NEONATAL JAUNDICE
NEONATAL JAUNDICE
NEONATAL JAUNDICE
WWW.SMSO.NET
Objectives
•
Understand etiology and pathophysiology of
neonatal jaundice and kernicterus
•
Identify high risk conditions
•
Understand limits of clinical exam
•
Describe appropriate evaluation
•
Apply appropriate treatment to term and near
term infants
JAUNDICE
JAUNDICE
Jaundice is the visible manifestation of
Jaundice is the visible manifestation of
increased level of bilirubin in the body.
increased level of bilirubin in the body.
It is not a disease rather a symptom of
It is not a disease rather a symptom of
diseases.
diseases.
In adults sclera appears jaundiced when serum
In adults sclera appears jaundiced when serum
bilirubin exceeds 2 mg/dl.
bilirubin exceeds 2 mg/dl.
Newborn skin >5 mg/dl.
Newborn skin >5 mg/dl.
BURDEN
BURDEN
Important problem in the 1
st
week of life.
Most neonates (60% Term and
80%
Preterm)
will have bilirubin > 5 mg/dl in the 1
st
week of
life and become visibly jaundiced, vast majority
being benign.
Some of the term babies (8 to 9%) have levels
exceeding 15 mg/dl in 1
st
7 days of life.
BILIRUBIN
BILIRUBIN
End product of hemoglobin metabolism that is
End product of hemoglobin metabolism that is
excreted in bile.
excreted in bile.
In neonates
In neonates
-75% :
-75% :
from catabolism of circulating RBCs
from catabolism of circulating RBCs
-25% :
-25% :
*from ineffective erythropoiesis
*from ineffective erythropoiesis
(bone marrow)
(bone marrow)
*from turnover of heme proteins &
*from turnover of heme proteins &
free heme( liver).
free heme( liver).
Hyperbilirubinemia
Hyperbilirubinemia
-Direct( Conjugated)
-Direct( Conjugated)
-Indirect( Un-conjugated)
-Indirect( Un-conjugated)
Conjugated Hyperbilirubinemia is present,
Conjugated Hyperbilirubinemia is present,
*
*
>20% of total bilirubin is conjugated
>20% of total bilirubin is conjugated
* >2mg/dl is conjugated
* >2mg/dl is conjugated
If neither criteria is met, hyperbilirubinemia is
If neither criteria is met, hyperbilirubinemia is
classified as Un-conjugated.
classified as Un-conjugated.
JAUNDICE APPEARING IN
JAUNDICE APPEARING IN
1
1
st
st
day
day
•
Hemolytic (Rh, ABO & minor group incompatibility,
Hemolytic (Rh, ABO & minor group incompatibility,
G6PD
G6PD
def. ,
def. ,
spherocytosis, thalassemia), Neonatal sepsis.
spherocytosis, thalassemia), Neonatal sepsis.
2nd & 3rd days
2nd & 3rd days
•
Physiological,
Physiological,
Neonatal sepsis, Polycythemia, concealed
Neonatal sepsis, Polycythemia, concealed
hemorrhages (cephalhematoma, SAH, IVH)
hemorrhages (cephalhematoma, SAH, IVH)
> 3 days (Prolonged)
> 3 days (Prolonged)
•
Neonatal sepsis, Hepatitis, Biliary atresia, Breast milk
Neonatal sepsis, Hepatitis, Biliary atresia, Breast milk
jaundice, metabolic disorders.
jaundice, metabolic disorders.
Prolonged Jaundice
Prolonged Jaundice
a)
Direct
›
Neonatal hepatitis (common)
Neonatal hepatitis (common)
›
Extra-hepatic biliary atresia
Extra-hepatic biliary atresia
›
Breast milk jaundice
Breast milk jaundice
›
Metabolic disorders
Metabolic disorders
›
Intra-hepatic biliary atresia
Intra-hepatic biliary atresia
b)
Indirect
> Criggler Najjar Syndrome
> Criggler Najjar Syndrome
> Breast milk jaundice
> Breast milk jaundice
>
>
Hypothyroidism
Hypothyroidism
> Pyloric stenosis
> Pyloric stenosis
> Ongoing hemolysis
> Ongoing hemolysis
Prolonged Jaundice
Prolonged Jaundice
Clinical classification:
Clinical classification:
Physiological jaundice
Physiological jaundice
Pathological jaundice
Pathological jaundice
Physiological jaundice
Physiological jaundice
•
First appears between 24-72 hours 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.
Pathological jaundice
Pathological jaundice
Presence of any of the following signs denotes
Presence of any of the following signs denotes
that the jaundice is pathological:
that the jaundice is pathological:
•
Clinical jaundice detected
before 24 hrs
of age.
•
Rise in serum total bilirubin by
more than 5 mg/dl/
day
(>5mg/dl on first day , 10 mg/dl on second day
and 12- 13 mg/dl thereafter in term babies).
Pathological jaundice
Pathological jaundice
•
Serum bilirubin
more than 15 mg/dl
•
Clinical jaundice persisting
beyond 14 days
of life.
•
Clay/white colored stool and/or dark urine staining
the nappy yellow.
•
Direct
bilirubin
>2
mg/dl at any time.
RISK FACTORS
RISK FACTORS
•
jaundice within first 24 hrs of life
•
a sibling who was jaundiced as neonate
•
premature infants and infants with low birth
weight.
•
Poor breastfeeding/suckling
•
delayed passage of meconium
•
deficiency of G6PD
•
Infection
•
Diabetic mother
COMPLICATIONS
COMPLICATIONS
KERNICTERUS
KERNICTERUS
•
=bilirubin encephalopathy
•
Brain damage caused by high levels of
bilirubin (Bilirubin≥25mg/dl)
•
Early signs:
Early signs:
Lethargy,
poor feeding,, loss of
Moro reflex.
•
Late signs:
Late signs:
Fever,
high pitched cry, Bulging
fontanel, paralysis of upward gaze,
hypo/hypertonia, seizures, opisthotonos.
KERNICTERUS
KERNICTERUS
•
If significant brain damage occurs before treatment,
If significant brain damage occurs before treatment,
a child can develop serious and permanent problems,
a child can develop serious and permanent problems,
such as:
such as:
•
cerebral palsy
cerebral palsy
(Permanent brain damage)
•
hearing loss
hearing loss
which can range from mild to
severe.
•
Death
Death
APPROACH TO A CHILD WITH
APPROACH TO A CHILD WITH
JAUNDICE
JAUNDICE
HISTORY
HISTORY
HPI
HPI
•
onset / duration
onset / duration
•
color of stool/urine
color of stool/urine
•
Associated symptoms: fever, poor feeding,
Associated symptoms: fever, poor feeding,
convulsions…
convulsions…
HISTORY
HISTORY
PREGNANCY AND DELIVERY
PREGNANCY AND DELIVERY
•
Term/preterm, Postnatal age in hours.
•
Maternal illness/infection during pregnancy:
diabetes; drug use, malaria, viral.
•
Traumatic delivery, delayed cord clamping.
•
Birth asphyxia, delay in meconium passage.
•
Breast feeding.
HISTORY
HISTORY
FAMILY HISTORY
FAMILY HISTORY
•
Family history of jaundice, liver disease
•
Previous sibling with jaundice in the neonatal
period.
•
Anemia, splenectomy, or bile stones in family
members or known heredity for hemolytic
disorders
ON EXAMINATION
ON EXAMINATION
•
Baby lethargic, poor feeding, temperature
instability, with apnea:
Sepsis
Sepsis
•
Small for gestation:
polycythemia
polycythemia
•
Cataract, rash:
TORCH infections
TORCH infections
•
Extra vascular bleed:
Cephalhematoma
Cephalhematoma
•
Pallor:
hemolysis
hemolysis
ON EXAMINATION
ON EXAMINATION
•
Petechiae:
Petechiae:
sepsis
sepsis
,
,
TORCH
TORCH
infections.
infections.
•
Hepatosplenomegaly:
Hepatosplenomegaly:
Rh
Rh
-isoimmunization,
-isoimmunization,
sepsis
sepsis
,
,
TORCH
TORCH
infections.
infections.
•
Dysmorphic features:
Dysmorphic features:
congenital Hypothyroidism
congenital Hypothyroidism
•
Look for evidence of
Look for evidence of
kernicterus
kernicterus
in deeply
in deeply
jaundiced NB (Lethargy and poor feeding, poor
jaundiced NB (Lethargy and poor feeding, poor
or absent Moro's, or convulsions)
or absent Moro's, or convulsions)
HOW DO YOU LOOK FOR ICTERUS?
HOW DO YOU LOOK FOR ICTERUS?
•
Dermal staining :progresses from head to toe
•
Examined in good day light skin of forehead,
chest, abdomen, thigh, legs, palms, and soles.
•
Blanched with digital pressure and the
underlying color of the skin and subcutaneous
tissue should be noted.
•
Trans-cutaneous bilirubinometer
?!!!
.
Clinical assessment of neonatal
Clinical assessment of neonatal
jaundice
jaundice
(Kramer’s rule)
(Kramer’s rule)
Diagnosis
28
> 12 mg/dl & infant < 24hr old
> 12 mg/dl & infant < 24hr old
< 12 mg/dl & infant > 24hr old
< 12 mg/dl & infant > 24hr old
Follow bilirubin level
Follow bilirubin level
Indirect
Indirect
Direct
Direct
MANAGEMENT
MANAGEMENT
Physiological jaundice
Physiological jaundice
•
Explain about benign nature of the disease
Explain about benign nature of the disease
•
Encourage to breastfeed frequently &
Encourage to breastfeed frequently &
exclusively
exclusively
•
Ask Mother to bring baby back if baby looks
Ask Mother to bring baby back if baby looks
deep yellow or palms & soles have yellow
deep yellow or palms & soles have yellow
staining.
staining.
Pathological jaundice
Pathological jaundice
2 modalities of Treatment:
2 modalities of Treatment:
•
PHOTOTHERAPY
PHOTOTHERAPY
•
EXCHANGE TRANSFUSION
EXCHANGE TRANSFUSION
PHOTOTHERAPY
PHOTOTHERAPY
•
ONLY
ONLY
if unconjugated hyperbilirubinemia.
if unconjugated hyperbilirubinemia.
•
Single/multiple phototherapy
Single/multiple phototherapy
•
Under blue-green light (460-490nm), insoluble
Under blue-green light (460-490nm), insoluble
bilirubin is converted into soluble isomers that
bilirubin is converted into soluble isomers that
can be excreted in urine & feces.
can be excreted in urine & feces.
•
To be effective, bilirubin must be present in skin;
To be effective, bilirubin must be present in skin;
hence no role for prophylactic phototherapy
hence no role for prophylactic phototherapy
PHOTOTHERAPY
PHOTOTHERAPY
•
The infant should be naked except for diaper ,
eye & gonads should be covered.
•
distance between the skin and light source
(35-50 cm) .
•
when used spotlight , the infant is placed in
center .
•
turn infant every 2 hours.
PHOTOTHERAPY
PHOTOTHERAPY
•
Ensure optimum breastfeeding as intermittent feeding
sessions.
•
routinely add 10-15% extra fluid.
•
Monitor temperature of the baby every 2-4hrs
Monitor temperature of the baby every 2-4hrs
•
Measure TSB every 12-24hrs.
Measure TSB every 12-24hrs.
•
Phototherapy is discontinued if
Phototherapy is discontinued if
2 TSB values 12hr apart
2 TSB values 12hr apart
<
<
10 mg/dl.
10 mg/dl.
•
Monitor for rebound bilirubin rise within 24hrs.
Monitor for rebound bilirubin rise within 24hrs.
Guidelines for phototherapy in hospitalized infants of 35 or more weeks’ gestation
Guidelines for phototherapy in hospitalized infants of 35 or more weeks’ gestation
Risk Factors:
Risk Factors:
iso-immune hemolytic disease, G6PD def, asphyxia, significant lethargy,
iso-immune hemolytic disease, G6PD def, asphyxia, significant lethargy,
temp. instability, sepsis, acidosis or albumin < 3.0 g/dL
temp. instability, sepsis, acidosis or albumin < 3.0 g/dL
COMPLICATIONS
COMPLICATIONS
•
Loose stools
•
Skin rash
•
hyperthermia
•
Retinal damage
•
Dehydration
•
Bronze baby syndrome
Exchange transfusion
Exchange transfusion
•
Remove excess bilirubin & maternal
antibodies.
•
Fresh blood, O -ve (or infant BG Rh -ve)
•
Umbilical venous route.
•
Double Volume Exchange Transfusion (DVET) :
160-180ml/kg; is to be performed if TSB levels
reach age-specific cut-offs or if the infant
shows signs of bilirubin encephalopathy,
irrespective of TSB levels.
Exchange transfusion
Exchange transfusion
Following exchange transfusion:
Following exchange transfusion:
•
maintain continuous multiple phototherapy
•
TSB every 6-8 hrs after procedure.
•
If baby shows signs of cardiac
decompensation at birth, partial exchange
transfusion with 50ml/kg of packed red cells
should be done to quickly restore oxygen
carrying capacity of blood.
Guidelines for exchange transfusion in infants of 35 or more weeks’ gestation
Guidelines for exchange transfusion in infants of 35 or more weeks’ gestation
Risk Factors:
Risk Factors:
iso-immune hemolytic disease, G6PD def, asphyxia, significant lethargy,
iso-immune hemolytic disease, G6PD def, asphyxia, significant lethargy,
temp. instability, sepsis, acidosis or albumin < 3.0 g/dL
temp. instability, sepsis, acidosis or albumin < 3.0 g/dL
COMPLICATIONS
COMPLICATIONS
•
Cardiac and respiratory disturbances.
•
Shock due to inadequate replacement of
blood.
•
Infection.
•
Clot formation.
Controversial Medications
Controversial Medications
Phenobarbital:
Phenobarbital:
•
an inducer of hepatic bilirubin metabolism,
has been used to enhance bilirubin
metabolism. Several studies have shown that
phenobarbital is effective in reducing mean
serum bilirubin values during the first week of
life.
Controversial Medications
Controversial Medications
Intravenous immunoglobulin (IVIG):
Intravenous immunoglobulin (IVIG):
•
500 mg/kg significantly reduce the need for
exchange transfusions in infants with iso-
immune hemolytic disease.
PREVENTION
PREVENTION
•
Ante-natal screening to detect Rh iso-
immunization & prompt administration of Anti
D after first obstetric event.
•
Ensure adequate breast feeding.
•
Educate parent about danger signs to ensure
immediate checkup.
•
Follow-up high risk babies( large cephal-
hematoma, family history of jaundice) for 2-3
days of discharge.
Neonatal jaundice, a common condition in newborns, results from elevated bilirubin levels. While often benign, high levels can lead to complications like kernicterus. Recognizing risk factors, limitations of clinical assessment, and appropriate evaluation and treatment are crucial in managing neonatal jaundice effectively.
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Presentation Transcript
NEONATAL JAUNDICE D.Amani Elgadal
Objectives Understand etiology and pathophysiology of neonatal jaundice and kernicterus Identify high risk conditions Understand limits of clinical exam Describe appropriate evaluation Apply appropriate treatment to term and near term infants WWW.SMSO.NET
JAUNDICE Jaundice is the visible manifestation of increased level of bilirubin in the body. It is not a disease rather a symptom of diseases. In adults sclera appears jaundiced when serum bilirubin exceeds 2 mg/dl. Newborn skin >5 mg/dl.
BURDEN Important problem in the 1st week of life. Most neonates (60% Term and 80% Preterm) will have bilirubin > 5 mg/dl in the 1st week of life and become visibly jaundiced, vast majority being benign. Some of the term babies (8 to 9%) have levels exceeding 15 mg/dl in 1st 7 days of life.
BILIRUBIN End product of hemoglobin metabolism that is excreted in bile. In neonates -75% : from catabolism of circulating RBCs -25% :*from ineffective erythropoiesis (bone marrow) *from turnover of heme proteins & free heme( liver).
Hyperbilirubinemia -Direct( Conjugated) -Indirect( Un-conjugated) Conjugated Hyperbilirubinemia is present, * >20% of total bilirubin is conjugated * >2mg/dl is conjugated If neither criteria is met, hyperbilirubinemia is classified as Un-conjugated.
Neonatal jaundice Conjugated bilirubin Unconjugated bilirubin Hepatic Pathological Physiological Extra-hepatic Biliary atresia or bile duct obstruction Hemolytic Non-hemolytic *Infections *Intrinsic (Spherocytosis, elliptocytosis, G6PD deficiency, Pyruvate kinase deficiency, Sepsis, thalassemia) Breast milk jaundice Hep A/B TORCH Cephalohematoma Polycythemia Sepsis *Metabolic Urinary tract infection Sepsis Galactosemia Hypothyroidism Alpha-1- antitrypsin def *Extrinsic (Rh, ABO & minor group incompatibility) Gilbert's syndrome Crigler-Najjar syndrome Cystic fibrosis High GI obstruction
JAUNDICE APPEARING IN 1st day Hemolytic (Rh, ABO & minor group incompatibility, G6PD def. , spherocytosis, thalassemia), Neonatal sepsis. 2nd & 3rd days Physiological, Neonatal sepsis, Polycythemia, concealed hemorrhages (cephalhematoma, SAH, IVH) > 3 days (Prolonged) Neonatal sepsis, Hepatitis, Biliary atresia, Breast milk jaundice, metabolic disorders.
Prolonged Jaundice a) Direct Neonatal hepatitis (common) Extra-hepatic biliary atresia Breast milk jaundice Metabolic disorders Intra-hepatic biliary atresia
Prolonged Jaundice b) Indirect > Criggler Najjar Syndrome > Breast milk jaundice > Hypothyroidism > Pyloric stenosis > Ongoing hemolysis
Clinical classification: Physiological jaundice Pathological jaundice
Physiological jaundice First appears between 24-72 hours 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.
Pathological jaundice Presence of any of the following signs denotes that the jaundice is pathological: Clinical jaundice detected before 24 hrs of age. Rise in serum total bilirubin by more than 5 mg/dl/ day (>5mg/dl on first day , 10 mg/dl on second day and 12- 13 mg/dl thereafter in term babies).
Pathological jaundice Serum bilirubin more than 15 mg/dl Clinical jaundice persisting beyond 14 days of life. Clay/white colored stool and/or dark urine staining the nappy yellow. Direct bilirubin >2 mg/dl at any time.
RISK FACTORS jaundice within first 24 hrs of life a sibling who was jaundiced as neonate premature infants and infants with low birth weight. Poor breastfeeding/suckling delayed passage of meconium deficiency of G6PD Infection Diabetic mother
COMPLICATIONS KERNICTERUS =bilirubin encephalopathy Brain damage caused by high levels of bilirubin (Bilirubin 25mg/dl) Early signs: Lethargy, poor feeding,, loss of Moro reflex. Late signs: Fever,high pitched cry, Bulging fontanel, paralysis of upward gaze, hypo/hypertonia, seizures, opisthotonos.
KERNICTERUS If significant brain damage occurs before treatment, a child can develop serious and permanent problems, such as: cerebral palsy (Permanent brain damage) hearing loss which can range from mild to severe. Death
APPROACH TO A CHILD WITH JAUNDICE
HISTORY HPI onset / duration color of stool/urine Associated symptoms: fever, poor feeding, convulsions
HISTORY PREGNANCY AND DELIVERY Term/preterm, Postnatal age in hours. Maternal illness/infection during pregnancy: diabetes; drug use, malaria, viral. Traumatic delivery, delayed cord clamping. Birth asphyxia, delay in meconium passage. Breast feeding.
HISTORY FAMILY HISTORY Family history of jaundice, liver disease Previous sibling with jaundice in the neonatal period. Anemia, splenectomy, or bile stones in family members or known heredity for hemolytic disorders
ON EXAMINATION Baby lethargic, poor feeding, temperature instability, with apnea: Sepsis Small for gestation: polycythemia Cataract, rash: TORCH infections Extra vascular bleed: Cephalhematoma Pallor: hemolysis
ON EXAMINATION Petechiae: sepsis, TORCH infections. Hepatosplenomegaly: Rh-isoimmunization, sepsis, TORCH infections. Dysmorphic features: congenital Hypothyroidism Look for evidence of kernicterus in deeply jaundiced NB (Lethargy and poor feeding, poor or absent Moro's, or convulsions)
HOW DO YOU LOOK FOR ICTERUS? Dermal staining :progresses from head to toe Examined in good day light skin of forehead, chest, abdomen, thigh, legs, palms, and soles. Blanched with digital pressure and the underlying color of the skin and subcutaneous tissue should be noted. Trans-cutaneous bilirubinometer ?!!!.
Clinical assessment of neonatal jaundice (Kramer s rule)
Diagnosis Lab Studies Total, conjugated & un- conjugated bilirubin. CBC + Retic. Peripheral blood film. Blood group. Direct coomb s test. Serum albumin * Osmotic Fragility test Radiology & US * TFT * LFTs * TORCH screening. * G6PD screening. 28
Clinical jaundice Measure bilirubin > 12 mg/dl & infant < 24hr old < 12 mg/dl & infant > 24hr old Direct Indirect Follow bilirubin level
Physiological jaundice Explain about benign nature of the disease Encourage to breastfeed frequently & exclusively Ask Mother to bring baby back if baby looks deep yellow or palms & soles have yellow staining.
Pathological jaundice 2 modalities of Treatment: PHOTOTHERAPY EXCHANGE TRANSFUSION
PHOTOTHERAPY ONLY if unconjugated hyperbilirubinemia. Single/multiple phototherapy Under blue-green light (460-490nm), insoluble bilirubin is converted into soluble isomers that can be excreted in urine & feces. To be effective, bilirubin must be present in skin; hence no role for prophylactic phototherapy
PHOTOTHERAPY The infant should be naked except for diaper , eye & gonads should be covered. distance between the skin and light source (35-50 cm) . when used spotlight , the infant is placed in center . turn infant every 2 hours.
PHOTOTHERAPY Ensure optimum breastfeeding as intermittent feeding sessions. routinely add 10-15% extra fluid. Monitor temperature of the baby every 2-4hrs Measure TSB every 12-24hrs. Phototherapy is discontinued if 2 TSB values 12hr apart < 10 mg/dl. Monitor for rebound bilirubin rise within 24hrs.
Guidelines for phototherapy in hospitalized infants of 35 or more weeks gestation Risk Factors: iso-immune hemolytic disease, G6PD def, asphyxia, significant lethargy, temp. instability, sepsis, acidosis or albumin < 3.0 g/dL
COMPLICATIONS Loose stools Skin rash hyperthermia Retinal damage Dehydration Bronze baby syndrome
Exchange transfusion Remove excess bilirubin & maternal antibodies. Fresh blood, O -ve (or infant BG Rh -ve) Umbilical venous route. Double Volume Exchange Transfusion (DVET) : 160-180ml/kg; is to be performed if TSB levels reach age-specific cut-offs or if the infant shows signs of bilirubin encephalopathy, irrespective of TSB levels.
Exchange transfusion Following exchange transfusion: maintain continuous multiple phototherapy TSB every 6-8 hrs after procedure. If baby shows signs of cardiac decompensation at birth, partial exchange transfusion with 50ml/kg of packed red cells should be done to quickly restore oxygen carrying capacity of blood.
Guidelines for exchange transfusion in infants of 35 or more weeks gestation Risk Factors: iso-immune hemolytic disease, G6PD def, asphyxia, significant lethargy, temp. instability, sepsis, acidosis or albumin < 3.0 g/dL
COMPLICATIONS Cardiac and respiratory disturbances. Shock due to inadequate replacement of blood. Infection. Clot formation.
Controversial Medications Phenobarbital: an inducer of hepatic bilirubin metabolism, has been used to enhance bilirubin metabolism. Several studies have shown that phenobarbital is effective in reducing mean serum bilirubin values during the first week of life.
Controversial Medications Intravenous immunoglobulin (IVIG): 500 mg/kg significantly reduce the need for exchange transfusions in infants with iso- immune hemolytic disease.
PREVENTION Ante-natal screening to detect Rh iso- immunization & prompt administration of Anti D after first obstetric event. Ensure adequate breast feeding. Educate parent about danger signs to ensure immediate checkup. Follow-up high risk babies( large cephal- hematoma, family history of jaundice) for 2-3 days of discharge.
