Presentation 3

Neonatal Jaundice (NNJ)

• History Taking
• Physical Examination
• Summary

Presented by: Haspreet Kaur Gill

 DEMOGRAPHIC DETAILS
Name : Nor Hasniza Waty binti Zainuddin
RN: 291861
Age: 34 weeks (preterm baby)
DOB: 10/5/2019
Gender: Male
Apgar score: 5 in 1 min , 10 in 5 min
Birth weight: 2.04 kg
Mode of delivery: Emergency c-section (EMLSCS)
DATE OF ADMISSION: 1 st day of life

Informant : mother
CHIEF COMPLAINT

• This is a case of preterm male newborn was referred to paediatrics

team standby for EMLSC due to mother having preeclampsia,
gestational diabetes mellitus (GDM) and 2 previous scar.
 HISTORY OF PRESENTING COMPLAINT

-Preterm male newborn @ 34 weeks of madam Nor Hasniza was kept in Nicu under
observation due to developing respiratory distress
- apgar score of 5 in 1 min, poor breathing effort, tachypneic of respiratory rate of
64 bp/m, heart rate of 100 bp/m
- weak cry, and cyanosis at post delivery.
-Baby was subsequently intubated and connected to ventilator support , vital signs
begin to improve , suction was done.
- Baby was checked for hypoglecemia due to mother had GDM during pregnancy.
-Intrapartum, there was was clear fluid, no meconium stained , no cod
around the neck .
- At 10 hours of life,baby was noticed to have yellow sclera and yellow
pigmented skin and was subsequently diagnosed with neonatal jaundice.
-Even after receiving phototheraphy as treatment the total billirubin as
still rising and baby was diagnosed with severe neonatal jaundice.G6PD
deficiency was investigated .

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 prenatal history:
• Mother is gravida 2 para 2, age 31 years old and 34 weeks period of gestation when she delivered her baby
• She was diagnosed with GDM at booking at 13 week @POG with pre prandial of 5.7 mmol/l and post prandial of
8.9 mmol/l and was on diet control till her delivery
• Apart from that she had essential hypertension before pregnancy and with significant proteinuria which was
diagnosed at booking and was on medication T. methyldopa 250 mg tds since 13 week booking.
• At 24 week POG , her 24 hour urine protein was 365 mg/day in 100 ml and was diagnosed with preeclampsia and
was kept on follow up regulary.
• Mother blood group B+, weight was 85kg , height was 155 making BMI 35 (overweight)
• Infective screning such as VDRL , Hepatitis B and HIV was not reactive. However mother had anemia during her
pregnancy and was on obimin

13/11/2019 7
She also had history of 2 previous cesearean section scar for her 2 previous pregnancy.

year Mode of delivery Term/preterm gender age weight Post-natal complication

2009 LSCS? Poor TERM male 10 years old 3.43 kg Neonatal jaundice
progress

2013 LSCS? Antenatal TERM female 6 years old 3.5 kg Neonatal jaundice

Both children is alive and healthy.There is no history of abortion or misccariage.

Infective screning such as VDRL , Hepatitis B and HIV was not reactive. However mother had
anemia during her pregnancy and was on obimin
• Intrapartum, there was was clear fluid, no meconium stained , no cod around
the neck.Baby was not born vigorously , had weak cry cyanosed, grunting,
poor breathing effort, flexed arm and leg.
APGAR scor was 5^1min, 9^10 min Heart rate was 100 bp/m, ppv was given heart rate improved
to 120 bp/m,colour of child improved.baby still had poor
breathing effort so second cycle PPV given , muscle tone
improved, pink, SPO2 95%, heart rate 158 bp/m.

Baby was subsequently intubated with ETT size 3 anchored at 8 cm and kept on ventilator
and admitted to NICU with Neopuff.

9
FEEDING HISTORY
• Mother started breast feed .
• Ideally we should ask about sucking history and how long baby can
suck, does the baby get cyanosed while sucking.etc
• In NICU, she has been fed through Ryle’s tube.
• Patient is fed 8 times a day, 3 hourly and is fed through Ryles tube.
• Each feeding is around (45cc/3hrly) of milk
• Total feeding is 176.47 cc/kg/day
• Her urine output is good(2.25cc/kg/hr), urine colour is yellow
• Bowel output is 4 to 6 times a day.
 IMMUNIZATION HISTORY
• Baby immunized with Hepatitis B , BCG during birth.
FAMILY HISTORY
33 years old 31 years old

It’s a non-consanguineous marriage. Ther is no history of consanguity

among parents.
There was no any respiratory disease in family.
There is no G6PD deficiency in family.
-There is no family history of congenital heart disease or anomaly.
-No history of family members died in young age.
- father is 33 years old a non-smoker and does not drink alcohol.
-There is no malignancy runs in family
SOCIAL HISTORY

• Mother is a housewife.
• Father is a lorry driver.
• They live in Kuala Kurau and transport provided by husband.
• They living in a single story house, and are financially stable.(>RM
2000)
• living in teres house has proper electrical or water supply.
PHYSICAL EXAMINATION
Physical examination:
-Baby was on ventiation.
-He was alert conscious ,yellow pigmented skin and yellow sclera , but was tachypneic with subcostal recession,
respiratory rate of 70 bp/m with grunting and nasal flaring
-Eyes and ears was normal and no presence of cleft lip or palate.
-No cyanosis ,No bruises,No caput or cephalo hematoma

Vital signs:
Bp: 71/45 mmhg
RR: 110 Bp/m
Pulse rate:158 bp/m
Spo2: 95%
ABDOMINAL EXAMINATION

• On inspection the abdomen moves with respiration and the abdomen is not
distended. There is no visible pulsations and no visible scars seen.
• Abdomen was soft and non- tender upon palpation. Soft umbilicus was
felt.Normal bowel sound was heard.

• On palpation, there is no tenderness, the liver is palpable 3cm below costal margin
and the kidneys are not ballotable.

• On auscultation there is normal bowel sound heard and no bruit heard.

 systemic
Respiratory system:
examinations:
There was no chest deformity but has subcostal recession.Equal bilateral air entry was heard. Vesicular breath
sound was appreciated.
Cardiovascular system:
S1 and s2 heart sound was heard. No murmur was heard. Apex Beatt was at 4 th intercostal space mid clavicular
line.
Gastrointestinal system:
Abdomen was soft and non- tender upon palpation. Soft umbilicus was felt.Normal bowel sound was heard.
Central nervous system:
Anterior fontanelle was intact.
Motor system:
-Tone was normal
-reflex was normal
-power was 3/5 atleast
There was no neurocutaneos stigmata
.Spine was normal
Moro reflex was complete, hips was stable . no CTEV.
SUMMARY
Baby , a Malay boy born preterm at 34 weeks through EMLSCS
weighing 2.04 kg in Hospital Taiping, was admitted to NICU on
the same day. She was admitted for yellowish discolouration of
sclera and skin. Systemic Examinations enlarged palpable liver.
G6PD dificiency was found.
• Differential Diagnosis
• Investigation
• Treatment
• Discussion

Presented by: Sukanya A/P Visvalingam

Issues
• Prematurity at 34 Weeks 1 Day
• Respiratory Distress Syndrome
(Started from First 1H OL)
• Hypotension
(Occurred during 1H OL)
• Neonatal Jaundice of severe prematurity
(Suspected on 10H OL)

• Infant of Mother with Essential Hypertension with significant proteinuria

• Infant of Mother with Gestational Diabetis Melitus on diet control
Differential Diagnosis
 Neonatal Jaundice
Investigation
• Prematurity at 34 Weeks 1 Day
• Birth Weight: 2.04kg
• Ballard Score: 32-34W
• Prem w/up: Normal
• USG Cranium on D4: Lateral Grade I IVH
• USG Cranium on D14: Normal
• Neonatal Jaundice of severe prematurity
• Basic laboratory studies
1. Total serum bilirubin
2. G6PD at 2H OL
3. Blood type and Rh status in both mother and infant
4. Direct antibody test
• Transcutaneous Bilirubinometry (TcB).
• Phototherapy
Reduces serum bilirubin level through photoisomerization and photooxidation of bilirubin
to an excretable form.
(Direct Antiglobulin Test [DAT]; also known as Direct Coombs Test)
• Exchange Transfusion on D8 OL
D1 D3 D4 D5 D6 D7 D8 POST ET D9 D10

Total Bilirubin 92.9 97.5 143.3 225.5 215.7 294.7 460.9 285.3 210.4 186.6 156.3 117.5 106

Direct Bilirubin 6.5 6.9 7.1 8.8 13.6 9.6 7.9

Photolevel 240 240 240 240 240 240 240

Intensive
291 291 291 291 291 291 291
Phototherapy
Exchange
340 340 340 340 340 340 340
Transfusion
• Full Blood Count
10/5 11/5 12/5 14/5 23/5
WBC 15.4 15.7 10.9 12.3 20.6
Hb 14.5 15.2 13.9 13.5 11.6
Hct 44.3 46.5 41.9 40.6 35
Plt 288 276 297 330 381
Retics 1056
Urea 4.1 2.8 3.5
Sodium 138 141 137
Potassium 5.5 3.9 5.4
Chloride 109 110 106
Creatinine 75 72 53
Calcium 1.88 1.87 2.72
Magnesium 0.8 0.95
Phosphate 2.01 2.15
AST
Total Protein 54
Albumin 34 31
ALP 1.7
AST
ALT 9
Management
• Child achieved full oral feeding at 13H OL (TF: 183cc/kg/Day)
• Hypotension: Required bolus NS 10cc/kg ×1
put nnj cpg page
discussion
 Discussion
Newborns appear
jaundiced when it is ≥7
mg/dL. Approximately
85% of all term newborns
and most premature
infants develop clinical
jaundice. Also, 6.1% of
well term newborns have
a maximal serum bilirubin
level ≥12.9 mg/dL. A
serum bilirubin level ≥15
mg/dL is found in 3% of
normal term babies.
Physical examination is
not a reliable measure of
serum bilirubin.
Phototherapy
Exchange Transfusion
• Exchange transfusion is required if the bilirubin
rises to levels which are considered potentially
dangerous.
• Blood is removed from the baby in small
aliquots, (usually from an arterial line or the
umbilical vein) and replaced with donor blood
(via peripheral or umbilical vein). Twice the
infant’s blood volume (2×80ml/kg) is
exchanged.
• Donor blood should be as fresh as possible and
screened to exclude CMV, Hepatitis B and C and
HIV infection. The procedure does carry some
risk of morbidity and mortality.
Biliblanket
• A biliblanket is a portable phototherapy device for the
treatment of neonatal jaundice (hyperbilirubinemia).
• Other names used are home phototherapy system, bilirubin
blanket or phototherapy blanket.
• Biliblankets exert a blue/white light of varying intensity that
permeates through a light fabric. The baby is placed close to
or on the blanket during treatment. This light helps break
down high levels of bilirubin in the bloodstream, which
causes the discoloration of the baby’s skin.
1. Kernicterus
A pathologic diagnosis and refers to yellow
staining of the brain by bilirubin together with
evidence of neuronal injury.
Most commonly seen in the basal ganglia, various
cranial nerve nuclei, other brainstem nuclei,
cerebellar nuclei, hippocampus, and anterior horn
cells of the spinal cord.
Microscopically, there is necrosis, neuronal loss,
and gliosis. Abnormal signal intensity may be
seen on brain magnetic resonance (MR) imaging,
and a metabolic signature on MR spectroscopy is
being investigated.
The term kernicterus in the clinical setting should
be used to denote the chronic and permanent
sequelae of bilirubin toxicity.
2. Acute bilirubin encephalopathy
The clinical manifestation of bilirubin toxicity seen in the neonatal period.

The clinical presentation of acute bilirubin encephalopathy can be divided into three
phases:
A. Early phase
Hypotonia, lethargy, high-pitched cry, and poor suck.
B. Intermediate phase
Hypertonia of extensor muscles (with opisthotonus, rigidity, oculogyric
crisis, and retrocollis), irritability, fever, and seizures. Many infants die in
this phase. All infants who survive this phase develop chronic bilirubin
encephalopathy (clinical diagnosis of kernicterus).
C. Advanced phase
Pronounced opisthotonus (although hypotonia replaces hypertonia after
approximately 1 week of age), shrill cry, apnea, seizures, coma, and death.
3. Chronic bilirubin encephalopathy (kernicterus)
Marked by athetosis, complete or partial sensorineural deafness (auditory
neuropathy), limitation of upward gaze, dental dysplasia, and sometimes,
intellectual defi cits.