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Group 14
 “Baby Low Birth Weight”
CASE
SCENARIO 2
A 3 days old baby boy, referred to Hospital’s emergency department with
note : the baby look yellow on the face and body. From Alloanamnesis, found
history of mother was on hyperemesis (heavy) and the pregnancy was terminated
on gestational age 8 months, birth weight was 1600 gram.

1. DIFFICULT WORDS
1) Termination

2. KALIMAT KUNCI
1) A 3 days old baby boy
2) The baby look yellow on the face and body
3) History of mother was on hyperemesis (heavy)
4) Pregnancy was terminated on gestational age 8 months
5) Birth weight was 1600 gram

3. PERTANYAAN
1) Is there any correlation between mother’s history of hyperemesis and
neonatal jaundice?
2) Is there any correlation between the termination and neonatal jaundice?
3) Is there any correlation between the neonatal jaundice and BLBW?
4) Is there any correlation between hyperemesis gravidarum and the
termination?
5) Is there any correlation between hyperemesis gravidarum and BLBW?
6) How to diagnose and interpretation of the scenario?
7) How is the first line management based on the scenario?

4. ANSWERS :
1) Is there any correlation between mother’s history of hyperemesis and
neonatal jaundice?
A. Hyperemesis Gravidarum

Nausea and vomiting complaints by about three-quarters of

pregnant women, usually occurs during the first trimester. Nausea and
vomiting usually accompanied by complaints of many spit
(hypersalivation), dizziness, flatulence, and the body feels weak. These
complaints are generally known as "morning sickness" because it feels
heavier in the morning. However, nausea and vomiting can last all day.
Flavor and intensity are often described resemble nausea, vomiting due
to chemotherapy for cancer.
Nausea and vomiting in pregnant women rarely can be
eliminated entirely. Fortunately the symptoms can be alleviated, for
example by restricting eating to satiety, eat little but often, avoid certain
foods, or giving antiemetics. However, in some cases nausea, vomiting
severe enough that the steps above do not work and there problems such
as weight loss, dehydration, acid-base balance disorders, and ketosis.
This condition is called hyperemesis gravidarum.
Hyperemesis gravidarum can be classified clinically into three levels,
namely:
• Level I
Hyperemesis gravidarum level I is characterized by continuous
vomiting accompanied by intolerance to eat and drink. There are weight
loss and epigastric pain. First of all contents are regurgitated food, then
mucus and a little bile, and when it's time to get out the blood. The pulse
rate increased to 100 beats / min and systolic blood pressure decreased.
Examination reveals sunken eyes, dry tongue, reduced skin turgor, and
the urine is slightly reduced.
• Level II
Hyperemesis gravidarum level II, patients regurgitate
everything you eat and drink, body weight rapidly decreases, and there
is a great thirst. Frequency pulse 100-140 beats / min and systolic blood
 pressure less than 80 mmHg. Patients look apathetic, pale, dirty tongue,
sometimes jaundice, and found acetone and bilirubin in urine.
• Level III
Level III condition is extremely rare, characterized by reduced
or even stopped vomiting, but decreased consciousness (delirium to
coma). Patients experience jaundice, cyanosis, nystagmus, heart
disorders, and found bilirubin in urine and protein.
Nausea and vomiting occurred in 50-90% of pregnancies.
Symptoms usually begins at 9-10 weeks' gestation, peaking at 11-13
weeks, and ends on Sunday 12-14. In 1-10% of pregnancies, the
symptoms may progress past 20-22 weeks. Hyperemesis severe that
hospitalization occurs in 0.3-2% of pregnancies.
B. Neonatal Jaundice
 Jaundice Physiology
Physiological jaundice is jaundice arising on the second day
and the third day and has no basis in pathology or do not have the
potential to be due to jaundice. As for the signs as follows:
1. Embossed on second and third day
2. The indirect bilirubin levels do not exceed 10 mg% in neonates at
term.
3. Speed bilirubin levels do not exceed 5% per day.
4. Bilirubin direct not exceed 1 mg%.
 Jaundice Pathology
Pathological jaundice is warranted pathological jaundice or
bilirubin levels reaches a value called hyperbilirubinemia. The signs
are as follows:
1. Jaundice occurs in the first 24 hours.
2. bilirubin level exceeds 10 mg% ON OR neonates Just months
exceeded 12.5% AT neonates Less months.
3. Appointment of bilirubin more than 5 mg% per day.
4. After 2 weeks Jaundice Residential First.
5. bilirubin direk exceed 1 mg%.
 6. Having Relationship WITH hemolytic process.

 Investigations
Review the history and perform a thorough physical
examination1 on a baby who requires phototherapy to treat jaundice.
examination.
 Early onset jaundice less than 24 hrs
Investigations should include:
• mother’s and baby’s blood group if not already known and DAT
• babies haemolytic screen which includes:
o full blood count (FBC) and film with reticulocyte count (to help
assess haemolysis)
o total serum bilirubin level
o G6PD if baby’s family history or ethnic/geographic origin is
suggestive of the possibility of deficiency (Mediterranean,
middle Eastern, African, South East Asian)1
• review of sepsis risk as a cause for the jaundice
 Jaundice approaching exchange level
Investigations as per 5.3.1 and in addition: direct
(conjugated) bilirubin liver function test (LFT) G6PD1 and screen
for Gilbert Syndrome
 Prolonged jaundice
Babies with prolonged jaundice (obvious persisting clinical
jaundice at greater than 2 weeks in term babies and greater than 3
weeks in preterm babies) require:
• clinical review including examination/enquiry regarding stool
colour
• total serum bilirubin and conjugated bilirubin level:
 o conjugated hyperbilirubinaemia or a jaundiced baby with pale
stools and dark urine requires urgent discussion with a

Zone 1 2 3 4 5

Lower Arms
Palms
Head and Upper trunk and
Definition and
neck trunk and lower
soles
thighs legs

TSB
100 150 200 250 >250
(micromol/L)

Neonatologist
• thyroid function tests (TFT)
• FBC to check for anaemia or signs of haemolysis (and full
haemolytic screen if not already done):
o consider Heinz body count for
oxidative causes of haemolysis
• review of results of newborn screening
test, specifically thyroid and
galactosemia screen
• review of any previous pathology
results relevant to jaundice
 Colour
Monitor all babies for jaundice
development by assessing them whenever vital signs are measured
or at least every 8 to 12 hours.
Always assess jaundice in a well-lit room or in daylight at a window
by blanching the baby’s skin with a finger and observing the
underlying skin colour. Jaundice appears first in the face and
progresses caudally to the trunk and extremities.
Kramer recognised the cephalocaudal progression of jaundice with
increasing total serum bilirubin levels and divided the baby into 5
 zones, with a total serum bilirubin level measurement associated
with each zone. This is known as Kramer’s rule (see Figure 1) and
has traditionally been used to visually assess the severity of jaundice.

C. Hyperemesis Gravidarum and Neonatal Jaundice

Nausea and vomiting are the clinical symptoms of hyperemesis
gravidarum, usually occurs in pregnancy months to two to four, severe
vomiting will cause dehydration, acidosis starvation, alkalosis due to
loss of hydrochloric acid and hipokanemia.
This disease can cause elevated levels of transaminases, BSP
retention, fatty infiltration of the liver, jaundice is rare and usually mild.
All the abnormalities in the liver will return to normal by
improving the balance of fluid, electrolyte and acid-base body (3). With
nausea, vomiting, and anorexia (lack of appetite) may occur lack of
fluids and nutrients, so there is an abnormality the liver with jaundice,
for their lobushepar central necrosis. Bilirubin levels increased to 2.0 to
5.5% 2).
2) Is there any correlation between the termination and neonatal jaundice?
A. Termination
Termination of pregnancy is terminating a pregnancy with fetal
spending efforts prematurely or before reaching the age of 36-40 weeks
gestation pregnancies with specific indications
Indication
• Abortion delayed
• Eggs empty (blighted ovum)
• hydatidiform mole
• Abortion insipiens
• Incomplete Abortion
• Membranes ruptured prematurely (KPSW)
• Pregnancy expiration
• The growth retardation (IUGR) weight
 • The death of the fetus in the womb
• Indications mother: diseases that endanger the mother if the
pregnancy is passed-like preeklampsi / eclampsia

Termination of pregnancy Gestation> 28 weeks

1. 50 mcg intravaginal misoprostol, which may be repeated 1 time 6
hours after the first administration
2. installation metrolia 100 cc 12 hours before the induction for the
installation of the cervix (not effective when performed in the
KPD)
3. The administration of oxytocin 5 IU drops in Dektrose 5% from 20
drops per minute to a maximum of 60 drops for primi and
multigravida, 40 drops of as much as 2 multigravida grande
pumpkin.
B. Termination and Neonatal Jaundice

Actually, there is no direct correlation between termination with

neonatal jaundice. But probably, there is some reasons why the patient
got terminated. This woman got a heavy hyperemesis during her
pregnancy. As we know, hyperemesis in pregnancy gives some effects
to maternal and fetal. If this hyperemesis occupy for a long time, it can
lead to complications such as Wernicke enchepalophaty to mothers. In
this case, the mother got terminated in 8 months pregnancy to prevent
those complications. The termination action causes the baby born with
low birth weight babies, in this case 1600 gram. LBWB causes the
jaundice on the baby’s body.
3) Is there any correlation between the neonatal jaundice and BLBW?
A. Baby Low Birth Weight
Weight loss is an indicator of the health of the newborn. The average
weight of normal infants (37-41 weeks gestation) is 3000-3600 grams.
Classification according to body weight at birth:
1. Infant birth weight over weight> 4000 grams;
2. The normal birth weight babies with birth weight 2500-4000
grams;
3. Low birth weight (LBW) babies are born with birth weight 1500-
2500 grams;
4. Very Low Birth Weight (VLBW infants), namely babies born with
birth weight <1,500 grams;
5. Extreme Low Birth Weight (BBLER), namely babies born with
birth weight <1,000 grams;
Classification of LBW babies can be divided into two categories,
namely
1. Pure Prematurity
Prematurity is pure neonates with a gestational age less than 37
weeks and have a weight corresponding to the period of pregnancy
or also called preterm neonates / LBW / vocational (corresponding
period of pregnancy).
2. Dysmaturity
Dysmaturity are babies born weighing less than weight should for
pregnancy, due to impaired growth in the womb.
Classification of gestation and infants according to gestational age were
divided into 3 groups
1. Pre-term infants with gestational age less than 37 weeks (259 days),
2. Term infants with gestation of 37 weeks up to 42 weeks (259 -293
days),
3. Post-term infants with gestation from 42 weeks or more.
Baby classification according to weight and gestational age were
divided into three groups, namely
1. Pregnancy small (SGA) that if a baby is born with BB below the
10th percentile of fetal growth curve.
2. In accordance Pregnancy (SMK) that if a baby is born with a BB
between the 10th percentile and 90th fetal growth curve.
3. Large Pregnancy (LGA) that if a baby is born with BB above the
90th percentile on fetal growth curve.
B. BLBW and Neonatal Jaundice
NEONATAL JAUNDICE PATHOPHYSIOLOGY
Neonatal physiologic jaundice results from simultaneous
occurrence of the following two phenomena :
 Bilirubin production is elevated because of increased breakdown
of fetal erythrocytes. This is the result of the shortened lifespan of
fetal erythrocytes and the higher erythrocyte mass in neonates.
 Hepatic excretory capacity is low both because of low
concentrations of the binding protein ligandin in the hepatocytes
and because of low activity of glucuronyl transferase, the enzyme
responsible for binding bilirubin to glucuronic acid, thus making
bilirubin water soluble (conjugation).

Bilirubin is produced in the reticuloendothelial system as the end

product of heme catabolism and is formed through oxidation-reduction
reactions. Approximately 75% of bilirubin is derived from hemoglobin,
but degradation of myoglobin, cytochromes, and catalase also
contributes. In the first oxidation step, biliverdin is formed from heme
through the action of heme oxygenase, the rate-limiting step in the
process, releasing iron and carbon monoxide. The iron is conserved for
reuse, whereas carbon monoxide is excreted through the lungs and can
be measured in the patient's breath to quantify bilirubin production.
Next, water-soluble biliverdin is reduced to bilirubin, which,
because of the intramolecular hydrogen bonds, is almost insoluble in
water in its most common isomeric form (bilirubin IXα Z,Z). Because of
its hydrophobic nature, unconjugated bilirubin is transported in the
plasma tightly bound to albumin. Binding to other proteins and
erythrocytes also occurs, but the physiologic role is probably limited.
Binding of bilirubin to albumin increases postnatally with age and is
reduced in infants who are ill.
The presence of endogenous and exogenous binding competitors,
such as certain drugs, also decreases the binding affinity of albumin for
bilirubin. A minute fraction of unconjugated bilirubin in serum is not
bound to albumin. This free bilirubin is able to cross lipid-containing
membranes, including the blood-brain barrier, leading to neurotoxicity.
In fetal life, free bilirubin crosses the placenta, possibly by a carrier-
mediated process, and excretion of bilirubin from the fetus occurs
primarily through the maternal organism.
When it reaches the liver, bilirubin is transported into liver cells,
where it binds to ligandin. Uptake of bilirubin into hepatocytes increases
with increasing ligandin concentrations. Ligandin concentrations are low
at birth but rapidly increase over the first few weeks of life. Ligandin
concentrations may be increased by the administration of pharmacologic
agents such as phenobarbital.
Bilirubin is bound to glucuronic acid (conjugated) in the
hepatocyte endoplasmic reticulum in a reaction catalyzed by uridine
diphosphoglucuronyltransferase (UDPGT). Monoconjugates are formed
first and predominate in the newborn. Diconjugates appear to be formed
at the cell membrane and may require the presence of the UDPGT
tetramer.
Bilirubin conjugation is biologically critical because it transforms
a water-insoluble bilirubin molecule into a water-soluble molecule.
Water-solubility allows conjugated bilirubin to be excreted into bile.
UDPGT activity is low at birth but increases to adult values by age 4-8
weeks. In addition, certain drugs (phenobarbital, dexamethasone,
clofibrate) can be administered to increase UDPGT activity.
Once excreted into bile and transferred to the intestines, bilirubin
is eventually reduced to colorless tetrapyrroles by microbes in the colon.
However, some deconjugation occurs in the proximal small intestine
through the action of B-glucuronidases located in the brush border. This
unconjugated bilirubin can be reabsorbed into the circulation, increasing
the total plasma bilirubin pool. This cycle of uptake, conjugation,
excretion, deconjugation, and reabsorption is termed 'enterohepatic
circulation'. The process may be extensive in the neonate, partly because
nutrient intake is limited in the first days of life, prolonging the intestinal
transit time.
Certain factors present in the breast milk of some mothers may
also contribute to increased enterohepatic circulation of bilirubin (breast
milk jaundice). β-glucuronidase may play a role by uncoupling bilirubin
from its binding to glucuronic acid, thus making it available for
reabsorption. Data suggest that the risk of breast milk jaundice is
significantly increased in infants who have genetic polymorphisms in the
coding sequences of the UDPGT1A1 or OATP2 genes. Although the
mechanism that causes this phenomenon is not yet agreed on, evidence
suggests that supplementation with certain breast milk substitutes may
reduce the degree of breast milk jaundice.
Neonatal jaundice, although a normal transitional phenomenon in
most infants, can occasionally become more pronounced. Blood group
incompatibilities (eg, Rh, ABO) may increase bilirubin production
through increased hemolysis. Historically, Rh isoimmunization was an
important cause of severe jaundice, often resulting in the development of
kernicterus. Although this condition has become relatively rare in
industrialized countries following the use of Rh prophylaxis in Rh-
negative women, Rh isoimmunization remains common in low- and
middle-income countries (LMICs).
DEVELOPMENTAL AND PHYSIOLOGIC IMMATURITY OF A
BABY LOW BIRTH WEIGHT
Late-preterm infants are physiologically and metabolically
immature. As a consequence, late-preterm infants are at higher risk than
are term infants of developing medical complications that result in higher
rates of mortality and morbidity during the birth hospitalization.
Jaundice and hyperbilirubinemia occur more commonly and are
more prolonged among late-preterm infants than term infants, because
late-preterm infants have delayed maturation and a lower concentration
of uridine diphosphoglucuronate glucuronosyltransferase. Late-preterm
infants are 2 times more likely than term infants to have significantly
 elevated bilirubin concentrations and higher concentrations 5 and 7 days
after birth.
Late-preterm infants also have immature gastrointestinal function
and feeding difficulties that predispose them to an increase in
enterohepatic circulation, decreased stool frequency, dehydration, and
hyperbilirubinemia. Feeding during the birth hospitalization may be
transiently successful but not sustained after discharge. Feeding
difficulties in late-preterm infants that are associated with relatively low
oromotor tone, function, and neural maturation also predispose these
infants to dehydration and hyperbilirubinemia.
4) Is there any correlation between hyperemesis gravidarum and the
termination?
A. Hyperemesis gravidarum
Hyperemesis gravidarum is a severe form of nausea and vomiting
which affects one in 200 pregnant mothers. The common clinical features
associated with hyperemesis gravidarum are persistent vomiting,
dehydration, electrolyte imbalance, ketonuria, and weight loss of more
than 5% of the body weight.
Symptoms and Signs of Dehydration in Pregnancy
a. Mild Dehydration
Thirst (not always), slight anxiety, slightly decreased
frequency of urination, slightly increased heart rate.
b. Moderate Dehydration
Severe thirst (not always), dry mouth, decreased frequency
of urination, dark yellow or tea-colored
urine, tiredness, dizziness, headache, nausea, constipation,
increased heart rate, prolonged skin recoil after pinch and release (up
to 2 seconds).
c. Severe Dehydration
Nausea and vomiting, usually in the first trimester (but
sometimes even in the third trimester), are the main causes of severe
dehydration in pregnancy.
Complications of Hyperemesis Gravidarum
Maternal Complications
a. Wernicke’s Encephalopathy
WE is typically identified by the symptom triad of ataxia,
confusion and oculomotor abnormalities. Persistent or prolonged
vomiting, confusion, and unintentional weight loss are red flags
indicating a high risk of WE.
WE develops rapidly when initiated by severe, short-term
thiamin deficiency (TD) in the presence of infection or an event that
rapidly increases thiamin requiremen. Chronic WE associated with
HG occurs subsequent to persistent or recurring mild TD. As HG
condition worsened, advanced WE signs were noted: elevated
transaminase levels, diffuse background slowing on EEG, seizure
activity, and high CSF protein levels. Consistent with the literature,
MRI findings involving the cerebellar and cerebral cortices. Thiamin
is an essential micronutrient only obtained from food or
supplements. TD is prevalent during pregnancy because the body
redirects maternal thiamin to the baby, especially during later
pregnancy, exacerbating maternal TD, and greatly increasing the risk
 of fetal loss and preeclampsia. TD adversely impacts the fetus as
well, increasing the risk of impaired brain development, neuromotor
immaturity, cranial malformations, low birth weight, and IUGR
In the offspring from perinatal thiamine
deficiency, hippocampal volume was reduced by almost a third
due to neural cell death. The neurons that survived were smaller
than normal and misshapen. The hippocampus is critical to memory.
Hippocampal damage in human adults causes all manner of
amnesias and aphasias (speaking and language comprehension
deficits) and is found in neurodegenerative disorders
like Alzheimer’s disease.
The neurons affected most by the thiamine deficiency, the
CA1 neurons, are especially susceptible to oxidative damage and
insult. Thiamine is integral to brain oxidation and so this makes
sense. What we have to remember though, is that in a fully developed
human brain, oxidative damage to the CA1 region is associated
with hippocampal ischemia, limbic encephalitis, status epilepticus,
and transient global amnesia – very serious conditions. To a
developing brain, requiring vast amounts of energy to grow, the
consequences of hippocampal deficits are largely under-recognized
except again in fetal alcohol syndrome.
b. Osmotic Demyelination Syndrome
Patients with hyponatremia present with nausea and
vomiting, headache, short-term memory loss, confusion, lethargy,
fatigue, anorexia, muscle weakness, spasms, seizures, and decreased
consciousness. Because sodium and thiamin are interdependent,
with thiamin involved in nerve impulse conduction, and its uptake
dependent upon sodium, deficiencies in either can cause severe
neurological sequelae.
Central pontine myelinolysis (CPM), or demyelination in the
pons, is induced by slight increases in osmotic pressure attributable
 to electrolyte infusions, especially in the presence of severe
infections, cachexia, and electrolyte imbalances.
Demyelination occurring both within and outside the pons is
termed ODS, and usually associated with significant osmotic shifts.
In this severely malnourished patient, numerous osmotic shifts
occurred due to alternating fluid restriction and rehydration,
diuretics, PN, and electrolyte replacement. TD and cachexia left her
with minimal osmolytes and inadequate amino acids for their
production, thus increasing the probability of demyelination
Fetal complications
The effects of Hyperemesis gravidarum on the fetus are mainly
due to electrolyte imbalances caused by Hyperemesis gravidarum in the
mother. Severe dehydration can affect the baby:
 Oligohydramnios,
The amniotic fluid is essential for the development of
muscles, limbs, lungs, and the digestive system. In the
second trimester, the baby begins to breathe and swallow the fluid to
help their lungs grow and mature. The amniotic fluid also helps the
baby develop muscles and limbs by providing plenty of room to
move around. Oligohydramnion can cause that the baby lies directly
on the uterus can lead to arm and leg deformities or other birth
defects.
 Premature Birth
Dehydration can lead to an irritable uterus, which means
contractions are much more painful. It can also trigger contractions
due to more concentrated blood volume, which then leads to a
buildup of oxytocin, which is a hormone that helps trigger
contractions. If all of this happens too early, the baby is at a higher
risk of premature birth.
B. Termination pregnancy
 Termination of pregnancy is the termination of pregnancy to
delivery, both the fetus alive or dead. Efforts termination of pregnancy
consists of:
a. Induction of labor
Induction of labor is a process utilizing a variety of chemicals
and mechanical methods to start uterine contractions before the
spontaneous onset of labor with the goal of achieving a successful
birth, or it can also be interpreted as the initiation of labor
artificially after the fetus is viable.
Induction is indicated only for patients whose health or the
health of her fetus at risk if the pregnancy continues. Induction of
labor may be necessary to save the fetus from intra-uterine
environment that is potentially harmful to the pregnancy for
whatever reason, or due to the continuation of pregnancy endangers
the mother
b. Induced abortion
Induced abortion is medically or surgical termination of
pregnancy before the fetus is viable (capable of living).

5) How to diagnose and interpretation based on the scenario?

 Interpretation based on the scenario
Neonatus terminated in 8 months gestational age, with weight 1600
gram, based on Lubchenco LO, and Searls DT curved. It’s indicate that
the baby is moderately preterm, appropriate for gestational age.
 How to dignose
Anamnesis
 Data identification : 3 days old baby boy, terminated in 8 months
gestational age, birth weight was 1600 gram
 Main complaint : look yellow on the face and body
 History complaint
 Antepartum history : severe hyperemesis gravidarum
 Obstetric history
 Intrapartum history
 Maternal disease history, family and social environment.
Physical examination
Inspection
 Skin Colour
 Breathing (frequency, retraction of the chest wall, chest movement)
 Note the edema / swelling as a result of birth trauma (caput
succadenum, cephal hematome)
 Abnormalities in the spine and extremities
 Pay attension on eye disorders, ear, umbilicus, anus
 Activity / movement
Auscultation
  Grunting
 Cry
 Heart sound
Palpation
 Palpate if there’s a Caput or cephalhematoma
 pulsation a.femoralis
 Capillary refill time (CRT)
 Lymph gland, abdominal, testis in baby boy
Additional examination
 Total serum bilirubin level >18 mg/dl
 Conjugated bilirubin level >2 mg/dl
6) How is the first line management based on the scenario?
Assessment

Colour
Monitor all babies for jaundice development by assessing them
whenever vital signs are measured or at least every 8 to 12 hours. Always
assess jaundice in a well-lit room or in daylight at a window by blanching
the baby’s skin with a finger and observing the underlying skin colour.
Jaundice appears first in the face and progresses caudally to the trunk and
extremities. Kramer recognised the cephalocaudal progression of jaundice
with increasing total serum bilirubin levels and divided the baby into 5
zones, with a total serum bilirubin level measurement associated with each
zone. This is known as Kramer’s rule (see Figure 1) and has traditionally
been used to visually assess the severity of jaundice.

Transcutaneous bilirubin level

Bilirubin levels can also be measured transcutaneously,1 by a
transcutaneous bilirubinometer. Available devices differ in accuracy, safe
use of this device requires knowledge of the accuracy of the particular
device being used. If a transcutaneous bilirubin level is approaching the
threshold for phototherapy (greater than 200 micromoles/L) then a total
serum bilirubin level measurement is recommended.
 USING PHOTOTHERAPY EFFECTIVELY IN THE LBW INFANT
Given that the mainstay of treatment for neonatal jaundice in
preterm infants is phototherapy, we review aspects of this treatment that
influence its effectiveness. Light source and dose. We use phototherapy in
the NICU at quite low TSB levels, to prevent the TSB from rising to a level
where exchange transfusion may be necessary. Like any therapeutic agent,
phototherapy should be administered in an adequate dose, and this can be
estimated quite easily using a radiometer obtained from the manufacturer of
the phototherapy device.

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