Neonatal medicine

Newborn examination
Normal variants and common disorders
When? after delivery and then 24 and 48 hours (blue book check)
Where? with mother
Who by? midwifery/ medical staff
o 1st week midwife
o 2nd week medical staff
o 6th week pediatrician/ GP

Newborn exam
take a history maternal anxieties, substances, significant events in pregnancy and delivery
o birth forceps use, injuries, complications

examination
o wash hands
o have a system and stick to it top bottom back
o quiet things first listen to heart early

ALWAYS DISCUSS YOUR FINDINGS WITH PARENTS

Normal variants
1) posture and colour
flexion of extremities well babies are flexed. If
unwell, they are extended and floppy.
pink with transient acrocyanosis hands and
feet purple in colour 2-3 days OK in term babies
o if cyanosed lips CENTRAL CYANOSIS
WORRY

2) skin appearance mild peeling normal. common in post term and IUGR infants

3) Growth restricted baby placental issues, maternal bleeding etc

scrawny
long and thin with relative large head
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absence of subcutaneous fat - wrinkly

skin dry/ cracked
umbilical cord: thin, reduced whartons jelly
thermoregulation and blood sugar issues!

4) Jaundice
day 1: pathological (unconjugated)
day 3-4, peaks day 5-6 then resolves by 2 weeks: physiological (unconjugated)
>2-3 weeks: pathological (conjugated) exclude hypothyroidism, biliary atresia

5) Vernix caseosa protect greasy white material, covers body of infants usually between 35-38weeks

6) Livedo reticularis
mottling/ marbling of skin
very common considering way baby maintains
thermoregulation
can last days

7) Lanugo
fine facial and body hair
seen mostly in preterm babies
lost during 1st month of life

8) Naevus flammeus (stork marks)

most common vascular birthmarks (50%)
irregular bordered, pink macule composed of dilated
distended capillaries
sites: nape of neck, upper eyelds, bridge of nose, upper lips
blanches with pressure
more prominent with crying
generally fade by 2 years, some may persist
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9) Mongolion blue spot

most common pigmented lesion in newborn especially
Asians
sites: buttocks, flanks or shoulders
colour: grey or blue-green
caused by melanocytes that infiltrate the dermis
fade over first three years of life some may persist
*** DOCUMENT THIS IN BLUE BOOK especially if Caucasian
THINK NAI

10) Milia
40% newborns
usually on face and scalp if in mouth = Epstein pearls
Yellow/ white papules about 1mm epidermal cysts caused by blocked sebaceous gland which
resolve spontaneously
may be present at birth or appear later

11) Erythema Toxicum

benign in up to 70% of newborns
small white. yellow papules with erythematous base
any part of the body
cause: unknown
peak incidence at 24-48 hours
may disappear then reappear

12) Harlequin phenomenon

reddening of one side of body and blanching of
the other half with sharp lien of demarcation
transient: seconds to minutes
occurs most often during first few days of life
thought to be a vascular manifestation due to
immaturity of the autonomic system in newborn

13) neonatal pustular melanosis

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begins: superficial vesiculopustular lesions

o rupture within 12-48 hours after birth
o leaves a spot of hyperpigmentation that may remain for up to 3 months after birth
freckling
benign
unknown cause
smears from pustules polymorphomuclear leukocytes with absence of organisms

14) staph skin sepsis

discrete pustules typically seen after few days of life
any part of body predilection to neck, axllla inguinal areas
mum may have wound/ episiotomy/ scar infection
almost always caused by staph aureus
TAKE SERIOUSLY treat with flucox for a few days otherwise babies
get unwell

15) caf au lait spots

tan or light brown macules/ patches with well define border
<3cm length and <6 in number = benign
o if LARGER SPOTS/ >6 cutaneous neurofibromatosis

16) strawberry hemangioma

bright red, raised lobulated
caused by dilated capillaries with associated endothelial proliferation
up to 10% newborns
o of this, 20-30% are present at birth
o remained apparent by 6 months
increase in size for approximately 9=12 months then gradually regress spontaneously complete
regression may take years
complicaitons: bleeding, ulceration, infection or compression of vital organs (affect vision or affect
cartilage, or cause trauma in nappy area)

17) pigmented naevus

dark brown/ black macule
most common on lower back/ buttocks but can occur
anywhere
generally benign
o malignant changes up to 10%
o observe closely for changes in shape and size
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18) cradle cap

waxy substance over scalp, can extend down to eyebrows
can cause little bleeding points
aspirin may help get rid otherwise advise:
o it is not irritating
o hair with grow over it, and the cradle cap will go away

19) port wine stain

pink/ reddish purple lesion
cosnists of dilated, congested capillaries directly beneath epidermis
often occurs on face or anywhere else
does not blanch with pressure
does not grow in size or spontaneously resolve
consider: Sturge Weber
Follow up

20) miliaria
vs. milia: these are due to obstruction of sweat and rupture of exocrine sweat ducts
o secondary to thermal stress/ overwrapped
o once heat stress removed, lesions quickly resolve
miliaria crystalline superficial vesicles 1-2cm in diameter. skin does not appear inflamed

miliaria rubra prickly heat papules and pustules from obstruction in mid epidermis
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Fontanelles

1) Caput succedaneum subcutaneous edematous, crosses suture lines

from constant compression in delivery
cone shaped head

2) cephalohematoma (big lump)

due to bleeding between periosteum and cranium
cause: shearing or tearing of communicating veins during delivery
often appears on 2nd day of life (slow bleeding)
often has a hard irregular bony margin surrounding
complications
o jaundice 2nd to resorption
o linear skull #
o calcification of the lump (takes longer time to reabsorb)

3) subgaleal hemorrhage (between periosteum and galea aponeurosis)

underneath scalp above periosteum
may result in large blood loss >250mls hypovolemic shock
most common after instrumental deliveries e.g. vacuum extraction
vague generalized scalp swelling/ fluctuance and can track down to neck
present with hemodynamic instability tachycardia, tachypnea, decreased activity and pallor

Positional plagiocephaly
Unilateral - more common in males, on the R side and present from birth
Bilateral - develops postnatally (brachycephaly)
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Both exacerbated by sleeping on back

Assessment
o HC = normal
o Palpate fontanelle and sutures = ridging
o Head shape from above (position of ear that is anterior in PP) and head from in front
o Look for torticollis to rule out
o Examine spine for curvature and sign of muscular asymmetry

Tongue tie
- associated with short frenulum
- difficult to latch onto breast
- interference with feeding and later speech development (uncommon)

Oral candiadias white patches on tongue, gums, lips and buccal mucosa
- both mum and baby needs to be treated with antifungal
- if bottlefed and has OC throw out bottles and start again

Periauricular skin tag

- usually anterior to ear
- may be associated with renal anomaly (do renal USS)

Facial asymmetry facial nerve palsy

- if does not resolve in 24-48 hours think why + investigate

Simian crease Down Syndrome/ 5-10% of normal population

Sacral dimple
- usually a bind pit in sacral region = no significance
- if pit is higher over lumbar or sacral region), discoloured or with hairy
tuft may be associated with spina bifida

Herpes vesiculo pustular lesions, grouped and often linear

- have to go into maternal history of cold sores/ genital herpes
- typically lesions develop by the end of first week or into second week of life (virus acquired at
time of birth)
o occasionally present at birth presumably they were exposed to virus several days prior to
delivery
- if eroded, shallow ulcer with erythematous base noted

Postural Tapies
- cramped pregnancy
- oligohydramnios
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- structural in syndromes, de novo (these need orthopod review) + must also check hips as
associated ith developmental dysplasia of hips

Polydactyly = extra digits

isolated or part of syndrome
most common form = extra little figner

Sucking blister
May be present at birth
Sites: over dorsal and lateral aspect of wrist or fingers
May appeara like well demarcated bruises or vesucilar
Infant often exhbiits XS sucking activity
Absence of lesions in other parts of body + well appearance
rule out pathological disorders like herpes/ bullous
impetigo

Pedal oedema = pathognomic for Turner syndrome + cardiac lesions

Napkin dermatitis contact, sparing skin folds and creases

- stagnant stools and urine
- like thrush lots of satellite lesions BUT DIFFERENCE IS: NOT IN
FLEXOR AREA
- cream + antifungal if not sure

Congenital hydrocele
- often transient
- transilluminable swellings surrounding testis
- associated with continuation of process vaginalis and contain peritoneal fluid
- spontaneous disappearance by 1 year
- ensure no hernia and that testes is in the scrotum

Hymenal tag
- common
- associated with protrusion of redundant vaginal mucosa
- often regresses without treatment over first 2 months of life

Blood on nappy in baby girls pseudomenses

- sorts itself out
- removal of maternal hormones
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Hypoglycemia
Fetal blood glucose
Babies need more glucose because of larger brain-to-body size ratio!
Normal production: 4-8mg/kg/min (3-6x more than adults)

What is normal
Fetal BGL closely related to maternal BGL
o umbilical venous BGL is estimated 2/3 value of mothers value
o maintained by facilitated diffusion across placenta
o GL and GN are not active prior to delivery
At delivery: Continuous diffusion of glucose by maternal circulation ceases abruptly baby
now needs to switch to GL and GN to maintain
o Transient fall in BGL in first 2hr after birth common in healthy infants
o Stabilizes by 4-8h
o Before counter-regulatory hormones (glucagon, adrenaline, GH and cortisol) induces
endogenous glucose production
o When BGL falls utilizes alternative fuels (KB & lactate)
Transient asymptomatic hypoglycemia is normal transition to extrauterine life!

what is normal? >2.6mmol/l

Maternal factors timing of last feed prior to delivery

duration of labour
IV glucose administration to mum
Maternal diabetes and insulin therapy
Fetal factors lack of glycogen stores & reduced ability to use alternative
fuels (IUGR babies and preterm)
increasing levels of circulating insulin (infants of diabetic
mothers and LGA infant >4.5kg, Beickwidth syndrome)
excess use of glycogen stores (tachypneic, tachycardiac,
hypo/hyperthermic any process that requires energy use)
o asphyxia
o thermal stress
o sick baby infection, hypermetabolic state
inadequate provision of substrate (constant vomiting, poor
feeding)
reduced ability to respond to low BGL with GN & GL

Importance of impact of low BSL on babies

- if prolonged/ recurrent acute systemic effects and neurologic sequelae (occipital lobe most
susceptible)
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Infant of diabetic mother/ - in both gestational diabetes and IDDM

LGA infant
Pathology:
Intermittent maternal hyperglycemia
fetal hyperglycemia premature maturation of fetal pancreatic
islets/ hypertrophy of beta cells neonatal hyperinsulinemia
hypoglycemia after interruption of the IU glucose supply from the
mother

ALSO because insulin is an anabolic factor makes baby big

Preterm infants Cause:
substrate deficiency secondary to immaturity of enzme
pathways e.g. impaired glucose metabolism
worse if baby is sick (HMD, infection, asphyxia)
SGA/ IUGR babies lack of substrate (adipose and glycogen)
may have increased insulin (a growth factor) we dont know
why this happens
after delivery a poorly coordinated response of counter
regulatory hormones may contribute to hypoglycemia in some
infants

Screening: when? all high risk infants!

Symptoms
Most are asymptomatic or have non specific sx:
jitteriness, irritability, poor feeding, lethargy, apnea and cyanosis, hypotonia and convulsions

screening test: rapid bed side test with glucometer

confirm low levels with formal lab test (blooD gas or formal blood sugar)

Management
ASYMPTOMATIC: feed ASAP (within 2h) continue every 3-4 hours +/- complementary feed
(EBM or formula) via bottle/OGT
o AIM: raise BGL >2.6mmol/L to provide a margin of safety BSL should be repeated 30
mins after feed
SYMPTOMATIC (significant symptoms)
o transfer urgently to NICU for assessment
o IV fluids 10% dextrose urgently
o BSL monitored frequent

BSL <1.2
establish IV access + bolus 2ml/kg 10% dextrose + commence IV fluids at 10% dextrose at
60ml/kg/day
IMI glucagon if IV access failures
recheck BSL 30 min after bolus
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o if still <1.2 additional bolus + monitor every hour till >2

o if still <2.6 increase dextrose flow rate

BSL 2 2.5 feed every 3-4 hours

Monitor BSL before feed for at least 24 hours an until 2 consecutive BSL are >2.6

Persistent hypoglycemia (low BSL >7 days)

if <2.6 after IV 10% dex graded increase in volume/ concentration of dextrose to achieve
>2.6
consider glucagon (not in babies with low fat stores) or hydrocortisone diazaoxide statins
surgery to remove pancreas

Before that determine cause of low BSL!

collect insulin, cortisol, GH, ammonia, lactate, pyruvate and formal BSL levels prior to
administration of hydrocortisone (only interpret at the time that BSL is low)
insulin level >10 when blood glucose is <2.6 is diagnostic of hyperinsulinism
If insulin normal urine metabolic screen, ketones, FFA, lactate, GH, cortisol, TFT and aBG
 Neonatal medicine

Respiratory distress in newborns

Signs of respiratory distress
- tachypnea >60/min (N=35-45
because smaller lungs and tidal
volume relative to mass to catch
up with sufiicent alveolar
ventilation to shift CO2)
- nasal flare
- subcostal / intercostal recession
- head bobbing
- expiratory grunt = PEEP,
PRODUCES BACKPRESSURE to stop
cllapsing alveoli
- cyanosis on pulse oximeter

Fetus is always born blue 45mmHg pO2

Examination
- listen to chest equal air entry + axilla to pick up dextrocardia
- scaphoid abdomen = diaphragmatic hernia

Parenchymal lung causes

Respiratory distress Hyaline membrane syndrome in preterm babies due to surfactant deficiency
syndrome atelectasis
Surfactant produced at 24-25 weeks of gestation, matures at 36-37 weeks
Develops within 4 hours of birth worsens over 24-36 hours
Improves over next 1-2 days
Coincide with marked diuresis (?)

Maternal risk factors significantly increase the risk of RDS:

Maternal Diabetes
Hypothyroidism
Caucasian race
Hypothermia

Fetal risk factors: prematurity, antepartum hemorrhage, second twin, hypoxia,

acidosis and shock

Complications: PTX, CP, BPD

CXR: small lung fields with reticulo-granular ground glass appearance (uniform,
spreading out to ribs) secondary to microatelectasis of alveoli + air
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bronchograms are radiolucent areas + indistinct cardiac border

Treatment
o TREAT with artificial surfactant prophylactically in at-risk (<27 GA) or
rescue when develop sx
o Manage with oxygen and CPAP
o Chest physiotherapy
o Antibiotics within 30 mins penicillin/ ampicillin and gentamicin
o use of antenatal steroid reduces this risk (RR:0.66) 20-30% babies at 32-36
weeks will develop this considered at 34-35 weeks gestationally (2 doses)

Transient tachypnea of Increased fluid retention in lungs tachypnea in the first few hours of life,
newborn wet lungs resolving in 2 days
- Normal:
o Increased fetal epinephrine concentration during labour
activates sodium channels leading to reabsorption of amniotic
fluid
o Fetal lung fluid is squeezed out during descent through birth
canal/ within first few breaths
- Pathology: build up of fluid in lungs due to reduced mechanical squeeze
and reduced capillary and lymphatic removal

RF: maternal asthma and diabetes, macroscomia, male sex, CS (lack of thoracic
compression reduced clearance of fluid), delivery <38 weeks, birth asphyxia,
excessive fluid administration to mother in labour

CXR: interstitial oedema and pleural effusions

streaky appearance and transverse fissure
prominence (fluid in fissure) Widening of
pleural space. Good lung volume, well inflated.
Normal by 48hrs postpartum

vs. RDS: RDS in preterm while TTN in preterm

and term

Treatment: Oxygen and artificial surfactant

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Meconium aspiration - seen in term babies, 1% of births

syndrome - 17% of pregnancies complicated by meconium not necessarily
pathological (pea soup thin meconium)
o pathological only if CTG changes indicating hypoxia
o babies excrete in stress
- sign: meconium stained liquor
- components:
o mechanical: clogging of airways
o chemical: chemical pneumonitis
o infective: though sterile lung fluid
Risk of ventilation perfusion mismatch and pulmonary hypertension

CXR: bilateral, patchy, coarse

infiltrates and hyperinflation of
lungs (ball valve effect) +/-
pneumothorax
- associated with persistent
pulmonary hypertension
very sick and requires
artificial ventilation
- increased incidence of
pneumothorax

Treatment:
- humidified inspired
oxygen + regular blood
gases
- suctioning not
recommended
- if need intubation & baby will deteriorate very fast

GBS Strep pneumonia Cause: Rupture of membranes >18 hours + positive GBS swab on mother or
previous baby with GBS
- Two onsets:
1. pneumonia SEPSIS AT BIRTH! 5% of those will have meningitis
at the same time
2. relapse at 6 weeks (second) significant risk
If colonized late in trimester, not enough time to produce IgG to cross placenta

Risk factors: previa, PPROM, offensive liquor, maternal infection markers,

positive swab

Signs: low temperature (sepsis in babies), hypotonia, respiratory signs, jaundice

and NEUTROPENIA (impending death)
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Treatment
Commence abx after blood cultures
cover gram + and (penicillin or cefotaxine
and gentamicin
Intrapartum treatment to to eliminate GBS

Pickup rate 1-2/7, need to do a rectal swab

with vagina swab

CXR: nonspecific; extensive bilateral (R>L) streaky interstitial pulmonary

opacities with airspace opacification at right base

Chronic lung disease presence of chronic respiratory signs (tachypnea and increased WOB),
persistent oxygen requirement or dependence on respiratory support +
abnormal CXR
Bronchopulmonary dysplasia
o Typically in long-ventilated premature neonates
Recurrent aspiration
Interstitial pneumonitis
Chromic pulmonary edema (PDA shunting)
Rickets of prematurity
Neuromuscular diseases e.g. SMA, MD, MG
CXR: honeycombing of lungs (fibrosis + cystic changes)

Congenital lung malformations pulmonary hypoplasia, congenital

emphysema

Extrapulmonary
pneumopericardium PTX can lead to this
serious condition, many do not survive

diaphragmatic hernia
mostly on left side, high mortality if R side, if
bilateral 1-5% survival rate
o pathology: during embryological development
foramen Bochdalek (posterolateral) herniation
of gut contents through incomplete diaphragm
during fetal development causing hypoplasia of
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lungs (structural and reactive pulmonary hypertension)

antenatally diagnosed: scaphoid abdomen
treat: gentle ventilation + agents to reduce pulmonary resistance
(nitrous oxide, sildenafil, magnesium) settle vascular tree before
definitive surgery
o outcomes depends on lung hypoplasia and pulmonary
hypertension
check for other congenital anomalies
CXR: bowel loops in thorax, if right after birth there is not much gas in the bowel so
more difficult to see, NG tube in thorax, lung and trachea displaced contralaterally

Esophageal atresia must have distal tracheoesophageal fistula air in

stomach
o RF: polyhydramnios in 3rd trimester, VACTERL
o Associated with excessive saliva and mucus production
coughing and cyanosis during feeds
o Main reason why newborn gets a NG tube (size 5)
o Aspiration main risk requires continuous suction otherwise
tracks into lungs

o Extraparenchymal lung causes/ pleural

pneumothorax causes: spontaneous/ infection/ meconium aspiration,
lung deformity, ventilation barotrauma
seen in immature lungs complicated by pneumomediastinum
0.8% air leaks occur spontaneously due to PPV
Small ones resolve spontaneously, or can aspirate from small
syringe
1. 20% oxygen to treat has NO evidence risk of oxygen
toxicity
Tension PTX - insert chest drain (intercostal drain)
transilluminates

Pleural effusion
Seen normally in hydrops fetalis
Chylothorax thoracic duct blending into pleura
Need chest drains

o intrapartum asphyxia
metabolic academia measured at birth which induces rapid deep
respirations in attempt to blow off CO2
leads to MOF and neonatal encephalopathy
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Tachypnea but no increased work of

breathing = Acidosis or Cardiac cause

Management
o maintain temperature
o provide oxygen if <92% O2Sat
nasal prongs
CPAP
o Fluids
o Test BGL, FBC, CRP (septic screen),
o Management depends on how much oxygen needed/ how much
respiratory support required
Mechanical ventilation
volume titrated use low tidal volume ventilation and keep
plateau pressure <30cm H2O to minimize volutrauma (over-
distension injury)
Appropriate inspiratory time minimize O2 toxicity by
maintaining FiO2 below 0.6
Permissive hypercapnia accept physiologic target outside normal
range
Optimal PEEP keep alveoli open (prevent de-recruitment)
reduces lung injury and pulmonary hypoplasia
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Once stabilized commence NG feeds

TEST INDICATION

Blood May indicate bacteremia Not helpful initially because

culture results may take 48 hours

Blood gas Used to assess degree of hypoxemia if arterial sampling,

or acid/base status if capillary sampling (capillary sample
usually used unless high oxygen requirement)

Blood Hypoglycemia can cause or aggravate tachypnea

glucose

Chest Used to differentiate various types of respiratory distress

radiography

Complete Leukocytosis or bandemia indicates stress or infection

blood count
with
differential Neutropenia correlates with bacterial infection

Low hemoglobin level shows anemia

High hemoglobin level occurs in polycythemia

Low platelet level occurs in sepsis

Lumbar If meningitis is suspected

puncture

Pulse Used to detect hypoxia and need for oxygen

oximetry supplementation
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Distinguishing Features of TTN, RDS, and MAS

CAUSE ETIOLOGY TIMING OF RISK FACTORS CLINICALFEAT CHEST TREATMENT PREVENTION
DELIVERY URES RADIOGRAPHY
FINDINGS

TTN Persistent Any Cesarean delivery4 Tachypnea Parenchymal Supportive, Prenatal

lung fluid infiltrates5 oxygen if corticosteroids
Macrosomia Often no
hypoxic before cesarean
hypoxia or Wet silhouette
delivery if 37 to 39
Male sex
cyanosis around the
weeks' estimated
heart5
Maternal asthma2 gestation (not
accepted U.S.
Intralobar fluid
Maternal
5 practice)19
accumulation
diabetes3

RDS Surfactant Pret Male sex7 Tachypnea Homogenous Resuscitati Prenatal

deficiency erm infiltrates5 on, oxygen, corticosteroids if
Maternal diabetes8 Hypoxia
ventilation, risk of preterm
Lung Air
surfactant delivery (24 to 34
Preterm delivery6 Cyanosis
under- bronchograms5
weeks' estimated
developme gestation)20(accept
Decreased lung
nt ed U.S. practice)
volumes

MAS Lung Term Meconium-stained Tachypnea Patchy Resuscitati Do not impede

irritation or amniotic fluid atelectasis5 on, oxygen, delivery for
Hypoxia
and post- ventilation, suctioning23;
Post-term delivery Consolidation5
obstruction term surfactant amnioinfusion of
no benefit27

Reading a chest x-ray

A: Name, Date, minimal/ presence of rotation,
appropriate exposure (= vertebral bodies), other
artefacts, position (AP/ PA?)
o AP = large heart and wider mediastinum,
more obvious
o PA = spine more obvious
o assess lordosis artefectual opacities along
spine if not perpendicular
o assess trachea deviation
B: Bone osteopenia (of prematurity), malignant
osteopetrosis, fractures
C: Cardiac cardiomegaly (>0.6),
pneumopericardium
o Assess cardiac borders, size, orientation
D: diaphragm flattened (hyperinflation)/ domed?
E: equipment: UVC, UAC, ECG, ETT, NG tube, drains
o UVC = on the R going straight into ductus
venosus/ thicker caliber/ higher than UAC
o UAC = seen on left, coiling up iliac artery and up into aorta/ thinner
caliber/ at level of diaphragm ideally
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F: Lung Fields
o Hetero/homogeneity hypodense and hyperdense areas? Reticular/
granular? Nodules or cysts? Diffuse or focal?
Honeycombing in CLD/ BPD cysts and fibrosis with
inflammation over time
Ground glass in HMD
o air brochograms
G: Gas bubble

Exam steps (OSCE skills)

1. Equipment required for this station:

Neonatal stethoscope
Opthalmoscope
Oxygen saturation monitor/pulse oximeter

2. Introduce yourself to mum and clarify her, and babys identity. Explain what you would
like to do, i.e. full examination of her new baby(s) and gain her consent. Congratulate her
on the birth as this will put her at ease and help gain your trust. New mums are protective
of their babies so trust and rapport is essential.

3. Whilst washing your hands you could ask mum to strip her baby down to its
nappy. Ensure you have a changing mat to do the examination on.

4. Start by asking mum a few questions:

How was the birth?

Good to know as forcep deliveries can cause facial bruising, subdural hematoma, c-
sections can occasionally cut the babys skin. Babys born by c-section are usually more
mucusy too.

Did your baby need any help after birth with breathing?

i.e. did the midwives or paediatric doctors have to give oxygen/rescue breaths.

How are you feeding your baby? Breast or bottle?

If breast feeding ask her

How is it going/baby latching ok, etc?

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If bottle feeding ask

Which milk are you giving your baby/is baby taking bottles ok, etc?

Dont criticise if mum has not opted to breast feed, this is an individual decision.

Are there any conditions that run in you or dads family e.g. congenital heart
problems?

Has anyone in your family (especially females) had problems with their hips at
birth?

Female babies are more likely to have clicky or dislocated hips due to the hormones that
are in mums body during pregnancy, these are the hormones which help to open up
mums pelvis prior to and during birth.

Has your baby passed its sticky black stool yet?

Parents often dont know the term meconium

5. Start by observing the baby. Does it look and behave normally, i.e. colour e.g.
jaundice, activity and posture. Is there any obvious bruising or marks from birth. Are
there any other marks such as strawberry naevus, stork marks or Mongolian blue spot.
Remember to turn the baby over and inspect its back too.

6. With the baby lying on its back feel the fontanelle gently with your hand. It should be nice
and soft, a tense/bulging or sunken fontanelle can suggest the baby is unwell.

7. Using both your hands gently feel the babys bones checking they are symmetrical on
both sides. Face, around ears, clavicles (these can be injured during birth if shoulder
dystocia occurs), both arms (e.g. Erbs palsy) down to legs and feet. Open up the babys
hand and look at the palm for normal palmar creases, count the fingers on each hand.
Look at the feet, is there any signs of a sandal gap or talipes and count the toes on each
foot.

8. If the baby has its eyes open at this point check for the red reflex using your
opthalmoscope. An absent reflex could suggest congenital cataracts.

9. Auscultate the babys heart using a neonatal/paediatric stethoscope. The normal rate is
120-150 so you will have to listen much more carefully for any murmurs as there is less
time between heartbeats to hear them. If you do pick up any murmurs assess whether it
radiates anywhere.
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10. Ausculate the lung fields. The normal respiratory rate is 30-60 in newborns. Are there any
extra sounds e.g. grunting or stridor.

11. Palpate the abdomen and check the umbilical stump/clamp to ensure no signs of
infection.

12. Turn the baby over and check down its spine and between buttock cheeks for the sacral
dimple.

13. At this point undo the babys nappy. Look for any obvious genital abnormalities. If its a
male infant you should check the scrotum to see if the testicles have descended. If not
you may be able to palpate them in the spermatic cord and gently bring them down
yourself. Check the patency of the anus at this point too.

14. Test the babys hips. This is done by two techniques, Ortolani and Barlow tests.
Essentially cup the babys hips in the palm of your hand and gently abduct the hips, this
should be smooth with no clicks. Next move your hands to the front of the baby and with
their knees flexed push gently downwards into the bed, again this should be smooth with
no clunks.

15. At this point redo the nappy and again wash your hands. With your hands freshly washed
you now want to assess inside the babys mouth. Use your little finger to feel the palate
of the mouth. Look to see if there is a tongue tie.

16. Again wash your hands. Attach the pulse/oxygen monitor to the babys foot. Remember
if a baby is sleeping or crying the heartrate may be higher or lower than the normal
range.

17. There are a number of primitive reflexes present in newborns which you should
elicit. Moro, grasp and sucking.

18. Thank mum, offer to dress the baby, although she will usually wish to do this herself.
Answer any questions she may have.

19. Again wash your hands and report your findings, if any, to the examiner, or doctor if on a
ward. Should you notice any abnormalities you may wish to suggest how to investigate
these further.

Neonatology
Neonatal medicine

Remember: BUGS BUGS BUGS

If mother withdrawals with sudden cessation of medication, give naloxone reversing
opiate effect baby has acute withdrawal reaction **** if suspect mother has been
taking illicits

Postnatal care
o mothercrafting support
o keep baby settled
o refer for hep C testing
o Postnatal ward NAS scoring
Develop at day 5 of life
Dosing: not related to if baby will withdraw or not
If loswer dose though, less likely

Neonatal scoring (normally done after a feed/ settled)

CNS
o cry
o sleep after feeding
o Moro reflex, tremors, tone, myoclonic jerks
o Perioral excoriation

METABOLIC
o Sweating
o Fever
o Frequent yawning
o Mottlng
o Nsaal stuffniess
o Sneezing
o Nasal flaring

GIT
o excessive sucking
Neonatal medicine

o poor feeding
o regurgitation
o loos stools
o
Jitteriness in preterm babies
o normal
o DDx: seizure
o test: hold the limb and flex it and it stops jitteriness
o observe for other clues of seizures
o jitteriness more high frequency vs. seizure slower

Withdrawal period
amphetamines 3-5 days
heroin 0-4 days
alcohol 3-12 hrs
methadone 12h to 14 days (even 1 month) peaking in first week

Treating withdrawal
o Drug of choice for opiate withdrawal morphine (acts on MG3 recptors
causing CNS symptoms)
o phenobarbiturates (sedative) for non opiates
** commence (/increase dose) if NAS scores
>= 8 for 3 consecutive scores (24 together)
OR
>= 12 (for 2 consequetive scores)

if 6 & 9 & 9 score again

encourage breastfeeding unless HIV positive, or not in best interest

WITH OPIATES, ENVIRONMENT AND DRUG EFFECTS ON THE CHILD

o Cannabis: behavioural
o Amphetamines later neuro effects
o Cocaine inhibits uterine blood flow ischemia

Hep C okay for breastfeeding unless CRACKED BLEEDING nipples or super high viral
load
 Neonatal medicine

SIDS
Definition Sudden Infant Death Syndrome = sudden death of an infant under one year of age,
during apparent sleep, which remains unexplained after a thorough case
investigation including review of the clinical history, examination of the death scene
and performance of a complete autopsy

Sudden Unexpected Death of Infant = an infant less than one year of age who died
unexpectedly

Epidemiology 504 children deaths in 2015

42 SUDI deaths in 2015
On average, cause of death determined only in 25% SUDIs.

Risk factors Explained and unexplained (including SIDS)

1. Non modifiable Male, indigenous (x6.5), low birth weight, preterm birth,
young mothers (16-21 years), disadvantaged bgs, preceding infectious illness,
child protection history/ NAI, geographic remoteness, tertiary education of other
2. Modifiable (MOSTLY unsafe sleeping environments)
- Admission to neonatal nursery
- prone sleeping
- bed sharing
- exposure to smoking
- excess bedding and clothing
- bedding and unsuitable environment
- unidentified infectious diseases *** (most common reason)

All deaths classified as SUDI were found to have at least one known risk factor, most
exposed to at least one modifiable one

Differences SIDS Explained SUDI

Peak age at death 2-4 months <1 month
Reported infant - Worse hx of
health 24 hours suggesting illness
before death
Smoking higher -
(maternal and
household)
Preventive Advice on preventing SIDS (Reduce the Risk campaign)
Factors - sleep baby on the BACK form birth, NEVER on tummy or the side
- sleep towards end of cot
- keep face and neck uncovered when sleeping blanket chin down/ swaddle
for the first 6 weeks when still not too active
- keep baby smoke free before and after birth
- make bedding tighter
- avoid bedsharing/ co sleeping (88% SUDI can be avoided)
- no cap on the head (baby controls temperature through head) heat is a risk
 Neonatal medicine

too
- cot environment: no pillows or soft toys or feather type doonas/ mattress
covered in plastic and not exposed foam (bed wetting can increase no)
- Room share until at least 6 months

Protective factors breastfeeding and not co-sleeping

Factors making co-sleeping unsafe

o rolling over/ smothering
o baby can fall out of bed
o baby trapped between wall and bed
o rolled on, arm slung across
o caught under bedding/ pillow
o less than 12 weeks old

Issues that Parents

impede risk of choking/ aspiration when supine when supine belief NO EVIDENCE
advice (laryngeal chemo reflex in first few months of life avoiding aspiration)
flat heads when supine belief risk is lower than SIDS
unsafe sleeping environments not recognised
Neonatal medicine

Neonatal jaundice
Definition: >10-15% direct bilirubin conjugated

Types:
Direct soluble and secreted sallow appearence
Indirect insoluble and likely to be absorbed in the skin very high
concentrations cause yellowing of skin

Clinical presentation: In neonates see in sclera and ear pinna

Newborns have very high hemoglobin 200 (in utero hypoxia)

RBC starts breaking down more total bilirubin higher indirect urine
Need to feed more so circulation is good indirect bilirubin gets excreted in
feces and urine after conjugation/ depends on enterohepatic pathway with
feeding (inhibited by breast milk glucuronidases that modifies bilirubin,
reducing excretion can prolong jaundice)

Complications: If bilirubin in serum is too high indirect bili can cross BBB (is neurotoxic)
in basal ganglia (kernicterus) CP (dystonic)

RF:
prematurity increased RBCs
sepsis hypoxia increased cell lines
albumin low (from sulphonamids and any illness/ SIRS) less binding of
the bilirubin to a protein
CAUSE:
increased RBC breakdown
blood group incompatibility
polycythemia
bruising/ cephalhematoma
premature (decrease life space of RBC)
decreased albumin binding sepsis, premature (immature liver function)
Decreased liver conjugation
changing liver function
breastfeeding (if glucorinyl transferase function) ask about
feeding and bowel habits
Decreased liver excretion dehydration, blood group incompatibility
sludging, obstruction
Increased reabsorption decreased GIT transit, breastfeeding
(glucoronidases effect)

TIMING
Day Unconjugated Conjugated
1 Hemolytic disease assumed until Neonatal hepatitis
proven otherwise Rubella
Neonatal medicine

Syphilis
CMV
Day 2-5 Hemolysis As above
Physiological
G6PD
Jaundice of prematurity
Sepsis
Extravascular blood
Polycythaemia
Spherocytosis
Day 5-10 Sepsis As above
Breast milk jaundice
Galactosaemia
Hypothyroidism
10+ Sepsis Biliary atresia
UTI Neonatal hepatitis
Pyloric stenosis

first day of life ASSUME PATHOLOGICAL and a hemolytic disease until

proven otherwise

blood group incompatibility (unconjugated due to HEMOLYSIS)

o Rh (-) mum and (+) baby
less likely in primigravida more likely in second
pregnancy because primed (more serious) IgM
crosses less easily cf IgG in subsequent pregnancies
can diagnose in utero fetal anemia (hydrops) on
USS Doppler
90% die in 3 months, 100% in 6 months
Rx: give anti-D binding antigen (forms complex)
preventing mum from recognizing it
o ABO-incompatability when maternal A/B/O antibodies
across and attack babys RBC (less aggressive and less
potent)
maternal O and baby A (most potent) because in O,
some anti-A antibodies are more potent (IgG = anti-
A) and crosses the placenta
this can happen in first pregnancy
o G6PD
o Sickle Cell less common because sickling does not happen
as easily in fetal hemoglobin
o Spherocytosis (gene mutation that occurs in any type of Hb)
o Thalessemia
o Pyruvate Kinase

congenital infection (conjugated)

o TORCH (normally conjugated) affects liver
Neonatal medicine

physiological jaundice is due to all five reasons peaks at 2-3 day of life, stabilizing
by 5th-7th day, disappears by day 14
o >65% NORMAL TERM INFANTS: SBR>80
o most common reason for readmission in first week
o peaking day 3-4 (formulae fed) ending 1st week, into 2nd
week (breast fed)
o plateauing of levels
day 5 in term baby
day 6-7 in preterm baby
causes
o physiological + feeding + sepsis + medications

prolonged jaundice unconjugated hyperbilirubinemic jaundice after 2 weeks of life

breast milk jaundice MOST common cause diagnosis of exclusion
inherited: Gilberts & Criger-Najal (type 1 > 2) diagnosis of
exclusion
TORCH sometimes unconjugated
Hypothyroidism - TFT
Urine infection culture

Conjugated causes
biliary atresia (before 6 months, must reconnect biliary tree)
choledodochal cyst
Hepatic hepatitis A/B/C/ congenital malformation
Metabolic disorders
Hypothyrdoism
idiopathic

Approach
Exam
for skin yellowing >120 total SBr
baby well?
General colour in natural light blanch skin and still yellow!
Bruising/ hematomas
Abdominal exam: distension and hepatosplenomegaly
Neurological effects: hypertonia, seizures, abnormal eye
movements
Extravascular blood
Lethargy
Investigations
- FBC & film hb, hemolytic screen
- Bilirubin total and conjugated
- Coombs test + G&H
- Weight feeding well or not
- Infection screen CRP, blood culture, urine culture
Neonatal medicine

Steps
If infant <24 hours old or bili >200 Coombs test positive = isoimmunisation
Coombs negative OR baby >24 hours or serum bili <200 measure conjugated
bilirubin (elevated = sepsis, TORCH)
o Normal conjugated bilirubin do FBC and Hct (high Hct TTTS,
materno fetal transfusion, delayed cord claming and SGA)
If Hct normal/ low blood smear to observe red blood morphology and
reticulocyte count
o If abnormal ABO incompatibility , G6PD, spherocytosis
o If normal extravascular blood e.g. cephalohematoma, hemrrohage,
increased enterohepatic circulation, Crigler Najjar, galactosemia,
hypothyroidism, drugs and hormones, transient familial
hyperbilirubinemia

Treatment

1. Supportive hydration
2. Phototherapy
photodegradation with 450mm blue light
serial SBR important to monitor
complications
- temperature instability
- fluid disturbances water los
- retinal damage
Neonatal medicine

- diarrhea decreases bowel transit time and induces lactose

intolerance
- bronze baby (if obstructive jaundice with PT)
1. Immunoglobulin
2. Exchange transfusion
o If >80 on day one exchange transfusion
o If >350 for any gestation worry! Check risk factors
o Preterm low rise (give phototherapy)
Blue phototherapy makes bilirubin soluble
(less toxic forms)
SE: darker skin tone, may damage eyes and
genitals
o Supportive feeding
o If incompatible give anti D to mum and baby (in baby, Ig
binds and does not allow maternal antibodies to attack)
buys time

Note on Coombs test:

Antenatal indirect Coombs to SCREEN pregnant women for ANTIBODIES that may cause
hemolytic disease of newborn
Postnatal direct Coombs used clinically when immune mediated hemolytic anemia
suspected
Neonatal medicine

Neonatal resuscitation

check if plugged to wall

check canisters
turn on light and heat for baby
ensure suction is attached and is working
ensure oxygen and room air is flowing
through attached tube to bagmask

take baby place in cot with head towards you with head in neutral position
turn on timer
call for help if needed
stimulate it by rubbing blanket over it

check airway suction secretions if needed

auscultate for FH sounds if <60
bagmask once per second over 30 mins and
then check
if HR<60 still call for help and start chest
compressions 3 to 1 breath (over 30 seconds)
intubate and give adrenaline
Neonatal medicine

Preterm issues

Intraventricular hemorrhage Germinal matrix is close to ventricles

Retinopathy of prematurity Hyperoxia after birth VEGF
downregulated with consequent
Osteopenia of prematurity

Neonatal Drug withdrawal

rug Risks

Smoking Increased risk of miscarriage

Increased risk of pre-term labour
Increased risk of stillbirth
IUGR
Increased risk of sudden unexpected death in infancy

Alcohol Fetal alcohol syndrome (FAS)

learning difficulties
characteristic facies: smooth philtrum, thin vermilion, small palpebral fissures
IUGR & postnatal restricted growth
microcephaly

Binge drinking is a major risk factor for FAS

Cannabis Similar to smoking risks due to tobacco content

Cocaine Maternal risks

hypertension in pregnancy including pre-eclampsia

placental abruption

Fetal risk

prematurity
neonatal abstinence syndrome
Neonatal medicine

rug Risks

Heroin Risk of neonatal abstinence syndrome

Timing of withdrawal onset

depends on time of last drug exposure/ metabolism/ excretion
o >-1 week incidence is low
alcohol first 3-12 hours
nacotics/ methadone first 48-72 hours
barbiturate 4-7 days
diazepam as late as day 12

Clinical Features of the Neonatal Narcotic Abstinence Syndrome

Neurologic Excitability Gastrointestinal Dysfunction

Tremors Poor feeding

Uncoordinated and
constant sucking
Irritability Vomiting
Increased wakefulness Diarrhea
High-pitched crying Dehydration
Increased muscle tone Poor weight gain
Hyperactive deep tendon Autonomic Signs
reflexes Increased sweating
Exaggerated Moro reflex Nasal stuffiness
Seizures Fever
Frequent yawning and Mottling
sneezing Temperature instability