Coovadia BOK 382 Neonatal Paediatrics

UNIVERSITEIT VAN PRETORIA
UNIVERSITY OF PRETORIA
YUNIBESITHI YA PRETORIA
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SEVENTH EDITION
COOVADIXS
PAEDIATRICS &
CHILD HEALTH
A manual for health professiona1s
in developing countries
Edited by Robin J Green
OXFORD
UNIVERSITY PRESS
SOUTHERN AFRICA
Contents
Preface vii
Tribute to HM Coovadia and WEK Loening viii
List of contributors ix
Part 1 Evaluation, growth and development

1 History-taking, physical examination, and
evaluation of the sick child 3
2 Growth and development 17
3 Medical genetics and congenital disorders 34
Part 2 Psychosocial and community paediatrics

4 Community paediatrics, child health and survival 55
5 Social paediatrics 66
6 Developmental, psychological and behavioural
disorders 87
Part3 Neonatal paediatrics

7 Care of the newborn 103
8 Surgical care of the newborn 155
9 Feeding and nutrition of babies and children 172
Part 4 Metabolic and nutritional disorders

10 Metabolic disorders 201
11 Poisoning 212
12 Rickets and metabolic disorders 224
13 Nutritional disorders 242
Part 5 Infections
14 Principles of infection 267
15 Childhood vaccines 296
16 Systemic infections 300
17 Parasitic and fungal infections 321
18 Tuberculosis 354
19 Human Immunodeficiency Virus infection 379
Part 6 Disorders of regulation and immune control
20 Endocrine disorders 403
21 Allergic disorders 421
22 Primary immunodeficiency diseases 433
23 Connective tissue disorders 448
24 Neoplastic disorders 468
Part 7 System-based disorders

25 Disorders of the blood 485
26 Gastrointestinal disorders 510
27 Respiratory disorders 537
28 Neurological and muscular disorders 564
29 Renal and urinary tract disorders 611
30 Cardiovascular disorders 646
31 Hepatic disorders 674
Parts Miscellaneous disorders and issues

32 Paediatric surgical disorders 697
33 Orthopaedic disorders 720
34 Skin disorders 729
35 Disorders of the eye 748
36 Ear, nose and throat disorders 758
37 Oral and dental disorders 769
38 Procedures 782
39 Ethical issues in paediatrics 795
Index 801
PART 3
Neonatal paediatrics
7 Care of the newborn

Iv! Adhikari, H Mackenjee and VA Davies
8 Surgical care of the newborn

GP Hadley
9 Feeding and nutrition of babies and children

N Rollins and DP V•littenberg
7 Care of the
newborn
Jvf Adhikari, II 1\1ackenjee
and VA Dauies
Introduction abortions, stillbirths, low birth weight,

complicated deliveries, neonatal deaths,
The first 28 days of life constitute the newborn and congenital abnormalities.
period. 1he baby is very vulnerable during this • Evaluation of the current pregnancy
time when adaptations to extra-uterine life take includes: the duration of pregnancy;
place. This is seen in the respiratory and gastro- smoking and substance abuse during
intestinal systems, in the haemodynamics of the pregnancy; maternal blood group;
cardiovascular system, and in the kidneys and counselling and testing for HN ·with a plan
the liver, which have to take on the full excretory of preventative management for the baby
and metabolic functions that were shared by the if necessary; syphilis serology; maternal
placenta during intra-uterine existence. diseases such as diabetes, cardiac, and
Illnesses occurring during this period are renal; pregnancy-related illnesses such
frequently associated with problems during as hypertension, abruptio placentae, and
pregnancy, during delivery, or during neona- placenta praevia; and abnormal maternal
tal care and can therefore often be prevented. weight gain.
Furthermore, many neonatal illnesses present • Labour and birth details must include
differently to those of older children. Early iden- the duration of the stages of labour and
tification of possible illness, and appropriate and of membrane rupture, the amount and
timely intervention decrease the risk of morbid- character of liquor, drugs administered
ity and mortality. Signs of illness in the neonate to the mother during labour and
are difficult to assess. The neonate reveals illness delivery, and the need for and extent of
by a limited number of non-specific physical resuscitation of the baby.
signs. Knowledge of these and the ability to eval- • Once a high-risk pregnancy and/ or fetus
uate them are important. are identified, the progress of labour and
delivery must be carefully monitored,
and appropriate action taken. Optimal
The high-risk pregnancy management of these babies requires
There are a number of conditions during preg- good communication between those
nancy, labour, and delivery in which serious neo- caring principally for the mother and the
natal problems must be anticipated. Early iden- delivery, and those responsible for the
tification of these conditions is the first step in baby.
the prevention of neonatal illness, thus reducing • Birth asphyxia is probably the most
morbidity and mortality. common neonatal condition associated
• They include poor socio-economic with a high-risk pregnancy, and therefore
conditions, an adolescent or single mother skilled resuscitation and correct
without a stable partner, and a history of equipment and drugs are essential.
103
PART THREE Neonatal paediatrics
Factors associated with, and which identify, the

high-risk pregnancy are outlined in Table 7.1. Practice point
Approximately 15 per cent of newborn babies re-

quire more than routine care as a result of illness
after birth.
Table 7.1 Factors identifying the high-risk pregnancy

Maternal obstetric Labour and delivery Fetal
Elderly primigravida Maternal hypertension Oligohydramnios
Anaemia Maternal hypotension Polyhydramnios
Poor weight gain, obesity Maternal sedation Multiple pregnancy
Previous abruption Prolonged rupture of membranes Fetal distress (acidosis, meconium-
Previous assisted delivery Prolonged first or second stage stained liquor, abnormal FHR)
Poor obstetric history (stillbirth, Caesarean section Growth retardation
>2 abortions) Breech Post-maturity
Previous LBW Cord compression Malformations
neonatal birth Preeipitate delivery
Illness: diabetes, cardiac. renal Pr:eterm labour
Pregnancy-induced hypertension Forceps or vacuum extraction
Social
Age <16 >35 years
Socio-economic deprivation
Alcohol consumption
Smoking
Child with cere0ral palsy
HIV status
Delivery room management However early clamping may facilitate

rapid resuscitation of the asphyxiated
Initial examination, resuscitation, and newborn.
management • The aim of the physical examination at
• Newborn babies loose heat rapidly due birth is to determine whether or not the
to their large surface area to body weight baby needs to be resuscitated. 1his is
ratio. Minimise heat loss by ensuring that assessed by answering three important
the temperature of the delivery room is questions:
kept at 23-28°C, and the area is free of • Is there normal breathing (not just
draughts. The newly born baby should be gasping)?
adequately dried and wet linen removed • Is the heart rate above 100 beats per
to prevent heat loss through evaporation. minute?
Placing the dried infant against the • Is the baby centrally pink?
mother's body with direct skin-to-skin • 1he absence of normal breathing indicates
contact \vill further minimise heat loss. the need for immediate resuscitation
Very low birth weight babies (< 1 500 g) and these three factors (breathing, heart
should be covered in plastic to prevent rate and colour) should be continuously
heat loss. Care must be taken not to cover assessed at nvo-minute intervals
the baby's head or airway. Hyperthermia throughout the resuscitation.
must be avoided. • 1he Apgar score (Table 7 .2) is done at one
• In term and preterm infants, delayed minute and at five minutes. The Apgar
clamping of the cord until after the infant score should not be used as the primary
has uttered its first cry is recommended. indicator for resuscitation. The Apgar
104
score should be used to determine the Birth asphyxia and resuscitation

response to resuscitation. A persistently
low Apgar score correlates ·with later poor
Practice point
neurological outcome.
• If the baby is well at delivery, the cord
Failure to initiate spontaneous, sustained respira-
is clamped and cut. The baby is then
tion after delivery is called birth asphyxia, and can
warmly wrapped and handed to the result in severe hypoxia. Fetal hypoxia refers to
mother for the first feed. Vitamin K1 inadequate oxygenation before delivery. This may
(1 mg, intramuscularly) and prophylaxis predispose to birth asphyxia.
for neonatal ophthalmia are given and the
Hypoxia during lab.our in term babies is the most
baby is identified.
common cause of neonatal brain damage and is
the leading cause of cerebral palsy in the develop-
Table 7.2 Apgar score ing world.
-
Sigrr/score 0 1 2
Factors causing delay in the onset of respiration at
Heart rate Absent <100 >100 birth are intra-uterine hypoxia, trauma to the brain,
Respiratory Absent Slow, Good, aml drugs depressing the respiratory centre.
effort irregular crying
Muscle tone, Limp Some Active
movement flexion Labour ward management of resus-
citation
Response Nil Grimace or Cry Ideally, every birth should be attended by a health
to nasal sneeze
professional skilled in neonatal resuscitation. In
1,
order to effect rapid and efficient resuscitation, all
catheter
the necessary equipment must be available and in
Colour Pale, Body pink, All pink
working order at all times (see Figure 7.1).
central extremities
The resuscitation algorithm is shown in
cyanosis blue
Figure 7.1.
Figure 7.1 Flow diagram of the resuscitation procedure
APGAR8-10 APGARS-7 APGAR3-S APGAR0-3
HR> 120/min HR> 100/min HR 80-100/min HR< 80/min

Rregular Rregular Apnceic Apnoeic
Normal tone Moderate tone Moderate tone Floppy
-v-
No resuscitation
- vo-
Face mask HR
-v-
Mask & bag HR
-v-
Intubate ~
Stimulation ' ~ Ventilation ~ IPPV : _____u___
-v- -v- ~ 1
HR>lOO/min
Regular R Naloxone Check technical R regular
error
-v-
No resuscitation
->v -
HR 100/min
-v-
External cardiac
~
Extubate
Regular R massage
Moderate tone Check perfusion
-v-
No further
-v-
Poor perfusion
resuscitation Faint pulses
HR<SO/min
Plasma
IV sodium
bicarbonate
~80/Jmin
Dextrostix
Correct if < 25 mg
Consider:
a) ICU
b) Discontinue
resuscitation
105
PART THREE Keonatal paediatrics
The algorithm follows the assumption that the circumstances such as diaphragmatic
previous step was unsuccessful and the newborn hernia or very low birth weight babies
infant is deteriorating. • External cardiac massage is indicated
The following should be noted when follnwing for bradycardia (heart rate <60 beats per
this algorithm: minute) and is performed at a ratio of
• A pulse oximeter should be applied if three chest compressions to one breath.
available to determine peripheral arterial • Adrenaline (0.1-0.3 ml/kg IVI of 1:10 000
oxygen saturations. Pre-ductal (right solution) is indicated for a persistent
hand) saturations may take 10 minutes or bradycardia despite adequate ventilation
longer to reach 85-95 per cent. and chest compressions.
• Gentle suctioning of the airway is done • Administer dextrose for hypoglycaemia
only if indicated. Overzealous deep (2 ml/kg of 10% dextrose solution
suctioning can cause laryngospasm and intravenously).
vagal bradycardia. This also applies to • Naloxone is administered only when
the vigorous infant who is born with indicated and when the airway has
meconium stained liquor. Suctioning been secured and effective bag-mask
in attempts to remove meconium is no ventilation is achieved.
longer advocated and these infants require • Ensure normothermia throughout
only clearing of the face and mouth of resuscitation. Avoid hyperthermia.
any obvious meconium. Aspiration of
meconium into the lungs may cause a
Table 7.3 Equipment requir:ed on resuscitation trolley
severe pneumonia but this is believed to
occur before birth and is not prevented by Laryngoscope - straight blade, plastic (e.g. Penlon®),
suctioning. In the depressed baby (absent infant size, spare batteries and bulbs
or depressed respiration, decreased Magill's forc~ps - paediatric size
heart rate) '"'ith meconium stained liquor Endotracheal tubes sizes 2.5-; 3.0; and 3.5 mm
endotracheal intubation and suctioning Neonatal Ambu-bag® and mask
the airway ofresidual meconium before Suction catheters sizes 8 FG and 6 FG
commencing ventilation is recommended. Umbilical catheters sizes 8 FG and 6 FG - tb be used
• In term infants administer bag-mask only if peripheral intravenous line is not possible
ventilation with air for 30 seconds. If there Feeding tubes sizes 8 FG and 6 FG
is no response give oxygen and as soon
Adhesive tape
as the colour or saturation improves, the
Dextrostix®
oxygen concentration should be reduced
Intravenous fluids
to room air.
Neonatalyte, 5%dextrose in 0.2% saline, 4%albumen
• Preterm infants should receive 100%
oxygen initially vvith reduction to room Syringes and needles of different s.izes
air as soon as saturations over 88% are Blood culture bottles, specimen containers and tubes
achieved. Ampoul~s of 4% sodium bicaroonate
• In the majority of cases successful Adrenaline 0.1-0.3 ml/kg of a 1:10 000 solution
neonatal resuscitation can be established
with effective bag-mask ventilation alone
and "vithout the need for intubation or The infant who does not respond to
cardiac massage or drugs. resuscitation
• Positive pressure ventilation can be If the response to resuscitation is poor but the
administered during resuscitation with baby is otherwise normal in appearance, tech-
a T-piece device (Neopuff®) which nical or mechanical problems must first be
is capable of delivering pre-set peak excluded (see Table 7.4).
inspiratory pressure (PIP) and positive Whenever possible, a chest radiograph
end expiratory pressure (PEEP). must exclude severe underlying lung disease.
• Endotracheal intubation is indicated in Only after all the above conditions have been
a prolonged resuscitation or in special excluded, and drug depression is not a possible
106
contributing factor, is it appropriate to consider Consequences of severe hypoxia

discontinuing life support.
Although the clinical manifestations of perinatal
hypoxia are, in the first instance neurological,
Table 7.4 The infant who does not respond to
. less obvious effects on other organs, such as the
resuscitation lungs and the kidneys, may manifest during the
T~chnical problem Possible solution ensuing days. Hypoxia, ischaemia, hypercapnia,
-
No air entry, O~ygen tube is disconnected, and acidaemia cause tissue injury.
the endotraGfleal tube is • Irritability, disturbances of tone and
kinked or blocked with convulsions herald the onset of hypoxic
seGretions: must replac·e tube ischaemic encephalopathy (HIE).
Neonates with severe asphyxia who have
· Breath sounds Endotracheal tube is probably
not established sustained respiration
are unequal in the placed in the right main
after 20 minutes frequently develop signs
lungs bronchus: withdraw tube until of severe HIE with a poor long-term
breath sounds symmetrical outcome.
Unequal breath Pneumothorax: e0nfirmed • Persistent cyanosis in the presence
sounds with a by an urgent chest X-ray or of a metabolic acidosis suggests the
displaced apex transillumination development of persistent pulmonary
beat An intercostal drain must be hypertension of the newborn (PPHN).
inserted if the diagnosis is • Acidaemia itself affects the myocardium,
confirmed ,vi.th a consequent drop in cardiac output.
and hypotension.
Diminished .breath Misplaced endotracheal tube
• Enlarging kidneys, decrease in urine
sounds and chest in the oesophagus: replace
output, and the presence of blood or
movements _, - protein in the urine suggest renal damage.
• Metabolic disturbances such as
Care following resuscitation .
hypoglycaemia, hyperglycaemia,
Once normal breathing has been established,
hypercalcaemia, and inappropriate
ongoing care of the infant who required resusci-
antidiuretic hormone secretion may occur.
tation includes the follm\ling:
• Maintain a clear airway.
1here may also be clotting disturbances resulting
• Give oxygen when necessary. Use
in disseminated intravascular coagulation.
a saturation monitor and maintain
saturation benveen 88-92 per cent.
• Monitor the temperature (avoid The normal newborn
hyperthermia). Therapeutic hypothermia
may be indicated in the infant with severe Examination of the newborn
birth asphyxia, prolonged resuscitation
and the onset of hypoxic ischaemic Practice poiRt
encephalopathy (HIE).
• Monitor the blood sugar level. Tube feeding The aims of the first routine physical examination
is advisable until the baby is stable. of the baby are to:
• Observe for developing complications. • Assess the bc;lbys gestatiohc;ll age.
• Ensure that the baby is not acutely ill.
• Establish a bas~line of normality and identify
Practice point any abnormality of development.
The infant who becomes pink and has a good A thorough physical examination is carried out
cardiac output with IPPV, but is unable to maintain soon after birth, preferably in the presence of the
respiration after 20 minutes is suffering from mother. The examiner's hands should be warm
severe hypoxic damage, 0rug depression, meta- and disinfected, and care must be taken to avoid
bolic acidosis, and/or shock.
hypothermia during the examination. After this
107
examination, the normal baby need not be re- • Low birth weight is a birth weight ofless
examined until just before discharge, when the than 2 500 g.
weight and any unusual findings are noted. • A preterm infant is one born prior to 37
weeks' gestation (259 days).
Birth weight and gestational age • Underweight for gestational age (UGA)
The routine physical examination of the vari- or light for dates (LFD) is a birth weight
ous systems is best performed after the baby has below the 10th centile for that period of
been fed, and each system should be observed gestation.
and examined. The examination can proceed • Ovenveight for gestational age (OGA) or
systematically from the head downwards. heavy for dates (HFD) is a birth weight
It is essential that all findings should be evalu- above the 90th centile for that period of
ated in terms of normal and abnormal, and it is gestation.
also important to know and recognise the nor-
mal appearances and values for the newborn, The gestational age (GA) is estimated by deter-
which are as follows: mining the Ballard Score as illustrated in
Figure 7.2.
Figure 7.2 Assessment of gestational 9ge using the Ballard Score
Neuromuscular maturity
-1 0 1 2 3 4 5
I
Posture ~ i~: '. ~ c}: ~
Square
window r r
~ ~ ~ r
(wrist) \ >90Y I 90Y 60Y j 45Y I 3(Jr OY
,..., ,...,,
~
I"',
Arm
recoil
0) A
180) 140¥180Y 110Y- 40)
y, 90~Y
u <90)
Popliteal
angle
p...,
'---'
180Y
~160) ......--.
~
'\...
140Y
CC)
120Y
c::)
100Y
2:> 90Y ~J
Scarf
sign --R---
u -~ -& -~ -& _g
Heel
to ce
-...
d5 £' ~~
CT3 c:9 ~--- C3"
ear
Maturity rating
score weeks
Physical maturity
-10 20
-1 0 1 2 3 4 5
-5 22
smooth SLperficial parchment
sticky gelatinous pink, peeling&/
cracking
deep
leathery 0 24
friable red, pale areas cracked
Skin transparent translucent
visible rash, rare veins crac_kling
veins few veins wrinkled
veins 5 26
bald mostly
Lanugo none sparse abudant thinning areas bald 10 28
heel -- toe >50mm anterior creases 15 30

Plantar 40-60mm:-1 no
faint
transverse creases over
red marks ant.2/3
surface <40mm:-2 crease crease only entire sole
20· 32
stippled raised full areola
imper- barely flat areola areola areola 5--10mm 25 34
Breast ceptible perceptible no bud 1-2mm bud 3-4mmbud bud
lids fused lids open sl. curved well-curved formed

thick
30 36
pinna flat pinna, &firm
Eye/Ear loosely:-1 pinna soft
soft but instant cartilage
tightly:-2 stays fo:ded slow recoil ear stiff
ready recoil recoil 35 38
scrotum scrotum testes in testes testes testes
Genitals flat, empty, upper canal descending
down pendulous 40 40
male smooth faint rugae rare rugae few rugae good deep rugae
rugae
clitoris prominent prominent majora& majora majora 45 42 Sourc~: JL Ballard et al. Pediatrics
Genitals prominent clltoris clitoris minora large cover
female labia flat small enlarging equally minora clitoris&
50 44 1991; 119:417-423. Copyright
labia minora minora prominent small minora
American Academy ofPediatrics.
108
1he appropriate weight for the gestational age Transient pustular melanosis is an eruption
that is determined in this way is obtained from that may be present at birth as small non-ery-
a Lubchenco chart, which gives standards for thematous vesiculopustules, which rapidly scale
size at birth. All those between the 10th and 90th and form hyperpigmented macules that fade in a
percentile are appropriate-for-gestational-age few weeks. These are sterile lesions and antibiot-
(AGA) babies. ics are not indicated.
Head
Practice point
Moulding of the head depends on the type of
• Average weight: mal~ 3 4-00 g, female 3 000 g delivery, leading to overlapping of the sutures
• Average length: 48 cm (range 46 to 52 cm) of the parietal, frontal, and occipital bones, and
• Average head circumferenc_ e: 35 cm ('range corrects itself. Asymmetrical moulding of the
33 to 37 cm) face occurs as a result of the intrauterine position
• Respiratory rate: 40 to 60/min of the baby during pregnancy.
• Heart rate: average 140-beats/tnin (range 120
Caput succedaneum is a soft, non-fluctuant
to 1€SQ/min).
swelling due to oedema of the presenting part of
the scalp caused by pressure during delivery.
1he full-term infant is fairly active, moves all
four limbs, has a good tone, and a pink colour. Mouth, tongue, palate, and teeth
The typical term infant's posture is that of the Occasionally babies are born \vith one or two
fetal position with flexion at hips, knees and teeth, which should be removed. Epstein's pearls
elbows. For additional information on the details are small white nodules on the hard palate on
of examination, see Chapter I, History-taking, either side of the midline. Retention cysts may
physical examination, and evaluation of the sick occur on the gum margins. A partial cleft of the
child. Only those aspects unique to the newborn posterior soft palate has to be excluded by palpa-
are dealt with here. tion.
Skin of the normal newborn Eyes

The skin is covered -with a thick, white substance,
Redness of the conjunctiva and oedema of the
vernix caseosa. It is not necessary to wipe or rub
eyelids due to chemical irritation are common
this off.
and subconjunctival haemorrhages may be seen
Stork bites, or telangiectatic naevi (fine, spider-
follm'\ing a difficult delivery.
like naevi), may be present over the nape of the
neck, the glabella, and the upper eyelids. They
Neurological system
are deep pink and flat, blanch easily and disap-
pear during the first years of life. A number of primitive reflexes can be elicited in
The mongolian spot is an irregular area of blue- the newborn and young infant (see Table 7.5).
grey slate pigmentation distributed over the sacral Abnormal responses include an absent or
and gluteal regions. It may, however, be so exten- asymmetric response, or persistence of a reflex
sive that it involves much of the infant's back. after the age at which it usually disappears.
Milia are white pinpoint spots over the bridge The neurological examination is similar to that
of the nose, chin, or cheeks and are epithelial- of older infants, but the plantar reflex always
lined cystic inclusions of sweat gland ducts. shows a Babinski (upgoing) response. The vision
Erythema toxicum are small macules on a red of a newborn infant is assessed by its ability to
base starting on the second or third day of life follow a face or a bright light, or by the opticoki-
and disappearing within a few days. The cause is netic response. Response to a noise by a startle
unknown. reaction suggests hearing ability.
109
-
Table.7.5 Neonatal primitive reflexes
-- - - - ·-
Ref!eX, Method of eliciting Re~p~,mse Disappearance
Grasp reflex Place finger in either the palm of Reflex flexion and grasping of the 4- 6 months of age ·
the hand from the ulnar side or the finger fr0m 26 weeks' gest-ational
sole of the foot age
Rooting reflex Stroke the cheek with the finger or Turning of the infant's head to the 4-6 months of age
mother strokes with the nipple side of the stimulus and opening
II
1,
of the mouth for insertion of the
II nipple. It develops from 28 weeks'
gestational age -·
Stepping/placing Stimalate the dorsum of the foot by The foot is raise_d and placeo on 4-6 months of age
reflexes bringing it in contact with the edge the table or couch
of a table or couch
Moro reflex Sudden supported extension Extension and abduction of 4-6 months of age
r:novemer::it of the head in relation to the arms and legs, followed by
the position of the spine adduction of the arms and flexion
of tl:le elbows and fingers across
the chest It develops from
..
28 weeks' gestational age
Sucking reflex Place baby's hand in the mouth or Strong sucking response in the Becomes a
offer mother's breast term infant, rather weaker in the voluntary response
preterm. Becomes well coordinated
11
with swallowing. It develops from
34 to 35 weeks' gestational age
Asymmetrical Infant spine and head should be Extensor tone occurs in the arm .on 7 months of age
tonic neck .reflex aligned. Tlie head is turned slowly the side to which the head is turned
to one· side and flexor tone in the opi;,osite
arm. Reflex appears by 35 weeks
Routine care of the healthy or spraying with a disinfectant before

handling any baby is very important.
term newborn • Urine should be passed within the first 24
hours and stool within 36 hours of birth.
Following delivery room procedures, the baby The latter is in the form of meconium for
should be with the mother: two to three days and is followed by a
• To encourage breastfeeding, and to transitional stool, which is green to black
·with milk curds for several days; after
promote her observation and caring skills
one week the normal non-offensive soft,
in keeping baby warm, dry and clean.
yellow, acid stools appear.
• The cord must be kept clean and dry
• The normal infant loses up to 10 per
by repeated application of an alcohol
cent of body weight in the first few
solution. Attention to drying the skin folds days but usually regains this within 1O
is essential, as moisture readily permits days. The rate of weight gain thereafter
monilial infection. Clothing should be is in the range of 200-300 g per week.
changed daily, with meticulous washing, Breastfeeding difficulties must be
rinsing, and drying of garments. anticipated and managed with expertise
• The biggest danger of infection arises to foster the mother's confidence and
from the contaminated hands of hospital success (see Chapter 9, Feeding and
staff members, so routine hand-washing nutrition of babies and children).
110
7 Care ofthe newborn
Routine care of the healthy low birth

Rractice poiAt
weight (LBW) baby
In highly developed countries no more than Healthy newl:w~n bab.ies should not be kept in
hospital er sep,arated fr@m tlileif rnott-,ers.
seven per cent of births fall into this category,
whereas in some underprivileged communities
more than 30 per cent of infants weigh less than 1he management of the healthy preterm baby is
2 500 g at birth. The majority of infants in the relatively simple, requiring very basic facilities
former group are truly preterm, whereas intra- and careful nursing.
uterine grmvth restriction makes a considerable • Minimal handling is important, especially
contribution to the latter. LBW constitutes up to if ill. Minor procedures such as a nappy
change may result in a sharp drop in
74 per cent of perinatal mortality, and the risk
oxygen saturation. Traumatic procedures
of dying during the first year of life is 20 times
should be kept to a minimum and in
greater in LBW than in appropriately grown
the event of apnoea, bradycardia, or
infants. They also tend to grow up to be malnour-
hypoxaemia occurring the procedure
ished, develop into short-statured adults, and in should be terminated.
turn produce LBW infants. • Meticulous monitoring of the respiration
Major factors contributing to LBW infants are: rate, heart rate, colour, peripheral
• Poor socio-economic circumstances perfusion, and temperature with timely
• Low maternal weight intervention in the case of abnormalities
• Adolescent pregnancy improves the overall prognosis for the
• Short birth intervals small baby. 1he blood sugar level should
• Physical exertion late into pregnancy be monitored regularly until feeding is
• Low-grade amniotic fluid infection. This established and maintained in the range
is more prevalent in undernourished 2- 7.5 mmol/1.
mothers and those who practise • Maintenance of a normal body temperature
unprotected coitus (without condom) is the first and most important step in the
during pregnancy. management. Day and night skin-to-skin
contact with the mother has been shmvn
In a large referral hospital one must anticipate to be very effective both in the prevention
12-20 per cent of births to be LBW. and management of hypothermia. More
sophisticated equipment can be used
where available.
• Early feeding, either orally or by gavage, is
Practice J}Oint the next stage of management. Frequent
small feeds or continuous nasogastric drip
The prevalence of low-birth weight (LBW) infants is feeds are essential to avoid complications,
a reflection of the health status of the commonity. starting with a total of 60 ml/kg/ day and
increasing by 25 ml daily to 200 ml/kg/ day
if tolerated.
Ideally, all LBW infants should be assessed for • Intravenous feeding is advisable for
special care. Some need intensive care, but these the sick preterm baby, giving 60 ml/
facilities are rarely freely available in developing kg/day on day one, and gradually
countries. Apart from efficient primary health increasing the volume to 150 ml/kg/
care, emphasis should be placed on meticulous day. Factors that increase insensible
routine nursing care, which in itself achieves a water loss, such as tachypnoea and high
great deal for these special infants. Sophisticated ambient temperature (overhead warmer,
monitoring and life-support systems make a phototherapy), need to be taken into
negligible contribution to overall survival, while account in calculating fluid requirements.
making crippling demands on personnel and the • 1he signs of respiratory distress must
budget. be noted and oxygen administered for
111
cyanosis. The airway must be kept clear at determined individually, dep~nding to

all times by correct positioning. Apnoeic some extent on available health services
episodes must be recognised early for and conditions at the unit of delivery.
appropriate management. Earlier discharge is possible with kangaroo
• Particular attention must be paid to mother care.
measures that prevent infection. Staff + The mother has been counselled on
hand hygiene is crucial if cross-infection general care and hygiene, particularly \vith
and hospital-acquired infection are to regard to washing hands, signs of illness,
be controlled. Regular hand-washing breast-feeding, preparation of the oral
before and after handling each baby, and rehydration fluid, and fertility control.
spraying the hands with a 70 per cent • The mother has been familiarised with
alcohol solution are essential. the most convenient primary health care
• EYen mild degrees of jaundice must facility for continued maternal and child
receive consideration ifbilirubin care with the Road-to-Health-Card.
encephalopathy is to be avoided. • Routine BCG and polio immunisation
• Haemoglobin levels must be checked have been given.
serially at weekly intervals, starting on the • Supplements should include
first day. multivitamins, iron, folate and vitamin D.
These aspects must receive particular emphasis

Once the clinical condition of the infant is stabi-
in mothers who are at risk, such as:
lised, and life-threatening complications of the
• Adolescents
first few days of life adequately dealt with, the
• Those with a poor obstetric history
preterm baby is observed, while taking continued
+ Those who have received counselling
precautions against infection. Time and patience
regarding antiretroviral therapy.
are required to support the mother in establish-
ing breastfeeding. Monitoring weight gain will
Wherever possible, home visits should be
assist in evaluating the baby's wellbeing. The
arranged. The mother and preterm baby must
environmental temperature can be decreased
be seen by an experienced health worker ,vithin
gradually, bearing in mind that failure to gain
a week of discharge. The Department of Health
weight is often an early sign of undue heat loss.
suggests all babies should be seen on ·day three
Promoting mother and baby contact to establish
post discharge.
bonding is an important aspect of preterm care.
The multiplicity of procedures and apparatus in
'Kangaroo mother care' of low birth
the nursery are often intimidating for the mother,
who is at risk of withdra\ving from involvement weight babies
,vith her baby. 'Kangaroo mother care' or 'skin-to-skin contact'
The process of bonding must be fostered care- is a simple, cost-effective method of keeping
fully, as failure may result in maternal rejection clinically stable, small preterm infants warm.
and reluctance to breastfeed and cuddle the The mother places her baby on her chest under
baby. Lack of maternal cooperation and interest protective clothing. This technique reduces cry-
in the baby are features suggestive of rejection. ing and promotes early breastfeeding by early
Any indication of this must be handled sensi- initiation of non-nutritive sucking. Kangaroo
tively. Where facilities exist, professional coun- mother care units are being established world-
selling must be called for. wide to provide supervised environments where
lhe baby is ready for discharge when: mothers can be supported in caring for their low
• Breast feeding has been fully established. birth weight babies before they are ready to be
• Temperature is maintained. discharged home. Such babies tend to breastfeed
• Weight gain of about one per cent of for longer periods, gain weight more readily, and
body mass per day is occurring. The are ready to leave the hospital sooner. Of course,
suitable weight for discharge should be fathers may also give their babies kangaroo care.
112
The preterm infant

Practice point
The clinical features consist of immaturity of
On discharge of normal, low birth external appearance and of neurological devel-
weight or very low birth weight babies opment, well described in the criteria for the
mother should be informed about: assessment of the gestational age (see Figure 7.2).
• Signs of illness - temperature change, The markedly preterm infant shows very obvious
behaviour change, failure to take two feeds clinical features. It is important, however, to con-
consecutively, irregular breathing, rapid sider intra-uterine grmvth restriction and wast-
breathing, convulsions, vomiting and diar- ing, which might make a greater contribution
rhoea. (IMCI: The sick young infant from birth to the baby's low birth weight than prematurity
to 2 months of age} alone. A rapid but superficial impression can be
• lmmunisat1on programme obtained by scrutinising the breast, nipple devel-
• Regular clinic visits with the RTHC - note
weight gain and development, feeding, opment, the plantar creases, and muscle tone.
report intercurrent illness
Risks and complications of prematurity
Mother should be informed about her In the appropriate-for-gestational-age (AGA)
health: preterm neonate, most organs are functionally
• Contraception and child spacing and metabolically immature. Risks and compli-
• Hand washing
• Diet cations arise because of immaturity and because
• Encouraged to ask any questions. of small body size (see Table 7.7(a)). Addition-
ally, there may be a reason for preterm labour
such as maternal infection, which predisposes
the baby to pneumonia at birth.
The high-risk neonate
Table 7.7(a) Risks of immaturity
Morbidity and mortality are appreciably reduced
by identifying risk factors both during pregnancy System Risks of immaturity
and after birth. All babies born from a high-risk
pregnancy or labour, as well as those outlined Respiratory Periodic pattern of respiration
centre or apnoeic episodes (i.e. 20
in Table 7.6, must be considered high-risk neo- immaturity
nates. The next step is careful observation during seconds or more}
the first few days or weeks and careful follow-up More sensitive to effects of
for long-term complications. hypoxia and maternal sedation
Lung Surfactant deiiciency and hyaline
immaturity membrane disease
Table 7.6 Factors identifying the neonate at risk
High risk Medium risk Liver Earlier development of neonatal

- - immaturity jaundice .and a tendency to
Pre-term or post-mature Birth weight bleed due to lack of vitamin
Small for gestational age 1.5-2.49 kg K-dependent coagulation factors
Large for gestational age Clinically stable (II, VII, IX, and X)
Birth weight after resuscitation
<1.5 kg or >4 kg Birth trauma Gastrointestinal Before 35 weeks of gestation
Neurological depression Abnormal CNS signs and feeding sucking and swallowing not
after resuscitation Cold exposure yet well coordinated leading to
Metabolic problems after low blood sugar significant feeding difficulties,
birth Jaundice with risk of regurgitation and
Any congenital Anaemia aspiration. Stomach emptying
abnormality Multiple births and gut motility is slower
113
-
Abdominal distension due of relatively poor iron and folate
to a retatively atonic bowel stores. Vitamin E deficiency may
aggravates feeding difficulties. contribute to the Elevelopment of
ii;1 Immaturity of digestive enzymes anae~ia in a preterm baby
affects feed tolerance in some
babies
- - The underweight-for-gestational-age
.Rena! A low glomeruJar 'filtration rate (UGA) baby
immaturity {GFR) and poor tubular function These babies can be classified as symmetrically
le.ad to the inabjlity to excrete growth-restricted or asymmetrically wasted. The
a water and so'lute l0ad. The former implies an early intra-uterine insult or
GFR is about 0,45 ml/min at other constitutional factors resulting in a small
28 weeks and 5 m1/min at baby with weight, length, and head circumfer-
term. During the first week the ence below the 10th centile.
plasma ereatinine levels are a Asymmetrical wasting is due to utero-placen-
reflection of the mother's levels. tal factors in the later stages of pregnancy; these
The preterm infant suffers cause failure to gain weight or even loss of weight
higM sodium losses; under 33
of the fetal trunk and limbs, while length and
head circumference are relatively spared.
weeks the fractional excreti0A
of sodium is 3 to 5 per cent
11
11 and ~etween 33 and 37 weeks Practice point
1 per cent. Th·e maxim1:1m urine
osmolality is 50Cf-700 mmo.f/1. Common causes of symmetrical intra-uterine
ii
11
Therefore oedema is frequently growth restriction (IUGR) are low maternal
seen in the preterm infant weight, genetic abnormalities, chromosomal
defects, chronic intra-uterine infection, and tera-
Neurological lntraventricular haemorrhage togenic agents such as alcohol.
immaturity is a constant hazard due to the
Asymmetrical wasting may be caused by preg-
rich network of unsupported
nancy-induced hypertension, placental infarction,
capillaries in the germinal partial separation of the placenta, poor nutrition
matrix. Fetal hyQ0xia, birth of the mother, severe physical exertion late into
a~phyxia, fluctuations in the pregnancy, and smoking during pregnancy.
blooa Qressure, and an unstable
metabolic status render these The essential clinical feature common to all these
delrcate vessels prone to babies is a birth weight under the 10th centile
rupture with ensuing 1:>eri- or for gestational age. The symmetrically gmwth-
intraventricular haemorrhage restricted infant may show features of the caus-
- -
ative disease such as a chromosomal defect or
Jmmatu're Shorter duration of last trimester
immunity intra-uterine infection. A high index of suspicion
means that less maternal
should be maintained for the features of the fetal
antibo.dy protection has been
alcohol syndrome (see Chapter 3, Medical genet-
transfer-red into baby. General
ics and birth defects).
immaturity increases risk of
Asymmetric wasting of late onset causes loss of
Gram-negative infections
,• -
subcutaneous fat and minimal or absent vernix
Bone marrow Anaemia is a common caseosa. The facial appearance is one of alertness,
immaturity problem due to exaggerated with a wizened expression. The skin is thickened
I phy,si0l0gical factors and and desquamating with a parchment-like qual-
sluggish erythropoietic ity. The muscle tone is generally increased. As the
response. Late anaemia OGcurs
liquor may well have been meconium-stained for
some considerable period, the skin and umbili-
with rapid growtb and depletion
cal cord may have a dirty green discoloration.
114
Risks and complications. Many problems are tal retardation in term UGA infants, and they are
similar to those experienced by preterm babies at increased risk of manifesting minor neuro-
and are related to the risks of small body size and logical disorders. On the other hand, the preterm
low stores (see Table 7.7b). UGA infant appears to have a higher incidence of
major handicap than the term UGA and the AGA
Table 7.7(b) Risks of small boc;ly size preterm infant.
Physiological Risks of small body size
Management. The mother \vith the growth-
paramej~r
restricted fetus must be regarded as having a
Temperature ~ Small stores of glycoge·n and high-risk pregnancy, which calls for the best
control fat predispose preter-m and attention available. Early delivery should be con-
underweight-for-gestatiorial-age sidered if there is continued evidence of fetal
(UGA) babies to poor temperature stress. During labour, careful monitoring of the
regulation. In addition, th-e large fetal heart will give an indication of the need for
surface area, poor muscle tone, oxygen and glucose infusion to the mother. Early
~nd inability to shiv.er compound intervention is called for if there is evidence of
the diffic;tJlty of temperature acute fetal distress.
control. Maintenance of a neutral During the delivery of a growth-restricted baby,
thermal environment is essential one must anticipate and prevent meconium aspi-
Blood sugar Hypoglyc;aemia occurs with gre_ater
ration, and institute early management.
control The neonate with symmetrical growth restric-
frequency in preterm babie$ due to
tion requires investigation for specific causative
uate stores of glycogen
inadeq_
factors. Feeding is not so problematic in UGA
babies - they are usually wide awake and take
As the UGA infant may have been exposed to
feeds avidly. Early feeding is essential. Every
chronic oxygen and nutritional deprivation in
effort must be made to ensure adequate nutri-
utero, the acute stress of the birth process is not
tion after discharge by making the mother aware
well tolerated. 1he infant is therefore additionally
of the deficit which must be made up and the
predisposed to a number of clinical problems.
risks to which the baby is predisposed.
• Fetal hypoxia is the most important, and
In other respects, the management corre-
can be detected by monitoring the fetal
sponds to that of the preterm baby.
heart rate during labour and delivery.
• There is a great risk of meconium
aspiration both in utero and at birth Practice point
in the term grm'Vth-restricted baby,
and pneumonia in the preterm baby. Careful observati0ns of the grnwth restricte€1
Hyaline membrane disease, in contrast, is infant must detect respirat0r,y distreS's_, hypogly-
relatively uncommon and less severe. caemia by frequent blood sugar monitoring, pre-
• Infections occur more readily in the UGA vention of hypothermia and signs of •infe.cti0n.
baby due to suppressed immunity.
• Chronic hypoxia stimulates erythropoietin
production, resulting in polycythaemia The very-low-birth-weight {VLBW)
and its complications. baby
Prognosis. The asymmetrically wasted baby is Babies weighing less than 1.5 kg at birth repre-
likely to do fairly well if adequately fed postna- sent a small percentage of live births (1-2 per
tally. Many UGA infants are not growth restricted cent), but they contribute more than 50 per cent
but only wasted. 1herefore intra-uterine growth to the overall neonatal mortality. Survival rate
restriction (IUGR) is not the same as UGA. The ¼rith tertiary care is about 80 per cent. However,
symmetrically small baby (IUGR) appears to the cost of intensive and high care of this group
have been programmed early in utero and in of babies is enormous. Furthermore, the social
general remains small after birth. There is a background is an important consideration for
slightly increased risk of cerebral palsy and men- the after-care. Many of these VLBW babies are
115
PART TH REE Neonatal paediatrics
born to adolescent or other disadvantaged moth- In the long term there are several problems. Gen-
ers. Often the pregnancy is unplanned and the eral health in the first year of life is likely to be
babies are frequently rejected. The VLBW baby affected by frequent infections, particularly of
therefore places a considerable financial and the respiratory tract. The mortality rate is high
social burden on the community in general. due to brain damage or acute respiratory ill-
ness. The sudden infant death syndrome (SIDS)
Prevention. Education and fertility control in occurs more often in the VLBW than in the full
the teenager must receive serious consideration. term. Neonatal problems cause a delay in regain-
Adequate antenatal care is essential so that early ing the birth weight for two to three weeks, but
detection and appropriate management of pre- following recovery, growth should proceed at the
term labour is effected to delay delivery where normal rate. Those who are appropriate for ges-
feasible. Women ·with threatened labour before tational age can be expected to grow at the same
32 weeks of gestation need early transfer, so that velocity as a full-term infant of the same concep-
optimal conditions for delivery and efficient tual age. Poor growth occurs in the UGA infant,
after-care can be provided. and those with prolonged undernutrition in the
early weeks of life. Visual, auditory, speech, and
Immediate problems in the neonatal other neurological deficits must be expected.
period Before discharge these vulnerable babies have
As the homeostatic balance of the VLBW baby is to be assessed carefully for neurological deficits,
even more precarious than the larger LBW baby, screened for hearing problems and for retinopa-
meticulous attention is essential. Prompt, skilled thy of prematurity.
resuscitation is the single most important deter- Retinopathy of prematurity (retrolental fibro-
minant of a favourable outcome. plasia) is emerging as one of the leading causes of
+ Temperature regulation is critical because childhood blindness in middle-income develop-
the thermo-neutral range in the smaller ing countries. It is an iatrogenic disease unknown
baby is narrow, ·with a marked tendency to in undeveloped countries and is caused by the
hypothermia. hyperoxygenation of small preterm babies. Oxy-
• Hypoxia and hyperoxia readily occur gen therapy in preterm babies should ideally be
in recurrent and prolonged episodes, monitored by pulse oximetry and arterial oxygen
as tissue levels of oxygen fluctuate saturation should be between 88-92 per cent.
widely. Poor respiratory excursion and ·where oximetry is not available, the least amount
apnoea occur spontaneously and are of oxygen required to keep the baby's tongue
often induced by handling. The most pink must be used with attempts to reduce the
serious effect of hypoxia is on the delicate oxygen concentration every few hours. Imma-
unsupported vessels of the periventricular ture babies requiring prolonged oxygen therapy
area, resulting in haemorrhage. should be transferred to specialised units where
Hyperoxia occurs as a result of over- monitoring is available. All babies of birth weight
zealous treatment of apnoeic episodes or less than 1250 g and gestational age of 30 weeks
respiratory distress, risking injury to the or less require examination by an ophthalmolo-
retina (retinopathy) and lungs (broncho- gist six weeks postnatally. Treatment \Vith cryo-
pulmonary dysplasia). therapy or laser in the early stages of the disease
+ The incidence of hypoglycaemia is higher, prevents blindness.
particularly if feeding is delayed.
• Fluid and electrolyte balance may be The overweight-for-gestational-age
difficult to achieve. The hazards of (OGA) baby
fluid restriction in these babies are well The best-known association of OGA babies with
established. Hyponatraemia, acidosis, a birth weight above the 90th centile for gesta-
hypoglycaemia, and hyperbilirubinaemia tional age (4.0 kg at term) is maternal diabetes.
are very real hazards unless close attention Large mothers and those with excessive weight
is paid to early feeding. Monitoring for gain during pregnancy can expect to have OGA
clinical signs of dehydration and for babies. The Beckwith syndrome is a much rarer
biochemical disturbances is essential to cause and has associated macroglossia, macro-
maintain homeostasis. somia, and small genitalia.
116
7 Care of the ne,vborn
The OGA infant is at risk of peripheral and Apnoea May be the first sign of a convulsion,
intracranial birth trauma. As shoulder dystocia severe respiratory disease,
is a further possibility, Caesarean section is often
hypoglycaemia or hypothermia
indicated.
Management of the OGA baby delivered vagi- Lethargy Maternal sedation and analgesia,
nally includes a careful search for cerebral birth hypoglycaemia, asphyxia, infection
trauma, fractured clavicle, or brachial plexus Failure to Important sign oJ serious disease,
injury. lhere is a need to monitor the blood feed particularly if feeding well before.
sugar level of the infant for the first 36 hours, and Meningitis, other serious infections
maternal diabetes must be excluded. and m0niliasis, metabolic disease. If
1here appears to be an increased risk of mental poor feeding from birth in term infant
subnormality in this group, which is thought to consider asphyxia
be related to cerebral complications. Delivery by
Fever Dehydration or, unusually, due to
Caesarean section and careful monitoring of the
blood sugar level after birth to prevent hypogly- serious infection - note herpes
caemia decreases this risk substantially. Hypothermia Exposure, severe infection, CNS and
circulatory disorders
Signs of illness in the neonate Jaundice A serious sign in the first 24 hours of
life due to blood group incompatibility
1he neonate reveals illness by a limited num- or infection
ber of non-specific physical signs. Knowledge of Vomiting Bile-stained is significant, always
these and the ability to evaluate them are impor- exclude obstruction, consider
tant (see Table 7.8 for a summary of these signs).
infection
Table 7.8 Signs of illness in the neonate Diarrhoea Acute gastroenteritis or a non-
Sign Causes and associations specific sign
Central Most commonly indicates severe Failure to Fracture/dislocation, nerve injury,
cyanosis respiratory distress. May be due to move a limb local infection, bone or joint infection
(tongue)
congenital heart disease. May be a
manifestation of a convulsion, sepsis Disorders of adaptation to extra-
or hypoglycaemia
uterine life
Peripheral Indicates a temperature change
cyanosis or hypotension. The peripheral Temperature instability
perfusion will be prolonged in both
Temperature regulation in the neonate is deli-
cases. Correction of hypotension is
cately balanced between heat loss (mainly by
best achieved by infusing crystalloid evaporation and radiation, and to a lesser extent
solutions by conduction to clothing and sheets and by
-
Grunting An expiratory sound made by the convection) and heat production. Brown fat is
baby with inadequate oxygen uptake an important site of heat production for which
at alveolar level. Associated with energy is obtained from metabolism of gly-
pneumonia, hyaline membrane cogen stored in the liver and myocardium. In
disease and pulmonary oedema, but the absence of further intake, these stores are
not with airtrapping depleted within four to eight hours. Both hypo-
and hyperthermia increase the metabolic rate.
Pallor Of face or extremities suggests
If there is associated hypoxia or hypoglycaemia,
anaemia, haemorrhage, hypoxia,
metabolic acidosis ,vill complicate the picture
shock, sepsis, hypoglycaemia
and cause tissue damage. In the care of neonates
Convulsions Suggests CNS disorder such as a neutral thermal environment, ·which will allow
asphyxia or meningitis. May occur as a normal temperature to be maintained at a
a non-specific sign of severe illness, minimum metabolic rate, is essential. There are
hypoglycaemia, or hypocalcaemia marked individual variations depending on the
117
size, maturity, and state of health of the baby. It cold injury. Not infrequently the temperature
is important to achieve this environment so that is 32°C or less. There is oedema, generalised
insensible water loss is kept to a minimum and redness, poor feeding, and lethargy. Sclerema,
energy can be utilised optimally for grmvth. hypoglycaemia, shock, hypoxia, decreased sur-
factant production, convulsions, uraemia, and
Hypothermia pulmonary haemorrhage may be encountered.
In LBW babies, hypothermia raises the mortality There is an increased risk of sepsis and haemor-
by at least 25 per cent. The most common cause rhage associated \vith cold injury. The mortality
of hypothermia is a low ambient temperature in this serious condition is very high. Treatment
at birth. The asphyxiated, hypotonic UGA baby is symptomatic and as for hypothermia.
requiring resuscitation is at greatest risk: hypoxia
interferes \vith heat production, while hypoto- Overheating
nia diminishes metabolism in the muscles and vVhen exposed to unnecessarily high environ-
increases exposure from extended limbs. Fur- mental temperatures the baby becomes over-
thermore, the LBW UGA baby has no brown fat heated. Term babies in incubators are par-
stores on which to draw. Hypothermia is particu- ticularly at risk. There is vasodilatation \vith
larly likely to occur if there is a need for resuscita- increased insensible water loss, which results in
tion and during transport. Associated sepsis fur- dehydration and hypernatraemia. Apnoeic epi-
ther interferes ,vith metabolism and hence heat sodes may occur, and heat stroke and death may
production. ensue.
The metabolic rate and oxygen demand Overheating is managed by lowering the envi-
increase rapidly \vith cooling. Vasoconstriction ronmental temperature, giving fluids either
occurs and apnoea may ensue. The adverse effects orally or by nasogastric tube, and correcting any
of hypothermia include metabolic acidosis, hypo- serious metabolic disturbances.
glycaemia, decreased surfactant production, and
a rise in free fatty acids. Slow or delayed weight Blood sugar control
gain may occur. The overall effects are reflected in
an increased morbidity and mortality. Hypoglycaemia
Hypoglycaemia (i.e. a blood sugar level (BSL)
Management. Prevention of heat loss is essential. less than 2.0 mmol/1 or a serum sugar level less
Rewarming the neonate is difficult, time-con- than 2.5 mmol/1) is an important risk in UGA,
suming, and fraught ·with further complications. preterm, and OGA babies. (For clinical features
At birth every baby must be dried and wrapped in and causes see Chapter 10, Metabolic disorders).
a prewarmed towel. The head must be included
as it is the site of appreciable heat loss. Skin-to-
skin contact ,vith the mother provides warmth Practice point
and prevents heat loss. When this is not possible
and additional risk factors are present, warmers, The blood sugar level (SSL) must b_e monitored
cotton wool, aluminium swaddlers, and incuba- within one hour of birth in infants at risk of hy-
tors can be used. poglycaemia, i.e. UGA and preterm neonates,
Rewarming of the cold baby is critical when those of diabetic mothers, and those that have
hypothermia has been prolonged, and must be been asphyxiated 0r hypothermic.
carried out as soon as possible. Again skin-to-
skin contact \vi th the mother is very effective. The Hyperinsulinism is responsible for the hypogly-
skin temperature must be monitored and meta- caemia of babies born to diabetic mothers and
bolic acidosis corrected. Complications such of those with severe erythroblastosis fetalis. An
as infection, haemorrhage, and cerebral insults increased rate of consumption of blood glu-
may develop. cose occurs in conditions such as hypothermia,
hypoxia, respiratory distress, and infection. There
Neonatal cold injury is also a distinct possibility of rebound hypogly-
Prolonged exposure to cold results in neonatal caemia if a glucose infusion is interrupted.
ll8
Thereafter it must be determined twu-hourly Cardiovascular disorders.) To prevent the latter

for the first eight hours and then six-hourly for it is critical to ensure preconceptual BSL control.
the rest of the first 24 hours. Reagent strips can 1he other major risk is due to maternal hyper-
be used for screening, but biochemical analysis glycaemia, which places the developing baby in a
is advisable to confirm hypoglycaemia. state of continuous hyperinsulinism and acceler-
ated gmwth. This causes an OGA baby with rela-
Management tive immaturity for gestational age.
• Commencing feeds within two hours of
birth in the at-risk infants will usually The problems include:
prevent hypoglycaemia. • Birth injuries because of the large size:
• A low blood sugar reading in an brachia! plexus injury and fractures of the
asymptomatic baby may be managed by humerus follov.ing shoulder dystocia are
an oral feed and monitoring of the BSL. the most common
• A 10 per cent glucose solution must be • Hypoglycaemia, which may develop
infused intravenously as soon as possible within the first one to 1:\vo hours after
in symptomatic infants or those with a BSL birth. This complication implies poor
of <1.5 mmol/1. The infusion is started at maternal blood glucose control during
65 ml/kg per 24 hours (0.5 g/kg/hr). pregnancy
• If the blood sugar does not reach normal • Poor feeding and sucking
levels, a 15% glucose infusion should be • Jaundice
considered. • Hypocalcaemia
• If control is not achieved, glucagon • Respiratory distress syndrome
0.1 mg/kg per dose may be given • Polycythaemia
repeatedly six- to twelve-hourly • Cardiomyopathy, which may lead to
intramuscularly. Consider referral if at cardiac failure
level one facility. • Small left colon syndrome, presenting as
• Investigations must be considered transient intestinal obstruction, which
to determine aetiology of prolonged resolves spontaneously
hypoglycaemia (see Chapter 10, Metabolic • Renal vein thrombosis, which presents as
disorders). macroscopic haematuria.
• Bolus infusions are generally not
recommended as the intravascular Management includes three-hourly monitoring
consequences of a hyperosmolar solution of the BSL from birth and early feeding.
and the effects on insulin levels cause
unacceptable metabolic stress. Hyperglycaemia
• The blood sugar is monitored hourly and Hyperglycaemia is defined as a BSL above
small volume milk feeds (breastmilk) are 7.5 mmol/1 with glycosuria. It may occur as a
commenced as soon as possible. consequence of severe stress, asphyxia, and sep-
• Whe:o. the patient is asymptomatic and sis, especially in the VLBW infant. Hyperosmolar
the BSL has stabilised, the infusion is solutions will induce an osmotic diuresis, which
decreased slowly, while the milk feeds are can result in significant dehydration.
slowly increased. Transient neonatal diabetes \·vithin the first six
weeks oflife occurs rarely in UGA babies. Usually
Infant of the diabetic mother there is failure to thrive with extreme hypergly-
Good diabetic control during pregnancy de- caemia and dehydration vdthout acidosis. Insu-
creases the risk of the majority of the problems lin corrects the hyperglycaemia.
which the infant of the diabetic mother (IDM) is
likely to suffer. Congenital malformations vary Management. The aim is to reduce the concen-
from 5-13 per cent and include neural tube or tration of glucose in any infused fluid. The blood
vertebral defects, sacral agenesis, and cardiac and urine sugar must be monitored carefully to
malformations such as ventricular septal defect, detect the fall in the glucose levels. If these simple
transposition, and coarctation. (See Chapter 30, measures fail and the blood sugar remains above
119
15 mmol/1, insulin is infused at a dosage of • Respiratory distress (tachypnoea >60

0.05-0.1 unit/kg/hr with very strict monitoring breaths per minute; intercostal and
of the BSL to prevent hypoglycaemia. The very ill subcostal recession expiratory grunting
infant may be exquisitely sensitive to insulin and and cyanosis)
the BSL may fall within 15 to 20 minutes of the • Central cyanosis
insulin injection. • Inspiratory stridor
• Apnoea.
Respiratory distress (RD)
It is not uncommon for newborns soon after
Respiratory problems are a leading cause of neo- birth to have transient mild respiratory distress.
natal deaths. It is important to recognise that This is an expression of adaptation from intra-
disturbances of almost any system may manifest uterine to extra-uterine conditions; the distress
with respiratory signs and symptoms. Respira- settles within one to two hours and does not war-
tory disturbances may present as: rant investigation. See Table 7.9 for the features
of respiratory distress.
Table 7.9 Clinical features of respiratory distress
Chest Rec-ession Xiphoid Alar flare Expiration
movement retraction grunt
Normal Synchronised No retraction/ None None None
recession
Mild Lag on inspiration Just visible Just visible Minimal Stethascope only
Severe See-saw Marked Marked Marked Naked ear I
!
The causes commonly encountered are listed in

Practice point Table 7.10.
• Central cyanosis is most commonly due
Respiratory distress is diagnosed when two or to pathology of the respiratory tract.
more of the following signs are present: Although parenchymal lung disease is
• Respiratory rate of 60/min or more the most common cause of cyanosis,
(tachypnoea) congenital heart disease must be
• Expiratory grunting suspected if the cyanosis is not relieved by
• lntercostal and/or sternal recession
oxygen (see Chapter 30, Cardiovascular
• Central cyanosis while breathing air.
disorders). Upper airway obstruction may
simply be due to secretions or meconium
Table 7.10 Causes of respiratory distress and is readily relieved by suction. Rarely it
is due to a structural abnormality such as
Pulmonary Extra- Congenital choanal atresia.
pulmonary abnormalities
• Inspiratory stridor indicates an upper
Respiratory Cold exposure Pneumothorax ainvay abnormality such as laryngeal
distress Cardiac failure Diaphragmatic webs or cysts or laryngomalacia. Mass
syndrome Cerebral hernia lesions at the base of the tongue may
Meconium damage Trachea- present \vith intermittent or positional
aspiration Metabolic oesophageal stridor.
Congenital disturbances fistula • Apnoea or poor respiratory effort may
pneumonia Acute blood Lung cysts be caused by failure or depression of the
Transient loss respiratory centre or severe respiratory
tachypnoea Septicaemia distress.
Acute I
pulmonary I
haemqrrhage -
120
Immediate respiratory difficulties Respiratory distress with diminished breath

Acute respiratory distress soon after birth requires sounds on one side of the chest, suggests a pneu-
careful clinical assessment to determine whether mothorax, which is readily confirmed radiologi-
it is due to parenchymal lung disease, extra-pul- cally or by chest transillumination. Other signs
monary conditions, or congenital abnormalities. include increasing respiratory difficulty, cyano-
Early diagnosis of congenital abnormalities in sis, restlessness, and apparent malposition of the
particular reduces mortality and morbidity, as cardiac apex.
surgical intervention is often required. Ideally, all newborns who are at risk of devel-
• Failure of the baby to breathe at birth oping respiratory problems should be delivered
suggests asphyxia or severe parenchymal at centres ·with special care facilities.
Transfer of selected infants to such centres
lung disease.
is warranted where there is moderate to severe
• Upper airway obstructive conditions
respiratory distress or if there is deterioration;
that may present at the time of birth
the latter is suggested by a need for increasing
are choanal atresia and Pierre Robin
amounts of oxygen, a steady increase in the heart
syndrome (see Chapter 36, Ear, nose,
and respiratory rate or repeated apnoeic or cya-
and throat disorders). A thick plug
notic attacks. Often seriously ill neonates, such as
of mucus in the nostrils may present
those in haemorrhagic or septic shock, may ben-
similar difficulties, but the obstruction
efit from respiratory support. Babies ·with severe
is immediately relieved by nasal suction.
asphyxia, convulsions, hypothermia, or hypogly-
The features of nasal obstruction are
caemia should not be transferred immediately,
cyanosis and suprastemal recession when but corrective management must be instituted
the mouth is closed, relieved by crying. first in consultation with the referral unit.
Cyanosis and respiratory obstruction
occurring in the supine position and
relieved immediately on turning the baby Principles of management of respira-
are indicative of the tongue falling back tory distress
and occluding the airway. These features,
From the list of causes of respiratory distress it
together \,vith micrognathia, are found in
can be seen that it is imperative to have a chest
the Pierre Robin syndrome.
radiograph.
• Stridor may follow resuscitation either as a
• Oxygen is administered by nasal cannula
result of vigorous suctioning or intubation.
in a concentration that abolishes cyanosis
Vocal cord paralysis or congenital
and keeps the oxygen saturation between
abnormalities of the larynx such as webs,
89-92%.
cysts, and laryngomalacia may also be
• Blood gas analysis (if available) should be
diagnosed by direct laryngoscopy. An performed approximately one hour after
urgent tracheostomy may be necessary clinical improvement and correction of
(see Chapter 36, Ear, nose, and throat any metabolic acidosis.
disorders). Persistent extension of the • A whole blood transfusion is indicated if
neck ·with stridor may be associated \vi.th the haemoglobin is below 12.0 g/dl (PCV
a retrosternal goitre or a vascular ring, below 35), giving 10-20 ml/kg over three
which can be confirmed by an X-ray hours.
with a contrast swallow. The baby who • A plasma or crystalloid (normal saline,
has increased secretions from the time Ringer's lactate) infusion should be given
of birth and chokes, coughs, or becomes if the peripheral perfusion and pulse
cyanosed with feeding must be regarded volume are poor.
as having oesophageal atresia. This is • Circulation is assessed by the capillary
easily confirmed by failure to pass a filling time while the renal function is
nasogastric tube into the stomach (see assessed by the urine output.
Chapter 8, Surgical care of the newborn). • Apart from the routine care, the blood
A chest radiograph with the tube in situ sugar level must be monitored.
will confirm the presence of a pouch ·with • Antibiotics are indicated in conditions
the coiled tube visible. such as congenital pneumonia.
121
Principles of, and indications for, Vasomotor instability may cause generalised
oxygen therapy mottling of the skin.
Apparent cyanosis may be due to the blue pho-
•Give as little oxygen as possible and as totherapy light or polycythaemia.
much as necessary to abolish central
cyanosis and grunting. The causes of cyanosis include:
• Oxygen administered indiscriminately, • Pulmonary pathology
particularly to the preterm infant, may • Congenital cardiac defects
lead to retinopathy and blindness (see • Hypothermia
Chapter 35, Disorders of the eye). However, • Metabolic disturbances, e.g.
too little oxygen leads to hypoxic brain hypoglycaemia
damage. • Infection, e.g. septicaemia, meningitis
• If at all possible, the percentage oxygen • Severe intracranial disturbances, e.g. intra
given and the blood oxygen saturation cranial haemorrhage, meningitis.
must be monitored. The saturation should
be kept between 88-92%. Management. With the infant supine, the head
+ Ch.-ygen therapy without additional should be slightly extended, the airway kept clear
ventilatory support is sufficient if the by suctioning, and oxygen administered. The
respiratory effort is good and there is temperature and blood sugar levels are moni-
reasonable tone and cry. Blood gas tored and enteral feeds discontinued or ,vith-
analysis should show no carbon dioxide held to avoid aspiration. Commence intravenous
retention and a PaO2 of 50-100 mmHg in fluids to maintain hydration and electrolyte bal-
an ambient oxygen concentration of up to ance. As is the case ,vi.th apnoea, further man-
60 per cent. agement depends on the cause of the cyanosis.
+ Nasal continuous positive airway pressure
(NCPAP) of 5 cm H 2O by nasal prongs is Hyaline membrane disease (HMD)
indicated if cyanosis cannot be corrected Th.is condition is the clinical manifestation oflung
with nasal cannula oxygen. immaturity. The lipoprotein, surfactant, which is
necessary for normal alveolar expansion is defi-
The main indication for oxygen therapy is cyano- cient, either because of lack of production or fail-
sis or a change in colour, such as pale extremities ure of release from alveolar Type II cells. The air
and a central duskiness. sacs collapse, the pulmonary capillary perme-
Oxygen should not be given for respiratory ability is increased and protein-containing fluid
distress alone. If the baby is obviously cyanosed and red cells ooze into the alveoli. The protein
or has had a cardiac arrest, 100 per cent oxygen (fibrin) coagulates to form a membrane, which
must be given. Th.is must be reduced once a clini- lines the alveolar sac; the sac itself contains
cal response occurs, which may take up to 20 oedema fluid and blood. Th.is eosinophilic stain-
minutes. ing material seen on histology is a non-specific
A baby with poor colour should be given 30-40 response of the lung to injury. Within a few days,
per cent oxygen via nasal cannula and once again the alveolar macrophages gradually remove the
reduced once clinical improvement is seen. membranes and, as surfactant is produced, the
normal physico-chemical properties of the gas-
Cyanosis liquid interface in the air sacs are restored and
the alveoli are able to maintain a spherical shape
Cyanosis of the skin and tongue is a guide to the in expiration.
state of oxygenation of the newborn. The degree The assessment of lung maturity and of alveo-
of cyanosis depends on the arterial oxygen satu- lar Type II cells is possible by measuring the ratio
ration, the haematocrit, the pH, the peripheral of lecithin to sphingomyelin (L-S ratio) in the
circulation, and the temperature of the baby. amniotic fluid. The more mature the fetus, the
Intermittent cyanotic episodes may occur dur- closer the L-S ratio approaches 2: 1.
ing vigorous crying; this is the result of right-to- The bubble or shake test is a simple bedside
left shunt through the ductus or foramen ovale. means of assessing lung maturity: 1 ml of amni-
122
7 Care of the nev,rborn
otic fluid obtained by amniocentesis and 1 ml Nasal continuous positive airway pres-
of absolute alcohol are shaken vigorously for 30 sure (NCPAP)
seconds in a clean 10 ml glass tube. After another NCPAP should be considered for babies ,.vi.th the
15 seconds the bubble score is read. The higher follo-wing:
the score the more mature the lungs: • Clinical: Moderate RDS tachypnoea (RR
O = no bubbles >60 breaths/min) recession - intercostal,
l+ = a single ring of bubbles subcostal and alae flare, grunting, apnoea,
2+ two rings of stable bubbles oxygen requirement >40-50% oxygen, a
3+ = more than two rings of bubbles and a pulse oximeter reading <88%. Good tone
clear centre and peripheral perfusion. (If poor tone
4+ = all of the miniscus covered in bub- and peripheral perfusion is present baby
bles. requires to be ventilated.)
• Arterial blood gases: PaO2 <8 kPa, PaCO2
A score of2+ can be considered 'safe' with regard >6 kPa, pH<7.3 (persistent respiratory
to lung maturity. The shake test can also be per- acidosis).
formed on a sample of clear gastric aspirate col-
lected within 30 minutes of delivery. If the baby does not settle on CPAP, SRT should
The pathophysiological effects of HMD on pul- be considered.
monary function are as follows: Prevention ofHMD includes the use of antena-
• Reduced lung compliance tal steroids. The effect of antenatal steroids is sig-
• Ventilation perfusion imbalance nificant if delivery occurs 48 hours after or '"'ithin
• Pulmonary vasoconstriction resulting in a seven days of the administration of the drug. A
large right-to-left shunt of blood secondary benefit is the reduction in intraven-
• Reduced alveolar ventilation and tricular haemorrhage and necrotising entero-
functional residual capacity colitis. There appears to be no increased risk of
infection to the mother or the baby. Administra-
• Increased minute ventilation and work of
tion of antenatal steroids will decrease or even
breathing.
prevent the incidence of HMD and thereby also
the use of the costly SRT.
These changes result in hypoxaemia, hypercap-
nia and eventually metabolic acidosis. The classi- Massive pulmonary haemorrhage
cal radiological findings are an air-bronchogram, This catastrophic situation most commonly arises
and reticulogranular pattern. However, this char- in the low-birth-weight infant during the acute
acteristic picture does not exclude infection. or recovery phase of an illness such as asphyxia,
The management is similar to that for respira- infection, or hypothermia. It occurs most fre-
tory distress and supportive care, and includes quently between the second and fourteenth day.
surfactant replacement therapy as discussed Treatment ,vi.th transfusion and ventilation is
below. unsatisfactory as the mortality rate is high. Prob-
Surfactant replacement therapy (SRT) is a ably of greater importance is the prevention of
major advance in the care of the preterm infant predisposing factors.
with respiratory distress syndrome. Mortality
and the incidence of air leaks are reduced by Meconium aspiration
this form of therapy. However, there has been This condition usually occurs in UGA, and term
no effect on the incidence of bronchopulmonary and post-term infants suffering from fetal dis-
dysplasia (BPD), intraventricular haemorrhage, tress before and during labour. The passing of
and patent ductus arteriosus. grade 1 meconium in utero is of doubtful signifi-
Two preparations of natural surfactant are cance. Although grade 2 and 3 meconium do not
commercially available in South Africa. Surfac- mean inevitable aspiration, the risk is high. The
tant is administered via an endotracheal tube, to monitoring oflabour to detect fetal compromise
preterm infants presenting ,vi.th respiratory dis- and its management are the most important
tress and not responding adequately to oxygen. factors in the prevention of this condition. The
123
aspiration of meconium may have a number of settles within a few days. Some may require oxy-
effects on the lungs and heart: gen or ventilation. Radiological changes are
• Small airways obstruction with areas of those of perihilar streaking, fluid in the lung fis-
atelectasis and air trapping sures, and a slightly enlarged cardiac silhouette.
• Acute pneumonitis presenting with
various degrees of severity, shock, and Apnoeic and cyanotic episodes:
acute pulmonary oedema or respiratory • Apnoeic episodes and periodic breathing
distress in the preterm infant are considered to
• Pneumothorax be one end of a spectrum of disturbed
• Persistent pulmonary hypertension of the respiratory regulation. The heart rate and
newborn. oxygenation remain normal with periodic
breathing, but apnoeic spells result in
If there has been severe hypoxia and hypo-ten- bradycardia and cyanosis after 20 seconds.
sion, cerebral oedema and renal problems with Should this persist, hypotonia and
fluid overload may readily occur. The natural his- unresponsiveness may develop.
tory is one of full clinical and pulmonary recov-
ery within weeks, unless of course severe hypoxia The following conditions may also be associated
or pneumonitis causes death. with apnoeic episodes:
Management is as for respiratory distress. • Immaturity
• Respiratory distress, particularly due to
Persistent pulmonary hypertension of obstructed airways
the newborn (PPHN) • Respiratory failure due to pulmonary
In this condition right-to-left shunting through pathology of any type
the foramen ovale and ductus arteriosus occurs • Central nervous system pathology,
as a result of high pulmonary vascular resistance e.g. convulsions, meningitis, raised
(persistent 'fetal circulation'). Profound hypoxia intracranial pressure due to cerebral
resulting in cyanosis occurs soon after birth. The haemorrhage or oedema
heart is structurally normal, the chest X-ray may • Septicaemia
show pulmonary oligaemia, and the ECG is most • Metabolic disturbances, e.g.
often normal. hypoglycaemia, hypocalcaemia,
PPHN may present as a primary disorder (the hyponatraemia, acidosis
lungs appear normal or oligaemic on chest X-ray) • Hyperpyrexia
or with HMD, meconium aspiration, polycythae- • Drugs given to the mother, particularly
mia, and diaphragmatic hernia. diazepam and magnesium sulphate.
Mechanical ventilation \vith a high Fi02 has lit-
tle effect on severe hypoxia. Correction of the aci- It is important to emphasise that apnoea attacks
dosis and systemic hypotension may be followed may indicate convulsions, as the typical features
by improving oxygenation as pulmonary vascular of a seizure are rarely seen in a neonate.
resistance improves. Maintenance of a normal to
high systemic blood pressure is important. The Management. The respiration of patients at risk
follmving options may be considered: MgSO 4 at of apnoeic episodes must be monitored care-
a dose of 200 mg/kg body weight M over 20 to fully. The basic management of an apnoeic or
30 minutes, followed by a continuous infusion of cyanotic episode is:
20-50 mg/kg per hour, surfactant replacement • Firstly gentle pharyngeal suction.
therapy, sildenafil or nitric oxide, which may be • Oxygen is given per mask.
available in some centres. • The baby is stimulated by flicking the foot.
• Intermittent positive pressure ventilation
Wet lung syndrome or transient tachy- has to be commenced ifbradycardia
pnoea of the newborn (TTN) persists.
This brief, self-limiting, relatively benign condi- • If the pulse rate increases but remains
tion follows a normal full-term pregnancy. 1he of poor quality, then plasma 10 ml/kg
infant usually has mild respiratory distress, which may be infused over 20 minutes and
124
respiratory support considered if a may reflect irritation of the gastric mucosa by

ventilator is available. swallowed blood or meconium. A gastric lavage
+ Once apnoea of immaturity is diagnosed will confirm this diagnosis and is therapeutic.
by exclusion of other causes, oral Vomiting may be the first sign of serious
theophylline 5 mg/kg is given, followed by organic disease, especially if it is persistent, bile-
2 mg/kg 12-hourly. stained, or associated \\Tith abdominal distension
or constipation (see Chapter 26, Gastrointestinal
Chronic lung disease disorders).
Infections, both enteral and parenteral, are
Chronic lung disease is diagnosed if a baby is
commonly associated ,\Tith vomiting.and include
ventilated and/ or oxygen dependent for 28 days
meningitis, septicaemia, urinary tract infections,
or more and has characteristic features on chest
and necrotising enterocolitis. Intestinal obstruc-
X-ray. Chronic lung disorder (bronchopulmo-
tion must be excluded (see Chapter 8, Surgical
nary dysplasia - BPD) may be associated with
care of the newborn). .
patent ductus arteriosus, pulmonary haemor-
Intracranial injury and congenital abnormali-
rhage, infection, and milk aspiration. The princi-
ties may cause persistent vomiting. Rarer causes
ples of management include prevention of noso-
include metabolic problems such as uraemia,
comial infection, adequate nutrition, treatment
congenital adrenal hyperplasia, and inherited
of cardiac failure if present, and maintaining
metabolic disturbances.
the haemoglobin above 12 g/1, and the oxygen
saturation between 88 and 92 per cent. The chest Abdominal distension
X-ray and electrocardiograph should be checked
This is a fairly common physical sign in the new-
regularly for the development of right heart
born. It may be a sign of serious illness. It should
involvement. Theophylline may help to wean the
be established whether the distension is due to
baby from oxygen therapy or the ventilator; in
gas, fluid, or organ enlargement, and whether
addition it may improve lung compliance. Dexa-
associated physical signs such as constipation
methasone must be used with great caution and
and vomiting are present.
as a short course. Nebulisation with ipratropium
+ Gaseous distension occurs as a result of
bromide or salbutamol may be of benefit.
the accumulation of air in the gut due to
In a population with a high prevalence of HIV
obstruction or paralytic ileus. The causes
infection, some babies with chronic lung disease
of intestinal obstruction are congenital
of infancy may be expected to also suffer from
abnormalities of the gut, hernias, volvulus,
vertically acquired HIV infection. Accordingly,
and malrotation (see Chapter 8, Surgical
a high index of suspicion should be maintained
care of the newborn). Meconium ileus is
for additional HIV infection in any baby show-
a pointer to cystic fibrosis and must be
ing unusual features or responses. 1hese babies
considered in babies of Caucasian origin
do not present \\rith the radiological features of who present \\ith partial or complete
chronic lung disorder of the newborn (BPD).
obstruction. Paralytic ileus occurs as
Tuberculosis or cytomegalovirus infection may
a result of hypoxia, shock, electrolyte
present in the neonatal period at about the sec- imbalance, and infection, which may be
ond or third week of life. systemic or confined to the gut.
+ Abdominal masses contributing to
Gastrointestinal disorders abdominal distension are most commonly
due to organ enlargement such as
Gastrointestinal disorders are common prob- hepatosplenomegaly, renal masses,
lems in the newborn. 1he major concern is to dilated bladder, liver cysts, tumours, and
exclude surgical conditions (see Chapter 8, Sur- ovarian masses. Rare causes include
gical care of the newborn). gut duplication, mesenteric cyst, and
retroperitoneal tumours. Urogenital causes
Vomiting are not uncommon so that abdominal
Vomiting is a very common sign in the first few ultrasound and urological investigations
hours of life. Regurgitation of the first few feeds may be required to detect these.
125
• Ascites is a rare clinical finding in the Clinical features. Abdominal distension is the
newborn and most commonly occurs in earliest sign. It may occur ·within a few hours of
babies with generalised oedema. This is birth and as late as one month of age. A poor
seen in severe anaemia (as in Rh disease), colour and shock may ensue 1,vith the full pic-
cardiac failure, nephrotic syndrome, and ture of septicaemia. Stools are usually scanty but
chronic intra-uterine infections. blood-streaked in 20-25 per cent of cases. Perfo-
ration of the gut may occur.
Management. Surgical conditions must be
Investigations. A low white count may be pres-
excluded first. An erect abdominal radiograph
ent; thrombocytopenia, particularly a falling
is obtained and an abdominal ultrasound per-
platelet count, is a poor prognostic sign and
formed in the case of an abdominal mass. A pae-
disseminated intravascular coagulation may be
diatric surgical opinion should be obtained.
present. An X-ray of the abdomen shows intesti-
nal distension ,vith thickened bowel walls, intra-
Diarrhoea mural air, and sometimes gas in the intrahepatic
The most common cause ofloose stools in a neo- portal venous system. Signs of pneumo-perito-
nate is dietary in origin. In the fully breastfed neum 1,vill be present if the gut has perforated.
infant a loose stool 1,vith each feed is not uncom-
mon and is due to a mild lactose maldigestion. Management. The general principles of treat-
This self-limiting condition clears 1,vithin days or ment of septic infants must be observed:
weeks and does not require a feed change if the • All feeds are stopped.
baby is thriving. • A nasogastric tube is passed and left open
Infective diarrhoea may occur and may be to drain to prevent accumulation of air
associated with parenteral infection (see Chapter and gastric content.
26, Gastrointestinal disorders). • Intravenous alimentation is mandatory
It is extremely difficult to differentiate paren- once the clinical condition is stable.
teral from enteral infection in the newborn. The • Monitor and correct electrolyte imbalance.
clinical presentation may vary from mild disease • Correct low Hb, and low platelet count.
to severe dehydrating disease 1,vith acidosis and • Broad spectrum antibiotics are
electrolyte imbalance. Many babies are afebrile, commenced once appropriate cultures
yet others become hypothermic or pyrexial. have been taken.
• Regular consultation 1,vith a paediatric
surgeon is essential as immediate
Necrotising enterocolitis intervention is necessary for perforation,
The incidence varies in different centres, being and strictures may develop later. ·
rare in some and reaching epidemic proportions
in others. It occurs more commonly in infants Prognosis. Prompt diagnosis, nasogastric drain-
weighing less than 1 500 g. age and intravenous alimentation have vastly
The pathogenesis is poorly understood but improved the outlook in this serious disease. In
ischaemia of the immature gut is a critical fac- the individual patient, however, the degree of
tor, followed by a combination of infection and prematurity and any associated conditions will
release of inflammatory mediators. Perinatal affect the prognosis. The prognosis depends on
hypoxia, prematurity, sepsis, artificial feeds, the staging of the disease as well. Bell's criteria
shock and exchange transfusions are contribut- is generally accepted. Stage 1 is suspected NEC
ing factors. Following the ischaemic insult, lumi- with mild distension, occult blood in the stool
nal gas enters the necrotic bowel wall to produce and a few systemic signs. Stage 2 is definite
classical pneumatosis intestinalis. Organisms NEC with systemic signs, abdominal distension,
associated with this disease include Escherichia pneumatosis intestinalis and definite blood in
coli, Klebsiella, Acinetobacter, Pseudomonas, the stools and stage 3 is a severely ill infant, with
and Clostridium difficile. Strict adherence to peritonitis and perforation.
exclusive breastmilk feeding has reduced the In some centres mortality rates have decreased
incidence in some units. from 75 per cent to less than 20 per cent.
126
Neonatal jaundice These result in raised unconjugated serum bili-

rubin levels in the first week of life. In physiologi-
Jaundice becomes apparent at 85-120 µmol/1 cal jaundice, the total serum bilirubin (TSB) level
(1 mg/dl of bilirubin = 17 µmol/1). Jaundice is does not exceed the upper limit of normal for age
pathological if: in days. In the term neonate it usually peaks at
• It occurs within the first 24 hours of life 150 µmol/1 on the third day, and in the preterm
• Total serum bilirubin exceeds 275 µmol/1 170-200 µmol/1 on the fifth to seventh day. The
or the upper limit of normal for the age in diagnosis of physiological jaundice is largely by
days exclusion.
• Bilirubin rises by more than 85 µmol/1 per
day. Bilirubin encephalopathy
Bilirubin encephalopathy occurs when the fat-
Or: soluble unconjugated free bilirubin crosses the
blood-brain barrier. Areas of the brain with high
• If the direct serum bilirubin exceeds blood flow and high metabolic rates are suscep-
34 µmol/1 tible to bilirubin toxicity. Kernicterus refers to
• If jaundice persists for more than a week the yellow staining of the basal ganglia and hip-
in the term and more than two weeks in pocampus seen at autopsy in infants dying of
the preterm baby. bilirubin toxicity.
Factors that interfere with albumin binding
The usual causes of jaundice in the first week of and allow a higher level of free bilirubin in the
life are shown in Table 7.11. circulation, are:
• A low serum albumin (<30 g/1)
Table 7.11 Usual causes of neonatal jaundice in the • Certain drugs such as sulphonamides,
first week of life which compete with bilirubin for binding
sites on albumin
Onset within the first 3 Onset after day 5 to day 7
to 5 days
• Non-esterified fatty acids (associated \vith
starvation or total parenteral nutrition
Blood group Infections, e.g. UTI, (TPN)
incompatibility hepatitis·; Gram-negative • Acidosis.
Blood collections, e.g. sepsis
cephalhaematoma Neonatal hepatitis The preterm infant is at risk of encephalopathy
Physiological jaundice syndrome at appreciably lower serum bilirubin levels than
Infection (intrauterine) Biliary atresia the term baby. Bilirubin encephalopathy is rarely
Immaturity Metabolic disorders, e.g. seen in term infants with total serum bilirubin
Maternal diabetes galactosaemia levels below 400 µmol/1 unless there is underly-
Endocrine, e.g. ing pathology or factors that enhance the deposi-
hypothyroidism tion of free bilirubin.
Miscellaneous, e.g. D0wn's Hypoxia, sepsis, acidosis, hypoglycaemia and
syndrome, pyloric stenosis hyaline membrane disease predispose to kernic-
terus.
Physiological jaundice In general, unconjugated hyperbilirubinaemia
Up to 50 per cent of normal newborns and con- originating from sources other than increased
siderably more preterm infants become jaun- haemolysis does not commonly cause bilirubiri
diced in the first week of life. The normal new- encephalopathy.
born has a number of factors involving bilirubin
metabolism and transport: Clinical features
• Increased breakdown of fetal red cells The clinical picture of bilirubin toxicity may
• Immature uptake, conjugation, and be transient or irreversible. The signs may not
excretion ofbilirubin develop for several hours after toxic levels have
• Increased enterohepatic circulation of been reached. Initially the signs are reluctance
bilirubin. to take feeds, temperature instability, irritability,
127
and cycling movements. An exchange transfu- Prevention. Antenatal investigation of Rh-nega-

sion at this stage may arrest the process. Pro- tive women for the presence of Rhesus antibody
gression of the disease shows up as generalised will detect potentially affected foetuses. Amnio-
increase in extensor tone with opisthotonus and centesis \vith the measurement of bilirubin
crossed extension of the legs. The cry is high- concentration and optical density has been the
pitched and paralysis of the extra-ocular muscles method of assessing severity. Recently tertiary
causes a 'setting sun' sign. In the surviving infant centres have been performing cordocentesis to
hypotonia eventually occurs ,vith developmen- measure the haematocrit and analyse the blood
tal delay. Long-term manifestations include groups. Direct fetal transfusion is performed if
choreoathetosis or spastic cerebral palsy, clum- indicated.
siness, intellectual impairment, and high tone All Rh-negative women must be given human
deafness. Dental dysplasia may occur. In the Rh-hyperimmune gammaglobulin (100 to 200
preterm infant the initial physical signs may be mg IM) within 48 hours of birth or any procedure
quite different with fisting, an increase in tone, which could result in sensitisation. The gamma-
and apnoea. globulin binds to the fetal~cells which are then
Bilirubin encephalopathy should now occur rapidly removed from the maternal circulation.
infrequently, reflecting an overall improvement This procedure has resulted in a dramatic decline
in care of the newborn. in the incidence of Rh-haemolytic disease.
Management of the infant. The jaundiced infant

Haemolytic disease of the newborn is managed as outlined below. Low-grade hae-
molysis may continue in the affected infant,
Rhesus haemolytic disease resulting in anaemia at two to four weeks and
may require a transfusion at that time. The early
Pathogenesis. There are five distinct Rhesus (Rh)
administration of iron and folate supplementa-
antigens c, C, D, e, and E. Incompatibility to the
tion may reduce the severity of the late anaemia.
D antigen is the most severe. About 85 per cent
of Caucasians have the D antigen. Rh negativity ABO incompatibility
denotes absence of the D antigen, indicated by
The frequency of ABO blood group incompatibil-
d. vVhen fetal cells carrying the D antigen leak
ity is similar in tropical and non-tropical areas.
across the placenta into the circulation of a Rh-
As Rh disease has become uncommon, ABO
negative mother, they stimulate antibody pro-
incompatibility assumes greater importance.
duction in the mother to the specific fetal anti-
The latter rarely presents with as severe manifes-
gen. 1hese antibodies, in turn, cross the placenta tations as Rh disease, e.g. hydrops fetalis, severe
causing haemolysis of the fetal red cells. anaemia, and early onset of jaundice. Although
Rhesus disease increases in incidence and the Coombs' test is often negative, sensitisation
severity if there has been prior sensitisation due may be suggested by the presence of immune
to feta-maternal bleeding at abortion, amnio- anti-A or anti-B antibodies in the baby's serum
centesis, external cephalic version, or delivery. or on the surface of the red cells. ABO incompat-
Severity of the disease is also related to parity and ibility can occur where the mother has the blood
to the stage of pregnancy during which the anti- group O and the baby either group A or B.
body crosses the placenta. The earlier the anti-
body crosses the placenta, the more severe the
disease. Haemolytic disease commencing in the
Management of hyperbilirubinaemia
second trimester may result in severe anaemia, Figure 7.3 gives guidelines for the management
hepatosplenomegaly, liver damage (hypopro- of hyperbilirubinaemia. The aim of therapy is
teinaemia, oedema), cardiac failure, and asci- to prevent bilirubin encephalopathy. Careful
tes (hydrops fetalis). When haemolysis occurs observation of the baby is important to detect
nearer to term the infant is born less anaemic but and correct any of the above-mentioned predis-
rapidly develops jaundice which may be severe. posing factors.
128
7 Care of tlw newborn
Figure 7.3 Phototherapy and total serum bilirubin {TSB) monitoring in the first week of life at primary care
Source: South African Neonatal Academic Hospitals 2006
• Refer/discuss all jaundiced infants who are: < 2 kg or< 35 weeks gestation.
• Refer all infants of mothers who have Rhesus antibodies on antenatal screening.
• Discuss ALL infants receiving phototherapy, daily, with MOU doctor (day) or referral hospital (night).
• Stop phototherapy when TSB > 50 µmol/1 below phototherapy line.
• If TSB continues to fall after phototherapy has been stopped, then no more TSB measurements
are needed.
Figure 7.3a
WELL TERM INFANTS> 3 kg
3 5 0 . - - - - - , - - - - - - , - - - - . . - - - - - - . - - - - - - - - ~ - - ~ - - - . - - - . . . . . . - - - ~---......-- - - ,
: . : .. ·-·-·•-·-••·-·
330 . .
310 ~:~~·: : :==~-!.::~~:·:-.- •------ f····--···· ---- ----r·-------
- - - - - - ;!-·· - - - - - - - ; - - - -
::::::
0 290 -·-· -·-··- ! -·--- -··-- i :
5_ 270 ·~:··::···:~::::···! ...... ·•···••--'. ...... ····-········'···
fn 250 ::::::::::::.:::::) ::=:=-~·-·-!·
g 230 ···-::.=:::::::::+·---· ··--··i··· -···-
: : i
I .. -··-········
....... --·-· .)' · •· .............i..........._. ·.....

--+---------- -·····
- - --·-······.
ACTION LINES - Take action if above these lines

-0- Referral line: start phototherapy and refer/discuss
110 _ . Phototherapy line: start phototherapy and repeat TSB daily
90 .. ,fl··· Repeat line: repeat TSB in 6h or start phototherapy and do TSB daily
·• ·· 2nd Repeat line: repeat TSB daily
70 If TSB is below the 2nd repeat line then monitor daily until it is falling or until
jaundice is resolving.
50 •--·······-·-•-•·;··· . ..
..
30..__________________ __________________________________________________
. •··-••· HO •·• --- - · - U - H - 0 0 0 0 0 ❖ • - • - • • - - - • • --4- •• • 00-0000_0 ____ _
~
6h 12h 24h 36h 48h 60h 72h 84h 96h 108h 120h
Age (hours)
Figure 7.3b
WELL INFANTS 2-3 kg and > 35 weeks
350 . - - - - - , - - - - - - , - - - - . . - - - - - - . - - -- ~- -- ~ - - ~ - -- . - - - ~ -- ~---......-----,
330 ·-· ·-··-········.L. i

310 ... . ·~-... ··-······· -···~-- - - .,_....-··--···-···1'-·······--· --,•~
·· - -- - - -
290 1--- -~'---- ---'-- - - - " ~ - - -- ' - -- ---'- - -
.. f t··
270 1--- - ~ - ········j··· i- --r~ --t-- - - -il;..--
250
··-·--·•·······-·······-········· - ----'.~-
'-.
230 -······ -· - i - - ... :··········-·····-· i.•. - .•

210 - ------+----- ~ - -~=.____ ..____ .... = .•. - - --'---- ---1
190 >----'---~--
- ---- -- - - -- - -- - - -~--- -----·
170 •- ·····--···-·······t - ~ - -- ···-····· ··-··-·1·····
150 1--- - - ' - - - -
130 I - -- - - ~< --< ACTION LINES - Take action if above these lines
-0- Referral line: start phototherapy and refer/discuss
_ . Phototherapy line: start phototherapy and repeat TSB daily
···!::..·.. Repeat line: repeat TSB in 6h or start phototherapy and do TSB daily
-e- 2nd Repeat line: repeat TSB daily
70 -···-··-··-· •,f\o,A" - - - - - - i - - ----,.- - If TSB is below the 2nd repeat line then monitor daily until it is falling or until
jaundice is resolving.
50 - - - -'---~---'----' ..... ..
30 ' - - - - - - - - - - - - - ' - - - --'------'-----------,.;...._----'----'---- - - - - - - ----'-- -- - - - - - - - '
6h 12h 24h 36h 48h 60h 72h 84h 96h 108h 120h
Age (hours)
129
PART THREE :-;eonatal paediatrics
Figure 7.3c
EXCHANGE TRANSFUSION
South African Neonatal Academic Hospital Guidelines: 2006
ln presence of sepsis, haemolysis, acidosis, or asphyxia,
use one line lower (gestation below) until <1 000 g.
If gestational age is accurate, use gestational age (weeks) rather than 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 hours of intensive phototherapy.
2. Immediate exchange is recommended if there are signs of bilirubin encephalopathy and
usually also if TSB is > 85 µmol/1 above the threshold at presentation.
3. Exchange if TSB continues to rise above 17 µmol/1/hour with intensive phototherapy.
r.===============.T - ---r--7 --r-- T -; - 7

-- ---····-··+··----
450
440 . - -0- - 38+ weeks or 3 000 g+
430 . -II- 37 - 38w6d or 2 500 - 2 999 g
420 · • • * ••
41 o . ,11 11111 .
400 · - D -
1111111
34 - 34w6d or 2 000 - 2 499 g
32 - 33w6d or 1 500 - 1 999 g
30 - 31 w6d or 1 2~0 - 1 499 g
l ,J--1--t·· ;---t --
390 · 28 - 29w6d or 1 000 - 1 249 g ,
380 · --+-- < 28w or < 1 000 g JJ'
C
:0
~ 310
i:n 300
E
::, 290
Q) 280
Cl)
270
260
... t···-····-··· :
200 t -- ~ ----- - - - - - ~- ---·-! ··············-··········-··
.
190 - - ~ - - ----;-,----+---,•·-·~~- ·-··--···••.0••··
180 ' - - - - - - -~ - ------ - - ---------------------~- - ------------------- - - '
6h 12h 24h 36h 48h 60h 72h 84h 96h 108h 120h
Age of baby (hours)
Phototherapy. This should be regarded as both Side-effects include hyperthermia, loose

prophylactic and curative. Optimal results are stools, and skin rashes.
obtained \vith blue light, but daylight is adequate. Intravenous immunoglobulin (MG) may be
Nappies should be left untied so that the maximum considered in haemolytic disease when the bili-
surface is exposed. Phototherapy should be given to rubin level is rising. The MG is given at 1 gm/
all LBW infants as soon as jaundice is noticed, to all kg over eight hours on three consecutive days.
infants 1,vith extensive bruising, to those 1,vith ceph- MG binds the red cell antibodies, preventing
alhaematomas, as well as to full-term infants ,vith further haemolysis. IVIG is not a substitute for an
TSB approaching exchange level. exchange transfusion.
Phototherapy should be discontinued as soon Exchange transfusion. Although the TSB
as there is a sustained fall in the unconjugated level gives an indication of the potential risk of
bilirubin level. Adequate hydration must be bilirubin encephalopathy, each baby has to be
maintained throughout the therapy with fre- assessed individually. An exchange transfusion
quent breastfeeds. 1he eyes must be covered may be required at a lower level of TSB if risk fac-
throughout the procedure. tors are present (see Chapter 38, Procedures).
130
The frequency of monitoring TSB levels Acute anaemia

depends on the severity of the jaundice, clini- Acute blood loss anaemia is a medical emer-
cal condition, and available facilities. Mild to gency. Pallor indicates hypoxia or, importantly,
moderate jaundice may require daily assess- anaemia due to acute blood loss before, during,
ment, whereas severe jaundice requires four- to or after delivery.
six-hourly determinations. If a bilirubinometer is The causes of acute anaemia may be related
being used, the standards must be checked regu- to the placenta, such as tearing of aberrant pla-
larly. cental veins, and feta-maternal or nvin-to-nvin
transfusion. Blood loss may occur during a trau-
Hydrops fetalis matic delivery with intracranial or intra-abdom-
inal haemorrhage. After birth, blood loss may
Hydrops fetalis describes a grossly oedematous occur if the cord is undamped, and the infant
fetus which is born anaemic, and has hepato- is held above the level of the placenta. Cephal-
splenomegaly, ascites, and pleural effusions. haematoma, soft tissue bruising, and bleeding
Besides Rh disease, congenital infections, most from the cord are other common causes. Rarely,
commonly syphilis, cytomegalovirus, and toxo- coagulation defects or thrombocytopaenia may
plasmosis may cause hydrops fetalis. Cardiac fail- cause bleeding.
ure, hypoproteinaemia due to hepatic and renal Initially the baby may be pale with normal
disease, nvin-to-twin transfusion, thalassaemia, heart rate and pulse volume. Some minutes or
and a host of miscellaneous conditions may be hours later peripheral vasoconstriction occurs
responsible for this condition. with tachycardia, a thready pulse, and low blood
1he management involves respiratory sup- pressure. During the second phase the baby
port, removal of the ascitic and pleural fluid (if becomes restless and finally lethargic and quiet.
they contribute to respiratory embarrassment) Without intervention death will ensue. When in
and slow correction of the anaemia by exchange doubt, serial haematocrit and haemoglobin esti-
transfusion. mations at hourly intervals will signify the need
Furosemide may be of assistance in controlling for transfusion.
the cardiac failure. Haemorrhage may be pre-
vented by the administration of vitamin K after Management. This depends on clinical assess-
birth and exchange transfusion \vi.th fresh whole ment of severity (see Table 7.12). Severely anae-
blood. Hypoglycaemia may also occur in these mic infants need oxygen and may need respira-
infants. tory support. It is \vise to check the prothrombin
index to exclude haemorrhagic disease of the
Haematological problems newborn. The blood sugar level must be moni-
tored before and during an emergency transfu-
(See also Chapter 25, Disorders of the blood.) sion.
- ~'"(er.
Table 7.12 Management of blood loss according t0 severity - .. -

- .
Colour Pulse BP -
Hb Haematocrit Management
Good N0rmal ~
Normal -
>15 65% Observe, check Hb/HCT 2 hours l9ter
Good Normal Normal 30-35% Transfuse - not ur~ent
Pale Normal Normal Irrespective Transfuse - urgent, Gross-match
--
Pale Thready Low Irrespective Transfl:.lse immediately. Use a plasma
expander while awaiting blood
- ·-
131
Chronic anaemia • Platelet disorders

Chronic anaemia at birth is suggested by pallor • Congenital deficiency of coagulation
and a well-compensated cardiovascular system, factors.
hepatosplenomegaly, and jaundice. Oedema
may be present if the anaemia is very severe. Haemorrhagic disease of the newborn
Blood group incompatibility, particularly Rh dis- This disease is more common in developing
ease, must be excluded. Chronic intra-uterine countries ,,vith poor socio-economic conditions.
infections, mainly congenital syphilis, may pres- Bleeding due to lack of vitamin K-dependent fac-
ent with anaemia. tors (II, VII, IX, X) classically occurs 48 hours after
Anaemia presenting late in the neonatal period delivery. Bleeding commonly occurs from injec-
may be due to frequent blood sampling or infection sites, cord stump, nose, and gastrointestinal
tion. The physiological anaemia of prematurity tract, but there may be intracerebral hae111-or-
presents at four to six weeks. Ideally, a record rhage. Multiple sites are commonly involved.
should be kept of blood volumes removed at each The diagnosis is confirmed by a prolonged pro-
venipuncture. Elemental iron 2 mg/kg is given thrombin time (International Normalised Ratio
daily once the baby is well. 1he VLBW infant or INR) which improves ,,11..in two to four hours
should also receive 25 IU of vitamin E daily. following the administration of vitamin K, 1 mg
IV. Preterm infants respond with a slower rise in
Polycythaemia the INR or prothrombin index and may require
Polycythaemia is diagnosed when the haema- fresh plasma or fresh whole blood in order to
tocrit is over 65 per cent, and is associated with control bleeding.
hyperviscosity, which may have serious con- Using Apt's test (see below) one can distin-
sequences, such as necrotising enterocolitis. guish fetal from maternal blood if the baby has
lhe infants at risk are those with hypovolaemia haematemesis and melaena. Similarly, if hae-
following twin-to-twin or materno-fetal trans- matemesis persists after a stomach washout, it is
fusion, underweight for gestational age, wasted almost certainly not maternal blood.
infants, and infants of diabetic mothers. Poly-
cythaemia is to be excluded by checking the
Apt's test
haemoglobin and haematocrit levels in at-risk
babies four to eight hours after birth. • 1 ml bloodstained vomitus or meconium +
Serious signs of hyperviscosity include central 1ml water; shake well and spin this mixture
cyanosis, respiratory distress, apnoea, convul- • 5 P.arts of supernatant + 1 part of 0.25%
sions, abdominal distension, cardiac decompen- NaOH
sation, and hypoglycaemia. Less ominous fea- • A pink eolour for more than 2 minutes = fetal
tures include poor feeding, vomiting, irritability, Hb; yellow/green = adult Hb.
lethargy, and hypotonia.
A partial exchange transfusion should be It is essential that all babies, including those of
performed, using 20 to 30 ml/kg of fresh frozen low birth weight, receive vitamin K1 1 mg IM at
plasma for any patient with a haematocrit over delivery in order to prevent this disease.
70 per cent, or 65 per cent plus any of the serious
signs. In view of the great risk of complications, Consumption coagulopathy (DIC)
such as cerebral infarcts, it is recommended Neonates ·with infection or hypoxia are liable
that the plasma is infused into a peripheral vein, to develop this form of bleeding disorder (see
while blood is withdrawn in equal volumes from Chapter 25, Disorders of the blood).
the umbilical vein. · Consumption coagulopathy may be associated
with systemic infection, asphyxia, hypothermia,
Bleeding disorders severe acidosis, and macerated twin. It usually
Bleeding disorders in the neonate include: presents in a seriously ill neonate, \'\11.th purpura,
• Haemorrhagic disease of the newborn bruising and bleeding from many sites, including
• Consumption coagulopathy haematuria and intraventricular haemorrhage.
132
7 ( :are of the newborn
Diagnosis. Clinical features are highly sug- Maintaining fluid and electrolyte homeostasis
gestive. 1he full blood count reveals anaemia, has revolutionised the care of the neonate at risk.
thrombocytopenia, and red cell fragmenta- As the baby adapts to the external environment
tion. Prothrombin, partial thromboplastin, and and independent existence, immaturity of gut,
thrombin times may be prolonged. In severe liver and kidneys together with delay in onset of
cases fibrinogen levels are reduced and fibrin feeding can result in a number of biochemical
degradation products are elevated. derangements.
Management. 1he baby must be treated vig- Water balance

orously for the underlying condition and the Basal fluid requirements are approximately
clotting defects corrected with fresh plasma 60 to 150 ml/kg/ day, increasing with age. 1he
10 ml/kg, platelet concentrates, and fresh whole less mature the baby, the greater are the losses,
blood. in particular with the use of the open incuba-
tor, radiant heaters, and phototherapy lamps.
Thrombocytopenia Osmotic diuresis (e.g. due to glycosuria in the
1he clinical expression of thrombocytopenia in stressed infant recehring a 10 per cent dextrose
the neonate is very variable. The platelet count is infusion), excess fluid losses from the gut, and
usually less than 50 000/mm3• Common causes diuretic therapy are examples of increased fluid
of thrombocytopenia are overwhelming bacte- losses. Fluid retention occurs in severely ill
rial infections, chronic intra-uterine infections, infants with asphyxia, poor renal function, and
consumption coagulopathy, maternal drugs, 'leaky' capillaries. Inappropriate antidiuretic
autoimmune disease, severe erythroblastosis hormone (ADH) secretion may occur in those
fetalis, repeat exchange transfusions, and con- with neurological and pulmonary problems.
genital leukaemia. Specific treatment for the Infants therefore vary greatly in their water
underlying condition ,vill reduce the bleeding requirements and need an assessment of fluid
tendency. Platelet transfusions may be consid- balance six- to twelve-hourly, depending on the
ered if the count is less than 10000/mm3 • An clinical state. The following are guidelines of nor-
exchange transfusion with whole blood is also mal urine values: urine volumes 50-100 ml/kg/
recommended. day, osmolality 75-300 mOsmol/kg, and specific
gravity 1005-1012.
Thrombasthenia The initial intravenous infusion should contain
A bleeding disorder ,vith the features of throm- 30-50 mmol/1 of sodium and 20 mmol/1 potas-
bocytopenia may occur in the presence of a sium with adjustments according to the electro-
normal platelet count and coagulation factors; lyte levels. 1he glucose requirement is adjusted
but platelet function may be defective. Chronic to the blood sugar level. Most infants are com-
ingestion of aspirin by the mother may give rise menced on a 10 per cent glucose infusion.
to this problem.
Congenital deficiency of coagulation Practice point

factors
1hese are rare conditions. The usual pr~entation In the following situahons J;>arenteral fluids
should be considered in place of oral feeds:
is one of prolonged bleeding from skin puncture
• At birth - severe birth asphyxia, weight less
sites in an othernrise well infant. Classical hae-
than 1.5 kg, major surgical conditions, se-
mophilia (Factor VIII) and Christmas disease vere respiratory distress
(Factor IX) are the most common deficiencies • Later - respiratory distress, apnoea, cyano-
(see Chapter 26, Disorders of the blood). The sis, intolerance of oral feed.s.
diagnosis rests on family history and demonstra-
tion of the relevant deficiency.
Oedema
Oedema is a common clinical problem. Accumu-
Fluid and electrolyte homeostasis
lation of oedema fluid can be brought about by
(See also Chapter 10, Metabolic disorders). decreased plasma oncotic pressure or decreased
133
tissue hydrostatic pressure. Immediately after ers with diabetes develop hypocalcaemia, which
birth the extracellular fluid mass is greater than may occur \vithin the first three days of life. In
the intracellular fluid compartment. During the infants fed unmodified milk hypocalcaemia may
first few days, however, the situation is reversed be seen after the end of the first week as a result
and weight loss occurs. Within a few days of birth of the high phosphate content of cow's milk.
the glomerular filtration rate rises with improved In term infants a serum calcium level of less
urinary concentration and no change in serum than 2 mmol/1 and in preterm infants less than
proteins. The body water may also be influenced 1.8 mmol/1 are regarded as hypocalcaemia.
by the amount of blood infused from the pla- Predisposing factors are:
centa and the mode of delivery: elective Caesar- + Relative hypoparathyroidism
ean section babies have a higher water content. + Preterm infants are relatively calciu1i;
The term baby tends to retain salt and may show deficient, and factors such as asphyxia,
oedema if challenged \vith a salt load. correction of acidosis, and exchange
1he preterm infant may have moderate transfusions may precipitate hypo-
oedema, probably due to increased capillary calcaemia.
permeability rather than hypoalbuminaemia.
Factors such as poor perfusion, acidosis, shock, Treatment. In babies \vith the predisposing
sepsis, severe respiratory distress, and hypother- factors, 3 ml of 10% calcium gluconate may be
mia aggravate this situation. added prophylactically to each 100 ml of glucose
Common causes of severe neonatal oedema infusion from the first day oflife, and the calcium
are Rh disease and severe haemolytic states, level monitored.
chronic intra-uterine infection, and congeni- Asymptomatic infants may be given oral cal-
tal nephrotic syndrome. In the VLBW baby cium carbonate, gluconate or lactate as elemen-
with HMD, fluid retention causes fairly severe tal calcium 30 mg/kg daily in divided doses, and
oedema. The syndrome of inappropriate ADH the blood level is then monitored.
(SIADH) secretion is commonly responsible for Symptomatic infants should receive 2 ml/kg of
oedema in hypoxic ischaemic encephalopathy 10% calcium gluconate diluted in 5 ml of 5% glu-
and severe parenchymal lung disease. This is cose and infused very slowly. Calcium may have
characterised by hyponatraemia. to be given intravenously or orally over days or
Careful assessment of salt and water intake is even weeks, and the dose gradually decreased
important in the oedematous baby. Maintenance and stopped.
fluids, plasma, or bicarbonate infusions should
be carefully administered. The weight, urine out- Hypomagnesaemia
put, peripheral perfusion, blood pressure, and This disturbance is very infrequent and diag-
temperature must be carefully monitored. The nosed when the serum magnesium level is below
known causes of oedema must be considered 0.62 mmol/1. Signs are indistinguishable from
and appropriate treatment instituted. hypocalcaemia and may occur in the UGA baby,
Fluid restriction is the first step in controlling the infant of the diabetic mother, or during
oedema. exchange transfusion. Hypomagnesaemia is cor-
A volume expander such as plasma and salt- rected by giving 0.1-0.3 ml/kg of 50% magnesium
poor albumin may be infused, followed by a sulphate IV or IM 12-hourly, \vith a maximum of
diuretic such as furosemide. three doses.
Underlying metabolic and temperature distur-
bances need to be corrected. Hypermagnesaemia
Oedema due to SIADH secretion frequently This uncommon disturbance occurs when
clears \vith fluid restriction. eclamptic mothers are treated \vith excessive
magnesium sulphate. Profound central ner-
Hypocalcaemia vous system depression \vith apnoea may occur,
(See Chapter 10, Metabolic disorders.) necessitating ventilation for a number of hours.
Approximately one-third of LBW babies and Hypernatraemia

about 50 per cent of the infants born to moth- (See Chapter 10, Metabolic disorders.)
134
Superficial abrasions on the infant's face, scalp,

Hypernatraemia is a serum sodium level above or other parts may be caused by blood sampling,
150 mmol/1. Insufficient fluid administration, rupture of the membrane by toothed forceps, or
and dehydration from excessive insensible water scalpel cuts during Caesarean section. Suturing
loss are the main causes. Phototherapy lamps may be necessary to prevent excessive blood
and radiant heaters tend to cause hyperthermia loss. These lesions should be kept clean and dry.
and diarrhoea. Excessive sodium bicarbonate Extensive bruising is often seen in the mark-
administration during resuscitation is a further edly preterm neonate. Oedema, bruising, and
iatrogenic element. haematomas may involve the vulva, scrotum,
and testes following breech delivery of the baby.
Hyponatraemia These injuries settle in a few days. This extrava-
(See Chapter 10, Metabolic disorders.) sation of blood may contribute to hyperbilirubi-
naemia and anaemia.
Hyponatraemia is a serum sodium level less than Subconjunctival haemorrhage follows on dif-
125 mmol/1. VLBW infants under 32 weeks' ges- ficult delivery. It usually clears spontaneously
tation are unable to conserve sodium and may ·within a week, requiring no therapy other than
lose more than 3 mmol/kg/ day in their urine. reassurance to the mother.
Severe asphyxia or respiratory distress may cause
SIADH, ·with water intoxication. Diarrhoea may Head injuries
be a cause of excess sodium losses.
Skull moulding denotes overriding of the cranial
Hyperkalaemia bones due to compression in the birth canal. It
1he causes are severe catabolism, acute renal does not necessarily imply intracranial injury.
failure, hypoxia, shock, acidosis, and congenital The skull bones assume a normal position within
adrenal hyperplasia. a few days.
Swelling of the head is caused by caput succe-
Birth trauma daneum, vacuum extraction, cephalhaematoma,
or sub-aponeurotic haemorrhage (see Table 7.13).
Minor superficial injuries
---
Tabl~ 7.13 Swellings of the head
- - - -
Caput succedaneum Vacuum extraction Cephalhaematoma Sub-aponeurotic
Haematoma haemorrhage
Site Diffuse over Lor.:alised at Localised, usually Diffuse over whole
presenting part site of vacuum over parietal bones, head underneath
application. Skin and under periosteum. cranial apoffe• rosis
subcutaneous tissue Extension limited by
involved periosteal a<ilhesion 0f
sutures
Cause Oedema and bruising Oedema± Haemorrage often Diffuse haemorrhage;
of presenting part haemorrhage at due to cephalo-pelvic sometimes follows
• vac1:.1um site disprop0rtion vacuum extraction
or poorly applled
forceps
Onse_t Present at birth Present at birth Often only detected May be present at
6-12 hours after birth; swelling often
birth. Becomes increases ouring first
11 progressivefy larger 2 days
- - - - over 1-2 days
135
PART TH REE l\"eonatal paediatrics
Distinguishing Diffuse. Petechiae Usually well defined. Well defined. Does Diffuse and
features over swelling Localised abrasions not cross suture lines. sometimes massive
at periphery of May be bilateral, haemorrhage.
I
swelling. Overlying but then a groove is Crosses suture lines.
skin may be purple present between the Bluish discoloration
two swellings. Skin of upper eyelids or
normal behind ears. Skin
normal
-
Course Disappears within 48 Subsides within 5- 7 Persists 6-8 weeks. Gradual reabsorption
hours days Centre may become •
of blood
fluctuant
Complications Nil Anaemia, infection, Anaemia, jaundice, Severe anaemia,
jaundice infection if aspirated. shock, jaundice
Rarely, underlying
skull fracture
-- -
Treatment Nil Local antiseptic to Usually nil. Observe Vitamin K. May
abrasions. Treat complications need urgent blood
complications transfusion
Skull fractures may be linear, stellate, or arm paralysis results from injury to cervical roots
depressed. Occasionally there is overlying soft 5 and 6 (Erb-Duchenne paralysis). The arm is
tissue swelling, but rarely intracranial dam- rotated internally and hangs limply at the shoul-
age. Nevertheless, observations for 36 to 48 der, the elbow is extended, the forearm pronated,
hours for signs of neuropathology are advisable. while the fingers are flexed in a 'waiter's tip' posi-
Depressed fractures resemble a ping-pong ball tion. Wrist action and grasp reflex are normal.
indentation and usually require elevation. Total arm paralysis (Klumpke paralysis) is due
to injury to the 7th and 8th cervical nerves.
Limb fractures Complete rupture of nerve roots results in per-
Fractures of the clavicle, humerus, and femur manent lesions. If the paralyses are due to bruis-
may occur during difficult deliveries. Move- ing of nerve roots, function returns within several
ments of the affected limb are restricted and months. Physiotherapy can be given to prevent
very painful. Splinting is usually not needed for contractures.
the upper limb, but femur fractures may require
traction. In every case the mother must be Spinal cord injury. This rare injury usually
,varned that a large callus is likely to form. results from traction on the legs in breech deliv-
ery. There is flaccid paralysis with loss of sensa-
Nerve injuries tion below the level of the lesion and bladder
Facial nerve paralysis, either due to forceps distension. The prognosis is poor.
application or occurring spontaneously, is
characterised by diminished movement of the Abdominal viscera
affected side of the face, with or ,,vith out ability to Occasionally a difficult delivery results in rupture
close the eye on the affected side. The baby may of the liver and/ or spleen. Large babies are par-
have difficulty in sucking. Treatment consists of ticularly prone to this serious injury. The first sign
keeping the affected eye clean by periodic instil- is usually shock, followed by anaemia and some
lation of sterile saline solution. The baby should abdominal distension. An urgent blood transfu-
be nursed on the unaffected side. 1he weakness sion and laparotomy are called for. An additional
usually resolves in hours to days. dose of vitamin K is advisable.
Brachia! plexus injury is a serious injury, which
is usually caused by excessive traction in cases of Intracranial haemorrhage
impacted shoulders or breech delivery. Upper The extent of the injury and the outcome depend
136
7 Care of the 11e,,vborn
on the underlying pathogenic factors. There are However, the chronic subdural collection is eas-
four major categories of haemorrhage in the ily tapped (see Chapter 38, Procedures). Chronic
newborn: subdural, primary subarachnoid, peri- collections may be tapped repeatedly over three
ventricular-intraventricular, and intracerebellar to four weeks and if they do not subside, surgical
haemorrhage. intervention is indicated, possibly ,vith a tempo-
rary subdural peritoneal shunt. In the acute vari-
Subdural fluid collections ety the blood must be evacuated.
This is the second most common cause of abnor-
mal head enlargement. The three main patholog- Hypoxic damage
ical types are haematoma, hygroma, and effusion
and all are managed along similar lines. Hypoxic ischaemic encephalopathy
Bleeding in the subdural space is due to dis- (HIE)
ruption of bridging veins from the cerebral sur- This results from significant hypoxia of the fetus
face to the major venous sinuses. Birth trauma or newborn. Hypoxia is due to the failure of gas
accounts for the majority of cases. Major factors exchange at placental level in the fetus and pul-
are cephalopelvic disproportion, the duration of monary level in the newborn. Perinatal hypoxia
labour, and the manner of delivery. Acute subdu- is predominantly an antenatal event, \Vith no
ral haemorrhages in the neonatal period gener- more than 10 per cent occurring postpartum.
ally have a poor prognosis. HIE is probably the major cause of cerebral palsy
Less commonly, bleeding disorders and in the developing world. The pathogenesis of
dehydration cause subdural bleeds. Hygromas brain damage resulting from hypoxia is illus-
result from laceration of the pia arachnoid and trated in Figure 7.4.
effusions as the result of infections. In an acute
subdural bleed the lysing blood clot creates an Figure 7.4 The cerebral consequences of asphyxia
osmotic gradient which draws fluid into the
space, enlarging the lesion and thus promoting Asphyxia Cortical necrosis
further bleeding.
Massive infratentorial haemorrhage manifests _'\_ _:f
from the time of birth. The signs are due to brain- Cerebral ischaemia
stem compression, namely deviation of the eyes, ;P
unequal pupils, rapid respiration, and opisthoto- Cerebral oedema
nus. If haemorrhage progresses coma ensues, the
pupils become fixed and dilated, ocular bobbing ~
appears, and finally respiratory arrest occurs. If Raised intracranial pressure
the haemorrhage is less catastrophic the infant
may survive with the late development of hydro- As fetal respiration is controlled by placental
cephalus. circulation, fetal hypoxia implies some degree
Minor subdural haemorrhage over the cere- of placental ischaemia. 1he systemic response
bral convexities may be asymptomatic. Focal sei- to hypoxia, hypercarbia, and mixed acidosis
zures may occur together ,vi.th other focal cere- is maintenance of cerebral blood flow at the
bral signs. expense of other organs. It follows that if an epi-
Hygromas do not expand because the pia is sode of hypoxia is sufficiently prolonged and
less vascular and the effusions are absorbed with severe, other organs such as the heart will be
resolution of the infection. affected. With further decreased cardiac output,
hypotension occurs and perfusion of the brain,
Diagnosis. In acute subdural bleeds, subhya- kidney, lung, and gut is compromised. 1he clini-
loid haemorrhage may be seen on fundoscopy. cal effects are those of ischaemia of these organs.
A computerised tomography (CT) scan is the The duration and severity of signs depend on the
investigation of choice. period of hypoxia and/ or ischaemia.
Treatment. Subdural clotted blood may be diffi- Clinical features. 1hese are caused by hypoxia
cult to drain by needling and require a burrhole. and ischaemia occurring simultaneously or in
137
sequence. Following severe intra-partum hypoxia • Feeding is by a nasogastric tube, the •

and/ or ischaemia, the infant goes into coma and volume not exceeding 80 ml/kg/ day for
has convulsions. Hypoxia during labour may the first two to three days.
be followed by a lucid interval of 12 to 18 hours, • Respiratory support for a limited period
before convulsions occur, which at times are sub- may be considered for the infant with
tle and expressed as apnoeic or cyanotic attacks. severe HIE.
The respiration is often irregular ·with a Cheyne- ' • Meningitis may be clinically
Stokes pattern suggesting diffuse bilateral hemi- indistinguishable from HIE. If in
sphere pathology. With a severe insult brain-stem any doubt, a lumbar puncture and
signs occur, such as fixed, dilated pupils, and examination of the cerebrospinal fluid
abnormal or absent eye movements. Motor weak- should be performed.
ness is the main clinical manifestation of primary • Babies ·with moderate HIE can benefit for
ischaemia. The fontanelle may become full as a a process of head or total body cooling
result of cerebral oedema. which requires special equipment.
1he clinical grades of HIE are mild, moderate,
or severe, depending on the severity and dura-
tion of neurological signs. Early improvement Practice point
suggests a good prognosis.
• Mild rllE manifests neurological signs such
as feeding and tone di~turbances for 24 to
Management. The most important aspect is pre- 48 hours.
vention, by identifying the fetus at risk of hypoxia • Mocl.erate HIE includes convulsions and signs
and taking the necessary steps to prepare for which last for four to five days.
prompt resuscitation. Where a baby has been • Severe HIE is diagnose<il if the physical signs
hypoxic, brain-oriented management is impor- are severe and persist for seven to 14 days
or more.
tant and is directed at relieving factors that aggra-
vate or contribute to hypoxia.
• Raise the head to 30 degrees above the A number of drugs, such as calcium channel
plane of the body. blockers, magnesium sulphate, prostaglandins,
• Adequate control of seizures is essential. and neurotransmitter inhibitors, are under
Some seizures are subtle. investigation but not yet recommended.
• Keep the infant's core temperature at Complications such as pneumonia, hypogly-
35°C for 48 hours. This reduces the risk of caemia, inappropriate antidiuretic hormone
progressive brain damage. secretion, must be borne constantly in mind.
• Avoid hypoglycaemia by maintaining the Long-term follow-up of the child is essential to
blood sugar level above 2.5 mmol/1. detect complications and developmental handi-
• Monitor the blood pressure. Hypotension cap. Appropriate rehabilitative measures must
occurs frequently in severely hypoxic be introduced.
infants. If fluid replacement does not Fortunately an appreciable proportion of
restore normotension, dopamine may be those ,.vho make rapid and early progress remain
used. Dopamine is of value in the baby free of any deficit.
with poor urine output as well.
• Routine administration of alkali is Convulsions
not recommended. Acidosis corrects Neonatal seizures result from an insult to the
spontaneously if the infant is adequately brain. In themselves they are also injurious to the
and efficiently resuscitated at birth. neurones. Furthermore, the concurrent respira-
• Clotting disturbances may occur and tory disturbance causes hypoxia and hypercap-
are most often due to disseminated nia (see Figure 7.5).
intravascular coagulation. Management The types of convulsions include:
is supportive, the infant should receive • Subtle convulsions are very common.
vitamin K, fresh frozen plasma, platelet The physical signs include deviation of
transfusion, and fresh whole blood as the the eyes, repetitive blinking or fluttering
clinical condition demands. of the eyelids, drooling, sucking, cycling
138
movements of the lower limbs, rowing Management:

movements of the upper limbs, tonic • Convulsions must be controlled as a
posturing of a limb, apnoea attacks, matter of urgency (see Table 7.14).
cyanotic episodes, an abnormal cry, and • Phenobarbitone is the drug of choice for
stertorous respiration. seizure control. Failing this midazolam
• Tonic seizures indicate severe infusion may be considered. This
encephalopathy. benzodiazepine has fewer side effects.
• Clonic convulsions may be focal or • Supportive care is provided as for any
multifocal. Lastly there are myoclonic unconscious neonate.
seizures, which are single or multiple • The ainvay must be kept clear with regular,
flex.ion jerks of groups of muscles. gentle naso- and oropharyngeal suction.
• Oxygen is administered if the baby is
Figure 7.5 The pathogenesis of brain damage in cyanosed.
neonatal convulsions • The baby is nursed prone or on the side
with regular changing of position to
REPEATED SEIZURE
facilitate drainage of secretions.
____k j_ • Monitor temperature, blood pressure,
apnoea
p-~ iAT~
oxygen saturation, and blood sugar levels.
• The baby must be tube-fed, commencing
tpC02 .J.. p02
with 80 to 100 ml/kg/ day.
V \/
tlCP CVS
Table 7.14 Anticonvulsant drug use
+
T J)-
collapse
Cerebral blood flow :::::::,..

Drag
Seizure control
Dose
--
-
- -
-- - ---- --
lnifial:
Phenobarbitone The dose is 30 mg/kg/IV
intravenously slowly over 20 minutes (not
Practice point
faster than l mg/kg/min)
The prognosis depends on the duri;itic;m and Subsequent seizure: 0.15 mg/kg IV bolus followed
severity of the cerebral insult. A neonate wrth
Midazolam by infusion of 0.1 to 0.4 mg/
prolonged loss of consciousness and gener-
alised hypotonia with severe convulsions very ~ -
kg/hour.
=
rarely makes a complete rec0very e-specially if Maintenance
-
the signs remain beyond seven days. Cerebral
palsy, microcephaly, and lesser degrees of
Phenobar0ital 3'-5 mg/kg/day in 1~2
neurological impairment are the sequelae of divided doses, started 12
profound cerebral hypoxia. hours after the loading dose.
-
When seizures have ceased for 24-48 hours, the

Jitteriness must be distinguished from convul- anticonvulsant dosage may be reduced gradually
sions: it is not accompanied by loss of conscious- over days.
ness or abnormal eye movements and stops as
soon as the limbs are held. However, it starts Prognosis. The nature of the underlying neuro-
again easily with stimulation. Bradycardia, pallor logical disease will determine the eventual out-
or cyanosis do not occur. come in the individual baby ·with seizures. Gen-
The most common causes of neonatal convul- erally:
sions are HIE, birth trauma, metabolic distur- • Babies with convulsions due to HIE have
bances such as hypoglycaemia and hypocalcae- only a 50 per cent chance of normal
mia, hypothermia, intracranial infections, elec- development.
trolyte disturbances (particularly sodium imbal- • Hypoglycaemia-associated convulsions
ance), and narcotic and alcohol withdrawal. have a similar outcome.
139
PART THREE .Neonatal paediat1ics
• Convulsions due to intracranial infection The pathogenesis has as yet not been fully clar-
are associated with permanent damage in ified. However, hypoxia and ischaemia are major
20-50 per cent of cases. factors; in addition, raised cerebral venous pres-
• Severe intraventricular haemorrhage sure occurring during resuscitation contributes.
causes 65-100 per cent morbidity\'\rith a Furthermore, there is marked fibrinolytic activity
mortality of 50-65 per cent. in the newborn, which promotes spread of the
haemorrhage.
Follow-up. It is essential that all babies who have 1he clinical presentation is variable and
had convulsions are assessed neurologically at depends on the size and rate of bleeding. Small
regular intervals in order to detect deficits, which haemorrhages may produce no signs. With large
usually manifest ·within 9-12 months. Minor prob- haemorrhages loss of consciousness, apnoea,
lems are often not detected during the pre-school convulsions, a full fontanelle, and anaemia may
period, but arise later as attention and learning occur. Altered muscle tone, behaviour distur-
difficulties. With expert counselling of the parents bances, and progressive head enlargement may
and correct management, many difficulties may be the only signs.
be overcome at home. Infants with significant The classical clinical features make the diagno-
neurological deficits may re-quire the assistance sis easy. Ultrasonography is used for confirma-
of a physiotherapist, occupational therapist, and tion; in difficult cases a CT scan may be indicated.
clinical psychologist. Hearing, vision, and speech These are also used for grading of the lesions.
assessments may be necessary. A unilateral Grade IV IVH may lead to a poren-
cephalic cyst and hemiplegia; bilateral lesions
Subarachnoid haemorrhage are usually fatal. No definite guidelines for treat-
This haemorrhage is related to hypoxia in term ment have been established. Intervention is not
infants. The development of the haemorrhage indicated for those with severe haemorrhage, as
probably occurs as a result of vascular injury the mortality is in the region of 90 per cent and
following hypoxia and ischaemia. Small bleeds the remaining patients have severe morbidity.
occur commonly \Vithout clinical manifesta- Blood transfusions, anticonvulsants, and even-
tions. Very few will have a structural lesion such tual shunting may be indicated. Approximately
as an aneurysm or a vascular malformation. 35 per cent of babies with MI develop post-
The clinical features are difficult to outline haemorrhagic hydrocephalus.
because of the associated manifestations of Recent evidence indicates that the outcome in
hypoxia. Convulsions may occur on the second the milder cases does not depend on the extent
day of life. Benveen seizures these babies appear of the haemorrhage but on the initiating events
very well and the prognosis is excellent. A mas- and circumstances. With steady improvement in
sive haemorrhage runs a fatal course and is often the management of these small babies, the inci-
associated with trauma. 1he cerebrospinal fluid dence and complications of IVH are decreasing.
is bloody, and later xanthochromic, \\'1th a high
protein and an increased cell count.
Practice point
Intraventricular haemorrhage (IVH)
1his classical haemorrhage of the preterm infant
Grade I (bleed into the germinal matrix only)
occurs within the first 72 hours of life, often in and Grade II (extension of the bleed into the
association with respiratory distress. It starts as a ventricles) can be expected to achieve a full
haemorrhage into the germinal matrix and then recovery. Grade Ill (ventricles dilated with blood)
may burst into the ventricles. The delicate vessels is associated with a risk of obstructive hydro-
of the germinal matrix form a large unsupported cephafus. An associated periventricular venous
network of capillaries, which ruptures easily. infarct is also called a Grade IV intraventricular
In 20-40 per cent of lesions the haemorrhage is haemorrhage.
confined to the brain tissue (germinal matrix)
and does not rupture into the ventricles. As the Periventricular leucomalacia (PVL)
fetus matures, the germinal matrix becomes less PVL occurs when ischaemia is prolonged or
vascular. 1his form of haemorrhage is therefore severe in a preterm infant. 1his degenerative
rare in the term baby. process may resolve or progress to multiple small
140
7 Care of the ne,vborn
cysts; clinical features are determined by the site 2 lntracri:lnial haemorrhage

and extent of the injury. The diagnosis is made
su0dural, subaraGhnoid, intraventricular,
by intracranial ultrasonography after the first few
intrpcerebral, and intracerebelli;ir
days of life.
3 Metabolic encephalopathy
Parasagittal cerebral damage hypoglycaemia, kernicterus, hypothyroidism
4 Infections
This typical cerebral lesion occurs in the term
infant. There is necrosis of the cerebral cortex
and subcortical white matter with characteristic A number of disorders of the CNS are preventable.
bilateral symmetrical distribution leading to leu- The risk of neural tube defects may be reduced by
comalacia of the parasagittal and supero-medial the administration of folate preconceptually, the
aspects of the cerebral hemispheres. 1he 'water- fetal alcohol syndrome by the avoidance of alco-
shed' infarct that follows cerebral hypoperfusion hol preconceptually and throughout pregnancy,
emphasises the ischaemic nature of the lesion. In and the screening of mothers over 35 years for
severe cases, necrosis extends to the lateral cere- chromosomal defects.
bral convexity. Clinically, spastic motor deficit, Only the commonly encountered conditions
seizures, and intellectual impairment occur. and those requiring urgent treatment vvill be dis-
cussed.
Focal ischaemic cerebral injury
Focal ischaemic lesions may also occur as a
Meningomyelocele
result of generalised cerebral hypoperfusion, This is the most common neonatal CNS disorder
with the middle cerebral arteries being most referred to neurosurgeons. This midline defect
frequently involved. Infarction occurs with sub- of the skin and vertebral arch containing both
sequent cystic development, which may or may meninges and neural tissue occurs most com-
not communicate vvith the lateral ventricles. 1he monly in the lumbosacral region. The aetiology
unilateral lesion results in hemiparesis and mul- is poorly understood. 1he prevalence is 0.2-0.4
tiple lesions may cause quadriparesis. per 1000 births with variation in different popu-
lation groups. 1here is evidence that adequate
folate supplementation preconceptually and
Congenital malformations of the cen- during the first trimester will reduce the risk of
tral nervous system this condition occurring. The risk of recurrence
is increased in subsequent pregnancies. The
The common disorders of the central nervous
Arnold Chiari malformation is the most common
system (CNS) in the neonate fall into nvo major
associated congenital abnormality and causes
categories, namely developmental defects and hydrocephalus.
perinatally acquired conditions (see Table 7.15).
Many cases are diagnosed by ultrasound
in early pregnancy when termination can be
Table 7.15 Lesions of the central nervous system offered. 1he diagnosis is usually quite obvious
I. Developmental defects at birth, with motor and sensory impairment,
1 Neural tube defects and bladder and bowel incontinence depending
encephalocele, myelomeningocele, spina bifida on the level of the lesion. Cranial ultrasound is
occulta, anencephaly used to demonstrate the initial ventricular size
2 Defects in growth and differentiation and to monitor subsequent distension. Associ-
chromosomal defects, porencephaly,
ated abnormalities can be excluded by CT scan.
Careful neurological assessment of the lower
hydranencephaly, megalencephaly,
limbs, bladder, and bowel function is important
holoprosencephaly
for prognostic purposes.
3 Defect in cerebrospinal fluid circulation
hydrocephalus, Dandy-Walker malformation,
Management. (See also Chapter 8, Surgical care
aqueduct stenosis of the newborn). Post-operatively the orthopae-
II. Perin•atally acquired conditions
dic, renal, and general problems must be evalu-
1 Hyp0xit ischaemic encephalopathy
ated. The head circumference must be closely
141
monitored as hydrocephalus is a common 3rd centile. The forehead tends to recede and may
sequel requiring ventricular shunting. The pre- appear relatively large. Initially, motor develop-
natal diagnosis of neural tube defects by means ment appears reasonable but as the head fails
of serum alpha feto-protein determination and to grow, motor and mental retardation become
antenatal ultrasonography must be offered to the more apparent. The outcome is better if the baby
mother for her future pregnancies. \vith a small head demonstrates head growth
along a particular centile without fall-off. Skull
Spina bifida occulta X-rays, serological tests, and a lumbar puncture
In this condition, which occurs most commonly assist in the diagnosis of microcephaly due to
at LS and Sl, there is a defect of the vertebral intra-uterine infection. Periventricular calci-
arch with failure of posterior fusion of the ver- fications occur in congenital cytomegalovirus
tebral laminae, and frequently absent spinous infection; diffuse cerebral calcifications occur in
processes. Associated vertebral body anomalies congenital toxoplasmosis.
such as hemivertebrae may occur. The overlying The fetal alcohol syndrome is a very important
skin may be quite normal or there may be a tuft of cause of microcephaly and growth retardation.
hair, telangiectasia, or subcutaneous lipoma. It is This condition must be suspected in a baby ,ivith
often an incidental finding. Less commonly there the following features:
are neurological signs including those associated + Small palpebral fissures and apparent
with meningomyelocele, e.g. unilateral leg and hypertelorism
foot lesions or bladder dysfunction. Diagnosis is + Smooth upper lip and absent philtrum
by X-ray of the spine, and further investigation is + Symmetrical growth retardation
indicated only if there is progression of neurolog- + Abnormalities of heart, skeleton, and
ical signs. Associated tumours may be removed palmar creases.
without neural tissue damage.
(See also Chapter 3, Medical genetics and con-
Anencephaly genital disorders).
Anencephaly is obvious at birth with absence of
the vault of the skull and cerebral hemispheres. Microcephaly must be distinguished from cra-
The brain stem and basal nuclei may be seen at nial synostosis affecting the sagittal and coronal
the base of the skull. 1hese infants are stillborn sutures which results in a small head. The pre-
or die \vithin hours or days of birth. Most cases maturely closed suture can usually be palpated
are now diagnosed ,vith routine antenatal ultra- clinically, and raised intracranial pressure is evi-
sound. dent as papilloedema and on skull radiograph.
This condition can be treated surgically.
Microcephaly
Isolated microcephaly is not associated with Hydrocephalus
destructive disease and is a disorder of cell pro- This term refers to an abnormally large head with
liferation, therefore brain growth as a whole is an increase in CSP, which is or has been under
defective and the resultant head size is belmv the increased pressure. 'Where the flow of CSF out of
3rd centile. The condition may occur in males the ventricular system is obstructed, the pressure
as an X-linked disorder. Developmental abnor- effect is from \vithin the brain. In the communi-
malities affecting the fetus or the young infant cating variety, on the other hand, there is inter-
may also lead to poor brain growth. Pathologi- ference \,vi.th CSP flow or absorption outside the
cally there is a decrease in total brain weight, a brain.
decrease in the number, size, and the complex-
ity of the gyri. The frontal lobes are usually more Aetiology. The aetiology is unknavvn in the
severely affected; follmving perinatal insults majority of congenital varieties of hydrocephalus
there may be associated gliosis and neuronal loss where there is a range of malfunctions. In a small
in the cerebral cortex. Often the cerebellum is proportion, congenital infections and genetic
relatively spared and appears disproportionately factors play a role. Meningitis, trauma, and intra-
large. Clinically the head is small compared to cranial haemorrhage are the common causes of
the body and the circumference well below the acquired hydrocephalus.
142
Clinical features. The big head may be obvi- These are:

ous at birth, or even diagnosed antenatally. At • Maternal infection, both acute and chronic:
times the head enlargement develops gradually • Amniotic fluid infection syndrome
with very few signs early on, but subsequently (chorioamnionitis) is a common
anorexia, vomiting, irritability, and lethargy are condition.
seen. A bulging fontanelle and separation of the • Newborn babies become colonised at the
sutures are invariably present. Superficial venous same time that they have to develop their
engorgement is variable, and the classical sign of O\'lln immunity.
the 'setting sun' eyes appears late. • Immature host defence mechanisms -
Benign enlargement of the head (or consti- both qualitative and quanitative:
tutional macrocephaly) must be differentiated • Newborns do not have IgM and IgA
from hydrocephalus. Once soft tissue swelling of antibodies; the latter protects the
the scalp has been excluded, serial head circum- mucosa! surfaces.
ference measurements will demonstrate propor- • Low birth weight and prematurity-
tional growth in the former. There ·will also be no passive transfer of antibodies occurs late
evidence of raised intracranial pressure. in gestation.
Subdural fluid accumulation must also be con- • Obstetric or resuscitative procedures.
sidered in the differential diagnosis. Rarely intra- • Anatomic: long cord stump, delicate or
cranial cysts or tumours present a similar clinical cracked skin.
picture. • Nursery environment: crowding, under-
staffing, poor hand-washing facilities.
Intervention. The prolonged pressure effect
causes CSP to leak into the surrounding white For these reasons, neonates become infected
matter ·with resultant atrophy. In the first with Gram-negative bacteria as well as all the
instance it is important to record and plot serial 'usual' infections, and if infected, they are par-
head circumference measurements. Early refer- ticularly likely to develop septicaemic illness.
ral for shunting is necessary as soon as excessive The prevention of infection is very important
head enlargement is demonstrated. If cranial and prompt recognition is necessary for opti-
ultrasonography is available and shows progres- mal management. It is equally important to stop
sive enlargement of the lateral ventricles, along antibiotic therapy when the investigations and
with the development of a full fontanelle, referral subsequent clinical picture do not support the
for shunting is indicated. diagnosis of infection. Antibiotic therapy is not
The prognosis depends on the severity of asso- only a discomfort to the patient and a consider-
ciated malformations and the extent of subse- able expense, but also increases the risk of devel-
quent brain damage. oping resistant organisms.
Complications are not uncommon and often
necessitate reinsertion of the shunt. Patients Common organisms
with arrested hydrocephalus require prolonged The common bacterial pathogens are the Gram-
observation for low-grade pressure build-up. positive organisms, such as Group B Strepto-
coccus, Streptococcus faecalis, Staphylococcus
Infection aureus, and Listeria monocytogenes. Gram-neg-
ative organisms are Escherichia coli and Kleb-
siella pneumoniae. Infection due to herpes,
Practice point enteroviruses, chlamydia, and Pneumocystis jir-
oveci may present in the same manner.
Newborn babies may be infected before birth,
at birth, or in the neonatal perio·d. Superficial infections
Constant vigilance for infections is essential in
Acquired neonatal infections the follmving areas: skin, umbilicus, eye, mouth,
The reported prevalence of infection in neonatal and perineum.
units varies from 7-30 per cent. Certain predis- Systemic antibiotics are rarely indicated. Any
posing factors increase the risk of infection in the pustules and abscesses of the skin should be
neonate. opened and the pus collected for a Gram stain
143
and culture. The lesions are cleaned with alcohol Investigations. To confirm suspected infection
or chlorhexidine and left exposed to air. Strict a full blood count and smear and blood culture
hand-washing should be observed and the baby are performed and material from superficial
isolated if possible. lesions is examined by Gram stain. Cerebrospi-
Conjunctivitis requires prompt treatment, pre- nal fluid (CSP) is examined and cultured if there
ceded by a Gram stain and culture (see Chap- is clinical suspicion of meningitis. Urinary tract
ter 35, Disorders of the eye). The eyes must be infections generally occur after the first week of
cleaned \vith saline and a broad-spectrum anti- life and may be considered in late-onset infec-
biotic instilled two- to four-hourly. If the eyelids tions. A C-reactive protein (CRP) estimation is
are red and swollen (blepharitis), ceftriaxone very useful; in conjunction with the white cell
125 mg IM or IV is given in a single dose. count it gives support to a clinical diagnosis of
For oral thrush, nystatin suspension is instilled sepsis. Both of these are also of value in assess-
after each feed. Nystatin cream must be applied ing response to treatment. A chest radiograph
to the perinea! area when this is involved. Monil- should be considered even in the absence of
ial infection of the mother often calls for con- signs of respiratory distress. A Gram stain of the
comitant therapy. gastric aspirate before the first feed is helpful if
An umbilical flare ,vithout induration may be chorioarnnionitis is suspected: the presence of
regarded as a superficial infection. Shortening organisms and pus cells is indicative of infection.
the stump and spraying the area frequently with In the tuberculosis-exposed infant chest radio-
alcohol is all that is required. Dressings should graph, lumbar puncture for the tubercle bacil-
not be applied but the area should be observed lus and a baseline full blood count, tuberculosis
for spread of infection. blood culture and liver function tests are done
(see Chapter 17, Tuberculosis).
Septicaemia Babies exposed to tuberculosis should receive
prophylaxis ,vith isoniazid and rifampicin for
The diagnosis of infection may be very difficult in three months.
the newborn because of subtle and non-specific
presentation. Certain clinical features, however, Management
are highly suggestive of infection, while others + Penicillin and an aminoglycoside are
indicate obvious sepsis. started early once infection is suspected
Septicaemia should be suspected when three until culture reports are available, when
of the follmving are present: antibiotics are either stopped or changed
• Predisposing factors as above according to microbial sensitivity.
• Unstable temperature • The duration of antibiotic therapy
• Lethargy depends on the nature of the organism
• Poor colour and the clinical condition of the patient,
• Apnoea but in general, proven septicaemia is
• Feeding difficulties treated for seven to 10 days.
• Vomiting • Supportive care of the infected neonate
• Abdominal distension in respect of metabolic derangements,
• Sclerema hypothermia, abdominal distension,
• Superficial sepsis. hypoxia, poor perfusion, and so on is as
important as the specific antibiotic.
A combination of the follmving signs is strongly
indicative of serious infection: Prevention
• Purpura • All personnel handling neonates must
• Anaemia be trained in the prevention of and the
• Jaundice dangers of infection. Contamination
• Hepatomegaly from the hands of attendants is the most
• Splenomegaly important source of infection. Hand-
• Full fontanelle washing before and after handling an
• A swollen joint. individual baby is recommended and
144
attendants' hands must be sprayed with Another form of nursery-acquired infection

antiseptic before touching a baby. occurs in babies supported by respirators. 1his
• Careful attention to the umbilical cord disastrous, often low-grade, chronic pneumo-
and meticulous cleaning of the skin before nia from organisms such as Klebsiella and Pseu-
venepuncture are mandatory. 1he use domonas contribute to mortality and chronic
of prophylactic antibiotics in newborn pulmonary disability. These organisms are
infants should be discouraged. harboured in equipment such as humidifiers
• Exclusive breastfeeding and kangaroo and suction apparatus. Once established, these
mother care are most important aspects in organisms are extremely difficult to eradicate.
the prevention of infection. Both colonise
the infant 1,vith community bacteria of low Meningitis
pathogenicity and protect against harmful
hospital bacteria. This is perhaps the most difficult diagnosis to
• Overcrowding must be avoided and make on clinical grounds alone. 1he classical
isolation facilities for highly infectious signs occur very late in the neonate. An added
illnesses, such as acute infective difficulty is the fact that a full fontanelle and con-
diarrhoea, must be available in all units. vulsions are frequently not due to meningitis.
Should these signs occur in the presence of men-
Pneumonia ingitis, the prognosis is poor.
Meningitis is therefore diagnosed on clini-
Pneumonia is an important cause of morbidity cal suspicion, and an examination of the CSF is
and mortality in the neonatal period. Infection recommended in any infant who is suspected of
may be transmitted via the placenta, by aspira- having sepsis. Ventriculitis is a characteristic fea-
tion during delivery, or acquired postnatally. ture of neonatal meningitis and is very resistant
The clinical features include those of respira- to treatment.
tory distress and the specific infection.
Aspiration pneumonia is acquired during the Osteitis and septic arthritis
last days of pregnancy or at birth by aspirating
infected material and can occur in the presence There are t\vo anatomical reasons why these
of intact membranes (chorioamnionitis) or rup- conditions occur together so frequently. Firstly,
tured membranes (if ruptured for more than 12 the capsules of the hip and shoulder joint are
hours). Sometimes aspiration of maternal fae- attached below the metaphysis of the femur and
cal material at the time of delivery may result in humerus respectively. Infection of the epiphy-
pneumonia. Clinically the liquor may be offen- seal cartilage will extend into the joint space,
sive and the onset of the illness occurs within causing purulent arthritis. Secondly, during the
minutes or hours of birth. Signs of respiratory first year of life capillaries perforate the epiphy-
distress may be mild or severe and delayed for seal plate of the long bones and provide a com-
a day or nvo. The microbes involved are group B munication between metaphysis and joint space
beta-haemolytic Streptococcus, Pneumococcus, so that spread readily occurs. The most common
and coliforms. organism is Staphylococcus aureus followed
In postnatally acquired pneumonia, the signs by Group B Streptococcus and Gram-negative
of respiratory distress usually appear after the organisms. This disease may follow certain inva-
first week of life. Common bacteria are coagulase sive procedures, such as femoral vein puncture
positive Staphylococci, Streptococci, Escherichia and umbilical catheterisation.
coli, and Klebsiella pneumoniae. Respiratory The most useful physical sign is decreased
syncytial virus, influenza A and B, adenovirus, movement of the affected limb; redness and
and echoviruses have been associated with out- swelling are late signs. Of all the serious infec-
breaks of pneumonia in nurseries. Chlamydia tions this is most often diagnosed late. Early
and Pneumocystis jiroveci may be responsible X-rays may still be normal (see Chapter 33,
for infection, particularly in premature babies. Orthopaedic disorders).
145
Specific infections Listeria monocytogenes

This facultative anaerobic Gram-positive bacillus
Chlamydia trachomatis may cause disease in a similar way to GBS. Infec-
The organism is acquired by the baby from the tion during pregnancy may be associated \vith
mother's birth canal and colonises the nasophar- spontaneous abortion, stillbirth, or disseminated
ynx in the majority of cases. disease in a premature baby. This frequently
Conjunctivitis occurs within five to 14 days presents \vith a diffuse pustular rash, hepato-
and may be mild or very severe \vith purulent splenomegaly and a very high mortality. This
discharge. organism may present early or late in infection.
Pneumonia develops in about 25 per cent of
babies with nasopharyngeal colonisation. The Treatment: Ampicillin and an aminoglycoside
onset is insidious about one to three months after are used together. Listeria are not susceptible to
birth. Cough and tachypnoea are present, but the the cephalosporins.
absence of fever and significant wheezing serves
to differentiate this infection from that caused by Chronic intra-uterine infection
respiratory syncytial virus. The peripheral blood
smear often shows significant eosinophilia. Congenital infections are acquired in utero
Diagnosis is by culture or serology. because of transplacental spread of infection
Treatment with erythromycin has to be pro- \vithin the mother's bloodstream, or because of
longed for 14 days for a response. direct spread from infected amniotic fluid. They
affect the fetus in two ways:
Streptococcus agalactiae ( Group B beta • By inducing organ damage, which persists
haemolytic Streptococcus - GBS) after the maternal infection has been
This common commensal of the genital and treated or overcome. These are teratogenic
gastrointestinal tract of pregnant women may influences for maldevelopment or
colonise their babies. The mothers are usually permanent changes.
asymptomatic but may have urine infection or • By blood-spread dissemination and
chorioamnionitis. persistence of the infection at the time
Early-onset infection (\vithin 72 hours to seven of birth. Such babies show pathology
days) is more common than late-onset disease. and dysfunction of many organ systems
Many babies are symptomatic at birth, indicating at birth together with a septicaemic
exposure in utero, which often arises in amniotic presentation.
infection. Immature, low-birth-weight babies are
particularly prone. Clinically, babies suffer from The prenatally acquired infections should be
pneumonia \vith respiratory distress which can diagnosed in the presence of a combination of
mimic hyaline membrane disease. This is often hepatosplenomegaly, jaundice, anaemia, and
complicated by pulmonary hypertension. Bacte- purpura in the newborn baby. Apart from the
raemia occurs frequently, and the patients may above, HIV infection, tuberculosis, hepatitis B
have disseminated disease, including meningitis and listeriosis should be considered. In syphi-
and septic shock. The mortality rate is high. lis, typical skin lesions and/ or metaphysitis may
Late-onset infection accounts for 20 per cent occur in isolation or together \vith this constella-
of cases. This can develop at any time, but after tion of signs.
one month of age is usually associated \vith pre- HIV-exposed neonates suffer an additional
maturity and immunodeficiency. This presents as burden of disease, especially in the small, wasted
bacteraemia or meningitis. Disseminated foci of preterm infant. These babies may experience a
infection can develop. number of co-infections, including tuberculosis,
Diagnosis is by culture of blood, CSP or other syphilis, cytomegalovirus, herpes simplex, fungal
fluids. infections and recurrent acute bacterial infec-
Treatment is \vith penicillin G. tions. 1hese babies present in the latter part of
the second week or in the third week of postnatal
life. The mode of presentation in infants infected
·with HIV during pregnancy is one of persistent or
146
recurrent pneumonia, fungal or bacterial infec- deafness, psychomotor retardation,

tions. These latter infections may be superficial microcephaly, and spastic quadriparesis.
or systemic.
Pregnant women who are exposed to rubella in
the first trimester in pregnancy should be tested
Pradice J:)Oint
and if found to be infected, therapeutic abortion
should be advised. Immunoglobulin therapy is
A number of pathogens are involved in causing of no value in such cases. Immunisation \vith the
similar clinical manifestation~. conveniently re-
live virus rubella vaccine is not advised in preg-
membered by the word, TORCHES:
• T: Toxoplqsmosis nancy.
• 0: Other viruses
• R: Rubella Congenital cytomegalovirus (CMV)
• C: CY,tomegatovirus infections
• He: Herp·es virus The incidence of congenital infection ranges
• S: Syphilis
from 0.2-2 per cent. Currently CMV infection
is the next commonest co-infection to tuber-
Fetal varicella syndrome culosis in the newborn. 1he exact incidence
This syndrome can occur in 10-13 per cent of in South Africa is not known. The majority are
fetuses whose mothers contract chickenpox in asymptomatic (only 5-10 per cent develop dis-
the first trimester of pregnancy, and in 5 per cent ease). Asymptomatic infants may subsequently
if the mother contracts chickenpox after the first develop deafness. In those \vith disease, hepato-
trimester. The major features are skin lesions, splenomegaly, jaundice, purpura, microcephaly,
cerebral atrophy, and eye abnormalities. Preg- cerebral calcifications, and chorioretinitis may
nant women in contact with varicella or who occur together or singly. Neurological involve-
contract varicella should receive varicella-zoster ment, (e.g. deafness, visual loss, cerebral palsy)
immuno-globulin (VZIG) within 96 hours of may not be evident for some time. Extraneural
exposure. disease is usually reversible.
Confirmation of diagnosis is by detection of
Congenital rubella large, inclusion-bearing cells in urine, specific
The main importance of the disease is the trans- IgM antibody in cord serum, CMV PCR on secre-
placental transfer of the virus to the fetus when tions and by virus isolation. The differential diag-
a pregnant woman contracts rubella. The virus nosis includes congenital toxoplasmosis, rubella
may spread ·widely in the fetus, damaging differ- and herpes simplex infection, as well as bacterial
entiating cells in many organs, leading to abor- sepsis.
tion, stillbirth, or a malformed child. The risk of
embryopathy is highest the earlier in pregnancy Congenital syphilis
the mother is infected: in the first month >80 Syphilis is most commonly acquired transpla-
per cent of fetuses exhibit embryopathy; by the centally, the fetus being infected by an infected
fourth month the risk has dropped to five per mother. Rarely, infection may occur from contact
cent. Congenital rubella is rare in South Africa, with infectious lesions during passage through
since most women in the reproductive age group the birth canal.
have protective antibodies. Serological diagnosis The incidence is not known, but the number
is by IgM specific antibody. of cases of congenital syphilis correlates with
Embryopathy consists of one or several of the the incidence of primary and secondary syphilis
follO\ving: J in women, and the adequacy of antenatal care.
• Temporary damage. Thrombocytopenia, There appears to be a world\vide resurgence.
hepatitis, skeletal -change, pneumonia, Sero-surveys from Africa indicate that 2-25
haemolysis, and small-for-gestational age. per cent of pregnant mothers are infected. The
• Permanent damage. Congenital heart spectrum of syphilis in childhood is outlined in
disease, cataracts, microphthalmia, Table 7.16.
147
PART THREE r\'.eonatal paediatrics
-
Table 7.16 Manifes!ations of congenital syphilis
-
Early Late
Skin Bullae
Desquamatkrn
Red maculo-papules
Condylomata
Muco.us membranes Fissures Scars at corners of mouth (rhi;!gades}
Scars Flat nasal bridge ('saddle nose'}
Rhinitis
Liver/spleen Hepatosplenomegaly
Jaundice
- Hepatitis
Haematological Anaemia
1, Haemolytic
1, Leuco erythroblastic
0
Normocytic, normochrornic
Leukaemoid reaction
Thrombocytopenia
DIC
Bone~ Metaphysitis Sabre tibia
Diaphysitis Bossing
Periostitis Deformities of maxilla
- -
CNS Meriingoencephalitis Chronic meningo-vascular disease
Convulsions Hydrocephalus
Hydrocephalus Mental retardation
Cranial nerve palsies
Hemiplegia
Paresis and tabes
Renal Nephrotic syndrome
--
Other SGA Malnutrition
Pseudoparalysis Hutchinson's teeth
Oedema Mulberry molars
Pancreatitis Caries
Gastrointestinal d.isease Nerve deafness
1, Pneumonia alba Painless synovitis
S.usceptibility to other infections Interstitial keratitis
Chorio-retinitis Argyll Robertson pupil
Optic atrophy
Pathogenesis. It has been shown that infection Clinical manifestations. Babies with congeni-
may occur as early as the first trimester, even tal syphilis are not infrequently small-for-gesta-
though histological evidence of syphilis is rarely tional age and many fail to thrive as a result of
seen until the second trimester. gastrointestinal involvement.
The placenta in congenital syphilis is large, Prenatal infection may be obvious at birth or
pale, and greasy. Vasculitis may lead to infarction signs and symptoms may be delayed for weeks or
and intra-uterine death, premature delivery, or months. The lesions correspond roughly to those
intra-uterine growth retardation. seen in the secondary stage of syphilis. lhose
148
7 ( :are of the newborn
occurring during the first two years of life are Figure 7.9 Bone changes in syphilis
referred to as early congenital syphilis and those
manifesting after this time, late congenital syphi- 2@
lis. Overlapping may occur.
Early congenital syphilis

(See also Chapter 34, Skin disorders.)
• The skin and mucous membranes are
commonly involved. The earliest sign
is often a transient bullous eruption
involving the palms and soles containing Metaphyseal translucent band
many spirochaetes (syphilitic pemphigus). 2 Wimberger's sign
• Condylomata lata may be seen and are 3 Diaphysitis
highly infectious. Mucous patches in the
4 Periostitis
mouth may lead to fissuring and scarring
at the angles of the mouth.
• Rhinitis frequently occurs after the first • Bone involvement causes pain which
week or two. 1he mucous discharge from is responsible for the irritability
the nose (snuffles) may become tinged with commonly found in infants suffering from
blood and is teeming \vith spirochaetes. congenital syphilis. In some instances,
• Hepatosplenomegaly is present in a pseudoparalysis of a limb occurs (Parrot's
very high percentage of affected infants. pseudoparalysis). The exact cause of this
Jaundice may occur but is less common. is not defined but may in part be due to
• Haematological involvement manifesting bone disease.
\Vi.th anaemia is very common. • Central nervous system (CNS)
Erythroblastosis, \'1rith many nucleated red involvement, when present, leads to
cells on a peripheral smear, together with convulsions and, if untreated, can cause
hydrops fetalis and haemolytic anaemia, mental retardation and hydrocephalus.
may produce a picture which has to be Routine examination of the cerebrospinal
differentiated from iso-immunisation. fluid \vill reveal abnormalities in more
A leucoerythroblastic picture \vith than one-third of patients.
immature white and red cells may be seen • Renal involvement should always be
on a peripheral blood smear. At autopsy sought in the presence of oedema.
extramedullary haemopoiesis involving The nephrotic syndrome is a well-
the liver and spleen is a common finding. recognised complication of syphilis.
• 1hrombocytopenia and disseminated The onset is usually within the first six
intravascular coagulation may lead to months, but may occur later without
purpura or bleeding from other sites. other clinical evidence of congenital
• Congenital syphilis is a rare cause of a syphilis. Immune complex deposition
leukaemoid reaction. leads to a membranous nephropathy.
• Bone involvement should be sought on Adequate antisyphilitic therapy results
radiographs of the long bones (see Figure in complete resolution of the condition.
7.6) in any infant suspected of being Pretibial oedema is a frequent finding in
syphilitic. early infancy and may occur as a result
• The long bones are most commonly of hypoproteinaemia unrelated to renal
involved but, rarely, the phalanges involvement.
(syphilitic dactylitis) and metacarpals • The pancreas and intestines frequently
may also be affected. Involvement of the reveal spirochaetes at autopsy, a fibrous
maxilla may lead to facial deformities and pancreatitis being a common finding.
involvement of the skull to bossing. In the • A pericellular fibrosis of the lungs may
newborn only 40 per cent may have long also be found at autopsy (pneumonia
bone involvement. alba). Pneumonia complicating congenital
149
syphilis is usually of intercurrent bacterial involvement, procaine penicillin G, 300 000 units
origin. IM daily for 10 days is essential. A symptom-
• Patients with congenital syphilis have atic infant with meningeal involvement is given
impaired cell-mediated immunity, and aqueous penicillin G, 50 000 units/kg/IV in two
secondary bacterial infections, including divided doses daily for 10 days.
septicaemia, occur frequently.
Follow-up. Ideally, all infants vvith congenital
Diagnosis. Symptomatic congenital syphilis syphilis should be seen at three-monthly inter-
may be mimicked by any of the causes of intra- vals after completion of treatment, for quanti-
uterine infection and by bacterial infections tative VDRL tests and clinical examination to
acquired after birth. The only ,vay to make a assess efficacy of treatment. Treatment should
definitive diagnosis of syphilis is through micro- be repeated if the VDRL remains positive 12
scopic identification of Treponema pallidum in months after therapy.
secretions, by dark ground illumination, or by The mother and father of the infant should be
examination of the pathological tissues. How- investigated and treated if necessary.
ever, although not foolproof, serological tests are
of great practical value in establishing the diag- Prevention. Adequate antenatal care of the
nosis. Treponemal infection leads to production mother should include serological testing and
of both non-specific antibodies knm,m as reagins treatment, where necessary, during the second
and specific anti-treponemal antibodies. Exam- and third trimester of pregnancy.
ples of the non-specific serum antibody tests
are the Wasserman, Kahn, and Venereal Disease Late congenital syphilis
Research Laboratory (VDRL) tests. The last-men- Scars of early syphilitic lesions and subsequent
tioned is one of the most commonly employed developmental changes give rise to stigmata.
as a screening test for syphilis and as a quantita- These include rhagades (scarring at corners of
tive serological method to assess the efficacy of the mouth), sabre tibiae, bossing of the skull,
treatment or activity of disease. A disadvantage 'saddle nose' and other deformities of the max-
is false positive reactions, which may be techni- illa, together \'\'1th characteristic deformities
cal or due to other infections or connective tissue involving permanent teeth. The upper central
disorders. incisors tend to be peg- or barrel-shaped, with
Specific antibody tests such as the fluores- convergent lateral borders and thickened bodies.
cent treponemal antibody (absorbed) test (FTA The cutting edge becomes notched with usage
Abs) have proved reliable. lhe FTA test detects (Hutchinson's teeth). Moon's mulberry molars
both IgG and IgM antibodies. A baby born to a have multiple small cusps instead of the normal
syphilitic mother may show a positive FTA IgG four. lhese deformities cause a predisposition to
test merely as a result of passive transplacental caries.
transfer of maternal IgG, but a positive IgM test A ,vide variety of neurological sequelae may
usually indicates infection of the infant. For prac-. result from chronic meningovascular syphilis,
tical purposes, a positive FTA IgM test in young including hydrocephalus, cranial nerve palsies,
infants is indicative of congenital syphilis infec- hemiplegia, juvenile paresis, and tabes (see
tion which requires treatment. Unfortunately, Table 7.16).
when syphilis is acquired by a mother late in Late hypersensitivity reactions include inter-
pregnancy, her baby may not produce IgM FTA stitial keratitis, nerve deafness, and painless
antibody until three months of age. synovitis (Clutton's joints) commonly involving
A cerebrospinal fluid examination should the knees.
always be done to exclude meningeal involve-
ment. HIV and the newborn
Treatment. An asymptomatic infant without The risk of HIV transmission to the newborn is
meningeal involvement requires benzathine the greatest concern. HIV positive mothers are
penicillin 50 000 units/kg/IM in a single dose. managed according to their CD4 count and stage
For a symptomatic infant ,Nithout meningeal of HN. lhe maternal stage of the disease predicts
150
the outcome and acquisition of co-infections in valcyclovir at this young age.

the baby. The HIV exposed baby as opposed to Pneumocystis jiroveci has not been seen in the
the infected baby is also at higher risk of acquir- neonatal period.
ing these infections. There is a concern that small, sick babies
who are HIV exposed or infected and fed for-
Prevention of mother-to-child transmission mula feeds may have a higher risk of necrotising
(PMTCT) based on WHO stages and CD4 count: enterocolitis.
+ HIV positive - stage 1 or 2 : CD4 > 350
+ AZT 300 mgs 12 hrlyfrom 14 weeks TB and the newborn
+ Labour - AZT 3 hrly + sd NVP
1he majority of pregnant women with TB are HIV
+ Post-delivery sd TDF + FTC (tenofovir +
positive.
emtricitabine)
+ The newborns born to mothers with
• Pre C/S 4 hrs before sd NVP + TDF+ FTC
TB tend to be lighter than expected
+ Post-delivery sdNVP to baby minimum 6
for gestational age, are more likely
weeks
to be premature and have a higher
• Exclusive breast feeding continue NVP
perinatal mortality. 1hese outcomes
>2.5 kg 15 mg daily, < 2.5 kg 10 mg daily
are significantly improved if mothers
• HIV positive - stage 3 or 4 CD4 count <350
are on the PMTCT programme, on
lifelong ARTs
anti-tuberculosis treatment and triple
antiretroviral therapy depending on their
Mothers who have a CD4 count > 350 and have CD4 counts.
the antiretroviral drugs for PMTCT have a mini- • The diagnosis of TB in the newborn is
mal HIV transmission rate of 1.9 per cent. Those based on a maternal history of persistant
mothers on triple antiretroviral therapy should cough of two weeks or more, an
have no HIV transmission to their babies. unresolving pneumonia, a previous history
All mothers must be screened for tuberculosis of TB, a history of current TB on therapy,
(TB) and be aware of the other co-infections, the a contact at home and positive HIV status.
acquisition of which is dependent on the stage of The baby usually presents in the second or
the their disease. A guideline to this staging is as third week oflife with non-specific signs
follows: of infection, unresolving pneumonia and
+ Stage 1 = asymptomatic and lymph nodes may develop hepatosplenomegaly and
• Stage 2 = moderate weight loss (<10%), lymphadenopathy.
recurrent URTI, skin and mucosa! lesions • Investigations are those done as a routine
- bacterial, viral, fungal and depend on the clinical features that
+ TB= stage 3 the newborn baby displays. These include
+ Any addition to these = stages 3 or 4 chest radiograph, three early morning
+ Respiratory - Pneumocystis pneumonia, gastric aspirates, induced sputum,
cytomegalovirus (CMV) endotracheal aspirate and / or bronchial
• GIT - chronic diarrhoea, CMV lavage if the baby is on a ventilator,
• Meningitis - TB, Cryptococcus cerebrospinal fluid, blood culture for TB,
• Fungal infections. liver and lymph node biopsy, cultures
of skin lesions or ear discharges. A
As indicated, the newborn baby born to the HIV- polymerase chain reaction (PCR) for TB
positive mother is at a risk of acquiring the co- may be done if available. Genexpertlt is
infections that the mother may experience. These being investigated in the young infant.
include CM\!, TB and acute bacterial infections. + Examination of the placenta histologically
Babies who have CMV infection present with and microbiologiocally is essential where
a clinical picture of generalised illness with or congenital TB is suspected in the infant
without pneumonia. Treatment is ,vith gancyclo- born to a mother ¼ri.th recently diagnosesd
vir for six weeks. An alternative is to use gancy- TB.
clovir until the viral load falls below 1 000 copies • Treatment of the baby and the mother is
per ml. There are safety concerns about the use of the standard anti-TB therapy.
151
Inherited errors of metabolism pre- In the preterm infant careful calculation of

senting in the neonatal period feed volumes is essential. Often insensible water
loss is underestimated, particularly in VLB\\-
(See also Chapter 10, Metabolic disorders.) infants and those nursed in incubators, urider
phototherapy units and radiant warmers.
Inherited metabolic disorders may present in Metabolic acidosis develops occasionally in
the neonatal period, when a previously healthy some artificially fed healthy preterm babies, par-
newborn baby may present severely ill and \vith ticularly during rapid growth when hydrogen
deranged metabolism. ions are produced, which may not be excreted by
The following patterns are seen: severe illness the immature kidney. This build-up of acidosis
\i\rith poor feeding, lethargy, vomiting, neonatal ivill in tum result in poor weight gain, which is
metabolic acidosis, recurrent or persistent hypo- easily corrected by giving oral sodium bicarbon-
glycaemia, coma and convulsions. These features ate 2-4 mmol/kg/24 hours for a short while. If
are indistinguishable from septicaemia or intra- acidosis persists, it should be investigated.
cranial haemorrhage, but occur in infants with Anaemia and occult infections such as urinary
a normal prior course and \vith no evidence of tract and chronic intra-uterine infections includ-
infection on investigation. Severely dysmorphic ing HIV and TB are not uncommon causes. Sub-
infants should also be investigated for inborn clinical cold stress occurs when babies nursed
errors of metabolism. in temperatures below thermoneutrality, use up
Prompt suspicion and laboratory diagnosis is energy in an attempt to maintain body tempera-
essential as many conditions can now be treated ture. Congenital heart defects, urinary and gas-
and the family appropriately counselled. trointestinal tract malformations, chronic chest
A number of congenital endocrine and meta- conditions, metabolic diseases, endocrine disor-
bolic disorders may not present in the neonatal ders, and brain damage may all cause failure to
period. Screening of the newborn may detect thrive.
some, allowing for the initiation of therapy and The common causes must be excluded by tak-
the prevention of damage. Congenital hypo- ing a careful history, particularly in respect of
thyroidism is the most important of these (see feeds, vomiting, and stools, and doing a detailed
screening programmes in Chapter 3, Medical relevant clinical examination. Special investiga-
genetics and congenital disorders; and hyper- tions must be selected with circumspection.
thyroidism in Chapter 20, Endocrine disorders). A very important aspect of thriving is the
mother-child relationship. Some infants with
Failure to thrive gmwth failure and developmental lag have been
shown to have suffered as a result of maternal
(See Chapter 9, Feeding and nutrition in babies psychosocial disturbances, such as maternal
and children.) depression. On correction of these problems the
babies improved both physically and develop-
Failure to thrive means that the baby fails to gain mentally. This form of failure to thrive is at one
weight adequately. Follo\ving initial weight loss end of the spectrum of child abuse a'nd neglect.
for a few days, the healthy term baby should Preterm babies and twins are at particular risk of
regain its birth weight by the tenth day and the this problem.
preterm baby by the fourteenth day. Thereafter
the expected weight gain is a minimum of 150 g Palliative care in the newborn
per week in a term infant or on average approxi-
mately one per cent of body weight per day; a 1he WHO definition of palliative care is an
baby who does not gain weight at this rate must approach that improves the quality of life of
be regarded as failing to thrive. patients and their families facing the problems
The most common cause is incorrect feeding associated with life-threatening illness, through
practices: firstly, those related to breastfeeding the prevention and relief of suffering by means of
such as difficulty \vith sucking, poor technique, early identification and impeccable assessment,
and inadequate frequency of feeding; secondly, treatment of pain and other problems - physi-
dilute or infrequent formula feeds. cal, psychosocial and spiritual.
152
Not uncommonly neonatal medicine deals • Tube: A nasogastric tube is placed to drain
·with life threatening conditions in small imma- gastric contents. This prevents vomiting
ture infants, severe life limiting congenital mal- and aspiration, decompresses the bowel
formations, failure of intensive care or cura- maximising intestinal mucosal blood flow,
tive treatment and circumstances under which reduces abdominal distension thereby
severe disability is predicted leading to the con- reducing resistance to diaphragmatic
sideration of withdrawal or withholding of care. descent and makes breathing easier.
With the increasing understanding of the None of these advantages are seen if the
newborn it has become clearer as specific infor- tube is spigotted, knotted or blocked by
mation became available from studies and from blood or dried mucus. It requires constant
parental feedback that this form of care was nec- supervision.
essary. Issues that became clear were the under- • Warmth: Keeping a warm baby warm
treatment of pain, overhandling of babies and is simply a matter of ,,vrapping him or
from parents, and 'not caring enough and being her, including the head, in insulation.
insensitive' In the earlier years of neonatal inten- Aluminium foil from the kitchen is
sive care parents were not granted adequate time perfectly adequate. If the baby has
and involvement with their babies leading to exposed viscera, e.g. gastroschisis, these
severe emotional difficulties. should be wrapped in non-adherent
This form of care is the active total care of plastic such as Klingfilm®. An incubator
patients whose disease is not responsive to cura- is not essential. Wrapping a cold baby in
tive treatment. This involves control of pain, con- insulation will, of course, keep him cold.
trol of other symptoms, discussions involving Cold babies must be rewarmed as part of
parents in decision making. the stabilisation prior to transfer.
1he common goals of care include physical • Oxygenation: Supplementary oxygen
comfort, emotional comfort for parents, address- improves oxygen delivery to the gut
ing family needs, considering spiritual/ cultural mucosa and is important in maintaining
values, bereavement counselling and prepara- the integrity of the mucosal barrier.
tion for death. • Stabilisation: Ambulance journeys are
not good for babies. Prior to transfer the
sending physician must ensure that the
Transportation baby is rewarmed, normovolaemic and
normoglycaemic.
The centralisation of neonatal intensive care and • Intravenous fluids: Fluid loss is almost
neonatal surgical services makes inter-hospital pathognomic of surgical pathology. The
transfer of neonates inevitable. However the small circulating blood volume of the
principles of neonatal transport are indepen- neonate means that fluid losses must
dent of distance and are as important when be replaced on a continuing basis or
transporting a baby betvveen the ward and the hypovolaemia ,.vill rapidly result. Surgical
X-ray department as they are when the transfer is babies lose isotonic fluid and replacement
between hospitals. ,-vith Ringer's Lactate is ideal.
Whenever a transfer is contemplated there • Documentation: All relevant X-rays and
must be direct communication between the blood results, as well as a detailed referral
sending and receiving staff and an appropriate letter must accompany all transfers.
level of care during transport must be arranged. Failure to do this compromises care in the
Speed is rarely, if ever, essential- care and plan- receiving institution.
ning is. • Escort: Care of a neonate during transport
All this is readily achieved \Nithout recourse to is the pinnacle of nursing achievement,
expensive technology and is ·within the ambit of and should be the domain of the most
any healthcare facility. skilled and experienced personnel
The mnemonic TWO SIDE is a useful aide available. It is never appropriate to
memoire when considering inter-hospital trans- dispatch a baby in the care of his mother
fer. only.
153
most efficient, but at times a transport

incubator is preferable.
• Monitor colour, respiration, and heart
£1:1rgicalltfill eabies n~ed t0 ee kepi warm, have rate.
their< st0mae"1 and small bowel decomRressed • Monitor the drip rate and volume
by a well-managed nasogastric tube, and have control if an intravenous line has been
tfieir circ,ulating" blood volume restored by intra- established.
venous infusion of an appropriate fluid. Supple- • Ensure that appropriate medical
me.ntary 9xygen is advised.
information accompanies the patient.
Transport of the high-risk patient Road or air?

Once the high-risk mother or baby has been In most parts of South Africa roads are adequate
identified and the immediate needs assessed, and transport by road is appropriate. In remote
the question of transfer to a referral centre arises. areas aero-med evacuation of sick babies may
Transport of the fetus is preferable in utero, but be needed. There are, however, difficulties \vith
delivery during transportation is hazardous. air transport, be it fixed \ving, or helicopter, and
Active maternal haemorrhage and fetal dis- this means of transport may not be suitable for all
tress are contra-indications to transporting the patients. Remember, in all aircraft gas expands.
mother in labour until appropriately managed 'Pressurised' aircraft have a cabin pressure set to
by maternal and fetal resuscitation. an altitude of around 3 600 m. Thus in any form of
Conditions requiring transfer of the mother air transport, the air \vithin an incarcerated her-
before delivery include eclampsia, severe preg- nia, pneumothorax, pneumoperitoneum, dia-
nancy-induced hypertension, abruptio placen- phragmatic hernia, or in a loop of intestine \vill
tae, multiple pregnancy, significant maternal expand and possibly harm the patient. The vol-
disease, and poly- or oligohydramnios. ume increase is related to the pressure according
The referral centre should always be informed to Boyle's Law, and the pressure is related to the
before transferring any patient. The escort must altitude (see Table 7.17). There are also problems
have adequate knowledge of the baby's condi- relating to turbulence and the displacement of
tion and must be able to care for the baby during tubes and lines. In helicopters lack of space and
transit. access make interventions difficult. Air transport
1he infant must be in a reasonably stable is also weather dependent.
condition to \vithstand the rigours of transport.
Therefore hypothermia, hypoglycaemia, and Table 7.17 Gas volyme relative to altitude
hypotension should be corrected. A nasogastric -
llltituae (m) Relative gas~ o!ume
tube should be passed. Monitoring equipment, - - ".
such as a saturation monitor and infusion con- 0 1.0

troller, are advisable. However, these may not be 1 500 1.2
available and clinical monitoring \vill be neces- -
3000 1.5
sary. - -- -
4 500 1.9
.
The following precautions must be taken in tran- 5 Zl-0.Q 2.0 -
sit: - - - - --
6QQU 2.4
• Ensure a clear airway.
• Ensure that suction and oxygen are Discussion with the receiving unit ¼'ill allow a
available. decision on the correct transport vehicle as well
• Prevent heat loss during transfer; skin- as any additional requirements for a specific
to-skin contact \vith the mother is baby\vith a specific pathology.
154

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UNIVERSITEIT VAN PRETORIA

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Edited by Robin J Green

Part 1 Evaluation, growth and development

Part 2 Psychosocial and community paediatrics

Part3 Neonatal paediatrics

Part 4 Metabolic and nutritional disorders

Part 7 System-based disorders

Parts Miscellaneous disorders and issues

7 Care of the newborn

8 Surgical care of the newborn

9 Feeding and nutrition of babies and children

Introduction abortions, stillbirths, low birth weight,

Factors associated with, and which identify, the

Approximately 15 per cent of newborn babies re-

Table 7.1 Factors identifying the high-risk pregnancy

Delivery room management However early clamping may facilitate

score should be used to determine the Birth asphyxia and resuscitation

APGAR8-10 APGARS-7 APGAR3-S APGAR0-3

HR> 120/min HR> 100/min HR 80-100/min HR< 80/min

contributing factor, is it appropriate to consider Consequences of severe hypoxia

heel -- toe >50mm anterior creases 15 30

lids fused lids open sl. curved well-curved formed

Skin of the normal newborn Eyes

Routine care of the healthy or spraying with a disinfectant before

Routine care of the healthy low birth

cyanosis. The airway must be kept clear at determined individually, dep~nding to

These aspects must receive particular emphasis

The preterm infant

High risk Medium risk Liver Earlier development of neonatal

Thereafter it must be determined twu-hourly Cardiovascular disorders.) To prevent the latter

15 mmol/1, insulin is infused at a dosage of • Respiratory distress (tachypnoea >60

The causes commonly encountered are listed in

Immediate respiratory difficulties Respiratory distress with diminished breath

respiratory support considered if a may reflect irritation of the gastric mucosa by

Neonatal jaundice These result in raised unconjugated serum bili-

and cycling movements. An exchange transfu- Prevention. Antenatal investigation of Rh-nega-

Management of the infant. The jaundiced infant

....... --·-· .)' · •· .............i..........._. ·.....

ACTION LINES - Take action if above these lines

330 ·-· ·-··-········.L. i

230 -······ -· - i - - ... :··········-·····-· i.•. - .•

r.===============.T - ---r--7 --r-- T -; - 7

Phototherapy. This should be regarded as both Side-effects include hyperthermia, loose

The frequency of monitoring TSB levels Acute anaemia

Table 7.12 Management of blood loss according t0 severity - .. -

Chronic anaemia • Platelet disorders

Management. 1he baby must be treated vig- Water balance

Congenital deficiency of coagulation Practice point

Approximately one-third of LBW babies and Hypernatraemia

Superficial abrasions on the infant's face, scalp,

sequence. Following severe intra-partum hypoxia • Feeding is by a nasogastric tube, the •

movements of the lower limbs, rowing Management:

Cerebral blood flow :::::::,..

When seizures have ceased for 24-48 hours, the

cysts; clinical features are determined by the site 2 lntracri:lnial haemorrhage

Clinical features. The big head may be obvi- These are: