Notes On The Newborn Infant+ 006

Notes on the
newborn infant
Notes_on_the_newborn_infant.indd 1 2018/09/05 16:00

Disclaimer
We have taken every care to ensure that drug dosages and related medical
advice in this book are accurate. However, drug dosages can change and are
updated often, so always double check dosages and procedures against a
reliable, up-to-date formulary and the given drug’s documentation before
administering it.
Notes on the newborn infant

First edition 1984
Second edition 1988
Third edition 1990
Fourth edition 1991
Fifth edition 1996
Sixth edition 2001
Seventh edition 2004
Eighth edition 2011
Ninth edition 2012
Tenth edition 2018
Contributors
Professor Michael Harrison, Professor Alan Horn, Dr Lucy Linley, Dr Max Kroon,
Dr Natasha Rhoda, Dr Niki Van Niekerk, Dr Yaseen Joolay, Dr Dave Le Roux, Dr
Mark Richards, Dr Candice Afonso, Dr Naana Brobby, Dr Shakti Pillay, Dr Kim
Prince, Dr Alex Stevenson, Dr John Kamenwa, Dr Lizel Jacobs, Dr Leigh-Ann Van
Balla, Lize van der Merwe.
Edited by Dr Lloyd Tooke and Professor Dave Woods

Text by The contributors 2018
Design by Lizette Watkiss
Cover photograph by Jo Splice, Newborns Trust
ISBN (paperback): 978-0-620-81204-7
All rights reserved. This publication may not be reproduced, stored in a

retrieval system, or transmitted in any form or by any means without the prior
permission of Lloyd Tooke.

Contents
Introduction.. . . . ............................................. 4 Apnoea. . ....................................................... 89
Abbreviations. .............................................. 5 Heart conditions........................................ 91
The infant at birth....................................... 6 Infection...................................................... 97
Resuscitation after birth............................ 9 Prevention of mother-to-child

transmission (PMTCT) of HIV.. ............... 104
Examination of the newborn.................. 17
Necrotising enterocolitis.. ...................... 108
Examination of the placenta. ................. 25
Intraventricular Haemorrhage and
Multiple births........................................... 26 Periventricular Leucomalacia................. 111
The healthy newborn infant and minor Hypoxic-Ischaemic Encephalopathy... 114
disorders. . . . . . . . . . . ........................................... 28
Neonatal Seizures.. .................................. 119
Fetal growth and size at birth................ 34
Blood disorders........................................ 121
Assessment of Gestational Age.............. 39
Neonatal hypocalcaemia....................... 128
Breastfeeding.. ........................................... 41
Birth injury. . .............................................. 132
Replacement feeding................................ 47
Congenital Disorders (CD).. .................... 135
Kangaroo mother care (KMC)................. 50
Down Syndrome (Trisomy 21)............... 137
Maternal Substance Abuse.. .................... 52
Procedures................................................ 139
Temperature control.. ............................... 54
Discharging infants and planning
Hypoglycaemia ......................................... 58 follow-up.................................................. 140
Infant of a diabetic mother (IDM).. ....... 62 Counselling bereaved parents. . ............. 143
Jaundice. . . . . . . . . . ............................................ 65 Burden of disease.................................... 146
Congenital Hypothyroidism. . ................... 75 Clinical Governance................................ 148
Respiratory distress.. ................................. 76 Ethics ........................................................ 151
Complications of prematurity. . ............... 85 Some drugs commonly used in newborn
infants. . ...................................................... 154

Introduction
These notes are not intended to be a comprehensive neonatal text as there are
numerous neonatal textbooks fulfilling this role. This is a concise guide, written by
practising professionals in neonatal medicine which can be used to provide core
knowledge. They are aimed at both the undergraduate student (medical or nursing)
as well as those already qualified.
While the views expressed in these notes are those of the authors, the readers will
appreciate that there are many areas that differing viewpoints may be held. The
contributors are affiliated with the Division of Neonatal Medicine, Department of
Paediatrics at the University of Cape Town. As far as possible, the content in this
book is evidence-based and up to date at the time of going to print.
Should readers wish to obtain a guide which is more focused on protocols and
medications, there is a pocket book available entitled ‘Neonatal Guidelines and
Drug doses’
Please contact the co-editor at Lloyd.tooke@uct.ac.za for any book orders,

suggestions or corrections.
Many thanks to Safeline Pharmaceuticals who provided sponsorship for the
set-up costs for this book.
This book is dedicated to our little patients and their families.
4 Introduction

Abbreviations
Many of the abbreviations used are intuitive, and not all are listed.
Abbreviation Term Abbreviation Term
μg microgram Max maximum
µmol micromol MCHC mean corpuscular haemoglobin
½ NS ½ normal saline MCV mean corpuscular volume
Aa alveolar arterial ratio MDI metered dose inhaler
ASD atrial septal defect Min minutes
BP blood pressure mg milligram
Bpm beats per minute mmol millimol
BSA body surface area NEB nebuliser
ng nanogram
corrected gestational age
CGA = gestational age at birth + nmol nanomol
postnatal age in wks. NS normal saline
CI contraindicated PDA patent ductus arteriosus
CNS central nervous system PIP peak inspiratory pressure
Conc concentration PJP Pneumocystis jiroveci pneumonia
PO per os (by mouth)
CVP central venous pressure
Proph prophylaxis
D day(s)
Q every (qua que)
D10W 10% dextrose water
RAD right axis deviation
D5W 5% dextrose water
RAH right atrial hypertrophy
Dly daily
Refs references
DW dextrose water (5 or 10%) RR respiratory rate
Elem elemental RSV respiratory syncytial virus
ETT endotracheal tube Rx treatment
FeNa fractional excretion of sodium SA South Africa
FiO2 fractional inspired oxygen S–U shoulder umbilicus
GA gestational age SC subcutaneous
GFR glomerular filtration rate SE potential side effects
GSH Groote Schuur Hospital Soln solution
HDN haemolytic disease of new born Susp suspension
hly hourly SW sterile water for injection
HR heart rate TA tricuspid atresia
hr hour Tab tablet
I/T ratio immature:total neutrophil ratio total anomalous pulmonary
TAPVD
venous drainage
IM intramuscular
T° temperature
IV intravenous
UAC umbilical arterial catheter
ℓ litre
LAD left axis deviation UVC umbilical venous catheter
LAH left atrial hypertrophy Vit vitamin
LH left heart wk(s) week(s)
LVH left ventricular hypertrophy wkly weekly
Maint maintenance ZAR South African rand
Abbreviations 5

The infant at birth
The normal infant should breathe well or cry within seconds of delivery. The
following routine procedures are carried out after an infant is born:
Heat conservation
Measures should be taken to prevent excessive cooling of the infant e.g. early drying,
warm towel, warm delivery room, prevention of unnecessary exposure, etc. Too often
the infant is left exposed in a cold draughty labour ward and forgotten, while the
attendant concentrates on the mother. All infants must be dried well immediately
after delivery. This often initiates breathing. Remember to dry the infant’s head. Wrap
the infant in a second warm, dry towel.
Assessing the infant

Breathing should be assessed immediately after birth while the infant is being dried.
If breathing is poor, resuscitation must be started. The aim is to start breathing
within the first “golden” minute. At the same time the infant can also be briefly
assessed for prematurity, respiratory distress or major congenital abnormalities. The
mother will want to know whether the infant is a boy or girl.
Give the infant to the mother

Infants that breathe well at birth should be dried and then placed on the mother’s
abdomen while waiting to clamp the umbilical cord. The infant can be dried and
covered by a warm towel. Once the cord is clamped the infant should be moved
into the kangaroo-care position (skin-to-skin) as this is a very effective method
of keeping newborn infants warm. The mother should be encouraged not only to
hold but also to suckle her infant. This is not only of psychological benefit but also
stimulates uterine contractions which facilitate delivery of the placenta. The sucking
reflex is at its height after birth. Other routine management of the newborn infant
can usually be delayed for 30 minutes while the mother gets to meet her infant.
Clearing the airway

Suctioning the mouth and pharynx is usually unnecessary, can cause damage or
stimulate a vagal response and should not be done routinely. It is only needed if
resuscitation is required. Infants with a lot of secretions should be turned on their
side so that the secretions can drain. Do not hold the infant upside down or attempt
to clear the mouth with a towel.
6 The infant at birth

Apgar score
This should be done at one minute in all infants to assess and document the infant’s
condition after birth. The infant can be scored while still with the mother. The Apgar
score should be repeated at five minutes if the one minute score is not normal in
order to document any improvement in the infant’s condition with resuscitation.
However, if the one minute score is normal the assessment at five minutes is not
usually required unless the infant deteriorates.
Umbilical cord
In the normal infant the umbilical arteries go into spasm within minutes of delivery.
It is advisable to delay clamping the cord until the infant has taken a few breaths
so as to encourage transfusion of blood via the umbilical vein into the infant’s
circulation from the placenta. Waiting one to two minutes will improve the infant’s
iron stores by significantly increasing the blood volume. If the infant has to be moved
for resuscitation, cord milking can be considered.
A sterile plastic umbilical clamp or tie is applied around the cord 2 cm from the skin,
and the cord above this is cut off. Beware of spraying blood into your eyes when
the cord is cut. Subsequent care entails cleaning the stump with saline, alcohol or
chlorhexidine. The stump will usually come away between 7 and 14 days after birth.
Eyes
Routine prophylaxis against gonococcal ophthalmia neonatorum is recommended
in high risk areas. Chloromycetin eye ointment is usually used. Erythromycin
or tetracycline ointment has the added advantage of preventing Chlamydia
conjunctivitis. This can be delayed while the mother first meets her infant and the
placenta is safely delivered.
Vitamin K1
Each newborn should receive an intramuscular injection (into the anterolateral thigh)
of 1 mg vitamin K1 (Konakion) to prevent haemorrhagic disease of the newborn. The
use of oral vitamin K1 is not recommended for routine use as repeated doses are
required, especially in the breastfed infant.
The infant at birth 7

Further care of the infant
Before leaving the labour ward the infant should be identified with name tags
on wrist and ankle before being weighed and the head circumference and length
measured. Normal term infants and bigger preterm infants delivered vaginally should
remain with their mothers from the time of delivery. If there is any doubt about
the well-being of the infant, observe the infant for a few hours in a nursery before
joining the mother once again. Healthy infants delivered by Caesarean section can
usually stay with the mother and need not be observed in the nursery for a few
hours. Every effort should be made to keep the mother and her infant together
The first feed

The normal infant should be put to the breast immediately after birth. This helps
to prevent hypoglycaemia, allows assessment of sucking ability and provides
antibodies in the colostrum. If not put to the breast at birth, let the infant suckle
as soon as possible.
The first bath

Early bathing soon after delivery is not recommended as it is of no physiological
advantage to the infant and should certainly be delayed in preterm or ill infants.
Infants born to HIV-positive women should be well dried after delivery to remove
contaminated blood and secretions but do not need an urgent bath. Vernix is
bacteriostatic and protects against skin infections.
8 The infant at birth

Resuscitation after birth
Not breathing well immediately after delivery is a neonatal emergency as it may lead
to hypoxia and possible brain damage or death if not correctly managed. There are
many causes of poor breathing including prenatal hypoxia, maternal anaesthesia or
sedation, and preterm or difficult delivery. Resuscitation may be required to assist the
transition from intra-uterine to extra-uterine life.
Anticipation is the key to good care, i.e. it is important to identify fetuses which are
likely to breathe poorly at birth, to monitor such high-risk pregnancies during labour,
to intervene appropriately, and to be adequately prepared for resuscitation. The goal
is to present each mother with a healthy newborn infant who has maximal potential
for growth and development. Resuscitation should be anticipated in a number of
clinical scenarios although any newborn infant may need resuscitation.
High-risk pregnancies associated with the need for

resuscitation after birth
Maternal status
• Teenage (< 16).
• Elderly (> 35).
• Low socioeconomic status.
Maternal illness
• Diabetes.
• Hypertension.
• Rh sensitisation.
• Severe anaemia.
Previous pregnancies
• Previous miscarriages.
• Previous stillbirths.
• Previous early neonatal deaths.
Resuscitation after birth 9

Present pregnancy
• No antenatal care.
• Certain medications, illicit drugs, alcohol and smoking.
• Pre-eclampsia.
• Antepartum haemorrhage.
• Multiple pregnancies.
• Severe fetal growth restriction (especially with poor umbilical flow on Doppler).
• Poor fetal movements in the last days of pregnancy.
• Polyhydramnios or oligohydramnios.
• Fetal abnormality.
• Abnormal presentation or position.
• Preterm or post-term labour.
• Poor progress in labour or prolonged labour.
• Cephalopelvic disproportion.
• Meconium staining or abnormal fetal heart rate.
• Instrument delivery or Caesarean section.
• Excessive maternal sedation.
• High-risk pregnancies should be delivered in hospitals where appropriate facilities
are available.
Fetal distress
If the fetus becomes hypoxaemic it develops bradycardia with shunting of blood
away from less vital organs to ensure an adequate blood supply to the myocardium
and brain despite a fall in cardiac output. This is an appropriate physiological
response to the stress of hypoxia to protect the brain and heart. Meconium may
also be passed and the fetus may make gasping respiratory movements, aspirating
amniotic fluid and meconium into the upper airways.
Fetal hypoxaemia during labour is usually transient, intermittent and occurs towards
the end of a uterine contraction when the placental oxygen content is lowest. This
results in a delayed deceleration which starts late in a contraction and continues
at least 30 seconds into the relaxation. If the placental blood flow from the mother
is able to recover and normalise placental oxygenation between contractions,
a fetal metabolic acidosis usually does not develop (the fetus is stressed rather
than distressed). However, if maternal blood supply to the placenta continues to
deteriorate, the fetus becomes hypotensive and tissue hypoxia results in a metabolic
acidosis (only now can the fetus be regarded as distressed and in danger of dying).
10 Resuscitation after birth

Fetal heart rate monitoring is used to screen for fetal distress. Repeated late
decelerations suggest the fetus is hypoxically stressed while persistent baseline
bradycardia or poor beat-to-beat variability on CTG suggest the infant is distressed
with severe hypoxia and a metabolic acidosis. This can be confirmed with a cord gas
immediately after birth (within 1 hr).
The distressed fetus must be delivered as soon as possible. If there is any delay
before a rapid vaginal delivery or Caesarean section is performed, fetal resuscitation
should be started by suppressing uterine contractions (intravenous salbutamol or oral
nifedipine) and turning the mother onto her side to optimize placental blood flow.
Giving the mother oxygen is not helpful. Fetal resuscitation is particularly important
if the mother has to be transported to hospital for delivery.
Confirming fetal hypoxia at birth

The best biochemical marker of hypoxia in the hours before delivery is the presence
of a metabolic acidosis in the infant at birth. Clinical suspicion of significant fetal
hypoxia (‘an acute intrapartum event’) can be confirmed if the base deficit is greater
than 10 mmol/l in a sample of arterial blood taken from the umbilical cord at birth or
the infant soon after delivery. However, the degree of the metabolic acidosis does not
indicate the severity or duration of fetal hypoxia nor the risk of cerebral damage. The
development of neonatal encephalopathy is the best measure of severe intrapartum
hypoxia and resultant cerebral ischaemia. If possible the acid-base status of
umbilical arterial blood should be determined in all cases of fetal distress or failure
to breathe well after delivery.
Helping Infants Breathe (HBB) and the golden minute

HBB is an evidence-based training program to teach neonatal resuscitation
techniques in resource-limited areas. HBB teaches the initial steps of basic neonatal
resuscitation to be accomplished within The Golden Minute (establishing adequate
breathing within the 1st minute of life) to save lives and give a much better start
to many infants who struggle to breathe at birth. It is an initiative of the American
Academy of Pediatrics (AAP) and a number of other global health stakeholders.
In addition to the practical steps needed to resuscitate an infant it includes the
following key strategies that improve neonatal outcome:
• Good communication between staff.
• Preparation and planning.
• Hand washing and cleanliness.
• Delayed cord clamping.

• Immediate skin to skin care.
• Breastfeeding.
The preparation in neonatal resuscitation is important as are the HBB principles of
providing a warm environment (no open windows or drafts, theatre temperature at
26 degrees), warm dry towels, a radiant heat source and clean hands.
Apgar score
The terms ‘birth asphyxia’ or ‘neonatal asphyxia’ are often defined as the failure
to initiate and sustain breathing after birth. Other authorities interpret ‘asphyxia’
to mean impaired fetal gas exchange during labour (intrapartum fetal hypoxia).
However, many infants who do not breathe well after birth have not suffered
intrapartum hypoxia, while some infants with intrapartum hypoxia still manage
to breathe spontaneously after delivery. It is therefore not surprising that the
association between poor breathing after birth (or a low Apgar score at one minute)
and abnormal neurological development is tenuous.
The Apgar score (if performed correctly) is an objective method of assessing an infant’s
clinical condition after delivery. The Apgar score is routinely assessed at 1 minute. If the
1 minute score is low, the Apgar score should be repeated every 5 minutes until normal
to objectively document the infant’s condition. If the 1 minute score is low, the 5 minute
score gives an indication of the success or failure of the resuscitation attempts. Do not
wait for the 1 minute score before deciding whether the infant needs resuscitation.
Table 1: The Apgar score
Sign Score
0 1 2
Heart rate Absent Under 100/min Over 100/min
Resp. effort Absent Weak/irregular Strong/regular
Muscle tone Limp Some flexion Active movement
Response to stimuli None Weak movement Cry
Colour Blue or pale Body pink, Completely pink
extremities blue
Score:
7–10 Normal
4–6 Moderately abnormal
0–3 Severely abnormal

A low score (below 7) at 1 minute confirms the need for resuscitation. With adequate
resuscitation the score should be normal (7 or above) by 5 minutes. A low score at
5 minutes, and especially at 10 minutes, suggests significant intrapartum hypoxia
or severe respiratory distress. The longer the score remains low the greater the
likelihood that the infant will die. A score of 10 at 1 minute is rare as all newborn
infants have peripheral cyanosis at birth.
Resuscitation
Neonatal cardiac arrest is due to hypoxia so initiation of ventilation remains the
focus of initial resuscitation. All delivery centers must have adequate resuscitation
equipment in working order which is routinely checked every day. A good overhead
light source and means of keeping the infant warm are essential. All medical and
nursing staff delivering infants should be able to perform basic resuscitation.
The majority of infants cry spontaneously at birth and need no intervention. If infants
do not breathe well, the aim of resuscitation is to establish breathing within one
minute of birth (the ‘golden minute’). It is important to document the timing and
response to each step in the resuscitation process.
Steps to resuscitate a newborn infant
Good drying to stimulate breathing and preventing hypothermia

All term and late preterm infants should be dried well immediately after delivery. This
stimulates the onset of breathing in 80% of infants. If the infant does not breathe
well or cry after drying, resuscitation is needed. Rubbing the infant’s back gently
(once or twice) is good way to provide stimulation. (Do not smack or shake the infant
or try to stimulate breathing by flicking the feet! )
Keep the infant warm. To maintain body temperature or prevent hypothermia during
transition (birth to 1–2 hours of life). Preterm infants <30 weeks gestation or
weighing < 1200g should be placed directly (without drying) into a clean food-grade
plastic bag (feet first, cover trunk and the back of the head but not the face). Continue
to resuscitate through the plastic bag. Cut holes in bag to expose umbilicus or limbs, if
required. Weigh the infant IN the plastic bag and transfer to the neonatal nursery. Only
remove the plastic bag once the infant is stabilized in an incubator.

The steps to resuscitate an infant after birth follow the ABCD format (Airways,
Breathing, Circulation, Drugs).
Airways
Routine suctioning of the airways is contraindicated. However, clear the airway first
if an infant is born through meconium stained amniotic fluid and needs resuscitation.
No further suctioning is needed if the infant breathes well.
Breathing
If the infant is still not breathing after being dried, some form of artificial ventilation
is required. The simplest method is mask ventilation using a resuscitator (mask and
self-inflating bag) with the mask applied tightly to the infant’s face or a T-piece with
5 cm PEEP. With the infant lying on his/her back position the head into the neutral
‘sniffing position’ with the face forward and the neck not hyper-extended. Mask
ventilation must produce good chest movement. If not the mask is not correctly
applied or the airway is blocked. Make sure the infant’s head is in the correct
position and the airways are not blocked with secretions, meconium or blood. Almost
all infants can be resuscitated with mask ventilation alone.
After 30 seconds of effective mask ventilation, palpate the base of the umbilical
cord or listen to the chest for heart sounds. If the pulse is good (above 100/minute)
continue ventilating until breathing starts. If the pulse is slow, reposition the mask
and ensure good air entry with mask ventilation.
If the bradycardia persists after a further 30 seconds, consider endotracheal
intubation (if skilled in intubation) with a 2.5 or 3.0 mm straight endotracheal tube
using a laryngoscope with a size ‘0’ straight blade. The ventilation bag can then be
connected to the endotracheal tube. 30-40 breaths a minute is recommended. The
chest should move well and air entry should be heard on both sides of the chest.
Only approximately 1 in 500 resuscitated newborns require intubation and bag-mask
ventilation is nearly always effective. The use of CPAP is now also encouraged if
ongoing respiratory distress is evident after the golden minute, in a spontaneously
breathing infant. The more severe the fetal hypoxia the longer it will take before the
infant starts to breathe spontaneously.
Administration of Supplemental oxygen
• Only give oxygen if the pulse remains slow despite good ventilation in room
air. The use of a pulse oximeter to measure heart rate and oxygen saturation in
complicated resuscitation is very useful. Saturations of 60% at birth steadily
increase to 85% at 5 minutes in well infants that breathe room air spontaneously.

Normal pre-ductal saturations after birth (right hand or ear)
1 min: > 60%
2 min: > 65%
3 min: > 70%
4 min: > 75%
5 min: > 80%
> 10 min: 90 - 95% (ILCOR – AAP guidelines, 2015)
• Most term infants can be adequately resuscitated in room air. New evidence
suggests that supplementary oxygen induces the release of free radicals which
may damage the brain.
• Preterm infants requiring resuscitation should be initiated with low oxygen
supplementation- 30% to 40% (Resuscitation Council of Southern Africa-2015),
and the oxygen concentration should then be titrated to achieve a preductal oxygen
saturation of 88-92%.
Circulation
The pulse rate, measured by palpating the base of the umbilical cord or auscultating
the heart, should be above 100 per minute. Peripheral pulses are often difficult
to feel. A persistent heart rate below 100 per minute is a good marker for
inadequate ventilation.
If the heart rate remains below 60 beats per minute, give external cardiac compressions
at approximately 120 times a minute while continuing with respiratory assistance.
A ratio of 3 sternal compressions to 1 breath is used (ratio 3:1). The sternum should
be depressed at a point 1cm below a line joining the nipples – well above the
xiphi-sternum. A two-handed technique is best with the palms and fingers behind
the infant’s back while the lower sternum is depressed with the thumbs a 1/3 of the
depth of the AP diameter. When giving cardiac massage it is very helpful if a second
person ventilates the infant. Pink peripheries with rapid capillary filling when the
skin over the chest is pressed are good indications of an adequate circulation. Blood
pressure is often difficult to measure in the delivery room.
Drugs
Only about 1 in 1000 infants needs drugs during resuscitation. Adrenaline 0.1 ml/kg
of a 1:10 000 solution (i.e. 1 ml adrenaline 1:1000 diluted in 9 ml saline or sterile
water) can be given intravenously via an umbilical catheter (or 0.25 ml/kg placed
down the endotracheal tube if an intravenous line cannot be started). The use
of sodium bicarbonate is controversial. Never give sodium bicarbonate down the
endotracheal tube.

If the infant fails to respond to resuscitation, check the blood glucose concentration.
If below 1.5 mmol/l (25 mg %) give 5 ml 10% dextrose water slowly intravenously
followed by a continuous intravenous infusion containing 10% dextrose at
60ml/kg/day. If the infant appears exsanguinated (e.g. from a snapped cord)
give 20 ml/kg of normal saline, or emergency O negative blood. There is no
role for atropine or calcium in neonatal resuscitation.
Naloxone only reverses the respiratory depressing effects of opiate analgesics given
to the mother within 4 hours of delivery. Routine naloxone (Narcan) 0.25 ml/kg IM/IV
(i.e. 0.1 mg/kg) is not recommended as evidence showed no difference in outcomes
compared to ventilation. IM naloxone may take a few minutes to act.
Post Resuscitation Care

• Maintain normothermia and appropriate oxygen saturations.
• If resuscitation has been prolonged or difficult, the infant should be transferred
to the nursery for observation and further assessment.
If there is no heartbeat after 10 minutes or bradycardia with no adequate respiratory
efforts persist after 20 minutes despite aggressive resuscitation, further attempts at
resuscitation are probably hopeless.
Delayed cord clamping

• Delay cord clamping 30-120 seconds in term and preterm infants who do not
require resuscitation at birth.
• The possible advantages and disadvantages of cord “milking or stripping” rather
than delayed cord clamping in infants who need resuscitation is still being
investigated.

Examination of the newborn
History
Maternal background
• Age, parity, blood group, VDRL and HIV status.
• Outcome of previous pregnancies.
• Any problems with previous infants.
Pregnancy
• Booked.
• Duration and fetal growth.
• Illness or complications e.g. diabetes, GPH.
• Drugs, smoking, alcohol.
• Feeding Choice.
Labour and delivery

• Duration of labour.
• Rupture of Membranes, Amniotic Fluid Clear, Meconium.
• Drugs given to mother.
• Method of delivery.
• Time and Date of Delivery.
• Fetal condition.
• Complications.
Infant
• Condition at birth – Apgar score.
• Need for resuscitation, Time to spontaneous Respiration.
• Passage of urine and meconium.
• Feeding.
• Problems since delivery e.g. hypothermia, jaundice.
Placenta
• Weight.
• Gross abnormalities.
Examination of the newborn 17

Physical examination
A brief initial examination should be done after delivery to detect major congenital
abnormalities or gross disease requiring immediate attention. A complete examination
should be performed within 24 hours of birth and before discharge home.
Remember
• Wash your hands.
• Undress the infant completely.
• Do not let the infant get cold.
Examine the infant in the mother’s presence if possible. This reassures her and
allows for an explanation of problems, such as mucoid vaginal secretion or milia. The
mother should be encouraged to ask questions.
Infants must always be examined gently with warm hands. The physical examination
of the newborn infant should be performed in a fixed order to ensure that nothing is
forgotten. First basic measurements are made, then the infant is inspected generally.
Thereafter the infant is examined by regions starting at the head and ending at the
toes. Finally, the neurological status is assessed. The step by step examination given
below lists what should be done and gives the normal and abnormal findings.
Table 2: Systematic examination of the newborn infant
Normal Abnormal
MEASUREMENTS
Birth weight 2500g or above. Between 10th Low birth weight (below 2500g).
and 90th centile for gestational Underweight (below 10th
age. centile) or overweight (above
90th centile) for gestational age.
Head Between 10th and 90th centiles Small head (below 10th centile)
circumference for gestational age. or large head (above 90th
centile) for gestational age.
Crown-heel Between 10th and 90th centile Short (below 10th centile or
length for gestational age. Measure long (above 90th centile) for
accurately with a measuring box. gestational age.
Skin Abdominal wall 36–36.5 °C Hypothermia (below 35 °C).
temperature (or axilla 36.5–37 °C)
18 Examination of the newborn

Normal Abnormal
GENERAL INSPECTION
Gestational Physical and neurological Immature features in preterm
age features of term infant. infant (below 37 weeks). Post-
Term (37–41.9 weeks). term infants (42 weeks and
above) have long nails and are
often wasted.
Wellbeing Active, alert. Lethargic, appears ill.
Wasting Well nourished. Soft tissue wasting.
Colour Pink tongue. Cyanosis, pallor, jaundice,
plethora.
Skin Smooth or mildly dry. Vernix and Dry, marked peeling. Meconium
lanugo. Stork bite, blue naevus, staining. Petechiae, bruising.
milia, erythema toxicum, salmon Large or many pigmented
patches. naevi. Capillary or cavernous
haemangioma. Skin infection.
Oedema.
HEAD
Shape Caput, moulding. Cephalhaematoma,
subaponeurotic bleed.
Asymmetry, anencephaly,
hydrocephaly, microcephaly,
encephalocoele.
Fontanelle Open, soft fontanelle with Full or sunken anterior
palpable sutures. fontanelle. Large or closed
fontanelles.
Sutures Palpable mobile sutures. Wide, fused or markedly
overlapping sutures.
Hair Wide familial variation. Low posterior hair line.
EYES
Position One eye space between the eyes. Hypertelorism or hypotelorism.
Size Microphthalmia or macrocornea
(glaucoma).
Lids Mild oedema common. Marked oedema, ptosis, bruising.
Narrow palpebral fissures in FAS.
Conjunctivae May have small subconjunctival Pale or plethoric. Conjunctivitis.
haemorrhages. Excessive tearing when
nasolacrimal duct obstructed.

Normal Abnormal
Cornea, iris Cornea clear, regular pupil, red Opaque cornea, irregular
and lens reflex. pupil, cataracts, no red reflex,
fixed squint, abnormal eye
movements.
NOSE
Shape Small with upturned nostrils. Flattened in oligohydramnios.
Nostrils Both patent. Easy passage of Choanal atresia. Blocked with
feeding catheter. dry secretions.
MOUTH
Lips Sucking blisters. Cleft lip. Long smooth upper lip,
no philtrum and thin pink border
in FAS.
Palate Epstein’s pearls. High arched or cleft palate.
Tongue Pink. Cyanosed, pale, macroglossia.
Posteriorly placed in Pierre-
Robin anomaly.
Teeth None at birth. Adventitious or primary teeth.
Gums Small cysts. Epulis.
Mucous Pink, shiny. Thrush, ulcers.
membranes
Saliva Excessive if poor swallowing or
oesophageal atresia.
Jaw Smaller than older child. Micrognathia in Pierre-Robin
anomaly.
EARS
Site Pinnae vertical at term. Ears rotated backwards with
poorly formed upper pinnae (low
set).
Appearance Familial. Pre-auricular skin tag or sinus.
Malformed ears. Hairy ears in
IDM.
NECK
Shape Usually short. Webbing, torticollis.
Masses No palpable lymph nodes or Cystic hygroma. Goitre.
thyroid. Sternomastoid tumour.
Clavicle Swelling or crepitus if fractured.

Normal Abnormal
BREASTS
Palpable breast nodules at term. Accessory or wide-spaced
0.5 to 1 cm. nipples. Mastitis. Enlarged,
lactating breasts.
HEART
Pulses Brachial and femoral pulses Pulses weak, collapsing, absent,
easily palpable. 120–160 beats fast or slow.
per minute.
Capillary Less than 3 seconds over chest Prolonged filling time if infant
filling time and peripheries. cold or shocked.
Precordium Mild pulsation felt over heart Hyperactive precordium.
and epigastrium.
Apex beat Heard maximally to left of Heard best in right chest in
sternum. dextrocardia.
Sounds Loud, single 2nd heart sound on Gallop, widely split-second
day 1. sound.
Murmurs Soft, short systolic murmur Systolic or diastolic murmurs.
common on day 1.
Heart failure Hepatomegaly, tachypnoea
or excessive weight gain.
Occasionally oedema
LUNGS
Respiration 40–60 breaths per minute. Tachypnoea – above 60 breaths
rate Irregular in REM sleep. Periodic per minute. Gasping. Apnoea
breathing with no change in with drop in heart rate, pallor or
heart rate or colour. cyanosis.
Chest shape Symmetrical. Hyperinflated or hypoplastic
chest.
Chest Symmetrical. Asymmetrical in pneumothorax
movement and diaphragmatic hernia.
Recession Mild recession in prems. Costal recession in respiratory
distress.
Grunting Expiratory grunt in respiratory
distress.
Stridor Inspiratory stridor a sign of
upper airway obstruction.

Normal Abnormal
Percussion Resonant bilaterally. Dull with effusion or
haemothorax. Hyper resonant
with pneumothorax.
Air entry Equal air entry over both lungs. Unequal or decreased.
Bronchovesicular.
Adventitious Transmitted sounds. Crackles, wheeze or rhonchi.
sounds
ABDOMEN
Umbilicus 2 arteries and 1 vein. 1 artery, 1 vein. Infection.
Bleeding or discharge. Hernia.
Exomphalos.
Skin Periumbilical erythema or
oedema.
Liver Palpable 1 cm below costal Enlarged, firm, tender.
margin, soft.
Spleen Not easily palpated. Enlarged, firm.
Kidneys Often palpable but normal size. Enlarged, firm.
Bowel sounds Heard immediately on Depressed or absent.
auscultation.
Anus Patent. Skin tags. Absent or covered. Displaced
anteriorly.
Stools Meconium passed within 48 Blood in or on stool. White
hours of birth. Yellow stools by stools in obstructive jaundice.
day 5. Breastfed stool may be Offensive watery stools.
green and mucoid.
SPINE
Coccygeal dimple or sinus. Sacral dimple or sinus. Scoliosis.
Straight spine. Meningomyelocoele.
GENITALIA
Penis Urethral opening at centre of Hypospadias. Epispadius.
glans. Micropenis.
Testes Descended by 37 weeks. Undescended.
Scrotum Well formed at term. Inguinal hernia. Fluid hernia.
Vulva Skin tags, mucoid or bloody Fusion of labia.
discharge.
Clitoris Uncovered in preterm or wasted Enlarged in adrenal hyperplasia.
infants.
Urine Passed in first 12 hours. Poor stream suggests posterior
urethral valve.

Normal Abnormal
ARMS
Flexed position in term infant. Erb’s palsy. Clavicle or humerus
fracture
HANDS
Extra, fused or missing digits.
Skin tags. Single palmar crease.
Hypoplastic nails.
LEGS
Mild bowing of lower legs Dislocatable knees in breech.
common.
FEET
Positional deformation. Clubbed feet. Abnormal toes.
NEUROLOGICAL STATUS
Behaviour Alert, responsive. Cries but Drowsy, irritable, jittery,
consolable. inconsolable.
Movement Active. Moves all limbs equally Absent, decreased or
when awake. Stretches, yawns asymmetrical movement. Jittery
and twists trunk. or convulsions.
Tone Some hypotonia in preterm Hypotonia or hypertonia.
infants. Asymmetrical tone.
Pull to sit Some initial head control. Totally floppy.
Supported Holds head erect briefly, moves Head flops back or forward. No
sitting head forward. attempt to elevate head.
Ventral Holds head in line with body Totally floppy or very
suspension momentarily. hyperextended.
Hands Intermittently clenched. Opens Permanently clenched.
hands and moves individual
fingers when relaxed.
Cry Good cry when awake. Weak, high pitch or hoarse cry.
Vision Follows a face, bright light or Absent or poor following. Fixed
red object for 90°. Alternating or squint.
intermittent squint.
Hearing Responds to loud noise. No response.
Sucking Good suck and rooting reflexes Weak suck at term. Biting.
after 36 weeks gestation.
Rooting Good symmetrical reflexes after Absent rooting.
36 weeks.
Moro reflex Full extension then flexion of Absent, incomplete or
arms and hands. Symmetrical. asymmetrical response.

When the history has been taken and the physical examination completed, an overall
assessment of the infant must be made and a list of the problems compiled. The
management of each problem in turn must now be addressed.
Examination of the hips

The hips must be examined in all newborn infants to exclude congenital dislocation
or an unstable hip.
The infant is examined lying on his/her back with the hips flexed to a right angle and
knees flexed.
Barlow’s test: demonstrates an unstable or dislocatable hip. One hand immobilises
the pelvis (thumb over pubic ramus, fingers over sacrum) while the other hand moves
the opposite thigh into mid-abduction. If the hip is unstable, backward pressure
on the lesser trochanter with the thumb on the inner side of the thigh causes the
femoral head to slip out of the acetabulum. Conversely forward pressure on the
greater trochanter with the fingers would tend to cause the head to spring back into
the acetabulum. The same procedure is then carried out for the opposite side.
Ortolani test: Both thighs are held so that the examiner’s fingers are over the greater
trochanters and both thumbs rest on the inner aspects of each thigh. The thighs are
then abducted: if a hip is dislocated, a ‘clunk’ can be felt and heard as the femoral
head slips forward into its normal position in the acetabulum.
Management of any hip abnormalities would include informing the parents and
referral to Orthopaedic services. Ultrasound is the most useful special investigation
early in life. The Pavlik Harness might be used for Congenital Hip Dislocation/
Developmental Dysplasia of the hip, and if that is unsuccessful surgery might
be needed.

Examination of the placenta
The placenta should always be weighed after delivery and then examined in a
systematic way: umbilical cord, membranes, then maternal and fetal surfaces of the
placenta. Remenber that the placenta is a fetal organ. At term a healthy placenta
weighs about 550 g (one-sixth of the infant’s weight). A relatively heavy placenta
suggests maternal diabetes, syphilis or Rhesus disease while growth-restricted or
wasted infants have relatively light placentas.
A single umbilical artery can be associated with major congenital abnormalities,
especially intestinal and renal, in 25% of cases while yellow staining of the cord
suggests Rhesus disease. A true knot may cause intrapartum hypoxia. Insertion of
the cord into the membranes may cause severe fetal bleeding with rupture of the
membranes (vasa praevia). The site of cord insertion into the placenta is not important.
A great deal of useful information can also be gained from a simple examination of
the placenta. Chorioamnionitis (clouding of the amnion, especially over the placenta)
and amnion nodusum (granularity of the amnion) due to severe oligohydramnios can
be diagnosed by looking at the membranes, especially if the amnion is peeled away
from the chorion and inspected.
Discreet, hard, pale infarcts on the maternal surface indicate poor uteroplacental
blood flow. Retroplacental clots with compression of the placenta are seen in
abruption. An area of extrachorial placenta on the fetal surface (membranes
attached a few cm from the placental edge) commonly causes painless vaginal
bleeding (APH of ‘unknown cause’).
Histology will confirm chorioamnionitis (acute), congenital intrauterine infection
(chronic) or uteroplacental ischaemia.
Chorionicity should always be assessed when like-sex twins with an apparant single
placenta are born. If the vessels of both infants anastomose with one another or
overlap the same territory on the fetal surface of the placenta then the placenta
is monochorionic and the twins are monozygous (identical). To distinguish arteries
from veins it is important to note that the chorionic arteries always cross over the
veins. With dichorionic placentation, a clear border (attachment of the chorion to
the placenta) is seen between the two halves of the placenta as the ‘single’ placenta
actually consists of two separate placentas, which have grown up against one
another. If the sex of the twins is the same, there is still a 30% chance that they are
monozygous even though they do not share the same placenta. Identical twins may
therefore have separate placentas.
Examination of the placenta 25

Multiple births
About 30 per 1000 births are twins and about 1 per 1000 births are triplets. Twin
births may be identical (monozygotic) and arise from a single fertilised egg (zygote)
or non-identical (dizygotic) and arise from two separate eggs. The rate of non-
identical twinning varies from 10 to 40 per 1000 in different communities while that
for identical twins is about 3 per 1000 in all communities. The risk of non-identical
twins increases in women over 35 years and in women receiving infertility treatment
as they both have a higher rate of polyovulation. There is an increased incidence of
dizygotic twins in the female line of some families. Most triplets are non-identical
and induced by fertility treatment.
Non-identical twins always have separate placentas although they may be attached
to each other and therefore falsely appear as a single placenta. These placentas are
called dichorionic as each of the two placentas has its own chorion. There are never
anastomoses between dichorionic placentas so twin-to-twin shunts cannot occur.
In identical twins 70% share a single placenta and therefore a single chorion
(monochorionic placentas). The remaining 30% of identical twins have dichorionic
placentas. The timing of the zygote split determines the type of placentation with an
early split resulting in dichorionic placentas. Therefore the twins must be identical
if the placenta is monochorionic. With dichorionic placentas the twins must be
non-identical if one twin is male and the other female. About 30% of same-sex
twins with dichorionic placentas will be identical. Therefore identical twins can have
separate placentas and DNA testing may be needed to decide if same-sex twins with
dichorionic placentas are identical or not. Clinical examination alone will not reliably
determine the zygosity in these infants.
Chorionicity can be diagnosed by ultrasonology at 12 weeks of gestation when the thick
dividing chorions can be identified in twins with dichorionic placentas. In contrast, there
is no chorion separating the placentas in identical twins. A monochorionic placenta
usually has two amnions (monochorionic-diamniotic). If both twins are in a single
amniotic sac (monochorionic-monoamniotic) have an increased risk of umbilical cord
entanglement and conjoint twinning. Twins with a monochorionic placenta always
have anastomoses and share the same blood pool allowing twin-to-twin transfusions.
Chorionicity is easily determined by examining the placenta after delivery.
26 Multiple births

Multiple pregnancy carries an increased risk of pregnancy complications, such as
miscarriage, pre-eclampsia, iron deficiency anaemia and diabetes while 50% of twins
and 90% of triplets are born preterm. The risk of major congenital abnormalities is
increased to 6% in identical but only 3% in non-identical twins which is the same
risk as singletons. The higher risk in identical twins is not surprising as monozygotic
twinning is an abnormal event due to splitting of a single zygote. Growth restriction
is common in twins due to the increased nutritional demand by two fetuses while
the twin-to-twin transfusion syndrome in monochorionic twins can result in a
larger polycythaemic twin with polyhydramnios (and sometimes heart failure due
to fluid overload) who is the blood recipient and a smaller anaemic twin with
oligohydramnios who is the blood donor. In contrast, with dichorionic placentation
and no possibility of twin-to-twin anastomoses it is the smaller, growth restricted
twin who has polycythaemia due to chronic hypoxia.
While the debate continues as to the safest method of delivery, many twins are
born by Caesarean section. Neonatal mortality and morbidity is higher in multiple
pregnancies, especially monochorionic twins, due to prematurity, growth restriction,
congenital abnormalities and complicated deliveries. Breastfeeding and bonding with
two or more infants can also be a challenge. Therefore all twins should be delivered
in a hospital with facilities for newborn care and their placentas need careful
examination at birth to assess, when possible, if they are identical or not.
Multiple births 27

The healthy newborn infant and minor disorders
Weight
A weight loss of up to 10% of birth weight may occur during the first 3 to 5 days
of life. Birth weight is usually regained by the seventh day. In preterm infants, the
weight loss may be greater (up to 15 %) and take longer to regain. Subsequent
weight gain is usually about 200 g a week (25–30 g/day) for the first three months.
Head and neck
Head circumference
• 33 to 37 cm (average 35 cm) at term.
• Average increase approximately 7 mm/week (range 5 – 10 mm).
Shape
• Caput succedaneum: oedematous thickening of the scalp in the presenting area,
and crosses suture lines. It disappears within a few days.
• Anterior fontanelle: diamond-shaped and variable size, normally slightly concave
and may be seen to pulsate. Normally closes by 18 months.
• Posterior fontanelle: small and triangle shaped. Closes by 4 months
• Moulding: altered head shape in response to pressure, sometimes with overriding
cranial bones.
• Craniotabes (softening of skull bones) is a normal finding in most newborns,
especially in the parietal region, and many infants up to 3 months. Metabolic
bone disease and osteogenesis imperfecta should be considered if it is severe
or prolonged.
Neck
• The newborn infant generally appears to have a short neck. Midline swellings
such as dermoid and thyroglossal cysts are uncommon.
• Sternomastoid ‘tumour’ – a hard lump in the body of the sternomastoid muscle
appearing some days after birth. Caused by trauma or avascular necrosis. It may
cause torticollis which usually improves with physiotherapy. Uncommon.
28 The healthy newborn infant and minor disorders

Eyes
• Examination may be difficult at first because of strong reflex closure. Infant often
opens eyes if held erect.
• ‘Red reflex’ should be present. Pupil should appear black and not grey. Cataracts
and retinoblastoma can cause a white pupil.
• Colour of iris indefinite and not predictable of colour in older infant.
• Sclerae often have a blue tinge in preterm infants because the darker colour of
underlying uveal tissue is transmitted through the underdeveloped sclerae. Darker
blue with osteogenesis imperfecta.
• Tears rare in first few weeks.
• Infants are able to see from birth and should follow a red or bright moving object.
• Subconjunctival haemorrhage: a bright red patch, often adjacent to the cornea
has no serious significance and disappears within a few weeks and may be more
common after traumatic delivery.
• Abnormally large eye/s may indicate congenital glaucoma (early treatment is very
important).
Ears
• Preauricular skin tags and sinuses are common and usually cause no problems.
• Hairy ears are common in the infant of a diabetic mother.
• Low set ears and unusual shapes are common in certain syndromes.
Nose and mouth

• The newborn infant is an obligatory nose breather. Nasal obstruction, congenital
(choanal atresia) or acquired (e.g. nasal secretions), may cause feeding problems
or respiratory distress. Try to pass a nasogastric tube if obstruction is suspected.
• Sucking blisters: thickened areas on the upper lip, usually in the midline.
• Epithelial (Epstein’s) pearls are small whitish inclusion cysts a few mm across,
usually visible in the midline on the hard palate. They are of no significance.
• Ranula. A cystic swelling in the floor of the mouth. Usually disappears
spontaneously.
• Tongue-tie, when the frenulum linguae is inserted into or near the tip of the
tongue, rarely interferes with sucking or future speech.
Teeth
Adventitious teeth may occasionally be present at birth. They are usually loose, do
not interfere with sucking, and fall out spontaneously. Rarely, primary teeth may also
be present at birth. They may pose potential aspiration risk.
The healthy newborn infant and minor disorders 29

Skin
Vernix caseosa
Protective greasy white substance secreted by fetal sebaceous glands. Not present in
preterm infants, and decreases in quantity after term.
Traumatic cyanosis of the face

Due to many small petechial haemorrhages in the skin after congestion of the head
with the cord around the neck.
Superficial skin peeling

Common during the first week. It is especially marked in post-term or wasted infants.
Hair
Colour at birth is poor guide to future shade. Lanugo is fine facial and body hair
which is a feature of preterm infants.
Milia
White pin-head sized papules which are made up of keratin and sebaceous material
in sebaceous glands, causing blockage. These are due to fetal oestrogen, frequently
found on the nose and cheeks and resolve within the first few weeks.
Blue spots (‘Mongolian spot’)

Flat blue-black areas over sacrum or buttocks, and occasionally on back, shoulders,
hands and feet. Usually disappear by 4 years.
Vascular naevi
Salmon patches: pink-red superficial capillary haemangiomata may occur over the
upper eyelids, upper lip, middle of forehead, and on the nape of the neck (stork-bite).
They usually fade by 1 year.
Strawberry naevus
A raised cavernous haemangioma with a surface resembling a strawberry. At birth,
the strawberry-to-be may show as a white (depigmented) patch of skin. Growth is
rapid and it may easily reach 4 cm in diameter. It usually starts to subside by 1 year
and most have disappeared by 7 years of age. Surgical removal is rarely necessary.

Port wine mark (capillary haemangioma or naevus flammeus)
Is a low-flow capillary malformation that can occur anywhere and may be extensive.
It persists for life. If situated over the ophthalmic division of the trigeminal nerve it
may be associated with a meningeal haemangioma (Sturge-Weber syndrome). Large
marks may require laser treatment later.
Erythema toxicum
Very common. Red blotchy rash with yellow central pin-head papules (which may
look like pustules but contain eosinophils) occurring between the second and eighth
days. Seldom seen in preterm infants and never on palms or soles. Cause unknown.
No treatment needed.
Transient neonatal pustular melanosis

A benign condition in a well infant with 3 stages – vesicles, ruptured vesicles and
hyperpigmented macules.
Fat necrosis
Localised areas of induration on back, thighs, or face (after forceps delivery). It has
a dark red appearance and may fluctuate. Resolves spontaneously but needs to be
differentiated from skin abscesses. Can be painful.
Sclerema
Very firm rubbery feel to the skin. Associated with severe infection, hypothermia or
severe hypoxia.
Wasting
Dry, loose skin hangs in folds due to loss of muscle and subcutaneous fat resulting
from recent intrauterine starvation.
Breasts
Breast enlargement is common in both male and female infants, usually lasting a
week or two (but may persist for months). It is due to the effect of fetal oestrogen
and progesterone. No treatment is necessary. Handling must be avoided as this may
cause mastitis.
Supernumerary nipples are common in approximately 1 in 40 newborn infants.

Gastrointestinal tract
Vomiting
Infants normally swallow a variable quantity of air when feeding and commonly
bring up a small amount of milk when winded. Occasional large vomits without
cause may occur. Persistent vomiting however, should be assessed carefully and
investigated, especially if bile is present.
Serious causes of vomiting
• Alimentary tract obstruction due to atresia, meconium ileus, volvulus,
strangulated hernia, inspissated cows’ milk, Hirschsprung’s disease and
necrotising enterocolitis.
• Marked gastro-oesophageal reflux.
• Infection (including urinary tract).
• Cerebral pathology (including intracranial bleed or meningitis).
• Metabolic disorders.
Umbilicus
• Usually has two arteries and one vein. There is a higher incidence of
chromosomal, gastrointestinal or renal abnormalities if there is only one artery.
• Umbilical hernias are common and usually close spontaneously by age 5.
Faeces
• Meconium is passed within 48 hours of birth in the majority of infants. (When
passed in utero it may indicate fetal distress). Obstruction may rarely be caused
by a firm meconium plug, and may be relieved by gently inserting a small
glycerine suppository into the anus.
• Stools replace meconium on day 3 or 4.
• Breast milk stools are usually bright yellow (vary from orange to green), may
vary from watery to pasty, and may contain mucus. Two to five stools are usually
passed each day, but the variation ranges from one stool a week to 12 a day.
• Cow’s milk (formula) stools are pale yellow, firmer and less frequent (up to 5 a
day or one stool every second day).
• ‘Starvation stools’ which occur in under-fed infants are characteristically small
and dark green.
• Blood in stools may be due to swallowed maternal blood (distinguished from fetal
blood by Apt test).
• Loose green stools are common with phototherapy.

Back
• A coccygeal sinus is common and normal.
• A simple sacral midline dimple with a visible intact base and less than 0.5 cm
diameter is usually benign. However, any sacral patch, dimple or sinus may
indicate an underlying occult spina bifida or tethering of the spinal cord.
Renal function
• Newborn infants should pass urine within the first 24 hours. Often at birth.
• Boys should pass urine with a good stream (dribbling suggests posterior
urethral valves).
• Physiological oliguria for first 3 days.
• In the first few weeks, the infant bladder is emptied up to 20 times a day.
• Urates may colour the urine heavily leaving a brick-red stain on the nappy
(sometimes mistaken for blood).
• The newborn kidney is less able to excrete a solute load and has a reduced
concentrating capacity in comparison with the older child.
• Urine collection: most easily done using a collecting bag, but contamination is a
risk. Uncontaminated urine may be obtained by suprapubic bladder puncture or
urethral catheterisation.
Genitalia
• Term male infants usually have testes in the scrotum at birth. The majority of
incompletely descended testes come down within the first month. Those infants
with undescended testes at 6 months should be referred for surgery at one year
of age.
• Preterm infants tend to have incompletely descended testes and a less
well-developed scrotum.
• Inguinal hernia: usually in males, especially if born preterm. Should be repaired to
prevent incarceration.
• Fluid hernia (soft swelling of scrotum which transilluminates easily) is common.
Most disappear spontaneously within the first year.
• Foreskin is normally adherent to the glans penis and cannot be pulled back
without trauma: 90% become fully retractable by the age of 3 years. Pulling
back the foreskin in infancy is therefore not advisable and routine circumcision is
medically unnecessary.
• A mucoid vaginal discharge is present in nearly all mature female infants at birth.
• Vaginal bleeding occasionally occurs at the end of the first week (a fetal hormone
withdrawal effect of no pathological significance).

Fetal growth and size at birth
Weight >4000g 2500g-4000g 1500g-2499g 1000g-1499g <1000g
Description Macrosomic* Normal Birth Low Birth Very Low Extremely
Weight Weight Birth Weight Low Birth
(LBW) (VLBW) Weight
(ELBW)
* The definition of macrosomia is contentious. Some use the I0th centile (aprox 4000g)
others the 97th centile (aprox 4500g). In Africa, maternal and neonatal mortality rises
at a birth weight of 4500g.
Broadly four factors affect birth weight:
1. Genetics: Some infants are constitutionally destined to be larger than others.
2. Gestational Age: Fetuses normally grow with age.
3. Fetal nutrition and placental function.
4. Environmental factors (e.g. alcohol or chronic infections).
Hence it follows that a infant with a low birth weight may be:
1. Constitutionally small.
2. Preterm.
3. Suffering from poor fetal nutrition.
4. Damaged by environmental factors.
Weight for gestational age vs. growth restriction

One can describe the weight with respect to the gestational age in terms of whether
the child is:
• Large (overweight) for Gestational Age (LGA): >90th centile on Intergrowth charts.
• Appropriate for Gestational Age (AGA) (10th to 90th centile).
• Small (underweight)for Gestational Age (SGA) <10th centile.
The term Intra-Uterine Growth Restriction (IUGR) describes a fetus who grows slower
than normal often from early pregnancy. Growth restricted infants, even if they
remain above the 10th centile for weight (i.e. AGA) are at increased risk of mortality
and morbidity.
34 Fetal growth and size at birth

Aetiology of underweight for gestational age
1. Maternal
• Teenager/Advanced Maternal Age.
• Short birth interval.
• Maternal undernutrition.
• Maternal diseases including hypertension, diabetes, cardiac and renal disease,
malaria, TB and advanced HIV.
2. Uterovascular inadequacy
• Abruption.
• Pre-eclampsia.
• Multiple Pregnancy.
3. Environmental
• Cigarettes.
• Alcohol.
• Illicit drugs.
• Licit drugs.
4. Fetal
• Chromosomal abnormalities.
• Genetic diseases.
• Intrauterine infections (TORCH).
• Inborn errors of Metabolism (IEM).
• Twin to twin transfusion.
Symmetrical vs. non-symmetrical underweight for gestational age

Fetuses who have previously been growing well but who suffer a late insult (such as
the mother developing pre-eclampsia), are acutely starved. Similar to older children
with Severe Acute Malnutrition (SAM) these fetuses use up their fat and glycogen
stores, resulting in a wasted (thin) infant with a small abdominal circumference
(because the liver is depleted of fat and glycogen). Hence these newborn infants
appear asymmetrical because their head and length remain the appropriate size
it had achieved when the insult occurred but the body appears relatively smaller
because of the wasting. These children often have good “catch up growth” if fed
appropriately after delivery.
Fetal growth and size at birth 35

Growth restriction which starts early in fetal life causes a growth restriction in all
organs resulting in a small but symmetrical newborn infant. These infants may have
severe concomitant pathology such as chromosomal abnormalities or intra-uterine
infections. They do not have good catch up growth and tend to have the worst long-
term prognoses. Constitutionally small infants have no pathology and good long-
term outcomes.
Complications of being underweight for gestational age

Some of the problems these infants face include:
• Hypoxic Ishaemic Encephalopathy.
• Meconium aspiration.
• Persistent Pulmonary Hypertension of the Newborn.
• Hypothermia.
• Hypoglycaemia.
• NEC
• Polycythaemia and jaundice.
• Cerebral Palsy, IVH and adverse neuro-developmental outcomes.
In I990 a British epidemiologist David Barker reported an association between low
birth weight, fetal nutrition and late onset coronary heart disease. This became
known as the Barker’s hypothesis, or Fetal Origins Hypothesis, which postulates
that being growth restricted as an infant has life long effects. Growth restricted
fetuses have an increased risk of hypertension, diabetes, dyslipidaemia, obesity and
ischaemic heart disease when they reach adulthood.

Weight, and head-circumference-for-gestational-age standards
INTERGROWTH-21st
International Newborn
Size Standards (Boys)
33 34 35 36 37 38 39 40 41 42 43
5.25 5.25
5.00 5.00
4.75 4.75
Birthweight (kg)
4.50 97th
4.50
4.25 90th 4.25
4.00 4.00
3.75 50th 3.75
Birthweight (kg)
3.50 3.50
3.25 10th 3.25
3.00 3rd 3.00
2.75 2.75
2.50
2.25 56
2.00 55
97 th
1.75 54
90th
1.50 53
1.25 52
50 th
Length (cm)
1.00 51
50
10 th
49 49
3rd
48 48
47 47
46 46
Length (cm)
45 45
44 44
43 43
42
41 39
40 38
97th
39 90th 37
Head circumference (cm)
36
50th
35 35
34 10th 34
3rd
33 33
32 32
31 31
30 30
29 29
28 28
27 27
33 34 35 36 37 38 39 40 41 42 43
Gestational age at birth (weeks)
Villar et al. Lancet 2014;384:857-68
Fetal growth and size at birth 37

INTERGROWTH-21st
International Newborn
Size Standards (Girls)
33 34 35 36 37 38 39 40 41 42 43
5.25 5.25
5.00 5.00
4.75 4.75
Birthweight (kg)
4.50 4.50
97 th
4.25 4.25
90th
4.00 4.00
3.75 3.75
Birthweight (kg)
3.50 50th 3.50

3.25 3.25
3.00 10th 3.00
2.75 3rd 2.75
2.50
2.25 56
2.00 55
1.75 54
97th
1.50 53
90 th
1.25 52
Length (cm)
1.00 51
50th
50
49 49
10th
48 48
3 rd
47 47
46 46
Length (cm)
45 45
44 44
43 43
42
41 39
40 38
39 37
97 th
90th 36
35 35
50th
34 34
10th
33 33
3rd
32 32
31 31
30 30
29 29
28 28
27 27
33 34 35 36 37 38 39 40 41 42 43
Gestational age at birth (weeks)
Villar et al. Lancet 2014;384:857-68

Assessment of Gestational Age
Terminology
By convention, gestational age is described in days or weeks after the last menstrual
period. Hence it usually 2 weeks longer than post-conceptual age.
The average duration of gestation is 280 days (40 weeks), although only 4% of
women actually deliver on this day.
Preterm is defined as birth before 37 completed weeks gestation (259 days) i.e. up
until and including 36 weeks and six days.
The World Health Organisation (WHO) categorises preterm birth according into:
• Extreme preterm: <28 weeks.
• Very preterm: 28–32 weeks.
• Moderate to Late preterm: 32– <37 weeks.
• Term: 37–<42 weeks Post term (=post dates): ≥42 weeks.
Prenatal Assessment of Gestational age
Antenatal
Early ultrasound (before fourteen weeks) is accurate within 5–7 days and is the
gold standard for gestational assessment. Ultrasound between I4 and 22 weeks is
accurate within 7–I0 days, but is affected by varying rates of intra-uterine growth
between individuals. Thereafter fetal size is not a good predictor of gestational age.
Other antenatal methods include the date of last normal menstrual period (LMP),
assessment of uterine size before 18 weeks and the measurement of Symphysis-
Fundal Height (SFH) from 18 weeks. These methods can be very unreliable.
Postnatal
Unfortunately no simple, reliable postnatal method for establishing a newborn
infant’s gestational age has been described.
All the current methods have limitations and wide confidence intervals.
Measurements of anthropometry (weight, head circumference, body length and foot
length) are all affected by varying rates of intrauterine growth and weight gain.
Assessment of Gestational Age 39

The regression of the anterior vascular capsule on the lens of the eye is reported
to be reliable between 27 and 34 weeks, but is technically difficult and not useful
outside that age window.
There are many described methods of trying to ascertain infants’ gestational age
through a composite score of external characteristics (e.g. nipple size and skin
texture) and neurological maturity (predominantly tone and posture). One of the
most widely used scores is the “New Ballard Score” However even in experienced
hands the New Ballard Score tends to over-estimate the gestational age in preterm
infants by 1–3 weeks and under-estimate the gestational age in post term infants.
Wasted infants underscore while fat infants overscore.
Prof. Ballard herself explains how to perform the Ballard Score in a series of training
videos available on Youtube.
40 Assessment of Gestational Age

Breastfeeding
Breastfeeding offers many benefits for both the mother and infant. Breast milk
facilitates a safe adaption to the extra uterine environment, provides the ideal
nutrition for growth and development and has immune enhancing properties. Short
term benefits include the reduced risk of gastrointestinal and respiratory infections
and allergy. In the long-term, it improves neurodevelopment and cognitive outcome
while reducing the risk of obesity, diabetes and cardiovascular disease. Breastfeeding
promotes bonding, is cost-saving and reduces the risk of ovarian and breast cancer in
the mother. Breastmilk provides particular benefit for preterm infants as it significantly
reduces the incidence of necrotizing enterocolitis (NEC) and sepsis.
Exclusive breastfeeding for the first six months of life is advised by the World Health
Organization (WHO). Thereafter infants should receive appropriate complementary
foods and continued breastfeeding up to 2 years and beyond should be encouraged.
Antenatal care
To be adequately prepared for breastfeeding, adequate and timely information during
the antenatal period is crucial. Breastfeeding education and support commenced during
pregnancy and continued during the intrapartum and postnatal period has been shown
to increase breastfeeding rates. In preterm infants, prenatal education focusing on
the benefits of breast milk and practical aspects of expressing breast milk has been
associated with longer breast feeding duration.
Breastfeeding immediately after delivery

Putting the infant to the breast as soon as possible after delivery has a profound
effect on successfully establishing and maintaining breastfeeding. Even after a
Caesarean section under spinal anaesthesia most healthy infants can be placed skin-
to-skin on the mother’s chest as soon as they are breathing well. The rooting and
sucking reflexes are particularly strong for the first hour after birth.
When mothers are physically separated from their infants, due to reasons such as
preterm delivery or when mother or infant need admission to the intensive care
unit, it will require special interventions to enable mothers to provide breastmilk
and eventually breastfeed their infants. In these cases, early (within 6 hours) and
frequent stimulation of lactation is associated with higher milk production later on.
Breastfeeding 41

Enable mothers and infants to remain together
The mother and infant must remain together unless there is a justifiable
medical reason.
Rooming-in (keeping mother and infant together 24-hours a day) encourages
mother–infant bonding, parental empowerment, and increases breastfeeding success.
Encourage early, continuous, and prolonged mother–infant skin-to-skin contact
(kangaroo mother care) without unjustified restrictions
Positioning and latching

Correct attachment positioning is vital to achieve adequate seal, sufficient negative
pressure and an adequate sucking mechanism for effective milk transition. It is
important that each mother finds a comfortable position to hold the infant during
feeds. The various positions to try are the cradle hold, cross-cradle hold or underarm
hold (“also known as ‘football’ hold). Ensure that the infant’s head and neck is
supported and that the infant’s whole body is facing the mother’s chest during
breastfeeding.
The mother should support the base of her nipple between second and third fingers
which allows the infant to take hold of the areola and nipple without the breast
obstructing the nose. When the infant’s mouth is wide open in response to the
rooting reflex, place the infant’s mouth over the whole nipple and areola. Do not
allow the infant to suck the nipple only as this rapidly results in a painful, cracked
nipple.
If the infant is correctly latched, the infant’s chin should touch the breast and the
lower lip should turn out. Most of the areola is taken into the mouth
Demand feeding
With demand feeding the infant is allowed to feed whenever hungry or thirsty.
Parents should be taught how to recognize hunger cues. If the milk supply is
adequate, most infants soon adopt a schedule of eight feeds daily. Infants should
be allowed to feed as long and as frequently as they want. Infants tend to feed
frequently for a short period for the first few days. Once the milk supply increases
they feed less frequently but spend a longer time with each feed.
In preterm infants, the ability to feed from the breast will mature with time. While
the infant is transitioning from tube-feeding to breastfeeding, nutritional adequacy
can be assured by providing expressed breast milk with cup or tube. The amount of
42 Breastfeeding

feed provided via cup or tube can gradually be decreased, while feeding from the
breast is established. Before discharge, the infant should be feeding well from the
breast and picking up weight from breastmilk alone.
Weight loss (5–10% of birth weight) is normal. Birth weight is usually regained by
5–7 days. Preterm infants may take longer to regain their birth weight. Exclusively
breastfed infants do not need water or other liquids.
Expressing breast milk

All mothers should learn how to express their milk. Either hand expression or a breast
pump can be used. To avoid infection, a breast pump should never be shared and
mothers should be educated on proper sterilization of breast pumps
Heat treating breast milk with the ‘flash pasteurization’ method is done in some HIV-
positive mothers who want to give their infants safe breast milk.
Donated pasteurised milk is used for infants whose mothers are absent or too
ill to produce milk or in preterm infants while mothers are establishing breast
milk production. Donated breastmilk is a finite resource and should be used with
discretion and in the most vulnerable infants.
Breastfeeding problems
Inadequate lactation
Many mothers stop breastfeeding because they erroneously believe that they have
insufficient or ‘weak’ milk. At each feed, the initial milk, or foremilk, contains little
fat and appears dilute, while the hindmilk at the end of the feed or expression
contains more fat and appears dense and white. Breast milk production is best
enhanced by putting the infant to the breast or express early on (to provide colostrum)
and at regular intervals, as frequently as 2-hourly during the day. The mother should be
educated on recognizing hunger cues and breast feed on demand, encouraged to relax
when feeding and to drink adequate fluids. Enough rest is also important.
Lactation is adequate if the mother’s breasts feel soft after feeds, the infant seems
satisfied after feeds, and gains weight well and passes stools and urine frequently (at
least 6 wet nappies in 24 hours). Make sure the mother is positioning and latching the
infant correctly and emptying one breast before feeding from the other. Successive
feeds should be started on the alternate breast. Test weighing after each feed is
controversial. Rather weigh the infant daily.
The best stimulus to increased milk production is frequent feeding.
Breastfeeding 43

Tender or cracked nipples
Demand feeding and correct positioning and latching are the best ways to prevent
injury to the nipples. Cracked nipples may follow engorgement or incorrect
attachment during feeds.
The nipples can best be treated with a few drops of colostrum after feeds. Do not use
surgical spirits as this dries out the nipple. Treatment consists of resting the nipple by
avoiding suckling on the affected side and expressing the milk at regular intervals for
a day or two. Breastfeeding can be gradually restarted after a few days. Lanolin or
sunlight/laser therapy are also treatment options
Breast engorgement and blocked milk ducts

If the breasts are not emptied regularly they may become very full and uncomfortable,
especially 3 to 5 days after delivery when full milk production occurs. Engorgements
can be prevented with correct positioning, latching and frequent feeds. Management is
aimed at emptying the engorged breasts by encouraging the infant to suck frequently
or by gently massaging and expressing the breast manually or with the help of a breast
pump. A warm shower or warm compresses before feeds reduces the discomfort. Cold
compresses between feeds and a mild analgesic help relieve the discomfort.
A blocked milk duct results in swelling and tenderness of a segment of the breast.
The obstruction can usually be resolved by gentle massaging towards the nipple
while feeding.
Mastitis and breast abscess

With simple engorgement the mother feels well, but with mastitis or abscess she
becomes ill and pyrexial. Usually only one breast is swollen, painful and inflamed.
Mastitis is treated with antibiotics, warm compresses and analgesics. It is usually
not necessary to stop breastfeeding as the inflammation is interlobular at this stage
and the milk is not necessarily infected. A breast abscess presents with a red, tender,
fluctuant mass in the breast. It must be incised and drained and the infant is often
temporarily taken off that breast while expressing regularly. It is safe for the infant
to breastfeed and feeding does not slow down healing.
44 Breastfeeding

Contraindications to breastfeeding
These are rare. Most drugs are excreted in the breast milk but usually not in
pharmacological amounts. Antineoplastic agents and radioactive drugs are
indications for stopping breastfeeding. Drugs such as iodine preparations and
tetracyclines should be avoided. Acute maternal illnesses rarely warrant stopping
breastfeeding. Even if the mother has pulmonary tuberculosis, breastfeeding can
continue if infant is given prophylactic INH. Breastfeeding is contraindicated in the
following inborn errors of metabolism: galactosaemia, phenylketonuria and maple
syrup urine disease.
Breastfeeding in HIV-positive mothers

With the correct use of antiretroviral prophylaxis or treatment the risk of HIV
transmission in breast milk is reduced to almost nil. In poor communities the benefits
of exclusive breastfeeding outweigh the increased risk of HIV infection. Each HIV-
positive woman should be individually counselled so that she can decide whether too
exclusively breastfeed or exclusively formula feed.
Promotion of breastfeeding
The WHO/UNICEF initiative of Baby-Friendly Hospitals promotes breastfeeding
through the ‘Ten Steps to Successful Breastfeeding’ and three additional items:
1. Have a written breastfeeding policy that is routinely communicated to all
healthcare staff.
2. Train all healthcare staff in the skills necessary to implement this policy.
3. Inform all pregnant mothers about the benefits and management of
breastfeeding.
4. Place infants in skin-to-skin contact and help mothers initiate breastfeeding
within an hour of birth.
5. Show mothers how to breastfeed and how to maintain lactation even if they are
separated from their infants.
6. Give newborn infants no food or drink other than breast milk unless medically
indicated.
7. Practise rooming-in to allow mothers and infants to stay together 24 hours a day.
8. Encourage breastfeeding on demand.
9. Give no artificial teats or dummies to breastfeeding infants.
10. Foster the establishment of breastfeeding support groups and refer mothers to
them on discharge from hospital or clinic.
Breastfeeding 45

Additional items
• Compliance with the International Code of Marketing of Breastmilk Substitutes &
Regulations relating to Foodstuffs for Infants and Young Children (SA).
• Mother-friendly care.
• Infant feeding in the context of HIV.
Breastfeeding support groups

Support groups of breastfeeding mothers or women who have successfully breastfed
before in the community are very helpful in assisting women who are breastfeeding
for the first time or having difficulties with breastfeeding. Breastfeeding advisors are
also very useful in clinics and hospitals. Breastfeeding associations play a valuable
role in promoting breastfeeding and helping mothers with problems.
46 Breastfeeding

Replacement feeding
Breastmilk is the first choice of feed and every effort must be made to promote and
support breastfeeding. However, in certain circumstances replacement feeding (or formula
feeding) may be necessary. Parents must be educated about the risks associated with
formula feeding and the family’s ability to safely formula feed should be considered.
The following conditions must be met for safe replacement feeding at home:
• Safe water and sanitation assured.
• Reliably provide sufficient infant formula for 12 months.
• Prepare infant formula freshly and cleanly with every feed.
• Exclusively give infant formula for the first 6 months of a infant’s life.
• Supportive family.
• Access to health care that offers comprehensive child health services.
Commercial milk products

Most formula feeds are based on cow’s milk which has been altered to a greater or
lesser extent to mimic breast milk. No modification of cow’s milk can ever reproduce
the unique properties of breast milk.
These milks are available as powder or ready-to-feed preparations. Consider the
following when deciding on which formula to use:
• Standard term formula are suitable for term or larger preterm infants.
• Preterm formulas for infants under 35 weeks (or less than 2000-2500g).
• Specialised formula i.e. amino-acid based or hydrolyzed formula may be needed
in malabsorption or allergy. Nutrient dense formula can be considered in infants
who are growth faltering.
• Socioeconomic status of the family.
• Local availability of the milk products.
Cow’s milk is not suitable for newborn infants but can be used after 12 months.
Fluid requirements
Most healthy, term infants can be fed ‘on demand’ deciding for themselves what
volume feed is needed. However, these are general guidelines for the first 24 hours:
Day 1 – 60 ml/kg
Day 2 – 75 ml/kg
Day 3 – 96 ml/kg
Day 4 – 132 ml/kg
Day 5 – 150 ml/kg
Replacement feeding 47

Continue at 150ml/kg thereafter for the first month of life.
In preterm infants <1500g, start feeds at 24ml/kg on day 1 of life and increase feeds
by 30-40ml/kg/day. Increase feeds to 150-200ml/kg. The volume of feeds will be
adjusted according to the nutritional content of the feeds (as preterm formulae vary
in calorie and protein content) and the infant’s growth.
Energy requirements
Calculate according to actual body weight. Breast milk and most modified and
partially modified milk contain 67 kcal/100 ml. Special preterm formulas contain 80-
85 kcal/100ml.
Recommended daily requirements:
Preterm: 110–135 kcal/kg/24 hours
Term: 100–115 kcal/kg/24 hours
If the appropriate volume of correctly mixed formula is used, the infant will receive
the required energy intake.
Reconstitution of milk products

Powdered infant formula is not sterile and may contain pathogens. Caregivers should
be informed about the potential risks associated with inappropriate preparation,
handling and use of powdered infant formula as it may result in serious illness.
Various brands have different reconstitution methods (e.g. 25mls water per 1 scoop
of powdered formula), therefore the preparation methods must be checked before
educating caregivers. Caregivers must be encouraged to cup feed their infants
at home, as bottles and teats are difficult to clean and put the infant at risk for
developing diarrhoea.
Frequency
Term infants: demand feed or 3-hourly feeds to start with i.e. 8 feeds a day
Preterm infants: 2 or 3-hourly feeds i.e. 8-12 feeds per day
Infants should be allowed to feed on demand and not be encouraged to “finish every
feed”. However, it is important to ensure nutritional adequacy, especially in preterm
infants transitioning from tube or cup to breastfeeding.
May require nasogastric tube or cup feeds at first, depending on clinical condition
and gestational age (use expressed breast milk).
48 Replacement feeding

Vitamins and iron
All preterm infants, whether breast or formula fed, should be given a multivitamin
supplement. Usually multivitamin drops are started daily when full volume feeds are
reached and then continued to when solids are introduced.
Iron should be given from 1 month in preterm infants to prevent later iron deficiency
anaemia.
Complimentary foods
Introduction of complementary foods is not recommended before 6 months of age
for the general population; however these recommendations are not intended for
special groups such as preterm infants. Individual recommendations must be made
based on the infant’s development (positioning, behavior and oral skills).
Introduce small amounts of iron-rich food, one at a time, starting with cereals, puree
fruits and vegetables. Gradually progress to a full mixed diet.
Assessment of satisfactory feeding

A helpful sign is when the infant is content after a feed coupled with a satisfactory
weight gain (according to the growth chart).
If there is failure to thrive:
• Examine to exclude disease.
• Assess adequacy of milk and energy and protein intake.
• Exclude abnormal losses, infection, acidosis and metabolic disturbances,
congenital or acquired conditions.
Feeding technique
Cup feeding is preferable to bottle feeding as a cup is far easier to clean.
No normal infants should be fed for longer than 20 minutes.
Give advice on cleanliness of cup, bottle and teat, sterilisation, storage of
reconstituted milk, correct temperature.
Warn mothers about common mistakes e.g. making feeds too strong or too weak and
the difference between thirst and hunger.
Replacement feeding 49

Kangaroo mother care (KMC)
The introduction of kangaroo mother care (skin-to-skin care) has brought an
enormous improvement to the management of small infants. With KMC the infant,
wearing only a nappy and woolen cap, is nursed naked against the mother’s bare
chest. The infant is kept upright between her breasts and the mother’s skin keeps
the infant warm. Numerous studies have documented the many advantages of KMC,
including better temperature control, less apnoea, faster growth, better bonding and
breastfeeding, less serious infection and shorter hospital stay. The father and other
family members can also give KMC.
KMC in the delivery room

Most mothers can give their newborn infants skin-to-skin care after delivery. Once
infants have been dried and are breathing well, and the cord has been cut, they should be
moved into the KMC position. Here the mother can meet her new infant while providing
a warm safe environment. KMC after delivery also helps with early breastfeeding.
KMC in the nursery

If the infant is clinically stable, the parents should be encouraged to sit beside the
incubator and provide KMC during visiting times (i.e. intermittent KMC). Colonisation
of the infant with maternal organisms reduces the risk of nosocomial (hospital)
infections. Every effort should be made to feed these infants with breast milk.
Mothers giving KMC often lodge in the hospital to spend as much time as possible
with their infants. Clean hands, breast milk and KMC are the most important and
cost-effective ways of preventing infection in preterm infants. Even the smallest
infants benefit from periods of KMC.
KMC ward
When healthy infants start sucking and are big enough to move out of the incubator,
the mother and infant should be admitted together to a KMC ward. Here mothers
provide KMC day and night under the supervision of the nursing staff (i.e. continuous
KMC). Once the infant is well, breastfeeding and gaining weight, and the mother can
manage her infant, the mother and infant can be discharged from hospital and advised
to continue KMC at home till 2500 g. These infants must be followed up at an infant
clinic to monitor their progress. A KMC ward allows earlier discharge and reduces
hospital costs. Every neonatal nursery should have a lodger and KMC ward nearby.
50 Kangaroo mother care (KMC)

KMC at home
Mothers of small infants should be encouraged to continue KMC after discharge from
the hospital, especially if the home is cold (ambulatory KMC). KMC is particularly
important in winter where the standard of housing is poor. With KMC at home and
frequent visits to the local well-infant clinic, many of the readmissions to hospital of
infants born preterm can be prevented. Many nurseries now discharge KMC infants
home at 1650 to 1750 g. For the first few weeks these mothers often visit the local
clinic each day or two.
KMC during transport

KMC can also be used when small but stable infants need to be kept warm during
transport to hospital or back to the clinic or home. The infant is secured to the
mother’s breasts over the vehicle’s safety belt. With the availability of KMC from any
adult, no newborn infant should ever be allowed to become hypothermic.
KMC is one of the most innovative and exciting recent developments in newborn
care. It is cheap, simple and is becoming widely used in both poor and industrialised
countries. Not only is it good care but it allows the mother to play a far more active
part in the care of her infant. KMC, starting immediately after delivery, is being used
in stable preterm infants where it helps to stabilise breathing and heart rate and
reduces the risk of apnoea. Small infants receiving KMC sleep more, cry less and
grow faster. KMC can also be used for term infants. However, some infants over 2500
g feel hot and uncomfortable receiving KMC.
In many small, rural hospitals with limited facilities and staffing, the neonatal
morbidity and mortality rates of preterm infants have fallen dramatically with the
introduction of KMC.
Kangaroo mother care (KMC) 51

Maternal Substance Abuse
Maternal drug use and abuse can have deleterious effects on the developing fetus.
Alcohol and cigarettes are probably responsible for the most harm.
Fetal Alcohol Syndrome Disorder

The Western Cape has one of the highest levels of Fetal Alcohol Syndrome (FAS) in
the world. FAS describes the most severe spectrum of alcohol teratogenicity with
a combination of growth restriction, dysmorphic facial features (short palpebral
fissures, smooth philtrum, thin upper lip), permanent neurological damage,
(intellectual impairment, behaviour disorders and microcephaly) and birth defects.
There is a spectrum of clinical presentations labelled Fetal Alcohol Spectrum Disorder
(FASD) which encompasses all the abnormalities associated with maternal alcohol
use; from subtle behavioural problems in children with a normal appearance to
severe neurocognitive disability and birth defects.
Tobacco Use
Maternal tobacco use is associated with many antenatal adverse outcomes including
miscarriage, stillbirth, prematurity and fetal growth restriction. There is an increased
risk of Sudden Infant Death Syndrome (SIDS) in infants who were exposed to tobacco
in utero. Maternal tobacco use may be associated with an increased risk of adverse
neurodevelopmental outcomes including learning and behavioural abnormalities.
Pregnancy is a time when women are highly motivated for change and every effort
should be made to educate and motivate pregnant women to give up cigarettes
and alcohol.
Neonatal Abstinence Syndrome (NAS)

Fetuses can become habituated to drugs when in-utero. When the drug is
“withdrawn” after birth they can undergo a withdrawal syndrome that is termed
Neonatal Abstinence Syndrome. This most commonly occurs after chronic opiate
exposure. The opiate may be illicit (e.g. heroin) or legal (e.g. chronic opiate painkillers
or methadone). Other drugs such as tobacco, benzodiazepines, SSRI antidepressants
and amphetamines (tik) may also cause withdrawal symptoms, although these tend
to be less severe than opiate withdrawal.
52 Maternal Substance Abuse

Signs of heroin induced NAS often start within 24 hours. The longer half-life of
methadone can cause later presentations of 24-72h.
The signs include irritability and fussing, poor sleep, feeding difficulties, excessive
(high pitched) crying, sneezing, yawning, scratching and vomiting.
The severity of the withdrawal signs can be graded using a Neonatal Abstinence
Score; infants are often assessed every four hours and interventions decided on their
total score.
Most infants with NAS can be managed with simple non-pharmacological methods
such as minimising stimulation, swaddling, holding the infant and keeping the infant
with the mother. She can reassure, give skin-to-skin care and breast feed the infant.
The amount of opiate passed on through the breast milk is very small and breast
feeding is now encouraged in NAS infants.
Rarely NAS infants may need pharmacological intervention, which can include
opiates such as oral morphine. The dose can be gradually reduced according the level
of the NAS severity score.
In addition to managing the pharmacological withdrawal, it is important to manage
the mother-infant dyad holistically with attention to bonding, breastfeeding, the
mother’s psychological status, the social situation and the wellbeing and safety of
the infant after discharge. A social worker is central to this process.
Maternal Substance Abuse 53

Temperature control
Newborn infants have inefficient temperature regulating mechanisms, which places
them at a high risk of hypothermia or hyperthermia. Infant temperature is routinely
measured on the abdominal skin (normal range 36–36.5 °C) or in the axilla (normal
range of 36.5–37 °C). Oral or rectal temperatures, are rarely used routinely in
newborn infants.
The optimal oxygen consumption and basal metabolic rate occurs when the infant
is normothermic, allowing for the infant’s energy to be used for growing. The
environmental temperature which is needed to maintain this state is variable,
depending on the weight and post-natal age of the infant, and is influenced by
humidity, air currents and clothing.
Most modern closed incubators and open radiant heaters are servo controlled (‘skin
mode’) to keep the skin temperature within the normal range. The telethermometer
probe should not be placed over the liver but on the left side of the abdomen or back.
The infant should not lie on the probe.
When incubators are used without probes (‘air mode’) the incubator temperature is
usually 33-35 degrees with the smaller infants requiring the higher temperatures.
As newborn infants cannot shiver, they use brown fat to generate heat if in a cool
environment. Milk is an important source of energy to produce heat. Preventing
hypothermia is one of the major advances in newborn care.
Hypothermia
This is defined as a temperature below 35 °C and is associated with an increased
morbidity and mortality.
Heat is lost by:
• Conduction: if the infant is laid on a cold surface or wrapped in cold blankets.
• Convection: to surrounding air especially if in a draught or if cold oxygen
administered.
• Evaporation: if the infant is not dried promptly or if the humidity is low.
• Radiation: especially if an ‘open’ incubator is used, when heat is lost to nearby
cold windows and walls.
The commonest cause of hypothermia in hospital is failing to dry the infant well
after birth.
54 Temperature control

The low birth weight infant (preterm or underweight for gestational age) is
particularly prone to hypothermia for the following reasons:
• Larger surface area for the body mass.
• Less subcutaneous tissue white fat resulting in less insulation.
• More evaporative heat loss from thin skin.
• Inadequate brown fat for non-shivering thermogenesis.
• Inadequate milk intake.
• Prone to hypoxia, hypoglycaemia and sepsis, all of which disturbs the
thermoregulatory mechanism which predisposes to hypothermia.
Hypothermia in a newborn infant may result in:
• Hypoglycaemia.
• Respiratory distress.
• Increased O2 consumption.
• Hypoxia and resultant metabolic acidosis.
• Increased energy requirement.
• Poor weight gain.
• Bleeding due to DIC.
• Neonatal cold injury.
• Neonatal death.
Failure to gain weight normally in an otherwise well LBW infant, who has a normal
temperature, may be the only indication that the infant is suffering a cold stress.
Excess energy is being used up to maintain a normal body temperature.
Management
Recognition
Use a digital or ‘low-reading’ mercury thermometer or telethermometer.
A severely cold infant can look pink and surprisingly healthy.
Prevention
At delivery:
• The theatre or delivery room should be maintained at an ambient temperature of
25 °C and be free of draughts.
• Immediately after birth, the infant should be dried and then wrapped in a second
warm dry towel and given to the mother for KMC or place in a warm cot or
incubator. The head should be dried well.
Temperature control 55

• If resuscitation or a procedure is required this should be done on a suitably
warmed surface with an overhead radiant heater switched on.
• Infants <1200g should be placed in a plastic polyethylene bag to minimise
evaporative heat loss during the initial resuscitation after birth, exposing only the
face. A woolen cap can be used to prevent heat loss from the head.
Postnatally:
• Small infants i.e. below 1800 g, should be nursed in an incubator and abdominal
skin temperature kept at 36.5 °C. Many of these infants can be kept warm with
KMC (skin-to-skin care).
• Perspex heat shields may be used in closed single-walled incubators to lessen
radiant heat loss.
• Use woolen caps in all low birth weight infants even if nursed in a closed
incubator. Dress infants when possible.
• Close curtains in the newborn nursery at night.
Treatment
Increase incubator temperature further or add overhead radiant heat source.
Increase room temperature if cold.
Use a perspex heat shield and put on a warm woolen cap to minimise radiant heat
loss from the scalp if not already in use.
Monitor and treat hypoglycaemia if present.
Give extra calories and oxygen while warming the infant. Feeding should be
continued to provide calories. If this is not possible a glucose infusion should be
commenced
Look for and treat any predisposing cause. Every hypothermic newborn should be
assessed for infection.
Neonatal cold injury

This refers to the unusual event of severe hypothermia. Risk factors include birth
during winter, home delivery and low birth weight
Clinical features include apathy and poor feeding. The cry is feeble and the infant is
lethargic with depressed reflexes, bradycardia and oliguria. The skin feels cold to the
touch and the skin temperature is usually below 32 °C (May drop as low as 27 °C).
Always use a low-reading digital thermometer or telethermometer in infants.
56 Temperature control

The mortality is high (25–35%) mainly due to:
• Hypoglycaemia (risk during re-warming).
• Hypoxia and metabolic acidosis.
• Pulmonary haemorrhage as a result of DIC.
Treatment
• Rapid re-warming in an incubator, preferably using a servo- controlled overhead
radiant heater. In emergencies KMC can be used to rewarm cold infants.
• Intravenous 10% dextrose water to prevent hypoglycaemia.
• Antibiotics in view of high risk of infection.
• Oxygen therapy may be necessary during re-warming.
Fever
• Fever (pyrexia) is defined as an axillary temperature > 37 °C. It is usually due to
overheating:
• Incubator or room temperature too high.
• Lying in direct sunlight, or phototherapy.
Over-dressing the infant or using too many blankets.
Once these errors have been corrected, the temperature should return to normal
within 1 hour.
Fever may also be due to dehydration. This is usually a term infant who has fed
poorly and lost more than 10% of his/her birth weight. The fever settles when extra
fluid is given.
Infection in a newborn infant usually results in hypothermia rather than fever
although it should always be considered, especially in term infants.
If untreated, severe pyrexia may lead to brain damage with hypothalamic injury.
Temperature control 57

Hypoglycaemia
Background
Following birth, transient low blood glucose concentrations may be a normal
phenomenon, as the source of glucose delivery transitions from a continuous
supply from the mother to an intermittent supply from milk feeds. In healthy term
infants, plasma glucose concentrations fall within the first two hours, reaching a
nadir at 2.2 mmol/l and then stabilising in the range of 2.5 – 4mmol/l by 4 to 6
hours. It is important to differentiate this normal physiological transitional process
from disorders that result in persistent and prolonged hypoglycaemia, which if left
untreated may lead to neurological and developmental sequelae. Hypoglycaemia
occurs when the rate of glucose utilization exceeds that of glucose production.
Definition
Hypoglycaemia
a. Whole blood glucose concentration < 2.6mmol/l
Severe hypoglycaemia
a. Whole blood glucose concentration < 1.5mmol/l
b. Any symptomatic hypoglycaemic newborn infant (seizures, apnoeas etc.) is
considered to have severe hypoglycaemia
Measuring blood glucose concentrations

Blood glucometers with reagent strips are used to measure whole blood glucose
concentrations (heel/finger prick). Laboratory blood glucose tests are a measure
of serum glucose concentrations (venous/arterial sampling of blood). Any severe
hypoglycaemia on whole blood measurement should be confirmed with a laboratory
sample. In the interim abnormal results should be acted on. Whole blood glucose
concentrations are approximately 15% lower than serum glucose concentrations and
may be further reduced in the face of an elevated haematocrit.
58 Hypoglycaemia

Aetiology
A. INADEQUATE GLUCOSE
SUPPLY
a. Inadequate intake i. Infant factors: poor suck/cleft palate/anatomical
abnormalities
ii. Maternal factors: poor milk supply
b. Inadequate glycogen i. Prematurity
stores ii. Low birth weight
c. Impaired glucose i. Inborn errors of metabolism (disorders of
production gluconeogenesis and glycogenolysis)
ii. Endocrine disorders (disorders of cortisol
and growth hormone e.g. congenital adrenal
hypoplasia and hypopituitarism)
iii. Other: maternal treatment with beta-
sympathomimetic agents/hypothermia/severe
hepatic dysfunction
B. INCREASED GLUCOSE
UTILIZATION
a. Hyperinsulinism i. Infant of diabetic mother
(may be transient or ii. Intrauterine growth restriction
persistent) iii. Perinatal hypoxia
iv. Persistent hyperinsulinemic hypoglycemia of infancy
v. Beckwith-Wiedemann syndrome
vi. Abrupt interruption of an infusion of a solution
with a high glucose concentration
vii. Polycythemia.
a. Without hyperinsulinism i. Sepsis
(situations of increased ii. Cardiac failure
metabolic demand) iii. Perinatal hypoxia
iv. Respiratory distress
v. Hypothermia
Clinical presentation
It is important to note that neonatal hypoglycaemia is frequently asymptomatic; in
these cases hypoglycaemia may be detected on routine screening of “at risk” infants
or as an incidental finding. It is important to identify situations of risk primarily for
screening purposes, in order to detect hypoglycaemia and institute treatment in a
timeous fashion so as to avoid adverse neurological outcomes. Normal term infants
in the postnatal wards do not require screening for hypoglycaemia.
Hypoglycaemia 59

“AT RISK” SCENARIOS
Prematurity
Small for gestational age (< 10th centile)
Intrauterine growth restriction or wasting
Infant of diabetic mother
Large for gestational age (> 90th centile)
Post-term particularly if wasted
Infants who have experienced perinatal and postnatal stress due to: perinatal
hypoxia/ meconium aspiration syndrome/severe Rhesus disease/polycythemia/
hypothermia/ fluid restriction
Symptomatic newborn infants have non-specific signs, which reflect nervous system
responses to glucose deprivation.
NEUROGENIC SIGNS NEUROGLYCOPENIC SIGNS
Jitteriness Poor suck or poor feeding
Irritability Weak or high-pitched cry
Tachypnea Change in level of consciousness (lethargy, coma)
Pallor Seizures
Sweating Hypotonia
Treatment
The goals of managing neonatal hypoglycemia are to:
i. Identify and prevent symptomatic hypoglycemia in at-risk infants.
ii. Correct blood glucose levels in symptomatic infants.
iii. Identify infants with a serious underlying hypoglycemic disorder, while avoiding
unnecessary treatment of infants with normal transitional low blood glucose,
which will resolve without intervention.
iv. The long-term goal is to prevent long-term neurologic complications.
Prevention
i. Identify infants at risk of hypoglycaemia.
ii. Depending on gestational age, institute feeds and fluids immediately within first
hour of birth.
iii. Place healthy term infants onto the breast.
iv. In cases of preterm or unwell newborn infants, tube feed if necessary.
v. Start intravenous fluids containing 10% glucose if full volume milk feeds are
contraindicated (prematurity).
60 Hypoglycaemia

vi. Monitor blood glucose levels every 1–3 hours for the first 24–48 hours in infants
at risk of hypoglycaemia.
vii. Avoid hypothermia.
Management of hypoglycaemia (1.5-2.6mmol/l)

i. Give a milk feed immediately or start intravenous fluids if milk feeds are
contraindicated.
ii. Keep infant warm.
iii. If blood glucose still below normal to consider increasing either volume or
frequency of feeds.
iv. If blood glucose persistently below normal to treat as per emergency treatment
of hypoglycaemia.
Emergency treatment of severe hypoglycaemia

Severe neonatal hypoglycaemia is an emergency when blood glucose concentrations
are < 1.5mmol/l and in any severely symptomatic newborn infant particularly
those who are having seizures. Severe hypoglycaemia is a well-known risk factor
for neuronal cell death and adverse neurodevelopmental outcome and must be
addressed immediately.
i. Admit to neonatal unit.
ii. Establish intravenous access and bolus 3ml/kg 10% glucose. If unable to establish
intravenous access, insert an umbilical venous catheter.
iii. If unable to obtain venous access, glucagon at 0.2mg/kg/dose intramuscularly
may be given.
iv. Start an intravenous infusion of 10% glucose at 60-90mls/kg/24 hours depending
on gestational age and day of life.
v. If hypoglycaemia persists options include increasing feed and fluid volumes or
increasing glucose concentration delivered. Never give 50% glucose intravenously
or orally due to its hypertonicity.
vi. Monitor blood glucose regularly with reagent strips.
vii. Start milk feeds as soon as it is safe to do so and gradually build up feeds while
decreasing intravenous fluids as blood glucose improves.
viii. Do not stop intravenous glucose until milk feeds are well established.
ix. It is important to consider sepsis in unwell newborn infants with persistent
hypoglycaemia. Other differential diagnoses include metabolic or endocrine
causes and one should investigate accordingly as guided by clinical and
laboratory parameters.
x. Any newborn infant with severe hypoglycaemia regardless of aetiology needs to
be followed up long term to assess neurodevelopmental outcome.
Hypoglycaemia 61

Infant of a diabetic mother (IDM)
Background
Diabetes in pregnancy is associated with an increased risk of fetal, neonatal, and
long-term complications in the offspring. In the first trimester and at time of
conception, maternal hyperglycemia may cause diabetic embryopathy resulting in
major birth defects and spontaneous abortions. The risk of congenital anomalies
increases with higher maternal HbA1c levels. This primarily occurs in pregnancies
with pregestational diabetes. Diabetic fetopathy occurs in the second and third
trimesters, resulting in fetal hyperglycemia, hyperinsulinemia, and macrosomia.
Neonatal effects
IDMs are at increased risk for mortality and morbidity compared to newborn infants
born to a non-diabetic mother, which includes:
i. Congenital anomalies.
ii. Prematurity.
iii. Perinatal hypoxia.
iv. Macrosomia, which increases the risk of birth injury (e.g. brachial plexus injury)
v. Respiratory distress.
vi. Metabolic complications including hypoglycemia, hypocalcemia and
hypomagnesimia.
vii. Hematologic complications including polycythemia and hyperviscosity.
viii. Low iron stores.
62 Infant of a diabetic mother (IDM)

Clinical features
SYSTEM SIGN PATHOPHYSIOLOGY
General Macrosomia Excess subcutaneous fat especially
examination Hirsutism over face and shoulders. Their
bodies are usually larger than their
heads. Consequence of maternal
hyperglycaemia leading to fetal
hyperglycemia, pancreatic islet cell
hyperplasia and increased insulin
levels (anabolic hormone).
Plethora Polycythemia occurs as a result
of increased fetal erythropoietin
concentration caused by chronic fetal
hypoxemia.
Jaundice Jaundice is associated with
polycythaemia, prematurity and
bruising
Respiratory Respiratory distress May be related to TTN or more
system commonly HMD. TTN may be as result
of reduced fluid clearance in the
diabetic fetal lung.
Reason for HMD is two fold – IDMs
are more likely to be delivered
prematurely than infants born to
non-diabetic mothers and neonatal
hyperinsulinism delays surfactant
production.
Central Examine for signs of In light of macrosomia, IDMs are
nervous encephalopathy with altered prone to shoulder dystocia and
system primitive reflexes. difficulty deliveries, which may be
Examine all limbs assessing associated with intrapartum hypoxia.
for reduced upper limb/hand Similarly they are at risk for brachial
movement. plexus injuries/clavicle fractures
Assess for abnormal during the birthing process.
movements/jitteriness (may be
an indicator of symptomatic
hypoglycaemia)
* Additional clinical findings are dependent on whether underlying congenital
anomalies are found.
Infant of a diabetic mother (IDM) 63

Congenital anomalies
SYSTEM ABNORMALITY
Cardiovascular system i. Cyanotic and acyanotic congenital cardiac lesions
(2/3 of anomalies in IDMs (VSD, PDA, TGA, Truncus arteriosus, Tricuspid
involve the cardiovascular atresia)
system and central nervous ii. Hypertrophic obstructive cardiomyopathy
system) (may be reversible in first 6–12 months)
Central nervous system i. Neural tube defects
ii. Anencephaly
iii. Holoprosencephaly
Gastrointestinal system i. Small left colon syndrome
ii. Duodenal atresia
iii. Imperforate anus
Skeletal system i. Caudal regression syndrome (sacral agenesis)
ii. Hemi-vertebrae
Urinary system i. Hydronephrosis
ii. Renal agenesis
iii. Ureteral duplication
Prevention
Because the critical period for teratogenesis is within the first 3-6 weeks after
conception, normal glycemic control must be instituted before pregnancy to prevent
birth defects. A target HbA1c of 6 to 6.5% is recommended in early pregnancy as
these levels in early gestation are associated with the lowest rates of adverse fetal
outcomes. Primary prevention is key and mothers need to plan for their pregnancies
and book early with early first trimester ultrasound scanning to assess for congenital
abnormalities.
Management
i. Thorough clinical examination to assess for congenital abnormalities.
ii. Monitor for complications particularly hypoglycaemia
iii. Prevent hypoglycaemia by immediate institution of milk feeds and one may need
to consider instituting intravenous fluids.
iv. In cases of persistent hyperinsulinism associated with hypoglycaemia one may
need to add hydrochlorothiazide and diazoxide in order to block insulin release
and maintain euglycaemia.
64 Infant of a diabetic mother (IDM)

Jaundice
Jaundice is a clinical sign of yellow discolouration of the skin and sclera. In adults
examining the sclera is the easiest way of detecting jaundice. Because of the difficulty
of seeing the sclera in the newborn, it is easier to detect jaundice in the skin. Clinical
jaundice only becomes evident when bilirubin levels are about 75 µmol; it is made
more difficult if the infant is dark-skinned. Press gently on the tip of the infant’s nose
and then examine the colour of the skin immediately upon releasing the pressure.
Jaundice in the newborn is extremely common: 60% of term infants, and 80% of
pre-term infants have visible clinical jaundice in the first week of life, and up to 10%
of breastfed infants at 1 month of age. It is essential to understand the underlying
physiology, recognize when jaundice may be pathological, and know how to investigate
and treat.
1. Bilirubin metabolism in the fetus and newborn

Red blood cells are removed from the circulation in the reticulo-endothelial
system (mainly spleen). Haemoglobin is broken down to haem and globin. Globin
is metabolized into amino acids; haem is metabolized into biliverdin, and then
to bilirubin. (Bilirubin is also formed during the breakdown of myoglobin and
cytochromes). In the plasma, unconjugated bilirubin is bound to albumin.
In the fetus most unconjugated bilirubin is rapidly removed by the placenta.
However, about 10% is still conjugated in the fetal liver and excreted into the gut,
where it is deconjugated by the enzyme beta glucuronidase and then reabsorbed
via the enterohepatic circulation. Thus most fetal bilirubin is maintained in the
unconjugated state to facilitate excretion across the placenta. In the newborn infant,
after separation from the placenta, progressively more bilirubin is taken up by the
liver and conjugated with glucuronic acid by the enzyme glucuronyl transferase.
Conjugated bilirubin is water-soluble and is not toxic to brain tissue. It is excreted
through the bile duct system into the duodenum. Most of the conjugated bilirubin
in the gut is broken down to stercobilin by bacteria, to be excreted in the stool; but
some is de-conjugated (back into unconjugated bilirubin) and reabsorbed, as the
enterohepatic circulation of bilirubin remains for a few weeks after delivery. The
intestinal enzyme beta glucuronidase, which is responsible for this enterohepatic
circulation, is also present in breast milk. Neonatal jaundice is therefore more
common in breastfed than formula-fed infants. If there is obstruction to the biliary
tree, conjugated bilirubin enters the plasma and may be excreted in the urine.
Jaundice 65

Bilirubin is an oxygen free radical scavenger. Mild jaundice may reduce the risk of
damage by free radicals generated during labour.
2. Physiological jaundice
All normal newborn infants have increased amounts of unconjugated bilirubin in
their blood, and more than half develop visible jaundice. In most infants this jaundice
is normal or ‘physiological’ and typically presents on the second or third day, peaks by
day 3 or 4 and has disappeared within 7 days. The total serum bilirubin (TSB) usually
does not usually exceed 200 µmol/l in formula-fed infants, although in some healthy
breastfed infants it might reach as high as 275 µmol/l. The diagnosis of physiological
jaundice is made by excluding pathological causes of jaundice in infants who are
active, feed well and show no sign of illness. Physiological jaundice never appears
within the first 24 hours of life and seldom lasts beyond 7 days. Physiological
jaundice does not need treatment other than reassuring the mother, encouraging
frequent feeds and monitoring the infant for abnormal signs.
Physiological jaundice is due to a combination of:
• The high haematocrit and shorter red cell survival time, which results in a high
bilirubin production.
• Slow hepatic conjugation (immature glucuronyl transferase enzyme).
• The enterohepatic circulation of bilirubin (beta glucuronidase in the intestinal
brush border).
Preterm and breastfed infants are especially likely to develop clinical jaundice.
Preterm infants have an immature liver with a limited ability to conjugate
bilirubin in the first weeks of life. Similarly, some term infants develop ‘idiopathic
hyperbilirubinaemia’ as they also have a slow rate of conjugation. Breastfed infants
may also develop prolonged unconjugated hyperbilirubinaemia with jaundice that
lasts several weeks and is referred to as ‘breast milk jaundice’. It is probably the
result of increased enterohepatic circulation of bilirubin, due to the presence of beta
glucuronidase in breast milk.
3. Bilirubin encephalopathy
Conjugated bilirubin is not toxic, and unconjugated bilirubin which is bound to
albumin crosses the blood brain barrier less readily. However, free unconjugated
bilirubin (not bound to albumin) penetrates cells as it is fat-soluble, and inhibits
mitochondrial activity. The cells of the basal ganglia, mid-brain and brain-stem are
particularly susceptible; damage may be fatal or may cause severe brain damage. An
intact blood-brain barrier reduces the risk of bilirubin encephalopathy. “Kernicterus”
66 Jaundice

is the autopsy description of brain tissue stained with bilirubin pigment; it should not
be used to describe neurological signs (encephalopathy) in live infants.
Risk of bilirubin encephalopathy is increased by:
• Very high levels of serum unconjugated bilirubin e.g. severe haemolysis.
• Low serum albumin (as present in preterm or septic infants).
• Very early jaundice (first two days of life).
• Competition for binding sites by drugs e.g. salicylates, sulphonamides, and by
non-esterified fatty acids (NEFA - increased by hypothermia).
• ‘Opening’ of the blood-brain barrier in sick infants with hypoxia, acidosis and
infection.
Clinical presentation of bilirubin encephalopathy:
• Severe jaundice, especially if jaundice becomes visible in hands and feet.
• Lethargy, with poor feeding and a depressed Moro reflex.
• High-pitched cry with increased tone.
• Tendency to retract head, progressing to opisthotonus and convulsions.
• Deconjugate eye movements with ‘setting sun’ appearance.
• Death.
Survivors may develop late signs of hypotonic or athetoid cerebral palsy, deafness,
stained teeth and some degree of intellectual disability.
4. Classification of jaundice
a) Non-pathological
Physiological jaundice and jaundice in breastfeeding infants. Mild, transient jaundice
in clinically well infants; never requires phototherapy.
b) Pathological
Jaundice can be considered pathological if it is:
1. Too early: jaundice in 1st 24 hours of life is always pathological.
2. Too late: prolonged jaundice (more than day 14 in a term infant, day 21
in pre-term).
3. Too high: any level above the “phototherapy line”.
4. Conjugated:
Causes of pathological jaundice
a) Unconjugated jaundice:
a. Excessive haemolysis.
Jaundice 67

1. Antibody mediated (blood group incompatibility): Rhesus disease, ABO
incompatibility, minor antigens).
2. Infection, sepsis.
3. Haemoglobinopathy (thalassaemia).
4. RBC enzyme deficiency (glucose 6 phosphatase deficiency, pyruvate kinase
deficiency).
5. RBC membrane defects (spherocytosis, ovalocytosis).
b. Excessive entero-hepatic circulation: breastfeeding jaundice.
c. Polycythaemia.
d. Defective conjugation (pre-term, infant of diabetic mother, hypothyroidism;
Gilbert syndrome, Crigler-Najjar).
e. Haematomas or haemorrhage (e.g. cephalohaematoma, bruising (traumatic
delivery, breech delivery); Internal haemorrhage (rare).
b) Conjugated jaundice:
a. Congenital infections with hepatitis: viral (herpes, CMV, rubella), spirochaetal
(syphilis), protozoal (toxoplasmosis).
b. Total parenteral nutrition.
c. Septicaemia, urinary tract infection.
d. Obstruction: Usually late onset. Choledochal cyst, biliary atresia.
e. Metabolic: Cystic fibrosis, galactosaemia (very rare), other inborn errors of
metabolism.
5. Measurement of jaundice and bilirubin

Jaundice can be screened for with a transcutaneous bilirubinometer (TCB). Local
protocols differ; some neonatal units will start phototherapy based on a TCB
value, others require confirmation with total serum bilirubin (TSB) before starting
phototherapy. Many blood gas machines can give a bilirubin value within minutes;
these are useful for clinical decision making, but do not have the medico-legal status
of a validated TSB from an accredited laboratory. A very high TCB reading should be
confirmed with a TSB.
6. Investigation
Not needed if the infant is asymptomatic, mildly jaundiced and feeding well.
If jaundice appears in the first 24 hours or is prolonged, or if the bilirubin level
approaches the exchange transfusion level, investigations should be done to exclude
haemolytic disease or infection. (Blood group, Coombs, haemoglobin, CRP). The level
of conjugated bilirubin and liver function tests are only done if obstructive jaundice
is suspected.
68 Jaundice

7. Treatment
Most infants have physiological jaundice which does not require treatment. Early feeding
lessens enterohepatic circulation of bilirubin and need for phototherapy. Most forms of
unconjugated hyperbilirubinaemia respond to phototherapy; exchange blood transfusion
is rarely required. Treatment of obstructive or conjugated jaundice requires treatment of
the underlying condition (surgery for biliary atresia, penicillin for congenital syphilis, etc).
A) Phototherapy
Unconjugated bilirubin in the skin is isomerised by visible light (NOT ultraviolet light) at
the blue end of the spectrum (420–460 nm) to a water-soluble non-toxic isomer known
as ‘lumirubin’ which is excreted in the stools and urine. Phototherapy reduces the risk
of kernicterus and minimises the need for exchange transfusions. Eyes must be properly
covered to prevent retinal damage; eye pads may be removed during feeds. Temperature
must be checked regularly to prevent over-heating or, less commonly, hypothermia.
Monitor response to phototherapy with TSB or blood gas machine bilirubin at least daily,
or more frequently if severe. Once phototherapy has been started, clinical jaundice of
the skin and TCB do not correlate with serum bilirubin due to the removal of bilirubin
from the skin, so monitoring must be done with blood tests, not assessment of cutaneous
bilirubin. If possible, phototherapy should be given beside the mother in the postnatal
ward and she should be encouraged to continue breastfeeding frequently. Phototherapy
lights have a limited lifespan: fluorescent and radiant lights may still emit visible light,
but stop emitting useful wavelength radiation after about 800 hours. LED lights last
longer; all lights should be assessed in accordance with manufacturer’s guidelines.
Phototherapy chart
A phototherapy chart is a guide to the use of phototherapy at different ages after
birth. Either the infant’s weight or preferably the gestational age can be used.
Phototherapy should be started when the appropriate line is crossed. If risk factors
for encephalopathy are present, use one line lower. Phototherapy may be stopped
when the TSB is more than 50 µmol/l below the line for that infant. Many infants
experience “rebound” jaundice after stopping phototherapy: must check bilirubin
level again 24-48 hours after stopping phototherapy.
b) Exchange blood transfusion

An exchange blood transfusion removes much of the infant’s blood and replaces it with
stable adult whole blood. This is usually done through an umbilical vein catheter or an
arterial line. Exchanging the infant’s blood helps remove bilirubin, corrects anaemia and
removes anti-red cell antibodies. It is only performed when there is high risk of bilirubin
encephalopathy. An exchange transfusion chart indicates when exchange is indicated.
Jaundice 69

As with the phototherapy chart, the next lower line should be used when additional
risk factors for bilirubin encephalopathy are present (haemolysis, sepsis, acidosis and
asphyxia). If required, usually perform a “double volume” exchange (replace twice the
infant’s circulating blood volume of 80 ml/kg over 4 hours). Risks include hypothermia,
hypoglycaemia, sepsis, and usual risks of blood transfusion (incompatibility reaction
and infection). This is considered a high-risk intervention: should only be performed in
a centre with expertise in this procedure.
PHOTOTHERAPY
WESTERN CAPE 2006 CONSENSUS GUIDELINES
In presence of risk factors use one line lower (the gestation below) until < 1 000 g
If gestational age is accurate, rather use gestational age (weeks) instead of body weight
Infants > 12 hours old with TSB level below threshold, repeat TSB levels as follows:
1–20 μmol/ℓ below line: repeat TSB in 6 hrs or start phototherapy and repeat TSB in 12–24 hrs
21–50 μmol/ℓ below line; repeat TSB in 12–24 hrs
> 50 μmol/ℓ below line: repeat TSB until it is falling and/or until jaundice is clinically resolving
Infants under phototherapy:
Check the TSB 12–24 hourly but if TSB > 30 μmol/ℓ above the line, check TSB 4–6 hourly.
STOP phototherapy:
If TSB > 50 μmol/ℓ below the line. Recheck TSB in 12–24 hrs.
340
320
300
280
260
Micromol/ℓ TSB (total serum bilirubin)
240
220
200
180
160
140
120
100 38+ wks or 3 000+ g
35–37 w6d or 2 500–2 999 g
80 34–34 w6d or 2 000–2 499 g
60 32–33 w6d or 1 500–1 999 g
30–31 w6d or 1 250–1 499 g
40
28–29 w6d or 1 000–1 249 g
20 < 28 w or < 1 000 g
0
6 h 12 h 24 h 36 h 48 h 60 h 72 h 84 h 96 h 108 h 120 h
Time (age of baby in hours)
Start intensive phototherapy when the TSB is ≥ the line according to gestation or weight
70 Jaundice

EXCHANGE TRANSFUSION
WESTERN CAPE 2006 CONSENSUS GUIDELINES
In presence of sepsis, haemolysis, acidosis, or asphyxia,
use one line lower (gestation below) until < 1 000 g
If gestational age is accurate, rather use gestational age (weeks) instead of body weight
Note: 1 Infants who present with TSB above threshold should have exchange done if the
TSB is not expected to be below the threshold after 6 hrs of intensive phototherapy
2 Immediate exchange is recommended if signs of bilirubin encephalopathy and
usually also if TSB is > 85 μmol/ℓ above threshold at presentation
3 Exchange if phototherapy continues to rise > 17 μmol/ℓ/hr with intensive
phototherapy
450
38+ wks or 3 000+ g
440
35–37 w6d or 2 500–2 999 g
430
420 34–34 w6d or 2 000–2 499 g
410 32–33 w6d or 1 500–1 999 g
400 30–31 w6d or 1 250–1 499 g
390 28–29 w6d or 1 000–1 249 g
380 < 28 w or < 1 000 g
Micromol/ℓ TSB (total serum bilirubin)
370
360
350
340
330
320
310
300
290
280
270
260
250
240
230
220
210
200
190
180
6h 12 h 24 h 36 h 48 h 60 h 72 h 84 h 96 h 108 h 120 h
Time (age of baby in hours)
8. Notes on specific causes of jaundice

1 Antibody-mediated haemolysis: ABO and Rh disease
2 Breastfeeding jaundice
3 Infection
4 Prolonged jaundice
5 Late onset jaundice
Jaundice 71

1. Antibody-mediated haemolysis
Haemolytic disease of the newborn most commonly arises with incompatibilities
between the mother and fetus in either the Rhesus or ABO blood groups. Less
commonly, other blood group incompatibility may be present such as Kell, Duffy and
Kidd.
A) Haemolytic disease due to ABO incompatibility
This is now the most common cause of haemolytic disease in the newborn. The
mother is group O and the infant group A or B. All group O mothers have both anti-A
and anti-B antibodies which result from exposure to A and B antigens on bacteria in
their gut. Normally these are IgM antibodies and do not cross the placenta. However,
some group O mothers also produce IgG type anti-A or B antibodies which are able
to cross the placenta and destroy fetal group A or B red cells. Since these antibodies
arise independently of pregnancy, even firstborn infants may be affected. Unlike
Rh disease, the disease process is milder and rarely causes hydrops fetalis (in utero
haemolysis, anaemia and cardiac failure).
ABO jaundice usually presents with early onset jaundice in the first 24 hours. The
haemoglobin is often in the low normal range and the direct Coombs test is positive
in about 30% of cases. The reticulocyte count is elevated and spherocytes are seen
on a peripheral blood smear. The TSB at 6 hours is usually above 80 µmol/l. Although
exchange transfusion may be necessary, in most cases phototherapy prevents
bilirubin rising to dangerous levels. Intravenous gamma globulin may be useful in
delaying haemolysis. If the mother’s blood group is known to be group O, infant
should have TSB measured at 6 hours after delivery, or before discharge from the
birth unit. If the mother’s blood group is not known, infants should have a clinical
examination 6-12 hours after delivery; if clinically jaundiced, should then have
bilirubin measured. Low grade haemolysis can occur for up to 2 weeks; late anaemia
is common, but usually self-limited, and requirement for blood transfusion is
very rare.
72 Jaundice

B) Haemolytic disease due to Rh incompatibility
Rhesus haemolytic disease occurs after an Rh-negative mother (D negative) has been
exposed to Rh-positive (D positive) red blood cells; her immune system is “sensitised”
to the Rh antigen, and starts to produce anti-Rh antibodies. The father of the fetus is
always Rh positive; fetal red cells may cross the placenta during labour and delivery
or at other times during pregnancy when the placenta is damaged. In a subsequent
pregnancy, maternal anti-D IgG antibodies pass across the placenta and, if the fetus
is Rh-positive, cause haemolytic disease. Anti-D antibodies may form in response to
a previous incompatible transfusion of Rh-positive blood, or by early pregnancy feto-
maternal blood mixing; thus, it is possible to get Rhesus disease in a first pregnancy,
but this is very rare. Other Rhesus blood groups (C, c, E and e) may cause less severe
haemolytic disease.
Group D incompatibility may present as:
1. Hydrops fetalis: severe anaemia causing heart failure; fetus is usually stillborn
with gross oedema, ascites and anaemia.
2. Early onset jaundice: due to progressive haemolytic anaemia.
3. Gradual onset of mild jaundice with severe anaemia during the first few weeks
after birth; may develop cardiac failure.
Antenatal care
Screen blood group at booking. If Rh-negative, test for anti-D antibodies at booking
and through pregnancy. If antibodies are present, refer to tertiary hospital. Fetal
anaemia is assessed by ultrasonography; may require intrauterine blood transfusion
or early induction of labour.
Postnatal management
Clinical features: Pale large placenta, anaemia, jaundice, enlarged liver and spleen,
oedema and ascites, ‘blueberry muffin rash’ due to extramedullary erythropoiesis
in the skin. Assist ventilation if required. Correct hypoxia, acidosis, hypoglycaemia,
hypothermia. Check blood group, direct Coombs test, serum bilirubin, haemoglobin.
Start phototherapy immediately while waiting for blood results; check TSB every
2–4 hours. IV immunoglobulin may slow haemolysis. Exchange transfusion may be
required to remove bilirubin and prevent bilirubin encephalopathy, correct anaemia
and remove anti-D antibodies. Indications include raised cord bilirubin, severe
anaemia, hydrops fetalis, rapidly rising bilirubin despite phototherapy – see exchange
transfusion chart. Straight blood transfusion: Late anaemia may occur in the weeks
following an exchange transfusion or in Coombs positive infants who did not require
exchange transfusions. Monitor serial haemoglobin over time and reticulocyte
counts; transfuse if symptomatic, or if Hb <6g.
Jaundice 73

Prevention of Rh disease
Rhesus-negative women should be given anti-D immunoglobulin by intramuscular
injection within 72 hours of delivery, or other potential times when feto-maternal
blood mixing could occur (miscarriage, amniocentesis, antepartum haemorrhage or
external cephalic version). This is very effective at preventing iso-immunization; Rh
disease is now uncommon.
2. Infection
Infection is an uncommon cause of jaundice in otherwise well infants. Bacterial
infection can cause haemolysis; may also impair hepatic conjugation of bilirubin or
obstruction the bile flow, causing increase in both conjugated and unconjugated
bilirubin. Unexplained jaundice, especially if associated with reluctance to feed,
drowsiness or vomiting, should raise suspicion of occult infection, often in
urinary tract.
3. Breastfeeding jaundice
Often occurs with a young mother who is unable to latch / feed her infant; the infant
is small, irritable, dehydrated, deeply jaundiced. Sometimes very hypernatraemic.
Responds to rehydration and establishment of adequate feeds.
4. Prolonged jaundice
Jaundice persisting more than 14 days (term) and 21 days (preterm).
a) Breast milk jaundice: A common cause of jaundice in well breastfed infants. The
jaundice is due to increased enterohepatic circulation of bilirubin. The infant
is usually thriving. No treatment is necessary as it rarely gives high levels of
bilirubin.
b) Hypothyroidism: Rare but treatable. Routine screening of TSH in the cord blood at
delivery makes early diagnosis possible.
c) Infection (UTI or other systemic infection) – common cause of prolonged jaundice.
5. Late onset jaundice

Jaundice starting after day 14 of life.
a) Obstruction to bile flow: intrahepatic (hepatitis); extrahepatic (biliary atresia,
choledochal cyst). Conjugated jaundice suggests bile duct obstruction: needs
urgent ultrasound, as surgical intervention must happen before hepatic
injury occurs.
b) Galactosaemia: Rare. Associated vomiting, poor feeding, failure to thrive with
prolonged jaundice. Check for reducing substances in the urine.
74 Jaundice

Congenital Hypothyroidism
The most common cause of congenital hypothyroidism is thyroid dysgenesis
(agenesis, hypoplasia or ectopy). Iodine deficiency can cause a transient
hypothyroidism. Thyroid dysgenesis may result in severe hypothyroidism and mental
retardation unless treated soon after delivery. The incidence is 1:4000 to 1:10000
with the condition more common in Caucasian infants.
The vast majority (more than 95 percent) of infants with congenital hypothyroidism
have few, if any, clinical manifestations of hypothyroidism at birth. This is because
some maternal thyroxine (T4) crosses the placenta. Clinical signs may include a large
tongue, umbilical hernia, prolonged jaundice and feeding problems. Bone age may be
reduced and cranial sutures wide.
Routine umbilical cord blood screening for thyroid agenesis should be done wherever
possible. The diagnosis must be suspected if a raised TSH and a low total T4 are
found. Some countries include thyroid screens as part of a more extensive metabolic
screen. If cord blood is not used, it is important to remember not to test for TSH
in the first 48hrs of life as there is typically a TSH surge during this time period.
TSH screening may also detect less severe forms of congenital hypothyroidism, e.g.
enzyme defects or ectopic thyroid.
Infants with abnormal results must be urgently referred to an endocrine service
for repeat testing. Treatment is daily thyroxin replacement for life. The sooner the
treatment is started the better the neurodevelopmental outcome, and infants started
on replacement therapy before 6 weeks of age should not be adversely affected.
Congenital Hypothyroidism 75

Respiratory distress
Respiratory distress is a common and important complication in newborn infants,
especially in infants born preterm. It presents with two or more of the following
cardinal signs:
• Persistent tachypnea (> 60 breaths per minute).
• Central cyanosis (tongue) in room air.
• Sternocostal (sternum and rib) recession.
• Expiratory grunting.
• Nasal flaring.
Predisposing factors
• Preterm delivery.
• Underweight for gestational age or wasting (especially if covered in meconium).
• Fetal distress or failure to breathe well at birth.
• Complicated labour e.g. prolonged rupture of membranes or vacuum extraction.
• Infant of diabetic mother.
• Clinical chorioamnionitis in the mother.
• Elective caesarean section.
Causes
The cause of respiratory distress must always be looked for:
Respiratory
• Hyaline membrane disease.
• Wet lung syndrome (transient tachypnea of the newborn).
• Meconium aspiration.
• Pneumonia.
• Chronic lung disease (bronchopulmonary dysplasia).
• Pneumothorax.
• Lung hypoplasia.
• Persistent pulmonary hypertension of the Newborn.
• Congenital diaphragmatic hernia.
76 Respiratory distress

Non-respiratory
• Hypothermia.
• Metabolic acidosis.
• Anaemia or polycythaemia.
• Patent ductus arteriosus.
• Congenital heart disease.
A chest X-ray may aid in identifying the cause of respiratory distress.
Hyaline membrane disease (HMD)

This is the most important cause of respiratory distress in newborn infants. It is
usually seen in preterm infants in whom it is the major cause of death. It may also be
seen in term infants born to poorly controlled diabetic mothers. Hyaline membrane
disease is due to a deficiency of surfactant in the infant’s lungs. Surfactant lowers
the surface tension in the alveoli and allows respiration with minimal physical effort.
Lack of adequate amounts of surfactant leads to progressive alveolar collapse.
Synthesis of surfactant is further inhibited by hypoxia, acidosis and hypothermia.
With preterm infants every effort must be made to avoid these factors.
Clinical signs
The features of respiratory distress (tachypnea, recession, grunting, and cyanosis) are
usually apparent at or soon after birth. Signs of respiratory distress become worse
for 72 hours before improving if left untreated. The infant is inactive and tends to lie
in the frog position. The chest X-ray typically shows an under-expanded chest with
a fine reticulo-granular appearance over both lung fields, ‘air-bronchograms’ extend
beyond the borders of the heart and thymus and the outline to the cardiothymic
shadow is indistinct.
As the disease progresses, the infant may develop ventilatory failure (rising carbon
dioxide concentrations in the blood), and prolonged cessations of breathing (“apnoea”).
Prevention
Preterm delivery and elective caesarean section before 39 weeks gestation should
be avoided if possible. Antenatal steroids should be given to all women at high risk
of preterm delivery before 34 weeks gestation to accelerate fetal lung maturity.
Whenever possible, delivery should be delayed for 48 hours while two doses of
betamethasone are given intramuscularly to the mother 24 hours apart. The use
of antenatal steroids has decreased both the incidence and severity of hyaline
membrane disease.
Respiratory distress 77

Management
The basic aim of treatment in the newborn infant is to prevent progressive alveolar
collapse, maintain oxygen saturation at 88 to 92%, keep body temperature and blood
glucose concentration within normal limits and provide adequate nutrition. The sick
infant should be handled as little as possible while regular and frequent observations
(skin temperature, colour, heart rate, and respiration) are recorded.
Relief of hypoxia is the most important aspect of treatment. Nasal prong CPAP
(continuous positive airway pressure) should be started as early as possible. If
facilities for nasal CPAP are not available, oxygen can be given by nasal cannula. Too
much oxygen is as dangerous as too little and can damage the eyes (retinopathy of
prematurity) and lungs. Thus when administering oxygen one must have adequate
facilities for measuring the inspired oxygen concentration (FiO2) and the arterial
oxygen tension (PaO2) and saturation (SaO2). The pulse oximeter has greatly
facilitated the monitoring of oxygen saturation. Blood samples for arterial blood
gas analysis are obtained by radial artery puncture or from an indwelling umbilical
or radial artery catheter. The aim is to maintain PaO2 between 7 and 10 kPa (50–80
mmHg). Raised PaCO2 (permissive hypercapnia) may be tolerated provided the pH
remains normal.
Surfactant replacement therapy

If the respiratory distress deteriorates, give ‘in-and-out’ surfactant via the
endotracheal route. The standard procedure for this is known as LISA (Less Invasive
Surfactant Administration). If the respiratory distress continues to deteriorate,
intermittent positive pressure ventilation or high frequency oscillation may be
needed. Infants with hyaline membrane disease should be transferred as soon as
possible to an intensive care unit. Usually the respiratory distress has resolved by a
week. The use of antenatal steroids, surfactant and early nasal CPAP prevents many
infants requiring ventilation. This has been a major advance in managing HMD.
Temperature control
Prevent hypothermia by nursing the infant under a radiant heat source or in a
closed incubator with the temperature controlled to maintain a neutral thermal
environment (to minimise oxygen requirements).
Nutrition
Fluid, electrolyte and energy requirements should be supplied by intravenous infusion
at first. Milk feeds by nasogastric tube should be started as soon as possible provided
the infant does not vomit. Total parenteral nutrition may be needed for a few days.

Correction of acidosis
Respiratory acidosis due to a high PaCO2 can be corrected by improving ventilation.
Mild respiratory acidosis is well tolerated and not an indication for ventilation.
Metabolic acidosis will usually improve with adequate oxygenation, normothermic
control and hydration.
Complications associated with HMD

The most important are:
Early
• Pneumothorax.
• Intraventricular haemorrhage.
• Heart failure due to a persistent patent ductus arteriosus.
Late
Chronic lung disease (Bronchopulmonary dysplasia)
Wet lung syndrome (transient tachypnoea of the newborn)

Transient tachypnoea of the newborn is a respiratory problem that presents in the
newborn shortly after delivery, most commonly following elective Caesarean section. It
is the commonest cause of respiratory distress in term newborn infants. It consists of a
period of tachypnoea and recession and is due to fluid remaining in the lungs after birth.
Within an hour or two of birth there are features of respiratory distress and the chest
is hyperinflated. Treatment is supportive and may include supplemental oxygen.
The chest x-ray shows hyperinflation of the lungs including prominent pulmonary
vascular markings, flattening of the diaphragm, and fluid in the horizontal fissure of
the right lung.
Most infants improve within 12 to 24 hours though tachypnoea may persist for several
days. It is important to differentiate wet lung syndrome from hyaline membrane disease
as the former does not require referral to an intensive care unit.
Meconium aspiration
This is due to the inhalation of meconium during or immediately after delivery. It
usually follows fetal distress during labour. It is limited to term or post-term infants,
especially if they are wasted or underweight for gestational age. Preterm infants
rarely pass meconium in utero. The inhaled meconium produces areas of emphysema
and atelectasis throughout the lungs. The chest is hyperinflated and there is risk

of pneumothorax, pneumomediastinum and persistent pulmonary hypertension. A
pneumonitis may be caused by chemical irritation of the inhaled meconium or by
secondary bacterial infection. Many infants with severe meconium aspiration die or
suffer severe lung damage.
At birth the meconium is present in the mouth and pharynx and may stain the skin,
nails, cord and placenta. Poor breathing after delivery is common.
On X-ray the lungs will show hyperinflation, diaphragmatic flattening, cardiomegaly,
patchy atelectasis and consolidation. The heart size may be increased and pneumothorax
or pneumomediastinum may be seen.
Treatment
• Every effort must be made to eliminate fetal hypoxia by good labour
management. It has been previously recommended that the throat and nose of
the infant be suctioned as soon as the head is delivered. However, this is not
useful and the revised Neonatal Resuscitation Guidelines no longer recommend it.
• Manage in the same way as severe respiratory distress. Nasal CPAP helps to
expand the collapsed alveoli and give better distribution of air in the lungs.
• Antibiotics only if secondary bacterial infection develops.
• Steroids are not helpful and may increase the risk of secondary pneumonia.
Pneumonia
Infection acquired before or during passage through the birth canal may cause early
onset (within the first 72 hours of delivery) bacterial pneumonia which is often
difficult to distinguish clinically from other causes of respiratory distress. E.coli
and the group B haemolytic Streptococcus are responsible for the majority of early
infections. The latter is commonly found in vaginal flora and may cause a clinical and
X-ray picture indistinguishable from that of hyaline membrane disease. Pneumonia
on day 1 usually results from chorioamnionitis caused by an ascending spread of
bacteria from the cervix with or without prolonged rupture of the membranes. The
mother usually has no clinical signs of infection.
Chronic fetal infections (e.g. syphilis) may cause early onset (congenital) pneumonia.
Acquired (nosocomial) pneumonia in the nursery presents after 3 days of life and is
usually due to Staph aureus, Klebsiella, Pseudomonas, and other ‘hospital bacteria’
which are often resistant to first-line antibiotics. This has become a major problem
in many intensive care units. Strict hand washing or spraying, good aseptic protocols,
use of breast milk and skin-to-skin care reduces the risk of nosocomial infections.

The newborn with pneumonia may present with poor breathing after delivery,
apnoeic spells or features of respiratory distress. The diagnosis is confirmed by chest
X-ray. The causative organism may be cultured from blood.
Treatment
• General measures as for respiratory distress.
• Specific therapy with appropriate antibiotics. It is important to know the
bacterial resistance pattern and antibiotics of choice in each nursery.
Pneumothorax
Common causes
• Meconium aspiration
• Vigorous resuscitation after birth
• Hyaline membrane disease, especially if on positive pressure ventilation or CPAP
• Spontaneous (idiopathic)
Pneumothorax is the presence of air in the pleural space (the space between the lung
and the chest wall). A small pneumothorax may have few clinical signs. These infants
are not particularly distressed and can be managed without needle aspiration.
In more severe cases, especially those with tension pneumothorax, there is a rapid
deterioration in condition. The infant becomes increasingly dyspnoeic or apnoeic
and is often shocked or cyanosed. The affected side will tend to be hyper-resonant
to percussion and breath sounds are diminished. The affected side will also trans-
illuminate with a bright cold light source. A diffuse glow will be seen on the
side of the pneumothorax. This is a rapid and reliable way of diagnosing a large
pneumothorax. A chest X-ray will confirm the diagnosis by showing absence of
lung markings and a collapsed lung on the affected side. Tension pneumothorax is
confirmed by mediastinal shift.
Treatment
Mild degrees of pneumothorax may resolve spontaneously. More severe cases will
need to have the air drained urgently and may be treated by needle aspiration or
chest tube placement. In severe cases do not wait for a confirmatory chest X-ray
before draining the air.

Persistent pulmonary hypertension
Persistent pulmonary hypertension of the newborn results when there is failure of
the normally high pulmonary artery pressures of the fetus to fall rapidly after birth.
Persisting high pulmonary vascular resistance in the newborn leads to hypoxia caused
by pulmonary under perfusion with right-to-left shunting from the pulmonary to
the systemic circulation via the patent ductus or patent foramen ovale. The infant is
usually term and presents with respiratory distress and hypoxia soon after birth. Often
there is a history of intrapartum hypoxia with meconium staining and poor breathing
at delivery. The diagnosis is confirmed on cardiac ultrasonography which shows a
normal heart structure but raised pulmonary artery pressure with a ductal shunt. The
chest X-ray may be clear or show features of vernix or meconium aspiration.
Treatment
Supplementary oxygen or ventilation may be needed. Sedate the infant and maintain
normal or suprasystemic blood pressure with inotropes to reduce the shunting. Sildenafil
or nitric oxide may be needed in severe cases to dilate the pulmonary arteries.
Diaphragmatic hernia
Herniation of abdominal viscera through the diaphragm (especially on the left side)
usually presents at birth with severe respiratory distress, cyanosis and a shift of
the mediastinum and interference with lung function. The main diagnostic clues
are polyhydramnios, shift of the maximal heart sounds to the right and a scaphoid
appearance of the abdomen. Bowel sounds may be heard in the chest. Today many
cases are detected by routine antenatal ultrasonography.
It involves three major defects:
• A failure of the diaphragm to completely close during development.
• Herniation of the abdominal contents into the chest.
• Pulmonary hypoplasia.
The timing of delivery should be planned with the surgeons informed beforehand. The
infant should be intubated at delivery if resuscitation is needed. Do not give mask
ventilation as this expands the gut and worsens the respiratory distress.
X-ray immediately confirms the diagnosis. Surgical repair should only be performed
once the infant is physiologically stable; however the prognosis in an infant with a
large diaphragmatic hernia remains poor due to pulmonary hypoplasia.

Bronchopulmonary dysplasia (Chronic lung disease)
Bronchopulmonary dysplasia (BPD) is a chronic lung disease in which preterm
infants, usually those who were treated with supplemental oxygen, require long-term
oxygen. It is more common in infants with low birth weight and those who receive
prolonged mechanical ventilation. It results in significant morbidity and mortality.
The definition of BPD has continued to evolve primarily due to changes in the nursery
population, such as more survivors at earlier gestational ages, and improved neonatal
management including surfactant, antenatal glucocorticoid therapy, and less
aggressive mechanical ventilation.
The new National Institute of Health (US) criteria for BPD (for newborn infants
treated with more than 21% oxygen for at least 28 days) is as follows:
Mild
• Breathing room air at 36 weeks post-menstrual age or discharge (whichever
comes first) for infants born before 32 weeks, or
• Breathing room air by 56 days postnatal age, or discharge (whichever comes first)
for infants born after 32 weeks gestation.
Moderate
• Need for <30% oxygen at 36 weeks postmenstrual age, or discharge for infants
born before 32 weeks, or
• Need for <30% oxygen to 56 days postnatal age, or discharge (whichever comes
first) for infants born after 32 weeks gestation.
Severe
• Need for >30% oxygen at 36 weeks postmenstrual age, or discharge (whichever
comes first) for infants born before 32 weeks, or
• Need for >30% at 56 days postnatal age, or discharge (whichever comes first) for
infants born after 32 weeks’ gestation.
There is evidence to show that steroids given to infants less than 8 days old can
prevent bronchopulmonary dysplasia. However, the risks of treatment may outweigh
the benefits. It is unclear if starting steroids more than 7 days after birth is harmful
or beneficial. It is thus recommended that they only be used in those who cannot be
taken off of a ventilator.
Whenever possible, CPAP should be used instead of assisted ventilation, especially in
very small infants. Chronic lung disease is a major problem in industrialised countries
where extremely low birth weight infants are offered intensive care with ventilation.

Respiratory support
There are a number of methods which can support respiration in infants with
respiratory distress:
• CPAP via nasal prongs (nCPAP) which includes bubble and flow driven.
• Humidified high flow nasal cannula (HHFNC).
• Nasal cannula.
• Conventional positive pressure ventilation.
• Oscillation.
Term infants with mild respiratory distress usually need nasal cannula only. Nasal
cannulas are often used in smaller infants to prevent alveolar collapse. The early
use of surfactant and nasal prong CPAP, to infants with HMD, often avoids the
need for ventilation. The indications for ventilation are failure to maintain adequate
oxygenation with other forms of respiratory support, respiratory acidosis with a high
PaCO2, and apnoea. The use of nasal CPAP with a pulse oximeter to monitor the
arterial oxygen saturation has revolutionised respiratory support in newborn infants.

Complications of prematurity
Infants born before 37 completed weeks of gestation is referred to as preterm.
Preterm infants have a higher rate of morbidity and mortality than term infants and
the more immature the infant, the more complications they may experience and the
higher the risk of mortality.
Complications of prematurity can be divided into:
• Immediate (At birth and within 24 hours of life).
• Early (1st 7 days of life).
• Late (1st month of life).
• Long term (Beyond 1st month of life).
*Some of the complications tend to overlap in between categories
Immediate Complications
1. Hypothermia
The target normal axillary temperature should be 36.5 – 37.5 °C. Hypothermia refers
to a temperature below 36.5 °C.
Preterm infants are prone to hypothermia on account of the following factors:
• Thin skin.
• Little subcutaneous fat tissue.
• Large surface area to body weight.
• Immature thermoregulatory centers in the brain and their inability to adjust to
temperature changes in their environment.
2. Hypoglycemia / Feeding problems
3. Respiratory Distress
Various causes:
• Hyaline Membrane Disease.
• Wet Lung Syndrome.
Complications of prematurity 85

Early Complications
4. Infections / Sepsis
• Early onset sepsis occurs <72hrs of life and late onset >72hrs.
• Preterm infants are at particular risk due to their immature immune system and
diminished antibody transfer from their mothers.
5. Jaundice
Physiological jaundice typically presents between days 2 and 5 after birth and occurs
as a result of the following factors
• Shortened life span of the red blood cell (RBC).
• Increased hemolysis after birth.
• Immaturity of the liver and low level of hepatic enzymes responsible for the
conjugation and excretion of bilirubin.
6. Apnea of prematurity
Cessation of breathing for 20 seconds, or less if associated with bradycardia and
or cyanosis. More common in preterm infants due to immaturity of the respiratory
center. Typically affects infants borne at < 34 weeks gestation.
Caffeine citrate is currently the drug of choice for the treatment of apnea in preterm
infants, and is preferred to other methylxanthines because it can be given orally as a
once a day dose and has a wide therapeutic window.
7. Patent Ductus Arteriosus (PDA)
8. Intraventricular hemorrhage (IVH) / Germinal Matrix hemorrhage.

This may lead to post haemorrhagic hydrocephalus.
Late complications
9. Necrotizing Enterocolitis (NEC)

Generally, the lower the gestational age, the later the NEC occurs.
10. Anemia of Prematurity

• The preterm infant tends to show signs of anemia by 4 – 8 weeks old.
86 Complications of prematurity

11. Metabolic Bone Disease (MBD)
Preterm infants are prone to poor bone mineralization. This is because most calcium
& phosphorus deposition occurs during the 3rd trimester. MBD is predominantly
caused by phosphate deficiency. Onset usually between 3 – 12 weeks of life. Alkaline
phosphatase (ALP) & phosphorus are the 2 most commonly used biomarkers for
assessing bone mineralization. In MBD, one expects a high ALP and low phosphorus.
Fortification of breast milk is recommended, and management involves giving
phosphate supplements.
12. Retinopathy of Prematurity (ROP)

One of the major causes of blindness in children worldwide.
The timing of the delivery of the preterm infant disrupts the normal development of
the retinal blood vessels. Typically seen at 31 – 34 Postmenstrual age.
Risk factors include
• GA < 32weeks or birth weight < 1250g.
• Infections.
• Supplemental oxygen.
• Hypoxia.
• Anemia.
Mode of management could be laser therapy or monoclonal antibodies that are
directly injected into the eyes. About 90% resolve without causing damage to the
retina. In severe cases, ROP causes the retina to detach itself from the wall of the eye
leading to blindness.
13. Periventricular leukomalacia (PVL)

Occurs as a result of injury to the white matter of the brain. Spastic diplegia is the
commonest complication of PVL. Diagnosis is by ultrasound or MRI.
14. Chronic Lung Disease (CLD) / Bronchopulmonary Dysplasia (BPD)

Oxygen use for at least 28 days and dependence at 36 weeks postmenstrual age.
Results from the arrest of the alveolarization process when the infant is born preterm
as well as postnatal damage to the lungs
15. Iron deficiency anaemia.

Usually at around 4-6months due to low iron stores. Prevented by delayed cord
clamping and supplementation from a month of age.
Complications of prematurity 87

16. Increased risk of respiratory illness and SIDS (sudden infant
death syndrome)
Long term complications

Long term complications are mainly neurodevelopmental in nature and includes the
following
17. Cerebral palsy, blindness, deafness
18. Cognitive and behavoural deficits
19. In growth restricted infants there is a higher chance of short

stature and metabolic syndrome (Barker hypothesis)
88 Complications of prematurity

Apnoea
Apnoea is a pause in breathing lasting long enough (usually more than 20 seconds)
to cause hypoxia (bradycardia and cyanosis or pallor). It is much more common in
preterm infants as a direct consequence of immature respiratory control that results
in an impaired respiratory drive (central cause) and/or inability to maintain upper
airway patency (obstructive cause). Sometimes there are both central and obstructive
elements (mixed cause). If severe or recurrent it may cause brain damage or death.
Not to be confused with ‘periodic breathing’ which is recurrent short periods of
interrupted respiration not associated with cyanosis and bradycardia.
Causes
• Immaturity.
• Respiratory distress or hypoxia.
• Aspiration of a feed or nasopharyngeal suctioning.
• Infection (especially meningitis or septicaemia).
• Hypoglycaemia.
• Pyrexia.
• Periventricular bleed.
• Convulsion.
• Sedation e.g. diazepam.
Treatment
• Stimulation may restart breathing, especially if done promptly.
• Gently clearing the airway and mask ventilation if stimulation is unsuccessful.
• Nasal CPAP may prevent further apnoea. Do not give added oxygen unless oxygen
saturation is low.
• Intubation and ventilation may be necessary in severe, recurrent apnoae.
• Look for and treat underlying cause.
Apnoea 89

Apnoea of prematurity
Apnea of prematurity is most widely defined as cessation of breathing for more than
20 seconds or a shorter respiratory pause associated with oxygen desaturation and/
or bradycardia in infants who are younger than 37 weeks gestation. The incidence
of apnea is inversely proportional to gestational age (GA), and almost all extremely
low birth weight (ELBW) infants (GA <28 weeks) are affected. Apnoea is usually first
noticed after the second day.
Although apnea of prematurity is the most common cause of apnea in preterm
infants, it is a diagnosis of exclusion.
Management includes minimal handling, close temperature control, monitoring
with an apnoea alarm or pulse oximeter and the administration of prophylactic
oral caffeine or theophylline until the infant is mature enough (usually 33 weeks).
Caffeine is the preferred drug due to the safety profile, however it is not always
available. If apnoea persists despite the theophylline or caffeine prophylaxis, nasal
CPAP will usually control the attacks. Mechanical ventilation is seldom necessary and
suggests another cause for the apnoea.
It is dangerous to provide added oxygen to very preterm infants with normal lungs
and recurrent apnoea as this may cause retinopathy of immaturity and damage
the lungs.
90 Apnoea

Heart conditions
Routine examination of the newborn infant should include looking for signs of
heart disease or dysmorphic features (many congenital cardiac abnormalities are
associated with specific syndromes). Assess pulses and peripheral perfusion in arms
and legs, palpate the precordium, listen for heart sounds and murmurs, and look for
signs of respiratory distress, heart failure and shock. If there is any doubt regarding
cyanosis or lower limb pulses measure the oxygen saturation and blood pressure in
all limbs. Pulse oximetry is a very helpful method of screening newborn infants for
hypoxaemia in cyanotic heart abnormalities. Many congenital heart defects may be
detected by antenatal ultrasonography.
Heart disease in the newborn infant is usually due to a congenital structural defect
and rarely due to an acquired abnormality in cardiac function and circulation. Heart
disease in the newborn infant usually presents with one or more of the following:
• Asymptomatic heart murmur.
• Cyanosis.
• Gradual onset of respiratory distress and heart failure, usually after 2-3weeks.
• Sudden, catastrophic heart failure with shock.
Asymptomatic heart murmur

A short, soft (<3/6), short systolic murmur (an ‘innocent’ or physiological murmur)
is very common in normal well infants soon after birth. These infants have no
other abnormal cardiac signs. The murmur disappears during the first days of life
and is usually due to flow through a patent ductus arteriosus (PDA) or tricuspid
regurgitation whilst the pulmonary pressures are still falling. Increased flow over a
normal pulmonary valve due to a hyperdynamic circulation (e.g. anaemia or fever)
may also give an asymptomatic murmur.
Peripheral pulmonary stenosis or a small persistent PDA may give a systolic murmur
heard well (<3/6) over both sides of the chest and back in an asymptomatic infant.
Both are common in preterm infants.
Small ventricular septal defect (VSD). The murmur usually becomes audible after
day 2, once the pulmonary vascular resistance (PVR) falls significantly and the right
heart pressure drops below that of the left heart. This allows a left to right shunt
through the VSD which causes a systolic murmur that is best heard at the lower left
sternal border. Most small VSDs close spontaneously with time. Larger VSD’s may
lead to pulmonary over circulation around 3 to 6weeks of age.
Heart conditions 91

Acyanotic Tetralogy of Fallot may present with a loud, harsh murmur (3/6 or more)
in an otherwise well acyanotic newborn. Adequate pulmonary blood flow prevents
the appearance of obvious cyanosis. The right ventricular outflow obstruction may
worsen in time as the ventricle and infundibulum hypertrophies.
Any loud or long systolic murmur (>3/6), any diastolic murmur or associated with
signs of respiratory distress, heart failure, cyanosis, shock or dysmorphic features
suggests a serious heart abnormality and must be urgently investigated.
Any <3/6 heart murmur in an asymptomatic infant, persisting after day 3 of life, needs
follow up.
Cyanosis
Most infants have peripheral cyanosis after birth (<10 minutes) or peripheral
cyanosis due to cold hands and feet. However persistent central cyanosis (blue
tongue) indicates hypoxaemia with inadequate arterial oxygen saturation and is
usually due to a pulmonary or cardiac condition.
Central cyanosis not responding to 100% oxygen (the hyperoxia test) is usually due
to persistent pulmonary hypertension or cyanotic congenital heart disease. There
are a number of severe congenital heart abnormalities which present with central
cyanosis (most start with a ‘T’). Important cardiac causes of cyanosis are obstructed
pulmonary flow with right-to-left shunting or common mixing of right heart
(deoxygenated) and left heart (oxygenated) blood. Often there is a single second
heart sound and often no murmur. All require urgent referral and surgery.
Persistent pulmonary hypertension presents with central cyanosis and may be
mistakenly diagnosed as congenital cyanotic heart disease. There is often a pre- and
post-ductal saturation difference of more than 7-10%. It’s usually seen in term
infants who have suffered intrapartum hypoxia often with meconium stained liquor,
but may be idiopathic. The significant fall in the pulmonary vascular resistance (PVR)
after delivery does not take place leading to persistent pulmonary hypertension,
with a right-to-left shunt through the ductus arteriosus and foramen ovale when
the pulmonary pressures exceed the systemic pressures. A dynamic pulmonary
vascular over reactivity component often results in clinical episodes of significant
desaturation with an ensuing viscous cycle. Treatment consists of oxygen (the most
potent vasodilator), respiratory support, blood pressure support (with inotropes and
intravenous fluids) and careful sedation. Oral sildenafil (Viagra) or inhaled nitrous
oxide reduces pulmonary resistance.
92 Heart conditions

Transposition of the great arteries (TGA): This is likely to be the diagnosis if a
newborn infant in the first few days of life presents with severe cyanosis, tachypnea
and cardiomegaly. As the aorta leaves the right ventricle and the pulmonary artery
the left ventricle, oxygenated blood is unable to reach the systemic circulation. There
may be some mixing at atrial and ductal level and pulmonary blood flow increases.
Chest X-ray shows congested lungs. Oral or intravenous prostaglandin therapy should
be started to improve arterial oxygen saturation by reopening the ductus. Urgent
referral is needed for possible atrial septostomy and early corrective surgery (“Arterial
Switch operation”).
Severe Tetralogy of Fallot with severe pulmonary outflow obstruction (pulmonary
atresia, severe valvar or sub-valvar (infundibular) stenosis) presents early with central
cyanosis. Chest X-ray shows oligaemic lungs and a boot-shaped heart. Pulmonary
flow can be maintained if the ductus is kept open with a prostaglandin E1 infusion
(or oral E2). An urgent shunt procedure (subclavian artery to the pulmonary artery)
or possible full repair is needed to establish blood flow to the lungs. Milder forms of
Tetralogy of Fallot may be acyanotic with a harsh murmur.
Other less common congenital heart abnormalities presenting with cyanosis include
Tricuspid atresia, Ebstein’s anomaly, Truncus arteriosus and Total anomalous
pulmonary venous drainage.
Respiratory distress and gradual onset of heart failure

(usually after week 2)
At birth, respiratory distress is usually due to a primary lung condition. However
cyanosis and tachypnea at birth not responding to oxygen may indicate cyanotic
heart disease.
Heart failure with respiratory distress developing after a week or more of life
(classically 3-6 weeks for a VSD), is usually due to pulmonary over circulation. Once
the PVR and right heart pressure has fallen significantly, the “left-to-right” shunt
at the level of the ductus arteriosus, ventricle or atrium increases and floods the
pulmonary vessels.
Clinical features of neonatal heart failure include:
• Signs of respiratory distress, especially fast breathing.
• Tiring with feeds and failure to thrive, with or without oedema.
• Excessive sweating, especially of the forehead, whilst feeding.
• Tachycardia or gallop rhythm.
• Hepatomegaly.
Heart conditions 93

The commonest cause of respiratory distress due to excessive pulmonary flow is a
large persistent ductus arteriosus in a preterm infant. In utero the ductus arteriosus
carries blood from the pulmonary artery to the aorta in order to bypass the non-
functional lungs. At birth, when the lungs replace the placenta as the respiratory
organ, a patent ductus is no longer required and it normally closes due to muscular
spasm in response to the higher PaO2 level. Occasionally, especially in the preterm
infant, the duct persists and does not close after delivery, because it is immature and
any episodes of hypoxaemia prevent the natural spasm. Due to the significant fall in
the PVR after delivery, blood will be shunted from the aorta to the pulmonary artery,
which now has a lower mean blood pressure. Over the first 6 weeks of life, as the
PVR falls even further, the left to right shunt into the lungs increase. With a large
left-to-right shunt, the flooded lungs become stiff and edematous causing respiratory
distress. The pulses are bounding or very easily felt with a wide pulse pressure. Usually
a systolic murmur is heard in the left subclavicular area after day 2-3 as well as over
the back. It is unusual to have a diastolic murmur in young infants with a PDA.
In the preterm infant, an elevated level of prostaglandin may also contribute to
the duct staying patent. With any underlying inflammatory condition such as
septicaemia, pneumonia, necrotizing enterocolitis bronchopulmonary dysplasia etc.
a high prostaglandin level will prevent the duct from closing. Therefore, treating the
underlying inflammatory condition and general supportive measures is usually all
that is needed. If not haemodynamically clinically significant, a “watchful waiting”
approach is advised.
A haemodynamically significant duct will lead to signs of increased pulmonary
blood flow such as tachypnea, tachycardia and poor growth. The clinical diagnosis
of haemodynamically significant PDA and the severity of the left-to-right shunt can
be confirmed by echocardiography: a large duct size, large ductal left to right shunt,
large left atrium and reversed diastolic flow in the aorta confirms a haemodynamically
significant shunt. Chest X-ray shows cardiomegaly and pulmonary plethora.
Intravenous fluid restriction, optimizing nutrition, maintaining a normal Hb and
small doses of diuretic are usually adequate to manage a haemodynamically
significant PDA until it closes spontaneously. Supportive nasal CPAP may be
needed in the short-term. In the rare newborn infant with a confirmed very large
ductal shunt and persistent severe respiratory distress, where infection has been
excluded: paracetemol or Brufen orally or indomethacin intravenously, which blocks
prostaglandin synthesis, can be considered in the first month of life as long as all
contraindications were excluded. Note: The evidence for the use of the agents is
equivocal and constantly reviewed. In extreme, ventilator dependent cases, where
medical treatment fails, the duct may be ligated surgically.
94 Heart conditions

A large ventricular septal defect causes excessive pulmonary blood flow when the
size of the left-to-right shunt increases as the pulmonary vascular resistance falls.
With a moderate to large defect, this leads to respiratory distress with poor feeding
usually around 3–6 weeks after birth and a diastolic flow murmur may be heard. VSD
is the commonest form of congenital heart disease. Failure to thrive and secondary
pneumonia is common with a large VSD. Infants with a symptomatic VSD must be fully
investigated and given anti-failure therapy. Large VSDs may require surgical closure.
A VSD may be part of an endocardial cushion defect (left axis on ECG) which is
common in children with trisomy 21. All trisomy 21 infants should have a cardiac
evaluation before 3 months of age since they’re at risk of accelerated pulmonary
hypertension developing, which increases the risks of later surgery.
Catastrophic shock and early heart failure

These infants usually have underdevelopment of the left side of the heart (hypoplastic
left heart syndrome), severe coarctation of the aorta or an interrupted aortic
arch or rarely severe aortic stenosis. Initially after birth the right ventricle maintains
systemic circulation via the patent ductus arteriosus. These infants usually present on
day 2 to 14 when the ductus closes with shock, heart failure, renal failure and often
sudden death follows. This usually occurs after the infant is discharged home and
may be misdiagnosed as sepsis (poor perfusion, mottled skin, hypotensive, poor pulses,
metabolic acidosis). The femoral pulses are usually palpable until the duct starts to
close but a saturation difference of >3% between right hand (preductal) and foot
(post-ductal) suggest the diagnosis. Prostaglandin E2 orally or a PG E1 infusion can
be lifesaving as they keep the ductus open. Urgent stabilization and early referral for
assessment is required with surgery if needed. Many of these infants die.
Heart failure at birth is rare and usually seen in severely anaemic infants (e.g.
Rhesus haemolytic disease, severe blood loss), infants after severe intrapartum
hypoxia, severe metabolic disturbances (e.g. hypoglycaemia) or arrhythmias,
especially paroxysmal atrial tachycardia or complete heart block and rarely with
myocarditis (e.g. Coxsackie).
Diagnosing congenital heart disease

With antenatal ultrasonography the diagnosis may be made during pregnancy. Most
of our population do not have access to fetal anomaly scanning or book too late to
have this and will only receive a growth scan in a busy clinic, where cardiac anatomy
may not be scrutinized. With a limited anomaly scan, where only the four chamber
cardiac view is looked at, less than 50% of congenital heart defects will be identified.
Heart conditions 95

The most important clue to the diagnosis in the newborn infant is the clinical
presentation.
Detailed examination of the cardiovascular system is essential.
Pre-discharge (>6hrs) oxygen saturation can screen for hypoxaemia.
Saturation should be ≥95%.
Chest X-ray to assess heart size and shape and whether the lung fields appear
plethoric or oligaemic.
ECG, especially QRS axis (Left axis + acyanotic=usually AVSD, + cyanotic=Tricuspid
atresia) and arrhythmias.
If a cardiology service not immediately available: clinical assessment and follow
up at 2 days post discharge and 7-10 days of life crucial for critical congenital
cardiac defects and at 4–6 weeks for left to right shunt lesions.
Detailed echocardiography (ultrasonography) which can usually be done at
the bedside and occasionally cardiac catheterization or a Magnetic Resonance
Angiography (MRA) may be needed.
Management of an infant with suspected congenital

heart disease
• Oxygen and respiratory support if necessary.
• If a cyanotic heart condition is suspected, give prostaglandin E2 orally or E1
intravenously to keep the ductus open. This should be given immediately in any
infant with suspected cyanotic congenital heart disease as it is often lifesaving.
The standard emergency dose of oral prostaglandin E2 is ¼ tablet crushed in 2 ml
water given via nasogastric tube 1 to 2 hourly.
• Inotropic support with dopamine, dobutamine or adrenaline in hypotensive failure.
• Diuretics (furosemide with or without spironolactone) and reduce fluid intake for
congestive heart failure.
• Correct anaemia and any correctable metabolic problems (Na+, K+, Ca2+, Mg2+, PO4).
• Optimize nutrition, consider tube feeds if infant is feeding well orally.
• Refer early for cardiologist confirmation and consideration for corrective or
palliative surgery.
• Parents should be counseled about the diagnosis, management and prognosis.
Management can be planned best if diagnosis is made before or soon after delivery,
ideally before the patient decompensates, hence the importance of early booking, a
good newborn clinical examination, pre-discharge pulse oximetry screening and the
day 2 and day 7-10 routine well infant checks.
96 Heart conditions

Infection
The newborn infant is more vulnerable than the older child to most infections.
The preterm infant is even less able to withstand infection and more liable to
suffer serious complications. The infection may be acquired from the mother
during pregnancy, labour, delivery or breastfeeding, or from the nursery or home
environment after birth.
Defence mechanisms
Specific factors
Humoral antibodies
IgG is transferred across the placenta especially in the last trimester, and protects
the infant (especially the term infant) against specific infections to which the mother
has been immunised, This passive immunity wanes after four to six months of age,
but may persist to 9 months e.g. measles.
Neither IgM nor IgA cross the placenta. These antibodies are normally only produced
by the infant after birth. The fetus can produce IgM in response to an intra-uterine
infection e.g. congenital syphilis.
Cell-mediated immunity
The lymphocytes at birth have not yet been exposed to antigens and therefore do not
function well.
Inflammatory reaction
In the newborn the inflammatory response is poor and phagocytosis of bacteria by
leucocytes is inefficient due to reduced opsonins (complement) and delayed chemotaxis.
All newborn infants, but especially preterm infants, are therefore at high risk of
infections due to their immature and inexperienced immune system.
General factors
Antenatal
The placenta filters out most organisms but not all e.g. Rubella virus, HIV,
Toxoplasma, CMV and Treponema pallidum (syphilis).
Amniotic fluid contains lysozymes and other antibacterial agents to reduce the risk
of bacterial infection.
Infection 97

Postnatal
Breastfeeding: Breast milk has IgG, IgM, IgA, lymphocytes, macrophages and
lysozymes. Lactoferrin and transferrin protect against Gram-negative organisms.
Breastfeeding promotes growth of Lactobacilli and inhibits E.coli.
Nursery care
• Infection may be prevented by hand-washing, good skin, cord and eye care.
Kangaroo mother care colonises the infant with maternal flora.
• Hand-washing, breast milk and KMC together can prevent many cases of
nosocomial infection in the nursery.
Sources
Antenatal
Transplacental spread of syphilis, HIV, Rubella, CMV, Varicella and other organsims
Ascending spread from cervix to cause bacterial chorioamnionitis.
Intrapartum
HIV, Herpes, Group B Streptococci, Gonococci, Candida, Chlamydia, Hepatitis B
(increased risk with prolonged labour).
Postnatal
Cross-infection: hands, feeds, inhalation.
Unsterile procedures, intubation, long lines.
Breast milk: HIV and CMV.
Contact at home
Tuberculosis.
Congenital Infection
Definition: Infection of the fetus anytime during pregnancy except the last 5 days of
pregnancy (this is peri-natal infection).
The ‘Torches’ acronym (toxoplasmosis, other, rubella, herpes and syphilis) is a good
reminder to think of congenital infection, however some of the organisms rarely
cause true congenital infection (eg: herpes) or are often geographically concentrated
(eg: toxoplasmosis). The ‘other’ category is large and includes organisms such as TB,
malaria, listeriosis etc.
98 Infection

Infants with congenital infection usually have widespread disease as the organisms
usually enter the bloodstream via the umbilical vessels. Features that may be
clinically obvious are: growth restriction, hepatosplenomegaly (HSM), pneumonitis,
petichiae, jaundice (conjugated) or microcephaly. As the placenta is usually also
infected, it is a valuable organ which can help with determining the diagnosis.
Syphilis
All pregnant women must be screened for syphilis at their booking visit with a
TPHA (Treponema Pallidum Haemagglutination Assay). If this is positive then a VDRL
(Venereal Disease Research Laboratory) or RPR (Rapid Plasma Reagin) should be done
to help determine present from past infection. A VDRL or RPR titre of 1:16 or above
is highly suggestive. Spirochaetes may affect the placenta and fetus resulting in a
first trimester abortion, stillbirth, clinically infected infant at birth, or an apparently
normal infant who develops signs of syphilis weeks or months after delivery. Infected
mothers should be treated with doses of 2.4 million units of benzathine penicillin
intramuscularly every week for three weeks.
Clinical signs of syphilis
• Heavy, pale placenta.
• Rash including on palms and soles. May be peeling.
• Hepatosplenomegaly (90%).
• Jaundice (conjugated), pallor or purpura.
• Oedema.
• Respiratory distress due to syphilitic pneumonia.
• X-ray examination of the long bones may show metaphysitis, especially around
the knee.
• The infant’s TPHA and VDRL/RPR is positive, whether infected or not, as the
maternal antibodies cross the placenta. If the infant titre is higher than the
maternal titre this suggests infection.
Treatment of congenital syphilis
Treatment of infants with clinical signs of syphilis consists of penicillin G 100 000
units IV 12-hourly for 10 days. If the mother has untreated or incompletely treated
syphilis and the infant is clinically normal, the infant should be treated with a single
dose of 50 000 units/kg benzathine penicillin IM. Symptomatic congenital syphilis is
notifiable and partners should also be treated.
Infection 99

Cytomegalovirus (CMV)
This is the most common congenital infection worldwide and usually occurs
when there is primary infection in the mother. Microcephaly, chorio-retinits,
thrombocytopaenia and deafness can occur. Symptomatic neurological CMV should
be treated with ganciclovir/valganciclovir for a minimum of 6 weeks to improve
hearing and neurological outcomes. Infection is confirmed by sending urine for PCR
within the first 3 weeks of life.
Rubella
Rubella (German measles) contracted during the first trimester usually has marked
implications for the fetus which can include cataracts, CNS damage, deafness,
cardiac malformations (especially patent ductus arteriosis) and a ‘blueberry muffin’
rash. There is no specific treatment for congenital rubella but the infant is infectious
and susceptible staff should take precautions. It is a vaccine preventable disease.
Infection can be confirmed by sending urine for PCR testing or looking for IgM
antibodies in the infant.
Tuberculosis
Although congenital TB can occur, this is relatively rare. The more common scenario
is that the infant is well but may be in close proximity to a mother or family member
who may have TB. Should the mother be sputum positive or recently diagnosed, the
infant should be placed on INH prophylaxis. Remember to delay the BCG until the
infant is no longer on INH.
Peri-natal infection
Varicella
Chickenpox very rarely affects the fetus. However, there is a vulnerable week in
which the infant is at higher risk of mortality (up to 30%) and morbidity. If the
mother develops a chickenpox rash from 5 days before delivery till 2 days afterwards,
then the infant would have received a large amount of virus from the mother’s
viraemia but without any protective antibodies. These infants should receive VZIG
(varicella zoster immunoglobulins) which should ameliorate the disease process.
Hepatitis B
The hepatitis B virus does not cross the placenta but may infect the infant at
delivery. If the mother is hepatitis B surface antigen positive, the infant should
100 Infection

receive the hepatitis B vaccine within 24 hours of birth. If the mother is HBe antigen
positive, or this is unknown, the infant should also receive passive antibodies
(Hebagam) within 72hrs of birth. Infected infants usually become chronic hepatitis
carriers and may decades later develop cirrhosis or hepatocellular carcinoma.
Herpes
Herpes is usually a perinatal and not a congenital infection. The infant is usually
infected during the birth process when he or she comes into contact with infected
vesicles. Due to the lack of antibodies, the greatest risk to the infant is when the
mother has a primary herpes infection and not re-activation or re-infection. The
infant usually becomes unwell 5-10 day after birth and may present with localised
skin/eye vesicles or more seriously with CNS or disseminated disease. Treatment is
with intravenous acyclovir.
Post-natal infection
Common minor infections

Conjunctivitis
Gonococcal conjunctivitis is a serious acute infection which usually presents in the
first few days after delivery. It may damage the cornea leading to blindness. The
onset is often rapid with red swollen conjunctiva and a copious purulent discharge.
The diagnosis can be made quickly with a Gram stain on a smear of pus (Gram-
negative diplococci in leucocytes). Chlamydia infection usually presents in the second
week of life.
Treatment of gonococcal conjunctivitis involves repeated irrigation with normal
saline to keep the eye free of pus. In addition give ceftriaxone 50 mg/kg as a
single intramuscular dose. Don’t forget to also treat the mother and have her VDRL
checked. Neonatal Gonococcal conjunctivitis is notifiable.
Gonococcal conjunctivitis can be prevented by putting chloromycetin eye ointment
into both eyes routinely after delivery.
Non-gonococcal conjunctivitis
Chloramphenicol ointment or drops applied 8-hourly for 5 days is usually sufficient
for most infections acquired after delivery.
Use tetracycline or erythromycin ointment if Chlamydia infection is suspected or
if inflammation recurs after chloramphenicol therapy. Proven Chlamydia infections
should also be treated with oral erythromycin 10 mg/kg 6-hourly for 10 days.
Infection 101

Skin infections
Mostly due to staphylococcus aureus and may present as one or more pustules,
infected vesicles, abscesses, etc. The diagnosis is made on Gram stain and culture,
the results of which will determine the form of treatment. Mild superficial infection
may be treated with chlorhexidine (Hibiscrub). Abscesses need incision and drainage.
More severe infections, e.g. cellulitis, require systemic antibiotic therapy.
Clear vesicles suggest Herpes infection. Small vesicles may also be due to miliaria
crystallinum (sweating on forehead usually) or pustular melanosis.
Thrush (moniliasis)
Moniliasis is caused by the fungus Candida and commonly affects the mouth or the
nappy area. The source is usually mother’s vagina or nipples, or contaminated hands,
bottles, etc.
Small white patches are found on the tongue and may spread to the inside of the
cheeks and lips. These white plaques resemble curds of milk but are difficult to
dislodge. The underlying mucosa is red and inflamed, and sucking is often painful.
In the nappy area, the insides of skin creases (groin) are affected.
Treat with mycostatin suspension (Nystatin) or micronazole (Daktarin) gel after
each feed for 5 days. If the mother is breastfeeding, mycostatin should be applied
to the nipples.
Umbilical infection (Omphalitis)
This is usually due to Staphylococci or Coliforms and is potentially serious as it may
result in peritonitis or septicaemia. With mild infections the cord is moist and smells
offensive, and a red flare may extend onto the skin of the abdominal wall. A purulent
or bloody discharge may be present. Severe infections have redness and oedema of
the anterior abdominal wall. Tetanus may complicate omphalitis. Infection can be
largely prevented by routinely cleaning all cords twice a day.
Septicaemia
Infection may begin before or after birth. Common organisms include the Gram-
negative organisms (especially E.coli and Klebsiella) and group B haemolytic
Streptococci (Streptococcus agalactiae). Hospital acquired infections usually present
after 72 hours of age.
Clinical signs: non-specific e.g. poor feeding, poor weight gain, lethargy,
hypothermia, jaundice, pallor, apnoea, abdominal distension. The temperature may be
raised but is more often normal or sub-normal. It is easy to miss the diagnosis.
102 Infection

Diagnosis: Confirmed on blood culture. CRP may be normal initially but then
increases above 10 mg/l.
Complications: meningitis, pneumonia, metabolic disturbances including acidosis,
hypoglycaemia, disseminated intravascular coagulation.
Treatment: suitable antibiotics to cover both Gram-positive and negative organisms
and depending on the organisms typically encountered. For early onset sepsis
(<72hrs) ampicillin and gentamicin are usually prescribed. Late onset sepsis is usually
treated with aminoglycosides (eg: amikacin) or carbapenems (eg meropenem). If
Staphylococcus is suspected vancomycin can be added. Review with blood culture
and CRP after 48 hours treatment. Antibiotics can usually be stopped at 48 hours if
clinically well, blood culture negative and CRP normal (<10).
Meningitis
Usually presents as a septicaemia. Later may show local signs e.g. full tense
fontanelle, squint, convulsions, increased tone or coma. Neck stiffness is unusual.
May complicate an open neural tube defect.
Diagnosis: Confirmed by lumbar puncture. Treatment is a prolonged course of
antibiotics for 14-21 days.
Infection 103

Prevention of mother-to-child transmission
(PMTCT) of HIV
Introduction
In 2016 an estimated seven million people were living with HIV in South Africa.
(Stats SA 2016)
The annual National Department of Health Antenatal HIV Seroprevalence Surveys
estimate that every year over 250 000 pregnant women are HIV positive (≈ 29% of all
pregnancies). The 2013 survey reported six districts (mostly in KZN) with antenatal HIV
prevalence greater than 40%! South Africa has rolled out the world’s largest PMTCT
program in response to this unusually high burden.
Without PMTCT, HIV may be transmitted from mother-to-child during pregnancy
(5%), during labour and delivery (15%), and through breastfeeding (15%). Without
intervention there would be about 80 000 new cases of childhood HIV every year in
South Africa.
The transmission risk increases in late pregnancy and peaks during the eight to 12
hours of labour and delivery. Risk during breastfeeding is low but the cumulative risk is
significant due to extended exposure. High maternal viral load is the primary determinant
of transmission at all stages. Maternal viral load is high with new infection or advanced
untreated HIV infection.
Women on antiretroviral therapy (ART) with suppressed viral loads are unlikely
to transmit HIV to their infants through pregnancy or extended breastfeeding.
Optimising maternal ART and supporting breastfeeding are critical to optimising HIV-
free survival.
In 2015, South Africa moved to a policy of Universal Test and Treat (UTT) with the
aim of identifying 90% of people with HIV, treating 90% of them and achieving a
90% rate of viral suppression (90-90-90 WHO).
This policy would automatically prevent MTCT but few pregnancies are planned and,
many pregnant women access antenatal care late, learn they are HIV positive during
antenatal care or are found to be failing ART. This reflects challenges in prevention,
policy implementation, uptake of testing, adherence to treatment programs and
human nature.
104 Prevention of mother-to-child transmission (PMTCT) of HIV

Infants who are infected in utero have rapid disease progression and high morbidity
and mortality unless treated promptly.
PMTCT has contributed significantly to the reduction in child and maternal mortality
in the last 10 years with transmission rates reduced to less than 1%.
Managing the mother

South African PMTCT policy requires repeated antenatal HIV testing (including poorly
implemented partner testing). Newly diagnosed and known HIV positive women are
initiated on ART and have viral load monitoring to identify those with poor viral control.
Fixed dose combination (FDC) ARVs (currently Tenofovir, Emtricitabine and Efavirenz)
have simplified treatment and improved adherence.
During pregnancy and breastfeeding, women with virological failure after 12
weeks of ART require intensified adherence support and, if still failing despite good
compliance, should be switched to 2nd-line ART.
Viral suppression is crucial for PMTCT and maternal health but, even when there has
been no prelabour ART and risk intensity is high, intrapartum rescue ARV regimens
(currently Nevirapine, Tenofovir, Lamivudine and three hourly oral Zidovudine)
followed by enhanced infant post exposure prophylaxis reduce transmission risk.
Strand integrase inhibitors (e.g. Dolutegravir) show promise for when there is poor
viral control but are not yet policy for prevention.
Managing the infant

• Risk classification
Infant management is by risk category.
In utero transmission risk is increased if disease is advanced, there is new
infection during pregnancy or ART was started less than 12 weeks before delivery.
Intrapartum transmission risk is increased if maternal viral load is greater than
1000 copies/ml at the time of delivery.
Postpartum transmission risk is increased if maternal viral load is unsuppressed or
there is viral rebound during breastfeeding.
Infants whose mothers are on ART with suppressed viral loads through pregnancy
have low risk for transmission.
Infant testing and prophylaxis regimens are boosted when risk is not low.
Prevention of mother-to-child transmission (PMTCT) of HIV 105

• Testing
Nucleic acid amplification testing (NAAT or PCR) is necessary as trans-placental
transfer of maternal antibodies invalidates antibody testing. Before 18 months, a
positive antibody test may suggest HIV-exposure only, rather than HIV infection.
Currently most PCR testing is by high throughput devices in centralised laboratories
but point-of-care NAAT may be an option where test turn-around-times are long.
NAAT is expensive and policy needs to carefully consider its cost-benefit.
In utero transmission is detected by routine testing of all HIV-exposed infants

at birth. Detected cases must start ART urgently to limit disease progression and
reduce mortality.
Intrapartum transmission is detected by repeat testing at ten weeks and, in high-

risk exposures, again after 18 weeks.
Breastfeeding transmission is detected by age appropriate testing six weeks after

the final breastfeed.
HIV-exposed infants who are malnourished, acutely unwell or growth faltering

should be tested by age appropriate test. After 18 months, antibody testing is
recommended as almost all infants will have cleared maternal antibody. Children
who are infected with HIV should initiate ART without delay.
Prophylaxis
Infant post-exposure-prophylaxis from soon after birth reduces frequency of
intrapartum transmissions but cannot reduce in utero transmission. Maternal ART
or extended infant ARV-prophylaxis reduce breastfeeding transmission to very
low rates.
If there has been no pre-labour ART, combination ARV infant post-exposure

prophylaxis has been reported to halve the frequency of intrapartum transmission
compared with a single agent.
Low risk prophylaxis: Infants whose mothers are virally suppressed on ART close
to delivery are given daily prophylactic Nevirapine syrup only until six weeks of
age. Thereafter maternal ART makes breastfeeding safe.
High-risk prophylaxis: Infants whose mothers are virally unsuppressed close to

delivery are given combination prophylaxis for 6 weeks to reduce intrapartum
transmission. Infant combination prophylaxis is currently Zidovudine and Nevirapine.
106 Prevention of mother-to-child transmission (PMTCT) of HIV

Formula fed infants stop ARV prophylaxis at six weeks whereas breastfed infants
should continue with Nevirapine monotherapy for a minimum of twelve weeks
until the maternal viral load is suppressed.
All HIV-exposed infants should be started on prophylactic co-trimoxazole from

6 weeks until HIV infection has been excluded. HIV-exposed and infected infants
should receive routine immunisations. BCG should not be given to infants known
to be HIV-infected.
• Feeding
Replacement feeding eliminates postnatal transmission but, in low resource
settings, never breastfeeding incurs significant mortality risk (malnutrition,
pneumonia and gastroenteritis) that is greater than the risk of HIV transmission.
Current default feeding policy in South Africa is exclusive breastfeeding for the
first 6 months of life and, thereafter, the addition of complimentary food while
continuing to breastfeed to 2 years or more (previously only 12 months). Mothers
should be taught correct latching and breastfeeding techniques to prevent
cracked nipples and mastitis.
The 2017 feeding policy update normalises infant feeding in HIV context and
recommends that ART and breastfeeding be supported systemically.
In addition, while promoting exclusive breastfeeding for six months, the update’s
two guiding practice statements discourage stopping breastfeeding if it is not
exclusive or only possible for a shorter duration.
Pasteurised own mother’s milk or donor milk can be used, especially in

neonatal units.
Formula feeding should only be considered if safety criteria are met or the
mother is failing 2nd or 3rd line ART. Feeding support is especially necessary for
mothers whose home circumstances are not safe for replacement feeding.
Prevention of mother-to-child transmission (PMTCT) of HIV 107

Necrotising enterocolitis
Background and Epidemiology

Necrotising enterocolitis or NEC is the most frequent and lethal gastro-intestinal
emergency in the preterm newborn infant. It is characterised by acute inflammation
and variable damage to the intestinal tract ranging from mucosal injury to full
thickness necrosis and perforation. NEC is a significant cause of morbidity and
mortality. Its incidence is about 6 to 7% in low birth weight (less than 1500g)
infants. The overall mortality is 30 to 50% despite advancements in neonatal care.
Risk factors
Antenatal
1. Maternal hypertension.
2. Maternal drug use (cocaine).
3. Maternal infection / chorioamnionitis.
4. Placental abruption.
5. Perinatal hypoxia.
These antenatal factors may lead to circulatory instability, reduced mesenteric blood
flow and bowel ischaemia.
Postnatal
1. Prematurity.
• Decreasing gestational age is associated with increased risk of NEC.
• Immature mucosal barrier with increased permeability and bacterial
penetration into the intestinal wall.
• Immature local host defences (reduced concentrations of IgA, mucosal
enzymes and protective factors such as lactoferrin).
2. Non-human milk formula / enteral feeding.
• Human milk compared with formula is more protective due to the decrease in
foreign antigens as well as protective factors
• Slow advancement and delayed initiation of feeds are NOT associated with
reduced risk of NEC.
3. Disruption of commensal gut bacteria and presence of pathogenic bacteria.
108 Necrotising enterocolitis

4. Blood transfusions.
• Transfusion-associated NEC has been described but a causal relationship is
yet to be established.
5. Patent ductus arteriosus.
• Left to right shunting results in reduced post-ductal and systemic blood flow.
Clinical features and investigations

Systemic signs
• Respiratory distress, apnoea, lethargy, irritability, poor feeding, temperature
instability, poor perfusion.
Abdominal signs
• Abdominal distension or tenderness, abdominal wall erythema or induration,
localised abdominal mass, ascites, large gastric aspirates, blood or bile-stained
vomitus, ileus and bloody stools.
Blood studies (not specific for NEC)
• Neutropaenia and thrombocytopaenia on FBC.
• Elevated C-reactive protein / CRP.
• Metabolic acidosis and increased lactate.
• Electrolyte abnormalities.
• Deranged coagulation profile.
• Blood and CSF culture.
Stool
• Stool occult blood.
Abdominal X-ray
• The radiological hallmark sign for NEC is pneumatosis intestinalis, which appears
as bubbles of gas in the bowel wall. Other radiological features include, thickened
bowel walls and abnormal bowel gas pattern, portal or hepatic venous air and
pneumoperitoneum.
Modified Bell’s Staging Criteria

stage I: suspected NEC
stage II: definite NEC
stage III: advanced NEC.
Necrotising enterocolitis 109

Medical management
Treatment should be prompt and resuscitative measures, including ventilatory
support, employed as appropriate. Most newborn infants with Bell’s stage I or II
are managed non-operatively. These measures include discontinuation of enteral
feeds, decompression of intestinal contents with nasogastric tube, bowel rest,
antibiotic treatment and correction of electrolyte or coagulation abnormalities.
Intravenous fluid or parenteral nutrition should be given during bowel rest and
feeds reintroduced slowly.
Surgical management
Indications for surgery include pneumoperitoneum with likely bowel perforation,
clinical deterioration despite aggressive medical therapy, presence of fixed dilated
loop of bowel and evidence of peritonitis or gangrenous bowel. The goals of surgery
are to resect necrotic bowel, decompress the intestine and free intraperitoneal air
and preserve as much of the bowel length as possible.
Late Complications
The most common complications of NEC include stricture formation and short
bowel syndrome.
Preventative strategies
Human milk instead of formula is the most important strategy to reduce the risk of
NEC. If mother’s own milk is unavailable pasteurised donated human milk should be
considered in preterm, low birth weight infants. Prophylactic probiotic administration
has been shown to reduce the risk of NEC. Strict infection control measures such
as handwashing and avoidance of overcrowding within the nursery, ensures a lower
NEC risk.
110 Necrotising enterocolitis

Intraventricular Haemorrhage and
Periventricular Leucomalacia
Cerebrovascular injuries in preterm infants are the most significant long term health
burden for prematurely born infants. They can cause devastating brain injuries and
may inform the decisions that neonatal teams and families make about care levels
for extremely preterm infants.
Prior to 34 weeks of gestation the fetal brain has a rich blood supply around the
base of the lateral ventricles where primitive neural cells migrate away to form
long corticospinal neurons or supporting cells. It is known as the germinal matrix.
It is a transient vascular system suited to intrauterine life with minimal capacity to
autoregulate for changes in flow or pressure.
In the event of preterm birth before 34 weeks these vessels are very vulnerable to
the many events in preterm infant’s life which can alter cerebral blood pressure and
vessel integrity- like intubation, a patent ductus arteriosus, sudden volume expansion
from IV fluids, septicaemia and artificial ventilation. These vessels can rupture with
resultant leak of blood:
i. Into brain parenchyma – damaging the evolution of long tracts and their
supporting stroma, especially those long tracts serving the legs which travel
closest to the ventricles (remember the homunculus!).
ii. Into ventricles – causing altered CSF production and flow- hydrocephalus at worst.
These are Germinal Matrix (GM) Haemorrhages (but frequently referred to as “IVH’s”-
Intraventricular Haemorrhages- they’re the same). There is a grading system used to
describe severity which grades volumes of blood in the parenchyma and ventricles
(Grades I-IV):
• Grade I – Bleeding is confined to the GM.
• Grade II – GMH and IVH occupies less than 50 percent of the lateral ventricle volume.
• Grade III – GMH and IVH occupies more than 50 percent of the lateral ventricle
volume and is associated with acute ventricular distension.
• Grade IV – Hemorrhagic infarction in periventricular white matter ipsilateral to
large IVH (also called periventricular hemorrhagic infarction [PVHI]).
The majority of bleeds will occur within the first 5 days of life.
Intraventricular Haemorrhage and Periventricular Leucomalacia 111

Clinical signs
• Small degrees of haemorrhage are usually asymptomatic.
• Reduced spontaneous movement.
• Apnoeas.
• Occasionally a full fontanelle with large haemmorhage.
• Coma and death.
Some associated metabolic features

• A drop in haemoglobin concentration.
• Hyperglycaemia.
• Metabolic acidosis from a shock like state if severe.
Diagnosis
The above signs might give a clue to the presence of haemorrhages but usually the
discovery is made with the routine cranial ultrasounds performed in neonatal units
looking after preterm infants.
Better definition is gained with CT scanning and MRI’s but practically these tests are
difficult to perform and seldom done.
Management
There remains little to mitigate the effects of haemorrhages and infarctions once
they have occurred. Hydrocephalus is shunted if it progresses or is causing raised
intracranial pressure.
Prevention may be possible by
• Antenatal steroids.
• Being aware of the precipitants above and avoiding them, including minimal and
gentle handling of the preterm infant during all aspects of care.
It is important to maintain careful long term neurodevelopmental follow-up of all
preterm infants to discover early evidence of neurological sequelae and start therapy
if needed.
112 Intraventricular Haemorrhage and Periventricular Leucomalacia

Outcome
The outcome depends on the grade of the haemorrhage. The neurological
development after small haemorrhages (grade I and II) seems to be no worse than
for infants of comparable gestation without haemorrhages. Extensive haemorrhages
have a high mortality and neurodevelopmental morbidity risk.
Peri-ventricular leukomalacia
This is a white matter injury characterised by ischaemic necrosis of the white matter
surrounding the lateral ventricles. Like IVH it is more common the more premature
the infant and the more complications were experienced. Infection, including
antenatal infection is also a risk factor.
PVL is diagnosed by neuroimaging – typically cranial ultrasound after a few weeks of
life when cysts can be seen in the periventricular region. MRI is a better modality but
seldom available in our setting.
Long term complications include cerebral palsy (spastic diplegia especially) and
seizures. Infants should be followed up carefully and therapies such as physiotherapy
initiated early if indicated.
Intraventricular Haemorrhage and Periventricular Leucomalacia 113

Hypoxic-Ischaemic Encephalopathy
Definitions and pathophysiology

Hypoxic-ischaemic encephalopathy (HIE) is neonatal encephalopathy (NE) occurring
in the first two days of life that is caused by intrapartum hypoxia and cerebral
ischaemia. Neonatal encephalopathy is characterised by an abnormal level of
consciousness, abnormal tone and abnormal primitive reflexes. Seizures and feeding
difficulties commonly occur in moderately or severely affected infants.
There are several other causes of NE, including hypoglycaemia, electrolyte
disturbances, sepsis, drug effects, haemodynamic disturbances, brain malformations,
inborn errors of metabolism and neonatal epileptic syndromes – these causes are less
common than intrapartum hypoxia, but must be considered during the assessment.
During intrapartum fetal hypoxia there is initially fetal bradycardia, and blood flow is
shunted towards the brain. The shunting compromises the perfusion of other organs.
If the hypoxia continues, the myocardium becomes critically hypoxic, cardiac output
decreases and cerebral ischaemia follows. In term infants the basal ganglia (due to
high metabolic rate) and subcortical white matter (due to being in the “water-shed”
zone) are most affected and spastic quadriplegic or diskinetic cerebral palsy is the
expected neurological outcome in some moderate and most severe cases.
It is important to diagnose HIE timeously so that appropriate supportive care can
be given and the moderately or severely affected infants can be considered for
therapeutic hypothermia which must be started within 6 hours of life.
The following findings suggest that the intrapartum hypoxia and ischaemia were of
sufficient severity to potentially cause brain damage:
• Metabolic acidosis with base deficit ≥ 10mmol/l in umbilical arterial blood or the
infant’s arterial blood within the first hour of life or the ongoing need for assisted
ventilation 10 minutes after birth.
• Intrapartum signs or events suggesting fetal compromise or Arterial Cord pH < 7.0.
• Severe or moderate encephalopathy during the first 48 hours of life.
114 Hypoxic-Ischaemic Encephalopathy

Clinical signs and neurological assessment
The clinical signs in infants with HIE vary with time. Signs in infants with moderate
or severe HIE typically become increasingly obvious or severe during the first 48 – 72
hours of life. Seizures are often clinically silent; they may also present as rhythmic
clonic movements, but are more frequently subtle seizures including buccal-lingual
movements, abnormal eye movements, cycling movements of limbs, abnormal tonic
posturing or grimacing. Cycling, posturing and myoclonus may alternatively represent
lack of inhibition/control at a brainstem level - EEG confirmation is required to
distinguish the aetiology.
Three stages of encephalopathy have been described. (Sarnat stages).
• Stage 1: Irritability, increased tone, poor sucking but an exaggerated moro reflex.
• Stage 2: Lethargy, decreased tone and primitive reflexes. Seizures are common.
• Stage 3: Stupor or Coma, flaccid tone and seizures often clinically less apparent.
Progression through the stages, represents the continuing damage that occurs after
birth because of reperfusion injury and oxidant damage caused by an excitotoxic
cascade at a cellular level. Some infants are born with established damage and
do not manifest a typical progression. Some infants may appear normal or mildly
affected in the first hours and may later deteriorate. Since there is much overlap
between the signs within the stages. The severity and prognosis may be more reliably
assigned using a more detailed HIE score known as the Thompson HIE Score.
Hypoxic-Ischaemic Encephalopathy 115

The Thompson HIE Score
Table 1 shows the signs that are assessed by the Thompson score. The maximum
score, based on the infant’s clinical signs in the previous 24 hours, is recorded in
each category and then totalled for the day.
Table 1: The Thompson HIE score
Score/
Grade 1 2 3 Score
Sign
Limb Tone Generally Generally Flaccid
Hypertonic Hypotonic
Level of Hyper-alert, Lethargic Comatose
Consciousness staring, or Stuporose
or excessive
irritability
Visible Fits Infrequent < 3/ Frequent > 2/day
day
Posture Fisting and / or Strong distal Decerebrate
Cycling flexion
Moro Partial Absent
Grasp Poor Absent
Suck Poor Absent and/or bites
Respiration Hyperventilation Transient apnoea Apnoea Req IPPV
Fontanelle Full Tense
TOTAL
aEEG Cerebral function monitor (CFM) evaluation
The aEEG is a time-compressed, processed EEG that has prognostic value; it is useful
in diagnosing subclinical seizures and is more objective than clinical examination. It
should be applied as soon as possible where available.
Cranial ultrasound may show established damage at birth (oedema, infarction,
ischaemia or haemorrhage) and/or evolving focal or global injury.
Seizures
See chapter on seizures for the diagnosis and management of seizures.
General assessment and management

Infants with HIE should be assessed and managed with the aim of minimising further
organ damage. Document antenatal history, intrapartum events and management at
delivery. Medicolegal investigation is increasingly occurring.

Assessment and management at birth.
Avoid over-heating and hyperoxia during resuscitation. An arterial blood gas should
be obtained from the umbilical cord or from the infant within the first hour of life.
The Apgar score should be recorded at 1, 5 and 10 minutes. The infant should be
admitted to a high or intensive care area. The placenta should be examined for signs
of abnormal bleeding, or abnormal vasculature and if resources allow, it should
ideally be sent for histology.
Respiratory system
Hypoxia can cause secondary surfactant deficiency and cerebral ischaemia can cause
respiratory failure. Monitor oxygen saturation and blood gases. Aim to keep CO2 and
PaO2 in the normal range.
Cardiovascular system
Hypoxic damage to the heart may occur, autonomic instability, and anaemia may also
be present. If Hb is < 10g/dl, investigate the cause and consider blood transfusion.
Monitor blood pressure and keep it in the normal range. Avoid multiple fluid boluses
unless the infant is obviously hypovolaemic, consider inotropic support.
Fluid Balance and electrolytes
Intrinsic renal failure, SIADH and cerebral oedema commonly occur. Initially fluid
restrict to 40 ml/kg/24 hours with potassium-free Neonatalyte. Monitor urine output,
electrolytes, blood glucose and blood gases. If hypoglycaemia occurs, use 12 or 15%
glucose as an infusion solution. Hypocalcaemia and hypomagnesia should also be
anticipated and treated.
Multi-organ failure
Almost all organs can be affected by intrapartum hypoxia and ischemia. Bone
marrow failure may manifest as thrombocytopaenia and hepatic failure may cause
coagulopathy, hypoglycaemia and hypoalbuminaemia. Intestinal ischaemia increases
the risk of necrotising enterocolitis, hence feeds should be introduced slowly over the
first few days and breastmilk is preferable.
Sepsis
Chorioamnionitis is associated with intrapartum hypoxia and sepsis can be difficult
to distinguish from encephalopathy. Screen for sepsis and treat empirically with
antibiotics until investigations exclude sepsis. If the history and investigations
suggest sepsis then a lumbar puncture is indicated.
Temperature control and neuroprotective hypothermia
Avoid overheating. If moderate or severe encephalopathy and evidence of intrapartum
hypoxia is present then induced hypothermia may improve the outcome if commenced
in term or near term newborn infants as soon as possible after birth and no later than
6 hours. Cooling should be discussed with a cooling centre if available.
Hypoxic-Ischaemic Encephalopathy 117

Parental counselling
Explain the clinical condition. Do not assign a final cause to the encephalopathy if
there is any doubt. Explain the management needed and the type of investigations
that will be done. Prepare them for a potential poor outcome if investigations and
signs are suggestive.
Prognosis and follow-up

Early neurological examination, aEEG and MRI all predict outcome, but they are only
reliable when abnormalities are severe.
Mild HIE
Infants who do not progress beyond Sarnat stage 1 and who are neurologically
normal within 7 days, usually do not develop cerebral palsy. These infants usually
have a peak Thompson score of < 7 in the first six hours of life and a normal CFM.
Therapeutic hypothermia is not usually offered to these infants, because there is no
evidence of benefit in this group.
Moderate and Severe HIE
Non-cooled infants
In the absence of therapeutic hypothermia, 25 – 40% of infants who progress to
Sarnat stage 2 develop cerebral palsy and around 90% of infants who progress to
stage 3 either die or develop severe cerebral palsy.
In non-cooled infants, a peak Thompson score of < 10 during the first 6 days with
a score of 0 by day 7 predicts a normal outcome in the majority. A peak Thompson
score of 11–15 at any time or a score above 0 on day 7 predicts an abnormal
outcome in 65%. A Thompson score above 15 at any time after 1 hour of life predicts
an abnormal outcome.
Cooled infants
Therapeutic hypothermia saves approximately 1 in 7 newborn infants with moderate
or severe HIE from death and disability. Neurological state only predicts outcome
in cooled infants when it is very abnormal: A Thompson score above 15 at any time
after 1 hour of life predicts a severely abnormal outcome, even in cooled infants.
Developmental follow up
Microcephaly, cerebral palsy and developmental delay are common in infants who
survive severe HIE and multidisciplinary specialist follow-up is required for affected
infants. Neurological assessment at 18–22 corrected weeks usually detects motor
abnormalities but longer-term follow-up to school age is required to detect all
developmental and behavioural abnormalities that may occur.

Neonatal Seizures
Definition
A seizure is an abnormal synchronous electrical discharge of a group of neurons in
the CNS lasting at least 10 seconds A seizure is usually accompanied by an abnormal
level of consciousness, abnormal movement or autonomic abnormalities, but in
newborn infants these clinical manifestations are very variable and are often subtle
or absent because of the immature CNS.
Clinical Signs
Subtle manifestations include: eye deviation, eyelid fluttering and bucco-lingual
movements. Complex repetitive movements such a pedaling of arms and legs may be
seizure activity or it may represent disinhibited brainstem activity. Newborn infants
may present with clonic focal or multifocal rhythmic twitching, generalized posturing
or myoclonic twitching. Increased jitteriness may be confused with convulsions.
Unlike jitteriness, convulsions cannot be induced or stopped by handling the infant.
Causes
Intrauterine hypoxia-ischaemia causing abnormal cellular metabolism and/or
infarction is the commonest cause of neonatal seizures in the first few days of life.
Other important causes are: biochemical abnormalities (hypoglycaemia,
hypocalcaemia, hypomagnesaemia, hypernatraemia, hyponatraemia); cerebral
haemorrhage/thrombosis; brain malformations; meningitis or encephalitis; bilirubin
encephalopathy; drug withdrawal after maternal opiate abuse; and neonatal onset
epilepsy syndromes.
Rare causes include inborn errors of metabolism and vitamin-responsive seizures
(pyridoxine dependency).
History
Pertinent history includes: family history, maternal medical history; drug/alcohol use;
antenatal, labour and birth complications; and clinical course since birth.
Neonatal Seizures 119

Investigations
• Serum glucose, magnesium, calcium and sodium are the most urgent as they are
the easiest to treat.
• Lumbar puncture and blood culture if causes other than sepsis are not obvious –
antibiotics should be commenced if these investigations are done.
• Confirm seizures on EEG or amplitude intergrated EEG (continual single or dual
channel EEG monitoring with a cerebral function monitor) if available.
• Head ultrasound may be diagnostic if intracranial bleeding, structural
abnormality or ventriculitis are present.
• If the cause is not clear and/or seizures do not respond to treatment, investigate
for inborn errors of metabolism (serum lactate, ammonia, amino acids and urine
organic acids).
Treatment
• Resuscitation: Airway management to ensure adequate ventilation and establish
intravenous access to optimize hydration/perfusion.
• Treat the cause (electrolyte/glucose abnormalities or sepsis) urgently.
• Treat seizures lasting > 3 minutes, recurrent seizures, or any seizure causing
cardio-respiratory compromise.
Follow the sequence of anticonvulsant treatment below if seizures persist:
• First line
• Phenobarbitone.
• Second line
• Midazolam.
• Third line (intractable seizures)
• Pyridoxine.
• Lignocaine infusion may be used in an intensive care setting if phenytoin has
not been used (care must be taken to use lignocaine suitable for intravenous
use – the lignocaine type that is used for injecting into tissues may cause
seizures).
• Alternative agents to lignocaine include levetiracetam, lorazepam or
Clonazepam.
120 Neonatal Seizures

Blood disorders
Bleeding disorders
The haemostatic mechanism in the newborn differs from that of an older child. In
newborns there is reduced activity of clotting factors, diminished platelet function
and suboptimal defence against clot formation.
Causes of bleeding include

1. Deficiency of clotting factors / coagulopathy
• Vitamin K deficiency / lack of administration (note: Vitamin K dependent
factors II, VII, IX and X).
• Maternal drugs (phenytoin, phenobarbitone, salicylates and warfarin).
• Disseminated intravascular coagulopathy / DIC secondary to infection, shock,
hypoxia, necrotising enterocolitis (NEC), renal vein thrombosis or use of
venous catheters.
• Inherited abnormalities (haemophilia, Turner syndrome, von Willebrand
disease).
2. Platelet problems
• Decreased production.
• Increased destruction.
• Dysfunction.
3. Vascular anomalies such as arterio-venous malformations and haemangiomas.
4. Other
• liver dysfunction.
• trauma.
Diagnostic work-up of the bleeding newborn infant

On history it is important to ask about familial bleeding disorders, maternal illness
including infection and HELLP syndrome and maternal drugs. On examination
determine whether the infant looks sick or well, shocked, anaemic or dysmorphic,
examine bleeding sites and determine if there is hepatosplenomegaly and jaundice.
Further investigations require a full blood count, smear and coagulation profile (INR,
PT, PTT).
Blood disorders 121

Clinical Laboratory investigations Likely diagnosis
picture Platelets INR (PT) aPTT
Sick ↓ ↑ ↑ DIC
↓ N N Platelet consumption (infection,
NEC, renal vein thrombosis)

N N N Altered vascular integrity
(extreme prematurity, hypoxia,
acidosis)
N ↑ ↑ Liver disease, heparinisation
Well ↓ N N Immune thrombocytopaenia,
occult infection or thrombosis,
abnormal bone marrow function
N ↑ ↑ Vitamin K deficient bleeding of
the newborn
N N ↑ Haemophilia

N N N Bleeding due to trauma,
anatomical abnormalities,
dysfunctional platelet disorders
Thrombocytopaenia
Thrombocytopaenia is defined as a platelet count of less than 150 X 109/L. It is mild
if 100 to 150 X 109/L, moderate if 50 to 99 X 109/L or severe if less than 50 X 109/L.
Thrombocytopaenia is classified as early (within 72 hours of life) or late (after 72 hours
of life) and its aetiology can be determined by assessing the infant as ill or well.
Causes of thrombocytopaenia
Early onset
In well infant
• Fetal hypoxia.
• Immune-mediated: autoimmune (mother has thrombocytopaenia / ITP or SLE) or
alloimmune (mother has normal platelet count and there is passive transfer of
maternal alloantibodies directed against paternally derived platelet antigens).
122 Blood disorders

In sick or dysmorphic infant
• DIC.
• Congenital infection.
• Genetic disorders or syndromes including (Trisomy 21, thrombocytopaenia-
absent-radii (TAR) syndrome, Wiskott-Aldrich syndrome and Fanconi anaemia)
• Tumour (Kasabach-Meritt syndrome).
• Thrombosis (renal vein).
Late onset
• The most common cause is bacterial or fungal sepsis and NEC.
• Thromboses secondary to umbilical catheters.
• Drug-induced.
• Less common causes include inborn errors of metabolism and Fanconi anaemia.
Management is directed at the cause. Guidelines for platelet transfusion:
If less than 30 X 109/L
• Transfuse all newborn infants.
If 30-49 X 109/L
• Transfuse if extreme low birth weight, less than one week of age, hypotensive
requiring inotropic support or bleeding tendency (major or minor).
If 50-99 X 109/L
• Transfuse only if bleeding.
If more than 99 X 109/L
• Don’t transfuse.
Disseminated intravascular coagulopathy

Newborn infants and particularly preterm newborn infants are vulnerable to DIC
because anticoagulants (antithrombin and protein C) are normally low at this stage.
Main causes of DIC
• Sepsis.
• Perinatal hypoxia.
• Respiratory distress syndrome.
• Necrotising enterocolitis.
Clinical manifestations
• Ill looking.
• Petechiae.
• Gastrointestinal haemorrhage.
Blood disorders 123

• Oozing from puncture sites.
• Signs of infection.
Investigations
• Decreased platelet count.
• Increased INR / PTT.
• Fragmented red blood cells on blood smear.
• Decreased fibrinogen.
• Increased D-dimers.
Management is focused on treating the underlying cause and ensuring that vitamin
K has been given. Platelets, fresh frozen plasma and cryoprecipitate should be
considered.
Vitamin K deficient bleeding of the newborn

This is also known as haemorrhagic disease of the newborn. Vitamin K is essential
for the production of coagulation factors II, VII, IX and X. Deficiency of vitamin K
leads to inadequate activity of these factors resulting in bleeding. Newborn infants
have reduced vitamin K stores due to poor placental transfer and deficient content in
breast milk. This deficiency may be classified as early, classical or late.
Causes
Early (within 24 hours)
• Placental transfer of maternal drugs (anticonvulsants) inhibiting vitamin K
activity.
Classical (2nd to 7th day)
• Inadequate supply of vitamin K in breastmilk.
Late (2nd to 12th week)
• Malabsorption secondary to liver dysfunction.
• Poor intake.
Clinical manifestations
• Bleeding from the umbilicus.
• Gastrointestinal bleeding.
• Intracranial bleeding.
Investigations
• Normal platelet count.
• Prolonged PT and PTT.
124 Blood disorders

After delivery all infants should receive 1mg of intramuscular vitamin K as
prophylaxis. If bleeding a further vitamin K 1mg can be given intravenously and fresh
frozen plasma considered. Oral supplements for late onset disease are shown to be
less effective.
Thrombosis
In newborn infants, factors affecting blood flow, blood composition and vascular
endothelial integrity can all contribute to thrombus formation. Thrombosis occurs
more frequently in the neonatal period than at any other age in childhood.
Main risk factors or causes for thrombosis include indwelling vascular catheters,
polycythaemia and surgery. Inherited thrombophilias can occur but are rare.
Doppler ultrasound is usually used as the first means of ascertaining the diagnosis
and angiography is the gold standard.
Management
Asymptomatic patients are managed with close monitoring and supportive care.
Severe symptomatic cases are treated with anticoagulants and fibrinolytic agents.
Surgical thrombectomy is rarely performed in newborns.
Anaemia
• The most common cause of anaemia in newborn infants is anaemia of
prematurity, which is an exaggeration of a normal physiological anaemia. This
typically occurs between 3 to 12 weeks of age and resolves by 3 to 6 months. In
the fetus, the oxygen levels are low, erythropoietin levels high and red blood cell
production rapid. The fetal liver is the major site of erythropoietin production.
HbF is higher in preterm infants and it has a high affinity for oxygen leading
to reduced tissue oxygen delivery. After birth, oxygen saturation improves
and erythropoietin levels drop markedly. The red blood cell production and
haematocrit drop over the next few weeks, with the more premature the infant,
the lower they fall. As the Hb drops, renal erythropoietin is produced. In addition,
the following factors also contribute to anaemia:
• Reduced red cell lifespan.
• Rapid rate of growth of the preterm infant.
• Frequent blood sampling.
• Lower haemoglobin nadir as erythropoietin is produced by the preterm infant
at Hb of 7 to 9 g/dL.
Blood disorders 125

Other causes of anaemia
Blood loss
1. Obstetric – abruption placentae, placenta praevia, rupture of the cord.
2. Occult – twin-to-twin transfusion, fetomaternal bleeding, fetoplacental bleeding.
3. Postnatal – intracranial, massive cephalophaematoma, ruptured liver or spleen,
bleeding from umbilicus or gastrointestinal system.
4. Iatrogenic – blood sampling.
Haemolysis
1. Immune haemolysis – rhesus or ABO incompatibility or minor blood group
incompatibility.
2. Hereditary RBC disorders – RBC membrane defects, metabolic defects,
haemoglobinopathies.
3. Acquired haemolysis – infection, DIC, vitamin E deficiency, microangiopathic
haemolytic anaemia.
Diminished red blood cell production
1. Diamond-Blackfan syndrome.
2. Congenital leukaemia or other tumour.
3. Infections.
4. Drug-induced suppression of RBC production (eg. AZT).
History and clinical features
• Always ask about family history including anaemia, jaundice, gallstones and
splenectomy.
• Review the obstetric history for clues.
• Clinically acute blood loss may result in shock, cyanosis, poor perfusion and
acidosis, while chronic blood loss produces pallor and mild distress and irritability.
Chronic haemolysis is associated with pallor, jaundice and hepatosplenomegaly.
Investigations
There are many investigations that can be done depending on the suspicion of the
underlying cause. Below are a few selected investigations:
• Blood smear: red blood cell morphology.
• Reticulocyte count: high with chronic blood loss and haemolysis and low with
infection and production defects.
• Coombs test: positive in the presence of immune haemolysis such as blood group
incompatibility.
126 Blood disorders

Apt test: is used to differentiate maternal from fetal blood. In a well infant when
“gastrointestinal bleeding” is noted this test can be done on gastric aspirates or
stool to rule out the presence of swallowed maternal blood. 0.1 ml of sampled
blood is added to a glass tube containing alkali and the tube is gently shaken for
two minutes. The sample is considered contaminated with maternal blood if the
colour of the mixture changes from pink to brown. Fetal haemoglobin resists alkali
denaturation and remains pink while adult haemoglobin denatures and changes
to brown.
Keihauer-Betke test: this is the main diagnostic test for detecting and quantifying
fetal-maternal haemorrhage. It is considered if there is fetal demise or stillbirth,
sinusoidal fetal heart rate pattern, non-immune fetal hydrops and severe neonatal
anaemia. Red blood cells from maternal circulation are fixed to a slide with acidic
solution and adult red blood cells become ghost cells as haemoglobin A is soluble at
this pH while fetal haemoglobin remain pink as it is stable at low pHs.
Management
It is important to determine and treat the cause. Healthy asymptomatic newborn
infants will self-correct a mild anaemia provided that there are sufficient iron
reserves. Blood transfusions are considered in infants with symptomatic anaemia,
significant respiratory disease or congenital heart disease. There are different
thresholds for transfusions depending on chronological age, oxygen requirements,
illness or need for surgery. Iron supplementation in preterm infants prevents late
iron deficiency. Delayed cord clamping or cord milking after delivery of the infant
has shown to facilitate placental transfer and therefore reduced need for blood
transfusions. Erythropoeitin has limited efficacy in reducing the number of blood
transfusions and donor exposures. It may in fact be a costly intervention and has
been associated with increased risk and severity of retinopathy of prematurity if
given early.
Polycythaemia
Polycythaemia is defined as haematocrit more than 2 standard deviations above
the normal value for gestational and postnatal age. Polycythaemia in a term infant
is defined as a haematocrit of more than 65% in a peripheral venous sample or
haemoglobin more than 22 g/dL. Most infants with polycythaemia are asymptomatic
but they may have features of thrombosis. Most patients (symptomatic or
asymptomatic) can be managed with intravenous hydration alone. Partial exchange
transfusion is controversial and is associated with certain risks, such as necrotising
enterocolitis and does not improve long-term neurodevelopmental outcomes.
Blood disorders 127

Neonatal hypocalcaemia
Background
Hypocalcemia is a common metabolic problem in newborns. The majority of fetal
calcium accretion occurs during the third trimester. After abrupt placental transfer of
calcium, levels drop within 24 hours and consequently rise, reaching levels in older
children by two weeks. The measurement of total calcium may be misleading. In
states of low albumin, total calcium may be low whereas the ionized calcium may be
normal. Whole blood ionized calcium should be measured.
Definition
Dependant on birth weight and gestational age:
• > 1500g
• Total calcium < 2mmol/l
• Ionised calcium < 1.1 mmol/l
• < 1500g
• Total calcium < 1.75 mmol/l.
• Ionised calcium < 0.9mmol/l
Signs are rare if ionized calcium > 0.8- 0.9 mmol/l.
Signs
• Jitteriness.
• Neuromuscular irritability.
• High pitched cry.
• Seizures.
• Stridor/ wheezing.
• Tetany.
• Decreased mycocardial function.
Some newborn infants may be asymptomatic.
Aetiology
Hypocalcaemia is common between 12 and 72 hours of life, especially in preterm
infants and may be related to PTH immaturity. After this period calcium levels are
dependent on feeding.
128 Neonatal hypocalcaemia

A. Early hypocalcaemia
Occurs in the first 2-3 days of life and is an exaggeration of a normal physiological drop.
Causes
1. Prematurity
• 1/3 of preterm infants have low calcium levels.
2. Infant of diabetic mothers (IDM)
3. Perinatal hypoxia
4. Di George syndrome
• Hypoplastic parathyroid glands.
• 1 in 4000 newborn infants.
• 90%: deletion of 22 q.
5. Intrauterine growth restriction
6. Maternal hyperparathyrodism
7. Hypomagnesemia
8. Hypoparathyrodism
9. Maternal Vitamin D deficiency
B. Late hypocalcaemia
Occurs at the end of the first week
Causes
1. Vitamin D deficiency
2. High phosphate intake
• Associated with cows milk/cows milk formula.
• Suppresses/antagonises PTH.
3. Transfusion with citrated blood
4. Lipid infusions (TPN)
5. Acute renal failure
• High phosphate.
Diagnosis
Most are asymptomatic therefore calcium, magnesium and phosphate may need to
be monitored in certain high-risk scenarios.
Measurement should be considered in the following scenarios:
i. Infants with congenital cardiac lesions (outflow tract lesions where there is a
concern of Di George Syndrome).
Neonatal hypocalcaemia 129

ii. Signs consistent with hypocalcaemia.
iii. HIE infants being cooled.
May need to consider further investigations if severely symptomatic (i.e. fitting)
or if persistent early hypocalcemia refractory to treatment or situations of late
hypocalcaemia.
Management
Most cases of early hypocalcemia are asymptomatic and resolve.
One should treat symptomatic newborn infants or those with total serum calcium
levels < 1.8mmol or ionised calcium levels < 0.9mmol/l.
Treatment is with 10% calcium gluconate intravenously (must be given slowly as
may cause bradycardia/asystole). Dose may be repeated as needed and maintenance
calcium may be initiated. Investigate for cause if persistent and prolonged neonatal
hypocalcaemia.
Hypomagnesaemia
• Serum magnesium < 0.65mmol/l.
• Unusual on its own.
• Associated with persistent hypocalcaemia.
• Seen most commonly in IDMs with associated hypocalcaemia.
• May be seen with rare disorders of intestinal/renal tubular magnesium transport.
• Treatment is with MgSO4 intramuscularly or slowly intravenously Treatment only
required if symptomatic.
Hyponatreamia
• Serum sodium < 130mmol/l.
Common causes
1. Prematurity.
2. Inadequate sodium intake.
3. Excessive fluid intake.
4. Diuretics.
5. Renal impairment.
6. Gastric losses.
7. SIADH.
8. Congenital adrenal hyperplasia.
130 Neonatal hypocalcaemia

Treatment
1. If weight gain or absence of weight loss + hyponatreamia:
• Consider dilutional causes from fluid overload or CCF or SIADH.
• Establish and treat the underlying cause.
• Restrict total fluid intake.
2. If weight loss + hyponatraemia:
• Consider sodium losses from osmotic diuresis, diuretics, GIT or renal losses.
• Establish the cause.
• Supplement sodium either orally or intravenously.
• Replace losses and deficit.
3. Symptomatic hyponatreamia (hypotonia/apnoea/seizures) or serum sodium
< 120mmol/l must be replaced over 24 hours with hypertonic saline after
correcting for sodium deficit. Do not correct too quickly due to risk of pontine
demyelination.
Hypernatraemia
• Serum sodium > 145mmol/l.
• Associated with cerebral venous thrombosis, and intracerebral bleeds.
Common causes
1. Excessive water loss.
2. Insensible losses from the skin.
3. Gastric losses.
4. Polyuria.
5. Excessive sodium intake.
Treatment
1. Review if infant dehydrated, if there is a source of fluid loss and if there are
sodium containing infusions or medications that the infant is receiving.
2. If weight loss + hypernatraemia:
a. Water loss.
b. Increase fluid intake or reduce sodium intake appropriately.
c. Reduce insensible losses.
2. Establish the cause.
3. Chronic hypernatreamia must be corrected over 24 hours.
Do not correct too quickly due to risk of cerebral oedema.
Neonatal hypocalcaemia 131

Birth injury
Birth injury is defined as an impairment of the newborn infant’s body function
or structure due to a traumatic event that occurred at birth. Injury may occur
during labour, delivery, or after delivery, especially in newborn infants who require
resuscitation in the delivery room.
Factors that increase the risk of birth injuries may be due to the fetus (fetal size
and presentation), the mother (maternal size and the presence of pelvic anomalies),
excess force used (impacted shoulders) or the use of obstetrical instrumentation
during delivery (vacuum and forceps deliveries).
Head
Superficial: abrasions, lacerations, bruises from forceps, vacuum cup or scalp clip
lesions are generally self-limited and resolve without any intervention and often seen
on the presenting portion of the newborn’s body. Some lacerations especially with
Caesarean deliveries may require repair with sterile strips.
Caput succedaneum is an edematous swelling of the scalp above the periosteum. It
presents at birth after prolonged engagement of the fetal head in the birth canal or
after vacuum extraction. Unlike cephalohematoma, it extends across the suture lines.
Cephalhaematoma: Subperiosteal collection of blood caused by rupture of vessels
beneath the periosteum (usually over the parietal or occipital bone), which presents
as swelling that does not cross suture lines. Usually reabsorbed within 3 months.
Leave well alone! (no treatment indicated). May cause jaundice.
Subaponeurotic (subgaleal) haemorrhage: develops when blood accumulates in the
loose tissue in the space between the periosteum of the skull and the aponeurosis.
The injury occurs when the veins between the scalp and dural sinuses are sheared
or severed as a result of traction on the scalp during delivery. The potential for
massive blood loss (20 to 40 percent of a newborn infant’s blood volume) into
the subaponeurotic space contributes to the high mortality rate associated with
this lesion. This is a potentially lethal condition that needs early diagnosis, close
monitoring and aggressive management.
Skull fracture: linear or depressed. Depressed skull fractures are due to direct
pressure to the skull from forceps delivery or the mother’s pelvis. Usually
asymptomatic though occasionally associated with brain injury. Urgent neurosurgical
consultation needed.
132 Birth injury

Intracranial bleeding: Intracranial hemorrhages (ICH) as a consequence of birth
injury include subdural, subarachnoid and intraventricular hemorrhages, and
less frequently, intracerebral and intracerebellar hemorrhages. Periventricular
haemorrhage is due to hypoxia rather than trauma. Clinical features may include full
fontanelle, splayed sutures, marked drop in PCV, irritability, hypotonia with poor suck,
hypertonia, vomiting, apnoea and convulsions.
Subconjunctival haemorrage: absorbed within 10 days.
Management
• Resuscitate if needed.
• May require blood and fresh frozen plasma.
• Nurse in incubator, feed with nasogastric tube if necessary and monitor.
• Depressed fractures should be elevated surgically.
• Subdural haematoma may need to be drained surgically.
Nerve injuries
• Brachial plexus: Erb’s palsy (arm extended and pronated). Initially the arm is
flaccid and may present as an asymmetrical Moro reflex. May recover fully. Refer
for surgery if no improvement by 1 month.
• Facial nerve palsy: due to pressure by prominent maternal sacral promontory
or secondary to forceps delivery. Weakness of upper and lower face accentuated
during crying where the mouth is drawn over to the unaffected side. Spontaneous
recovery within 2 weeks is usual.
Fractures of long bones

• Clavicle: Usually mid-clavicula and often missed and causes few signs. Heals
spontaneously.
• Humerus and femur: bruising, swelling, immobility and crepitus. May follow a
difficult delivery of a breech or impacted shoulders. Natural repair occurs with
eventual return to normal shape in spite of severe displacement. Brachial plexus
injury is a common associated finding in infants with humeral fractures. Humerus
should be immobilised by strapping arm to side to reduce pain. Femur: The Pavlik
harness is generally used to treat neonatal femoral fractures (in consultation with
the orthopaedic surgeons). Analgesia may be needed.
Birth injury 133

Bruising
• Common after a difficult delivery, especially breech.
• Common in preterm infants.
• Tight cord around the neck may cause facial bruising with petechiae due to
capillary rupture.
• Bruising can result in jaundice due to breakdown of extravascular blood.
Abdomen
Rupture of the liver following a traumatic breech delivery with traction on
the abdomen
134 Birth injury

Congenital Disorders (CD)
One in every 15 live births (6.8%) in South Africa is affected by a physical or
functional congenital disorder. About 25% of physical disorders should be easily
recognizable on day one of life. CDs are responsible for 4% of deaths in children
younger than five years of age. The burden of long term disability and care is
also important.
Internal abnormalities may manifest themselves at birth or remain occult. External
abnormalities should be noted and recorded at birth.
Congenital physical disorders can be classified as a single defect alone or a
single defect (initiating factor) resulting in a sequence of problems or as multiple
abnormalities resulting from two or more separate defects.
Abnormality sequences resulting from a single defect

• Malformation sequence (abnormal tissue formation) e.g. Pierre Robin sequence
with small chin and cleft palate due to posterior positioning of the tongue
• Deformation sequence (normal tissue acted on by an external force) e.g.
oligohydramnios deformation sequence with clubbed feet, flat face and
hypoplastic chest due to being squashed in the uterus
• Disruption sequence (destruction of previously normal tissue) e.g. amniotic bands
amputating fingers and toes
Abnormalities due to multiple defects

These are usually syndromes e.g. Down syndrome and fetal alcohol syndrome with
abnormalities of the heart, face and brain.
Aetiology of congenital disorders

• Hereditary – sex-linked, dominant or non-recessive genetic disorders,
or multifactorial.
• Non- hereditary e.g. trisomy 21 due to non-disjunction in older mothers.
• Infections, e.g. CMV, Rubella, Toxoplasmosis.
• Drugs e.g. alcohol, warfarin, anticonvulsants.
• Maternal illness e.g. diabetes.
• Unknown – majority.
Congenital Disorders (CD) 135

Early diagnosis of congenital disorders
Indications for increased vigilance

• Family history of hereditary disorders.
• Excess or deficiency of amniotic fluid.
• Polyhydramnios:
• Anencephaly.
• High intestinal obstruction.
• Maternal diabetes.
• Oligohydramnios:
• Renal disease.
• Persistent fetal malposition and presentation.
• Maternal ill-health in the first trimester e.g. rubella.
• Drugs taken in the first trimester e.g. alcohol, warfarin.
• History of recurrent fetal loss.
• Increased maternal age.
Definitive prenatal diagnosis

• Ultrasound scanning is a useful tool in detecting a wide variety of abnormalities
e.g. hydrocephalus, bowel atresias, renal tract and cardiac anomalies, etc.
• Nuchal translucently or ‘triple test’ in first trimester for trisomies.
• Radiological diagnosis: bone disease, e.g. osteogenesis imperfecta and various
forms of dwarfism.
• Auscultation e.g. fetal heart block.
• Prenatal sexing for sex-linked abnormalities e.g. haemophilia.
• FISH or chromosomes on amniotic cells e.g. prediction of trisomy 21.
Today emphasis is placed on the screening and early diagnosis of fetal abnormalities
between 12 and 20 weeks gestation.
The management of the situation and the family is of the utmost importance:
• Counsel, advise and support the family.
• Discuss and explain reason for abnormality. Confirm diagnosis if possible.
• Correct abnormality where possible, usually only after delivery.
• Consider termination e.g. anencephaly.
• Discuss future pregnancies.
• Close co-operation between the paediatrician, obstetrician, ultrasonologist,
geneticist and pathologist is essential (a ‘fetal abnormality team’) to plan timing
and method of delivery and care from birth.
136 Congenital Disorders (CD)

Down Syndrome (Trisomy 21)
This is one of the most common chromosomal syndromes diagnosed in the neonatal
period. The incidence is approximately 1:800 - 1:1000 live births with the risk
increasing with increasing maternal age (1:400 at 35 years and 1:60 at 42 years).
However, due to the much larger number of births in young women, most infants
with Down syndrome are born to mothers <30years old.
Genetics
• Non-disjunction 95%.
• Translocation 4%. These could influence the risk in future pregnancies.
• Mosaicism 1%.
Clinical features most commonly found in newborn infants

• Hypotonia.
• Upslanting palpable fissures.
• Flat nasal bridge.
• Brachcephaly (short, wide head).
• Short neck.
• Protruding tongue.
• Single palmer crease.
• Clinodactyly (incurved fifth finger).
• Sandle gap.
Complications in newborn infants

• Cardiac: 40-50% have cardiac abnormalities of which AVSD and VSD are the
most common.
• GIT: Duodenal atresia (double bubble on AXR) is the most common.
• Endocrine: Hypothyroidism can be present but is more common later in childhood.
All infants with suspected Down syndrome should have

the following
• Full karyotype (unless done antenatally).
• Thyroid test (unless cord thyroid done).
• Cardiac evaluation (even if asymptomatic).
Down Syndrome (Trisomy 21) 137

• Follow-up for development, vision, hearing etc.
• Counselling for parents.
Trisomy 13 (Patau) and Trisomy 18 (Edward) are the other two syndromes with an
extra chromosome, but these infants are usually born with multiple abnormalities
and seldom survive longer than a few months.
138 Down Syndrome (Trisomy 21)

Procedures
All procedures should be done with the maximum amount of sterility that the
urgency of the procedure allows. Correct immobilization and care of all these
catheters is extremely important to prevent displacement or infection
Procedures relating to umbilical vessels are unique to neonatology.
Umbilical Vein Catheterization (UVC): The umbilical vein can remain patent for up
to 14 days after birth. It serves as a vascular access during emergency resuscitation,
exchange transfusions and central venous access. Complications of UVCs include air
embolism, infection, and thromboembolism. Non-emergency UVCs should have their
position checked with an x-ray to ensure the catheter is not too deep (in the heart)
or in the wrong place (hepatic or other smaller vessels.
Umbilical Arterial Catheterization (UAC): The umbilical artery can be used
for arterial access during the first week of life. Umbilical artery catheterization
affords direct access to the arterial blood supply and allows accurate measurement
of arterial blood pressure and serves as a source of arterial blood sampling.
Complications associated with intra-arterial catheters include thrombosis and
infection.
Peripheral Long-Line (Peripherally inserted central catheter (PICC line): This is
a form of intravenous access that can be used for a prolonged period of time (e.g.
extended antibiotic therapy, or total parenteral nutrition) or for administration of
substances that should not be done peripherally (e.g. inotropes). It is a catheter that
enters the body through the skin (percutaneously) at a peripheral site, extends
to the superior vena cava (or other large vein), and stays in place (dwells within
the veins) for days or weeks.
Endotracheal intubation: Intubation refers to placement of a tube in the airway
to support the work of breathing. This can be done through the nose or the mouth
into the trachea. The depth of the tube into the trachea is measured to ensure that
the tip of the endotracheal tube rests above the carina. The diameter of the tube
is also an important consideration to ensure maximum effectiveness. Non-urgent
intubations should be performed using sedation.
Procedures 139

Discharging infants and planning follow-up
Clear local guidelines are needed to help decide when infants can safely be
discharged home and when they should come back to a hospital or clinic for follow-
up assessment. It is best to plan discharge a few days in advance to avoid having
infants go home over the weekend. This also allows time to discuss discharge and
follow-up plans with the parents. Advanced arrangements should also be made
to book the follow-up appointments. Good follow-up allows many infants to be
discharged home earlier. There must be excellent communication between the
discharge and follow-up facilities.
Most healthy term infants with no problems and weighing 2000 g or more can be
discharged home 6 hours after vaginal delivery provided the mother has no problems.
After an uncomplicated Caesarean section, most well mothers and infants can go
home after 72 hours. These infants are usually seen on day 2 and 7 after discharge
by nurses in the district clinic or the MOU in keeping with the postnatal care plan for
mother and infant.
If all is well they can then be referred to a Well Baby Clinic in their area for
continued growth monitoring, supplementation and immunisations.
When should infants be discharged from a newborn

nursery?
• All major problems should have been resolved.
• The infant should be feeding well from breast or cup.
• The infant should be gaining weight.
• Weight should have reached 1750g or more.
• Gestational age plus duration after delivery should be 36 weeks or more.
• The mother must be managing and confident that she can look after her infant at
home. She must keep her infant in kangaroo care if discharge weight is less
than 2500 g.
• Follow-up plans must have been made.
What should be done before discharge?

• Make sure that the results of all investigations have been received.
• Check that BCG and oral polio immunisations have been given as well as any
immunisations due whilst an inpatient.
140 Discharging infants and planning follow-up

• Check that HIV-exposed infants are receiving daily nevirapine, the result of the
PCR taken at birth checked and a booking made for follow up in the community.
• Arrange any medicines which are needed to take home.
• Provide the mother with clear (preferably written) instructions for all aspects of
caring for her infant, especially feeding and any medication.
• Provide the mother with a plan of action if her infant should become sick
at home.
• Check that follow-up arrangements have been made and that the mother
understands them. Find out which clinic is most convenient for the mother.
• Enter follow-up plans into the hospital notes and the Road-to-Health booklet.
Enter these on the PMTCT letter for communication with the referral clinic.
• Check that the Road-to-Health booklet has been completed, including a list of
the infant’s problems and the infant’s HIV status.
• Write a discharge summary for the follow-up visit in the Road-to-Health
booklet. It is important that this is a thorough history so that those following the
infant up in the community or at the neurodevelopmental clinic understand the
neonatal course.
• Don’t forget to enter the date of discharge with the weight and head
circumference measurement, cranial ultrasound results, relevant blood results
such as the haemoglobin result.
• Fill in the appointment card giving the date and place of the visit.
Timing of follow-up
• All infants discharged at 1750 to 2000 g should be seen 2 days later to make sure
that the infant is feeding well, there is no weight loss, the infant’s condition is
satisfactory, and the mother is keeping the infant in kangaroo care as much as
possible until 2500 g. The visit also gives the mother and the follow-up health
provider (usually a nurse) an opportunity to meet. The next routine visit is usually
at a week after discharge.
• Infants with medical problems (e.g. respiratory, cardiac, gastrointestinal) are
usually seen by a doctor at a clinic or hospital at a date decided at discharge.
Discharging infants and planning follow-up 141

Some infants may need a follow-up appointment at a special clinic e.g.
cardiac clinic.
• Neurodevelopmental follow-up is usually planned at 20 weeks ‘corrected age’ as
this is the earliest age at which developmental abnormalities can be confidently
diagnosed. This allows for early intervention. The age corrected for preterm
delivery must be carefully calculated e.g. an infant born at 28 weeks gestation
needs to be seen at 20 weeks ‘corrected age’ (40-28=12 plus 20 weeks = 32
weeks) after the birth date. This standardises the assessment to 20 weeks after
term. If this date is not convenient, it is better to make the appointment later
rather than earlier than 20 weeks.
• Infants with moderate or severe HIE, convulsions, grade 3 or 4 IVH, severe
NEC, prolonged ventilation, meningitis, severe neonatal jaundice or who were
extremely preterm are at particular risk for neurodevelopmental impairment and
should be closely followed.
Always book the follow-up appointment for twins on the same date. Make sure that
the staff at the follow-up clinic know why the infant has come for assessment and
that the clinical summary and investigation results are available.
142 Discharging infants and planning follow-up

Counselling bereaved parents
Most deliveries result in the birth of a healthy newborn infant, but sadly newborn
infants sometimes die. This is an extremely difficult time for the parents, the family
and for the staff who have cared for the infant. It is helpful to have a structured
approach when counselling the bereaved parents.
Before speaking to the parents, read the clinical notes if you are not familiar with
the details of the infant’s clinical course. If necessary, examine the infant. Then
take the parents to a private space together with a family member of their choice if
requested. Speak first to both parents together, where possible. The sooner you can
speak to the parents the better. Involve an interpreter where necessary, rather than
using a child or other family member to interpret.
Speaking to parents
• Transparency in a face to face interaction is the only rule. Be yourself: eg ‘I am
really sorry that your infant died’.
• If the cause is apparent, state it simply and clearly. If not, tell them. Say whether
or not special investigations e.g. postmortem or placental histology or other tests
would be helpful. Then offer the option of those special investigations.
• Explain the grief process to parents. Tell them that the whole process takes a long
time and that it is normal to feel numb at first. Normal healthy reactions include
shock, anger, sadness, guilt, loss of appetite, interrupted sleep, extreme tiredness,
sense of isolation from the rest of the world (worse at night when the bereaved
patient is alone and thinking). The initial agony gradually subsides, but then there
are recurrent, intermittent episodes of acute sadness just when one ‘seems to
be getting better’. This is normal. The mother often experiences intense pain for
a longer period than the father, probably because she has felt the infant’s life
within her.
• Encourage the parents to express their feelings to each other. It is appropriate for
them to cry.
• Be sensitive to different cultural or religious beliefs.
• Address any guilt (almost inevitable). Allow parents to speak about anything that
is worrying them. Reassure the parents that the infant’s death was not their fault.
• Give the parents a formal opportunity to ask questions. Be patient and listen.
Then answer to the best of your ability. Honesty is the best policy. Allow them to
voice their anxieties and any questions arising from their experience as simply
and accurately as you can. Refer them to an informed obstetrician if necessary.
Counselling bereaved parents 143

• Encourage the parents to see and hold their infant. If there are visible congenital
abnormalities then mention these to prepare the parents, but also emphasize the
normal aspects, e.g. ‘Your little boy has a beautiful face, but his arms and legs are
not properly formed’. Be there to support the parents as they inspect their infant.
They may well have questions that occur at this time. Encourage them again to
hold and cuddle their infant, and to name him or her. Parents often want private
time with their infant: it is important to facilitate this for them.
• Encourage them to keep a memento e.g. a photograph, lock of hair, name-band.
Offer footprints and handprints. Respect cultural and /or personal beliefs that
view these practices as inappropriate.
Funeral or memorial service

Encourage these. Even if the parents have requested pauper burial, encourage a
memorial service of sorts. These provide an official time and place at which the
parents can focus on the loss of their infant and express their grief. Arrange a pauper
burial or help the parents with their choice of undertaker. Issue a death certificate.
Tell the parents where the infant will be kept in the meanwhile.
Suppression of lactation
Oral pyridoxine (Lactosec) 200 mg 8-hourly. Binding of breasts may help. Also advise
the mother to contact her doctor or clinic if she has physical problems subsequently.
Support groups
Encourage the parents to identify people with whom they can freely discuss their
loss and resultant feeling:
• Family or friends.
• Religious leaders or groups.
• Bereavement support groups where available.
• Encourage parents to inform their other children honestly about what has
happened. Encourage open.
• Discussion within their family about their loss, and expression of their feelings
about it.
144 Counselling bereaved parents

Follow up
Six weeks is a good time for a follow up visit. This allows the parents time to come
to terms with the reality of their loss. In addition, post mortem results should be
available. Allow the parents to ask questions. Ask if the mother has any physical
problems. Make sure that the health worker involved in follow-up has all the
necessary information about the mother and infant and the birth. Be alert to
dysfunctional grieving patterns:
• No expression of grief.
• Excessive anger with spouse, health workers, community.
• Severe depression.
• Psychosis.
• Refer for skilled counselling where appropriate.
Do not forget support and debriefing of staff involved in the perinatal loss
(including yourself).
Counselling bereaved parents 145

Burden of disease
In 2000, the WHO in its Millennium Declaration set a two-thirds reduction in
under-5 mortality between 1990 and 2015 as a key millennium development
goal (MDG 4). Approximately one-third of under-5 deaths (childhood deaths),
and two-thirds of under-1 deaths (infant deaths) occur during the first 28 days
of life (neonatal deaths). There are more than million newborn infants who die on
their first and only day of life. The post 2015 development agenda is now called
the Sustainable Development Goals (SDGs). South Africa did not meet the MDG 4
goals by 2015 (2015 data: U5MR 37/1000, NMR 12/1000), but have committed to
support the SDG global strategy of Every Woman, Every Child and Every Adolescent
everywhere to Survive, Thrive and Transform their communities. RSA has aligned their
National Development Plan Vision 2030 with the SDG targets and aims to reduce
U5MR to 25/1000 by 2030.
The major causes of neonatal deaths in South Africa and most other developing
countries are complications of preterm delivery, intrapartum hypoxia and infection. It
is difficult to quantify the burden of subsequent illness and disability in children who
had problems during the neonatal period but survived. Every effort must be made to
reduce both neonatal morbidity and mortality by improving all aspects of maternal
and newborn care. Interventions likely to have most impact include:
• Improved access to early booking and good antenatal care.
• Prevention of mother-to-child transmission of HIV (PMTCT).
• Screening and treatment of syphilis during pregnancy.
• Antenatal triage protocols to ensure birth at appropriate levels of care.
• Antenatal steroids for women likely to deliver before 34 weeks gestation.
• Good fetal monitoring and care in labour.
• Neonatal resuscitation training.
• Kangaroo Mother Care.
• Exclusive breastfeeding.
• Early use of CPAP for respiratory distress.
• Good aseptic technique, especially hand washing, in newborn nurseries.
• Audit of all neonatal deaths with attention to the avoidable factors.
• Continuing education and training of all maternal and neonatal health workers.
• Appropriate management protocols and medical technology.
• Accelerated national and provincial programs to introduce and roll out these key
interventions are urgently needed to address neonatal morbidity and mortality.
146 Burden of disease

References/websites
http://sustainabledevelopment.un.org/
http://www.worldwewant2015.org/
Burden of disease 147

Clinical Governance
Clinical governance is the method by which health care organisations monitor, assure
and improve the quality and safety of services. Neonatal units and allied networks,
require robust clinical governance and accountability arrangements.
Clinical Governance Frameworks establish a collective duty to ensure that specified
objectives and clinical standards are met and that all clinicians and allied health care
workers strive to improve quality and standards of care available to the mothers,
infants and their families.
Reporting and management of a “Serious Untoward

Incident” (SUI)
Definition of a “serious untoward incident” (SUI):
• An incident or accident when a patient or member of staff suffers serious injury,
major permanent harm or unexpected death (or risk of death or injury).
• A major health risk such as an outbreak of infection which has resulted in
complete closure of the neonatal unit.
• Serious damage to property e.g. though fire, natural disaster, criminal activity or
any other reason which has resulted in complete closure of the neonatal unit.
• Apparently trivial incidents which may have disproportionate ramifications,
including those which could attract media attention.
An element of judgment as to what constitutes a serious untoward incident is
inevitable, however where any doubt exists, it is safer to err on the side of caution
and report it.
Analysis of a SUI
A structured root cause analysis approach should be used.
• This may include review of case records, interviews with staff involved in the
incident or other staff with local management responsibility, interview with
parents, review of policy guidelines etc.
• Prioritize issues for analysis.
• Identify causal and contributory factors.
• Identify root causes or fundamental issues.
• Develop recommendations to strengthen support systems, prevent future
recurrence and reduce impact in there is a recurrence.
148 Clinical Governance

Writing good clinical notes
Keeping good, clear, concise and readable notes is an essential part of newborn
care. Systematic notes greatly facilitate the identification of problems, making
correct diagnoses, planning management and documenting progress. Poor care,
miscommunication, ‘lost’ problems and incorrect diagnoses are often the result of
bad note-keeping.
After taking a full history, completing a detailed examination and obtaining any
side-room investigations needed, a problem list should be constructed. Problems (e.g.
respiratory distress, hypothermia or suspected sepsis) must be identified even if the
precise diagnosis cannot yet be made.
Each problem on the problem list must now be individually addressed. Is additional
history or further examination needed? What investigations are required? What
management is planned for each problem?
Every time notes are written, record the date (possibly time) and person making
the notes. Common patient notes should be used by all health professionals –
doctors, nurses, social workers, physiotherapists. Follow-up notes must always be
problem orientated: list the active problems and then address the current findings,
investigations, results and management of each problem. Only the relevant positive
and negative facts should be recorded. No one ever reads pages and pages of
irrelevant records. Confused notes indicate confused thinking! Good notes save time
and lives. Good note-keeping is both a science and an art which must be mastered by
anyone caring for newborn infants.
With good notes it should immediately be obvious to a colleague what the problems
are and how they are being tackled. Once a problem is resolved it should be dropped
from further problem lists. At discharge from hospital, any remaining problems form
the basis for planning follow-up management.
Clinical notes form an important legal record. Many civil cases have been lost
because of poor record-keeping. The habit of keeping daily problem-orientated
records is excellent practice for passing professional examinations and managing
years of future practice. It teaches the skill of condensing a wide range of facts
into a simple, understandable clinical problem which can then be tackled logically
and effectively.
A very useful method of writing systematic notes is to turn a page on its side and
then divide it vertically into suitable wide columns for the date, problem list, clinical
findings, investigations, results and management. At a glance, the management of
Clinical Governance 149

each problem can be determined. Errors or outstanding results can be identified.
What is not wanted is a combined list of problems followed by a muddled account of
the findings, investigations, results and management. Address each problem one at a
time. The quality of care can be accurately assessed by the standard of note keeping.
Patient notes should be written with pride and read with pleasure.
How to keep out of court!

Write the patient’s name and unit number on the top of each side of paper
Time and date each entry.
Sign and write your name legibly after every entry.
Document acknowledgement of results of all investigations (including radiology).
Document all interactions including discussions with parents (and who was present).
150 Clinical Governance

Ethics
In neonatal care the mother infant dyad is unique, with the infant (unlike the fetus)
is entitled to full human rights under the Children’s Act. The mother is the primary
decision maker provided she makes it in the best interest of the child. Ethics has
allowed us to shift from a “disease orientated” to “person orientated” approach with
an increasing realization of the benefits of a shared decision-making model with an
informed parent.
THE 4 PRIMARY AND FUNDAMENTAL ETHICAL

PRINCIPLES
1. The Principle of Respect for autonomy

“Aim is to respect the individual’s right to make his or her own decisions”
This right to self-determination includes veracity (the principle of truth telling),
disclosure/informed consent, confidentiality and promise keeping. However, infants
cannot make autonomous decisions and therefore we must include the role of the
parent as the primary decision-making authority with the role of the health care
provider as a child health advocate. From birth- all children have rights as described
by the South African Bill of Rights section 28 and the Children’s Act (2005) and thus
all decisions must take these legal implications into consideration.
Recommendation
• Evidence based objective information to parents.
• Consideration of family values.
• Culturally sensitive manner.
• Allows engagement of parents as equal partners.
2. The Principle of Beneficence

“Aim is to benefit the individual and to promote their welfare”
Beneficence is the “intention of doing good” and includes promoting the best
interest of the infant - this is different to preventing harm. Data provides a relative
understanding of outcomes and expectations but individual factors determine
outcomes for each newborn infant. Therefore acting in beneficence can differ from
case to case.
Ethics 151

3. The Principle of Non-Maleficence
“ Aim is to avoid the causation of harm”
Maleficence refers to non-harming or inflicting the least harm possible to reach a
beneficial outcome and it includes short and long-term harm. It should be used with
beneficence to promote the best outcome and should include the “the possibility of
future harm to potential patients”. Corollary principle: It is wrong to waste resources
that could be used for good. The application in an NICU setting would include
withdrawal of life saving treatment and/ or institution of palliative care.
4. The Principle of justice

“Aim is to create fairness and equity between individuals and communities”
The principle of justice refers to acting out of fairness for individuals, groups,
organizations and communities. It includes four main areas: 1) Equitable and fair
allocation of health care services and resources, 2) Competing needs, 3) Rights and
obligations and 4) Potential conflicts with established legislation. The corollary
principle: Impose no unfair burdens.
Examples include:
• Providing compassionate, quality and dignified care to all newborn infants and
families regardless of parental or family values, lifestyles or social circumstances.
• Limitation of resources creates ethical conflict.
• Act within the resources allocated.
• Create equitable distribution of these resources and services within a facility.
• Advocacy for equitable allocation of resources and services at a national and
global level.
THE 5 SECONDARY ETHICAL PRINCIPLES

1. Tell the truth.
2. Keep your promise.
3. Respect confidences.
4. Use the principle of proportionality – risk benefit ratio (how much harm can be
justifiably risked to effect good.
5. The wedge principle – an attempt to avoid undesirable exceptions (going down a
slippery slope).
For every case, ask:
1. Who is making the decision?
2. Is this of benefit to the patient?
152 Ethics

3. Are we causing more harm than good?
4. Does the decision affect the equity in the unit?
CHALLENGES TO APPLYING THESE PRINCIPLES TO

DECISION MAKING IN THE NICU
• Parents and health care providers each have their own personal experience, value
system and interpretation of medical data.
• Self reflection and self awareness needed by health care providers.
• Power dynamics: difficult to have true dialogue and gain real insights into family
value systems.
• Expertise and knowledge of the most recent evidence based practices and
guidelines are needed to make recommendations.
Practical recommendations for approaching ethical issues in the NICU

1. Understand the four primary principles of ethics: autonomy, beneficence, non-
maleficence, and justice and their application in the NICU setting.
2. Survey the ethical beliefs and values of self and health care colleagues, and use
the information as a basis for discussion of ethical decision-making practices.
3. Consider staff debriefing sessions after an ethical issue is encountered.
4. Understand and respect cultural differences in ethical beliefs and values.
5. Regularly comply with professional ethical standards and best practices in the
clinical setting to guide decision-making.
6. Comply with federal and legal standards for ethical care.
7. Adopt a family-centered approach to ethical decision-making.
8. Consider regular use of an ethics committee comprised of all stakeholders
including family representatives.
Ethics 153

Some drugs commonly used in newborn infants
DRUG DOSE ROUTE FREQUENCY COMMENTS
Adrenaline (for 0.1 ml/kg of IV stat Can be given via ETT if
resuscitation) 1:10 000 no venous access but
solution higher volumes should
be considered.
Amikacin 15 mg/kg IV 24-36 hrly Nephro- and oto-toxic.
Levels should be taken
for monitoring. Second
line antibiotic
Ampicillin 50-100 mg/kg/ IV, IM, 6-12 hourly First-line antibiotic.
dose orally Treats Group B
Streptococcus
Caffeine (base) 10 mg/kg load Orally daily To prevent or treat
then 2.5-5 mg/ apnoea of prematurity.
kg/day Caffeine Citrate
requires double the
dose of caffeine base.
10% Calcium 1-2ml/kg IV Slow IV
gluconate (for diluted 1:1 infusion
symptomatic with saline
hypocalcaemia)
Cefotaxime 50 mg/kg/dose IV or IM 6-12 hourly Second line antibiotic.
Better CSF penetration
than some other
antibiotics
Ceftriaxone 50-100 mg/kg/ IV/IM daily Rarely used but useful
dose for infants in postnatal
wards as it can be
given IMI. Should not
be given IV if infant
receiving IV fluids
containing Calcium
Ferrous lactate 0.3 ml then orally daily To prevent late iron
0.6 ml after deficiency anaemia in
discharge preterm infants
154 Some drugs commonly used in newborn infants

DRUG DOSE ROUTE
FREQUENCY COMMENTS
Folic acid 0.5 mg orally
daily Consider if there has
been a large amount of
haemolysis
Furosemide 1 mg/kg orally 12-24 hrly. Beware of rapid fluid
or IV Stat for shifts and electrolyte
severe abnormalities
cardiac
failure
Gentamicin 5 mg/kg/day IV Daily (longer First line antibiotic –
in preterm) treats most community
acquired gram negative
organisms. Nephro-
and ototoxic. Levels
should be done if
prolonged use
Glucagon 0.2 mg/kg IV or IM stat For symptomatic
hypoglycaemia
especially in an infant
of a diabetic mother
Ibuprofen 10 mg/kg load IV Daily Can be used for closure
then 5 mg/kg x of a PDA especially
2 daily when the infant is very
symptomatic
Isoniazid (INH) 10 mg/kg/day orally daily Prophylaxis for the
infant when the
mother has infectious
TB
50% Magnesium 0.2 ml/kg IM stat
sulphate
Meropenem 20-40 mg/kg IV 8-12 hrly Second line antibiotic.
Good CSF penetration
Morphine 0.1 mg/kg IV infuse slowly For sedation and/or
pain control. Can be
reversed with naloxone
Multivitamin 0.3 ml–0.6 ml orally daily To prevent vitamin
drops (preterm) deficiencies in preterm
infants
Some drugs commonly used in newborn infants 155

DRUG DOSE ROUTE FREQUENCY COMMENTS
Naloxone 0.1 mg/kg IV or IM stat Should be used with
caution in resuscitation
scenarios
Nystatin drops 1 ml orally 6-hourly Oral candida
Penicillin G 100 000 u/kg/ IV 12-hourly The first choice
dose antibiotic for
symptomatic
congenital syphilis
Benzathine 50 000 u/kg IM only stat Asymptomatic
penicillin congenital syphilis
Phenobarbitone 20 mg/kg IV stat First line treatment for
slowly seizures
Probiotics 0.1-0.2 mls PO dly Helps prevent NEC
Prostaglandin E2 1/4 tablet orally hourly To keep the ductus
arteriosus open for
certain cyanotic
congenital heart
conditions
Surfactant 100-200mg of tracheal stat There are two
phospholipid main types of
surfactant (porcine
and bovine). The
porcine phospholipid
concentration is
higher which allows
greater amounts of
phospholipid to be
given
Vitamin K 1mg IM after birth To prevent
haemorrhagic disease
of the newborn.
156 Some drugs commonly used in newborn infants

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Notes on the

Notes_on_the_newborn_infant.indd 1 2018/09/05 16:00

Notes on the newborn infant

Edited by Dr Lloyd Tooke and Professor Dave Woods

ISBN (paperback): 978-0-620-81204-7

All rights reserved. This publication may not be reproduced, stored in a

Notes_on_the_newborn_infant.indd 2 2018/09/05 16:00

Introduction.. . . . ............................................. 4 Apnoea. . ....................................................... 89

Abbreviations. .............................................. 5 Heart conditions........................................ 91

The infant at birth....................................... 6 Infection...................................................... 97

Resuscitation after birth............................ 9 Prevention of mother-to-child

Notes_on_the_newborn_infant.indd 3 2018/09/05 16:00

Please contact the co-editor at Lloyd.tooke@uct.ac.za for any book orders,

This book is dedicated to our little patients and their families.

Notes_on_the_newborn_infant.indd 4 2018/09/05 16:00

Notes_on_the_newborn_infant.indd 5 2018/09/05 16:00

Assessing the infant

Give the infant to the mother

Clearing the airway

6 The infant at birth

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The infant at birth 7

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The first feed

The first bath

8 The infant at birth

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High-risk pregnancies associated with the need for

Resuscitation after birth 9

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10 Resuscitation after birth

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Confirming fetal hypoxia at birth

Helping Infants Breathe (HBB) and the golden minute

Resuscitation after birth 11

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12 Resuscitation after birth

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Steps to resuscitate a newborn infant

Good drying to stimulate breathing and preventing hypothermia

Resuscitation after birth 13

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14 Resuscitation after birth

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Resuscitation after birth 15

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Post Resuscitation Care

Delayed cord clamping

16 Resuscitation after birth

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Labour and delivery

Examination of the newborn 17

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18 Examination of the newborn

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Examination of the newborn 19

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20 Examination of the newborn

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Examination of the newborn 21

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