function tests
• Thyroid function tests
• Blood gas measurements:
• The risk of bilirubin CNS toxicity is
increased in acidosis,
particularly respiratory acidosis.

• Reducing substance in urine
• Screening test for galactosemia
• Tests for viral and/or parasitic infection
• In infants with hepatosplenomegaly, petechiae, thrombocytopenia, or other
evidence of hepatocellular disease.
• Total serum protein and serum albumin.
• Provide information about the nutritional status of a neonates. Poor feeding
increases enterohepatic circulation and can result in an increase in the levels
of unconjugated bilirubin.
• G6PD activity

• IMAGING
• Ultrasonography:
• U/S of the liver & bile ducts in infants with
laboratory or clinical signs of cholestatic
disease.
• Radionuclide Scanning:
• Indicated if extrahepatic biliary atresia is
suspected.
• Intraoperative Cholangiography:
• The GOLD STANDARD for diagnosing
biliary atresia and histologic evaluation
of the duct remnant.

• OTHERS
• Percutaneous liver biopsy
• Adequate biopsy specimen can differentiate between obstructive and
hepatocellular causes of cholestasis, with 90% sensitivity and
specificity for biliary atresia.
• Biopsies are not usually diagnostic in those younger than 2 weeks.

MANAGEMENT
Physiological
Reassurance
No Treatment Is Required
Pathological
Conjugated
Treat the underlying etiology
Phototherapy is contraindicated
may lead to Bronze Baby syndrome.
Unconjugated
Phototherapy
Exchange Transfusion
Immediate exchange transfusion
in
( Acute bilirubin encephalopathy)
Hydration
IV Immunoglobulin
4.MANAGEMENT

4.MANAGEMENT
PHOTOTHERAPY
Primary treatment
in neonates with
unconjugated
hyperbilirubinemia.

4.MANAGEMENT
• Phototherapy Indications :
• For infants born ≥ 35 weeks gestation, threshold bilirubin levels for treatment
are based on the American Academy of pediatrics
(AAP) phototherapy nomogram, which divides the infants into three risk groups:
• Low-risk infants : ≥ 38 weeks and well
• Medium-risk infants : ≥ 38 weeks with risk factors (e.g., isoimmune
hemolytic disease, G6PD deficiency, sepsis), or 35-37 weeks and well
• High-risk infants : 35-37 weeks with risk factors.
• For infants born < 35 weeks gestation, threshold bilirubin levels for treatment
are lower because premature infants are at a greater risk of neurotoxicity.

4.MANAGEMENT(Cont.)
• Guidelines for Phototherapy
in Hospitalized Term and
Near-Term Newborns
• Term and late preterm infants
(gestational age ≥35 weeks)
• Neurotoxicity risk factors

4.MANAGEMENT(Cont.)
• Phototherapy Procedure
• Exposure to blue light (non-UV, wavelength: 420–480 nm) → Absorption of light through
the skin converts unconjugated bilirubin into bilirubin photo- products that are excreted in
the stool and urine.
• Continued until total bilirubin levels < 15 mg/dL.
• Adequate fluid supplementation to prevent dehydration.
• Eye protection to prevent retinal damage.
• Phototherapy Contraindications
• Concomitant use of photosensitizing medications.
• Congenital erythropoietic porphyria.
• Family history of porphyria.

4.MANAGEMENT(Cont.)
• When to discontinue phototherapy ?
• Although no standard is noted for the discontinuation of phototherapy,
current guidelines suggest stopping phototherapy on infants 35 or more
weeks’ gestation at birth readmitted after their birth hospitalization when
the levels of total bilirubin fall below 13-14 mg/dL.

4.MANAGEMENT(Cont.)
• EXCHANGE TRANSFUSION
• Most rapid method for lowering serum bilirubin concentrations
• Indications
• Threshold in a 24-hour-old term baby is a total serum bilirubin value > 20 mg/dL
• Inadequate response to phototherapy, or a rapid rise in the total serum
bilirubin level (> 1 mg/dL/hour in less than 6 hours)
• Acute bilirubin encephalopathy.
• Hemolytic disease, severe anemia
• Procedure
• Exchange blood in quantities of 5–20 mL via an umbilical venous catheter until total
serum bilirubin is < 95th percentile on nomogram.

4.MANAGEMENT(Cont.)
• Guidelines for exchange transfusion
in infants 35 or more weeks’ gestation.

4.MANAGEMENT(Cont.)
• Intravenous Immune Globulin (IVIG)
• Evidence is inconclusive on the benefit of IVIG in the management of
neonates with severe hemolytic disease of the newborn.
• reserved the use of IVIG for infants with Rh-isoimmune hemolytic
disease who fail to adequately
respond to intensive phototherapy.
• Dose 0.5 to 1 g/kg over two hours.

CASE APPROACH
• Amy, a 4-day-old infant, is brought to clinic because “she is yellow.” She was
born at term to a 25-year-old woman. Maternal lab results are as follows: blood
type A+, syphilis negative, rubella immune, group B streptococcus (GBS)
negative.
• Amy has been breastfeeding every 3 to 5 hours. She has had one stool and three
wet diapers per day. Her weight is 15% less than her birth weight. On your
examination, you notice jaundice from the head to the thighs. Her total bilirubin
level is 21.6 mg/dL.The conjugated (direct) fraction is 0.4 mg/dL.

CASE APPROACH (Cont.)
HISTORY :
• Onset of jaundice :
• 4th day (physiological vs. pathological)
• jaundice in a term newborn less than 24 hours old is always pathologic.
• Risk factors :
• Breast feeding + weight loss > major risk factor
• Decrease caloric intake as first milk supply is inadequate in first several days of birth
> major risk factor
• Evidence Amy is not receiving adequate breast milk feedings :
• < 6 wet diapers/day and < 2-5 stools/day
• Mother age is 25-year-old > minor risk factor

EXAMINATION :
• weight is 15% less than her birth weight
• well-hydrated infant of Amy’s age should
generally lose no more than 10% of birth
weight
• jaundice from the head to the thighs.

LABS :
• Total bilirubin level is 21.6 mg/dl
• Pathological rather than physiological as it is higher than would be expected with
physiologic jaundice (which should not be higher than 17 mg/dl in a term infant).
• The conjugated (direct) fraction is 0.4 mg/dl.
• Unconjugated bilirubin is not high >2 gm/dl so this is unconjugated
hyperbilirubinemia.
• Maternal blood group :
• Rh factor : positive
• Rh incompatibility is impossible due to the mother being rh+.
• ABO : blood group A
• ABO incompatibility is unlikely in a mother whose blood type is something
other than O.

MCQ
• Amy, a 4-day-old infant, is brought to clinic because “she is yellow.” She was born at term to
a 25-year-old woman. Maternal lab results are as follows: blood type A+, syphilis negative,
rubella immune, group B streptococcus (GBS) negative. Amy has been breastfeeding every 3
to 5 hours. She has had one stool and three wet diapers per day. Her weight is 15% less than
her birth weight. On your examination, you notice jaundice from the head to the thighs. Her
total bilirubin level is 21.6 mg/dL. The conjugated (direct) fraction is 0.4 mg/dL.
Of the following, the infant most likely is experiencing:
A. Breast feeding failure jaundice
B. Physiological jaundice.
C. Biliary atresia; you must consult pediatric gastroenterology.
D. Alloimmune hemolysis due to ABO incompatibility

MCQ
Which of the following is the most appropriate initial treatment for this patient (remember
the conjugated [direct] fraction is 0.4 mg/dL)?
A. Admission for exchange transfusion.
B. Admission for IV fluids alone to improve hydration.
C. Admission for phototherapy.
D. Discharge to home with recommendations for formula feeding, light exposure, and
follow-up bilirubin tomorrow.

MCQ
Which of the following is the most appropriate initial treatment for
this patient (remember the conjugated [direct] fraction is 0.4 mg/dL)?
A. Admission for exchange transfusion.
B. Admission for IV fluids alone to improve hydration.
C. Admission for phototherapy.
D. Discharge to home with recommendations for formula
feeding, light exposure, and follow-up bilirubin tomorrow.

FOLLOW UP
• Recommendations for follow-up range from as early as prior to 72 hours of
life (if discharged before 24 h) to no later than 120 hours (5 d) if discharged
before 72 hours.
• The follow-up assessment should include the infant’s weight and percent
change from birth weight, adequacy of intake, the pattern of voiding and
stooling, and the presence or absence of jaundice (evidence quality C )

FOLLOW UP (Cont.)
• For some newborns discharged before 48 hours, 2 follow up visits may be
required, the first visit between 24 and 72 hours and the second between
72 and 120 hours.
• Clinical judgment should be used to determine the need for a bilirubin
measurement. If there is any doubt about the degree of jaundice, the TSB
or TcB level should be measured. Visual estimation of bilirubin levels can
lead to errors, particularly in darkly pigmented infants (evidence quality C
)

Infant Discharged Should Be Seen by Age
Before age 24 h
72 h
Between 24 and 47.9 h 96 h
Between 48 and 72 h 120 h
FOLLOW UP (Cont.)
• Follow-up should be provided as follows:

COMPLICATIONS
COMPLICATIONS
Acute Bilirubin
Encephalopathy
Chronic Bilirubin
Encephalopathy
Phototherapy
Exchange Transfusion

COMPLICATIONS (Cont.)
• Acute Bilirubin Encephalopathy:
• Data on progression of acute bilirubin encephalopathy to kernicterus are
limited.
• A high index of suspicion of possible bilirubin induced neurological
damage that leads to prompt intervention can halt the progression of the
illness, significantly minimizing long-term sequelae.
• Neuroimaging has no major diagnostic benefit. can help to R/O other
diagnoses.
• Treatment :
• Immediate exchange transfusion. (evidence quality D ) AAP
• Phototherapy and/or exchange transfusion. BMJ

Acute
Bilirubin
Encephalopathy
PHASE 1
(Initial)
First few days of life
Decreased alertness,
hypotonia, and poor feeding
PHASE 2
(Intermediate)
Variable onset & duration
•Hypertonia of the extensor muscles is a typical sign.
Opisthotonos (backward arching of the back).
Retrocollis (backward arching of the neck)
High pitched cry.
Infants Who Progress To This Phase Develop
Long-term Neurologic Deficits.
PHASE 3
(Advanced)
Infants aged >1 wk
Hypotonia is a typical sign.
Coma / stupor.

• Chronic Bilirubin Encephalopathy (Kernicterus):
• Rare condition
• Pathophysiology:
• Deposition of unconjugated bilirubin in the
basal ganglia and/or brain stem nuclei.
• Clinical features :
• extrapyramidal, visual, auditory, dentition
abnormalities & cognitive deficits.
• Kernicterus can be prevented by early and
aggressive phototherapy and/or exchange
transfusion.

Chronic
Bilirubin
Encephalopathy
(
kernicterus
)
Extrapyramidal abnormalities
Athetosis is the most common movement disorder
Chorea
The upper extremities > the lower extremities
Visual abnormalities Ocular movements are affected, most commonly resulting in upward gaze
Auditory abnormalities
Hearing abnormalities are the most consistent feature of chronic bilirubin encephalopathy
high-frequency hearing loss which can range from mild to severe
Cognitive deficits Cognitive function is relatively spared in chronic bilirubin encephalopathy
Abnormalities of dentition
dental enamel hypoplasia
GREEN-stained teeth

• Phototherapy :
• Short-term
• Diarrhea
• Interference with maternal–infant
bonding
• Intestinal hypermotility
• Skin rash / Bronze baby syndrome.
• Temperature instability
• Long-term
• Increased risk of childhood asthma
• Increased risk of type 1 DM

• Exchange Transfusion:
• Higher mortality & morbidity from
infections
• Cardiac arrhythmias
• Necrotizing enterocolitis
• Electrolyte imbalances
• Thrombosis
• Hypotension
• Acidosis
• Graft-versus-host disease
• Avoided by irradiation of blood prior using
it for exchange transfusion.

PROGNOSIS
• Most neonates with neonatal unconjugated
hyperbilirubinemia do well after phototherapy and/or
exchange transfusion.
• Kernicterus should be preventable if recommendations
for hyperbilirubinemia management are carried out in
timely manner.
• Neonates with conjugated hyperbilirubinemia prognosis
depend on the etiology of the condition.

SCREENING
• The American Academy of Pediatrics:
• recommends pre-discharge bilirubin universal screening with total serum
bilirubin (TSB) or transcutaneous bilirubin (TcB) levels or targeted
screening based on risk factors ( evidence quality C )
• For assessing the risk of subsequent significant hyperbilirubinemia in
healthy term and near-term newborns.

SCREENING (Cont.)
• US Preventive Surface Task Force:
• The U.S. Preventive Services Task Force and the American Academy of
Family Physicians found insufficient evidence that screening for
hyperbilirubinemia is associated with improved clinical outcomes.

PREVENTION
• 1ry Prevention :
• Clinicians should advise mothers to nurse their infants at least 8 to 12
times per day for the first several days (evidence quality C ).
• The AAP recommends against routine supplementation of
nondehydrated breastfed infants with water or dextrose . (evidence
quality B&C).
• 2dry Prevention :
• Clinicians should perform ongoing systematic assessments during the
neonatal period for the risk of an infant developing severe
hyperbilirubinemia.

SUMMERY
1. Jaundice is the most common condition that requires medical attention
and hospital readmission in newborns.
2. Jaundice in the first 24 hours of life is pathologic & usually due to
hemolytic disease such as ABO incompatibility.
3. Physiological neonatal jaundice is a diagnosis of exclusion. Laboratory tests
should first rule out all pathological causes of neonatal jaundice.
4. In breast milk or breastfeeding jaundice a temporary interruption is usually
not necessary, but it can be advised if serum bilirubin level >20 mg/dl.
5. Kernicterus is the chronic, rare and permanent clinical sequelae of bilirubin
toxicity.

SUMMERY
6. Physicians should encourage optimal breastfeeding (8 to 12 feedings per
day) to decrease the incidence of hyperbilirubinemia.
7. Pre-discharge all newborn should undergo bilirubin universal screening
with total serum bilirubin (TSB) or transcutaneous bilirubin (TcB) levels or
targeted screening based on risk factors.
8. TcB measurement is as accurate as TSB measurement.
9. Bronze baby syndrome (rare) complication of phototherapy Occurs
in infants with elevated direct bilirubin (conjugated bilirubin > 2mg/dL)
following phototherapy.
10. Prognosis is Favorable in most cases.

References :
• Graber & Wilbur’s Family Medicine 5th Edition.
• American Academy of Family Medicine.
• U.S. Preventive Services Task Force.
• Children’s Hospital of Philadelphia.
• Illustrated Textbook of Pediatrics.
• American Academy of Pediatrics.
• BMJ Best Practice.
• UpToDate.
• Medscape.
• AMBOSS.
• BiliTool.

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