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LONG CASE REPORT
Preterm Baby, Low Birth Weight Baby with Respiratory Distress

Syndrome Grade I, Early-Onset Sepsis, Apnea of Prematurity,
Hyperbilirubinemia of Prematurity, and Feeding Intolerance Neonatal
Jaundice, Small Patent Ductus Arteriosus, and Feeding Intolerance
Kartika Sari WiduriResita Sehati
National Board Examination

SemarangJakarta, August 11th-12May 5th-6tth, 2018
INDONESIAN CHILD HEALTH COLLEGE
TIMELINE DIAGRAM
Mayrch 2823thrd, 2018 May 24th, 2018 April 12thJune 6th,

March 29th, 2018 2018 2018
Initial observation Reporting

Patient was born
by the candidate
in X Hospital
1
PATIENT’S STATUS FOR NATIONAL BOARD EXAMINATION
Augist 11th-12MayFebruary 611thst, 2018
Candidate: Resita SehatiKartika Sari WiduriEllen Wijaya
Identity
Patient’s name : Baby Mrs. NL Father’s name : Mr. RA

Gender : FemMale Father’s age : 1837 years old
Chronological age : 1 day Father’s education : JuSenior high school
trdh
Birth date : May 23March 28 ,2018 Father’s occupation :
Entrepreneurmployee
Hospital admission : May 23rd,2018March 29th,2018 Mother’s name : Mrs. NL
Mother’s age : 3619 years old
Mother’s education : JunioSenior high school
Mother’s occupation : Housewife
Initial observation by candidate from Mayrch 2490th,2018

Source of Information: parents and medical record
Chief Complaint
Premature baby with respiratory distress followingsince birth.
History of Present Illness

The patient was born preterm at 323 weeks age of gestation (AOG) by Ccesarean section
(C-section) from a G13P01A01 mother due oligohydramnion (amniotic fluid index/AFI 4) and
preterm premature rupture of membranes (PROM). to preterm contractions and breech
presentation. ShHe was born at X Hospital on Mayrch 238trdh,2018 at 05.158.40 APM with an
Apgar score (A/S) of 56 at the first minute and 87 at fifth minutes. Hiser birth weight (BW)
was 15580 gram (g), birth length (BL) was 4038 cm and head circumference (HC) was 29
cm. Maternal risk factors include preterm PROM for 3 days, leucocytosis (17.2407.400/µL),
urinary tract infection, and flour albus without foul smelling and itchiness. There was no
(suspected bacterial vaginosis) without signs of chorioamnionitis..
T The mother was referred from a private practice midwife nearby her house due to preterm
PROM for 3 days. a nearby primary health center because preterm contractions. At X hospital,
the mother had uterine contraction anda cardiotocography (CTG) ) examination which
revealed no sign of fetal distress. The ultrasound (US) examination revealed low amniotic
fluid index (AFI) 4 score, which was considered oligohydramnion, butThere was no fetus
congenital abnormalitiesy seen. from ultrasound. The mother was hospitalized After the
parents received explanation about the pregnancy’s condition, the emergency C-section was
performed. 2 days pPrior to C-section the mother delivery and got the antibiotic ampicillin-
sulbactam and one shot steroid (dexamethasone) injections. administration of tocolytic agents
as well as a complete course of steroid injection for fetal lung maturation.
At birth, there was inadequate volume of amniotic fluid, clear colorgreenish and non-foul
smelling. The neonateHe did not cried slowly with some flexion of the extremities and
acrocyanotic. Her muscle tone was normal with heart rate (HR) more than 100 beats per minute
(bpm), but she grimaced when stimulated. There were no signs of respiratory distress.y She was
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brought to the infant warmer, covered with transparent plastic sheet, and a hat was put on. The
patient was properly positioned, stimulated, and simultaneously assessed (vital signs). On
evaluation, her respiratory rate (RR) was 60 cycles per minute (cpm) without nasal flaring nor
epigastric-intercostal retractions. Oxygen (O2) saturation on the right hand was 68%, HR was
140 bpm with temperature of 36,5OC.
and there was no respiratory effort. His muscle tone was weak, heart rate (HR) was less than
100 beats per minute (bpm). He was brought to the infant warmer, covered with transparent
plastic sheet, put on a hat, positioned, stimulated. There was still no respiratory effort and HR
was less than 100 bpm, positive pressure ventilation (PPV) was given with peak inspiratory
pressure (PIP) of 25 cmH2O, positive end expiratory pressure (PEEP) of 5 cmH 2O, and 30% of
fraction of inspired oxygen (FiO2). At 30 seconds of life, there was still no respiratory effort and
HR was less than 100 bpm. The PPV was continued, patient was checked for the body
temperature and the peripheral oxygen (O2) saturation on the right hand. Positive pressure
ventilation was continued, PIP increased to 30 cmH2O while PEEP was maintained at 5 cmH2O.
At fifthrst minute of life, there were nasal flaring, intercostal retraction and grunting. The
respiratory rate was 70 cpm, O2 saturation 78%, and HR 160 bpm. Patient was subsequently
treated with continous positive airway pressure (CPAP) with positive end-expiratory pressure
(PEEP) 7 mmH2O and 21% of fraction inspired oxygen (FiO 2). The respiratory distress was
improving, with RR 54 cpm, HR 140 bpm, and O2 saturation of 88-90%. In the post-resuscitation
care, random blood glucose (RBG) of the patient was 113 mg/dL, no temperature instability,
and capillary refill time (CRT) was shorter than 3 seconds. Vitamin K1 0.5 mg intramuscular (IM)
injection and oxytetracycline 1% eye ointment were being given. The patient was transported
with transport incubator and admitted to special care for neonatus (SCN) with CPAP.
HR was 120 bpm and there was slight breathing effort. His respiratory rate (RR) was 65 cycles
per minute (cpm), with nasal flaring and epigastric-intercostal retractions. Oxygen (O2)
saturation on the right hand was 55%. Patient was subsequently treated with continuous
positive airway pressure (CPAP) with positive end-expiratory pressure (PEEP) of 7 mmH2O and
30% of fraction of inspired oxygen (FiO2). At
the second minute of life, the patient’s condition did not completely improve with RR at 70 cpm,
retractions, O2 saturation 60% and HR 160 bpm. He was not crying vigorously, the arms and
legs were slightly flexed, grimaced when stimulated and cyanotic. Thus, the PEEP was increased
to 8 mmH2O and the FiO2 was gradually increased to 40%. At fifth minute, he still had retraction
with RR at 65 cpm, O2 saturation was 75%. Finally, patient was treated with non-invasive
positive pressure ventilation (NIPPV) with peak inspiratory pressure (PIP) of 20 mmH2O, PEEP
of 5 mmH2O, RR of 40 cpm and FiO2 of 30%. He cried and grimaced when stimulated with RR of
60 cpm, HR of 160 bpm, O2 saturation of 88% and cyanosis was seen only at her extremities. In
the post-resuscitation care, random blood glucose (RBG) of the patient was 56 mg/dL, no
instability of temperature and capillary refill time (CRT) was less than 3 seconds. Vitamin K1 0.5
mg intramuscular (IM) injection and oxytetracycline 1% eye ointment were given right after
resuscitation. The patient was transported with transport incubator and admitted to neonatal
intensive care unit (NICU).
On physical examination, patient had active and symmetrical movement. New Ballard
score was appropriate for 323 weeks AOG. There was no head deformity and the anterior
fontanelle was opened and flat. Hiser heart, abdomen and back were all within normal
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limits. There were nNo chest retractions, rales nor wheezing were found on lungs
auscultation, peripheral O2 saturation was steady at greater than 9290%. Hiser urogenital
was normal with anal and female genital appearance. Blood gas analysis (BGA), septic
work-up and chest radiography were evaluated. The diagnosis of the patient were
preterm baby, 323 weeks AOGage of gestation with BW of 15580 g, appropriate for
gestational age (AGA), low birth weight (LBW), respiratory distress syndrome (RDS) and
early onset sepsis (EOS). TheHis parents were informed regarding their baby’s condition
and heris management plan.
The patient was placed on incubator, ordered for nothing per oral (NPO), decompression
orogastric tube (OGT) was being placed, and she was being given total parenteral nutrition
(TPN) which contained dextrose 10% with glucose infusion rate (GIR) of 5,6
mg/kg/minute, protein of 2 g/kg/day, lipid of 1 g/kg/day, and electrolytes [potassium (K),
calcium (Ca) and magnesium (Mg)] with total calories of 34 kcal/kg/day, protein of 2.5
g/kg/day, lipid of 1 g/kg/day, and electrolytes [potassium (K), calcium (Ca) and magnesium
(Mg)] with and total fluid 80 mL/kgBW/day. Ventilation was supported by NIPPV with PIP 20,
PEEP of 5 mmH2O, RR of 40 cpm, and FiO2 of 30%. . First line antibiotics which consisted of
ampicillin 75 mg IV every 12 hours (50 mg/kgBW/dose every 12 hours) and gentamicin
7.5 mg IV every 36 hours (5 mg/kgBW/dose every 36 hours) were given. Ventilation was
supported by CPAP with PEEO of 7 mmH2O, and FiO2 of 21%. Nystatin 100.000 IU/mL per oral
(po) was also given to prevent fungal colonization (1 mL every 8 hours). The patient already
urinated within the first 12 hours of life, but not yet defecated. Laboratory examination for
complete blood count (CBC), immature:total (I/T) ratio, C-reactive protein (CRP) and blood
culture was performed. At 12th hour, patient started to get oral care with donor human milk
along with TPN via peripherally central line catheter (PICC).
At first day at SCN, there was no episode of temperature instability, the respiration gradually
improved and oxygen therapy was ceased. Chest radiograpy reticulogranular pattern in both
lung field.
At first day at NICU patient had two episodes of apnea, aminophylline was given 9.5 mg (loading
dose 6 mg/kgBW and gave maintainance dose 2.5 mg/kgBW every 12 hours) to treat apnea of
prematurity (AOP). His respiration gradually improved, the PIP and FiO2 of NIPPV could be
weaned to 15 mmH2O and 21%, with RR 30 cpm respectively. Patient also started to get oral
care with human milk and administer TPN via peripherally central line catheter (PICC).
Gestational History
Patient is the only child in the family. Mother’s menstruation period was regular. Her pregnancy
was actually unwell planned. She had no routine antenatal care (ANC)during pregnany (4 times)
at nearby primary health care. There was no history of fever, rash and itchiness. She never
smoked, drank herbs, nor took any specific medication during the pregnancy except for vitamins
prescribed by her physician. Nutritional intake throughout pregnancy was inadequate in
quantity and quality. She gained 8 kg during the pregnancy, her body weight at labor was 50 kg
and her height was 155 cm.
Patient is the second child in the family. There was history of abortus and preterm delivery in
the pass pregnancy. Mother’s menstruation period was irregular and she often forgot to take her
contraceptive pills. Mother had no routinely antenatal care (ANC) at nearby primary health care.
There was no history of fever, rash and itchy. She never smoked, drank herbs, nor took any
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specific medication during the pregnancy except for vitamins prescribed by her physician.
Nutritional intake throughout pregnancy was inadequate in quantity and quality. She gained 5
kg during the pregnancy, her body weight at labor was 56 kg and her height was 155 cm.
Two days prior to delivery, she was referred from a nearby primary health care to X hospital due
to contractions. No history of sexual intercourse. She was hospitalized to get tocolytic agents and
fetal lung maturation. Blood work up revealed anemia (Hb 10.5 g/dL), leucocytosis (17.400/µL)
and her urinalysis result was consistent with urinary tract infection. She had been given an
antibiotics broad spectrum since the admission. Her blood type was O+ and her hepatitis B
surface antigen (HbsAg) was negative. The family had been educated about the condition of
their baby. Three days prior to delivery, she felt constant leaking fluid which at first was thought
as urine leakage. She did not seek for medical advice. Third day after complaint of fluid leakage,
she felt uterine contraction and went to the nearest midwife. Blood work up revealed no anemia
with leucocytosis (17,240/µL) and normal urinalysis result. She had been given injection of
broad spectrum antibiotics since the admission. Her blood type was B+ and her hepatitis B
surface antigen (HbsAg) was negative. The family had been educated about the condition of
their baby.
Impression: mother with preterm labor and infection caused by premature PROM., history
of abortus and preterm delivery in pass pregnancy, irregular ANC, urinary tract infection,
anemia, and leucocytosis.
Family History
NoThere was history of previous preterm labor and abortus, no history of hypertension,
atopy, nor diabetes mellitus. No history of neonatal jaundice in siblings nor jaundice
particularly after consuming drugs.
Impression: no significant family history.
family history of preterm labor and abortus.
Nutritional History
Patient was orderred on NPO since birth and she was being given TPN.
Growth and Development History

Growth
The patient was born with BW of 1.5850 g and BL of 4038 cm. At chronological age of 1
day old, anthropometric measurements were status quo.
Impression: premature, appropriate for gestational age, low birth weight baby, but
increment in body weight and height were not expected in the first day of life.
Development
Not possible to be evaluated yet.
Impression: development can not be evaluated at this point of time.
Immunization History
The patient was not being given any immunization since birth. Hepatitis B vaccine can not
be administered to this patient since her weight has not reached 2..000 g.
Impression: no immunization given yet.
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Socioeconomic and Environmental History
 Patient’s father and mother age are 18 and 19 years old, respectively. They are both of
Javanese descent and Moslems. The father works as a entrepreneur with average income of
2.000.000 IDR per month. Mother is a housewife. Patient is the first child in the family. The
patient’s health expenses is covered by government through Badan Penyelenggara Jaminan
Sosial (BPJS).
 The parents live in a crowded area. A total of 4 persons live in the rental house with spacious
10x5m2. It has a kitchen area, with place of dish washer and bathroom in same area. The
tiles are made from ceramics and it had permanent roof with brick walls. Ventilation and
sanitation are inadequate. Clean water source is available from a soil water with fair quality,
drinking water supply is using mineral water and power supply is provided from
Perusahaan Listrik Negara (PLN). Midwives and local primary health care are easily
accessed (less than 30 minutes) by motorcycle. Other public facilities such as mosque and
school are available nearby. Relationship with neighbours are close.
 Patient’s father and mother age are 37 and 36 years old, respectively. They are both of
Javanese descent and Moslems. The father works as a private employee with average income
of 4.000.000 IDR per month. Mother is a housewife. The patient’s has 1 brother and now in
health condition. His brother is already 7 years old. The patient’s health expenses is covered
by government through Badan Penyelenggara Jaminan Sosial (BPJS).
 The parents live in a crowded area. A total of 4 persons live in the rental house with spacious
7x5m2. It has a kitchen area, with place of dish washer and bathroom in same area. The tiles
are made from ceramics and it had permanent roof with brick walls. Ventilation and
sanitation are inadequate. Clean water source is available from a ground water with fair
quality, drinking water supply is using mineral water and power supply is provided from
Perusahaan Listrik Negara (PLN). Midwives and local primary health care are easily
accessed (less than 20 minutes) by motorcycle. Other public facilities such as mosque and
school are available nearby. Relationship with neighbours are close.
Impression: patient’s family is considered of low socioeconomic class that lived in a
crowded environment. Primary health care is easily accessed and health expenses are
covered by the government.
Impression: patient’s family is considered teenage couple with low socioeconomic status
who lived in a crowded environment. Primary health care is easily accessed and health
expenses are covered by the government.
PHYSICAL EXAMINATION (NICU, March 29th, 2018)(SCN 4, May 23rd, 2018)
General survey: alert, moderately ill looking, quite active, no respiratory efforts.
Vital Signs
No signs of cardiorespiratory distress
HR : 130-155 bpm, regular, adequate pulses
RR : 50 cpm, regular, good chest rise, no intercostal, no epigastrium retraction
Temperature : 36.8oC (axillary)
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O2 saturation : 98% supported with NIPPV PIP 15/PEEP 5 mmH2O, RR 30 cpm, FiO2 21%
RR : 50 cpm, regular, adequate chest rise, no intercostal nor epigastrium retraction
Temperature : 36,7oC (axillary)
O2saturation : 92-95% supported with CPAP PEEP 7 cmH2O and FiO2 21%
Anthropometrics status
BW = 1580 g (P25-50 Lubchenco’s curve)
BL = 38 cm (P10-25 Lubchenco’s curve)
HC = 29 cm (P25-50 Lubchenco’s curve)BW =1.550 g (P50-90Lubchenco’s curve)
BL = 40 cm (P50-90Lubchenco’s curve)
HC = 29 cm (P50-90Lubchenco’s curve)
Impression: appropriate for gestational age.
System Description
Skin Reddish and smooth skin, veins were seen. No jaundice, no cyanosis. N,
no meconium stain. No petechiae nor any skin lesion.
Head No cephalhematoma, caput succedaneum nor other deformity, open and flat
anterior fontanelle, 2.5 x 3 cm size. Head circumference was 29 cm
(normocephalic).No cephalhematoma, caput succedaneum nor other
deformity, open and flat anterior fontanelle, 2.5 x 2 cm size. HC was 29 cm
(normocephalic)
Hair Black, abundant lanugo was seen.
Face Symmetric, no dysmorphic, no cranial nerve paralysis seen.
Eyes Pink palpebral conjunctivae, anicteric sclerae, round and isochoric pupils,
diameter 3 mm/3 mm, reactive to light, good eye movements to all directions.
Nose No nasal flaring, no mucus secretion, septum in midline position, no anomaly
seen.
Ears Well curved pinna, soft but ready recoil, no deformity was seen. Tympanic
membranes were difficult to assess.
Mouth No cyanosis was seen, moist buccal mucosa. Inadequate sucking reflex and
rooting reflex.
Hair Black, abundant lanugo was seen.
Face Symmetric, no dysmorphic, no cranial nerve paralysis seen.
Eyes Pink palpebral conjunctivae, anicteric sclerae, round and isochoric pupils,
diameter 3 mm/3 mm, reactive to light, good eye movements to all directions.
Nose No nasal flaring, no mucus secretion, septum in midline position, no anomaly
seen.
Ears Well curved pinna, soft but less recoil, no deformity was seen. Tympanic
membranes were difficult to assess.
Mouth No cyanosis was seen, moist buccal mucosa. Inadequate sucking reflex and
rooting reflex.
Neck No palpable neck mass.
Chest Symmetrical chest expansion, no intercostal retraction. Barely perceptible
areola, no bud.
Lungs Vesicular breath sounds, no rhales, no wheezing.
Heart Distinct S1 and S2 heart sound, no murmur, no gallop.
Abdomen Flat, supple, normoactive bowel sounds, hepar just palpable.
Abdominal circumeference (AC): 23 cm.
Back No sacral dimple, no hair bundle.
Genital area Prominent clitoris, bulging labia minora.
Anus No deformity, anal hole seen
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Extremities Pulses were full and equal, no edema no cyanosis, CRT less than 2 seconds.
Anterior-transverse crease was seen only on the plantar surface. Normal
muscles tone, no paralysis, and normal physiologic reflexes in all extremities.
Positive babinsky bilateral. Positive moro reflex. Positive palmar and plantar
grasp reflexes
Lymph nodes No enlargement.
Lungs Vesicular breath sounds, no rhales or wheezing.
Heart Normal S1 and S2, no murmur, no gallop.
Abdomen Flat, supple, normoactive bowel sounds, hepar just palpable. Abdominal
circumeference (AC): 25 cm
Back No sacral dimple nor hair bundle
Genital area Grossly male, palpable testes in the upper canal, with rare rugae seen at the
scrotal area.
Anus No deformity, anal hole seen
Extremities Pulses full and equal, no edema, no cyanosis, CRT less than 2 seconds. Normal
muscles tone, no paralysis and normal physiologic reflexes in all extremities.
Positive babinsky bilateral. Positive moro reflex. Positive palmar and plantar
grasp reflexes
Lymph nodes No enlargement.
DIAGNOSTICS
Laboratory Examination
May 23rd , 2018
Normal value
(age of 6 hours)
Hemoglobin (g/dL) 17.5 14.5 – 24
Hematocrite (%) 51.6 41 – 70
Red blood cell count 4.61 3.0 - 5.4 x 106
MCV (fL) 111.9 99 – 105
MCH (pg) 38.0 33 – 39
MCHC (g/dL) 33.9 32 – 36
WBC (/µL) 17,080 9,100–34,000
Basofil 0.4 0-1
Eosinofil 0.9 1-3
Neutrofil 64.8 52-76
Limfosit 19.3 20-40
Monosit 14.6 2-8
Platelet (/µL) 261,000 150,000–400,000
C-reactive protein (mg/L) 0.2 <0.6
I:T ratio 0.12 <0.20
Albumin 3.11
Blood culture No result yet
Impression: normal infection marker
Laboratory Examination
March 28th, 2018
Normal value
(age of 12 hours)
Hemoglobin (g/dL) 15.5 15 - 24
Hematocrite (%) 45.9 44 - 70
8
Red blood cell count 4.58 3.0 x 106 – 5.4 x 106
MCV (fL) 100.2 99 - 115
MCH (pg) 33.8 33 - 39
MCHC (g/dL) 33.8 32 - 36
WBC (/µL) 9.750 9.100–34.000
Platelet (/µL) 245.000 150.000–400.000
I :T ratio 0.05 <0.20
May 23rd , 2018March

Capillary blood gas Normal value
28th, 2018
pH 7.454 7.25 - 7.45
pCO2 (mmHg) 41,68.3 35 - 60
pO2 (mmHg) 40,937.3 60 - 80
SO2 (%) 78,05.3 92 - 94
BE (mmol/L) +4,31.9 -2 - +2
HCO3- (mmol/L) 28,64.9 22 - 26
Impression: normal BGA (on CPAP PEEP 7 mmH2O FiO2 21%) (on NIPPV PIP 20/PEEP 5
mmH2O, RR 30 cpm, and FiO2 21%)
Chest radiography (May 23rd, 2018March 28th, 2018):

Reticulogranular pattern on both lung fields. Heart within normal limit.
Impression: consistent with respiratory distress syndrome grade I.
SUMMARY
The patient was born on May 23rd, 2018, 5.15 am at X Hospital from a G1P0A0 mother via C-
section due to oligohydramnion and PROM. She was 33 weeks AOG, with A/S 6 at the first
minute and 8 at the fifth minute. Her birth weight was 1.550 g, birth lenght was 40 cm and HC
was 29 cm. Maternal risk factors include PROM for 3 days, leucocytosis (17,240/µL), and flour
albus without foul smelling and itchiness. There was no sign of chorioamnionitis. The mother
had been given one shot antenatal corticosteroid, and broad spectrum antibiotic at the delivery
day.
The patient was born on March 28th, 2018, 8.40 pm at X Hospital from a G3P1A1mother via
cesarean due to preterm contractions and breech presentation. He was 32 weeks age of
gestation, with Apgar score of 5 at the first minute and 7 at the fifth minute. His birth weight was
1580 g, birth lenght was 38 cm and head circumference was 29 cm. Maternal risk factors of
infections were urinary tract infection, bacterial vaginosis, anemia and leukocytosis of
17.400/uL without signs of chorioamnionitis. The mother had given antitocolytic, antenatal
corticosteroid and broad spectrum antibiotic from two days prior to delivery.
At birth, amniotic fluid volume was sufficient, clear and non-foul smelling odour. He did not cry
and there was no respiratory effort. His muscle tone was weak, HR was less than 100 bpm.
Patient was subsequently treated with PPV with peak PIP 25-30 cmH2O, PEEP 5 cmH2O, and FiO2
30% for 60 seconds. After being supported by PPV, the condition was improved, HR was 120
bpm and there was slight breathing effort with nasal flaring and epigastric-intercostal
retractions. Patient was subsequently treated with CPAP PEEP of 7 mmH2O and 30% of FiO2, but
the condition was not completely improved even after being supported with PEEP 8 mmH2O and
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the FiO2 that had been increased to 40%. After supported with NIPPV PIP 20 and PEEP 5
mmH2O, RR 40 cpm, and FiO2 30% she could cry and grimace. At the post-resuscitation care, his
RBG was 56 mg/dL, and CRT was less than 3 seconds. Other physical examinations were within
normal limits. Ballard score was consistent with 32 weeks of gestational age. amniotic fluid
volume was insufficient, greenish with foul smelling odour. The neonate cried slowly with some
flexion of the extremities There were no cyanosis and respiratory distress at the beginning. At
fifth minute of life, there were nasal flaring, intercostal retraction and grunting. The respiratory
rate was 70 cpm, O2 saturation 68%, and HR 140 bpm. Patient was subsequently treated with
CPAP with PEEP 7 mmH2O and 21% of FiO2. The respiratory distress was improving, At the post-
resuscitation care, his RBG was 113 mg/dL, and CRT was less than 3 seconds. Other physical
examinations were within normal limits. New Ballard score was consistent with 33 weeks of
gestational age.
During observation, patient started to get oral care with donor human milk along with
administration of TPN via PICC. There was no episode of temperature instability, the respiration
gradually improved and the oxygen therapy was ceased. Laboratory work up revealed normal
result while chest radiograph showed bilateral reticulogranular pattern. Patient was diagnosed
as preterm, AGA, LBW, with RDS, and EOS. She was ordered NPO, given TPN, and antibiotics.
During observation, patient had two episodes of apnea, but his respiratory distress improved
with PIP and FiO2 of NIPPV gradually decreased. Laboratory work up revealed no anemia, no
elevation of infection markers level, while chest radiograph was consistent with RDS grade I.
Patient was diagnosed as preterm, AGA, LBW, with RDS, EOS and AOP. He was ordered NPO,
given TPN, antibiotics, aminophylline and antifungal prophylaxis.
LIST OF PROBLEMS
1. Prematurity with low birth weight
2. Respiratory distress syndrome grade I
3. Early onset sepsis
4.
5. Apnea of prematurity
6. Low socioeconomic status
7. Infant with teenage parents
WORKING DIAGNOSIS
1. Preterm baby (33 weeks), appropriate for gestational age (AGA) P 07.3
with low birth weight (1550 g) P07.1
2. Respiratory distress syndrome grade I P 22.0
3. Early onset sepsis P
36.9Preterm baby (32 weeks), appropriate for gestational age (AGA) P 07.3
with extremely low birth weight (980 g) P 07.1
Respiratory distress syndrome grade I P 22.0
Early onset sepsis P 36.9
Apnea of prematurity P 28.4
MANAGEMENT
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1. Preterm baby, AGA, LBW
 Diagnostics:
o Screening of high-risk baby morbidities, such as retinopathy of prematurity
(ROP) screening, hearing screening, anemia, osteopenia of prematurity,
congenital heart disease, evaluation of check TSH level after 48 hours
 Therapeutics:
o Patient maintained inside the incubator for thermoregulation with body
temperature target between 36.5 - 37.5 °C.
o Oral care 8 x 0.1 mL, continued with trophic feeding 8 x 1 mL/OGT after 12 hours; as
soon as the baby was stable.
o Total fluid 80 mL/kg/day, given parenterally [GIR 5.6 mg/kg/minute, protein 2
g/kg/day, lipid 1 g/kg/day, and electrolytes (K, Ca, Mg)] with total calories of 34
kcal/kg/day
o Hospital admission until patient was capable to fulfil her basic needs (breathing
without support, enteral full feed and maintain her body temperature) and body
weight target of ≥1.800 g.
o Patient maintained inside the incubator for thermoregulation with body
temperature target between 36.5 - 37.5 °C.
o Oral care 8 x 0.1 mL, continued with enteral feeding 8 x 3 mL/OGT (~15 mL/kg/day)
after 24 hours; as soon as the baby was stable.
o Total fluid 80 mL/kg/day, given parenterally [GIR 6 mg/kg/minute, protein 2.5
g/kg/day, lipid 1 g/kg/day, and electrolytes (K, Ca, Mg)].
o Fungal prophylaxis with nystatin 100.000 IU/mL po, 1 mL every 8 hours.
 Hospital admission until patient was capable to fulfil his basic needs (breathing without
support, enteral full feed and maintain his body temperature) and weight target: ≥1.800
g.
 Monitoring :
o Vital signs every 1 hour.
o Feeding tolerance.
o Weekly evaluation of weight, length and HC.
o
o Serial RBG.
o Cranial ultrasound (cUS), echocardiography.
 Education:
o Morbidityies in very preterm baby to the parents.
o Management plan and requirements for sending home.
o Long-term follow up for growth and developmental care plan and their
importance.
o Motivation and emotional support to the mother and the family regarding
breastfeeding and taking care of premature infants.
2. Respiratory distress syndrome grade I

 Diagnostics:
o Chest radiography evaluation if there was any respiratory function worsening.
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o Serial BGA if necessary.
 Therapeutics:
o NIPPV PIP CPAP PEEP 7 mmH2O and FiO2 21%.15/ PEEP 5 mmH2O, RR 30 cpm and
FiO2 21%.
 Monitoring :
o Work of breathing, O2 saturation target between 88 - 92%.
o HR and RR.
 Education:
o Regarding RDS and the possibility of complications, management, monitoring
and prognosis.
3. Early onset sepsis

 Diagnostics:
o Complete blood count (CBC), C-reactive protein (CRP), immature:total (I:T)
ratio (septic screening) at 4848 hours after administration of antibiotics for
evaluation.
o Blood culture and sensitivity (C/S) follow up.
 Therapeutics:
o Ampicillin IV 75 mg every 12 hours (50 mg/kg/dose) and gentamicin IV 7.5 mg
every 36 hours (5 mg/kg/dose).
 Monitoring:
o Vital signs, work of breathing.
o Feeding tolerance.
 Education:
o Regarding sepsis, the possibility of complication, management, monitoring and
prognosis.
o Prevention of nosocomial infection by implementing five5 moments of hand
hygiene.
4. Apnea of prematurity
 Diagnostics:
o Episodes of apnea, bradycardia.
 Therapeutics:
 Apnea of prematurity treatment with aminophylline 9.5 mg (loading dose 6 mg/kg),
12 hours after loading 4 mg every 12 hours (2.5 mg/kg/dose).
 Monitoring:
o Frequency and duration of apnea
o Vital signs, and peripheral oxygen saturation
 Education:
o Regarding apnea of prematurity, management, monitoring and prognosis.
12
OBSERVATION AND FOLLOW-UP
May 24rch 30 th – 31st, 2018 (day-2-3 hospitalization)

S Baby was active without temperature instability of temperature. No respiratory distress and apnea.
NIPPV CPAP was weaned to CPAP lower PEEP, from 7 become 6 and then 5 respectively with FiO 2 of
21% at age of 29 hours. and maintained at 7 cmH 2O FiO2 21% at age of 48 hours. Patient had
priming with human milk/standard formula (SF) at age of 24 hours, 3 mL every 3 hours with
good tolerance.
Spontaneous meconium was at the age of 36 hours. Normal infection marker at 24 hours of age,
but the patient still needed CPAP for respiratory support, hence the antibiotic therapy was
continued.CPAP could be weaned to 6 cmH2O FiO2 21% at age of 72 hours.
O Patient is awake, active, no pale, no cardiorespiratory distress, no cyanotic.
HR : 140 - 150 bpm, regular, adequate pulses
RR : 50 - 55 cpm, good chest rise, no respiratory effort
Temperature : 36.5-37.3o C
O2 saturation : 95-99% (on CPAP PEEP 65 FiO2 21%.)
BP : was not observed
BP : 67/46-71/54 mmHg
Weight: 1.5580 g Length: 3840 cm HC: 29 cm
Physical examination status quo.
Balance -44,756 until + 25 mL/24 hours Urine output 4.8-5.52,1 mL/kg/hour
Laboratory result:
May 24th, 2018 (24 hours) Normal value
Hemoglobin (g/dL) 13,3 14.5 – 24
Hematocrite (%) 38,5 41 – 70
WBC (/µL) 9.950 9.100 – 34.000
Platelet (/µL) 206.000 150.000 – 400.000
I :T ratio 0.07 <0.20
Impression: normal infection marker in 24 hours of age respiratory alkalosis ( March 30th), normal
blood gas analysis (March 31st)
Cranial ultrasound (May 24th, 2018):

No ventricle enlargement, sign of hemorrhagic, nor focal lesion intra/extra axis
Impression: normal
Blood C/S: 1x24 hours: no growth yet

A 1. Preterm baby (332 weeks), AGA, LBW (15580 g) (P 07.3) (P 07.0) (P 07.1)
2. RDS (P 22.0)
3. EOS (P 36.9)
4. Apnea of prematurity (P 28.4)
P  Thermoregulation, maintain body temperature 36.5°C-37.5°C
 Oxygen therapy : CPAP PEEP 65 mmH2O FiO2 21%
13
 Diet:
Diet Day-2 Information
Total fluid mL/kg/day
9110
= 17540 mL
Enteral:
 Hhuman breast 8 x 3 ml
milk ~ 15 mL/kg/day
~10.2 kcal/kg/day
Parenteral
 dextrose 102,5% mg/kg/min
5,47.3 kcal/kg/day
31,6542
 protein 2.5 g/kg/day
10 kcal/kg/day
 lipid 2 g/kg/day
18 kcal/kg/day
Total of calories kcal/kg/day
59,6580
 Medications:
o Ampicillin IV 75 mg/12 hours, gentamicin IV 7.5 mg/36 hours (day-2-3)
o
o Aminophylline IV 4 mg/12 hours (2.5 mg/kg/dose)
o Nystatin PO 100.000 IU/8 hours
 Further examination:
 radiology: cranial US (day-3)
 Follow up : blood C/S result.
 Monitor :
o General survey and vital signs
o Balance and urine output
o Body weight, length and HC once a week
 Parental education regarding current condition and plan management.

May April 1st - 25nthd, 2018 (day- 34-5 hospitalization)

S Baby was active, no temperature instability. No respiratory distress. CPAP PEEP 5 FiO2 215 could be
weaned to high flow nasal (HFN) 4 lpm. There was an episode of apneu, desaturation, and
bradycardia once. and apnea, CPAP weaned to PEEP 5 FiO2 21%. His skin started to look jaundice
from head to abdomen since ….. hours.The patient vomitted two times when being given enteral
feeding @ 3 mL (15 mL/kg/day) and the abdomen was distended, she then being given nothing per
oral. Enteral feeding was increased 15 mL/kg/day with good tolerance. No vomit or abdomial
distended, and dDefecation frequency was 2-13x/ day. The abdominal x-ray showed sepsis rather
than NEC sign, the patient was planned to get NPO for 3 days afterwards. She got only oral care with
human milk 4x0,5 mL
O2 saturation : 95 – 98 % (CPAP PEEP 5 FiO2 21%)
BP : 68/45-70/48 mmHg
14
Abdomen : distended, minimum bowel sounds, AC 26 cm (↑3 cm) Skin : jaundice from
head to abdomen (Kramer III)
Other Other general physical examination status quo
Balance 33 until -+ 37 mL/24 hours Urine output 4.1 - 4.23,9 mL/kg/hour
Laboratory results:
Nor
April 1st, 2018
al value
Total bilirubin (mg/dL) 6.53 <1.20
Direct bilirubin (mg/dL) 0.66 <0.3
Indirect bilirubin (mg/dL) 5.87 0.30-0.90
Albumin (g/dL) 3.83 2.8-3.4
Blood type O+
Impression: unconjugated hyperbilirubinemia
April 1st, 2018 Normal value

pH 7.45 7.25 - 7.45
pCO2 (mmHg) 46.8 35 - 60
pO2 (mmHg) 50.2 60 - 80
HCO3- (mmol/L) 26 22 - 26
O2 saturation (%) 85.7 92 - 94
BE -2 -2 - +2
CPAP settings CPAP PEEP 5 FiO2 21%
Impression: normal blood gas analysis
Blood C/S: 24x24 hours: no growth yet
Abdominal x-ray (May 25th, 2018)

No reduction of intestinal air, no intestinal dilatation, no visible free-air, no intestinal pneumatosis,
no ascites, positive intestinal wall thickening.
Impression: sepsis
Cranial ultrasound (March 31st, 2018):
No ventricle enlargement, sign of hemorrhagic, or focal lesion intra/extra axis
Impression: normal
2. RDS (improved) (P 22.0)
3. EOS (improved) (P 36.9)
4. Apnea of prematurity (AOP) (P 28.4)
5. Apnea of prematurity (improved) (P 28.4)
6. Hyperbilirubinemia associated preterm delivery dd/sepsis (P 59.0)
P  Thermoregulation, keep body temperature 36.5°C-37.5°C
 Oxygen therapy CPAP PEEP 5 FiO2 21%HFN 4 lpm
 Diet: TPN (included maintainance of electrolyte Na/K/Cl/Mg)
Total fluid 1040 mL/kg/day
= 155221
Enteral:
 human milk 8x6 mLNPO (oral
care) mL/kg/day
kcal/kg/day
15
4x0,5 mL~30
~20
Parenteral
 dextrose 12,5% 8.20 (12,5%) mg/kg/min
467 kcal/kg/day
 protein 3 g/kg/day
12 kcal/kg/day
 lipid g/kg/day
23 kcal/kg/day
1827
Total of calories 7106 kcal/kg/day
 Medications:
o Ampicillin IV 75 mg/12 hours, gentamicin IV 7.5 mg/36 hours (day- 34-5)
o
o Aminophylline IV 4 mg/12 hours (2.5 mg/kg/dose) 10 mg (loading dose 6 mg/kg), 12
hours after loading 4 mg every 12 hours (maintenance dose 2,5 mg/kg/dose).
o
 Phototherapy not indicated
 Further examination: toracoabdominal radiography echocardiography.
 Follow up : blood C/S results.
 Monitor:
o Abdominal circumference and signs of NEC
o t
o Feeding tolerance
o Body weight, length, and HC once a week
May 26April 3rthd -4 th, 2018 (day-4 6-7 hospitalization)

S The baby was quite active. NNo temperature instability nor, episodes of breathing difficulties.
There was an episode of apneu, bradycardia, and desaturation once, HFN used then returnedy,
apnea, nor desaturation. to CPAP PEEP 5 FiO2 21%. No vomit (NPO day-2). weaned to HFN 6 lpm
FiO2 21% and 4 lpm FiO2 21%. Abdominal distention stqa. Neither sign of sepsis nor growth of
bacteria on blood culture so antibiotics were stopped after given for five days. Patient was vomit No
defecation. Oral care still being given 4x0,5 mL. The skin looked jaundice (face, chest, and partial
abdomen area) since the age of 72 hours, the patient got light therapy after the bilirubin level
checked.2 times when feeding increased to 70 mL/kg/day, but no abdominal distended, feeding
volume was decreased to last tolerable volume (60 ml/kg/day).
O Patient is awake, active, no pale, no cardiorespiratory distress, no cyanotic
HR : 140 – 160 bpm, regular, adequate pulses
RR : 55 – 60 cpm, good chest rise
O2 saturation : 95-98% (CPAP PEEP 5HFN 4 lpm FiO2 21%)
BP : 60/35-66/40 mmHg
Weight: 148550 g (100 g) Length: 40 cm (↥ 2 cm) HC: 2930 cm (↥ 1 cm)
Abdomen : suppledistended, normoactive minimum bowel sounds. AC 26.0 cm (stqa)
16
Skin : jaundice (Kramer II)
Other physical examination status quo.
Balance -8,3+22 - 30 mL/24 hours Urine output 3,57-3.9 mL/kg/hou
Blood C/S: no growth (sterile)Blood C/S: 3x24 hours: no growth yet
Laboratory results:
May 26th, 2018 Normal value
Total serum bilirubin/TSB (mg/dL) 12.22 <1.20
Direct bilirubin (mg/dL) 1.16 <0.3
Indirect bilirubin (mg/dL) 11.04 0.30-0.90
Albumin (g/dL) 2.97 2.8-3.4
Blood type B+
Impression: unconjugated hyperbilirubinemia
2. Feeding intolerance (P 92.9)
4. EOSUnproven sepsis (P 36.9)
5. Apnea of prematurityOP (improved) (P 28.4)
6. Hyperbilirubinemia of prematurityHyperbilirubinemia associated preterm delivery dd/sepsis
(improved) (P 59.0)
 Oxygen therapy: HFN 4 lpmCPAP PEEP 5 FiO2 21%
= 170 mL237
Enteral:
 human milk/SF NPO (oral care)
4x0,5 mL8x12 mL/kg/day
~ 60 kcal/kg/day
~ 40
Parenteral
 dextrose 1015% 7.2 mg/kg/min
401.4 kcal/kg/day
 protein 32.5 g/kg/day
120 kcal/kg/day
189 kcal/kg/day
 Medications:
o Antibiotics stopped
o Ampicillin IV 75 mg/12 hours, gentamicin IV 7.5 mg/36 hours (day-4)
o Aminophylline IV 4 mg/12 hours (2.5 mg/kg/dose)
o Caffeine citrate PO 30 mg (20 mg/kg/day) loading dose (at day 7)
o Nystatin PO 100.000 IU/8 hours.
 Phototherapy stoppedLight therapy (day-1)
 Monitor :
o Feeding tolerance
o Body weight, length and HC once a weekGeneral survey and vital signs
17
April 5th - 9 th, 2018 (day 8-12 of hospitalization)
S No temperature instability, episodes of breathing difficulty, apnea, nor desaturation. Aminophylline
was already switched to caffeine citrate. HFN weaned to 2 lpm FiO2 21% and no oxygen therapy at
age of 9 day with no respiratory distress. Kangaroo mother care (KMC) intermittently done to the
patient. Baby’s feeding gradually reached 126 mL/kg/day at age of 11 day with good tolerance.
Weight increment was inadequat, so enteral feeding was changed to breastmilk fortifier and preterm
formula.
Sucking reflex was still inadequate so patient was consulted to Department of Physical Medicine and
Rehabilitation.
At age of 12 day, patient looked lethargy with recurrent episodes of hypothemia (peak 36.1 oC) and
hyperthermia (peak 37.8oC). There was no respiratory distress, but desaturation until 54% without
periode of apnea or bradycardia. The abdomen looked distended, but there was no vomitting., and
defecation was 2x/day. Feeding volume was maintained in 126 ml/kg/day, and given by drip in 1
hours and with proper positioning.
O Patient is awake, quite lethargy, no pale, no cardiorespiratory distress, no cyanotic
O2 saturation : 96-99% (room air)
Weight: 1435 g (↧ 45g) Length: 40.5 cm (↥ 0.5 cm) HC: 30 cm
Head : open and flat anterior fontanelle, 2.5 x 2 cm size

Heart : normal S1 and S2, no murmur, no gallop.
Abdomen : supple, normoactive bowel sounds, AC 26 cm
Reflex : sucking reflex and rooting reflex were inadequate
Balance + 18 - 27 mL/24 hours Urine output 3.5-4.9 mL/kg/hour
Echocardiography April 6th, 2018

Patent foramen ovale (PFO), LR shunt
Small PDA, 2 mm, LR shunt
Impression: small PDA
Laboratory result:
March 9th, 2018 Normal value
Hemoglobin (g/dL) 14.2 14.5 – 24
Hematocrite (%) 41.3 41 – 70
Red blood cell count 4.52 x 106 3.0 x 106 – 5.4 x 106
MCV (fL) 86.5 99 – 105
MCH (pg) 30.2 33 – 39
MCHC (g/dL) 35 32 – 36
WBC (/µL) 11.500 9,100 – 34,000
Platelet (/µL) 410.000 150,000—400,000
RET-HE (pg) 26.5 25.69-34.77
C-reactive protein (mg/L) 0.3 <5
I :T ratio 0.12 <0.20
18
A 1. Preterm baby (32 weeks), AGA, LBW (1580 g) (P 07.3) (P 07.0)
2. Feeding intolerance ec prematurity (P 92.9)
3. Small patent ductus arteriosus (PDA) (Q25.0)
5. Unproven sepsis (P 36.9)
7. Hyperbilirubinemia associated preterm delivery (improved) (P 59.0)
 Oxygen therapy: none
Diet Day-8 Day-9 Day-10 Day-11 Day-12 Information
Total fluid 150 150 150 150 150 mL/kg/day
= 237 = 237 = 237 = 237 = 237
Enteral: Human milk/SF Human

milk+HMF/
preterm
formula
8x15 8x18 mL 8x21 mL 8x25mL 8x25mL
~ 76 ~ 91 ~ 106 ~ 126 ~ 126 drip 1 hr mL/kg/day
~ 51 ~ 61 ~ 71 ~ 85 ~ 101.2 kcal/kg/day
Parenteral
 dextrose 6,4 5.1 3.8 2 2 mg/kg/min
12.5% 37 29.4 21.8 11.7 11.7 kcal/kg/day
 protein 2.5 2 1.5 - - g/kg/day
10 8 6 - - kcal/kg/day
 lipid - - - - - g/kg/day
0 - - - - kcal/kg/day
Total of calories 98 98.5 99 96.5 112.9 kcal/kg/day
 Medications:
o Aminophylline IV 4 mg/12 hours (2.5 mg/kg/dose)  stopped at day 9
o Caffeine citrate PO 7.2 mg (5 mg/kg/day) every 24 hours, maintenance dose
 Stimulation: kangaroo mother care, oromotor stimulation
 Further examination: echocardiography for PDA evaluation, 2 weeks later
 Monitor :
o Feeding tolerance
April 10th -12rd, 2018 (day 13–15 of hospitalization)

S Patient looked more active, no instability of temperature, no respiratory distress, no dasaturation or
apnea. The abdomen looked more distended, AC (↥ 0.5 cm), but no vomitting with the same volume by
drip in 2 hours and proper positioning. Feeding volume was decreased to 111 ml/kg/day.
Patient was also consulted to Ophthalmology Department to evaluate retinopathy of prematurity (ROP)
and Ear Nose and Throat Department for hearing screening.
19
At age of 15 day, the conditon was improved. Feeding tolerance was good by drip 2 hours, the abdominal
distended was getiing better. Slow progression feeding was given to this patient. The feeding volume was
increased to 121 ml/kg/day with good feeding tolerance.
O Patient is awake, quite lethargy, no pale, no cardiorespiratory distress, no cyanotic
Weight: 1480 g (↥ 45g) Length: 41 cm (↥ 1 cm) HC: 31 cm (↥ 1 cm)
Head : open and flat anterior fontanelle, 2.5 x 2 cm size

Heart : normal S1 and S2, no murmur, no gallop.
Abdomen : distended, supple, normoactive bowel sounds, AC 26.5 cm (↥ 0.5 cm)
Reflex : sucking reflex and rooting reflex were inadequate
Balance + 25 - 79 mL/24 hours Urine output 3.0-4.5 mL/kg/hour
Cranial ultrasound (March 11st, 2018) : normal

Hearing screaning (March 12nd, 2018) : otoacoustic emission (OAE) PASS bilateral
ROP screening (March 12nd, 2018) : bilateral immature retina
A 1. Preterm baby (32 weeks), AGA, LBW (1580 g) (P 07.3) (P 07.0)

2. Small patent ductus arteriosus (PDA) (Q25.0)
3. Feeding intolerance ec prematurity (improved) (P 92.9)
7. Hyperbilirubinemia associated preterm delivery (improved) (P 59.0)
 Oxygen therapy: none
Diet Day-13 Day-14 Day-15 Information
Total fluid 150 150 150 mL/kg/day
= 237 = 237 = 237
Enteral:
 Human milk+HMF/
preterm formula
8x22 mL 8x22 mL 8x24mL

~ 111 drip 2 hr ~ 111 drip 2 hr ~ 121 drip 2 hr mL/kg/day
~ 89 ~ 89 ~ 97 kcal/kg/day
Parenteral
 dextrose 12.5% 3.4 3.3 2.5 mg/kg/min
23 23 14.2 kcal/kg/day
 protein 1 1 - g/kg/day
4 4 - kcal/kg/day
 lipid - - - g/kg/day
- - - kcal/kg/day
Total of calories 112 112 111.2 kcal/kg/day
 Medications:
o Caffeine citrate PO 7.2 mg (5 mg/kg/day) every 24 hours, maintenance dose
20
 Further examination: screening osteopenia of prematurity (OOP), echocardiography for PDA
evaluation
 Monitor :
o Feeding tolerance
 Parental education regarding
o Current condition and plan management
o Planning for long-term follow up high risk baby
 Family counseling to other family (grandmother, aunty etc) to help mother in carriying patient.
May 27th, 2018 (day-5 hospitalization)

S Baby was active without temperature instability. No respiratory distress, no desaturation, nor
apneu. CPAP PEEP 5 FiO2 21% was stopped at 3.00 PM, no respirarory distress seen. Nothing per
oral day-3. On light therapy day-2. OGT decompression, no bleeding from OGT. The patient still got
oral care 4 x 0,5ml. No defecation day-2. Light therapy day-2, jaundice was improving.
HR : 150 bpm, regular, adequate pulses
RR : 50 cpm, good chest rise, no respiratory effort
Temperature : 36,6 0 C
Weight: 1.550 g Length: 40 cm HC: 29 cm
Skin : Pink color, jaundice (kramer I)
Abdomen : supple, minimum bowel sounds, AC 26 cm (stqa)
Other general physical examinations status quo.
Balance -4,2 ml/24 hours Urine output 4,2 mL/kg/hour
Blood C/S: 4x24 hours no growth

2. RDS (improved)(P 22.0)
3. EOS (P 36.9)
4. AOP (improved) (P. 28.4)
5. Hyperbilirubinemia of prematurity dd/sepsis (P 59.0)
 Oxygen therapy: CPAP PEEP 5 FiO2 21% stopped
= 187 mL
Enteral:
 Human/ breast milk Oral care 4x0.5 mL
Parenteral
 dextrose 10% 7,7 mg/kg/min
44 kcal/kg/day
12 kcal/kg/day
21
18 kcal/kg/day
 Medications:
o Ampicillin IV 75 mg/12 hours, gentamicin IV 8 mg/36 hours (day-5)
o Aminophylline IV maintenance dose 4 mg/12 hours
 Light therapy (day-2)
 Monitor:
o General survey and vital sign
May 28th, 2018 (day-6 hospitalization)

S No temperature instability, episodes of breathing difficulties, apnea, nor desaturation. There was
bleeding from decompression of OGT (red-brownish coloured, volume of 1 mL). No vomit nor
abdominal distention. Still NPO day-4. Jaundice diminished, light therapy ceased after 48 hours. No
bacterial growth from blood culture examination and clinical manifestation was considered
improving, so antibiotics were stopped after given for 6 days.
HR : 150 bpm, regular, adequate pulses
RR : 50 cpm, good chest rise, no respiratory effort
Temperature : 36,6 0 C
O2 saturation : 98-99% (on CPAP PIP 5 FiO2 21%
Weight: 1550 g Length: 41 cm HC: 30 cm
Skin : Pink color, no jaundice
Abdomen : supple, minimum bowel sounds, AC 26 cm (stqa)
Other general physical examinations status quo.
Balance +71,5 ml/24 hours Urine output 2,2 mL/kg/hour
Blood C/S: no growth (sterile)

2. History of RDS (P 22.0)
4. AOP (improved) (P 28.4)
5. Hyperbilirubinemia of prematurity dd/sepsis (improved) (P 59.0)
 Diet: TPN (included maintainance of electrolyte Na/K/Cl/Mg/P)
= 210 mL
Enteral:
 Human milk Oral care 4x0.5 mL
Parenteral
 dextrose 10% 8,4 mg/kg/min
48 kcal/kg/day
16 kcal/kg/day
22
27 kcal/kg/day
 Medications:
o Antibiotic stopped
o Aminophylline IV maintenance dose 4 mg/12 hours
 Light therapy stopped
 Monitor
o General survey and vital sign
May 29th – 30th, 2018 (day 7-8 hospitalization)

S Patient looked more active. No temperature instability. episodes of breathing difficulties, apnea, nor
desaturation. Aminophylline therapy was stopped at the age of 7 days (chronological age of 34
weeks). OGT decompression produced minimum brownish blood (±1-2 mL) and subsequently
become clear in color. Patient got NPO for 5 days. At 8 th day of hospitalization she started to get
trophic feeding with human milk 4x1 mL per OGT with good tolerance. No vomit nor abdominal
distention
RR : 48- 50 cpm, good chest rise
Temperature : 36.5-37o C
O2 saturation : 95 – 98 % (room air)
Weight: 1540 g (↓10 g) Length: 41 cm HC: 30 cm
Skin : Pink color, no jaundice
Abdomen : supple, normoactive bowel sounds, AC 25,5 cm (↓0,5 cm)
Other physical examinations status quo
Balance + 29.3 mL/24 hours Urine output 2.8 - 3.8 mL/kg/hour
A 1. Preterm baby (33 weeks), AGA, LBW (1,550 g) (P 07.3) (P 07.0) (P 07.1)
4. AOP (improved) (P 28.4)
5. History of hyperbilirubinemia of prematurity dd/sepsis (P 59.0)
Diet Day-7 Day-8 Information
Total fluid mL/kg/day
145 145
= 223 ml = 223
Enteral:
 human milk 8x0.5 mL 4x1 ml
(oral care) (trophic feeding)
Parenteral
 dextrose 11,3 11,3 mg/kg/min
12,5% 64,5 64,5 kcal/kg/day
23
 protein 3 3 g/kg/day
12 12 kcal/kg/day
 lipid 3 3 g/kg/day
27 27 kcal/kg/day
Total of calories 103,5 103,5 kcal/kg/day
 Medications:
o Aminophylline stopped
 Monitor:
o Feeding tolerance
May 31st – June 1st, 2018 (day 9-10 hospitalization)

S Baby was active, no temperature instability, respiratory distress, nor apnea. Oral gastric tube was
clear. Previous trophic feeding (human milk 4x1 mL per OGT) was well tolerated. No vomit nor
abdominal distention The volume of trophic feeding was increased 8x1 – 12x1 mL respectively.
Kangaroo mother care (KMC) was intermittently done to the patient at 10th day.
RR : 48- 52 cpm, good chest rise
Temperature : 36.5-37oC
O2 saturation : 95 – 98 % (room air)
Abdomen : supple, normoactive bowel sounds, AC 25,5 cm (stqa)
Other physical examination status quo
Balance + 28.8 mL/24 hours Urine output 4.3 – 5.9 mL/kg/hour
Laboratory result:
Capillary blood gas May 31st,2018 Normal value
TSH (µIU/mL) 5.0 <20
Impression: normal TSH (May 31st)

4. History of AOP (P 28.4)
 Diet: TPN (included maintainance of electrolyte Na/K/Cl/Mg/P)
Total fluid 150 150 mL/kg/day
= 237 ml = 237
Enteral:
 human milk 8x1 mL 12x1 ml
(trophic feeding) (trophic feeding)
24
Parenteral
 dextrose 12,5% 12,1 10,9 mg/kg/min
69 62,1 kcal/kg/day
 protein 3 3 g/kg/day
12 12 kcal/kg/day
27 27 kcal/kg/day
Total of calories 108 101 kcal/kg/day
 Medications:
o Stimulation: kangaroo mother care (KMC)
 Monitor:

o Feeding tolerance
 Parental education regarding current condition and plan management.
June 2nd to 3rd 2018 (day 11-12 hospitalization)

S Baby was quite active without any temperature instability. No respiratory distress. Previous trophic
feeding (human milk 8x1 mL per OGT) was well tolerated. No vomit nor abdominal distention. She
defecated 2 times a day. The feeding volume was increased to 27 mL/kg/day and 66 mL/kg/day at
the age of 11 dan 12 day.
Abdomen: normoactive bowel sounds
Balance + 10,5 mL/24 hours Urine output 2,5 mL/kg/hour
 Oxygen therapy : room air
Total fluid 150 150 mL/kg/day
Enteral:
 human milk 2x2 - 5x3 – 5x5 ml 6x7 - 6x10 mL
~ 27 ~ 66 mL/kg/day
~ 17 ~ 44 kcal/kg/day
Parenteral
 dextrose 12,5% 10,9 6.5 mg/kg/min
25
62,1 37 kcal/kg/day
 protein 3.5 2.5 g/kg/day
14 10 kcal/kg/day
27 18 kcal/kg/day
Total of calories 103,1 109 kcal/kg/day
 Medications:
 Stimulation: kangaroo mother care (KMC)
 Monitor:

o Feeding tolerance
June 4th to 6th 2018 (day 13-15 hospitalization)

S Baby had no episode of temperature instability. No respiratory distress. Baby defecates routinely 1-
2x/day.
At age of 12 day: There were 1 episode of vomiting, (when given feeding volume of 6x10 – 6x12
mL ~ 85 mL/kg/day), the feeding volume being lowered to 12x6 mL ~ 55 mL/kg/day and the
feeding was given via OGT by continuous drip 1-hourly, still there were vomit episodes 2 times. The
duration of continuous drip was slowered by 2 hours.
At age of 13 day: There were 3 episodes of vomiting (when given feeding volume of 12x15 mL ~
116 mL/kg/day), the feeding volume then lowered to 4x15 mL, 8x10 mL ~ 90 mL/kg/day by 2-
hour continuous drip, the baby was also properly positioned when being fed.
Sucking reflex was still inadequate, patient was then consulted to Department of Physical Medicine
and Rehabilitation.
At the age of 15 day: the condition was improved. Slow progressive feeding was given to this
patient. Two-hourly continuous drip still continued. Feeding tolerance was improving, no vomit nor
abdominal distention. The feeding volume of 12x10 mL ~ 77 mL/kg/day was properly achieved.
Patient was also consulted to Ophthalmology Department to evaluate retinopathy of prematurity

(ROP) and Ear Nose and Throat Department for hearing screening.
Weight: 1605 g( ↑ 65g) Length: 41 cm HC: 30 cm
Abdomen: normoactive bowel sounds
Balance 11 - 65 mL/24 hours Urine output 2,5 mL/kg/hour
ROP screening (June 5th, 2018) : bilateral immature retina

Hearing screaning (June 6th, 2018) : otoacoustic emission (OAE) PASS bilateral
26
2. Feeding intolerance ec prematurity(P 92.9)
Diet Day-13 Day-14 Day-15 Information
Total fluid 150 150 150 mL/kg/day
Enteral:
 human 3 x10, 9x6 ml 4x15. 8x10 mL 12x10 ml
milk/preterm ~ 55 ~ 90 ~ 77 mL/kg/day
formula ~ 36 ~ 60,5 ~ 52 kcal/kg/day
Parenteral
 dextrose 12,5% 5.8 5,8 5.8 mg/kg/min
34 34 33 kcal/kg/day
 protein 2 1 2.3 g/kg/day
8 4 9.2 kcal/kg/day
 lipid 0 0 0 g/kg/day
0 0 0 kcal/kg/day
Total of calories 78 98,5 94,2 kcal/kg/day
 Medications:
o Nystatin PO 100.000IU/8 hours
 Monitor:

o Feeding tolerance
 Further examination: screening osteopenia of prematurity (OOP)

 Parental education regarding
o Current condition and plan management
o Planning for long-term follow up high risk baby
 Family counseling to other family (grandmother, aunty etc) to help mother in carrying patient
PROGNOSIS
 Ad vitam : bonam
 Ad functionam : dubia ad bonam
 Ad sanationam : ad bonam
27
CLINICAL COURSE DIAGRAM
At birth 1st day of hospitalization
 32 weeks AOG, BW 1580 g  No respiratory effort, weak muscle tone  Weaned off oxygen therapy (NIPPV 15/5
 A/S 5 at first minute and 7 at 5 minutes  HR <100 bpm PPV PIP 25 PEEP 5 FiO2 30% FiO2 30%)
 Mother: PPV PIP 30 PEEP 5 FiO2 30%  HR 120 bpm,  Septic screening : normal infection
o 36 years old G3P1A1 retractions CPAP PEEP 7 FiO2 30%  CPAP marker  1st line of AB
o preterm labor, history of abortus and PEEP 8 FiO2 40%  NIPPV PIP 20 PEEP 5 FiO2  Thoracoabdominal x-ray: RDS grade 1
preterm delivery 30% RR 40 cpm  respiratory distress  PICC inserted
o Anemia, lLeucocyte 17.400/uL improved  Two episodes of apnea aminophylline
o (+) urinary tract infection  Normal RBG  Oral care with human milk
o (-) chorioamnionitis  Normal temperature  Nystatin prophylaxis
o (+) IV antibiotics  Stable hemodynamic
 Education and emotional support
o (+) antenatal steroid
 Give vitamin K1 (IM) and topical antibiotic on
o Prenatal Doppler US: normal
both eyes
 Amniotic fluid clear and non foul smelling
 admitted to NICU
 Initial steps in stabilization
2nd-3rd day of hospitalization 4-5th day of hospitalization
 Baby was quite active  No respiratory distress, no instability of temperature

 Weaned oxygen therapy (CPAP PEEP 6 FiO2 21%)  Weaned oxygen therapy (CPAP PEEP 5 FiO2 21%)
 Age of 24 hours: Priming with human milk good tolerance  Jaundice (Kramer III) unconjugated hyperbilirubinemia (total
 Age of 36 hours: Spontaneous meconium 6.53 mg/dL) phototherapy not indicated
 Age of 48 hours: TSH normal  BGA: normal
 BGA: normal  Cranial ultrasound: normal
 Total fluid: 110-120 mL/kg/day  Total fluid: 140-150 mL/kg/day
o Enteral: human milk/SF 15 ml/kg/day o Enteral: human milk/SF 30 ml/kg/day
o Parenteral: GIR 7.3-7.8 mg/kg/min, prot 2.5-3 g/kg/day, o Parenteral: GIR 7.2-8.2 mg/kg/min, prot 2.5-3 g/kg/day,
lipid 2-3 g/kg/day lipid 1-3 g/kg/day
 Total calories: 80-94 kcal/kg/day  Total calories: 106-109 kcal/kg/day
28
6-7th day of hospitalization 8-12th day of hospitalization
 No instability of temperature, no apnea, nor  More active, no temperature instability

desaturation  Supported with HFN 2 lpm FiO2 21%  no oxygen therapy at day 9
 BW 1480 g (100 g)  Aminophylline switched to caffeine citrate at day 7, and stopped at day 9
 Weaned oxygen therapy (HFN 4 lpm FiO2 21%)  Start KMC intermittent, inadequate sucking reflex  oro-motoric stimulation
 Stop AB (total 5 days after blood C/S sterile)  Enteral feeding 126 mL/kg/day at age of 11 day
 Kramer II  Inadequate weight increment (1435 g (↧ 45g)) changed to breastmilk fortifier and
 Age of 7 days: vomit 2 times, no abdominal preterm formula.
distended feeding volume was decreased to last  Age of 12 day: lethargy, temperature instability, desaturation 54%, no of apnea or
tolerable volume bradycardia, distended abdomen, no vomitting normal infection marker
 Total fluid: 150 mL/kg/day  Echocardiography: small PDA
o Enteral: human milk/SF 60 ml/kg/day  Maintained enteral feeding in 126 ml/kg/day, drip 1 hours and with proper positioning.
o Parenteral: GIR 7.2 mg/kg/min, prot  Total fluid: 150 mL/kg/day
2.5 g/kg/day, lipid 1 g/kg/day o Enteral: breastmilk fortifier/preterm formula 76-126 ml/kg/day, drip 1 hour
 Total calories: 101 kcal/kg/day o Parenteral: GIR 2-6.4 mg/kg/min, prot 0-2.5 g/kg/day, lipid stopped
 Total calories: 96.5-112.9 kcal/kg/day
13-15th day of hospitalization
 No instability of temperature, no respiratory distress, no apnea

 Abdomen more distended, AC (↥ 0.5 cm), no vomitting
 Enteral feeding drip in 2 hours and proper positioning slow progression feeding
 At age of 15 day, the conditon was improved  feeding volume was increased (121 ml/kg/day), good tolerance.
 Weight: 1480 g (↥ 45g)
 Cranial US (age of 14 days): normal
 ROP screening: bilateral immature retina
 OAE screening: PASS bilateral
 KMC intermittent, oro-motoric stimulation
 Total fluid: 150 mL/kg/day
o Enteral: breastmilk fortifier/preterm formula 111-121 ml/kg/day, drip 2 hour
o Parenteral: GIR 2.5-3.4 mg/kg/min, prot 0-1 g/kg/day, no lipid
Total calories: 111-112 kcal/kg/day
29
CASE ANALYSIS SCHEME
30
CASE ANALYSIS
This patient was a preterm baby (33 weeks of gestation with birth weight 1550 g) who
experienced respiratory distress a birth. According to birth weight and gestational age, this baby
was classified as a moderate to late preterm baby (gestational age 32 - <37 weeks) with low
birth weight (birth weight less than 2.500 g). Many factors had been identified as risk factors of
premature birth. Mothers age (<20 or > 35 years old), low socioeconomic status, poor antenatal
care (<6 controls), history of previous premature birth, preeclampsia, anemia, infection, and
antepartum haemorrhage were among the risk factors identified. 1 TheOur patient was born
from a 18 year-old mother with history of 3-day preterm PROM with low socioeconomic status
as the risk factors for preterm labor.
The complications of preterm birth arise from immature organ systems that are not yet
readyprepared to support life in the extrauterine environment. Although the mortality rate for
preterm infants and the gestational age-specific mortality rate have dramatically improved
over the last 3 to 4 decades, infants born preterm remain vulnerable to many complications,
including RDS, chronic lung disease (CLD), injury to the intestines, a compromised immune
system, cardiovascular disorders, hearing and vision problems, and neurological insult. Infants
born at the lower limit of viability have the highest mortality rates and the highest rates of all
complications. Careful consideration should be done, especially in detecting and treating specific
organs/system organ complications, since these complications when being left undetected and
untreated, could cause significant impact on baby’s long-term growth and development.2
At the delivery day, the patient’s mother laboratory examination showed leukocytosis up to
17.240/μL with history of 3-days PROM. Intravenous broad-spectrum antibiotics were then
given to treat the infection and to decrease risk of sepsis. The mother had already been given
one shot antenatal corticosteroid to enhance fetal lung maturation. A single course of
corticosteroids is recommended for pregnant women < 34 weeks of pregnancy and with
multiple gestations. Subsequent trials have shown that antenatal corticosteroid therapy
improves circulatory stability in preterm neonates, resulting in lower rates of IVH and NEC
compared with unexposed preterm neonates.The mechanism of antenatal glucocorticoids in
reducing the risk of RDS in premature infant is by accelerating development of type-1 and type-
2 pneumocytes thus improving neonatal lung function by enhancing maturational changing in
lung architecture and inducing enzymes that stimulate phospholipid synthesis and release of
surfactant.3,4 A Cochrane Database review published that antenatal corticosteroids associated
with an overall reduction in RDS (RR 0.66, 95% CI 0.56-0.77). Corticosteroid treatment was also
associated with a significant reduction in the risk of intraventricular haemorrhage (IVH) (RR
0.55, 95% CI 0.40-0.76) and neonatal mortality (RR 0.69, 95% CI 0.59-0.81), compared with
neonates whose mothers did not receive antenatal corticosteroids.3 (Level of evidence 1a)
One of the most common complication in preterm infants is respiratory problems/distress at

birth which is due to failure in rapid transition process from intrauterine to extrauterine life. A
successful transition is characterized by alveolar fluid clearance, lung expansion and circulatory
changes.5-7 However, respiratory distress in premature infants is not exclusively caused by lung
problem. Other condition such as infection (sepsis), heart disease, cardiovascular problems
(shock), hypoglycemia and hypo/hyperthermia could manifest as respiratory distress as well.
The patient presented with increased work of breathing (chest retractions) at birth which were
31
characteristics of respiratory distress.6 Several differential diagnosis as the cause of respiratory
distress are RDS, transient tachypnea of the newborn (TTN) and neonatal pneumonia (sepsis).8
Diagnosis of RDS established in this patient supported by her gestational age without history of
thick-greenish amniotic fluid. Respiratory distress syndrome or previously called hyaline
membrane disease (HMD), is caused by deficiency of surfactant, the phospholipid mixture that
reduces alveolar surface tension, which decreases the pressure needed to keep the alveoli
inflated and maintains alveolar stability especially during end expiration phase.3,5-7 EuroNeoStat
annual reports for very low gestational age infants 2010 indicates a rate of 92% for RDS in
newborn babies 24-25 weeks gestational age (GA), 88% in 26-27 weeks GA, 76% in 28-29
weeks GA and 57% in 30-31 weeks GA. In moderate to late preterm baby, the frequency of RDS
was 33,1%; 18,2%; 9,9%; 4,6% and 1,6% in 32, 33, 34, 35 and 36 weeks of gestation,
respectively.9 Chest radiographs may be useful in differentiating the aetiology of neonatal’s
respiratory distress. In this patients, the classical findings of RDS/HMD are found, which are
diffuse, reticulogranular and ground glass appearance/pattern.6,7,10 Nevertheless, sepsis still
could not be ruled out at that time due to presence of maternal and neonatal risk factors.
Mandatory aspects in the treatment strategy for RDS consists of prenatal care, delivery room
stabilization, respiratory support, surfactant and supportive care. 6,7 Her RDS was managed with
CPAP. Randomized clinical trials suggest that nasal CPAP is acceptable as an alternative of
surfactant administration in preterm infants with RDS. Prophylactic nasal CPAP given within 15
minutes after birth regardless of respiratory status in preterm infants reduces the need for
mechanical ventilation (RR 0.50, 95% CI 0.42 to 0.59) and surfactant (RR 0.54, 95% CI 0.40 to
0.73) and also reduces the incidence of bronchopulmonary dysplasia at 36 weeks (RR 0.89, 95%
CI 0.79 to 0.99) and death or BPD (RR 0.89, 95% CI 0.81 to 0.97)10 (Level of evidence 1a)
Administration of antenatal glucocorticoids along with the use of nasal CPAP had helped
resolving the RDS problems in this patient.
Normal BGA in this patient could be a result of successful early oxygen therapy so that
subsequently, CPAP use could be changed/weaned to high flow nasal (HFN) use at 3 rd and
oxygen therapy could be stopped at 5 th day. High flow nasal oxygen use has similar rates of
efficacy to other forms of non-invasive respiratory support in preterm infants for preventing
respiratory failure, and chronic lung disease. High flow nasal oxygen is associated with less nasal
trauma, and may be associated with reduced pneumothorax complication compared with nasal
CPAP.10,11 In this patient, CPAP therapy was stopped at fifth day, as known that after the age of 72
hours the endogenous surfactant was already produced so the oxygen therapy was no longer
needed, along with the improvement of sepsis condition.
At birth, the patient showed respiratory distress which could lead us to a symptom of neonatal
sepsis. Patient was born from a mother with history of preterm PROM for 3 days and
leukocytosis up to 17.400 /μL. This patient has few risk factors of getting sepsis, such as
prematurity and low birthweight and ROM > 18 hours. Chorioamnionitis is the main risk factors
of neonatal sepsis. Although there were no other clinical signs of chorioamnionitis except
maternal leukocytosis (such as maternal fever, maternal tachycardia, fetal tachycardia, uterine
tenderness, and/or foul odor of the amniotic fluid), but along with clinical presentation and
other risk factors found, we conclude her of having early onset sepsis (EOS).14,15 Early onset
sepsis term is used when the onset of symptoms appear within the first 3 days of life.
32
Chorioamnionitis, colonization of grup B streptoccus (GBS), preterm premature rupture of
membrane (PPROM) >18 hours, and gestational age <37 weeks are the main risk factors of EOS
Organisms causing EOS ascend from the birth canal resulting in intra-amniotic infection. The
signs of sepsis are non-specific, therefore diagnosis of EOS is frequently based on constellations
of perinatal risk factors along with clinical signs that are neither sensitive nor specific.
The patient was immediately being given empirical first line antibiotics and a complete septic
work up was carried out. Initial septic markers were within normal limits.?? After 5 days of
treatment, the patient was clinically stable. Based on her improving clinical condition, supported
with sterile blood culture, the least diagnosis was unproven sepsis, the administration of
antibiotics was stopped after 5 days then. Combination of two serial normal I:T ratios and a
negative blood culture at 24 hours is indicative of noninfective neonates (negative predictive
value 100%).15 (Level of evidence 2b) Her infection marker at 24 hours of age were normal,
but she still needed CPAP for respiratory support, hence the antibiotic therapy was
continued.The patient’s mother was given IV antibiotics on admission which may help reduce
the risk of EOS in her infant. This patient was also treated with prophylaxis fungal infection with
nystatin oral. This therapy aimed to prevent invasive fungal infection later on. Based on the
latest meta-analysis, nystatin significantly reduced the incidence of invasive fungal infection in
low birth weight baby compared to placebo or no drug (RR 0.20, 95% confidence interval 0.14
to 0.27).16 (Level of evidence 1a)
Apnea of prematurity is a common problem affecting premature infants, its incidence is

inversely correlated with GA and BW. Seven percent of neonates born at 34 to 35 weeks
gestation, 15% at 32 to 33 weeks, 54% at 30 to 31 weeks [50], and nearly all infants born at
<29 weeks gestation or <1,000 g exhibit AOP. The cause of AOP are delayed CNS development
and excessive bradycardic response. It usually begins at the first 7 days of life and self-limiting
once the baby reach mature age. 12 Symptoms of AOP can be a result of sepsis, significant patent
ductus arteriosus (PDA), hypoxic ischemic encephalopathy (HIE), abdominal distention (NEC),
nasal obstruction, hypoglycemia, hypo or hyperthermia and severe anemia. Prone position, use
of CPAP and HFN subsequently, and administration of xanthine derivate (aminophylline) was
already done to this patient. Pharmacological effects of methylxanthines include stimulation of
the respiratory center in the medulla, increase minute ventilation, CO 2 sensitivity, and neural
respiratory drive while decreasing hypoxic depression of breathing. Methylxantine also improve
diaphragmatic contraction and respiratory muscle function. 11-13 During observation, after
aminophylline administration, there was no apneic episode. Aminophylline therapy was
continued until the patient reach 34 weeks of correctional age.
Neonatal hyperbilirubinemia is a common problem. Approximately 60-70% of term and 80% of

preterm infants develop jaundice in the first week of life, which is called hyperbilirubinemia of
prematurity, and 5-10% of them require intervention for pathological jaundice. 17 The patient
looked jaundice at the age of 72 hours. In premature infants, visible jaundice caused by
predominant unconjugated bilirubin usually appears between 24-72 hours of age and reach its
peak at the 5th day of life.17,18 Babies with gestational age of 32 0/7 – 33 6/7 weeks are suggested
to have phototherapy when TSB ach 10-12 mg/dL and exchange transfusion when TSB level
reach 15-18 mg/dL.18 Blood examination showed hyperbilirubinemia (TSB 12,22 mg/dL),
dominated by unconjugated serum bilirubin, which reached phototherapy cut-off. The cause of
hyperbilirubinemia in this patient were physiological immaturity of the body to manage the
33
increasing bilirubin production and also sepsis. Sepsis could decrease the binding affinity of
albumin toward bilirubin. There were no risk for hemolitic condition such as rhesus and ABO
incompatibility in this patient. Other hemolitic condition such as G6PD as one of the differential
diagnosis of pathologic hyperbilirubinemia, usually happens at the first 24 hours of age and
wasn’t being checked in this patient due to financial problem. 18 Phototherapy in most infants
less than 35 weeks of gestation is generally used in a prophylactic mode. The mandatory goal is
to prevent further elevation of TSB which can cause severe bilirubin induced neurological
damage, ie. kernicterus.19,20 The jaundice was improving after 48 hour of phototherapy along
with the improving condition of sepsis, so the photothetapy was stopped then. The TSB level
wasn’t being checked again to minimize the invasive procedure along with clinical improving
jaundice.
The goal of nutritonal support in preterm infants is not only to achieve basal metabolic needs
but also to support postnatal growth. Low birth weight infants are well known with their
significant weight loss in the first early days and weeks due to catabolic illness and insufficient
protein energy supply. Aggressive nutrition should be initiated from birth as this is known not
only to fulfill basal metabolic needs, but also to support postnatal growth. Low birth weight
infants are characterized by significant weight loss in the initial days and weeks because of
catabolic illness and insufficient protein energy supply. 21-23 Early aggressive parenteral
nutrition (PN) is mandatory to fulfill energy, protein, lipid, mineral and micronutrients
requirements along with introduction of minimal enteral nutrition (MEN).
Preterm infants loose more weight and rneed more time to regain birth weight compared with
term infants. Weight gain generally begins by the second week of life. Early aggressive TPN is
defined when total of 4 g/kg/day of amino acid is administrated via standardized TPN to
neonates over first week of life. 24 There is no agreement on the ideal age at which to introduce
amino acid (AA) and intralipid (IL) to the feeding regimen of a preterm infant. Infants who
have respiratory distress syndrome have a range of estimated resting energy expenditure of 40-
60 kcal/kg per day, with caloric needs directly proportional to the severity of the illness. From
the available data it is suggested that VLBW neonates require a daily minimum of 60
kcal/kilo-day (including 2.5 g/kilo-day of AA) to prevent catabolism, and 80 to 90
kcal/kilo/day (including 2.7 to 3.5 g/kilo-day) of AA to maintain the rate growth they would
have had in utero. 25,26 When parenteral AA and IL started after the first 48 hours of life, 80 to
90 kcal/kilo-day can be achieved by 5 to 7 days after birth like we found in this patient.
Nutritional support has been made since birth. Patient was supported by aggressive parenteral,
after the PICC inserted, lipid could given until 3 g/kg/day, protein 3,5 g/kg/day, the GIR could
increased to 12,1 mg/kg/min, and the total calory also maintained almost 2 times of her resting
energy expenditure.In this patient at the first 10-day of life she has status quo of body weight,
altough still suboptimal, but she did not experience weight faltering as usually seen in previous
era of aggressive TPN. And in the setting of the hospital, we couldn’t do the weight-height
examination everyday, so we couldn’t intensively monitored the rate of growth velocity. At the
age of 14 days she showed increment of body weight of 3,5% (1550 to 1605 g), this was still
suboptimal, but along with the increment of enteral feeding, we could hope a better weight
increment. Beside that, comorbidities of this patient such RDS, sepsis were also managed
properly so further complication could be avoided and we hope the growth velocity is
increasing adequately.
34
Trophic feeding which is termed early enteral nutrition or also known as MEN, refers to the
commencement of feeding of preterm infants (using either human breast milk or formula)
within the first 72 hours of life, which feedings is being given at small volumes to stimulate
development of the immature gastrointestinal (GI) tract of the preterm infant. It used 10–20
ml/kg/day milk (breast milk preferrable) to improve GI disaccharidase activity, hormone
release, blood flow, motiliti, and microbial flora. The clinical benefits include improved milk
tolerance, greater postnatal growth, reduced systemic sepsis and shorter hospital stay. 27
Cochrane reviews show no increase in the risk of necrotizing enterocolitis (NEC) with trophic
feeding, earlier initiation of feeding or more rapid advancement of feeds. The latest study
revealed that early feeding in preterm IUGR neonates as a standardized feeding initiation and
advancement plan does not increase the risk of NEC or feeding intolerance in very preterm
infants (p=0.636, RR 1.58; 95% CI 0.236-10.605).28
As mentioned before, it is essential to start nutrition early to preterm infants by giving small
amount of milk (preferably human milk) to ensure that metabolic homesotasis is kept stable
and to prevent postnatal growth retardation. Increasing feeding volumes to reach “full enteral
feeding” is limited by individual feeding tolerance.29,30 Feeding intolerance is extremely
common in premature infants. The most frequent signs of a suspected feeding intolerance are
the presence of gastric residuals, abdominal distension, the onset of apnea/bradycardia after
oral/enteral feeding and failure to reach enteral full feed of 140 mL/kg/day within 10 days since
the beginning of oral/enteral feeding. Abdominal girth and gastric residual volume was not good
indicator of feeding tolerance. 29,30 The patient had reccurent vomiting 12 days after birth, when
oral intake increased to 85 mL/kg, feeding volume was decreased to the last tolerable volume,
slow bolus feeding (60 minutes) were applied, and proper position maintanined while the
patient being fed. At the age of 13 day, she vomitted again when the feeding volume increased.
The feeding volume was lowered to the last tolerable volume, slow bolus feeding lengthened to
120 minutes, and proper position when the baby being fed was done. She alsobeing consulted to
Department of Physical Medicine and Rehabilitation. To promote sucking-swallowing
coordination this patient had oral motor intervention using non-nutritive sucking and oral
stimulation.30 The feeding tolerance was improving then.
Preterm infants lack the rapid fetal iron accretion during the third trimester of pregnancy and
also susceptible to zinc deficiency because of low body stores (60% of fetal zinc is acquired
during the third trimester of pregnancy).31-33 It caused by limited capacity to absorb and retain
micronutrients, coupled with increased endogenous losses associated with organ immaturity,
high nutrient demand to support catch-up growth and inadequate intakes. As a consequences,
disturbation development of brain structure and neurotransmission could happen. Hence, an
elemental iron intake of 2–4 mg/kg/day and zinc intake from 1 to 2.5 mg/kg/d up to 3 mg/kg/d
for LBW infants is recommended for stable growing preterm infants.31,34 In this patient, Fe and
Zn was not yet fully supported from preterm formula and no preparation of parenteral route. Fe
and zinc supplementation was planned to be given once the the patient got full oral/enteral
feeding.
Kangaroo mother care (KMC), which initiated as soon as her condition clinically stable, could
promote bonding, better regulation in HR, breathing, and temperature, also help to achieve
rapid growth with positive impacts on baby’s brain and emotional development.35
35
Impaired neurodevelopmental outcome is a major long-term complication of premature
infants. The neurodevelopmental sequelae that can be found in these survivors are impaired
cognitive skills, motor deficit including mild one, gross motor delay, and cerebral palsy (CP),
sensory impairment including vision and hearing losses, behavioral and psychological
problems.36,37 Preterm infants had 20 times higher risk of hearing loss, either sensorineural or
conductive, than full terms with normal weight. Generally, all neonates, especially with the birth
weight less than 2,000 g are indicated for hearing and visual evaluation after discharge. This
patient had normal result (pass) on the first hearing screening test and was planned to do
auditory brainstem response test (ABR) evalution at 3 months of age as recommended by
American Academy of Pediatrics (AAP).38 Hypoxia, arterial carbon dioxide pressure changes,
arterial pH and oxygen consumption with high concentration are influential factors for visual
defects in infants with LBW. A study reported that the prevalence of visual impairment is 5.21%
and blindness is 0.5% in preterm neonates.39 Retinopathy of prematurity (ROP) is one of the
most common causes of visual loss in preterm infants, which is preventable. Retinopathy of
prematurity screening is recommended for infants with BW of ≤1.500 g or GA of 30 weeks or
less, selected infants with BW between 1.500 and 2.000 for GA > 30 weeks with unstable clinical
course which done by an experienced ophthalmologist. In this patient, screening for ROP is
recommended because there were history of unstable clinical course and the use of oxygen
therapy for several days.39 Screening for ROP was already performed and showed immature
retina on both eyes. Re-evaluation is scheduled two weeks afterwards.
Screening for heart problem in preterm baby without any significant symptoms should be done
with echocardiography, as it is known that every third preterm infant with a BW of 501-1.500 g
can be expected to have a persistent PDA that can lead to pulmonary edema, loss of lung
compliance, and deterioration of respiratory status which ultimately leads to chronic lung
disease (CLD).40,41 Unfortunately, the echocardiography machine was out of order at that time so
the evaluation could not be done at the moment, but special consideration has to be kept in
mind about the risk of having heart disease (PDA) in every preterm infants, though no clinical
signs of PDA were found in this patient.
Significant advancements in the nutritional care of preterm infants such as the initiation of early
intravenous nutrition, early enteral feeds, breastmilk fortifier and preterm formula have been
associated with a declining incidence of metabolic bone disease (MBD) in preterm infants. MBD
presents between 6 and 12 weeks of age but may remain asymptomatic for weeks until overt
rickets or fractures develop.42 Symptoms may include poor weight gain, growth faltering, and
respiratory difficulties or failure to wean off ventilatory support due to excessive chest wall
compliance. Serum calcium values may remain normal until late course of the disease. Low
concentrations of inorganic phosphate (<1.8 mmol/L with elevated alkaline phosphatase (>900
IU/L) were choices of laboratory examination in diagnosing inadequate intake and low bone
mineral density.42 Patient was planned to do complete electrolytes, alkaline phosphatase and
inorganic phosphate examinations after the chronological age of 28 days.
Preterm infants’ brain is vulnerable of having hemorrhagic and ischemic injury during the late
second and early third trimester. Early diagnosis is important for prognostication, optimal
treatment and accessing possible neurological outcome. 43,44 Cranial ultrasound (cUS) is a simple
bedside tool to evaluate intracranial haemorrhage. It has high sensitivity (100%) and specificity
(93.3%) in detecting grade III intraventricular haemorrhage (IVH), but poor sensitivity in
36
detecting IVH with normal-sized ventricles. 44 Cranial US examination in patient were within
normal limit. Infants without cUS abnormality had the lowest probability (23% and 26%) of
having delayed mental or psychomotor development. However, sensitivity of cUS as predictors
of later neurodevelopmental abnormalities only 16% at first and second weeks after birth, and if
re-examined at sixth weeks its sensitivity increase to 53%.44
Preterm and low birth weight (LBW) babies are at increased risk of experiencing complications
from vaccine-preventable diseases but are less likely to receive immunizations on time due to
high rates of medical complications related to premature birth and practitioner concerns of the
infant’s minimum ability to develop protective immune response after receiving routinely
recommended vaccines.45-47 This patient was born from HbsAg-negative mother with birth
weight less than 2.000 g, therefore no immunization was given early after birth. The observer
planned to give the patient first Hepatitis B vaccine later after she reaches 2.000 g body weight
or after she turns 1-month old of chronological age. Oral polio vaccine will be given to the
patient at time of discharge from the hospital in order to prevent the dissemination of polio
virus infection; otherwise inactivated polio vaccine is indicated. The rest of the immunization
will be given in accordance with the reccommended schedule.
At the end of the observation, life threatening condition has been reduced, so the ad vitam
prognosis of this patient is dubia ad bonam. 48 As a high-risk baby, a long-term follow up is
mandatory to detect any growth-development disorders and make appropriate early
intervention. Therefore, her ad functionam prognosis is dubia ad bonam. Nevertheless in this
patient, after 2 weeks of hospitalisation, the condition was improved, there was no deteriorate
condition. So her ad sanactionam prognosis is bonam. 49,50
Table 1. Planning for long-term follow up this patient
Every child has the rights to survives and thrives, learns, be protected from violence and
exploitation, lives in a safe and clean environment, and has a fair chance in life. UNICEF’S
commitment to data for children is guided by the fact that the Sustainable Development Goals
(SDGs) in 2030 will impact every aspect of a child’s well-being. 51 The goal is to achieve a 30%
reduction in the number of infants born with a weight lower than 2.500 g by the year 2025. In
this case, patient is the first chuld in the family, with teenage parents, both mother and father
had low educational background, low socioeconomic status, and who lived in crowded home
environtment. These factors could increase psychological distress to parents, particularly for
mother and increasing the risk of neglection to the patient.52 Family counseling to other family
37
member is crucial to support mother in carrying her children. The information given to the
families are related to feeding, hygiene, bathing, affective bonding, signs and symptoms of
baby’s sickness and other warning signs that needed to get early medical assistance. Families
were also orientated about outpatient clinic visits, use of vitamins, vaccination schedule,
growth, and development monitoring.
CASE ANALYSIS
This patient was a preterm baby (32 weeks of gestation and birth weight of 1580 g) with
respiratory distress at birth. Based on birth weight and gestational age, this baby was classified
as a moderate to late preterm baby (gestational age 32- <37weeks) with low birth weight
(birth weight <2500 g). Unfortunately, the etiology in most cases of preterm labor is unknown.
Mothers age (<20 or >35 years old), low social status, inadequate antenatal care (<6 controls),
history of premature birth, preeclampsia, anemia, infection and antepartum hemorrhage are the
factors to get preterm birth in Indonesia. 1 Our patient was born from a 36 years old mother with
preterm labor, urinary tract infection, inadequate ANC (only 3 times) and low social economic
status as the risk factors for preterm labor. Preterm infants are particularly vulnerable to
complications due to immature organ systems that are not yet prepared to support life in the
extrauterine environment. The risk of acute neonatal illness decreases with gestational age,
reflecting the fragility and immaturity of the brain, lungs, immune system, kidneys, skin, eyes
and gastrointestinal system. In general, more immature preterm infants require more life
support. There is controversy about how infants at the border of viability should be managed.
Specific complications such as central nervous system, haemorrhage and/or ischaemia,
respiratory distress syndrome (RDS), necrotizing entercolitis (NEC), retinopathy of prematurity
(ROP), hearing impairment, patent ductus arteriosus (PDA), nosocomial infection and chronic
lung disease must be evaluated, as they have a significant impact on long-term growth and
development outcome.1,2
Two days prior to delivery, the patient’s mother laboratory work up indicated the presence of
urinary tract infection, anemia and leukocytosis up to 17.400/μL. Intravenous broad-spectrum
antibiotics were then given to treat the urinary tract infection and to decrease risk of sepsis. The
mother had already given a course of antenatal corticosteroid to enhance fetal lung maturation
two days before delivery due to preterm labour and no improvement with anti-tocolytic agent. A
single course of corticosteroids is recommended for pregnant women < 34 weeks of gestation
and multiple gestations. The mechanism of antenatal glucocorticoids in reducing the risk of RDS
in premature is by improved neonatal lung function with enhance maturational changing in lung
architecture and induced enzymes that stimulate phospholipid synthesis and release of
surfactant.3 A Cochrane Database review published that antenatal corticosteroids associated
with an overall reduction in RDS (RR 0.66, 95% CI 0.56-0.77). Corticosteroid treatment was also
associated with a significant reduction in the risk of intraventricular haemorrhage (IVH) (RR
0.55, 95% CI 0.40-0.76) and neonatal mortality (RR 0.69, 95% CI 0.59-0.81), compared with
neonates whose mothers did not receive antenatal corticosteroids.3 (Level of evidence 1a)
Respiratory problems/distress at birth are still the most common complications because of a
failure in rapid transition process from intrauterine to extrauterine life. A successful transition is
38
characterized by alveolar fluid clearance, lung expansion and circulatory changes.2,4,5 However,
respiratory distress is not exclusively due to lung problem. Other condition such as heart
disease, cardiovascular problems (shock), hypoglycemia and hypo/hyperthermia could manifest
as respiratory distress as well. The patient presented with increased work of breathing (chest
retractions) at birth which were characteristics of respiratory distress. 4 There are several
differential diagnosis etiology of his respiratory distress, such as RDS, transient tachypnea of the
newborn (TTN) and neonatal pneumonia (sepsis).
Diagnosis of RDS was established in this patient supported by his gestational age, no history of
thick-greenish amniotic fluid. Respiratory distress syndrome which is previously called
hyaline membrane disease (HMD), is caused by deficiency of surfactant, the phospholipid
mixture that reduces alveolar surface tension, which decreases the pressure needed to keep the
alveoli inflated and maintains alveolar stability especially during end expiration. Respiratory
distress and possibly cyanosis at or shortly after birth and increases in severity over the first 2
days of life. 2-5 EuroNeoStat annual report for very low gestational age infants 2010 indicates a
rate of 92% for RDS in newborn babies with a gestational age (GA) of 24-25 weeks, 88% at 26-
27 weeks, 76% at 28-29 weeks and 57% at 30-31 weeks. In moderate-late preterm baby, the
frequency of RDS was 33.1%, 18.2%, 9.9%, 4.6% and 1.6% in 32, 33, 34, 35 and 36 weeks of
gestation, respectively.6
Chest radiography may be useful in differentiating among the disorders neonatal respiratory
distress which its classical findings are diffuse, reticulogranular and ground glass appearance.4,5,7
In this case from chest radiography showed a reticulogranular pattern. Nevertheless, sepsis
could not be ruled out at that time due to presence of maternal and neonatal risk factors.
Principal aspects in global approach strategy for RDS consist of prenatal care, delivery room
stabilization, respiratory support, surfactant and supportive care. 4,5 His RDS was managed with
non-invasive respiratory support. The earlier continuous positive airway pressure (CPAP) was
applied to avoid chance to get mechanical ventilation and reduce the need for surfactant
therapy.7 Randomized clinical trials suggest that nasal CPAP is acceptable as an alternative to
surfactant administration in preterm infants with RDS. Prophylactic nasal CPAP given within 15
minutes after birth regardless of respiratory status in preterm infants reduces the need for
mechanical ventilation (RR 0.50, 95% CI 0.42 to 0.59) and surfactant (RR 0.54, 95% CI 0.40 to
0.73) and also reduces the incidence of bronchopulmonary dysplasia at 36 weeks (RR 0.89, 95%
CI 0.79 to 0.99) and death or BPD (RR 0.89, 95% CI 0.81 to 0.97). 7 (Level of evidence 1a)
Unfortunately, after CPAP already increased to positive end expiratory pressure (PEEP) 8
mmH2O and FiO2 up to 40% the patient still had mild respiratory distress, it was indicated
failure of CPAP support and continued with nasal intermittent positive pressure ventilation
(NIPPV). Nasal intermittent positive pressure ventilation had less duration of oxygen therapy
than conventional ventilator (7.77 vs 9.28 days; p=0.05) and shorter length of stay (41.7 vs 48.7
days; p=0.097) in preterm infants with CPAP failure. 8 (Level of evidence 2b) Administration of
antenatal glucocorticoids and use of NIPPV shortened the RDS problems.
Normal BGA in this patient could be a result of successful of early oxygen therapy so that his
oxygen therapy could progressively weaned off to high flow nasal (HFN). High flow nasal oxygen
use has similar rates of efficacy to other forms of non-invasive respiratory support in preterm
39
infants for preventing treatment failure, death and chronic lung disease. High flow nasal oxygen
is associated with less nasal trauma, and may be associated with reduced pneumothorax
compared with nasal CPAP.7,8
Beside RDS, preterm baby who born before 34 weeks GA had risk of apnea of prematurity
(AOP). The incidence of recurrent apnea is increased with decreasing GA and factors implicated
in the pathogenesis are delayed central nervous system development and excessive bradycardic
response. It usually begins at the first 7 days of life and self-limiting once the baby reach mature
age.9 Symptoms of AOP can be a result of sepsis, significant ductus arteriosus, hypoxic ischemic
encephalopathy (HIE), abdominal distention (necrotizing enterocolitis), nasal obstruction,
hypoglycemia, hypo or hyperthermia and severe anemia. Prone position, use of HFN and NIPPV
and administration of xanthine derivate (aminophylline) was already given to this patient for
AOP treatment. Pharmacological effects of methylxanthines in AOP include stimulation of the
respiratory center in the medulla, increased sensitivity to carbon dioxide, increased skeletal
muscle tone, enhanced diaphragmatic contractility and increased minute ventilation.8,9,10 During
observation, after aminophylline administration, there was no apneic episode.
Patient was a preterm baby who born from a mother with urinary tract infection and
leucocytosis up to 17.400 /μL. Although there were no other clinical signs of chorioamnionitis,
he was still considered at risk for early onset sepsis (EOS).11,12 Early onset sepsis (EOS) term is
used when the onset of symptoms appear within the first 3 days of life. Organisms causing EOS
ascend from the birth canal resulting in intra-amniotic infection, which commonly referred as
chorioamnionitis. Chorioamnionitis, colonization of grup B streptoccus (GBS), preterm
premature rupture of membrane (PPROM) >18 hours, and gestational age <37 weeks are the
main risk factors of EOS.11 The signs of sepsis are non-specific, therefore identification of
neonates at risk for EOS is frequently based on a constellation of perinatal risk factors that are
neither sensitive nor specific.
At birth, the patient showed respiratory distress which could lead us to a symptom of neonatal
sepsis until proven otherwise. He was immediately given empirical first line antibiotics and
complete septic work up was carried out. Initial septic markers were within normal limits. After
5 days of treatment, the patient was clinically stable. Based on his condition, supported by a
sterile blood culture, administration of antibiotics was stopped. Combination of two serial
normal I:T ratios and a negative blood culture at 24 hours is indicative of noninfective neonates
(negative predictive value 100%).12 (Level of evidence 2b) The patient’s mother was given IV
antibiotics on admission for 2 consecutive days which may help reduce the risk of EOS in the
patient. This patient was also given prophylaxis of fungal infection with nystatin oral. This
therapy was given to prevent invasive fungal infection later on. Based on the latest meta-
analysis, nystatin significantly reduced the incidence of invasive fungal infection in low birth
weight baby compared to placebo or no drug (RR 0.20, 95% confidence interval 0.14 to 0.27). 13
(Level of evidence 1a)
Neonatal jaundice is the most common morbidity in the neonatal period and 5-10% of all
newborns require intervention for pathological jaundice. 14 The patient was jaundice on the age
of 4 days. In premature infants, visible jaundice cause by predominant unconjugated bilirubin
usually appears between 24-72 hours of age and the peak on the 5 th day of life.14,15 Patient in
gestational age 32 0/7 – 33 6/0 weeks should initiate phototherapy if TSB 10-12 mg/dL and
40
exchange transfusion is recommended if TSB reach 15-18 mg/dL. 15 Blood examination showed
hyperbilirubinemia (total bilirubin 6.53 mg/dL), predominated by unconjugated bilirubin. This
TSB level did not indicate phototherapy. There was no risk for rhesus and ABO incompatibility in
this patient. Hemolitic condition such as G6PD, was one of the differential diagnose in this early
neonatal jaundice. Unfortunately, this enzyme was not checked due to family financial problem. 15
Patient with risk factors of sepsis. Therefore, the cause of hyperbilirubinemia was probably
caused by not only physiological immaturity to manage the increasing of bilirubin production
but also sepsis. Sepsis could decrease the binding affinity albumin for bilirubin. 15
In normal infants, endogenous surfactant reduced the need for oxygen therapy in the first 72
hours after birth. This patient depended on oxygent therapy for almost 7 days. We suspected the
patient had a heart condition. Patent ductus arteriosus (PDA) is the most common cardiac
condition among preterm infants.2,16 We evaluate the patient’s echocardiography and showed
small PDA with duct diameter less than 1.4 mm/kg (<2.2 mm: 2 mm) and hemodynamically
insignificant.17 This condition did not need special treatment.
Intensive nutrition should be initiated from birth as this is known not only to achieve basal
metabolic needs, but also to support postnatal growth. Low birth weight infants are
characterized by significant weight loss in the initial days and weeks because of catabolic illness
and insufficient protein energy supply.20-22 Parenteral nutrition is necessary to meet energy and
nutrient requirements while enteral feeds are introduced and progress together with minimal
enteral nutrition (MEN). Oral care with colostrum can help in promoting the health and
development of preterm infants. There is a significant increase of the gram-negative flora in
patients without oral care. Minimal enteral or ‘trophic’ feeding using 10–20 ml/kg/ day of
breast milk, should be provided to enhance maturation and function of the gastrointestinal
tract.21,23 Cochrane reviews show no increase in the risk of necrotizing enterocolitis (NEC) with
trophic feeding, earlier initiation of feeding or more rapid advancement of feeds. The latest
study revealed that early feeding in preterm IUGR neonates as a standardized feeding initiation
and advancement plan does not increase the risk of NEC or feeding intolerance in very preterm
infants (p=0.636, RR 1.58; 95% CI 0.236-10.605).24
Feeding intolerance is common in premature infants. The most frequent signs of a suspect
feeding intolerance are the presence of gastric residuals, abdominal distension, the onset of
apnea/bradycardia and failure to reach the full enteral feed of 140 mL/kg/day within 10 days of
starting feed. Abdominal girth and gastric residual volume was not good indicator of feed
tolerance.26,27 The patient had reccurent vomiting 7 days after birth, when oral intake increase to
70 mL/kg, then positioning and feeding volume was decreased to the last tolerable volume.
Feeding was reached 126 ml/kg/day, but at 12 days of life patient looked lethargy, desaturated
54%, abdominal distended but no vomitting. Patient was checked for infection marker, and the
result was normal, so late on sepsis was excluded. Then enteral feeding was adjusted to patient’s
conditon, positioning and slow bolus feeding (1-2 hours) were applied to reduce
gastroesophageal reflux. To promote sucking-swallowing coordination this patient had oral
motor intervention using oral stimulation.27
Preterm infants lack the rapid fetal iron accretion during the third trimester of pregnancy and
also susceptible to zinc deficiency because of low body stores (60% of fetal zinc is acquired
41
during the third trimester of pregnancy).29-31 It caused by limited capacity to absorb and retain
micronutrients, coupled with increased endogenous losses associated with organ immaturity,
high nutrient demand to support catch-up growth and inadequate intakes. As a consequences,
disturbation development of brain structure and neurotransmission could happen. Hence, an
elemental iron intake of 2–4 mg/kg/day and zinc intake from 1 to 2.5 mg/kg/d up to 3 mg/kg/d
for LBW infants is recommended for stable growing preterm infants.29,32 In this patient, Fe and
Zn was not yet fully supported from preterm formula and no preparation of parenteral. Target
will be achieve when patient got full oral feeding.
Preterm infants lose more weight and regain birth weight slower than term infants. Weight gain
generally begins by the second week of life. A premature infant should given 50–60 kcal/kg/day
to maintain weight and 110–140 kcal/kg/day to achieve weight gain. Infants who have
respiratory distress syndrome have a range of estimated resting energy expenditure of 40-60
kcal/kg per day, with caloric needs directly proportional to the severity of the illness. 20,21 In this
patient, the weight lose was 9.2% of his birth weight and couldn’t catch up to birth weight less at
10 day of life. This could happen because of several factors. His mother couldn’t support
breastmilk for enough volume and feeding intolerance in preterm infant. The enteral feeding
was changed to breast milk foritfier and combined with preterm formula. After that his weight
gain was 10 g/kg/day. Nutritional support has been made since birth. Patient was supported by
aggressive parenteral nutrition even his enteral nutrition was increased. After the PICC inserted,
lipid could given until 3 g/kg/day, protein 3 g/kg/day, the GIR could increased to 8 mg/kg/min,
and the total calory also maintained almost 2 times of his resting energy expenditure. Beside
that, comorbidities of this patient such RDS, sepsis were also managed properly so further
complication could be avoided. Kangaroo mother care (KMC), which initiated as soon as his
condition clinically stable, could promote bonding, better regulation in HR, breathing, and
temperature, also to achieve rapid growth with positive impacts on their brain and emotional
development.33
Impaired neurodevelopmental outcome is a major long-term complication for premature

infants. The neurodevelopmental sequelae that can be found in these survivors are impaired
cognitive skills, motor deficit including mild one, gross motor delay, and cerebral palsy (CP),
sensory impairment including vision and hearing losses, behavioral and psychological
problems.34,35 Preterm infants had 20 times higher risk of hearing loss, either sensorineural or
conductive, than full terms with normal weight. Generally, all neonates, especially with the birth
weight less than 2,000 g are indicated for the hearing and visual evaluation after discharge . This
patient had normal result (pass) on first hearing screening test and plan to evaluate with ABR at
3 months of age as recommended by American Academy of Pediatrics. 36 Hypoxia, arterial carbon
dioxide pressure changes, arterial pH and oxygen consumption with high dosage are influential
factors in visual defects in infants with LBW. A study reported that the prevalence of visual
impairment is 5.21% and blindness is 0.5% in preterm. 37 Retinopathy of prematurity (ROP) is
one of the most common causes of visual loss in preterm infants, which is preventable.
Retinopathy of prematurity screening is recommended for infants with a BW of ≤1.500 g or GA
of 30 weeks or less, selected infants with a BW between 1.500 and 2.000 for GA > 30 weeks with
an unstable clinical course by an experienced ophthalmologist. In this patient, screening of ROP
is recommended because history of an unstable clinical course and need oxygene therapy for
several days.37 Screening for ROP was already performed and showed immature retina on both
eyes. Re-evaluation is scheduled for two weeks afterwards. 38,39
42
Significant advances in the nutritional care of preterm infants such as the initiation of early
intravenous nutrition, early enteral feeds, breastmilk fortifier and preterm formula have been
associated with a declining incidence of metabolic bone disease (MBD) in preterm infants. MBD
presents between 6 and 12 weeks of age but may remain asymptomatic for weeks until overt
rickets or fractures develop.40 Symptoms may include poor weight gain, faltering growth, and
respiratory difficulties or failure to wean off ventilatory support due to excessive chest wall
compliance. Serum calcium values may remain normal until late in the course. Low
concentrations of inorganic phosphate (<1.8 mmol/L with elevated alkaline phosphatase (>900
IU/L) were choices of laboratory examination in diagnosing inadequate intake and low bone
mineral density.40 Patient was planned to check complete electrolytes, alkaline phosphatase and
inorganic phosphate after chronological age of 28 days.
The preterm infants’ brain is vulnerable to both hemorrhagic and ischemic injury during the late
second and early third trimester. Early diagnosis is important for prognostication, optimal
treatment and neurological outcome.41,42 Cranial ultrasound (cUS) is a simple bedside tool to
evaluate intracranial haemorrhage. Cranial US had high sensitivity (100%) and specificity
(93.3%) in detecting grade III intraventricular haemorrhage, but poor sensitivity in the
detection of intraventricular hemorrhage with normal-sized ventricles. 42 Cranial US examination
in patient were in normal limit. Infants without cUS abnormality had the lowest probability
(23% and 26%) of delayed mental or psychomotor development. However, sensitivity of cranial
ultrasound examinations as predictors of later neurodevelopmental abnormalities only as 16%
at one and two weeks after birth, and if re-examined at six weeks its sensitivity increase to
53%.42
Preterm and low birth weight (LBW) babies are at increased risk of experiencing complications
of vaccine-preventable diseases but are less likely to receive immunizations on time due to high
rates of medical complications related to premature birth and practitioner concerns for the
premature infant’s fragility and ability to develop protective immunity after receiving routinely
recommended vaccines.45-47 This patient was born preterm to HbsAg negative mother with birth
weight less than 2.000 g, therefore no immunization was given early after birth. The observer
has planned to give the patient first Hepatitis B vaccine later after he reaches 2.000 g or after
she turns 1 month old. Oral polio vaccine will be given to the patient after discharged from the
hospital in order to prevent the dissemination of polio virus; otherwise inactivated polio vaccine
is indicated. The rest of the immunization will be given in accordance with the schedule.
At the end of observation, life threatening condition has been reduced, so his ad vitam prognosis
of this patient is dubia ad bonam.48 As a high risk baby, a long-term follow up is needed to early
detection of any growth and development disorders and make appropriate intervention.
Therefore, his ad functionam prognosis is dubia ad bonam. Nevertheless in this patient, after 2
weeks of hospitalisation, the condition was improved, there was no deteriorate condition. So
that his ad sanactionam prognosis is bonam. 13,14
Table 1. Planning for long-term follow up this patient
43
Every child has the rights to survives and thrives, learns, protected from violence and
exploitation, lives in a safe and clean environment, and has a fair chance in life. UNICEF’S
commitment to data for children is guided by the fact that the Sustainable Development Goals
(SDGs) in 2030 will impact every aspect of a child’s well-being. 47 The goal is to achieve a 30%
reduction in the number of infants born with a weight lower than 2500 g by the year 2025. In
this case, parents have 3 children and this patient was actually unplanned pregnancy, mother
had low education background, low socioeconomic and live in crowded home environtment.
That factors could increase psychological distress to parents, particularly for mother and caused
the risk of neglect or abuse either to patient or her siblings. 49
Family counseling to other family is needed to support mother in carriying his children. The
information dispensed to families are related to feeding, hygiene, bathing, affective bonding and
signs and symptoms of sick. Families were also orientated about outpatient clinic, use of
vitamins, vaccination schedule, growth, and development.
44
LIST OF ABBREVIATIONS
A/S : Apgar score IV : intravein

ABR : auditory brainstem response KMC : kangaroo mother care
AC : abdominal circumference LBW : low birth weight
AGA : appropriate for gestational age LOS : late-onset sepsis
ANC : antenatal care MBD : mineral bone disease
AOG : age of gestation MH : morbus hirschsprung
AOP : apnea of prematurity NEC : necrotizing enterocolitis
ARR : absolute risk ratio NICU : neonatal intensive care unit
BGA : blood gas analysis NIPPV : non-invasive positive pressure
BL : birth length ventilation
BPJS : Badan Penyelenggara Kesehatan NNT : number needed to treat
Nasional NPO : nothing per oral
bpm : beats per minute O2 : oxygen
BW : birth weight OGT : orogastric tube
C/S : culture and sensitivity OR : odd ratio
CBC : complete blood count PEEP : positive end expiratory
CI : confidence interval pressure
CNS : central nervous system PICC : peripherally inserted central
CP : cerebral palsy catheter
CPAP : continuous positive airway PLN : Perusahaan Listrik Negara
pressure po : per oral
cpm : cycles per minute PPROM: preterm premature rupture of
CRP : C-reactive protein membrane
CRT : capillary refill time RBC : red blood cells
CTG : cardiotocography RBG : random blood glucose
cUS : cranial ultrasound RDS : respiratory distress syndrome
ELBW : extremely low birth weight ROP : retinopathy of prematurity
EOS : early-onset neonatal sepsis RR : respiratory rate
EPO : erythropoietin SDGs : Sustainable Development Goals
FiO2 : fraction of inspired oxygen SIMV : synchronized intermittend
GA : gestational age mandatoryl ventilation
GE : gastroesophageal TPN : total parenteral nutrition
GIT : gastrointestinal tract TSB : total serum bilirubin
GIR : glucose infusion rate TTN : transient tachypnea of the
HbsAg : hepatitis B surface antigen newborn
HC : head circumference UNICEF: United Nations International
HFN : high flow nasal Children's Emergency Fund
HR : heart rate UVC : umbilical vein catheter
IM : intramuscular WBC : white blood cells
I:T : immature:total
45
REFERENCES
1. Hidayat, ZZ, Ajiz EA, Achadiyani, Krisnadi SR. Risk factors associated with preterm birth at Hasan
Sadikin General Hospital in 2015. OJOG. 2016;6:798-806.
2. Ward RM, Beachy JC. Neonatal complications following preterm birth. BJOG. 2003;110:8-16.
3. Roberts D, Brown J, Medley N, Dalziel S. Antenatal corticosteroids for accelerating fetal lung
maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2018;3:CD004454.
4. Sweet DG, Carnielli V, Greisen G, Hallman M, Ozek E, Plavka R, et al. European consensus
guidelines on the management of neonatal respiratory distress syndrome in preterm infants--
2013 update. Neonatology. 2013;103:353–68.
5. Grappone L, Messina F. Hyaline membrane disease or respiratory distress syndrome? a new
approach for an old disease. J Pediatr Neonat Individual Med. 2014;3:e030263.
6. Condo V, Cipriani S, Colnaghi M, Bellu R, Zanini R, Bulfoni C, et all. Neonatal respiratory distress
syndrome: are risk factors the same in preterm and term infants? J Matern Fetal Neonatal Med.
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7. Subramaniam P, Ho JJ, Davis PG. Prophylactic nasal continuous positive airway pressure for
preventing morbidity and mortality in very preterm infants. Cochrane Database Syst Rev.
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8. Bediee Z, Nekooie B, Mohammadizadeh M. Noninvasive positive pressure ventilation or
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J Prev Med. 2014;5:1045-53.
9. Eichenwald EC, AAP Committee on Fetus and Newborn. Apnea of prematurity. Pediatrics.
2016;137:e20153757.
10. Armanian AM, Badiee Z, Afghari R, Salehimehr N, Hassanzade A, Sheikhzadeh S, et al. Prophylactic
aminophylline for prevention of apnea at higher-risk Preterm neonates. Iran Red Crescent Med J.
2014;16:1-6.
11. Polin RA, AAP Committee on Fetus and Newborn. Management of neonates with suspected or
proven early-onset bacterial sepsis. Pediatrics. 2012;129:1006–15.
12. Murphy K, Weiner J. Use of leukocyte counts in evaluation of early-onset neonatal sepsis. Pediatr
Infect Dis J. 2012;31:16-9
13. Austin N, Cleminson J, Darlow BA, McGuire W. Prophylactic oral/topical non-absorbed antifungal
agents to prevent invasive fungal infection in very low birth weight infants. Cochrane Database
Syst Rev. 2015;10:CD003478.
14. Ullah S, Rahman K, Hedayati M. Hyperbilirubinemia in neonates: types, causes, clinical
examinations, preventive measures and treatments: a narrative review article. Iran J Public
Health. 2016;45:558–68.
15. Maisels MJ, Watchko JF, Bhutani VK, Stevenson DK. An approach to the management of
hyperbilirubinemia in the preterm infant less than 35 weeks of gestation. J Perinatol.
2012;32:660–4.
Daftar Pustaka
1. Hidayat, ZZ, Ajiz EA, Achadiyani, Krisnadi SR. Risk factors associated with preterm birth
at Hasan Sadikin General Hospital in 2015. OJOG. 2016;6:798-806.
2. Ward RM, Beachy JC. Neonatal complications following preterm birth. BJOG. 2003;110:8-
16.
3. Roberts D, Brown J, Medley N, Dalziel S. Antenatal corticosteroids for accelerating fetal
lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev.
2017;3:CD004454.
4. Smolders-de Haas H, Neuvel J, Schmand B. Physical development and medical history of
children who were treated antenatally with corticosteroids to prevent respiratory
distress syndrome: a 10- to 12-year follow up. Pediatrics. 1990;86:65.
5. Ward RM, Beachy JC. Neonatal complications following preterm birth. BJOG. 2003;110:8-
16.
6. Sweet DG, Carnielli V, Greisen G, Hallman M, Ozek E, Plavka R, et al. European consensus
guidelines on the management of neonatal respiratory distress syndrome in preterm
infants--2013 update. Neonatology. 2013;103:353–68.
7. Grappone L, Messina F. Hyaline membrane disease or respiratory distress syndrome? a
new approach for an old disease. J Pediatr Neonat Individual Med. 2014;3:e030263.
46
8. Reuter S, Moser C, Baack M. Respiratory distress in the newborn. Pediatr Rev. 2014;
35:417-29.
9. Condo V, Cipriani S, Colnaghi M, Bellu R, Zanini R, Bulfoni C, et all. Neonatal respiratory
distress syndrome: are risk factors the same in preterm and term infants? J Matern Fetal
Neonatal Med. 2017;30:1267-72.
10. Subramaniam P, Ho JJ, Davis PG. Prophylactic nasal continuous positive airway pressure
for preventing morbidity and mortality in very preterm infants. Cochrane Database Syst
Rev. 2016;6:CD001243.
conventional mechanical ventilation for neonatal continuous positive airway pressure
failure. Int J Prev Med. 2014;5:1045-53.
12. Eichenwald EC, AAP Committee on Fetus and Newborn. Apnea of prematurity.
Pediatrics. 2016;137:e20153757.
13. Armanian AM, Badiee Z, Afghari R, Salehimehr N, Hassanzade A, Sheikhzadeh S, et al.
Prophylactic aminophylline for prevention of apnea at higher-risk Preterm neonates.
Iran Red Crescent Med J. 2014;16:1-6.
14. Polin RA, AAP Committee on Fetus and Newborn. Management of neonates with
suspected or proven early-onset bacterial sepsis. Pediatrics. 2012;129:1006–15.
15. Murphy K, Weiner J. Use of leukocyte counts in evaluation of early-onset neonatal sepsis.
Pediatr Infect Dis J. 2012;31:16-9
16. Austin N, Cleminson J, Darlow BA, McGuire W. Prophylactic oral/topical non-absorbed
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50
Appendix 1. Lubchenco’s Curve
51
Appendix 2. Fenton Curve
52

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LONG CASE REPORT

Preterm Baby, Low Birth Weight Baby with Respiratory Distress

Kartika Sari WiduriResita Sehati

National Board Examination

Mayrch 2823thrd, 2018 May 24th, 2018 April 12thJune 6th,

Initial observation Reporting

Patient’s name : Baby Mrs. NL Father’s name : Mr. RA

Initial observation by candidate from Mayrch 2490th,2018

History of Present Illness

Growth and Development History

PHYSICAL EXAMINATION (NICU, March 29th, 2018)(SCN 4, May 23rd, 2018)

May 23rd , 2018March

Chest radiography (May 23rd, 2018March 28th, 2018):

2. Respiratory distress syndrome grade I

3. Early onset sepsis

May 24rch 30 th – 31st, 2018 (day-2-3 hospitalization)

Cranial ultrasound (May 24th, 2018):

Blood C/S: 1x24 hours: no growth yet

May April 1st - 25nthd, 2018 (day- 34-5 hospitalization)

April 1st, 2018 Normal value

Blood C/S: 24x24 hours: no growth yet

Abdominal x-ray (May 25th, 2018)

May 26April 3rthd -4 th, 2018 (day-4 6-7 hospitalization)

Blood C/S: no growth (sterile)Blood C/S: 3x24 hours: no growth yet

Head : open and flat anterior fontanelle, 2.5 x 2 cm size

Echocardiography April 6th, 2018

Enteral: Human milk/SF Human

April 10th -12rd, 2018 (day 13–15 of hospitalization)

Head : open and flat anterior fontanelle, 2.5 x 2 cm size

Cranial ultrasound (March 11st, 2018) : normal

A 1. Preterm baby (32 weeks), AGA, LBW (1580 g) (P 07.3) (P 07.0)

8x22 mL 8x22 mL 8x24mL

May 27th, 2018 (day-5 hospitalization)

Blood C/S: 4x24 hours no growth

May 28th, 2018 (day-6 hospitalization)

Blood C/S: no growth (sterile)

May 29th – 30th, 2018 (day 7-8 hospitalization)

May 31st – June 1st, 2018 (day 9-10 hospitalization)

Impression: normal TSH (May 31st)

o Balance and urine output

June 2nd to 3rd 2018 (day 11-12 hospitalization)

o Balance and urine output

June 4th to 6th 2018 (day 13-15 hospitalization)

Patient was also consulted to Ophthalmology Department to evaluate retinopathy of prematurity

ROP screening (June 5th, 2018) : bilateral immature retina

o Balance and urine output

 Further examination: screening osteopenia of prematurity (OOP)

2nd-3rd day of hospitalization 4-5th day of hospitalization

 Baby was quite active  No respiratory distress, no instability of temperature

 No instability of temperature, no apnea, nor  More active, no temperature instability

13-15th day of hospitalization

 No instability of temperature, no respiratory distress, no apnea

One of the most common complication in preterm infants is respiratory problems/distress at

Apnea of prematurity is a common problem affecting premature infants, its incidence is

Neonatal hyperbilirubinemia is a common problem. Approximately 60-70% of term and 80% of

Table 1. Planning for long-term follow up this patient

Impaired neurodevelopmental outcome is a major long-term complication for premature