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TIMELINE

January 29th, 2020 February 10th, 2020 February 11th, 2020 February 17th, 2020 February 18th, 2020

Patient was Initial Observation Final


born at K observation started observation Reporting
hospital by candidate

PATIENT’S RECORD
Candidate: Irene Aurelia Santoso
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I. IDENTITY
1.1. PATIENT’S IDENTITY
Registration number : 00.71.55.XX
Name of patient : NM
Date of birth : January 29th, 2020
Gender : Male
Nationality : Indonesia
Date of admission : January 29th, 2020

1.2. PARENT’S IDENTITY


FATHER MOTHER
Name : RM NM
Age : 42 years old 39 years old
Occupation : Employee Housewife
Education : Diploma Diploma

II. HISTORY
(Allo-anamnesis was taken from parents, physician, and medical record on
February 10th, 2020 in Neonatal Intensive Care Unit).
Chief complaint: shortness of breath.

2.1. HISTORY OF PRESENT ILLNESS


A male infant, NM, was delivered trough a cesarean section delivery because
his mother has a history of severe pre-eclampsia and previous cesarean
section. The delivery was assisted by obstetrician at K hospital on January
29th, 2020 at 06.00 am. Infant’s birth weight was 1,650 gram and body length
was 42 cm with Apgar score at first, fifth, and tenth minutes were 3-5-7. He
was born from a 39-year-old mother, G3P2A0 with 34-35 weeks of gestational
age. He did not cry immediately after birth. He had breathing difficulty and
seemed weak. He had rapid respiratory rate and grunting. During the first
hour of life, chest retraction was observed. Risk factors of sepsis on this
patient were gestational age less than 37 weeks and low Apgar score. New

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Ballard Score was 34-36 weeks. Patient was given CPAP Fi02 40% PEEP 7
cmH2O O2 flow 8 lpm, ampicillin and gentamicin antibiotics.

2.2. HISTORY OF PREGNANCY AND LABOR


Patient was born from a 39-year-old mother, G3P2A0, on 34-35 weeks of
pregnancy. Patient’s mother had more than 6 times antenatal examinations at
primary health care and received one dose of tetanus toxoid (TT)
immunization. During pregnancy, mother had hypertension induced
pregnancy in late trimester and did not consume any drugs or alcohol. His
mother was a non-smoker. The only medication she took was some vitamins
from the midwife. There was no history of trauma during pregnancy. Mother
never had any complaint on micturition or vaginal discharge associated with
pruritus or foul odor. Before delivery, mother was given two shots of
dexamethasone injection before giving birth. Mother did not have fever during
pregnancy and labor. Right after birth, infant got intramuscular vitamin K 1
injection on the left thigh and chloramphenicol eye drops for both eyes.

2.3. HISTORY OF FAMILY’S HEALTH


Patient’s mother had been tested for Hepatitis B infection before delivery and
the result was negative. There were no family members who had congenital
abnormalities. Patient’s siblings did not have similar complaints after birth.

FAMILY TREE

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STRUCTURE OF FAMILY MEMBERS

No Name Relation Gender Age Information


1 RM Father M 42 years Healthy
2 NM Mother F 39 years Healthy
3 WM Brother M 10 years Healthy
3 TM Brother M 9 years Healthy
5 MK Patient M 12 day Patient

2.4. PERSONAL/SOCIAL HISTORY


A. SOCIO-ECONOMIC AND ENVIRONTMENT CONDITION
Socio-economic
Patient’s father works as an employee and her mother is a housewife. Healthcare
expenses are covered by class III National Healthcare Insurance.
Environment
Patient’s family lives in their own house. Their house has tin roof, concrete wall, and
tiles floor. The house has two bedrooms, which are inhabited by 5 persons, consists
of 2 adults and 3 children. Bathroom is located inside the house. Water source is
coming from government owned water company and electricity source is coming
from the government owned electricity company. Waste is handled by dumping it to
a local waste disposal center.

B. HISTORY OF FEEDING
Patient hasn’t had any enteral feeding.

C. HISTORY OF IMMUNIZATIONS
Patient hasn’t gotten any vaccine.

D. HISTORY OF BASIC NEEDS


Patient is the third born child from a happy marriage family. Since his condition
hasn’t possible to be roomed-in, he was treated in level 3 Neonatal Intensive Care
Unit. His parents had given consent to take care of their child with maximal effort. It
showed that they love and care for their newborn

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PATIENT’S HOSPITAL ADMISSION SUMMARY
Prior to candidate’s initial observation (January 29 th- February 10th, 2020)
A male infant, NM, was delivered trough a cesarean section delivery because
his mother has a history of severe pre-eclampsia and previous cesarean section.
The delivery was assisted by obstetrician at K hospital on January 29 th, 2020 at
06.00 am. Infant’s birth weight was 1650 gram and body length was 42 cm with
Apgar score at first, fifth, and tenth minute were 3-5-7. He was born from a 39 years
old mother, G3P2A0 with 34-35 weeks of gestational age. He did not cry immediately
after birth. He had breathing difficulty and seemed weak. He had rapid respiratory
rate and grunting. During the first hours of life, chest retraction was observed. Risk
factor of sepsis on this patient include gestational age less than 37 weeks and low
Apgar score. New Ballard Score after birth was 34-36 weeks. Patient had received
intramuscular vitamin K1 injection and chloramphenicol eye drops right after birth.
Vital sign examination showed pulse rate 162 bpm (regular, full pulses),
respiratory rate 72 cpm, and body temperature 36.8°C. Oxygen saturation was 84%.
From head and neck examination, frontal fontanel was open and flat, no anemic
conjunctiva, no icteric sclera, but there was nasal flaring. On chest examination,
there was subcostal and intercostal retraction. Murmur was not found. The abdomen
was flat, soft on palpation, with normal bowel movement sound. There was no
hepatomegaly or splenomegaly. Umbilical cord examination was normal. Extremities
appeared normal without any cyanosis or deformities, and capillary refill time (CRT)
was less than 3 seconds. Total Downes score was 4. He was also examined for
babygram photo and complete blood test, then she transferred to level 3 NICU.
Babygram photo examination showed apparent, distinct, and coarse granularity to
the lung fields. Heart margin were clearly visible. Complete blood count examination
showed that Hb 17.0 g/dL, Ht 49.8%, Leukocyte 13,500/mm 3, Platelet 284,000/mm3,
CRP <6 mg/L, and differential count were: 3/0/0/54/30/13, I/T ratio 0, Ureum 14
mg/dL, Creatinine 0.8 mg/dL, ALT 51 U/L, AST 5 U/L, random blood glucose 86
g/dL. Blood gas analysis showed pH 7.29, pCO 3 53 mmHg, PaO2 78 mmHg, HCO3
26 mEq/L, base excess 0. Infant was diagnosed with preterm infant appropriate for
gestational age with grade I Hyaline Membrane Disease. The Infant was treated with
early initial continuous positive airway pressure (CPAP) FiO2 40% PEEP 7 cmH2O
and O flow 8 lpm, nothing per oral with nasogastric tube on, total parenteral nutrition
at the rate of 6 ml/hour and Ampicillin and Gentamicin antibiotics. Two hours after
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initial CPAP oxygenation patient was examined for blood gas analysis. The result
was normal with pH 7.39, pCO2 42.5mmHg, pO2 80mmHg and HCO3 22 mmol/L,
base excess 0.
On the third day of treatment, shortness of breath was improved and the
patient appeared icteric and he was started to received enteral trophic feeding. From
vital sign examination showed pulse rates of 156 bpm (regular, full pulses),
respiratory rate 62 cpm, body temperature 37⁰C, oxygen saturation was 95%. On
physical examination, there was no nasal flare and retraction, icteric was from head
to lower abdomen and thigh (Kramer III). The laboratory result showed Hb 16.8 g/dL,
Ht 50.4%, Leukocyte 8,100 /mm3, Platelet 244,000/mm3, CRP <6 mg/L, and
differential count were: 1/0/0/56/31/12, I/T ratio 0, total bilirubin 11.4 g/dl and direct
bilirubin 0.6 g/dl. Blood culture examination is awaiting result. The patient was
treated with CPAP FiO2 30%, PEEP 5 cmH2O, O2flow 8 lpm, given parenteral
nutrition at a rate of 8ml/hour, fed via orogastric tube 5ml breastmilk every 3 hours
and planned for phototherapy. Patient was diagnosed with preterm infant appropriate
for gestational age with grade I Hyaline Membrane Disease and hyperbilirubinemia.
On the fifth day of treatment, patient shortness of breath was decreased. Vital
sign examination found pulse rates 156bpm (regular, full pulses). Respiratory rates
55 cpm, body temperature 36.8°C, oxygen saturation 97%. Physical examination
found no nasal flaring or retraction, and icteric was reduced. From laboratory
examination found blood culture was negative and decreased total bilirubin from 11.4
to 5.6 g/dl. The patient was treated with discontinued of CPAP and continue with
nasal oxygen 0.5l/m, parenteral nutrition at the rate of 8 ml/hour and breastmilk via
orogastric tube and increased volume according to patient tolerance, antibiotics and
phototherapy was stopped. On initial candidate examination, the infant was 12 days
old.

III. PATIENT’S DATA AND CONDITION AFTER TAKEN AS A CASE REPORT

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Examination was done in Neonatal Intensive Care Unit, on February 10 th, 2020.
Complaint : No shortness of breath
General condition : Appeared active
Anthropometric status
Weight : 1.690 grams
Length : 43 cm
Vital signs : pulse 144 bpm (regular, full pulses), respiratory rate 44 cpm,
body temperature 36.6°C (axilla)
oxygen saturation 98%
Skin : light brown, no efflorescent

Head and Neck


Head : head circumference 32 cm (normocephal), open flat fontanel, no
dysmorphic facies
Eyes : no anemic conjunctiva, no icteric sclera, round and isochoric
pupils, diameter 2-2 mm, reactive to light, centered eyeballs,
clear lenses, normal eye movements to all directions
Nose : no secretion, nasal flaring (-)
Ears : no secretion, no deformities, both pinna formed completely
ready to recoil
Mouth : no cyanosis, moist buccal mucosa and lips
Throat : pharynx not hyperemic
Neck : centered trachea, no palpable lymph node enlargement
Chest : normal shape, symmetrical chest expansion, subcostal and
intercostal retraction (-)
Heart
Inspection : ictus cordis not visible, no precordial bulging
Palpation : ictus cordis palpable on left midclavicular line, 5th intercostal
space, no thrill
Percussion : right border at right parasternal line, left border at left
midclavicular line, upper border at 3rd left intercostal space
Auscultation : heart rate frequency 144 bpm, regular, no murmur

Lungs

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Inspection : symmetrical movement of breathing, no retraction, raised areola
3-4 mm bud
Palpation : symmetrical vocal fremitus
Percussion : normal, symmetrical resonant sounds
Auscultation : decreased bilateral bronchial breath sounds, symmetry, no rales,
no wheezing
Abdomen
Inspection : flat, no venectation
Palpation : soft, there was no hepatomegaly or splenomegaly
Percussion : tympanic
Auscultation : normal bowel sounds

Vertebrae : no deformity
Genitalia : male, testes down
Anus : intact
Extremities : warm, no cyanosis, CRT ≤ 3 seconds, no deformity,
plantar crease on 2/3 anterior
Muscles : normal muscle tone for all four extremities
Reflexes : almost good physiological reflexes (Moro, sucking,
rooting, graps, tonic neck reflex)

Cranial Nerves Examination:


NI : can’t be assessed yet
N II : he turns toward soft lights and able to fix and follow bright objects
N III, IV, VI : round, isochoric pupils, normal pupillary light response, doll’s eye (+),
normal extra-ocular movements
NV : almost good sucking reflex
N VII : symmetrical face when he was inactive like sleeping and active like
crying
N VIII : he responded well to sound stimulus
N IX, X, XII : almost good sucking reflex, normal gag reflex, tongue protrude in the
mid-line
N XI : his sternocleidomastoids and trapezoid muscle are symmetrical, with
normal size and fasciculation
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IV. SUMMARY
A male infant, NM, was delivered trough a cesarean section delivery because
his mother has a history of severe pre-eclampsia and previous cesarean section.
The delivery was assisted by obstetrician at K hospital on January 29 th, 2020 at
06.00 am. Infant’s birth weight was 1650 gram and body length was 42 cm with
Apgar score at first, fifth, and tenth minute were 3-5-7. He was born from a 39 years
old mother, G3P2A0 with 34-35 weeks of gestational age. He did not cry immediately
after birth. He had breathing difficulty and seemed weak. He had rapid respiratory
rate and grunting. During the first hours of life, chest retraction was observed. Risk
factor of sepsis on this patient include gestational age less than 37 weeks and low
Apgar score. New Ballard Score after birth was 34-36 weeks. Patient had received
intramuscular vitamin K1 injection and chloramphenicol eye drops right after birth.
Vital sign examination showed pulse rate 162 bpm (regular, full pulses),
respiratory rate 72 cpm, and body temperature 36.8°C. Oxygen saturation was 84%.
From head and neck examination, frontal fontanel was open and flat, no anemic
conjunctiva, no icteric sclera, but there was nasal flaring. On chest examination,
there was subcostal and intercostal retraction. Murmur was not found. The abdomen
was flat, soft on palpation, with normal bowel movement sound. There was no
hepatomegaly or splenomegaly. Umbilical cord examination was normal. Extremities
appeared normal without any cyanosis or deformities, and capillary refill time (CRT)
was less than 3 seconds. Total Downes score was 4. He was also examined for
babygram photo and complete blood test, then she transferred to level 3 NICU.
Babygram photo examination showed apparent, distinct, and coarse granularity to
the lung fields. Heart margin were clearly visible. Complete blood count examination
showed that Hb 17.0 g/dL, Ht 49.8%, Leukocyte 13,500/mm 3, Platelet 284,000/mm3,
CRP <6 mg/L, and differential count were: 3/0/0/54/30/13, I/T ratio 0, Ureum 14
mg/dL, Creatinine 0.8 mg/dL, ALT 51 U/L, AST 5 U/L, random blood glucose 86
g/dL. Blood gas analysis showed pH 7.29, pCO 3 53 mmHg, PaO2 78 mmHg, HCO3
26 mEq/L, base excess 0. Infant was diagnosed with preterm infant appropriate for
gestational age with grade I Hyaline Membrane Disease. The Infant was treated with
early initial continuous positive airway pressure (CPAP) FiO2 40% PEEP 7 cmH2O
and O flow 8 lpm, nothing per oral with nasogastric tube on, total parenteral nutrition
at the rate of 6 ml/hour and Ampicillin and Gentamicin antibiotics. Two hours after
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initial CPAP oxygenation patient was examined for blood gas analysis. The result
was normal with pH 7.39, pCO2 42.5mmHg, pO2 80mmHg and HCO3 22 mmol/L,
base excess 0.
On the third day of treatment, shortness of breath improved and the patient
appeared icteric and he was started to received enteral trophic feeding. From vital
sign examination showed pulse rates of 156 bpm (regular, full pulses), respiratory
rate 62 cpm, body temperature 37⁰C, oxygen saturation was 95%. On physical
examination, there was no nasal flare and retraction, icteric was from head to lower
abdomen and thigh (Kramer III). The laboratory result showed Hb 16.8 g/dL, Ht
50.4%, Leukocyte 8,100 /mm3, Platelet 244,000/mm3, CRP <6 mg/L, and differential
count were: 1/0/0/56/31/12, I/T ratio 0, total bilirubin 11.4 g/dl and direct bilirubin 0.6
g/dl. Blood culture examination is awaiting result. The patient was treated with CPAP
FiO2 30%, PEEP 5 cmH2O, O2flow 8 lpm, given parenteral nutrition at a rate of
8ml/hour, fed via orogastric tube 5ml breastmilk every 3 hours and planned for
phototherapy. Patient was diagnosed with preterm infant appropriate for gestational
age with grade I Hyaline Membrane Disease and hyperbilirubinemia.
On the fifth day of treatment, shortness of breath was decreased. Vital sign
examination found pulse rates 156 bpm (regular, full pulses). Respiratory rates 55
cpm, body temperature 36.8°C, oxygen saturation 97%. Physical examination found
no nasal flaring or retraction, and icteric was decreased. From laboratory
examination found blood culture was negative and decreased total bilirubin from 11.4
to 5.6 g/dl. The patient was treated with discontinued of CPAP and continue with
nasal oxygen 0.5l/m, parenteral nutrition at the rate of 8 ml/hour and breastmilk via
orogastric tube and increased volume according to patient tolerance, antibiotics and
phototherapy was stopped. On initial candidate examination, the infant was 12 days
old.

V. DIAGNOSIS
- Preterm infant appropriate for gestational age (P07.38)
- Grade I Hyaline Membrane Disease (P22.0)
- Hyperbilirubinemia (E80.6)

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VI. PROBLEM
Prognosis in preterm infant appropriate for gestational age with Hyaline
Membrane Disease.

VII. MANAGEMENT PLANS


1. Treatment plans
- Placed inside the incubator
- Nutritional care until reach targeted body weight
2. Pediatric nutritional care
A. Nutritional status assessment
According to Lubchenco curve, an infant with 34-36 weeks of gestational
age, 1,650 grams birth weight and 42 cm body length is defined as
Appropriate for Gestational Age.
B. Nutritional status assessment
According to Lubchenco curve, an infant with 34 weeks of gestational age,
1,650 gram birth weight and 42 cm body length is defined as appropriate
for gestational age.
C. Nutritional requirements
Ideal body weight = 2.300 grams (based on 2013 Fenton Growth Chart for
Boys)
Each 100 mL of preterm breast milk consists of 71 kcal, 1.5 grams of
protein and 3.5 grams of fat.
Calories : 115-120 kcal/kgBW/day = 265 - 276 kcal/day
D. Nutritional route: oral
E. Nutrition in this infant were given with solution of:
Breast milk 50 ml every 3 hours via oral (@35 kcal, 0.8 gr protein and 1.8

gram of fat)

F. Monitoring and evaluation: acceptability, body weight, and urine


production.

3. Counselling plan
Progress of the disease, therapy and prognosis, immunization, growth and
development.

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4. Monitoring plan
- Oxygen support
- General state and vital signs monitoring
- Body weight daily monitoring until reach 1,800 grams
- Nutrition, fluid, and calories intake monitoring everyday
- Monitoring of hygiene for parents, doctors, and nurses
- Do the screening for retinopaty of prematurity and hearing function

6. Education plan
- Describes the illnesses of the patient: causes, treatment, prognosis,
complications and treatment plans.
- Education to maintain personal and environmental hygiene, and avoid any
infectious environment
- Education on immunization plans
- Education on how to give a proper stimulation for growth and development

Nursing care
1. Vital sign monitoring
2. Nutrition and growth development
3. Hygiene control of parents, doctors and nurses
4. Input and output monitoring

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VIII. FOLLOW UP

February 11th, 2020 (1st observation day, 13th day of hospitalization)


S Shortness of breath (-), icteric (-), intake (+)
O Body weight: 1,700 grams
- General condition: appeared active
- Pulse: 150 bpm
- Respiratory rate: 48 cpm
- Body temperature: 36.9ºC (axilla)
- SpO2 : 98%
Head : no anemic conjunctiva, anicteric sclera, no nasal flaring
Chest : symmetrical movement, no retraction
Heart : no murmur, no gallop
Lungs : bronchial breath sounds, no rales, no wheezing
Abdomen : flat, soft, normal bowel sound, there was no hepatomegaly or
splenomegaly, clean umbilical cord
Extremities : warm, CRT ≤ 3 seconds
A - Preterm infant appropriate for gestational age (P07.38)
- Grade I Hyaline Membrane Disease (P22.0)
P Medications :
-
Nutritional care :
Breast milk 50 ml every 3 hours via oral (@35 kcal, 0.8 gr protein and 1.8

gram of fat)

Nursing care : same as before

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February 12th, 2020 (2nd observation day, 14th day of hospitalization)
S Shortness of breath (-), icteric (-), intake (+)
Body weight: 1,720 grams
- General condition: appeared active
- Pulse: 144 bpm
- Respiratory rate: 50 cpm
- Body temperature: 36.8ºC (axilla)
- SpO2 : 98%
Head : no anemic conjunctiva, anicteric sclera, no nasal flaring
Chest : symmetrical movement, no retraction
Heart : no murmur, no gallop
Lungs : bronchial breath sounds, no rales, no wheezing
Abdomen : flat, soft, normal bowel sound, there was no hepatomegaly
or splenomegaly, clean umbilical cord
Extremities : warm, CRT ≤ 3 seconds
A - Preterm infant appropriate for gestational age (P07.38)
- Grade I Hyaline Membrane Disease (P22.0)
P Medications :
-
Nutritional care :
Breast milk 50 ml every 3 hours via oral (@35 kcal, 0.8 gr protein and 1.8

gram of fat)

Nursing care : same as before

February 13th, 2020 (3rd observation day, 15th day of hospitalization)


S Shortness of breath (-), icteric (-), intake (+)
Body weight: 1,745 grams
- General condition: appeared not active
- Pulse: 142 bpm

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- Respiratory rate: 42 cpm
- Body temperature: 36.6ºC (axilla)
- SpO2 : 97%
Head : no anemic conjunctiva, anicteric sclera, no nasal flaring
Chest : symmetrical movement, no retraction
Heart : no murmur, no gallop
Lungs : bronchial breath sounds, no rales, no wheezing
Abdomen : flat, soft, normal bowel sound, there was no hepatomegaly or
splenomegaly, clean umbilical cord
Extremities : warm, CRT ≤ 3 seconds
A - Preterm infant appropriate for gestational age (P07.38)
- Grade I Hyaline Membrane Disease (P22.0)
P Medications :
-
Nutritional care :
Breastfeeding
Nursing care : same as before

February 14th, 2020 (4th observation day, 16th day of hospitalization)


S Shortness of breath (-), icteric (-), intake (+)
Body weight: 1,760 grams
- General condition: appeared active
- Pulse: 147 bpm
- Respiratory rate: 42 cpm
- Body temperature: 36.9ºC (axilla)

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- SpO2 : 98%
Head : no anemic conjunctiva, anicteric sclera, no nasal flaring
Chest : symmetrical movement, no retraction
Heart : no murmur, no gallop
Lungs : bronchial breath sounds, no rales, no wheezing
Abdomen : flat, soft, normal bowel sound, there was no hepatomegaly
or splenomegaly, clean umbilical cord
Extremities : warm, CRT ≤ 3 seconds
A - Preterm infant appropriate for gestational age (P07.38)
- Grade I Hyaline Membrane Disease (P22.0)
P Medications :
-
Nutritional care :
Breastfeeding
Nursing care : same as before

February 15th, 2020 (5th observation day, 17th day of hospitalization)


S Shortness of breath (-), icteric (-), intake (+)
Body weight: 1,775 grams
- General condition: appeared active
- Pulse: 147 bpm
- Respiratory rate: 42 cpm
- Body temperature: 36.9ºC (axilla)
- SpO2 : 98%
Head : no anemic conjunctiva, anicteric sclera, no nasal flaring

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Chest : symmetrical movement, no retraction
Heart : no murmur, no gallop
Lungs : bronchial breath sounds, no rales, no wheezing
Abdomen : flat, soft, normal bowel sound, there was no hepatomegaly
or splenomegaly, clean umbilical cord
Extremities : warm, CRT ≤ 3 seconds
A - Preterm infant appropriate for gestational age (P07.38)
- Grade I Hyaline Membrane Disease (P22.0)
P Medications :
-
Nutritional care :
Breastfeeding
Nursing care : same as before

February 16th, 2020 (6th observation day, 18th day of hospitalization)


S Shortness of breath (-), icteric (-), intake (+)
Body weight: 1,790 grams
- General condition: appeared active
- Pulse: 147 bpm
- Respiratory rate: 42 cpm
- Body temperature: 36.9ºC (axilla)
- SpO2 : 98%
Head : no anemic conjunctiva, anicteric sclera, no nasal flaring
Chest : symmetrical movement, no retraction
Heart : no murmur, no gallop

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Lungs : bronchial breath sounds, no rales, no wheezing
Abdomen : flat, soft, normal bowel sound, there was no hepatomegaly
or splenomegaly, clean umbilical cord
Extremities : warm, CRT ≤ 3 seconds
A - Preterm infant appropriate for gestational age (P07.38)
- Grade I Hyaline Membrane Disease (P22.0)
P Medications :
-
Nutritional care :
Breastfeeding
Nursing care : same as before

February 17th, 2020 (7th observation day, 19th day of hospitalization)


S Shortness of breath (-), icteric (-), intake (+)
Body weight: 1,810 grams
- General condition: appeared active
- Pulse: 147 bpm
- Respiratory rate: 42 cpm
- Body temperature: 36.9ºC (axilla)
- SpO2 : 98%
Head : no anemic conjunctiva, anicteric sclera, no nasal flaring
Chest : symmetrical movement, no retraction
Heart : no murmur, no gallop
Lungs : bronchial breath sounds, no rales, no wheezing
Abdomen : flat, soft, normal bowel sound, there was no hepatomegaly

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or splenomegaly, clean umbilical cord
Extremities : warm, CRT ≤ 3 seconds
A - Preterm infant appropriate for gestational age (P07.38)
- Grade I Hyaline Membrane Disease (P22.0)
P Medications :
-
Nutritional care :
Breasfeeding
Nursing care : same as before
Plan : discharge from the hospital, screening for hearing before discharge
and retinopathy of prematurity at 4 weeks of chronological age, Hepatitis B
immunization when weight reached 2,000 grams

IX. PROGNOSIS
- Ad vitam : ad Bonam
- Ad functionam : ad Bonam
- Ad Sanationam : ad Bonam

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DISEASE COURSE TIMELINE

When chosen as a
case Follow up

January 29th – February 10th, 2020 February 11th – 12th, 2020 February 13th – 14th, 2020 February 15th – 16th, 2020 February 17th, 2020
February 9th, 2020

Baby was delivered through Caesarean Shortness of breath (-) Shortness of breath (-) Shortness of breath (-) Shortness of breath (-) Oral intake (+)
section due maternal history of severe pre-
eclampsia and previous Caesarean section Icteric (-) Icteric (-), intake (+) Icteric (-), intake (+) Icteric (-), intake (+)
on January 29th, 2020, gestational age 34-35
weeks, APGAR 3-5-7, BW 1,650 gram. He PE: active (+)
had breathing difficulty and grunting.
BW: 1,810 gr
PE: active (+) PE: active (+) PE: active (+) PE: active (+)
HR: 147 bpm RR:42 cpm
BW: 1,690 gr BL : 43 cm BW: 1,700 gr – 1,720 gr BW: 1,745 gr - 1,760 gr BW: 1,775 gr – 1,790 gr
PE: inactive, nasal flaring, tachypnea, BT: 36.9C SpO2: 98%
HR: 144 bpm RR: 44 cpm HR: 150 bpm RR: 48 cpm HR: 150 bpm RR: 48 cpm HR: 147 bpm RR: 42 cpm
grunting, chest wall retraction. New  Nasal flaring (-)
Ballard Score 34-36 weeks. Downes BT: 36.6C SpO2 98% BT: 36.9C SpO2: 98% BT: 36.9C SpO2: 98% BT: 36.9C SpO2: 98%  Retraction (-)
 Nasal flaring (-), retraction  Nasal flaring (-), retraction  Nasal flaring (-), retraction
Score 4. On 3rd day: shortness of breath
improved; icteric Kramer III.
 Nasal flaring (-), retraction (-), icteric (-)
(-), icteric (-) (-), icteric (-)
(-), icteric (-)
 Diagnosis:
(January 29th, 2020) Preterm infant
Laboratory: Hb 17.0 g/dL, Ht 49,8%, Leu
13,500/mm3, Plt 284,000/mm3, CRP <6 mg/L, Diagnosis: Diagnosis: Diagnosis: Diagnosis: appropriate for
diff count: 3/0/0/54/30/13, I/T ratio 0, Ur 14 Preterm infant appropriate Preterm infant appropriate Preterm infant appropriate Preterm infant appropriate gestational age + Grade I
mg/dL, Cr 0.8mg/dL, BG 86 g/dL. BGA: pH for gestational age + Grade for gestational age + Grade for gestational age + Grade I for gestational age + Grade I Hyaline Membrane
7.29, pCO3 50 mmHg, PaO2 78 mmHg, HCO3
26 mEq/L, BE 0. I Hyaline Membrane I Hyaline Membrane Hyaline Membrane Disease Hyaline Membrane Disease Disease
Babygram: apparent, distinct, coarse Disease Disease
granularity to the lung fields. Heart margin
were clearly visible.
(Feb 1st) Tot. bil 11.4g/dL, dir. bil 0.6g/dL
(Feb 3st) Tot. bil 5.6 g/dL, blood culture: Therapy:
negative Therapy: Therapy: Therapy: Therapy:
- Breastfeeding
Breastfeeding
Breast milk 8 x 50 ml via Breast milk 8 x 50 ml via Breastfeeding
oral oral Plan : discharge from
Working diagnosis: the hospital, screening
Preterm infant, appropriate for gestational for hearing before
age + Grade I Hyaline Membrane Disease
+ Hyperbilirubinemia
discharge and
retinopathy of
prematurity at 4 wk of
chronological age, Hep
Therapy: B immunization when
- CPAP weight reached 2,000 gr
- Nothing per oral with NGT on
- Total parenteral nutrition  trophic
feeding
- Phototherapy

20
Case Analysis Diagram

Risk Factor Prematurity (34-35 weeks)


Low Apgar score
Low birth weight
Maternal severe pre-eclampsia

Problem Neonatology

Diagnosis Preterm infant, appropriate for gestational age


Grade I Hyaline Membrane Disease
Hyperbilirubinemia

Clinical manifestation Inactive, tachypnea, grunting, nasal flaring, chest wall


retraction. Jaundice Kramer III.

Supporting New Ballard Score 34-36 weeks. Downes Score 4.


Hb 17.0 g/dL, Ht 49,8%, Leu 13,500/mm3, Plt 284,000/mm3, CRP <6 mg/L,
examination diff count: 3/0/0/54/30/13, I/T ratio 0, Ur 14 mg/dL, Cr 0.8mg/dL, BG 86
g/dL.Blood culture negative, BGA: pH 7.29, pCO3 50 mmHg, PaO2
78mmHg, HCO3 26 mEq/L, BE 0.

Management CPAP, nutritional support, phototherapy

Prognosis  Initial response of Ad vitam : ad Bonam  Education plan


therapy Ad functionam : ad Bonam  Breast milk
 Laboratory result Ad Sanationam : ad Bonam  Immunization
evaluation  Hearing and ROP screening
 Complication  Growth and development monitoring

Anwaar O, Hussain M, Shakeel M, Baig MMA. J Ayub Med Coll Abbottabad. 2018. Level of evidence 2b, Recommendation B
Carns J, Kawaza K, Liaghati-Mobarhan S, et al. Pediatrics. 2019. Level of evidence 2b, Recommendation B
Manandhar SR. J Nepal Med Assoc. 2019. Level of evidence 2b, Recommendation B
Kawaza K, Machen EH, Brown J, et al. Malawi Med J. 2016. Level of evidence 1b, Recommendation B
21
DISCUSSION
The American Academy of Pediatrics recommends that all newborn to be
classified by gestational age and birth weight. Gestational age can be determined
prenatally by the following techniques: date of last menstrual period, date of first
reported fetal activity (quickening usually occurs at 16-18 weeks), first reported heart
sound (10-12 weeks by Doppler ultrasound examination), and ultrasound
examination (very accurate if obtained before 20 weeks gestation). Gestational age
or menstrual age is the time elapsed between the first day of the last normal
menstrual period and the day of delivery. Consistent definitions to describe the
length of gestation and age in neonates are needed to compare
neurodevelopmental, medical, and growth outcomes. 1,2,3
The infant can be classified based on gestational age; infant born <37 weeks
is classified as preterm, 37-41 weeks as term, and > 42 weeks as post term.
Birthweight (extremely low birth weight [ELBW],very low birthweight [VLBW], low
birthweight [LBW], etc.), and gestational age and birthweight combined (small for
gestational age [SGA], appropriate for gestational age [AGA], large for gestational
age [LGA]). Appropriate for gestational age is defined as weight between 10 th – 90th
percentile in Lubchenco curve.3
This patient was born from mother with gestational age 34-35 weeks by last
menstrual period and confirmed with ultrasonography. From physical examination we
founded that birth weight was 1650 gram, birth length was 42 cm, and Ballard score
was 34-36 weeks. By Lubchenco curve it was defined as preterm infant with
appropriate gestational age.
Hyaline membrane disease (HMD), the pathologic correlate of respiratory
distress syndrome (RDS) of the newborn, is an acute lung disease of premature
infant caused by inadequate amounts of surfactant. Decreased surfactant result in
insufficient surface tension in the alveolus during expiration, leading to atelectasis,
decreased gas exchange, severe hypoxia and acidosis. Insufficient surfactant results
in increased surface tension in the alveolus during expiration leading to alveolar
collapse, atelectasis, decreased gas exchange, severe hypoxia with acidosis,
leading to respiratory failure.
HMD refers to the histological aspect of the most frequent pulmonary
pathology in preterm neonates. The lung of the preterm baby is morphologically and
functionally immature. This definition is presently used to indicate surfactant deficit
22
alone and should not be used for other causes of respiratory distress. Surfactant is a
complex lipoprotein composed of 6 phospholipids and 4 apoproteins. Surfactant
recovered by alveolar wash from most mammals contains 70-80% phospholipids, 8-
10% protein, and 10% neutral lipids, primarily cholesterol. The components of
pulmonary surfactant are synthesized in the Golgi apparatus of type II alveolar cells.
Its production is regulated by different hormones and growth factor as
glucocorticoids, insulin, prolactin, thyroxine and transforming growth factor beta
(TGF-β). Its production generally starts around the 24 to 28 weeks of pregnancy, and
surfactant is found in amniotic fluid between 28 and 32 weeks. By about 35 weeks of
gestation, most babies have developed adequate amounts of surfactant. Surfactant
deficiency may not be the sole cause of HMD formation. 4,5
HMD predominantly occurs in infants younger than 32 weeks of gestation and

weighing less than 1200 grams. The incidence of Hyaline Membrane Disease (HMD)

is inversely proportional to gestational age with disease occurring in nearly all


preterm neonates born at 22–28 weeks’ estimated gestation. The Incidence of HMD
is 80% of babies born at 28 weeks’ gestation and increasing to 90% at 24 weeks’
gestation, approximately 3% of late preterm neonates born at 34–36 weeks’

gestation, and 0.12% of term neonates born at >37 weeks’ gestation. 6-8
The risk of developing HMD increases with maternal diabetes, multiple births,
Caesarean section delivery, precipitous delivery, asphyxia, cold stress, and a history
of previously affected infants. The incidence is highest in preterm male or white
infants. The risk of HMD is reduced in pregnancies with chronic or pregnancy-
associated hypertension, maternal heroin use, prolonged rupture of membranes, and
antenatal corticosteroid prophylaxis.4,5,8
The assessment of a neonate with respiratory distress should always begin
with the compilation of a detailed perinatal history, a review of the maternal-perinatal
history and a complete diagnosis. The historical information such as the duration of
membrane rupture, the presence of meconium-stained amniotic fluid also included
as a important pieces of information that can be helped to assesed the newborn with
respiratory distress. A working diagnosis should be made as fast as possible to give
a immediately life saving management. 9-10
Clinical symptoms of respiratory distress in neonate is diagnosed when one or
more of the following is present; tachypnea or respiration rate of more than 60 cpm,

23
retractions or increased chest in drawing on respirations (subcostal, intercostal,
sternal, suprasternal) and noisy respiration in the form of grunt, stridor or wheeze.
The respiratory distress may or may not associate with cyanosis and desaturation on
pulse oximetry.9
As the disease progresses, the infant may develop ventilatory failure (rising

carbon dioxide concentrations in the blood), and prolonged cessations of breathing

or apnea. Whether treated or not, the clinical course for the acute disease lasts

about 2 to 3 days. During the first day the patient worsens and requires more
support. During the second day the patient may be remarkably stable on adequate
support and resolution is noted during the third day, heralded by a prompt diuresis.
Despite huge advances in care, HMD remains the most common single cause of
death in the first month of life in the developed world. Complications include
metabolic disorders (acidosis, low blood sugar), patent ductus arteriosus, low blood
pressure, chronic lung changes, and bleeding in the brain. The disease is frequently

complicated by prematurity and its additional defects in another organ functions. 4,5
On x-ray, the lungs may have a characteristic, but not pathognomonic
appearance that includes a fine reticular granularity of the parenchyma and air
bronchograms, which are often more prominent early in the left lower lobe because
of superimposition of the cardiac shadow. The basic defect causing the idiopathic
HMD in preterm babies is represented by immaturity of the lungs, particularly type II
pneumocytes. The immature type II pneumocytes cannot produce surfactant and
make lung compliance is low, the critical negative pressure needed to allow influx of
air into the lungs cannot be attained. The collapse of alveoli (atelectasis) that not
adequately coated with surfactant reduces the pulmonary surface and allowing
exchange of gases only through the walls of alveolar ducts and terminal bronchioles
structures that are not suitable for that purpose anoxia and hypercapnia cause
acidosis, leading to peripheral vasodilatation and pulmonary vasoconstriction.
Hypoxia adversely affects pulmonary cells, and necrosis of endothelial, alveolar, and
bronchial cells takes place. Vascular disruption causes leakage of plasma into the
alveolar spaces and layering of fibrin and necrotic cells arise from type II
pneumocytes (“hyaline membrane”) along the surface of alveolar ducts and
11
respiratory bronchioles partially denuded of their normal cell lining.

24
This patient was showed with clinical symptoms of respiratory difficulties such
are tachypnea, grunting, retraction, and nasal flaring. The severity of respiratory
distress is assessed by Downes score.In this patient, total Downes score is 4 which
is categorized by moderate respiratory distress. He was delivered by gestational age
<37 weeks, confirmed with Ballard score as 34-36 weeks old, with history of
corticosteroid administration during pregnancy. From the x-ray features showed
apparent, distinct, and coarse granularity to the lung fields. These conditions
supported Hyaline Membrane Disease, which also categorized as grade I HMD.
Prenatal corticosteroid therapy is recommended in all pregnancies with
threatened preterm birth before 34 weeks’ gestation where active care of the
newborn is anticipated. Prenatal corticosteroid therapy decreases the severity of
HMD and reduces the incidence of other complications of prematurity, such as
patent ductus arteriosus (PDA), pneumothorax, and necrotizing enterocolitis, without
adversely affecting postnatal growth, lung mechanics or development, or the
incidence of infection. According to a number of studies on prenatal corticosteroid
therapy, it is assumed that pre-birth steroids reduce the rate of death and morbidity
in premature infants with very low birth weight. In meta-analysis of corticosteroid
prophylaxis studies, it was concluded that the intrauterine corticosteroid effect
resulted in a 50% reduction in neonatal HMD. Administration of dexamethasone to
women 48 hours before the delivery of fetuses between 24 and 34 weeks of
gestation significantly reduces the incidence, mortality, and morbidity of HMD.
Corticosteroid administration is recommended for all women in preterm labor (24–34
weeks gestation) who are likely to deliver a fetus within 1 week. Repeated weekly
doses of dexamethasone until 32 weeks may reduce neonatal morbidities and the
duration of mechanical ventilation.12-14
This patient’s mother had been administrated with corticosteroid before
delivery, which can bring less complications during natal period.
Those with RDS will develop progressively worsening lung disease, clinically
presenting as increased work of breathing, sternal retractions and increasing oxygen
requirements to maintain normal saturations. Surfactant is necessary for inflation of
lung alveoli by reducing its surface tension. Clinical trials have confirmed that
surfactant replacement therapy is effective in improving the immediate need for
respiratory support and the clinical outcome of premature newborns. Surfactant is
25
composed of a complex mixture of approximately 90% lipids and 10% proteins.
These lipids include 80%–90% phospholipids, 5% neutral lipids, and cholesterol. The
phospholipids are mainly composed of 80% phosphatidyl-choline, 5%–10%
phosphatidyl-glycerol (PG), and other phospholipids. Surfactant is administered to all
newborn patients FiO2 >0.30 for very immature babies and >0.40 for more mature

infants based on thresholds used in the early clinical trials . The surfactant storage
pool in term newborn infants is 100 mg/ kg whereas that in preterm infants is 4–5
mg/kg at birth. Thus, exogenous surfactant replacement therapy in preterm infants is
crucial until endogenous surfactant levels are sufficient to stabilize the alveoli and
reduce surface tension. The use of surfactant is to be timely and possibly followed
by non-invasive ventilation (NIV) so as to reduce the risks of mortality and short and
long-term morbidity. If intubation is required as part of the stabilisation, then
surfactant should be given immediately.15-16
Early initial Continuous positive airway pressure (CPAP), when applied to
premature infants with HMD have various functions such as re-expands collapsed
alveoli, splints the airway, reduces work of breathing and improves the pattern and
regularity of respiration and reduced the risk for intubation and mechanical
ventilation in premature baby with HMD. Many preterm infants with HMD will
transition successfully on CPAP. Bubble CPAP, when used appropriately, is more
cost effective, less intensive, requires less training and has lower risk of
complications. However, not all preterm infants with HMD respond to CPAP. Bubble
CPAP was considered to be successful if the respiratory distress improved and the
baby could be successfully weaned off from CPAP. The criteria for weaning was
absence of respiratory distress (minimal or no retractions and respiratory rate
between 30 and 60 per minute) and, SpO2>90% on FiO2 <30% and PEEP <5 cm of
water. Infants were diagnosed to have failed CPAP and were started on mechanical
ventilation when they: (a) remained hypoxic, i.e. SpO2<87% despite FiO2>70% and
PEEP >7cm of water; (b) had severe retractions on PEEP >7cm of water; (c) had
prolonged (>20 seconds) or recurrent apnea (>2 episodes within 24 hours
associated with bradycardia) requiring bag and mask ventilation; and, (d) had severe
metabolic acidosis or shock requiring inotropic support (dopamine and or
dobutamine) >20μg/kg/min. Infants failing CPAP in the first 1 week of life were

considered to be CPAP failures.13,17

26
In this patient, total Downes score is 4 which is categorized as moderate
respiratory distress; therefore, this patient give early initial CPAP as soon as
possible. There is standard setting of CPAP, in this case we used FiO2 40%, PEEP
7 cmH2O and O2 flow 8 litre/minutes. In this case we used bubble CPAP. The
preterm infants show good response and fulfil the criteria of weaning, so in the next
day observation the CPAP settings consider to be weaned. The early used of CPAP,
giving good response for preterm baby.
Jaundice attributable to physiological immaturity which usually appears
between 24 – 72 hours of age, and between 4 th and 5th days can be considered as its
peak in term neonates and in preterm at 7 th day, which will disappear by 10 – 14
days of life. Jaundice can be detected clinically with a tactile blanching of the skin
that can reveal the underlying yellow color of the skin. Examination should be done
in light conditions that are not too bright and not too dark. Jaundice usually begins on
the face and develops toward the body and extremities. The appearance of
jaundiced sclera should be assessed, generally the further the jaundice progresses
to the lower part of the body the higher the total serum bilirubin level. The more
intense the color (which can approach the yellow-orange), the higher the total serum
bilirubin is. Jaundice in dark-skinned newborns in particular can be difficult to assess.
Whenever there is suspicion in the appearance of jaundice in the neonate, the
recommendation is to examine total serum or transcutaneous bilirubin. Clinical
jaundice will be detected if serum bilirubin is a total of 5 mg%. Unconjugated bilirubin
is the predominant form and usually its serum level is less than 15 mg/dL. Based on
the recent recommendations of the AAP, bilirubin levels up to 17–18 mg/dL may be
accepted as normal in term and healthy newborns. 18-19
Among 13 studies conducted in countries such as India, Nigeria, Pakistan,
Nepal, and Egypt, the risk factors for primordial hyperbilirubinemia are ABO
incompatibility, rhesus incompatibility, low-birth-gestation, less weight and sepsis. In
jaundiced infant is always necessary to perform a clinical assessment. Assessment
of the degree of jaundice on physical examination can be done with the Kramer
scale method. Kramer set limits on serum levels of unconjugated bilirubin according
to the development of jaundice: when seen only in the head and neck (4-8 mg/dL),
chest (5-12 mg/dL), abdomen to thigh (8-16 mg/dL), arms and legs (11-18 mg/dL),
on the palms and feet (>15 mg/dL). This examination has clinical significance
because when jaundice appears on the hands or feet it indicates elevated serum
27
bilirubin levels so it should be considered for checking serum bilirubin levels. On the
Kramer scale when icteric jaundice is found in the legs of serum bilirubin levels
ranging from 16-20 mg/dL. Sharanabasappa et al conducts research on the
effectiveness of clinical judgment through the Kramer index and estimation of
bilirubin levels as a predictor of hyperbilirubinemia in infants. Within the first 48 hours
postpartum it is said that the Kramer index has a significant relationship to total
serum bilirubin level which is a gold standard of hyperbilirubinemia diagnosis 20,21
Bilirubin levels with a deviation from the normal range and requiring
intervention would be described as pathological jaundice. Pathological jaundiced
define as appearance of jaundice within the first 24 hours due to increase in serum
bilirubin beyond 5 mg/dL/day, peak levels higher than the expected normal range,
presence of clinical jaundice more than 2 weeks and conjugated bilirubin (dark urine
staining the clothes).22
Several types of hypebilirubinemia have been reported in neonates including
physiological jaundice, pathological jaundice, jaundice due to breastfeeding or breast
milk and hemolytic jaundice including three subtypes due to Rh factor incompatibility,
ABO blood group incompatibility and Jaundice associated with glucose-6-phosphate
dehydrogenase (G6PD) deficiency. Physiological jaundice is the most abundant type
of newborn hyperbilirubinemia, having no serious consequences. The physiological
process of breastfeeding in this jaundice can be due to dehydration and caloric
deficiency at the beginning of breastfeeding. Early jaundice is caused by inhibition of
bilirubin metabolism by β-glucuronidase and fatty acids contained in non-esterified
milk and pathological jaundice. Although most newborns with healthy yellow skin,
however, they need to be monitored because bilirubin has the potential to damage
the central nervous system. Increased levels of unconjugated bilirubin in the blood
can cause bilirubin encephalopathy and then kernicterus. Neurodevelopmental
abnormalities including as athetosis, loss of hearing, and in rare cases intellectual
deficits, may be related to high toxic level of bilirubin.. 22-23
The goal of jaundice therapy is to decrease the circulating bilirubin
concentration or inhibit its increase. Phototherapy is used because it uses light
energy to change the shape and structure of bilirubin, turning it into a molecule that
can be excreted even when the normal conjugation process does not work
properly.21

28
On his 3rd day of age, the patient started to look yellowish on his face,
abdomen and upper thigh (Kramer 3). From the laboratory findings, total bilirubin
level was 11.4 mg/dL and conjugated bilirubin 0.6 mg/dL. According to Maisles et al,
phototherapy was suggested in preterm infants 32-33 weeks when total billirubin
level was 10-12 mg/dl. Thus this patient immediately given phototherapy for 2 days.
After phototherapy administered for 2 days, the jaundice has mostly subsided, with
no other complaints.
The chief rationale of treating jaundiced newborn is the prevention of
kernicterus, a devastating and often fatal outcome attributed to bilirubin’s effects on
the basal ganglia. In the late 1950’s phototherapy emerged as another potential
treatment of jaundice after exchange transfusion. Current practice supports
considerably more conservative use of exchange transfusion. For example, a term
healthy neonate with hyperbilirubinemia above threshold (set at 25 mg/dl). Right
now, phototherapy has become the standard of care for jaundiced neonates.
Intensive phototherapy in neonatal hyperbilirubinemia rapidly decreases serum total
bilirubin (STB) below the threshold for treatment. 24
Nutritional assessment should be considered in premature infants, careful
assessment of fluid administration in meeting the theological needs and should have
a positive impact on cardiovascular and intestinal function, without causing
significant dehydration. The recommendation of parenteral fluids nutrition in preterm
infants for birth weight ≥1,500 grams: starting with 60-80 mL/kgBW/day gradually
increasing from 10-20 mL/kgBW/day the next day to a maximum of 140-160
mL/kgBW/day, While recommendation for enteral nutrition: 135-200 mL/KgBW/day.
Calories intake should also be monitored in preterm infants. Calorie intake on the
first day after birth must be able to meet the needs of the basal metabolic rate (BMR)
which is 50 kcal/kgBW/day and then increases gradually 25-30 kcal/kgBW/day until
calorie adequacy is achieved during the administration of total parenteral nutrition,
which is 90-100 kcal/kgBW/day. An optimal calories intake to achieve optimal growth
during enteral nutrition is 115-120 kcal/kgBW/day. 25
Trophic feeding is given within the first 48 hours of fresh breast milk from 5-10
mL/kgBW/day which is increased gradually to a volume of 25 mL/kgBW/day. The
transition from parenteral nutrition to enteral nutrition is done in stages by calculating
the total amount of fluid adequacy. Then parenteral nutrition can be stopped if the
intake of oral or enteral nutrition reaches 2/3 (two third) of the adequacy calories
29
based on actual body weight. Full target enteral nutrition (full feed), which is 150-180
ml/kg/day: ≥28 weeks or >1,500 grams, strive to be achieved within 7-10 days. 25
Breast milk is the first choice for premature babies both oral and enteral
administration. If breast milk is not available, donor breast milk that can meet safety
requirements can be given. The target of nutritional therapy in premature babies is to
achieve the same growth rate as normal fetuses that are appropriate for gestational
age, resemble fetal body composition, and achieve functional outcomes similar to
term infants, namely: weight gain of premature infants 15 g/kg/day, Increase in body
length: 0.8-1.0 cm / week and head circumference: 0.5-0.8 cm / week. 25
In this patient, total parenteral nutrition was given starting with 60-80
mL/kgBW/day and increased gradually. Enteral nutrition was started at third day of
treatment and increased in volume according to patient’s tolerance and acceptability.
Then parenteral nutrition has been stopped when oral or enteral nutrition reaches 2/3
of the adequacy calories. Nutrition in this patient already achieved full feed (180
ml/KgBW/day) and was given through breast milk 50 ml every 3 hours via oral and
proceed to breastfeed.
Anwaar O et al in the study of 60 neonates with mean gestational age was
33.35±2.59 weeks and mean weight was 2113.3±580.32 g. Total 52 (86.7%) babies
were successfully weaned off from nCPAP while only 8 (13.3%) neonates required
mechanical ventilation. Main indication of use of CPAP was RDS (65%). This study
concluded that nasal CPAP can be safely and easily used as primary support for
neonates with respiratory distress even in resource limited developing countries.
(Level of evidence 2b , recommendation b). 26
Carns J et al during their observational study, they monitored CPAP usage
and outcomes in newborn wards admitted with respiratory distress and for those
diagnosed with respiratory distress syndrome at 26 government hospital in Malawis.
On implementation of CPAP, survival to discharge improved for all neonates
admitted with respiratory distress (48.6% vs 54.5%; P=.012) and for those diagnosed
with respiratory distress syndrome (39.8% vs 48.3%; P=.042). Neonates with normal
mean temperatures during CPAP treatment experienced the highest survival rates
(65.7% for all neonates treated with CPAP and 60% for those diagnosed with
respiratory distress syndrome). (Level of evidence 2b, recommendation b). 27
Manandhar SR, studied 63 babies with mean gestational age was 36.67±3.4
weeks who receiving Bubble CPAP. The Bubble CPAP was started at 8.05±2 hours
30
of life and duration of Bubble CPAP required for settling respiratory distress due to
hyaline membrane disease was 95.71±3 hours. Out of 63 babies, improvement of
respiratory distress in neonates with Bubble CPAP was 39 (61%) wit CI of 38% to
62% whereas 24 (39%) babies required mechanical ventilation and other modalities.
This study concludes usefulness of Bubble CPAP in neonates with respiratory
distress. (Level of evidence 2b , recommendation b). 28
Kawaza K et al studied 87 neonates weighing >1,000 g and presenting with
severe respiratory distress were recruited at Queen Elizabeth Central Hospital
Malawi, 62 were treated with bCPAP therapy and 25 received oxygen therapy (62
bCPAP, 25 controls). The survival rate in the control group was 44.0% (95% CI: 26–
63%); survival in the bCPAP group was 71.0% (95% CI: 59–81%) (p = 0.018).
Without adjustment, bCPAP is associated with a 3.1 fold increase in odds of survival
(95% CI: 1.2–8.1, p = 0.02). For neonates with RDS, survival was 23.5% (95% CI: 9–
49%) in the control group, compared to 64.6% (95% CI: 50–77%) in the bCPAP
group (p = 0.006). (Level of evidence 1b, recommendation b).29

31
REFERENCES

1. Lee AC, Panchal P, Folger L, et al. Diagnostic Accuracy of Neonatal Assessment


for Gestational Age Determination: A Systematic Review. Pediatrics.
2017;140(4):e20171423.
2. Damanik SM. KlasifikasiBayiMenurutBeratLahir dan Masa Gestasi. In: Kosim MS,
Yunanto A, Dewi R, Sarosa GI, Usman A, editors. Buku Ajar Neonatologi.
Jakarta: Badan Penerbit IDAI. 2008. P. 11-30.
3. Gomella TL, Cunningham MD, Eyal FG. Assessment of gestational age. In:
Gomella TL, Cunningham MD, Eyal FG, editors. Neonatology management,
procedures, on-call problem, diseases and drug. USA: McGraw-Hill. 2010. P. 23-
30.
4. Grappone L, Messina F. Respiratory DrstressSyndome or Hyaline Membrane
Disease? A new approach for an old disease. JPNIM. 2014;3:1-7.
5. Martin R, Fanaroff A. The preterm lung and airway: past, present, and future.
PediatrNeonatol. 2013;4:228-34.
6. Anadkat JS, Kuzniewicz MW, Chaudhari BP, Cole FS, Hamvas A. Increased risk
for respiratory distress among white, male, late preterm and term infants. J
Perinatol. 2012;32:780–785. http://dx.doi. org/10.1038/jp.2011.191.
7. Sweet D, Carnielli V, Greisen G, Hallman M, Ozek E, Plavka R, et al. European
Association of Perinatal Medicine. European Consensus Guidelines on the
Management of Neonatal Hyaline Membrane Disease in Preterm Infants-2019
update. Neonatology. 2019;115:432–450.
8. Locci G, Fanos V, Gerosa C, Faa G. Hyaline membrane disease (HMD) : the role
of perinatal pathologist. J Pediatr Neonat Individual Med.2014;3(2):e030255.
9. Morley C. Hyaline Membrane Disease. In: Polin RA, Yoder MC, editors.
Workbook in Practical Neonatology, 4th edition. Philadelphia: Elsevier; 2014.
p.129-52.
10. Lott JW. Cardiovascular system. In: Kenner C, Lott JW, editors. Comprehensive
Neonatal Care an InterdiciplinaryApproach, 4th edition. Philadelphia:Elsevier.
2015. p.32-9.
11. Manandhar SR. Outcome of surfactant replacement therapy in preterm babies
with Hyaline Membrane Disease at Neonatal Intensive Care Unit of atertiary

32
hospital. BJHS.2018;3:537-541.
12. Roberts D, Brown J, Medley N, Dalziel SR. Antenatal corticosteroids for
accelerating fe- tal lung maturation for women at risk of pre- term birth. Cochrane
Database Syst Rev. 2017 Mar;3:CD004454.
13. Ehret DE, Edwards EM, Greenberg LT, Bern- stein IM, Buzas JS, Soll RF, et al.
Association of antenatal steroid exposure with survival among infants receiving
postnatal life support at 22 to 25 weeks’ gestation. JAMA Netw Open. 2018
Oct;1(6):e183235.
14. Holme N, Chetcuti P. The pathophysiology of Hyaline Membrane Disease in
neonates. Paed Child Health. 2015;22:507-12.
15. El-GendyN, Kaviratna A, Berkland C, Dhar P. Delivery and performance of
surfactant replacement therapies to treat pulmonary
disorders.TherDeliv.2013;4:10.4155/tde.13.72.
16. Jeon GW. Surfactant preparations for preterm infants with Hyaline Membrane
Disease: past, present, and future. Korean J Pediatr. 2019;62:155-161.
17. Lu-Ann, Richard Polin, Waldemar Carlo, Rosemarie Tan, Praven Kumar, William
Benitz, et al. Respiratory support in preterm infants at Birth. Pediatrics.
2014;133:1-8.
18. Olusanya BO, Osibanjo FB, Slusher TM. Risk factors for severe neonatal
hyperbilirubinemia in low and middle-income countries: a systematic review and
meta-analysis. PLoS One. 2015;10:1-16.
19. Maisels MJ, Kring E. The contribution of hemolysis to early jaundice in normal
newborns. Pediatrics. 2006; 118:276-9.
20. American Academy of Pediatrics Subcommittee on Hyperbilirubinemia.
Management of hyperbilirubinemia in the newborn infant 35 or more weeks of
gestation. Pediatrics. 2004;114:297-316.
21. Sharanabasappa S, Rasalam C, Masood Z. Effectiveness of early clinical
assessment and bilirubin estimation for prediction of neonatal hyperbilirubinemia.
Int J ContPed. 2016;3:477-84.
22. Sukadi A. Hiperbilirubinemia. In: Kosim MS, Yunanto A, Dewi R, Sarosa GI,
Usman A, editors. BukuAjar Neonatologi, 1 st edition. Jakarta: Badan Penerbit
IDAI. 2008. p. 147-69.
23. Mishra S, Agarwal R, Deorari AK, Paul VK. Jaundice in the newborns. Indian J
Pediatr. 2008;75:157–163.
33
24. McKiernan PJ. Neonatal jaundice. Semin Neonatol J. 2002;7:153-65.
25. Kadim M, Rosalina D. In: Asuhan Nutrisi pada Bayi Prematur. UKK Neonatologi
dan UKK Nutrisi dan Penyakit Metabolik, Ikatan Dokter Anak Indonesia. 2016.
26. Anwaar O, Hussain M, Shakeel M, Baig MMA. Outcome of use of nasal
continuous positive airway pressure through infant flow drivers in neonates with
respiratory distress in a tertiary care hospital in Pakistan. J Ayub Med Coll
Abbottabad 2018;30(4):511–5.
27. Carns J, Kawaza K, Liaghati-Mobarhan S, et al. Neonatal CPAP for Respiratory
Distress Across Malawi and Mortality. Pediatrics. 2019;144(4):e20190668
28. Manandhar SR. Outcome of Respiratory Distress in Neonates with Bubble CPAP
at Neonatal Intensive Care Unit of a Tertiary Hospital. J Nepal Med Assoc
2019;57(216):92-97.
29. Kawaza K, Machen EH, Brown J et al. Efficacy of low-cost bubble CPAP system
in treatment of respiratory distress in neonatal ward in Malawi. Malawi Med J.
2016 Sep; 28(3): 131-7.

34
CLINICAL SEARCH REFERENCE

1. Anwaar O, Hussain M, Shakeel M, Baig MMA. Outcome of use of nasal


continuous positive airway pressure through infant flow drivers in neonates with
respiratory distress in a tertiary care hospital in Pakistan. J Ayub Med Coll
Abbottabad 2018;30(4):511–5.
2. Carns J, Kawaza K, Liaghati-Mobarhan S, et al. Neonatal CPAP for Respiratory
Distress Across Malawi and Mortality. Pediatrics. 2019;144(4):e20190668.
3. Manandhar SR. Outcome of Respiratory Distress in Neonates with Bubble CPAP
at Neonatal Intensive Care Unit of a Tertiary Hospital. J Nepal Med Assoc
2019;57(216):92-97.
4. Kawaza K, Machen EH, Brown J, et al. Efficacy of low-cost bubble CPAP system
in treatment of respiratory distress in neonatal ward in Malawi. Malawi Med J.
2016 Sep; 28(3): 131-7.

35
ABBREVIATIONS

% Percent
o
C Degree of Celsius

AAP American Academy of Pediatrics

ALT Alanine aminotransferase

AST Aspartate aminotransferase

am Ante-Meridiem

BW Body Weight

cm Centimeter(s)

bpm Beats per minute

cpm Cycles per minute

CRP C- Reactive Protein

CRT Capillary Refill Time

F Female

g Gram(s)

g/dL Gram(s) per deciliter

Hb Hemoglobin

Ht Hematocrit

I/T Immature to Total

JVP Jugular Vein Pressure

kcal Kilo Calories

kg Kilogram(s)

36
kgBW Kilogram(s) Body Weight

lpm Liter(s) per minute

M Male

mg Milligram(s)

mg/dL Milligram(s) per deciliter

mg/L Milligram(s) per liter

mL Milliliter(s)

mm Millimeter(s)

mmHg Milimeter mercury

mm3 Millimeter cubic

O2 Oxygen

N Nervus

PE physical examination

pH Potential Hydrogen

RDS respiratory distress syndrome

TT Tetanus Toxoid

uL Microliter

U/L Unit per Liter

37
APPENDIX

PATIENT’S PHOTO

38
LUBCHENCO CURVE

1650 g

39
NEW BALLARD SCORE

40
FENTON PRETERM GROWTH CHART

41
DOWNES SCORE

GUIDELINES FOR MANAGEMENT OF HYPERBILIRUBINEMIA FOR


PRETERM BABY

Total Serum Bilirubin (mg/dL)


Weight Phototherapy Exchange transfusion

Preterm
<1000 g On the first 24 10 - 12
hour

1001-1500 g 7-9 12 - 15

1501-2000 g 10 - 12 15 - 18

2001-2500 g 13 - 15 18 - 20

42
BABYGRAM
January 29th, 2020

43
BLOOD GAS ANALYSIS

January 29th, 2020

44
Oxford Centre for Evidence-based Medicine Levels of Evidence

Differential
Therapy /
diagnosis /
Lev Prevention, Economic and
Prognosis Diagnosis symptom
el Aetiology / decision analyses
prevalence
Harm
study
SR (with
SR (with homogeneity*)
homogeneity*) of SR (with SR (with
SR (with of Level 1 diagnostic
inception cohort homogeneity*) of homogeneity*) of
1a homogeneity*) studies; CDR”  with 1b
studies; CDR”  prospective Level 1 economic
of RCTs studies from different
validated in different cohort studies studies
clinical centres
populations

Analysis based on
Individual inception Validating** cohort clinically sensible
Individual RCT Prospective
cohort study with > study with good” ” ”  costs or alternatives;
(with narrow cohort study with
1b 80% follow-up; reference standaHMD; systematic review(s)
Confidence good follow-
CDR”  validated in a or CDR”  tested within of the evidence; and
Interval”¡) up****
single population one clinical centre including multi-way
sensitivity analyses

Absolute better-
All or none case- Absolute SpPins and All or none case-
1c All or none§ value or worse-value
series SnNouts” “ series
analyses

SR (with
homogeneity*) of SR (with SR (with
SR (with SR (with homogeneity*)
either retrospective homogeneity*) of homogeneity*) of
2a homogeneity*) of Level >2 diagnostic
cohort studies or 2b and better Level >2 economic
of cohort studies studies
untreated control studies studies
groups in RCTs

Analysis based on
Retrospective cohort Exploratory** cohort
clinically sensible
Individual cohort study or follow-up of study with good” ” ” 
costs or alternatives;
study (including untreated control reference standaHMD; Retrospective
limited review(s) of
2b low quality RCT; patients in an RCT; CDR”  after derivation, cohort study, or
the evidence, or
e.g., <80% Derivation of CDR”  or validated only on poor follow-up
single studies; and
follow-up) or validated on split- split-sample§§§ or
including multi-way
sample§§§ only databases
sensitivity analyses

“Outcomes”
Research; “Outcomes” Ecological Audit or outcomes
2c
Ecological Research studies research
studies

SR (with SR (with
SR (with
homogeneity*) SR (with homogeneity*) homogeneity*) of
3a homogeneity*) of 3b
of case-control of 3b and better studies 3b and better
and better studies
studies studies
Analysis based on
limited alternatives
or costs, poor quality
Non-consecutive study; Non-consecutive
estimates of data,
Individual Case- or without consistently cohort study, or
3b but including
Control Study applied reference very limited
sensitivity analyses
standaHMD population
incorporating
clinically sensible
variations.
Case-series
Case-series (and Case-control study, Case-series or
(and poor quality
poor quality poor or non- superseded Analysis with no
4 cohort and case-
prognostic cohort independent reference reference sensitivity analysis
control
studies***) standard standaHMD
studies§§)
Expert opinion
Expert opinion
without explicit Expert opinion Expert opinion without Expert opinion
without explicit
critical appraisal, without explicit explicit critical without explicit
critical appraisal,
or based on critical appraisal, or appraisal, or based on critical appraisal, or
5 or based on
physiology, based on physiology, physiology, bench based on economic
physiology,
bench research bench research or research or “first theory or “first
bench research
or “first “first principles” principles” principles”
or “first principles”
principles”

45
Categories of Recommendations

Level

Good scientific evidence suggests that the benefits of the clinical


A service substantially outweigh the potential risks. Clinicians
should discuss the service with eligible patients.

At least fair scientific evidence suggests that the benefits of the


B clinical service outweighs the potential risks. Clinicians should
discuss the service with eligible patients.

At least fair scientific evidence suggests that there are benefits


provided by the clinical service, but the balance between benefits
C and risks are too close for making general recommendations.
Clinicians need not offer it unless there are individual
considerations.

At least fair scientific evidence suggests that the risks of the


D clinical service outweighs potential benefits. Clinicians should not
routinely offer the service to asymptomatic patients.

Scientific evidence is lacking, of poor quality, or conflicting, such


that the risk versus benefit balance cannot be assessed.
I Clinicians should help patients understand the uncertainty
surrounding the clinical service.

46

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