With all due respect to :

CASE REPORT
To be presented on August 18th 2014

Hyperbilirubinemia et causa ABO Incompatibility

By:
Shekina Rondonuwu
Supervisor:
Dr. Johnny Rompis, Sp.A

Department of Child Health

Medical Faculty of Sam Ratulangi University
Prof. Dr. R. D. Kandou General Hospital Manado
2014
1

INTRODUCTION
Jaundice occurs in most newborn infants. Most jaundice is benign, but
because of the potential toxicity of bilirubin, newborn infants must be
monitored to identify those who might develop severe hyperbilirubinemia
and, in rare cases, acute bilirubin encephalopathy or kernicterus. 1
Neonatal jaundice is a clinical symptom on neonates marked by
jaundice of skin and scleral because of the accumulation of unconjugated
bilirubin. Clinically, jaundice is visible on a newborn baby if the bilirubin
level reached 5-7 mg/dL. Hyperbilirubinemia is a term used to explain the
increase of plasma bilirubin level over 2SD or more than te level expected
based on neonates age or more than 90th percentile. 2 Neonatal jaundice
can be best understood as a balance between the production and
elimination of bilirubin, with a multitude of factors and conditions affecting
each of these processes.3
Risk factors that known to be the cause of neonatal jaundice in Asia
and South East Asian region are ABO incompatibility, G6PD defficiency,
low birth weight, neonatal sepsis, and prematurity.4,5 ABO hemolytic
disease is the most common blood group incompatible hemolytic
processes

of the newborn period and is the major cause of neonatal

jaundice attributed to maternal

and infant blood incompatibility.6 Foeto

maternal ABO incompatibility exist in about of 25% pregnancies, but

hemolytic disease develops in only 1:10 of such offsprings. 7 On first week
of age, almost 60% term babis got neonatal jaundice, and almost 80% of
preterm babies.8
ABO hemolytic disease can develop in any pregnancy including the
first, but it is restricted to group A and group B infants born to group O
mothers. ABO

incompatibility is

one

of

pathologic

unconjugated

hyperbilirubinemia. ABO incompatibility occurs in 3% of all infants.

Antigens present on the surface of RBCs react with antibodies in the
plasma of opposing blood types, resulting in ABO incompatibility.
Hemolytic disease related to blood groups is generally limited to group A

or B infants born to group O mothers. Risk of recurrence of ABO hemolytic

disease is reported to be as high as 8% in those infants with the same
blood type as their index sibling. ABO incompatibility is somewhat
protective of Rh sensitization because th fetal ABO-incompatible RBCs are
rapidly destroyed in the maternal circulation thereby decreasing the
opportunity of Rh antigen to mount an immune response 9.
In this case report, the author present a report of a male newborn with the
diagnosis of hyperbilirubinemia because of ABO incompatibility.

CASE REPORT
A male newborn, MP, admitted to NICU RSUP Prof. Dr. R. D. Kandou
Manado on July 15th, 2014 at 22.30 p.m. The baby was referred from
Ratumbuysang hospital with the diagnosis of hyperbilirubinemia. He was
admitted with the chief complaint of jaundice and pale since one day
before admitted. He was born on July 13th, 2014, at 12.35 p.m in
Ratumbuysang hospital. Born from a 38 year old mother, with a term
pregnancy, helped by midwife. He weighed 2400 grams, with 44 cm long,
and Apgar score 8-10.
History of pregnancy and labor
A few hours after he was born, the parents started to notice that the babys
skin looked yellowish. The morning he was admitted, he looked more
yellow than the day before, and also looked pale. Along the treatment in
Ratumbuysang hospital, his intake is good, and he was breastfed and
formula milk fed. The baby was active and cried loudly. Vomit was never
found, and there was no seizure. While the mother was pregnant, she
routinely checked up her pregnancy at an obstetrician, got Tetanus shot
twice, and along the pregnancy, she never complained about any illness,
no history of hypertension nor any kind of infections. The mother also
known had no history of troubled pregnancy. The brother was born by
spontaneous vaginal delivery, and never had a complain about jaundice as
a newborn.
History of feeding
Breast feeding

: birth until now

Formula milk

: birth until now

Soft rice porridge

: -

Rice

: -

Immunizations
BCG

: 0 time

Polio

: - time

DTP

: - time

Measles : - time
Hepatitis : - time
History of social-economics and family
He is the second child of the family. He has a brother. His father is 41
years old, a senior high school, a government company employee while
her mother is 38 years old, a senior high school graduation, a housewife.
They live in a permanent house, consist of 2 bedrooms, occupied
by 3 adults and 1 children. They had electrical source from the electrical
company of government and water supply from local state water company.
Their bathroom and lavatory were inside the house. The rubbish is
collected and thrown away. Inside their room, there were no closet filled
with naphthalene balls.
Pedigree

= patient

Physical examination
Body weight

: 2,4 Kg

Body height

: 44 cm

Head circumference : 34 cm (normal)

General condition

: activity (+) . Reflex (+)

Heart rate

: 150 beats per minute

Respiratory rate

: 54 times per menute

Body temperature

: 36,8C

Skin

: jaundice (+)

Head

: oval shape, no caput succadeneum

Eyes

: Conjunctiva was anemic and sclera was icteric,

pupil was round, isochors, 2-2 mm, light reflex was
normal

Ears

: Formed and firm instant recoil

Nose

: There was no secretes and no flare

Mouth

: no cyanotic lips

Neck

: trachea at the middle line

Chest

: Symmetrical respiratory movements, no retraction

Heart

: Normal rate, regular heart rhythm, no thrill, no

murmur

Lungs

Symmetrical

movement,

symmetrical

vocal

fremitus, bronchovesicular breath sound, without

rales and wheezing
Abdomen

: soft and flat, liver and spleen were not palpable,

peristaltic movement was normal

Extremities

: warm, no cyanotic, capillary refill time less than 3

seconds, no deformity

Genitalia

: Male, testis down (+/+), good rugae, penis length

2,3 cm

Laboratory findings
Complete Blood Count (13/07/2014) Laboratory in Ratumbuysang hospital
Haemoglobin
: 11,1 g/dl
Haematocrit
: 33,5%
Leukocyte
: 13.400/mm3
Platelets
: 321.000/mm3
ESR
: 18 mm/hr
Total bilirubin
: 23,7 mg/dL
Direct bilirubin
: 1 mg/dL
Indirect bilirubin
: 22,7 mg/dL
14/07/2014 in Ratumbuysang Hospital
AST

: 13 U/L

ALT

: 59 U/L

CRP

: (-)

Na

: 132 mmol/L

: 5,7 mmol/L

Cl

: 112 mmol/L

Working diagnosis:
Hyperbilirubinemia et causa suspected of ABO incompatibility
Differential diagnosis:
G6PD defficiency
Rhesus incompatibility
Treatment
Phototherapy
Breast milk

Planning

Complete blood count, serum electrolytes, CRP, Blood smear

7

Total protein, albumin, globulin

Reticulocyte count, Coombs Test

G6PD level

PCV/24hrs

FOLLOW UP
July 16th, 2014 (2nd day care)
Complaint
: generalized jaundice, good intake, no tight breath
nor tachypneu
General conditions : activity (+) , reflex (+)
Heart rate

: 128 beats/minutes

Respiratory rate

: 40 times/minutes

Body temperature : 37C

CNS

: rounded pupils, isochors, 2mm-2mm, light reflex

(+/+)

CV

: no murmurs, warm extremities, no cyanotic lips,

CRT<3

RT

: symmetrical, no retractions, no rales, no wheeze

GIT

: flat belly, supple, positive intestinal sound

Hemato

: anemic conjunctiva and icteric scleral

Skin

: jaundice

PCV

: 30%

Working diagnosis:
Hyperbilirubinemia ec suspected of ABO incompatibility

Differential diagnosis:
G6PD defficiency
Rhesus Incompatibility

Treatment
Phototherapy (day 2)
Breast milk
PCV/24 hours
Planning

Coombs Test, G6PD level

PCV/24 hrs

July 17th, 2014 (3rd day care)

Complaint
: generalized jaundice, good intake, no tight breath
nor tachypneu
General conditions : activity (+) , reflex (+)
Heart rate

: 140 beats/minutes

Respiratory rate

: 40 times/minutes

Body temperature : 36,5C

CNS

: rounded pupils, isochors, 2mm-2mm, light reflex

(+/+)

CV

: no murmurs, warm extremities, no cyanotic lips,

CRT<3

RT

: symmetrical, no retractions, no rales, no wheeze

GIT

: flat belly, supple, positive intestinal sound

Hemato

: anemic conjunctiva and icteric scleral

Skin

: jaundice

Laboratory Result (17/07/2014)

Total bilirubin
: 27,78 mg/dL
Direct bilirubin
: 1,40 mg/dL
Indirect bilirubin
: 26,53 mg/dL
Total protein
: 6,44 g/dL
Albumin
: 3,57 g/dL
Globulin
: 2,87 g/dL
9

Reticulocyte Index : 15%

Blood smear
: bleeding/haemolytic (G6PD defficiency?)
Coombs test
: direct (-), indirect (-)
Babys blood group : A, rh(+)
Mothers blood group : O, rh(+)
PCV
: 26%
Working diagnosis:
Hyperbilirubinemia ec suspected of ABO incompatibility
Anemia ec hemolysis
Differential diagnosis:
G6PD defficiency
Treatment
Phototherapy (day 3)
Breast milk
Planning

G6PD level

Exchange transfusion

PCV/24 hrs

July, 18th, 2014 (4th day care)

Complaint

: generalized jaundice, good intake, no tight breath nor

tachypneu

General conditions : activity (+) , reflex (+)

Heart rate

: 140 beats/minutes

Respiratory rate

: 40 times/minutes

Body temperature : 36,5C

10

CNS

: rounded pupils, isochors, 2mm-2mm, light reflex

(+/+)

CV

: no murmurs, warm extremities, no cyanotic lips,

CRT<3

RT

: symmetrical, no retractions, no rales, no wheeze

GIT

: flat belly, supple, positive intestinal sound

Hemato

: anemic conjunctiva and icteric scleral

Skin

: jaundice

Laboratory Result (18/07/2014)

Total bilirubin
: 27,1 mg/dL
Direct bilirubin
: 1,03 mg/dL
Indirect bilirubin
: 26,22 mg/dL
PCV
: 28%
Working diagnosis:
Hyperbilirubinemia ec suspected of ABO incompatibility
Anemia ec hemolysis
Differential diagnosis:
G6PD Defficiency

Treatment
Phototherapy (day 4)
Breast milk
Planning
-

G6PD level
Exchange transfusion
PCV/24hrs

July, 19th, 2014 (5th day care)

11

Complaint

: generalized jaundice, good intake, no tight breath nor

tachypneu

General conditions : activity (+), reflex (+)

Heart rate

: 136 beats/minutes

Respiratory rate

: 48 times/minutes

Body temperature : 36,8C

CNS

: rounded pupils, isochors, 2mm-2mm, light reflex

(+/+)

CV

: no murmurs, warm extremities, no cyanotic lips,

CRT<3

RT

: symmetrical, no retractions, no rales, no wheeze

GIT

: flat belly, supple, positive intestinal sound

Hemato

: anemic conjunctiva and icteric scleral

Skin

: jaundice

PCV

: 29%

Working diagnosis:
Hyperbilirubinemia ec ABO incompatibility
Anemia ec hemolysis

Differential diagnosis:
G6PD Defficiency
Treatment
Phototherapy (day 5)
Breast milk
Planning
-

G6PD level
Bilirubin serum level
PCV/24 hrs

12

July, 20th, 2014 (6th day care)

Complaint

: generalized jaundice, good intake, no tight breath nor

tachypneu

General conditions : activity (+) , reflex (+)

Heart rate

: 150 beats/minutes

Respiratory rate

: 48 times/minutes

Body temperature : 36,6C

CNS

: rounded pupils, isochors, 2mm-2mm, light reflex

(+/+)

CV

: no murmurs, warm extremities, no cyanotic lips,

CRT<3

RT

: symmetrical, no retractions, no rales, no wheeze

GIT

: flat belly, supple, positive intestinal sound

Hemato

: conjunctiva not anemic and icteric scleral

Skin

: jaundice

PCV

: 32%

Working diagnosis:
Hyperbilirubinemia ec ABO incompatibility
Anemia ec hemolysis
Differential diagnosis:
G6PD Defficiency
Treatment
Phototherapy (day 6)
Breast milk
Planning

13

Exchange transfusion
G6PD level
Bilirubin serum level

July, 21th, 2014 (7th day care)

Complaint

: generalized jaundice, good intake, no tight breath nor

tachypneu

General conditions : activity (+) , reflex (+)

Heart rate

: 138 beats/minutes

Respiratory rate

: 48 times/minutes

Body temperature : 37,3C

CNS

: rounded pupils, isochors, 2mm-2mm, light reflex

(+/+)

CV

: no murmurs, warm extremities, no cyanotic lips,

CRT<3

RT

: symmetrical, no retractions, no rales, no wheeze

GIT

: flat belly, supple, positive intestinal sound

Hemato

: conjunctiva not anemic and icteric scleral

Skin

: jaundice

PCV

: 32%

Working diagnosis:
Hyperbilirubinemia ec ABO incompatibility
Anemia ec hemolysis
Differential diagnosis:
G6PD Defficiency
Treatment
Phototherapy (day 6)
Breast milk

14

Planning
-

G6PD level
Bilirubin serum level
PCV/24 hrs

July, 22nd, 2014 (8th day care)

Complaint

: generalized jaundice, good intake, no tight breath nor

tachypneu

General conditions : activity (+) , reflex (+)

Heart rate

: 138 beats/minutes

Respiratory rate

: 48 times/minutes

Body temperature : 37,3C

CNS

: rounded pupils, isochors, 2mm-2mm, light reflex

(+/+)

CV

: no murmurs, warm extremities, no cyanotic lips,

CRT<3

RT

: symmetrical, no retractions, no rales, no wheeze

GIT

: flat belly, supple, positive intestinal sound

Hemato

: conjunctiva not and icteric scleral

Skin

: jaundice decreased

PCV

: 35%

Laboratory findings:
Total bilirubin serum : 11,0 mg/dL
Direct bilirubin
: 0,3 mg/dL
Indirect bilirubin
: 10,7 mg/dL
G6PD
: 19.7 U/gHb
Diagnosis:
Hyperbilirubinemia ec ABO incompatibility
Anemia ec hemolysis ec ABO incompatibility
Treatment
Stop phototherapy

15

Breast milk
Planning
-

Plan to discharge tomorrow

July, 23rd, 2014 (9th day care)

Complaint

: generalized jaundice, good intake, no tight breath nor

tachypneu

General conditions : activity (+) , reflex (+)

Heart rate

: 132 beats/minutes

Respiratory rate

: 44 times/minutes

Body temperature : 36,8C

CNS

: rounded pupils, isochors, 2mm-2mm, light reflex

(+/+)

CV

: no murmurs, warm extremities, no cyanotic lips,

CRT<3

RT

: symmetrical, no retractions, no rales, no wheeze

GIT

: flat belly, supple, positive intestinal sound

Hemato

: not anemic conjunctiva and icteric scleral

Skin

: jaundice decreased

Diagnosis:
Hyperbilirubinemia ec ABO incompatibility
Anemia ec hemolysis ec ABO incompatibility
Treatment
Breast milk
Planning
-

Discharge today from the hospital

16

17

DISCUSSION
Hyperbilirubinemia is one of the most often clinical phenomenon
found in newborns. More than 85% of term neonates that readmitted to
hospital was because of hyperbilirubinemia. Hyperbilirubinemia caused
the baby looked yellow, because the accumulation of bilirubin pigment that
has icteric color on skin and scleral.The isomer of this bilirubin came from
the degradation of heme from hemogolobin. On the transcient period
shortly after birth, liver has not reached its maximum function, therefore
the process of bilirubin glucuronidated did not happen optimal. This
condition wiil cause the domination of unconjugated bilirubin inside the
bloodstream. On most newborns, unconjugated hyperbilirubinemia is an
usual transitional period, but to some newborns occurs the excessive
increase of bilirubin, thus it becomes toxic and can cause death, even if
the newborns survived, will cause neurological sequelae. Thus, every
newborn with jaundice should be differentiated whether it is physiological
or pathological, and closely monitored, as if there were tendency to grow
into severe hyperbilirubinemia.2
Neonatal jaundice is categorized into two, physiological jaundice and
pathological

jaundice.

Physiological

jaundice

generally

occurs

in

newborns, where level of unconjugated bilirubin on first week of life is

greater than 2mg/dL. On term formula fed babies, the bilirubin level will
reach its peak approximately 6-8mg/dL on the third day of life, then rapidly
decrease within 2-3 days followed by slower decrease 1 mg/dL in 1 -2
weeks. On term breastmilk fed babies, the peak level of bilirubin will be
higher (7-14 mg/dL) and the decrease occurs slower, even need 6 weeks
to reach the normal level.10,11
Pathological jaundice are not easily diferred with the physiological
one. The following conditions are categorized as pathological jaundice,
and need further follow up. The conditions are:
1. Onset of jaundice occurs before 24 hours of age
2. Any elevation of bilirubin level that need phototherapy
3. Increase level of total bilirubin serum > 0,5 mg/dL/hour
18

4. Any other symptoms of diseases like vomiting, lethargic, poor

feeding, excessive weight loss, apneu, tachypneu, or temperature
instability
5. Jaundice still seen after 8 days of age for term babies, and 14
days for preterm babies.11
To diagnose a jaundice, the examiner should do a thorough examination.
Jaundice appearance is determined by checking the baby through tactile
blanching, inside a room with a sufficient lighting, by pressing the skin
gently in order to see the color of the skin and subcutaneous tissue.
Physical examination should be focused in identifying one of the cause of
pathologic jaundice. Conditions should be considered are pale, petechiae,
blood extravasation, skin bruising, hepatosplenomegaly, weight loss, and
evidence of dehydration.12,13
Risk of hyperbilirubinemia is increasing in breastfed neonates and preterm
neonates. Hyperbilirubinemia occured in first 36 hours usually caused by
the increase of bilirubin production, especially because hemolysis,
because in this period hepatic clearance seldomly produced bilirubin
greater than 10 mg/dL. One percent destruction of haemoglobin will
increase bilirubin level 4 times.10
In this patient, found that jaundice was firstly seen just a few hours after he
was born. Thus we conclude it was a pathological jaundice and need
further care. Laboratory examination was done and the result suggested
that the patient got an anemia because of the haemoglobin level was 11,1
g/dL. Diagnosis of hyperbilirubinemia was concluded from the anamnesis,
physical examination, and laboratory results. From the anamnesis, found
that jaundice had been observed since first day of life in this patient,
followed by pale noticed in palms and plantar feet. From the physical
examination, noticed that jaudice had reached the whole body. According
to bilirubin serum level, that shown total bilirubin level 23,7 mg/dL, direct
bilirubin level 1 mg/dL, and indirect bilirubin level of 22,7 mg/dL. From the
lab result, we found an increase in total serum bilirubin and indirect
blirubin level. Because we could not rule out the cause of hemolytic

19

process,

it

is

needed

to

trace

the

etiology

of

the

patients

hyperbilirubinemia and anemia, thus we planned to do Coombs test, blood

smear, and reticulocyte count to detect any signs of hemolytic process.
Coombs test was done in the following day, given a negative result. And
from the blood group test, we got the blood group of the baby was A with
rh (+), and the mother was O with rh (+). The reticulocyte count shown an
increase, 15% (N: 0.5 1.5%), and the blood smear concluded a
suspected of hemolytic (G6PD defficiency?). From the laboratory result,
we diagnosed this patient wih hyperbilirubinemia et causa suspected of
ABO incompatibility dd/ G6PD defficiency and anemia ec hemolysis from
the blood smear result. The most common cause of unconjugated
hyperbilirubinemia are physiological process, breastmilk jaundice, ABO
incompatibility, cephalhematoma, G6PD defficiency, and mostly occured in
Asian ethnicity.14 From the amount measured, G6PD defficiency had
greater risk of kerincterus, but ABO incompatibility is often used as a
reason to do exchange transfusion.15,16
In this patient, the cause of hyperbilirubinemia was determined based on
the clinical evidence and laboratory results. ABO incompatibility was
diagnosed from the laboratory result, where the blood group examination
shown an incompatibility on mother and babys blood group. Mother was
O(+) and baby was A(+). The Coombs test result came back negative but
we still did not rule out the diagnosis of incompatibility, because not every
ABO incompatible cases, analyzed as Coombs test negative. 17,18 Based
on blood smear examination and reticulocyte count found the evidence of
haemolysis, so the diagnosis considered were ABO incompatibility with the
differential diagnosis of G6PD. The differential diagnosis ruled out after the
result of G6PD enzyme given a normal result.
ABO hemolytic disease results from the action of maternal anti A or anti B
antibodies on fetal erythrocytes of the corresponding blood group.
Haemolysis in maternal-fetal ABO blood group incompatibility, in which the
mother has blood group O and the newborn has blood group A or B,
occurs in 15-20% of all pregnancies. 19 Hemolytic disease develops in
20

approximately 10% of such newborns and may be associated with

clinically significant neonatal hyperbilirubinemia 20. The hemolytic process
results from maternal anti-A or anti-B immunoglobulin G (IgG) antibodies
crossing the placenta and attaching to the appropriate antigens on the
neonatal red cells. Resultant heme catabolism causes an increased
indirect

bilirubin

(IB)

production,

leading

to

neonatal

jaundice. 21

Considering that maternal-fetal ABO incompatibility can cause severe

neonatal jaundice requiring an exchange transfusion and even kernicterus,
the prediction of probable risk factors for hyperbilirubinemia, such as the
degree of hemolysis, gains importance.
Hemolysis associated with ABO incompatibility is similar to Rh hemolytic
disease in that maternal anti A or anti B antibodies enter the fetal
circulation and react with A or B antigens on the erythrocyte surface. In
type A and B individuals, naturally occurring anti B and anti A isoantibodies
largely are IgM molecules that does not cross placenta. In contrast, the
allo-antibodies present in type O individuals are predominantly IgG
molecules. For this reason ABO incompatibility is largely restricted to type
O mothers with type A or B fetus. The presence of IgG anti A or anti B
antibodies in type O mothers also explains why hemolysis caused by ABO
incompatibility frequently occurs during first pregnancy without prior
sensitization.22
Therapy given in this patient were phototherapy and closely monitor
the haemoglobin by doing a daily PCV. In hyperbilirubinemia babies,
phototherapy usually done using the guideline published by AAP 2004.
This guideline not only consider the total serum bilirubin level, but also the
babys age and risk factors including haemolytic isoimmune diseases,
G6PD defficiency, asphyxia, lethargic, temperature instability, sepsis,
acidosis, and hypoalbuminemia. On preterm babies, phototherapy applied
in lower level of bilirubin serum, and in few centers, used as prophylaxis in
neonates with birthweight less than 1000gr.23
The therapy of hyperbilirubinemia in ABO incompatibility can be done

21

alsi

by

giving

intravenous

immunoglobulin

(IVIG).

Intravenous

immunoglobulin (IVIG) has been found to decrease hemolysis in neonatal

jaundice due to blood group incompatibility, but a consensus on its usage
has not been reached. IVIG therapy, single or multiple, did not affect
exchange transfusion, need of erythrocyte transfusion and hospitalization
time when used in combination with LED phototherapy in the treatment of
ABO hemolytic jaundice in neonates. 24
Exchange transfusion was planned to be done in this patient to
prevent further complications like kernicterus. In this case, we should use
a group O blood with a compatile rhesus to mother and baby, Rh (-), with
the lowest titer of anti-A and anti-B. And the blood should be crossmathed
before. The exchange transfusion will cast off neonates red blood cells
that had been sensitisized with maternal antibodies (antibodies coated
RBCs), lower the bilirubin serum level, and also corrected the anemia
occured due to the hemolysis.25
Complications that can happen in this patient are kernicterus and late
anemia in infancy. The prognosis on this patient was good, because he
shown a better clinical condition after receiving treatment with intensive
phototherapy. But a routine follow up still needed to determine the better
outcome and to make sure that no complications happened.

22

REFERENCES
1. American
Academy
of
Pediatrics.
Subcommittee
on
hyperbilirubinemia. Management of hyperbilirubinemia in the newborn
infant 35 or more weeks of gestation. Clinical Practice Guidelines.
Pediatrics 2004; 114: 297-316.
2. Sukadi, Abdurrahman. Hiperbilirubinemia. In Kosim MS, Yunanto, Ari.,
Dewi, Rizalya., Sarosa, Gatot I., Usman, Ali., eds. Buku Ajar
Neonatologi. 1st ed. Jakarta: UKK Neonatologi Ikatan Dokter Anak
Indonesia. 2008; p. 147-70.
3. Cohen Ronald S., Wong Ronald J., Stevenson, David K. Inderstanding
neonatal jaundice: aa perspecctive of causation. Pediatr and
Neonatol. Vol. 51. 2010; p. 143-8.
4. Zabeen B, Nahar J, Nabi N, Baki A, Tayyeb S, Azad K, et al. Risk
factors and outcome of neonatal jaundice in a tertiary hospital. Ibrahim
Med Coll J 2010;4(2):70-73.
5. Aina YT, Omoigberale AI. Risk factors for neonatal jaundice in babies
presenting at the university of benin teaching hospital, benin city. Niger
J Paed 2012;39(4):159-163.
6. Madan, Ashima., McMahon James B., Stevenson, David K. Neonata
hyperbilirubinemia. In Taeusch, William H., Ballard, Robert A.,
Gleason, Christine A., eds. Averys diseases of the newborn. 8th ed.
Philadelphia: Elsevier Saunders. 2004; p.1226-56.
7. Nadig, Naveen., Basavaraj, AC. Early predictors of pathological
jaundice due to ABO hemolytic disease. Int J Pharm Bio Sci 2013 July;
4(3): (B) 125 - 130
8. Kliegman RM. Ikterus dan hiperbilirubinemia pada bayi baru lahir.
Dalam: Behrman, Kliegman, Arvin, Wahab AS, editor. Ilmu kesehatan
anak nelson. Edisi ke-15. Jakarta: Penerbit Buku Kedokteran EGC.
2000. 610-6.
9. Gomella
Tricia L., Cunningham MD., Eyal, Fabien G., eds.
Neonatology: Management, procedures, on-call problems, diseases,
and drugs.. 7th ed. New York: McGraw-Hill. 2013; p.547-9.
10. Blackburn ST, penyunting. Bilirubin metabolism. Maternal, fetal, &
neonatal physiology, a clinical perspective. Edisi ke-3. Saunders.
Missouri; 2007.
11. Martin CR, Cloherty JP. Neonatal hyperbilirubinemia. Dalam: Cloherty
JP, Eichenwaald EC, Stark AR, penyunting. Manual of neonatal care.
5th ed. Philadelphia: Lippincott Williams & Wilkins. 2004; p.185-221.
12. Helen AC, Kevin S, David RH. Thrombocytopenia. In: Cloherty JP,
Eichenwald EC, Stark AR. Editors. Manual of neonatal care. 6th ed.
Philadelphia: Lippincot Williams & Wilkins. 2008; p.455-62.
13. Johnson LH, Bhutani VK, Brown AK. System-based Approach to
Management of Neonatal Jaundice and Prevention of Kernicterus. J
Pediatr. 2002;140:396-403.

23

14. Nkhoma ET, Poole C, Vannappagari V, Hall SA, Beutler E. The global
prevalence of glucose-6-phosphate dehydrogenase deficiency: a
systematic review and meta-analysis. Blood Cells Mol Dis.
2009;42:267-78.
15. Melton K, Akinbi HT. Neonatal jaundice: Strategies to reduce bilirubin
induced complications. Postgrad Med. 1999;106:167-8.
16. Wennberg RP, Ahlfors CE, Bhutani VK. Toward understanding
kernicterus:a challenge to improve the management of jaundiced
newborns. Pediatrics.2006;117:474-85.
17. Al-Swaf, Faris., Jumaa RS., Saeed, Isam S. Hemolytic disease of newborn
due to ABO incompatibility. Tikrit Medical Journal 2009; 15(2):70-78.

18. Stoniene D, Buinauskiene J, Markuniene E, Tameliene R,

Kudreviciene. The value of diagnostic tests in predicting
hyperbilirubinemia in ABO incompatibility. Pediatric Research.
2011;70:735-6.
19. Yigit S, Gursoy T, Kanra T, et al. Whole blood versus red cells and
plasma for exchange transfusion in ABO haemolytic disease. Trans
Med 2005; 15: 313-318.
20. Yaseen H, Khalaf M, Rashid N, Darwich M. Does prophylactic
phototherapy prevent hyperbilirubinemia in neonates with ABO
incompatibility and positive Coombs' test? J Perinatol 2005; 25: 590-4.
21. Kaplan M, Na'amad M, Kenan A, et al. Failure to predict hemolysis
and hyperbilirubinemia by IgG subclass in blood group A or B infants
born to group O mothers. Pediatrics 2009; 123: 132-137.
22. Mentzer WC, Glader BE. Erythrocyte disorder in infancy. In Averys
disease of the newborn. Taruseh HW, Ballard RD Eds. 7th Ed.
Philadelphia, WB Saunders Co. 1998:1080-1111.
23. Maisels MJ, Watchko JF. Treatment of jaundice in low birth weight
infants. Arch Dis Child Fetal Neonatal. 2003;88:F459-F463.
24. Demirel, Gamze., et al. Single versus miltiple dose intravenous
immunoglobulin in combination with LED phototherapy in the
treatment of ABO hemolytic disease in neonates. Int J of Hemato.
2011;93:p.700-3.
25. Dewi, Rizalya. Prosedur medik pada bayi baru lahir: transfusi tukar. In:
Kosim MS, Yunanto, Ari., Dewi, Rizalya., Sarosa, Gatot I., Usman, Ali.,
eds. Buku Ajar Neonatologi. 1st ed. Jakarta: UKK Neonatologi Ikatan
Dokter
Anak
Indonesia.
2008;
p.411-20.

24

ATTACHMENTS

25

1 American Academy of Pediatrics. Subcommittee on hyperbilirubinemia. Management of

hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Clinical Practice Guidelines.
Pediatrics 2004; 114: 297-316.
2 Buku ajar neo
3 Cohen Ronald S., Wong Ronald J., Stevenson, David K. Inderstanding neonatal jaundice: aa
perspecctive of causation. Pediatr and Neonatol. Vol. 51. 2010; p. 143-8.
4 Zabeen B, Nahar J, Nabi N, Baki A, Tayyeb S, Azad K, et al. Risk factors and outcome of neonatal
jaundice in a tertiary hospital. Ibrahim Med Coll J 2010;4(2):70-73.
5 Aina YT, Omoigberale AI. Risk factors for neonatal jaundice in babies presenting at the university of
benin teaching hospital, benin city. Niger J Paed 2012;39(4):159-163.
6 Madan, Ashima., McMahon James B., Stevenson, David K. Neonata hyperbilirubinemia. In Taeusch,
William H., Ballard, Robert A., Gleason, Christine A., eds. Averys diseases of the newborn. 8th ed.
Philadelphia: Elsevier Saunders. 2004; p.1226-56.
7 Nadig, Naveen., Basavaraj, AC. Early predictors of pathological jaundice due to ABO hemolytic
disease. Int J Pharm Bio Sci 2013 July; 4(3): (B) 125 - 130
8 Kliegman RM. Ikterus dan hiperbilirubinemia pada bayi baru lahir. Dalam: Behrman, Kliegman,
Arvin, Wahab AS, editor. Ilmu kesehatan anak nelson. Edisi ke-17. Jakarta: Penerbit Buku Kedokteran
EGC. 2004. 610-6.
9 Gomella Tricia L., Cunningham MD., Eyal, Fabien G., eds. Neonatology: Management, procedures,
on-call problems, diseases, and drugs.. 7th ed. New York: McGraw-Hill. 2013; p.547-9.
10Blackburn ST, penyunting. Bililrubin metabolism. Maternal, fetal, & neonatal physiology, a clinical
perspective. 3rd ed. Saunders. Missouri; 2007.
11 Martin CR, Cloherty JP. Neonatal hyperbilirubinemia. In: Cloherty JP, Eichenwaald EC, Stark
AR,eds. Manual of neonatal care. 5th ed. Philadelphia: Lippincott Williams & Wilkins. 2004; p.185221.
12 Helen AC, Kevin S, David RH. Thrombocytopenia. In: Cloherty JP, Eichenwald EC, Stark AR.
Editors. Manual of neonatal care. 6th ed. Philadelphia: Lippincot Williams & Wilkins. 2008; p.455-62.
13 Johnson LH, Bhutani VK, Brown AK. System-based Approach to Management of Neonatal
Jaundice and Prevention of Kernicterus. J Pediatr. 2002;140:396-403.
14 Nkhoma ET, Poole C, Vannappagari V, Hall SA, Beutler E. The global prevalence of glucose-6phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood Cells Mol Dis.
2009;42:267-78.
15 Melton K, Akinbi HT. Neonatal jaundice: Strategies to reduce bilirubininduced complications.
Postgrad Med. 1999;106:167-8.
16 Wennberg RP, Ahlfors CE, Bhutani VK. Toward understanding kernicterus:a challenge to improve
the management of jaundiced newborns. Pediatrics.2006;117:474-85.
17 Al-Swaf, Faris., Jumaa RS., Saeed, Isam S. Hemolytic disease of newborn due to ABO incompatibility.
Tikrit Medical Journal 2009; 15(2):70-78.

18 Stoniene D, Buinauskiene J, Markuniene E, Tameliene R, Kudreviciene

19 Yigit S, Gursoy T, Kanra T, et al. Whole blood versus red cells and plasma for exchange transfusion
in ABO haemolytic disease. Trans Med 2005; 15: 313-318.
20 Yaseen H, Khalaf M, Rashid N, Darwich M. Does prophylactic phototherapy prevent
hyperbilirubinemia in neonates with ABO incompatibility and positive Coombs' test? J Perinatol 2005;
25: 590-4.
21 Kaplan M, Na'amad M, Kenan A, et al. Failure to predict hemolysis and hyperbilirubinemia by IgG
subclass in blood group A or B infants born to group O mothers. Pediatrics 2009; 123: 132-137.

22 Mentzer WC, Glader BE. Erythrocyte disorder in infancy. In Averys disease of the newborn.
Taruseh HW, Ballard RD Eds. 7th Ed. Philadelphia, WB Saunders Co. 1998:1080-1111.
23 Maisels MJ, Watchko JF. Treatment of jaundice in low birth weight infants. Arch Dis Child Fetal
Neonatal. 2003;88:F459-F463.
24 Single vs double phototherapy LED with IVIG
25 Dewi, Rizalya. Prosedur medik pada bayi baru lahir: transfusi tukar. In: