CHBH NEONATAL

PROTOCOLS
2010
 Foreword

This booklet has been prepared to help interns, medical officers, registrars and
others in the performance of their duties, and to maximise learning opportunities,
during their rotation through the neonatal unit at Chris Hani Baragwanath Hospital.

This booklet represents work in progress. Protocols are constantly being updated
and will therefore change with time. Suggestions from our junior staff are always
welcome.

Contributors

Pinky Chirwa
Hitesh Diar
Cheryl Mackay
Khakhu Mathivha
Ramatsimele Mphahlele
Mantoa Mokhachane
Firdose Nakwa
Reenu Thomas
Haroon Saloojee
Gail Sherman
Sithembiso Velaphi
CHBH Neurodevelopmental team

Edited by: Sithembiso Velaphi and Haroon Saloojee

September 2010

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 CONTENTS

DUTIES OF INTERNS, MEDICAL OFFICERS AND REGISTRARS ...................................................6

INFECTION CONTROL POLICY........................................................................................................ 10
ADMISSION POLICIES....................................................................................................................... 11
DISCHARGE POLICIES..................................................................................................................... 14
INTRAPARTUM HYPOXIA/ ASPHYXIA: RESUSCITATION.............................................................16
ASPHYXIA: POST-RESUSCITATION MANAGEMENT – GENERAL .............................................18
CRANIAL ULTRASOUND.................................................................................................................. 29
SPINA BIFIDA..................................................................................................................................... 30
HYDROCEPHALUS............................................................................................................................ 32
SURFACTANT REPLACEMENT THERAPY......................................................................................40
VENTILATOR MANAGEMENT........................................................................................................... 42
PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN (PPHN)..................................45
USE OF NITRIC OXIDE...................................................................................................................... 48
CHRONIC LUNG DISEASE/ BRONCHOPULMONARY DYSPLASIA...............................................50
APNOEA............................................................................................................................................. 53
RETINOPATHY OF PREMATURITY.................................................................................................. 57
ABNORMAL HEART RATE/ RHYTHM (ARRHYTHMIAS)................................................................64
PATENT DUCTUS ARTERIOSUS...................................................................................................... 66
ABDOMINAL WALL DEFECTS.......................................................................................................... 68
............................................................................................................................................................ 69
NECROTISING ENTEROCOLITIS...................................................................................................... 70
ENTERAL FEEDING OF PRETERM INFANTS..................................................................................72
Suggested Guidelines of Feeding Well Neonates...........................................................................74
NUTRITIONAL SUPPLEMENTATION................................................................................................ 75
PARENTERAL NUTRITION................................................................................................................ 77
FLUID THERAPY................................................................................................................................ 79
HYPONATRAEMIA............................................................................................................................. 81
HYPERKALAEMIA............................................................................................................................. 85
HYPOCALCAEMIA............................................................................................................................. 86
HYPERGLYCAEMIA........................................................................................................................... 94
FUNGAL INFECTION....................................................................................................................... 107
CHICKEN POX/ VARICELLA........................................................................................................... 113
HUMAN IMMUNODEFICIENCY VIRUS............................................................................................ 115
CYTOMEGALOVIRUS...................................................................................................................... 120
HERPES SIMPLEX VIRUS............................................................................................................... 122
RESPIRATORY SYNCYTIAL VIRUS (RSV).....................................................................................124
HEPATITIS B VIRUS........................................................................................................................ 126
INFLUENZA VIRUS ......................................................................................................................... 127
(with specific reference to Pandemic Influenza; H1N1)................................................................127
THROMBOCYTOPAENIA ................................................................................................................ 131
ANAEMIA ......................................................................................................................................... 133
POLYCYTHAEMIA............................................................................................................................ 135
PROLONGED NEONATAL JAUNDICE........................................................................................... 147
GUIDELINES FOR REFERRAL TO NEURODEVELOPMENT TEAM, DIETICIAN AND SOCIAL
WORKER ......................................................................................................................................... 157

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 GENERAL INFORMATION

Neonatal service at CHBH

• The neonatal service consists of the rooming-/lying-in wards (Wards 57, 64, 65,
67 and 68), Ward 40, Ward 66, Transitional Care Unit (TC) and Neonatal
Intensive Care Unit (NICU).
• The wards that cater for admitted patients are NICU, TC, ward 66 and ward 40.
• In lying-in wards the babies room-in with their mothers, which means they do not
require admission. The beds in these wards are not counted under the neonatal
unit, though some of the babies are still under the neonatal service.

Capacity or Size of the Neonatal unit

• There are 120 authorized beds in the neonatal unit; 12 in NICU, 18 in TC, 50 in
ward 66 and 40 in ward 40.
• There are 150 usable beds; 12 in NICU, 33 in TC, 80 in ward 66 and 25 in ward
40.

Medical Staff in the Neonatal Unit and Allocation of Duties

• The medical personnel assigned to the neonatal unit consist of 9-10 registrars
and 5-7 medical officers (MOs)/ interns.
• There are 3 registrars and 2 MOs/ interns in ward 66, 3 registrars in TC and
1MO/ intern, 2 registrars in NICU and 1 MO/ intern, 1 registrar and 1 MO/ intern
in the labour ward nursery or admission/ observation nursery, 1 registrar in ward
40, and 1 MO/ intern in lying-in wards.
• The registrar and MO/ intern who were on call the previous night are given a day
off post-call, but this might be cancelled if there are not enough people to cover
the wards during the day.
• The GEMP 4 students or final year medical students join the MO/ intern allocated
to work in the lying-in wards to examine patients.

Rosters or Time Tables or Work Schedules

There are 3 Rosters:
• The weekly roster- This roster is drawn up weekly with morning and afternoon
duties allocated.
• The night call roster- This roster is drawn up monthly and shows the names of
people who will be on call at night covering different areas of the neonatal unit
• The weekend call-in roster- This roster is drawn up monthly and shows the
names of people who will be covering the different wards during the day on
weekends and public holidays.

Meetings/ Clinics
• Morbidity and mortality meetings with obstetricians are held every weekday at
08h15 to discuss neonatal cases that have morbidities or died from the previous
night. MO/ intern on call in LW and/ or registrar on call for TC must give names of
patients to be discussed to the obstetric registrar by 07h30 of the morning of the
meeting.
• Registrar tutorial- Tuesdays 14h30-15h30, held in the lecture room

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• Grand round- Wednesdays 12h00-13h00, commonly in NICU/ TC, could be in
ward 66
• Neonatal follow up clinic- Thursdays 12h30, until all patients have been seen, this
clinic is held in the Antenatal Care (ANC) area
• Neonatal morbidity and mortality meetings- Fridays 13h00-14h30, held in the
lecture room
• Unit/ Neonatal Wards statistics- Last Friday of the month, 13h00-14h30

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 DUTIES OF INTERNS, MEDICAL OFFICERS AND REGISTRARS

Duties are divided into morning (07h30-12h00) and afternoon duties (12h00-16h00)
during the weekdays.
All patients should have been seen and ready to be presented to consultants
(consultant ward rounds) by 10h00 in all wards.

Morning duties: Medical Officer/ Intern

• Handover in NICU, TC and LWN starting at 07h30
• Check resuscitation equipment in LWN, and in the obstetric theatre and sign the
resuscitation equipment book if everything is available and complete, if the
equipment is not complete let the charge nurse in LWN and theatre get the
missing equipment.
• Check with the nurse in charge that equipment in the LW delivery rooms or
cubicles has been checked by the relevant midwives (midwives working in LW)
• Ward rounds in all wards start at 07h30
• In labour ward nursery (LWN) the MO/ Intern
o attends deliveries as requested by obstetricians,
o resuscitate newborns as needed in labour ward, labour ward nursery and
theatre
o assesses and admits patients referred to sick baby labour ward nursery/
triage nursery.
• On the morning post-call in LWN, the MO/ Intern collects cases from the previous
day and night (including deaths in LWN, asphyxias- anyone who required
resuscitation, VLBW infants requiring more than 40% oxygen) for the M&M and
submit their names to one of the obstetric registrars who was on-call the previous
night. These names should be submitted to the obstetric registrar by 07h30.
• Post-call doctor in LWN must attend the M&M meeting with obstetricians at
08h15 before starting ward rounds or going off.

Morning duties: Registrars

• Handover in NICU, TC and LWN starting at 07h30
• Check resuscitation equipment in the ward in which you are allocated and sign
the resuscitation equipment book if everything is available and complete, if the
equipment is not complete let the charge nurse get the missing equipment.
• Ward rounds in all wards start at 07h30
• Registrar in LWN to supervise and assist interns with resuscitation of all babies
requiring resuscitation and with admission of very low birth weight infants, any
baby with severe respiratory distress and any baby with moderate to severe
asphyxia/ encephalopathy.
• Registrar in LWN to help in TC if LWN is quiet.
• On the morning post-call in TC, to collect cases from the previous day and night
(including asphyxias- anyone who required resuscitation, VLBW infants requiring
more than 40% oxygen and were admitted in TC or NICU) for the M&M and
submit their names to one of the obstetric registrars who was on-call the previous
night. These names should be submitted to the obstetric registrar by 07h30.

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• Post-call doctor in TC to attend the M&M meeting with obstetricians at 08h15
before starting ward rounds or going off.
• Registrars doing the night calls in NICU and TC are given a day off post-call after
the handover round and the morning mortality meeting with obstetricians if there
are enough registrars to cover the day duties.

Afternoon duties- Medical Officer/ Intern

• Start at 12h00 and if late because one was still finishing the morning duties, one
should not be later than 13h00.
• Attends deliveries as called by obstetricians, resuscitating newborns in labour
ward or labour ward nursery.
• Examining and admitting patients in labour ward nursery as necessary
• Afternoon cover for Exchange transfusion (does exchange transfusion/s as
required, to be assisted by a registrar)
• Afternoon cover for Insertion of central lines (inserts umbilical and PICC lines as
required, to be assisted by a registrar)
• To check outstanding results (laboratory and X-rays) and act appropriately on all
abnormal results, if not sure what to do with abnormal results, call the registrar.
• Afternoon cover for all problems that require a doctor in lying-in wards & ward 66
• Covers ward 40, including discharges
• Attends neonatal follow up clinic on Thursdays
• Do bed-side C-reactive protein (CRP) when equipment is available

Afternoon duties- Registrar

• Starts at 12h00 and if late because one was still finishing the morning duties, one
should not be later than 13h00.
• Attends deliveries as called by obstetricians, resuscitating newborns in labour
ward or labour ward nursery.
• Examining and admitting patients in labour ward nursery
• Exchange transfusion cover
• Insertion of central lines cover
• NICU or TC cover
• Lying-in wards and ward 66 cover
• Covers ward 40, including discharges
• Attends neonatal follow up clinic on Thursday
• Do bed-side c-reactive protein (CRP) when equipment is available
• ROP screening on Tuesday to identify patients (see ROP for details) for
screening on Wednesday afternoon, the list should be handed to sister assisting
ophthalmologist by Tuesday afternoon. To assist the ophthalmologist on
Wednesdays if the sister is not available.
• The afternoon handover round in NICU and TC starts at 15h30 both registrars
covering NICU and TC are expected on both handover rounds.

Night duties- Medical Officer/ Intern

• Start at 16h00 and ends at 08h00 the following day
• Attends deliveries as called by obstetricians, resuscitating newborns in labour
ward or labour ward nursery.
• Examining and admitting patients in labour ward nursery.

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• Lying-in wards and ward 66 night cover.

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Night duties- Registrar
• Start at 15h30 and ends at 08h00 the following day.
• Registrar on call for TC supervises and assists MO/ intern in LWN with
resuscitation and assessing infants especially those with severe illness e.g. those
requiring ventilation, and those with major congenital abnormalities.
• Exchange transfusion cover.
• NICU and TC cover.
• If allocated in LWN do duties similar to those of MOs/ interns.
• The night call in NICU starts at 15h30, therefore the handover round in NICU and
TICU starts at 15h30.
• Both registrars doing their night calls in NICU and TC must attend the handover
rounds in both areas (TC and NICU).
• The NICU/TC registrars work as a team. Though one is allocated in TC and other
in NICU, they must assist each other. For example, if there is a resuscitation in
progress both registrars are expected to be present, assisting each other and
should notify the consultant on call immediately that a resuscitation is in progress.

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 INFECTION CONTROL POLICY
Aim
To prevent infections and eradicate the spread of infection especially those due to
resistant organisms such as Acinetobacter, Methicillin-Resistant Staphylococcus
Aureus (MRSA), extended spectrum beta lactamase (ESBL) producing organisms,
Candida and others. This helps in reducing antibiotic costs, blood investigations,
shortens hospital stay and reduces mortality.

CONTROL MEASURES

Universal precautions
• Everyone entering NICU/TC should wash their hands at the sink at the entrance
of the ward.
• Everyone entering ward 66 or ward 40 should apply D-germ on their hands as
they enter the ward.
• All infants must be considered as colonized therefore one of the potential sources
of infection.
• Hand decontamination is the single most important preventative measure for
cross infection. This can be achieved through hand washing or use of hand rubs.
• Wash your hands using long acting antiseptic detergent such as chlorhexidine
hand scrub or povidone iodine. Wash your hands for at least 20 seconds,
washing your palms, back of your hands, web spaces, fingers including thumbs,
web spaces, and tip of your fingers.
• Use chlorhexidine-based alcohol hand rubs e.g. D-germ. Ensure that all surfaces
of your hands are wet with the D-germ. Rub your hands together in the same way
as for hand-washing until the hands are dry. In the absence of secretions
contaminating your hands, use of hand-rub is as effective as hand-washing.
• Wipe your stethoscopes with alcohol (Webcol®) swab before examining each
patient.
• All invasive procedures must be performed under sterile conditions, using sterile
gloves, masks, sterile gowns and sterilized equipment.
• Do not bring bags inside the wards.
• Remove wrist watches.
• Roll your sleeves if wearing clothes with long sleeves before examining patients.
Take off overcoats before entering the ward.

Isolation
• Infants infected with resistant organisms such as Acinetobacter, ESBL producing
bacteria, MRSA, Fungi/Candida must be isolated in the isolation cubicle (cubicles
7 and 8 in NICU, procedure room in TC and chosen isolation cubicle in ward 66).
• If the isolation cubicle is not available the patient can be nursed in a corner within
a strictly demarcated area using relevant precautions.
• Non-sterile, clean gloves must be used when examining these patients and must
be discarded after each use.
• A stethoscope must be allocated to the isolated infant. Do not use your own
stethoscope. Wipe stethoscopes with alcohol swab in between patients.

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 ADMISSION POLICIES

All babies requiring admission should be admitted to the appropriate ward as soon
as possible. No baby should wait or stay in the labour ward nursery or triage
area for more than two hours irrespective of the underlying condition or
diagnosis. A decision on whether to admit or not to admit the patient must be made
within the first hour after the patient has been referred to the doctor.

Temperature should be checked on all babies immediately post-resuscitation on

those requiring resuscitation or on arrival to the triage or labour ward nursery in
those not requiring resuscitation. Dextrostix/ glucose (haemoglucotest) should be
checked on all babies immediately post-resuscitation on those requiring resuscitation
or within an hour of arrival to the triage or labour ward nursery in those not requiring
resuscitation. Thereafter these should be monitored every hour while the baby is in
labour ward nursery. All babies should either be fed or having intravenous fluids
within two hours being in the triage area or labour ward nursery.

The decision as to which ward the baby is admitted to, is based on the criteria listed
below.

Neonatal Intensive Care Unit (NICU)

It should be noted that in all instances each patient and his/her problems should be
individualised and the availability of appropriate nursing staff determined.
Required nurse to infant ratio should be 1:1-2. Only professional nurses should work
in NICU, preferably nurses who are neonatal trained or experienced. Professional
nurses who are not neonatal trained or experienced should go through an
introductory training or internship as agreed by the unit. Enrolled nurses/ staff nurses
can only work in NICU after they have gone through a unit agreed training for staff
nurses.

Indications for admission to NICU

• All infants should have had a birth weight of ≥900 grams, or are currently
weighing ≥900 grams.
• For infants weighing between 899 and 1000 grams, NICU admission will be
mainly for those whose primary indication is respiratory problem and have no
associated severe lactic/ metabolic acidosis (BD>10) in absence of dehydration,
no neonatal encephalopathy.
• Intubated infants requiring ongoing respiratory support or mechanical ventilation.
• Infants receiving an oxygen concentration (FiO2) of >60% to maintain pulse
oximetry saturations between 86 and 93%, and/or PaO2 >50 mmHg.
• Infant with PaCO2 >60 mmHg and/or PaCO2 >55 mmHg with a pH<7.25.
• Definite necrotizing enterocolitis (during acute phase), especially those with a
tense abdomen who might have respiratory compromise.
• Infants in shock requiring inotropic agents.
• Suspected congenital heart disease requiring intensive care.
• All preoperative or postoperative infants requiring intensive care.
• Need for chest tube (intercostals drain) insertion.
• Need for arterial line.

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High Care/ Transitional Care (TC) Nursery
Required nurse (professional nurse) to infant ratio is 1:2-3. With a shortage of
professional nurses, enrolled nurses (EN)/ staff nurses or nursing assistants (NA)
may assist the professional nurse with 1 professional nurse supervising 3 NAs
allocated 2 patients each, or supervising 2 ENs allocated 3 patients each.

Indications for admission to TC

• All infants weighing ≤1200g
• Infants with Apgar score <7 at 5 minutes or who required resuscitation (bag mask
ventilation and more) for ≥5 minutes.
• Infants of diabetic mothers
• Any infant who requires ≥ 40% oxygen to maintain pulse oximetry saturations 86
to 93%.
• Infants with a subaponeurotic haemorrhage
• Infants discharged from NICU
• Infants with apnoea and bradycardia or those requiring monitoring
• Infants with congenital abnormalities with a potential for airway obstruction, or
those requiring cardio-respiratory monitoring or those who are being prepared for
surgery.
• Well term infants requiring a second exchange transfusion
• Preterm infants requiring exchange transfusion
• Infants with central venous lines including umbilical venous line
• Infants on parenteral nutrition
• Infants admitted in the neonatal unit who are recovering post-surgery and not
requiring intensive care.
• Hypoglycaemia requiring an intravenous bolus of glucose more than once.
• Persistent hyperglycaemia
• Infants with seizures
• Infants on Amphotericin B

Ward 66
Required nurse (registered nurse) to patient ratio is 1:4-6. With a shortage of
professional nurses, enrolled nurses (EN)/ staff nurses or enrolled nursing assistants
(ENA) may assist the professional nurse with 1 professional nurse supervising 3
ENAs allocated 4 patients each, or supervising 2 ENs allocated 5-6 patients each.

Indications for admission to 66

• Infants requiring less than 40% of supplemental oxygen
• Infants weighing between 1200 and 1800g at birth
• Babies weighing less than 1200g will only be admitted to ward 66 if there is
shortage of beds in TC and meet the following conditions: weighing above 900g,
are on full feeds, regained their birth weight, and continuing to gain weight, no
apnoeas, if on supplemental oxygen the estimated oxygen concentration
delivered to the baby should be less than 40% on nasal prongs, and their transfer
is countersigned by the consultant.
• Infants being transferred from TC including those with:
a. Birth asphyxia
b. Congenital abnormalities

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 c. Evolving chronic lung disease on supplemental oxygen estimated to be
less than 40% on nasal prongs.
d. Awaiting weight gain
e. Recovering from NEC
• Well newborn infants with jaundice and a bilirubin >20 mg/dL

Ward 40
This is mainly a KMC ward, where infants stay with their mothers all the time.
Indications for admission to 40
• Infants weighing more than 1000g, not on oxygen or antibiotics, on full feeds and
gaining weight over the previous week and ward Hb >8g/dL
• Because this is a KMC ward, mother must be present 24 hours a day
• Well infants with jaundice requiring phototherapy, admitted from home or another
hospital

Lying in wards (57, 64, 65, 67 and 68)

These infants are cared for by their mothers but need to be reviewed by medical staff
from the neonatal unit.
Patients that need to be reviewed in the lying-in wards
• Birth weight between 1800g and 2500g, and well.
• Babies born to mothers with no antenatal blood results (WR and HIV) (awaiting
mother’s results).
• Infants born to mothers who are Rh negative.
• Genetic conditions and congenital abnormalities that do not compromise the
infant has no cardio-respiratory compromise, e.g. a well Trisomy 21 and club feet.
• Asymptomatic term or near-term infants born to mothers with obstetric risk factors
• Infants weighing above 1800g with cardiac murmurs but otherwise well with no
other signs like cyanosis or signs of cardiac failure

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 DISCHARGE POLICIES

Before discharging an infant check the following:

Lying-in Wards
• Ensure that all mother’s antenatal blood results (WR, HIV and Rh) are available
and have been acted upon appropriately e.g. if mother is HIV positive make sure
that the baby has received and discharged on the appropriate drugs to prevent
mother to child transmission of HIV; or if the mother is WR positive make sure
that the baby has received Bicillin before discharge.
• Infant is well and has passed urine, stools, is feeding well and has no jaundice.
• Those who were admitted for monitoring of glucose (LBW and LGAs) check that
they have normal glucose levels (≥ 2.6 mmols/L) for at least 12 hours before
discharge.
• For those admitted with birth weight <2000g, re-check weight before discharge
and if weight loss is predicted to be more than 15% in 7 days of life then do not
discharge but admit to ward 66, check if feeding well and check hydration status
and discuss patient with consultant. Weight must be at least 1650g before
discharge.
• Infants born to mothers with tuberculosis must be prescribed prophylaxis and
given an appointment to come to Dr. Mathivha’s follow up clinic or come back to
neonatal follow up clinic.
• Each infant’s details must be included in the statistics form before discharge.

Ward 66
• Infant is well and weighs at least 1650g, is feeding well and on full feeds,
maintaining temperature and glucose, and is passing urine and stools.
• Ensure that all mother’s antenatal blood results are available and have been
acted upon appropriately.
• All infants must have a standard neonatal discharge summary completed.
• Give an appointment for neonatal follow up clinic for infants with the following:
o Birth weight <1800g
o Required mechanical ventilation during his or her stay in hospital.
o Perinatal asphyxia with HIE II or more
o Neonatal jaundice requiring exchange transfusion or SB >20 mg/dL.
o Major congenital abnormalities
o Chronic lung disease
o Congenital infections (mainly STORCH group)
o Infants born to mothers with tuberculosis
• All infants must be immunised on discharge.

High care or Transitional Care Unit

• Generally most patients will not be discharged directly from TC, but term infants
who were admitted to TC for observation but not on any treatment and have no
major congenital abnormalities can be discharged directly from TC, e.g. those
born to diabetic mothers and were admitted for monitoring of glucose. Follow the
same policy as in ward 66 for all discharges.

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• Infants transferred from other hospital must not be sent to Ward 66, but
transferred back to their original hospital.
• NICU discharges, including those transferred to TC must have the NICU
discharge summary completed.
• NICU discharges and transfers to other hospitals or neonatal theatre and deaths
must have both the NICU discharge summary, and the standard neonatal
discharge summary completed.
• All deaths in TC and NICU must have the standard neonatal discharge summary
completed.

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 INTRAPARTUM HYPOXIA/ ASPHYXIA: RESUSCITATION

Provide warmth
Position, clear airway
Dry, stimulate, reposition A
Give oxygen as necessary
Connect to pulse oximeter if available

Evaluate
Breathing,
HR and Colour

Apnoea or Irregular breathing or HR <100

Provide PPV (BMV) B

Assess BHC after 30sec

HR <60 HR ≥60
Provide PPV + Chest Compressions
C
Assess BHC after 30sec

0sE3
HR <60 HR ≥60
Provide PPV + Chest Compressions + Adrenaline D

Note:
• BHC - stands for evaluate Breathing, Heart rate and Colour

• Infants born to mothers with meconium staining of amniotic fluid/ liquor (MSL)
must be intubated and suctioned through the meconium aspirator only if they
require resuscitation or are not vigorous (poor respiratory effort, HR <100/min,
decreased tone). If infant is vigorous the management should be the same
like any other baby irrespective of consistency of the meconium. Vigorous
infants should not be intubated for suction.

16
 • Re-assess colour, heart rate & breathing after every 30 seconds of action.

• To assess heart rate: listen over heart for 6 seconds, then multiply by 10 to
get heart rate in beats per minute.

• For adrenaline (ivi)- dilute 1:1000 to 1:10 000, by taking 1 mL adrenaline

into 9 mLs of normal saline and give 0.1-0.3 mLs/kg every 3-5 minutes,
always give a flush or 0.5-1ml of normal saline after giving the adrenaline.

• For adrenaline (ETT): Use 10 times the ivi dose. That means use
adrenaline as it is, without diluting it (neat adrenaline) and still give a
dose of 0.1-0.3 mLs/kg, follow it by a flush of 0.5 ml of normal saline.

• Continue PPV+Chest compressions for 30 seconds, before next

colour, heart rate & breathing assessment after giving adrenaline to
allow adrenaline time to be circulate.

Reference
South African Handbook of resuscitation of the Newborn. July 2009; 3.

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 ASPHYXIA: POST-RESUSCITATION MANAGEMENT – GENERAL

Definition of asphyxia: Lack or inadequate exchange of respiratory gases. This

results in hypoxia with or without ischaemia. It can occur prepartum, intrapartum or
immediately postpartum hence the term intrapartum or perinatal asphyxia is
preferred rather than birth asphyxia. Biochemically, there is hypoxaemia, hypercarbia
and acidosis.

The following are essential characteristics to make a diagnosis of intrapartum

asphyxia:
1. Umbilical cord arterial blood metabolic or mixed acidemia (pH < 7.0)
2. Apgar score ≤5 at 10 minutes
3. Clinical neurologic sequelae in immediate neonatal period (encephalopathy)
4. Evidence of multi organ dysfunction (e.g. CNS, renal)

Post resuscitation management - Immediate

• Ensure effective airway and ventilation.
• Ensure good circulation, give circulatory support if needed.

Ventilation
• Limit inspired oxygen to keep oximeter saturation between 86-93%.
• Maintain pCO2 between 35-55 mm Hg.

Perfusion
• Limit fluid intake to about 80% of usual recommendations for the first 48-72
hours, or until renal function recovers.

• Acidosis frequently accompanies significant perinatal asphyxia. Usually,

correction of the acidosis occurs spontaneously over a few hours after birth with
the initiation of adequate resuscitatory procedures. Hence, non/ free- potassium
Neonatalyte or 10% dextrose water, with no added alkali is recommended.

• Persistence of a base deficit of >12 mmol/l in the presence of persistent

hypoxaemia/ hypoxia/ pulmonary hypertension, despite adequate ventilation and
perfusion, may be an indication to give sodium bicarbonate. Give one to two
boluses of 8.4% sodium bicarbonate 0.5-1 mls/kg mixed with equal volume of
sterile water, infuse it slowly and repeat a blood gas 30 minutes after the bolus. If
acidosis persists add 8.4% sodium bicarbonate (usually 4 ml per 100 ml) to the
dextrose solution being used. This cocktail may be discontinued once the
standard bicarbonate is normal.

• Vasopressors, such as dopamine (5-20 µg/kg/min) and dobutamine (5-20

µg/kg/min) are effective in normalising blood pressures in asphyxiated infants.
Pressors should be used before fluid boluses in managing hypotension, unless
there is clear evidence of acute volume loss, e.g. vasa praevia or the presence of
a large subaponeurotic haemorrhage.

18
Other
• Post-resuscitation ensure that the patient is not hyperthermic, therefore switch off
the radiant warmers and consider using induced hypothermia when equipment is
available and is appropriate for the patient. To avoid hyperthermia, if the infant is
nurse under a radiant warmer or incubator, switch them off and monitor
temperature hourly. Aim to maintain rectal temperature at 34-35.5ºC.

• Start antibiotics as infection may be the underlying cause of asphyxia. The

potential for aminoglycoside toxicity is high in asphyxiated neonates (because of
diminished renal function). Consider whether antibiotics are necessary after 48
hours. Monitoring of the serum aminoglycoside level is essential if its use is to be
continued beyond three doses.

• Postpone feeding for 24-48 hours especially if has convulsions or has neonatal
encephalopathy. Start and increase feeds by 20-40mls/kg/day.

• Admit to TC (high care) if there are any signs of neonatal encephalopathy or

required resuscitation for 5 minutes or more.

• Put patient on aEEG within two hours of resuscitation, especially those who are
encephalopathic post-resuscitation.

• Monitor for development of seizures and treat convulsions promptly if they

develop. If have convulsions give Phenobarbital 20mg/kg loading dose, followed
by a second and third dose of 10 mg/kg if no response. If convulsions continue,
consider use of Phenytoin, Clonazepam or Lorazepam or Midazolam or
Lidnocaine. Start on maintenance Phenobarbital if has more than 2 episodes of
convulsions. Maintenance dose can be given intravenously or orally.

• Temperature fluctuations (particularly hyperpyrexia) are noted in severely

encephalopathic neonates and may be attributed to the effects of the insult on the
hypothalamus. Pyrexia usually requires the discontinuation of supplementary
heating, e.g. a warm incubator, and occasionally requires the use of an anti-
pyretic agent (paracetamol).

• Prevent hyperthermia. Hypothermia has been shown to improve neurological

outcome.

• Consult Allied health workers (namely speech therapists, physiotherapists and

occupational therapists) so that they can be involved early in management of
these infants especially for those with moderate to severe hypoxic ischaemic
encephalopathy (HIE II and III) (see staging below).

Admission to NICU
• Ideally, all infants with asphyxia and require respiratory support should be put on
mechanical ventilation for at least 24-48 hours and then reassessed.

19
 • This might not always be possible because of limited resources in our hospital.
The infants with any of the following criteria may not be offered mechanical
ventilation,
o Took >10 minutes to first spontaneous respiration/ gasp (must exclude
effect of maternal anaesthesia or pethidine use first) with a base deficit of
>16 mmol/L
o Developed convulsions requiring more than one drug to control
o Comatosed (HIE 3)
• A decision not to ventilate an asphyxiated infant should be discussed with the
consultant on-call.

Investigations
• Do FBC and Blood Culture at birth to exclude infection
• Do U&E, Cr around 24 hours of life, generally day 2 of life to check for renal
function and electrolyte abnormality mainly hyponatraemia
• Do CRP on Day 2 to decide on whether to stop antibiotics or not. Stop antibiotics
if CRP is <16 mg/dL.
• Do serum Glucose, Calcium, Magnesium and Phosphate if having seizures
(hypomagnesaemia tends to occur on the first day, whereas hypocalcaemia
tends to occur day 2-3 of life).
• Do Lumbar Puncture in those with seizures and/ or those with CRP >20 mg/dL
and/ or those with encephalopathy and history not compatible of asphyxia.
• LFTs (in those with jaundice) and Cardiac enzymes (in those with hypotension/
tachycardia) may be done only after discussing with the consultant

Table 1. Features of Sarnat and Sarnat Stages Hypoxic Ischaemic Encephalopathy (HIE)

Stage I Stage II Stage III

Level of Hyperalert; irritable Lethargic or obtunded Stuporous, comatose
consciousness
Neuromuscular control Overeactive Diminished Diminished or absent
Posture Mild distal flexion Strong distal flexion Intermittent decerebration

Muscle tone Normal Mild hypotonia Flaccid

Stretch reflexes/ Deep Overactive Overactive Decreased or absent

tendon reflexes
Primitive reflexes Normal Suppressed Absent
Suck Weak Weak or absent Absent

Moro Strong, low threshold Weak, incomplete high Absent

threshold
Autonomic function Sympathetic Parasympathetic Both systems depressed
Pupils Mydriasis Miosis Midposition, often unequal;
poor light reflex
Respirations Spontaneous Spontaneous, occasional Periodic, apnoea
apnoea
Heart Rate Tachycardia Bradycardia Variable
Seizures None Common (onset 6-24 hrs Uncommon (excluding
of age) decerebration)
Outcome About 100% normal 80% normal; abnormal About 50% die; remainder
if signs last >5-7 days with severe sequelae

20
Table 2. Thompson Scoring of Hypoxic Ischaemic Encephalopathy

Category Signs of HIE

Normal/ mild Moderate Severe
Level of 1 2 = Lethargic 3 = Stupor/ Coma
Consciousness
Spontaneous activity 1 2 = Decreased activity 3 = No activity
Posture 1 2 = Distal flexion or 3 = Decerebrate
complete extension
Tone 1 2 = Hypotonia (focal or 3 = Flaccid
general)
Primitive reflexes
(any)
Suck 1 2 = Weak 3 = Absent
Moro 1 2 = Incomplete 3 = Absent
Autonomic nervous
system (any)
Pupils 1 2 = Constricted 3 = Deviation/ dilated/
non-reactive to light
Heart rate 1 2 = Bradycardia 3 = Variable heart rate
Respiration 1 2 = Periodic breathing 3 = Apnoea

Signs of moderate or severe HIE in at least 3 of the following 6 categories

Reference
1. 1. Fanaroff Textbook- pages on post resusc management. In Fanaroff and Martin’s neonatal-
perinatal medicine: diseases of the fetus and infant (8 th ed.). Philadelphia, Elsevier, 2006,
p1108-1118

21
ASPHYXIA: POST-RESUSCITATION MANAGEMENT- INDUCED HYPOTHERMIA

Introduction
• Cooling of asphyxiated infants to body temperatures between 33-35ºC
(induced hypothermia) started within 6 hours of life has been shown to reduce
mortality and disability associated with asphyxia 1-4.
• Therefore induced hypothermia should be considered post-resuscitation of
asphyxiated infants.

Criteria for starting induced hypothermia

• If induced hypothermia is considered, infants must fulfil the following criteria:

i. Infant born at ≥34 weeks and/ or weighing ≥ 2000 grams.

ii. Apgar score ≤ 5 at 10 minutes or continued need for
resuscitation (including endotracheal and bag mask ventilation)
for 10 minutes
iii. Metabolic acidosis with pH <7.00 or base deficit ≥16 mmol/L
from an arterial blood gas done within 60 minutes of life
iv. Have encephalopathy defined as
Lethargy or stupor or coma and at least one of the
following:
a. Hypotonia
b. Abnormal reflexes
c. Absent or weak suck
d. Clinical seizures
v. Abnormal amplitude-intergrated electroencephalography (aEEG)
for at least 30 minutes. Abnormalities could be any of the
following
• Moderate abnormal background (upper margin of the
band above 10µV and lower margin below 5 µV)
• Severe abnormal background (upper margin of the band
below 10µV and lower margin below 5 µV)
• Normal background with seizure activity

• It is appropriate not to offer induced hypothermia in infants with the following

conditions:
o Infants with no spontaneous respiratory effort after 30 minutes post-
resuscitation (after excluding possible effect of anaesthesia), heart rate
below 100 per minute at 15 minutes post-resuscitation in a baby who
has normal temperature.
o Infants expected to be more than 6 hours of age at the time of starting
cooling, and those with congenital abnormalities or have signs
suggestive of syndromes or chromosomal abnormalities that involve
brain dysgenesis should not be put on induced hypothermia

22
Protocol

• The following protocol should be followed:

 Start hypothermia as soon as possible but not later than 6hours
of life
 Nurse patient on a servo-controlled radiant warmer that is off or
regulated to maintain hypothermia
 Check skin and rectal temperature
 Switch off the warmer
 Put the patient on the cooling machine, set up the thermostat
 Aim to keep rectal temperature between 33 and 34ºC
 Put on the servo-controlled radiant warmer once the rectal
temperature reaches 35 ºC
 Set the radiant warmer to servo-control to keep the rectal
temperature between 33 and 34ºC
 Check rectal temperature every 30 minutes until have
established hypothermia and thereafter 1 hourly, monitor skin
temperature hourly.
 Monitor vital signs hourly
 Give sedation, Morphine if BP is normal (loading dose 50 µg/kg
followed by infusion of 10-40 µg/kg) or a combination of
Fentanyl infusion (1-2 µg/kg/hr) and Midazolam (0.1 mg/kg/hr) if
hypotensive.
 Treat patient according to unit protocol as problems are
detected.
 Rewarm after 72 hours of hypothermia
• Rewarm at not faster than 0.5ºC per hour
• Increase radiant warmer set temperature 0.5ºC higher
than skin temperature
• Continue monitoring rectal temperature for the next 4
hours post cooling
 Patient must be followed up for at least 18 months post
discharge

o Other management
 Start on fluids of 60 mls/kg and regulated according to urine
output, electrolytes and creatinine.
 Keep NPO during hypothermia up to 12 hours after rewarming
 Most patients on hypothermia will maintain HR at about 100/ min
and mean BP >40 mmHg. If mean BP is <40 mmHg, give one
bolus of Normal Saline 10—20 mls/kg, and if BP is still low start
on dopamine, followed by dobutamine and adrenalin as
necessary.
 Ventilation, keep pH >7.25, paCO2- 35-45 mmHg, paO2- 45 –
70
 Do electrolytes, creatinine, and FBC+platelets from 24 hours of
life and 48 and 72 hours on hypothermia, PI/ PTT day 2 and day
3 on hypothermia, LFTs once at 48 hours of life.

23
  Manage seizures according to the standard unit protocol

References
1. Gluckman PD, Wyatt JS, Azzopardi D, et al. Selective head cooling with mild systemic
hypothermia after neonatal encephalopathy: multicentre randomised trial. Lancet
2005;365:663-70.
2. Shankaran S, Laptook A, Ehrenkranz RA, et al. Whole-body cooling for neonates with
hypoxic-ischaemic encephalopathy. N Engl J Med 2005;353:1574-84
3. Jacobs S, Hunt R, Tarnow-Modi W, et al. Cooling for newborns with hypoxic ischaemic
encephalopathy. Cochrane Database Syst Rev 2007;4:CD003311
4. Azzopardi DV, Strohm B, Edwards AD, et al. Moderate hypothermia to treat perinatal
asphyxial encephalopathy. N Engl J Med 2009;361:1349-58
5. Edwards AD, Brocklehurst P, Gunn AJ, et al. Neurological outcomes at 18 months of
age after moderate hypothermia for perinatal hypoxic ischaemic encephalopathy:
synthesis and meta-analysis of trial data. BMJ 2010;340:c363.

24
 AMPLITUDE ELECTRO-ENCEPHALOGRAPH (aEEG)

INTRODUCTION

• aEEG is used to monitor cerebral function.

• The aEEG uses two channels F3-P3 and F4-P4 which corresponds to the EEG
10-20 classification of a standard EEG. This provides information about
symmetry, helpful in identifying unilateral brain injury. The signal is amplified,
filtered and rectified and smoothed. The signal is then displayed on a
semilogarithmic scale at 6cm/hr.

• Handling, ECG and HFOV may cause a baseline drift. Antiepileptics may depress
background (wide band). Morphine infusion can also depress background.

• aEEG gives limited information when it comes to seizure detection but a good
reliability when detecting an abnormal background which is predictive of an
abnormal neurodevelopmental outcome.

• aEEG is a monitoring device and does not replace the standard EEG. There are
five important background patterns (see Figures).

• Pattern recognition is important in aEEG. The patterns that predict poor outcome
are
o Burst Suppressions (BS),
o Continuous Low Voltage (CLV), and
o Isoelectric (IE) tracing.

• To get a better idea of prognostication it is important to leave patient on monitor

for at least 12-24 hrs. But a trace within the first 3-6 hrs can also aid in
prognostication.

Uses of aEEG

1. Infants with neonatal encephalopathy (NE).

2. Causes of neonatal encephalopathy include the following:
- Asphyxia
- Meningitis/ Meningo-encephalitis
- Electrolyte abnormalities
- Metabolic disorders
- Congenital malformations
3. In predicting outcome after brain injury.
4. Detection of seizures – clinical and subclinical.
5. Aids in identifying patients for neuro-protective strategies e.g. induced
hypothermia.

25
DESCRIPTION OF DIFFERENT PATTERNS OF aEEG

a. Continuous normal voltage (Normal aEEG)

Upper part of the tracing (broad band) is >10 and the lower part of the tracing is >
5mV

b. Discontinuous normal voltage (Moderately Suppressed)

Upper part of the tracing (broad band) is >10 and the lower part of the tracing is
<5mV

c. Burst Suppression (Abnormal)

Upper part of the tracing (broad band) is >5 and the lower part of the tracing is
<5mV, interspersed with bursts >25mV

d. Continuous low voltage (Abnormal)

26
Both upper part and lower part of the tracing (broad band) are <5 mV; raw EEG
shows low amplitude background.

e. Isoelectric tracing (Abnormal)

Both Upper and Lower amplitude <5mV; raw EEG – inactive background

27
f. Seizure activity
Identified as a rapid increase in the upper and lower margins. Be aware of electro-
clinical dissociation or uncoupling. Usually occurs after antiepileptic drug is given.
Antiepileptic drug dampens the clinical seizure but still see electrographic seizures.
Focal seizures and those of low amplitude and brief seizures may be missed with
aEEG. Impedance may hinder the tracing.

g. Recurrent seizures/ Status epilepticus. The repetitive seizures or status

epilepticus may give a saw-tooth appearance (see the tracing below- lower band or
right side).

References
1. Toet MC, van Rooij LGM, de Vries LS. The use of amplitude-integrated
electroencephalography for assessing neonatal neurology injury. Clin Perinatol 2008;35:
6665-678.
2. Al NaqeebN, Edwards AD, Cowan F, et al. Assessment of neonatal encephalopathy by
amplitude integrated electroencephalography. Pediatrics 1999;103:1263-71.
3. Toet MC, Hellstrőm-Westas L, Groenendaal F, et al. Amplitude integrated EEG 3 and 6
hours after birth in full term neonates with hypoxic-ischaemic encephalopathy. Arch Dis
Child Fetal Neonatal Ed 1999;81(1):F19-23.

28
 CRANIAL ULTRASOUND

Indications
• Preterm infants, especially if weighing <1500g
• Birth asphyxia with stage II-III HIE- early sonar to exclude oedema or
periventricular echodensities (PVEs), haemorrhage or structural abnormalities;
later sonar for cystic changes
• Seizures- to exclude similar findings as in birth asphyxia and IVH
• Macrocephaly or microcephaly- to exclude hydrocephalus or structural
abnormalities
• Dysmorphic infants with involvement of CNS or midline defects like hypotelorism-
to exclude structural abnormalities
• Suspected congenital infections, namely cytomegalovirus and toxoplasmosis- to
exclude intracerebral calcifications

Screening cranial ultrasound in preterm infants

Routine ultrasound must be done in all infants weighing <1500g
Head ultrasound schedule for preterm infants:

1. First ultrasound: Within the first 7 days of life

a. Will identify >90% of cases of IVH;
b. Identify increased periventricular echodensities

2. Second ultrasound: At 10-14 days of life

a. Will identify progression of PVEs,
b. Periventricular cysts may become apparent.
c. May identify early development of post haemorrhagic hydrocephalus

3. Last ultrasound at 28 days and beyond or before discharge

a. Periventricular cysts may become apparent
b. Post haemorrhagic hydrocephalus will be apparent by this time

Grading of IVH
• Grade I Germinal matrix haemorrhage
• Grade II Blood within ventricular system without distension
• Grade III Blood within ventricular system with distension
• Grade IV/ III+IPE IVH + Intraparenchymal bleed (echodensity)

Reference
1. Intracranial hemorrhage: germinal matrix-intraventricular hemorrhage of the premature infant.
In Volpe JJ. Neurology of the newborn, 4th Edition p428;2000
2. Van Wezel-Meijler G, Steggerd SJ, Leijser M. Cranial ultrasonography in neonates: role and
limitations. Semin Perinatol 2010;34:28-38

29
 SPINA BIFIDA

Introduction: A meningocoele is a cystic dilation of the meninges associated with

spina bifida and a defect of the underlying skin. Meningomyelocoele is identical to
meningocoele but with associated abnormalities in the structure and position of the
spinal cord or cauda equine (nerve roots). Spinal dysraphism includes the overall
group of defects. Spina bifida occulta refers to non-fusion of one or more posterior
arches of the spine. This lesion is significant if associated with underlying
abnormalities. Its presence may be signalled by the presence of a haemangioma, a
patch of abnormal hair, a dimple/ sinus, or a lipoma in the lumbar-sacral area.

Presentation:
Approximately 80% of lesions occur in the lumbar (thoracolumbar, lumbar,
lumbosacral) area. There is dorsal displacement of the neural tissue such that a sac
is presented. The level and extent of neural tissue involvement determines the
severity of the deficit in motor & sensory function, involvement of bladder and bowel
function. Typically, infants with lesions at L5-S1 will ambulate with or without short
leg braces; L3-L4 might be ambulatory with assistance of long leg braces and
crutches, prone to paralytic hip dislocation, L1-L2 or above are completely paraplegic
with no functional ambulatory ability. Hydrocephalus is a frequent associated
complication. Always do a full neurological examination. Examine other systems:
Cardiac, Gastro-intestinal tract, Genito-urinary tract and Skeletal to exclude other
abnormalities.

Management
Approaches to Management
1. An aggressive, non-selective approach is recommended as these infants might
survive months with an open lesion which might become infected and worsening
hydrocephalus making it difficult for the parents to take care or handle the infant.
Early closure is recommended because it decreases the incidence of infection
and subsequent loss of motor function.

2. A selective approach (advising against early surgery) may be used for infants
with major cerebral anomalies, severe HIE, associated gross anomalies,
haemorrhage or infection, high cord lesions and severe hydrocephalus.

3. Whatever approach is used, an open discussion with parents must take place
before surgery.

Immediate Management
1. Keep infant in the prone position
2. Cover the defect with a sterile saline-moistened gauze or plastic wrap. Do not
use Betadine (neurotoxic) or any other sticky substance
3. Start on antibiotics (Ampicillin and Gentamicin) and continue until closure.
4. Consult paediatric surgeons (paediatric surgeons have agreed to assist us with
early closure of meningomyelocoele in infants delivered at CHBH), or
neurosurgeons if paediatric surgeons are not available
5. If the sac is not leaking, closure within 24 to 72 hours should be undertaken
6. If the sac is leaking, prompt closure within 24 hours is indicated

30
Postoperatively Management
1. Position the infant on abdomen or either side, avoiding compression of the back
2. Observe wound daily for signs of leakage, infection or wound breakdown
3. Observe for signs of progressive hydrocephalus, do serial cranial ultrasounds
and monitor head circumference, needs shunt if hydrocephalus develops
4. If hydrocephalus is present at birth, it is recommended not to put shunt at the
same time as correcting the defect.
5. If has or develops hydrocephalus, neurosurgeons will usually request brain CT
scan before placing a shunt, therefore order brain CT scan.
6. Monitor for bladder function, palpate for the bladder or catheterise the bladder
looking for residual volume of urine, may need intermittent catheterization if not
able to empty bladder. Palpate for the kidneys.
7. Start on prophylactic antibiotics against urinary tract infection if infant requires
intermittent catheterization.
8. Order renal ultrasound and voiding cystourethrogram.
9. Consult the following specialities for further management
o Physiotherapist and Occupational therapists
o Nephrologist and/or Urologists for renal or bladder dysfunction
o Orthopaedic surgeons for lower limb function
o Social workers

Prevention:
1. Most neural tubes can be prevented by folic acid supplementation of 0.4mg/day
before 28th day of pregnancy .
2. Mothers with affected infant are at higher risk than the normal population. They
should receive 4mg/day of folic acid if considering falling pregnant months before
conception and during the first trimester. They should also be advised to start
antenatal care early, preferably at a referral center and be referred to the fetal
medicine unit.

References
1. Kaufman BA. Neural tube defects. Pediatr Clin N Am 2004;51:389-419.
2. Neural tube formation and prosencephalic development. In Volpe JJ. Neurology of the
newborn, 4th Edition p9-19;2000

31
 HYDROCEPHALUS

Introduction: Hydrocephalus indicates either a state of progressively expanding

ventricles, or enlarged ventricles, and increased intracranial pressure. Congenital
hydrocephalus refers to a state of progressive ventricular enlargement apparent from
the first day of life.

Causes
Major causes of congenital hydrocephalus are aqueduct stenosis (33%),
myelomeningocoele (28%), communicating hydrocephalus (22%), Dandy-Walker
malformation (7%), Others (10%): intrauterine infection (toxoplasmosis and
cytomegalovirus), tumour (choroids plexus papilloma), intraventricular haemorrhage
and malformation of the vein of Galen.

Post haemorrhagic hydrocephalus is the common acquired form of hydrocephalus in

neonates. May evolve over weeks following intraventricular haemorrhage. Usually
occurs because of obstruction of CSF outflow or impairment of CSF resorption.

Management
Congenital hydrocephalus:
1. Do a full examination looking for other abnormalities.
2. Order a cranial sonar.
3. Order brain CT scan.
4. Consult neurosurgeons for possible shunt insertion.

Post haemorrhagic hydrocephalus

Approximately 35% of infants with IVH will develop slowly progressive ventricular
dilatation. Of these 65% arrest spontaneously, arrest generally occurs within 4
weeks. Of the remaining 35%, the majority (30%) continue to progress for >4weeks
and if not treated will progress rapidly; the remaining 5% develop rapid progression
even before 4 weeks. Rate of head growth >1.5-2cm/ wk signals rapid progression.
• Slow progressive ventricular dilatation (moderate dilatation, appropriate head
growth) and duration <4 weeks
1. Observe closely for 4 weeks
• Slow progressive ventricular dilatation, duration >4 weeks
1. Call neurosurgeons, CT scan brain as neurosurgeon will ask for it.
2. Serial lumbar punctures on alternate days for a week in attempt to arrest
progression and decrease ventricular size by removing adequate quantity
of CSF (10-15 mLs/kg), but watch for hyponatraemia. Reassess head
growth for a week. Duration of serial LPs will depend on the response
usually 3-4 wks. Measure opening pressure when doing LPs. Send CSF
for MCS and biochemistry. (Note: serial LPs will only help if it is a
communicating hydrocephalus)
3. There are drugs that decrease CSF production like acetazolamide
100mg/kg/d and Lasix 1mg/kg/d. However, drug therapy may not have
extra benefit compared to serial LPs, also have side effects.
• Rapidly progressive ventricular dilation (moderate to severe dilation, excessive
head growth)

32
 1. Serial lumbar punctures, Call neurosurgeons, CT scan brain as
neurosurgeons will ask for it.
2. Ventricular drainage
3. Ventriculoperitoneal shunt

• Spontaneous arrest of ventricular dilation or arrest following serial LPs or drugs

1. Follow up for 1 year

References
Intracranial hemorrhage: germinal matrix-intraventricular hemorrhage of the premature infant.
In Volpe JJ. Neurology of the newborn, 4th Edition p457-481;2000

33
 SEIZURES

Introduction: Four essential neonatal seizure types can be recognized: subtle,

clonic, tonic and myoclonic, tonic-clonic rarely occurs in neonates. Subtle seizures
are more common in preterm than in full term infants. Most common presentation of
subtle seizures in both preterm and term infants are ocular phenomena, sustained
eye opening with fixation in preterms and horizontal deviation in term infants.
Jitteriness, a movement disorder is often confused with a seizure. Jitteriness is a
tremor, compared to clonic jerking of a seizure, is stimulus sensitive, ceases with
passive flexion, not associated with abnormal eye movement and autonomic
changes.

Management:
Investigation
1. Check glucose level (dextrostix) immediately
2. Electrolytes: Sodium and potassium
3. Ionised calcium, magnesium and phosphorus
4. Lumbar puncture
5. Cranial ultrasound
6. Focal seizures will need a CT scan as focal ischaemic lesions may not be
detected by cranial sonar
7. Monitor with aEEG, assists to diagnose seizures, monitor response to treatment
and to detect subclinical seizures.

Treatment: Immediate
Step 1. Maintain airway and breathing, stabilize vital signs

Step 2. Look for metabolic disturbances and correct them if found

a. Hypoglycaemia
• Give glucose iv. {10% dextrose 2-3mLs/kg (200-300 mg/kg)} if
hypoglycaemia is present. Give continuous infusion at 6-8
mg/kg/min.
b. Hypocalcaemia
• Give 10% calcium gluconate- 1-2 mls/ kg diluted with equal
volume of sterile water, give it over 5 minutes. Monitor heart rate
and iv site.
c. Hypomagnesaemia
• Give 50% magnesium sulphate- 0.1-0.2 mls/ kg diluted with
sterile water iv slowly. Can also be given intramuscular. Monitor
heart rate. Intramuscular dose may cause tissue necrosis.
Step 3. Phenobarbital - a loading dose of 20 mg/kg over 5-10 minutes
• If no response to loading dose give additional doses of 5-10 mg/kg
until seizures have ceased or reached a total dose of 40 mg/kg.
Step 4. Phenytoin- a loading dose of phenytoin 20 mg/kg as infusion over 20-30
minutes in normal saline.
• Heart rate and rhythm should be monitored during infusion
• May give a repeat dose of 5 mg/kg to total dose of 30 mg/kg
Step 5. Lorazepam (long acting benzodiazepine)- 0.05 mg/kg iv.

34
 • May repeat to total dose of 0.1 mg/kg.
• If Lorazepam is not available give Dormicum/ Midazolam (short
acting benzopiazepine)- 0.02-0.1 mg/kg. Because is short acting it
is better to give it as a continuous infusion of 0.06 to 0.4 mg/kg/ hr.
Be prepared to provide mechanical ventilation, especially with
previous doses of Phenobarbital, because of its effect on respiration
(causes depression). diac rate and rhythm monitored during
infusion. Rivotril 0.1 mg may also be used (NOTE: not per kg)
repeated 3 hourly.
Step 6. Pyridoxine dependency should be considered in infants with no asphyxial
history and having uncontrollable seizures.
• This is diagnosed by rapid cessation of seizures on EEG to an iv
dose of 50-100 mg of pyridoxine.
• If diagnosis is made maintenance oral dose of 10-100 mg/kg/day is
started.

Treatment: Maintenance
1. Phenobarbital 3-8 mg/kg daily iv or p.o.
2. Phenytoin 3-8 mg/kg daily iv or p.o

Duration of therapy:
1. Depends on the likelihood of recurrence of seizure if drug is stopped and risk of
subsequent epilepsy.
2. This depends on the neurological examination, cause of seizures and EEG. For
example, in asphyxiated infants should treat for 7 days. There is approximately
50% risk of recurrence of seizures if neurological examination is abnormal on
discharge.
3. If neurological examination is normal, stop treatment. If abnormal discharge on
treatment and reassess in 1-2 months, if no seizure activity wean off treatment.

Investigations of a neonate with seizures

• Serum Glucose, Calcium, Magnesium and Phosphate, U&E
• Lumbar puncture
• FBC+Plat+Diff, CRP
• Amplitude EEG

References

1. Silverstein FS, Jensen FE. Neonatal seizures. Ann Neurol 2007;62:112-20.

2. Glass HC, Wirrell E. Controversies in neonatal seizure management. J Child Neurol
2009;24:591-9
3. Jensen FE. Neonatal seizures: an update on mechanisms and management. Clin
Perinatol 2009;36:881-900
4. Neonatal Seizures. In Volpe JJ. Neurology of the newborn, 4th Edition p178;2000

35
 RESPIRATORY DISTRESS

Introduction: Signs of respiratory distress include tachypnoea (RR >60/min),

recession, nasal flaring, grunting and cyanosis. These signs may occur on their own
or in various combinations. These signs may also be manifestation of non-respiratory
causes, e.g. cardiac disease, metabolic acidosis, infection, anaemia and
polycythaemia.

Causes: Common causes of respiratory distress in the newborn are hyaline

membrane disease (HMD), pneumonia, meconium aspiration syndrome (MAS) and
transient tachypnoea of the newborn (TTN).

Guidelines to differential diagnosis: HMD is the most likely cause in preterm

infants (<37 weeks). However, prematurity is a risk factor for infection, therefore
pneumonia is also a consideration. An infant born from a mother with meconium
staining of amniotic fluid (MSAF) and develops respiratory distress, has MAS until
proven otherwise. Respiratory distress in a term infant without a history or evidence
of MSAF is most likely due to pneumonia or TTN. Other pulmonary causes of
respiratory distress to consider are pneumothorax, congenital pulmonary
abnormalities such as congenital diaphragmatic hernia, and obstruction to the
airways.

Management:
1. General
If having good respiratory effort ensure adequate oxygenation by checking
saturation using pulse oximeter.
If supplemental oxygen is required administer it via nasal prongs or headbox if
nasal prongs are not available.
If assisted ventilation is required, use positive pressure devices which provide
positive end expiratory pressure (PEEP) and measures or limits inspiratory
pressure (i.e. Neopuff, set at PEEP 4 -5 cm H2O, start with PIP of 15-20
cmH2O) or self-inflating resuscitation bag/ “Ambu bag” if Neopuff is not
available.

Temperature must be maintained within normal to minimize oxygen

consumption and requirements.

2. Oxygen Delivery/ Administration

• The best way to administer oxygen is through a blender/ mixer so that one
can regulate the concentration of oxygen administered. Unfortunately
oxygen blenders are not always available especially in labour ward nursery.

• Oxygen can be administered by nasal prongs or headbox. Headbox allows

delivery of a wide range of oxygen (21% to 100%). If using head box and do
not have blenders/ mixers one can use the Venturi system connecters. If
using headbox oxygen please ensure that oxygen flow rate is not less than
2-3 L/min/kg to avoid re-breathing of carbon dioxide 1. Using headbox
requires large amounts of oxygen that are used compared to nasal prongs
therefore cost is a major disadvantage. It is also difficult for the staff and

36
 mothers to handle babies on headboxes compared to those on nasal
prongs.

• Nasal prongs give marked variations in concentration of oxygen that the

baby is actually getting, due to mixture with inspired environment/ room air
that the baby is also breathing. Using nasal prongs, the concentration of
oxygen delivered to the baby depends on the body weight, nasal prong flow
rate, oxygen concentration and nasal prong diameter. The rule of thumb is
that if flow in L/min is equal to or greater than the baby’s weight in kilograms,
then delivered oxygen concentration equals the oxygen concentration set on
the blender or coming from the oxygen source 2. Advantage of nasal prongs
is use of low flows of oxygen, therefore less costs, may generate some
positive airway pressure, easy to handle babies.

• To avoid damage from inadequate oxygen or too much oxygen, all patients
on supplemental oxygen should be attached to a pulse oximeter so that
oxygen levels (saturations) in the baby’s body can be monitored to enable
one to deliver the appropriate amount/ concentration of oxygen.

3. Specific Management of Infants with Respiratory Distress

i. All babies with any form of respiratory distress should be admitted to the
appropriate ward as soon as possible. No baby should wait or stay in
the labour ward nursery or triage area for more than two hours
irrespective of the underlying condition or diagnosis. A decision on
whether to admit or not to admit the patient must be made within the first
two hours after the patient has been referred to the doctor.

ii. All babies with respiratory distress weighing less than 1000 grams should
be put on nasal prongs at flows of 1 L/min and those above 1000 grams
on flows of 1-2 L/min to achieve maximum concentration of oxygen. Big
term babies with moderate to severe respiratory distress who are dropping
Sats on nasal prong oxygen might need to be put on oxygen headbox to
improve their Sats.

iii. All babies on oxygen should be put on pulse oximeter and aim to keep
Sats between 86 and 93. For those on head box wean flow by 2L/min
every 5-10 minutes if Sats are >93% to not below 2-3 L/min/kg. For those
on nasal prongs wean flow by 0.25 L/min every 5-10 minutes if Sats are
>93% to not below 0.25 L/min.

iv. If infant requires <40% oxygen (a guide is a baby who is on 6L/min

headbox or nasal prong flow at 0.3 or less for those weighing ≥1250
grams) to maintain oxygen saturation >90% admit to ward 66 (Level 2
nursery) and put on nasal prong oxygen at 1L/min on 35% FiO2 if blenders
are available or at 0.3 L/min if there are no blenders and low reading flow
meters are available. If the above equipment is not available give
incubator oxygen at 4 L/min through the incubator oxygen filter port, NOT
in the main incubator openings or ports.

37
 v. If infant requires ≥ 40% oxygen do arterial blood gas and admit to TC, or
NICU if requires ventilation.

vi. Indications for mechanical ventilation are PaCO2 >55 mmHg,

especially when associated with pH <7.25; or PaCO2 >60 with any pH; or
require FiO2 >0.6 to maintain PaO2 ≥50 mmHg or O2 saturations between
86 and 93%. Mechanical ventilation can be given as continuous positive
airway pressure (CPAP) or conventional mechanical ventilation (CMV).

vii. VLBW infants weighing between 800 and 1000 grams should be offered
CPAP with or without surfactant in TC if they require more than 40%
oxygen. All preterm infants who are on CPAP for respiratory distress and
are within 48 hours of life and cannot be weaned below 40% oxygen give
in and out surfactant. Infants requiring CPAP or CMV and weighing ≥1000
grams should be admitted to NICU.

viii. All patients with respiratory distress requiring >40% oxygen should be put
on CPAP soon after delivery, and be kept on CPAP, especially those
weighing between 800 and 1500 grams. They can be tried off CPAP when
oxygen requirements are less than 30%, have no or mild respiratory
distress and no apnoeas.

ix. Start antibiotics. Pneumonia may mimic respiratory diseases such as

HMD or meconium aspiration, both clinically and on chest X-ray.
Therefore, start all infants with newly diagnosed (within 72 hours of life)
respiratory distress on antibiotics – Ampicillin and Gentamicin (Gentamicin
dose should be calculated according to gestational age. Always take
bloods for blood culture and FBC (Wbc + diff count, Hb, Platelets) before
starting antibiotics. In those who develop RD after they have been in
hospital for >72 hours use second-line antibiotics.

x. Feeds and fluids: Infants with severe respiratory distress may not be able
to co-ordinate breathing and swallowing therefore they are at risk of
aspiration if fed orally. Infants with mild to moderate respiratory distress
should be started on feeds either orally or through nasogastric tube
depending on gestational age and severity of distress. Infants with severe
respiratory distress should be kept nil per mouth. Start intravenous fluids
for maintenance in those who cannot be fed or are not on full feeds.

xi. Investigations of infants with respiratory distress at birth.

a. FBC+Plat + Differential count on admission

b. Blood culture on admission before starting antibiotics
c. Do CRP at 12-24 hours of life only if still having respiratory distress and/ or
requiring supplemental oxygen.
d. Chest-ray on admission if having moderate to severe respiratory distress
or requiring intubation. If having mild to moderate respiratory distress, only
do CXR if is still having respiratory distress and/ or on supplemental
oxygen by day 2 of life.

38
Reference
1. Frey B, Shann F. Oxygen administration in infants. Arch Dis Child Fetal Neonatal Ed
2003;88:F84-F88.
2. Walsh M, Engle W, Laptook A, et al. Oxygen delivery through nasal cannulae to preterm
infants: can practice be improved? Pediatrics 2005;116:857-61
3. Ho JJ, Subramaniam P, Henderson-Smart DJ, Davis PG. Continuous distending pressure for
respiratory distress syndrome in preterm infants. Cochrane Database Syst Rev 2002;
(2):CD002271
4. Stevens TP, Harrington EW, Blennow M, Soll RF. Early surfactant administration with brief
ventilation vs. selective surfactant and continued mechanical ventilation for preterm infants
with or at risk for respiratory distress syndrome. Cochrane Database Syst Rev
2007;4:CD003063
5. Morley CJ, Davis PG, Doyle, et al. Nasal CPAP or intubation at birth for very preterm infants.
N Engl J Med 2008;358:700-8.
6. Verder H, Bohlink, Kamper J, et al. Nasal CPAP and surfactant for treatment of respiratory
distress syndrome and prevention of brochopulmonary dysplasia. Acta Paediatr
2009;98:1400-8
7. Finer NN, Carlo WA, Walsh MC, et al. Early CPAP versus surfactant in extremely preterm
infants. N Engl J Med 2010;362:1970-90

39
 SURFACTANT REPLACEMENT THERAPY

Introduction
Effects of surfactant therapy include an increase in functional residual capacity, rapid
improvement in oxygenation, increase in lung compliance, decrease in pulmonary
ventilation-perfusion mismatch and a decrease in pulmonary artery pressures. It
results in a reduction in pulmonary air leaks and mortality 1. In combination with
nCPAP it reduces the need for mechanical ventilation 2.

Surfactant Therapy
Prophylaxis :
• With this approach, the infant is given before the infant develops signs of
respiratory distress, ideally before the infant takes a breath. This is often not
possible as one must ensure that the infant does not need resuscitation first.
• It is usually given after resuscitation and stabilisation usually within the first hour
and is usually followed by putting baby on nCPAP. We are currently unable to
give surfactant prophylactically because of cost reasons.

Rescue:
• With this approach, surfactant is only given to those who have developed signs of
respiratory distress.
• CHBH uses this approach, babies are only given surfactant if they develop
respiratory distress and require more than 40% oxygen on nCPAP or invasive
mechanical ventilation. The sooner the rescue therapy is administered (preferably
within 2 hours of life) the better the outcomes 3.

When to consider giving surfactant therapy?

• Preterm infant (<37 weeks) and postnatal age ≤ 48 hours
• Changes suggestive of HMD on chest X-ray when available.
• Ventilated infant requiring ≥ 40% oxygen to keep O2 saturations at 86 to 93%.
• Expanded use of surfactant in newborns includes its use in meconium aspiration
syndrome (MAS).
• Administration of surfactant must be discussed with the consultant on call
in NICU or TC.

Administration
• Stabilization: Not to be used during resuscitation. Stabilize the infant first, correct
hypotension, significant metabolic acidosis (get pH<7.25) and maintain normal
temperature.
• Type of surfactant: Exogenous surfactants available at CHBH include Curosurf
and Survanta.
• Timing of initial dose: Preferably within the first two hours of life. This may not be
possible, but attempts must be made to administer it as soon as the requirements
for surfactant therapy are established.
• Dose: Survanta- 100 mg/kg (4mLs/ kg), Curosurf- use the dosing chart or 100-
200mg/kg. Make sure surfactant is warmed before administration
• Route: Through endotracheal tube, preferably using side-port adapter. A catheter
or feeding tube fed through the endotracheal tube may also be used.

40
• Procedure: Administer as fast as it is tolerated (not blocking the tube, infant not
desaturating) (this applies only if using side-port. May increase ventilator rate to
60/min during the procedure.
• Subsequent dose: At least 6 hours from the previous dose. Only one repeat
dose. Indications for repeat dose are the same as the first dose. Discuss with
consultant

References
1. Suresh GK, Soll RF. Lung surfactants for neonatal respiratory distress syndrome: animal-
derived or synthetic agents. Paediatric Drugs 2002;4:485-92.
2. Stevens TP, Harrington EW, Blennow M. Early surfactant administration with brief ventilation
versus selective surfactant and continued mechanical ventilation for preterm infants with or at
risk for respiratory distress syndrome. Cochrane Database Syst Rev 2007; Oct 17
(4):CD003063.
3. Yost CC, Soll RF. Early versus delayed selective surfactant treatment for neonatal respiratory
distress syndrome. Cochrane Database Syst Rev 2000;(2):CD001456.

41
 VENTILATOR MANAGEMENT
Introduction: Conventional positive pressure ventilation remains the mainstay of
assisted ventilation in neonates despite the development of new ventilatory
techniques. Management of infants on mechanical ventilation require specialized
personnel. A registrar or consultant should be available at all times. Ideal nurse to
patient ratio for infants on assisted ventilation is 1:1. Because of limited human
resources we accept ratios of 1:2 in our unit.

Indications for ventilator therapy: Mechanical ventilation is often required for

primary lung disease or central respiratory failure (apnoea).
1. Respiratory failure:
• PaCO2 >55 mmHg when associated with falling pH <7.25 and/ or
• PaO2 <50 mmHg or pulse oximeter saturations (O2 Sats) <90% on >60%
oxygen or require >60% oxygen to maintain O2 Sats between 86 & 93% or
PaO2 >50 mmHg.
2. Increasingly severe work of breathing
3. Severe or recurrent apnoeas
4. Post operative
5. Definite NEC with peritonitis- for pain control
6. Shocked, not responsive to fluids

Choice of ventilatory strategy

The choice between continuous positive airway pressure (CPAP) and conventional
mechanical ventilation (CMV) depends on the goal to be accomplished.
• CPAP is generally used to recruit collapsed or fluid filled alveoli, thereby
improving ventilation-perfusion mismatch. Therefore, it will improve oxygenation
but may or may not significantly improve ventilation (CO2 removal). It may
actually impair CO2 removal at high pressures.
• The use of nasal CPAP is advantageous because it is relatively atraumatic,
causes less barotrauma, avoids the need for an endotracheal tube, and is simple
to setup and maintain.
• Therefore, start infant on CPAP if the main problem is oxygenation, especially if
preterm.
• CMV is generally used when improved ventilation or improved oxygenation and
ventilation are required.
• High Frequency Oscillatory Ventilation (HFOV) is reserved for use in
circumstances when conventional ventilation has failed, or in the management of
significant air leaks. HFOV is efficient in removal of CO2 and permits oxygenation
without overdistention of the lungs. Therefore consider HFOV if infant on CMV
requires PIP >30 mmHg and/or rates >60 to maintain oxygenation (despite 100%
oxygen) and/ or ventilation or Oxygen Index (OI) = (MAP X FiO2 X 100 ÷ PaO2)
is >15; in presence or risk of pulmonary air-leaks and diaphragmatic hernia.

Initiation of ventilation
• CPAP: Start CPAP at pressures of 4-6 cmH2O and can increase up to 8-10
cmH2O if O2 saturations are not improving. Because CPAP has variable effect
on PaCO2, do arterial blood gas 30-60 minutes after putting infant on CPAP. If

42
 respiratory failure ensues (PaCO2 >55 mmHg and pH <7.25) consider change to
CMV. Order CXR.
• CMV: Start on PIP of 15-20 mmHg, PEEP of 4-5, Rate of 30-40/ min, inspiratory
time of 0.4 seconds. Note that it is better to use low pressures and high rates
than the opposite to achieve adequate ventilation and oxygenation. Aim for tidal
volumes of 4-8 mls/kg. The Mode of ventilation to start with is Assist Control
(A/C) and then can change to Synchronized Intermittent Mandatory Ventilation
(SIMV) when the patient is recovering and weaning. (Note: A/C and SIMV can
only be used if one is the machine has a sensor). Do arterial blood gas 30-60
minutes after putting patient on ventilator. Order CXR to check ET tube position.
• HFOV: Starting mean airway pressure of 1-2 cmHO 2 above the one used while
on CMV, Frequency 10–15 Hz (10-12 Hz for bigger babies and 12-15 Hz for
infants <1.6 kg). Occasionally one may need to use Hertz as low as 6-9 Hz to get
rid of CO2. The amplitude should be based on the clinical assessment of chest
wall movement (wiggle), or start at amplitude of PIP-PEEP + 20. The inspiratory
time is generally fixed at 33%. After 2-4 hours of HFOV get a Chest X-ray. The
level of the diaphragm should be ideally at T8-T9. Do arterial blood gas 30-60
minutes after putting patient on ventilator. Order CXR.
• Always check an arterial blood gas 30-60 minutes after putting infant on the
ventilator including CPAP.

Monitoring of oxygenation and ventilation of patients on mechanical

ventilators
• The gold standard for assessing oxygenation and ventilation is the arterial blood
gases.

• Note that arterial puncture also known as arterial stab may not reflect the resting
state because if the infant is crying the PaO 2 may decrease and PaCO2 may
increase or decrease.

• Umbilical arterial catheter (UAC) can serve as an easy access in obtaining

frequent arterial blood gas samples without disturbing infant. Therefore, it should
be inserted in all ventilated infants, especially those on CMV and HFOV. If the
UAC is inserted the tip of the catheter should be at level between T6 and T10.

• If UAC cannot be inserted, a peripheral arterial line must be inserted using radial
or posterior tibial arteries.

• Capillary blood samples for blood gas can be obtained, as they are less invasive
than arterial stabs. If the heel is warmed appropriately, the capillary pH and
PaCO2 usually correlate with arterial samples, but capillary PaO 2 is unreliable,
usually considerably lower. Therefore, capillary gas can only be used to assess
pH and PaCO2, and use pulse oximetry to assess oxygenation. If PaCO 2 is high
on capillary gas, repeat blood gas using arterial stab before making changes on
the ventilator.

• Pulse oximetry allows continuous non-invasive monitoring of oxygenation. Aim to

keep saturations between 86 to 93% unless ordered otherwise.

43
• For most infants with acute pulmonary disease on mechanical ventilation aim for
a pH of 7.25-7.40, PaO2 of 45–60 mmHg, PaCO2 of 45 – 55 mmHg, unless a
different range is preferred for conditions such as persistent pulmonary
hypertension of newborn, chronic lung disease and congenital heart
disease.

• To improve oxygenation can adjust (increase) FiO 2, PIP, PEEP and inspiratory
time on CMV and adjust FiO2 and MAP on HFOV.

• To improve ventilation (CO2) can adjust ventilator rate, PIP and PEEP on CMV
and adjust Amplitude and Hertz on HFOV. Remember effect of increasing
ventilator rate on IE ratio.

Weaning
• Wean FiO2 based on pulse oximetry saturations. Remember to keep oximeter
saturations between 86-93%.

• The approach is to decrease PIP as tolerated until 16-18 cmH2O is reached.

Remember is better to ventilate with low pressures and high rates than the
opposite.

• Wean PIP by 2 at a time if PaO2 and PaCO2 are within accepted range or higher
for PaO2 or lower for PaCO2. Wean rate by 5 at a time if PaCO2 <45 mmHg.

• Most infants can be extubated at a PIP of 16-18, a FiO2 of <40%, PEEP of 4-5
and a rate of 15-20/min.

• For HFOV, wean FiO2 first and start weaning MAP by 1-2 at a time once the
FiO2 is 40-60%, can switch to CMV when MAP is <12 and Amplitude <30; and
extubate directly from HFOV if MAP <8 and Amplitude <25. Wean amplitude by
2-4 at a time. When transitioning patient from HFOV to CMV start on PIP
calculated from HFOV settings- namely MAP and Amplitude. Starting PIP on
CMV from HFOV= MAP + half of Amplitude.

References
1. Carlo WA, Martin RJ, Fanaroff AA. Assisted ventilation and complications of respiratory
distress. In Fanaroff and Martin’s neonatal-perinatal medicine: diseases of the fetus and infant
(8th ed.). Philadelphia, Elsevier, 2006, p1108-1118
2. Bhandari A, Bhandari V. Pitfalls, Problems and Progress in Bronchopulmonary dysplasia.
Paediatrics, Vol 123 (2009): pp 1562-1573

44
 PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN (PPHN)

Definition: Persistence of high pulmonary vascular resistance, therefore pulmonary

blood pressure with resultant cyanosis due to right to left shunting across PDA and/
or foramen ovale. It may be associated with birth asphyxia, meconium aspiration,
congenital pneumonia, RDS, congenital diaphragmatic hernia and pulmonary
hypoplasia.

Diagnosis
1. Suspect it if there is cyanosis or low pulse oximeter saturation (sats) on
supplemental oxygen with or without respiratory distress.
2. Confirm if there is a transcutaneous oxygen saturation gradient >10% between
the right arm- preductal (higher sats) and that from the lower limbs- postductal
circulations, or a PaO2 gradient >20mmHg between the preductal (R radial artery
and post ductal circulation- umbilical artery or via an echocardiogram (need to
consult cardiologist).

Risk Factors
1. Perinatal asphyxia
2. Meconium aspiration syndrome (MAS)
3. Congenital diaphragmatic hernia

Management
1. Start on higher concentrations of oxygen. Mild PPHN may respond to high
supplemental oxygen.

2. Initiate mechanical ventilation with 80-100% of oxygen, with a goal of

maintaining pH- >7.25, PaCO2 of 35-45 mmHg, and PaO2 of 45–70 mmHg or
preductal pulse oximetry saturations >85%.

3. Mechanical ventilation should aim to recruit atelectatic segments while

avoiding over distension, which leads to lung injury and increased resistance
to pulmonary blood flow.

4. HFOV is a useful mode of ventilation if patients require high mean airway

pressures or remain hypoxic despite optimising conventional ventilation and
systemic blood pressure.

5. Maintain normal to slightly higher mean arterial blood pressure in term infants
that is MAP around 50mmHg or more, may give fluid boluses and then
continue with inotropic support the choice of inotropes should be directed at
the underlying cause. If sepsis is the underlying problem use dopamine/
dobutamine with adrenalin and might require multiple boluses of normal
saline, if asphyxia is the predominant problem use dobutamine, if cause
unknown start with dopamine at 10µg/kg/min and escalate from there.

6. Refractory hypotension may require the use of hydrocortisone using stress

dose of 20-40mg/m2/day in 2-3 divided doses .

45
7. Minimal stimulation and sedation of infant as needed, if hypotensive use
Fentanyl 1-2µg/kg in combination with Midazolam (Dormicum) 0.1 mg/kg 1-2
hourly as required. Use morphine if normotensive at a dose of 0.1mg/kg 1-2
hourly as necessary, try to avoid muscle relaxants unless absolutely
necessary. These can be given as infusions, check dose under ANALGESIA
& SEDATION section.

8. If PPHN is due to MAS or RDS and infant remains on high FiO2 despite
optimising above, you may give bolus of surfactant 100mg/kg phospholipid via
the endotracheal tube.3 The aim is to improve oxygenation by treating the
underlying condition.

9. If unable to maintain saturation >80%, try to get pH > 7.45 by either giving
sodium bicarbonate 1-2mmoL/kg of 4.25% Sodium bicarbonate (dilute 8.5%
sodium bicarbonate with sterile water 1:1 ratio) over 30 minutes and using a
bicarbonate infusion, if repeated boluses are required.

10. When alkalinising infants ensure that normal calcium values are maintained
on blood gases, as alkalinisation may result in hypocalcaemia which may
affect cardiac contractility.

11. Consider HFOV if not able to get PaCO2 levels to the required levels. At this
stage accept PaO2 40-60mmHg or preductal oxygen saturation >80%. May
try to get PaCO2 in low 30s. Try to avoid hyperventilation or very low PaCO2
(PaCO2<30) as this may decrease cerebral perfusion.

12. If still unable to maintain Sats >80% despite above manoeuvres, at times one
might have to accept Sats in the 70s as long as there is no metabolic acidosis
(that is pH>7.25 and base deficit <6).

13. Be aware that hypocarbia, and alkalosis have been associated with hearing
loss in infants surviving PPHN and should therefore be reserved for refractory
cases of PPHN.4

14. If infant remains hypoxic despite above measures and blood pressure is
within normal limits start Sildenafil 0.5 mg/kg 3 hourly for 3 doses, if no
improvement and systemic BP remains normal increase dose to 1 mg/kg 6
hourly to a maximum dose of 2 mg/kg hourly as oral dose.

15. If no response to the above start the infant on inhaled NITRIC OXIDE (iNO)
as per protocol and ideally after an echocardiograph has been done to rule
out a cyanotic congenital heart lesion as the cause of the PPHN.

16. If infant is septic and hypotensive consider broadening antibiotic cover to

cover other possible virulent maternal acquired infections like Klebsiella and
community acquired MRSA using a combination of Cefotaxime, Vancomycin
and Ampicillin.

17. Other therapies that have been tried in the absence of Nitric Oxide but are not
routinely recommended are MgSO4 at a dose of 20 - 50mg/kg/hr provided the

46
 mean arterial blood pressure is within normal limits, and Prostglandin E1 at a
dose of 0.05-0.01µg/kg/min.

References
1. Konduri GG, Kim UO. Advances in the diagnosis and management of persistent
pulmonary hypertension of the newborn. Pediatr Clin N Am 2009:56;579-600.
2. Steinhorn RH. Neonatal pulmonary hypertension. Pediatr Crit Care Med 2010;11 (Suppl.):
S79-S84
3. Lotze A, Mitchell BR, Bulas DI, et al. Multicenter study of surfactant (beractant) use in the
treatment of term infants with severe respiratory failure. J. Pediatr 1998;132:40-7
4. Marron MJ, Crisafi MA, Driscoll JM Jr, et al. Hearing and neurodevelopmental outcome in
survivors of persistent pulmonary hypertension of the newborn. Pediatrics 1992;90:392-6

47
 USE OF NITRIC OXIDE

Indications for use of inhaled NITRIC OXIDE IN PPHN

• Confirmed diagnosis of PPHN (Preferably on echocardiograph, otherwise
differential saturation >10% gradient between pre-and post ductal circulations.)
• Oxygen index >20 [Oxygen Index (OI) = Mean Airway Pressure (MAP) X FiO 2 X
100/ PaO2 (mmHg)] on 2 arterial blood gases done at least 15 minutes apart
• Example of calculation of OI: MAP- 12 mmHg, on 80% oxygen, PaO 2- 60 mmHg;
OI= 12 X 0.8 X 100/60 = 16
• All other strategies have been maximised e.g. on 100% oxygen on a ventilator
(does not have to be on HFOV), normal blood pressure, acidosis corrected and
trial of Sildenafil
• Infant must be ≥34 weeks gestation or weighing >2000 grams, and less than 14
days old.

Contraindications for use of inhaled NITRIC OXIDE

• Uncertain diagnosis in term infants
• Infants with congenital diaphragmatic hernia
• Structural heart lesion other than PDA and ASD
• Preterm infants without proof of PPHN confirmed on echocardiography

INITIATION: Dose and Administration of inhaled NITRIC OXIDE

• Obtain baseline ABG and Methaemoglobin (MetHb) level before starting iNO
• Start with 20 ppm (approximately 400 mL/ min if ventilator flow is at 10L/ min)
• FiO2 and ventilator settings should not be changed during initiation phase.
• Assess response after 30 min by doing ABG.
o If increase in PaO2 is >10 mmHg above baseline PaO2 leave on 20
ppm and plan for weaning (see next session).
o If increase is ≤10 mmHg increase iNO to 40 ppm and repeat ABG in 30
minutes.
o If no response on 40 ppm, that is PaO2 increase is ≤10 mmHg above
baseline stop/ discontinue iNO.
o If on 40 ppm the increase is >10 mmHg above baseline continue with
40 ppm and follow the weaning plan (see next session).
• Obtain MetHb at 6 hours, 12 hours, 24 hours, 36 hours and 48 hours, then every
24 hours and 24 hrs after stopping iNO.
o If MetHb is 5-10% wean iNO by 50% and repeat MetHb in 2 hours, and
repeat weaning by 50% until MetHb is <5%.
o If MetHb is >10% stop iNO and consider treating with ascorbic acid- 50
mg/kg iv 6 hourly.
• Monitor NO2- check on the analyser.
o If NO2 is 3-5ppm, decrease iNO by 50%, and recheck after 15 minutes,
if NO2 remains 3-5 ppm continue decreasing iNO by 50% until NO2 is
<3ppm.
o If NO2 is >5ppm discontinue iNO.

48
Weaning of inhaled NITRIC OXIDE
• Weaning should be attempted after 6hrs of iNO if the PaO2 is >60 mmHg, repeat
ABG 30 minutes after weaning iNO. Weaning must be done every 6 hours until
get to 5 ppm then every 3 hours. Weaning should be done if PaO2 is >60 ppm
• Wean iNO by 50% until iNO is 5ppm, then decrease iNO by 1 until reach 1ppm
and then stop iNO.
• Succesful wean is defined as PaO2 not decreasing by >40% of the pre-wean
PaO2 if the PaO2 was ≥100 mmHg or >20% if PaO2 was <100 mmHg.
• If no arterial line, successful wean should be defined as postductal pulse
oximeter sats remaining ≥93%

Adverse effects of inhaled NITRIC OXIDE

• Combines with haemoglobin to form MetHb. Measure MetHb before starting iNO
and every 24 hours. Need to keep MetHb <5%.
• Affects platelet function, therefore use it with caution when there is
thrombocytopaenia or bleeding diathesis
• NO converts to NO2 when mixed with oxygen in ventilator circuit therefore
monitor NO2 levels. The NO2 levels should remain <1.5 ppm at all times

References
1. Greenough A, Khetriwal B. Pulmonary hypertension in the newborn. Paediatr Respir Rev
2005;6:111-6.
2. Konduri GG, Kim UO. Advances in the diagnosis and management of persistent pulmonary
hypertension of the newborn. Pediatr Clin N Am 2009:56;579-600.
3. Finer NN, Barrington KJ. Nitric oxide for respiratory failure in infants born at or near term.
Cochrane Database Syst Rev 2006 Oct 18;(4):CD000399

49
 CHRONIC LUNG DISEASE/ BRONCHOPULMONARY DYSPLASIA

Introduction: Chronic lung disease affects predominantly premature babies who

have needed mechanical ventilation and O2 therapy for respiratory distress. Can
also occur in infants born at term who need aggressive ventilator therapy for severe
lung disease. Liberal definition of chronic lung disease is persistent oxygen
requirements up to 36 weeks postmenstrual age in preterm infants or up to 28 days
in term infants with abnormal chest X-rays

Diagnostic criteria for BPD

Gestationa Mild Moderate Severe

l age at
birth
< 32 weeks Supplemental O2 for Supplemental O2 for Supplemental O2 for
28d and in RA at 36w 28d and <30% FiO2 at 28d and > 30%
corrected age or at 36w corrected age or FiO2/IPPV at 36w
discharge at corrected age or at
discharge discharge

> 32 weeks Supplemental O2 for Supplemental O2 for Supplemental O2 for

28d and RA 28d and <30% FiO2 by 28d and >30%
by postnatal day 56 Postnatal day 56 or at FiO2/ IPPV by
or at discharge discharge postnatal day 56 or
at discharge

Most neonates with acute lung disease recover within the first week. The
development of chronic lung disease is often suspected when mechanical ventilation
and oxygen dependence extend beyond 10 to 14 days. Definitive X-ray features of
chronic lung disease often do not develop until later in the course, usually 3 rd or 4th
week of life.

Management
Prevention:

• Limit O2 duration and concentration: accept O2 sats between 86 – 93%

• Non-invasive ventilation (nCPAP) preferably.
• Ventilatory strategies:
o Permissive hypercapnia: accept PaCO2 45-55mmHg if Ph > 7.25
o Permissive hypoxemia: accept PaO2 40-60mmHg if Ph > 7.25
o Faster ventilatory rates: 40-60 breaths/min to avoid high pressures
o Use lowest peak inspiratory pressure (PIP- 15-20)/ Mean airway
pressure (MAP) to obtain adequate ventilation.
o Use shorter inspiratory time between 0.3-0.4 seconds, flow 5-10 L/min
and moderate PEEP between 4-5 cm H2O .
o Low tidal volumes: 3-6 mls/kg
• Avoid excessive intravenous fluid administration in the first week.

50
• Treat patent ductus arteriosus once diagnosed.
• Use of Methylxanthines:
o Caffeine- 20mg/kg (10mg/kg- caffeine base) loading dose and then
maintenance 10mg/kg (5mg/kg- caffeine base).
o Aminophylline i.v. 5-6 mg/ kg loading dose followed by 2mg/kg p.o. 8
hourly as maintenance.

Treatment of evolving or established chronic lung diseae :

• Ventilation-
o Keep PaCO2 at 50-65 mmHg and PaO2 50-70 mmHg, with pH >7.25.
Maintain O2 saturations at 86%-93%, may need to maintain higher sats if
there are signs of pulmonary artery hypertension
o PEEP 4-5cmH2O, Ti 0.35-0.45s, Tidal volume 3-6ml/kg, low PIP/MAP to
maintain adequate ventilation.
• Maintain fluids at 140-160 mls/kg/day to supply sufficient calories for growth, but
avoid pulmonary oedema.
• Adequate nutrition: Infants may require 120-140 kcal/kg/d to gain weight (15-20
g/kg/day). May need to discuss nutritional requirements with the nutritionist/
dietician
• Vitamin A supplementation in ELBW: 5000IU IMI 3 X weekly for 4 weeks may be
considered.
• Diuretics: Start on lasix 0.5-1mg/kg/dose 12 hourly intravenously combined with
spironolactone 1mg/kg/dose p.o. 12hourly for 5-7 days and then stop. Monitor
electrolytes while on diuretics. Note chronic use of diuretics is associated with
complications. No patient should be discharged on diuretics

• Bronchospasm:
o Use bronchodilators: Nebulize- salbutamol – 0.1-0.5 mg/kg 2-6 hourly or
berotec or use MDI (salbutamol or berotec). Note bronchospasm may not
manifest as audible wheezing. A trial of bronchodilators can be used even
if there is no wheezing, and assess the infant before and after treatment to
evaluate changes in breath sounds and work of breathing.
o Bronchial reactivity may be increased because of infection including viral
infections. Therefore, consider infection in an infant whose respiratory
status is deteriorating.
o Consider adding theophylline: load with aminophylline – 5-6 mg/kg over 30
minutes followed by Neulin 2mg/kg/dose 8 hourly.

Steroids:
o There is evidence that steroid therapy is associated with a reduction in
days on the ventilator. Potential side effects- hyperglycaemia,
hypertension, gastrointestinal perforation, cardiomyopathy, failure to gain
weight and abnormal neurodevelopmental outcome.
o Decision to use steroids should only be made by the consultant. Consider
use of steroids at 7-14 days of life if infant is ventilator dependent with X-
ray changes suggestive of development of chronic lung disease.
o Steroid to use is dexamethasone; dose 0.1-0.2mg/kg/dose 12 hourly X 3
days, 0.05-0.1mg/kg/dose 12 hourly X 2 days, 0.05-0.1mg/kg/dose daily X
2 days and then stop (this will give a maximum dose of 0.85-1.8

51
 mg/kg/course). If there is deterioration after stopping, steroids continue
with the low dose for 5-7 days. If no response (not able to wean) do not
continue with steroids beyond 3 days.
• If not on ventilator, administer oxygen through nasal prong and keep SaO2
between 86%-93%.
• If unable to wean FiO2, look for signs of cor-pulmonale, do ECG and consult
cardiologists for echocardiography.
• Keep Hb >12g/dL if ventilated and >10g/dL if on oxygen only. If infant requires
blood transfusion, give Lasix 1-2mg/kg half way through the transfusion.
• Infant can be discharged on home oxygen if infant has good social background,
not on ventilator, weighing >2000g, and gaining weight on full oral feeds.
• Immunization: prophylaxis against RSV and Influenza (if postnatal age >6
months) to reduce re-hospitalizations where possible.

References:
1. Bhandari A, Bhandari V. Pitfalls, Problems and Progress in Bronchopulmonary dysplasia.
Pediatrics 2009;123:1562-1573
2. Ambalavanan A, Carlo WA. Ventilatory strategies in the prevention and management of
bronchopulmonary dysplasia. Semin Perinatol 2006;30:192-199
3. Jobe A. Postnatal corticosteroids for bronchopulmonary dysplasia. Clin Perinatol
2009;36:177-188
4. Onland W, De Jaegere AP. Effects of higher versus lower dexamethasone doses on
pulmonary and neurodevelopmental sequelae in preterm infants at risk for chronic lung
disease: A meta-analysis. Pediatrics 2008;122:92-101
5. Biniwale M, Ehrenkranz R. The role of nutrition in the prevention and management of
bronchopulmonary dysplasia. Semin Perinatol 2006;30:200-208
6. Schmidt B, Roberts RS, Davis P, et al. Caffeine therapy for apnea of prematurity, N Engl
J Med 2006;354:2112–2121.

52
 APNOEA

Definition: Cessation of breathing for >20 seconds or for any duration if associated
with cyanosis, desaturation and/or bradycardia. Usual age at onset is 12 hours to
one week, usually resolves by the 35-40th week post conceptual age.

Types;
1. Central: cessation of airflow and inspiratory efforts simultaneously
2. Obstructive: absent airflow in the presence of inspiratory efforts
3. Mixed: In which a central pause is either preceded by or followed by airway
obstruction

Causes: Include hypoxia, metabolic abnormalities e.g. hypoglycaemia/

hypocalcaemia, infection, electrolyte abnormalities, circulatory disorders e.g.
hypotension, anaemia, PDA, temperature instability and intracranial pathology. In
premature infants, apnoea of prematurity is considered once other causes have
been excluded.

Monitoring: All preterm infants born at less than 33 weeks or those weighing less
than 1500 grams should be placed on apnoea monitors or cardio-respiratory
monitors when available.

Prevention:
Although there is no conclusive evidence that prophylactic use of
methylxanthines like caffeine and theophyllines is of benefit, early use of
methylxanthines in preterm infants may result in reduction in episodes of apnoea and
therefore need for supplemental oxygen, may facilitate extubation and reduce the
incidence of BPD1, and has been shown to be associated with improved long term
neurological outcome2. Early use of intravenous caffeine has been associated with
reduction in need for mechanical ventilation 3. (We currently do not have intravenous
caffeine).
All infants ≤32 weeks gestational age/ birth weight <1500g should receive a
loading dose of IV aminophylline 5-6mg/kg over 30minutes and start maintenance
dose 8 hours later at 2 mg/kg 8 hourly p.o. Other treatment that can be used when
available is caffeine citrate starting with loading dose of caffeine citrate 20mg/kg
(10mg caffeine base) orally and followed with a daily maintenance dose of 10mg/kg
(5mg caffeine base).

Management:
• Acute management: Stimulate infant, give supplemental oxygen (100%) while
maintaining patent airway (chin lift), bag & mask ventilation if still not breathing.
Consider intubation and ventilation if still no response on repositioning and bag
mask ventilation. All infants who had apnoea must be admitted to TC or NICU, to
be put on apnoea monitor or cardiorespiratory monitor for at least 48 hours. If
apnoea required bag & mask ventilation for ≥5 minutes to respond, omit feeds for
12-24 hours.
• Ongoing management: If infant required bag & mask ventilation to respond
investigate; check glucose (HGTs) and electrolytes, septic work-up including LP
and start on antibiotics. Keep on oxygen using nasal cannula at rates of 1-2 litres

53
 per minute and adjust oxygen concentrations to maintain saturation between 86
and 93%. Start on theophylline or caffeine (when available) if was not on it
already, loading and maintenance dose as for prevention. If already on
theophylline, send serum levels and continue giving theophylline. If apnoeas are
recurrent and not requiring intubation, consider putting the infant on nasal CPAP.
• Monitoring: Ideally, theophylline levels should be checked with the 5 th dose, but
because of limited resources, check levels if apnoeas persist, especially those
who are already on nCPAP, or presence of signs suggestive of theophylline
toxicity namely vomiting, irritability, tachycardia or seizures. Target levels 8-10
mg/L.
• When to stop treatment or prophylaxis : Consider stopping theophylline or
caffeine if the infant has had no apnoeas for 7-14 days but continue to monitor for
apnoea. Stop monitoring for apnoea if infants has had no apnoea for 7-14 days
off theophylline or caffeine in VLBW.
• Apnoea in term infants is less common, usually secondary to infection; CNS,
e.g. haemorrhage, seizures, meningitis; maternal anaesthesia and analgesia;
upper airway obstruction; gastro-oesophageal reflux; metabolic e.g.
hypoglycaemia. Management: Treat the primary cause, and manage with
stimulation, supplemental oxygen, bag –mask ventilation nasal CPAP,or
mechanical ventilation as required.

Investigation to be done on a patient presenting with Apnoea

a. Exclude metabolic causes: Serum glucose, calcium, magnesium,
phosphate, electrolytes and ABG
b. Exclude sepsis and anaemia: FBC+Plat+Diff count, Blood culture, LP and
Urine for MC&S (suprapubic).

References
1. Bhatt-Mehta V, Schumacher RE. Treatment of apnea of prematurity. Paediatr Drugs
2003;5:195-210
2. Henderson-Smart DJ, Davis PG. Prophylactic methylxanthines for extubation in preterm
infants. Cochrane Database Syst Rev 2003;(1):CD000139.
3. Schmidt B, Roberts RS, Davis P, et al. Caffeine therapy for apnea of prematurity, N Engl J
Med 2006;354:2112–2121.
4. Schmidt B, Roberts RS, Davis P, et al. Long-term effects of caffeine therapy for apnea of
prematurity, N Engl J Med 2007;357:1893–1902.
5. Davis PG, Schmidt B, Roberts RS, et al. Caffeine for Apnoea of Prematurity Trial: Benefits
may vary in subgroups. J Pediatr 2010;156:382-7
6. Henderson-Smart DJ, Steer PA. Caffeine versus theophylline for apnoea in preterm infants.
Cochrane Database Syst Rev 2010 Jan 10;(1):CD000273.

54
 PNEUMOTHORAX

• A pneumothorax occurs when the pleural surface is ruptured with subsequent

leakage of air into the pleural space.

• Suspect in an infant with;

o poor chest wall movement
o sudden acute deterioration in condition while being mechanically
ventilated
o respiratory acidosis
o hypotension

• Diagnosis:
o Based on an high index of suspicion, supported by the clinical findings
of a worsening respiratory distress, chest asymmetry and reduced
breath sounds over affected chest (if unilateral).
o Transillumination of chest (using the pneumo-light)
o Chest radiograph

• Management
o In the case of a small pneumothorax where the clinical condition of the
infant remains stable, one may adopt a wait and watch conservative
approach whilst being closely monitored, or,
o Consider nitrogen washout, which involves administration of 100%
oxygen; not feasible for preterm infants and infants with a tension
pneumothorax.
o A tension pneumothorax is a medical emergency and should not await
confirmation by chest radiograph.
 Needle aspiration (landmark: 2nd or 3rd intercostal space in the
mid-clavicular line on the affected side), followed by,
 Insertion of intercostal drain (landmark: 5 th intercostal space in
the mid axillary line on the affected side) with an under water
drainage system (water level: 100mLs).
• Ensure sterile conditions
• Use:
o local anaesthesia- lignocaine 1% to infiltrate skin
o systemic analgesia- morphine or fentanyl
o 10 – 12 Fr chest tube (10- smaller size, 12- big
size).
• Make a small skin incision (0.5-1cm) with a scalpel blade.
Dissect the subcutaneous tissue with a small curved
artery forceps/ haemostat. Push the artery forceps/
haemostat through the intercostals muscles and parietal
pleura. Listen to gush of air or feel a give to indicate
muscle and pleural penetration. Spread the tips of artery
forceps to widen the opening, leave the artery forceps in
place and feed the chest tube through the hole. You
could also push the artery forceps through the

55
 intercostals muscles and pleura with the chest tube
attached to it. Try to avoid using a trochar as this may
increase the risk of lung perforation and forming pleural
fistula.
• Advance chest tube only a few centimetres ensuring that
the side hole is inside the chest wall, using the curved tip
of an artery forceps.
• Secure the chest tube in place with suture and tape
• Loop the chest tube over the chest wall to minimise
tension on the skin wound.
• Confirm placement with chest radiograph.
o Following clinical (drain stopped bubbling or swinging) and radiological
resolution of pneumothorax, consider removal of intercostal drain after
being clamped for 6 hours.

• In cases of persistence of pneumothorax, consider:

o redirecting/ adjusting chest tube placement (check lateral chest
radiograph for position of chest drain in relation to the pneumothorax)
o reducing mean airway pressures and/ or peak inspiratory pressures, if
mechanically ventilated.
o using/ extubating to a non-invasive mode of ventilation
o inserting 2nd intercostal drain
o putting the underwater drainage system on additional suction (wall
suction: 10 – 20 cmH20)
o an untreated pulmonary infective process (send tracheal aspirates for
microscopy and culture)
o an underlying structural lung abnormality either congenital such as
CCAM or bronchopleural fistula (consider CT scan of chest).
References:

1. Donn SM, Sinha SK. Manual of Neonatal Resiratory Care. 2006. 2:445 – 49.
2. Cloherty JP, Eichenwald EC, Stark AR. Manual of Neonatal Care. 2004; 5:371 – 75.

56
 RETINOPATHY OF PREMATURITY
Definition: Is the interruption of the normal progression of retinal vascularization.

Implicated aetiology: Exposure of immature retina to high oxygen concentration

resulting in vasoconstriction and obliteration of the retinal capillary network followed
by vasoproliferation.

Classification: based on location, extent and stage of disease

Stage 1: Demarcation line separates avascular from vascularized retina
Stage 2: Ridge forms along demarcation line
Stage 3: Extra-retinal fibrovascular proliferation tissue forms on the ridge
Stage 4: Partial retinal detachment
Stage 5: Total retinal detachment

Prevention:
1. Antenatal steroids to mothers in preterm labour
2. Aggressive weaning of FiO2, aim to maintain oxygen saturation between 86-93%.
3. Adequate nutrition
4. Screening

Screening (eye examination for ROP)

1. Screening for ROP must begin from 4 weeks after birth.
2. In our hospital screening for ROP is performed weekly by an ophthalmologist
from St John’s Eye Hospital on Wednesdays at ±1pm.
3. Patients for screening must be identified by Tuesday afternoon, there is a
registrar allocated for ROP examination, it is the responsibility of this registrar to
make sure that patients have been identified and names handed over to the
sister helping the ophthalmologist by Tuesday afternoon. Names of patient
identified to be due for ROP exams should be given to this registrar by Tuesday
afternoon.
4. The following groups of infants must be identified for screening at a postnatal
age of 4 weeks:
• All infants with birth weight <1500g
• Any infant born weighing 1500 to 2000g who required mechanical ventilation
for more than 7 days.
• Any infant born weighing 1500 to 2000g who required supplemental oxygen
for more than 2 weeks.
• Any infant of any birth weight with supplemental oxygen requirements for
more than 6 weeks.
5. Follow up screening may be necessary as per the ophthalmologist’s orders.

References:
1. Smith L. Pathogenesis of retinopathy of prematurity. Semin Neonatol, 2003;8:469-473.
2. An international committee for the classification of retinopathy of prematurity. The
international classification of retinopathy of prematurity revisited. Arch Opthalmol,
2005;123:991-999
3. O’Keefe M, Kirwan C. Screening for retinopathy of prematurity. Early Human Development,
2008;84:89-94.

57
 SHOCK HYPOTENSION

Definition: Mean arterial blood pressure (MAP) less than the 10 th percentile for
gestational age, birth weight and postnatal age. Hypotension can also be defined as
MAP less than gestational age of the infant in weeks. This usually applies only
during the first 72 hours of life. Beyond 72 hours most preterm infants weighing
>750g should have a MAP of ≥30 mm Hg. Term infants should have a MAP ≥40 mm
Hg.

10th Percentile Oscillometric MAP (in mmHg) for Birth-weight & Postnatal age 1

age(hrs)
3 12 24 48 72 96 ≥120
800-900 25 26 27 30 32 35 ≥35
901-1200 27 28 29 33 34 36 ≥36
Weight
1201-1400 28 29 30 33 35 37 ≥37
(grams) 1401-2400 29 30 31 33 36 37 ≥37
≥2401 30 32 34 36 36 36 ≥36

Causes: These include blood loss, sepsis, hypoxia, high ventilating pressures,
pneumothorax and cardiac failure. Note that most hypovolaemic infants are
asphyxiated but most asphyxiated infants are not hypovolaemic.

Management:

Hypotension is not necessary for the clinical diagnosis of septic shock, therefore
initiation of treatment should be based on the clinical suspicion of infection with any
one of the following clinical signs of poor tissue perfusion;
• altered/ diminished neurological status
• mottled cooled extremities
• diminished pulses
• prolonged capillary refill time: > 2 seconds
• tachycardia: heart rate >180/ min or bradycardia: heart rate <120/ min
• oliguria/ anuria: urine output<0.5mls/kg/hr (age>48hrs)
• metabolic acidosis: pH<7.25 and/or base deficit>10

Blood pressure can be improved by increasing cardiac output and systemic vascular
resistance. Cardiac output is influenced by end diastolic volume and contractility.
Inotropes will affect the cardiac output and some will also affect systemic vascular
resistance. Fluids will improve end diastolic volume. Which of these factors has led
to hypotension may not be known at presentation, therefore can either start with
fluids or inotropes. The decision on whether to start fluids or inotropes must be
based on the most likely cause of hypotension and must be done in discussion with
the consultant on-call. Be careful of using fluids in asphyxiated infants without a
history of hypovolaemia.
• In the setting of acute blood loss, use packed red blood cells as volume
expander.

58
• Crystalloid is the fluid of choice in neonates. Use 10 mL/kg of normal saline
infused over 15-20 minutes. Up to 60 mL/kg may need to be infused in the setting
of septic shock whilst observing for signs of fluid overload.
• If no response to fluid resuscitation, start inotropes. Inotropes, especially
adrenaline, must be given through a central line e.g. umbilical venous catheter,
as far as possible.
• Start dopamine if no response to fluids, dose: 5-20 µg/kg/min. Start at 10
µg/kg/min and increase in increments of 5 µg/kg/min at 20-30 minute intervals, to
a maximum dose of 20 µg/kg/min.
• If no response to dopamine, add dobutamine, dose: 5-20 µg/kg/min. Start
adrenaline (0.1-2 µg/kg/min) in place of dobutamine if sepsis is the most likely
cause of hypotension.
• Consider starting hydrocortisone at 20 mg/m 2/day given 12-hourly, after doing
baseline random cortisol level if a second inotrope is required.
a. Note: surface area (m2) = [0.05 X weight (kg)] + 0.05.
• Continue steroid for 3-5 days then wean over 48-72 hours, whilst monitoring
response.
• If there is no response after maximum dose of 2nd inotrope, increase
hydrocortisone to 40mg/ m2/day given 8-hourly.
• In the case of refractory shock, exclude unrecognised morbidities (eg.
pneumothorax, hyperkalaemia, hypocalcaemia)
• Therapeutic end points include;
a. capillary refill ≤ 2 seconds
b. normal pulses
c. warm extremities
d. urine output >1 mL/kg/hour
e. <5% difference in preductal and postductal arterial oxygen saturation
f. mixed venous oxygen saturation (Scvo 2) >70% (please explain as to
when or how to use it before putting it as therapeutic endpoint)
g. normal blood pressure for age
h. normal glucose and ionized calcium concentration
i. normal neurological status
j. normal anion gap and lactate
• Start weaning inotropes once the normal blood pressure has been achieved and
has been maintained for at least 6-12 hours.
• If more than one inotrope had to be used, wean the inotrope infant was put on
last. If adrenalin is used at the same time as dopamine, wean dopamine first
before adrenalin.
• If cause of hypotension is due to cardiac failure treat with Lasix and start digoxin,
and exclude congenital heart disease that may benefit from ivi prostaglandin, in
consultation with cardiologists.

Formula for calculation of infusion of inotropes

Use rule of six.
Equation 1: mg of inotrope to add in 100mLs= 6 X weight X dose (µg/kg/min)
drip rate (mL/hr)
or
Equation 2: mg of inotrope to add in 20mLs= 1.2 X weight X dose (µg/kg/min)
drip rate (mL/hr)

59
Remember to change mg to mL: divide the above calculated amount in mg by
concentration (mg/mL) of the inotrope usually 40 mg/mL for dopamine, 12.5mg/mL
for dobutamine and 1 mg/mL for adrenaline.

For example for an infant weighing 2kg and the drip rate of 0.5 ml/hr, starting
dopamine or dobutamine at 10 µg/kg/min:
- mg of inotrope to add in 20mLs = 1.2 X wt (2 kg) X dose (10 µg/kg/min) = 48mg
Drip rate (0.5 ml/hr)
To change mg of dopamine to mLs = 48mg/ 40mg/mL=1.2 mLs, therefore 1.2 mLs
will be added to 18.8 mLs 5% dextrose water, to make up 20 mLs.
To change mg of dobutamine to mLs = 48mg/ 12.5mg/mL=3.8 mLs, therefore 3.8
mLs will be added to 16.2 mLs 5% dextrose water, to make up 20 mLs.
Note: Do not infuse inotropes with sodium bicarbonate.

Drug Dose Range Remarks

Adrenaline 0.05 -2 µg/kg/min • Has inotropic and chronotropic effect.
(endogenous • Causes marked peripheral vasoconstriction
catecholamine, potent and may result in metabolic acidosis and
α & β adrenergic hyperglycaemia
effect) • Extravasation may cause tissue necrosis.
Dopamine 5-20 µg/kg/min • Inotropic and chronotropic effect
(endogenous • High doses may cause vasoconstriction
catecholamine, has • Extravasation may cause tissue necrosis.
predom. α1 effect) • May cause arrhythmias
Dobutamine 5-20 µg/kg/min • Inotropic and chronotropic effect
(synthetic • Extravasation may cause tissue necrosis
catecholamine, • May cause tachy-arrhythmias
selective action at β1)

REFERENCES

1. Watkins AM, West CR, Cooke RW. Blood pressure and cerebral haemorrhage and
ischaemia in very low birth-weight infants. Early Human Development 1989;19:103-
10.

2. Cunningham S, Symon AG, Elton RA, et al. Intra-arterial blood pressure reference
ranges, death and morbidity in very-low-birth-weight infants during the first seven
days of life. Early Human Development. 1999;56:151-165.

3. Brierley J, et al. Clinical practice parameters for haemodynamic support of pediatric

and neonatal septic shock: 2007 update from the American College of Critical Care
Medicine. Critical Care Medicine. 2009; 37(2): 666-68.

4. Dempsey EM, Barrington KJ. Treating hypotension in the preterm infant: when & with
what: a critical & systematic review. J Perinatol 2007;27:469-78.

5. Paradisis M, Osborn DA. Adrenaline for prevention of morbidity & mortality in preterm
infants with cardiovascular compromise. Cochrane Database Syst Rev 2005; 3.

6. Subhedar NV, N.J. Shaw NJ. Dopamine versus dobutamine for hypotensive preterm
infants. Cochrane Database Syst Rev 2005; 3.

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61
 HYPERTENSION

Definition: Systemic hypertension is defined as a blood pressure (systolic or mean)

that persistently exceeds the mean + 2SD for normal subjects of similar gestational
age, size and postnatal age.
• Hypertension is likely if BP exceeds 90/60 in term infants and 80/50 mmHg in
preterm infants.
• Mean arterial BP >70 mmHg in term infants and > 60 mmHg in preterm infants
should be considered as hypertension.
• Significant hypertension is systolic BP >96 mmHg and severe hypertension is BP
>106 mmHg in term infants within the 1st week.
• Beyond 1st week within the neonatal period significant hypertension is systolic BP
>104 and severe hypertension is systolic BP >110.

Causes
• Iatrogenic: Excessive administration of fluids or sodium, steroids, pancuronium
(pavulon), post-surgical repair of abdominal wall defects.
• Renovascular: Aortic or renal artery thromboembolism related to umbilical artery
catheterization, renal venous thrombosis, external pressure of renal artery;
congenital vascular anomalies.
• Coarctation of the aorta: Hypertension limited to the upper limbs.
• Renal causes: Polycystic kidney disease, renal dysplasia, hydronephrosis, acute
tubular necrosis and interstitial nephrosis
• Neurogenic: postoperative pain, intracranial hypertension, seizures and drug
withdrawal
• Endocrine: Congenital adrenal hyperplasia, hyperthyroidism, hypercalceamia

Management
Determine if infant is truly hypertensive, check cuff size, check if BP is raised only
during periods of agitation or crying. Check BP in all limbs. Complete examination of
the infant looking for abnormalities like absent femoral pulses, renal masses, bruits,
and ambiguous genitalia.
1. Investigation: Urine for MC&S, U&E, creatinine, calcium, renal ultrasound with
Doppler. If associated with persistent tachycardia consider hyperthyroidism - do
T4 and TSH. Consult nephrologists and cardiologists as required.
2. Treatment: Aim is a decrease in BP of not less than 75% of initial value, followed
by progressive normalization.
• Restrict fluids and sodium with or without diuretics (Lasix 1-4 mg/kg/day 6-12
hourly) if hypertension is related to fluid or sodium overload.
• The first-line antihypertensive include vasodilators or beta-blockers.
• Vasodilators available include Prazosin (Minipress) 0.1-0.15 mg/kg/day 12 hourly
p.o.
• Beta-blockers include propranolol 0.25mg/kg/dose p.o. given 6-8 hourly to a
maximum dose of 5 mg/kg/day.
• Severe hypertension should be corrected immediately to prevent intracranial
haemorrhage. Treatment should include fluid and sodium restriction, a loop
diuretic and a potent short term vasodilator.

62
References
1. Flynn JT. Neonatal Hypertension: diagnosis & management. Pediatric Nephrology. 2000;14:332-
41.

2. Watkinson M. Hypertension in the newborn. Arch Dis Fetal Neonatal Ed 2002;86:F78-F81.

63
 ABNORMAL HEART RATE/ RHYTHM (ARRHYTHMIAS)

Introduction: Heart rate alone may not be enough to make a diagnosis of

arrhythmia, therefore, also look at the QRS complex on cardiac monitor. Confirm it
by doing ECG.
• The most common neonatal abnormal heart rates are sinus tachycardia and
sinus bradycardia.
• Sinus tachycardia is heart rate >180/min, and may be as high as up to 220/min.
Rates above 220/min are most likely to be tachyarrhythmias.
• Transient sinus bradycardia is associated with activities such as crying and
straining or micturition.
• Healthy infants might have a heart rate close to 80/min. Sustained bradycardia
<70 /min or a dropping heart rate with desaturation is abnormal.

Causes
• Infant can develop sinus tachycardia in response to serious illness, hypotension,
myocarditis, pain, fever, anaemia, drugs like inotropic agents and theophylline.
• A common cause for sinus bradycardia is hypoxia. Other causes of sinus
bradycardia include electrolyte abnormalities, hypothyroidism, vagal stimulation
due to procedures like intubation and feeding tube insertion and drugs like
digoxin and beta-blockers.
• Significant arrhythmias are commonly due to congenital abnormalities, e.g. an
extranodal accessory atrioventricular connection, tumours, and prenatal damage
due to transplacental antibodies e.g. maternal SLE.
• Ventricular fibrillation, tachycardias and severe bradycardia usually occur in
association with severe hypoxia, acidosis, electrolyte disturbances (e.g.
hyperkalaemia) or drug toxicity.

Management
Congenital heart block: sustained heart rate <70/ min
• Continuous cardiac monitoring, check BP, do ECG
• Treat correctable causes (hypoxia and electrolyte abnormalities)
• Consider Neonatal Lupus (as a manifestation of maternal SLE)
a. Do Ro and La antibodies on both the baby and the mother
b. Do antinuclear factor (ANA) on the mother
• Consult and manage as per cardiologist, depending on actual heart rate and
metabolic status and/ or other intra-cardiac abnormalities (if present).
• May need pacing.

Supraventricular tachycardia: Is the most common symptomatic arrhythmia,

usually has a rate >200/min, with narrow QRS complex.
• Continuous cardiac monitoring, check BP, do ECG, and get defibrillator.
• Consult cardiologist
• Vagal stimulation by covering infant’s face with crushed ice in a glove or plastic
bag for 1-2 minutes (Do not obstruct the airway).
• DO NOT use ocular pressure or carotid massage in infants.

64
• If have vascular access give a rapid bolus of intravenous adenosine, starting at
50 µg/kg, increasing to 100 µg/kg after 2 minutes if no response. Maximum total
dose is 300 µg/kg.
• If infant is hypotensive and there is no vascular access or no response to
maximum dose of adenosine, start synchronus DC shock (defibrillation) starting
at 0.5 J/kg increasing to 1 J/kg and to 2 J/kg if no immediate response.
• Other drugs that can be used include digoxin, beta-blockers and amiodarone.

Ventricular tachycardia: Usually has wide QRS complexes. Causes include

congenital heart disease, hyperkalaemia and drug toxicity. Relatively rare in
neonates, it is sometimes associated with hypoxia, shock, electrolyte abnormalities
and digoxin toxicity.
• Continuous cardiac monitoring, check BP, do ECG, and get defibrillator.
• Consult cardiologist.
• If no pulse present, start resuscitation (CPR) and give asynchronous DC shock
(defibrillation) 2 J/kg, repeat dose and increase to 4 J/kg if no response.
• If no response to defibrillation continue CPR including adrenaline.
• If pulse present, but infant shocked, give asynchronous DC shock 0.5 J/kg
increasing to 1 and to 2 J/kg if no response.
• If pulse present and infant not shocked, give amiodarone 5 mg/kg over 30
minutes or consider synchronous DC shock.
• Check electrolytes, especially potassium, calcium and magnesium

Ventricular fibrillation usually occurs in a patient who is dying from another cause.
Management is similar to management of ventricular tachycardia with no pulse.

Sinus tachycardia: Identify and treat the cause.

Sinus bradycardia: If the blood pressure and oxygen saturation are normal, this is
not of major concern. Identify and treat the cause

Reference
1. Wren. Cardiac arrhythmias in the fetus & newborn. Seminars in Fetal & Neonatal Medicine.
2006; 11:182-90.

65
 PATENT DUCTUS ARTERIOSUS
Definition: Failure of the ductus arteriosus to close within 48-96 hours of postnatal
age.

Presentation
• The earliest sign in neonates is a full pulse with an ejection systolic murmur best
heard at the 2nd left intercostal space, unlike that of infant or child in whom the
murmur is often continuous.
• The diastolic flow into pulmonary artery causes bounding pulses and widening
(estimated as pulse pressure >50% of systolic BP) of pulse pressure (systolic
minus diastolic BP).
• Increased pulmonary blood flow causes pulmonary oedema, increased oxygen
requirement, CO2 retention, unexplained metabolic acidosis, recurrent apnoeas
and difficult in weaning off ventilator.
• Increased risk of pulmonary hemorrhage and chronic lung disease.
• Increased left ventricular volume produces a hyperdynamic precordial impulse.
• Serial chest X-rays show an increase in heart size and signs of oedema.
• Echocardiogram clarifies the diagnosis and excludes ductal-dependent
congenital heart lesions.

Management
• Restrict fluids to 120 - 140 mLs/kg/day in preterm infants
• Give diuretics (Lasix 1-2 mg/kg 12hourly) if in cardiac failure or has pulmonary
oedema. Careful monitoring of hydration and electrolytes during treatment with
Lasix.
• Two drugs have been shown to be effective in closure of patent ductus arteriosus
that is Indomethacin and Ibuprofen, Ibuprofen has less renal side effects.
• Indomethacin (Indocid) to close PDA: diagnosis of PDA to be confirmed on
Echocardiograph first. Dose- 0.2 mg/kg/dose 12 hourly X 3 doses p. o., or 0.1-0.2
mg/kg/dose 12 hourly i.v. (iv form currently not available at CHBH). The full
course should be completed even if closure is achieved before the 3 rd dose.
Indomethacin results in ductal closure in approximately 80-85% of patients. Best
results if treated in 1st week of life.
• Ibuprofen (Brufen) to close PDA: diagnosis of PDA to be confirmed on
Echocardiograph first. Dose- 10 mg/kg, then 5 mg at 24 hrs and 48 hours after
the 1st dose p.o. or i.v. (iv form currently not available at CHBH).
• Failure of PDA to close on treatment may be related to extreme prematurity and
greater postnatal age.
• If there is renal dysfunction, you may use low dose Indocid if Ibuprofen is not
available - 0.1mg/kg/dose p.o. daily for 5 days.
• Surgery (ductal ligation) if duct remains clinically significant after second course
of treatment or Indomethacin and/ or Ibuprofen are contra-indicated and the
patient cannot be weaned of the ventilator. Decision to be taken in consultation
with cardiologists.
• Intravenous Ibuprofen (not currently available at CHBH) is as effective as
Indomethicin in achieving PDA closure but it has less renal side effects 2.

66
Monitoring
• Before administration: Check urine output, do U&E, creatinine; platelet count and
cranial sonar.
• Repeat U&E, creatinine after completing the course of therapy if they were
normal before administration, or repeat them between doses if they were
abnormal.

Contraindications for Indomethacin/ Ibuprofen therapy

• Urine output <0.6ml/kg/hr over the preceding 8 hours,
• Serum creatinine >120 µmols/L and/ or Serum Urea > 10mmols/l
• Platelet count <60 X 109
• Evidence of bleeding diathesis
• Clinical and radiologic evidence of necrotizing enterocolitis
• Active and untreated infection
• Suspected congenital heart disease
• Evidence of new intraventricular haemorrhage grade III with or without
intracerebral bleed

References:
1. Agarwal R, Deorari A, Paul V. Patent Ductus Arteriosus in Preterm Neonates. Ind J
Paediatrics 2008;75:277-280.
2. Sekar KC, Corff KE. Treatment of patent ductus arteriosus: indomethicin or ibuprofen? J
Perinatol 2008;28:S60-S62.
3. Hermes-DeSantis ER, Clyman RI. Patent Ductus Arteriosus: pathophysiology and
management. J Perinatol 2006;26:S14-S18
4. Chiruvolu A, Jaleel MA. Therapeutic management of patent ductus arteriosus. Early Hum
Dev 2009, doi: 10.1016/j.earlhumdev.2008.12.
5. Thomas RL, Parker GC, Van Overmeire B, Aranda JV. A meta-analysis of ibuprofen
versus indomethacin for closure of patent ductus arteriosus. Eur J Pediatr 2005;164:135-
40.
6. Herrera C, Holberton J, Davis P. Prolonged versus short course of indomethacin for the
treatment of patent ductus arteriosus in preterm infants. Cochrane Database Syst Rev
2007;2:CD003480
7. Ohlsson A, Walia R, Shah SS. Ibuprofen for the treatment of patent ductus arteriosus in
preterm and/ or low birth weight infants. Cochrane Database Syst Rev 2010;4:CD003481.

67
 ABDOMINAL WALL DEFECTS

Introduction: Major defects of abdominal wall are gastroschisis and omphalocoele,

occur in approximately 1 in 6000 live births. As a general rule, gastroschisis has no
covering sac, defect in the abdominal wall is small, is lateral and to the right of
umbilical cord. Omphalocoele is covered with sac (unless is ruptured) and the
insertion of the cord is on the omphalocoele sac.

Associated anomalies: Diagnostic distinction between omphalocoele and

gastroschisis is important because of differing spectrum of associated anomalies.
Omphalocoele has a higher incidence of associated malformations including cardiac,
genitourinary, skeletal, neurologic and chromosomal (30%) abnormalities.
Gastroschisis is rarely associated with serious non-gastrointestinal malformations.
Although intestinal atresias occur commonly in gastroschisis, they may be
associated with either anomaly. Abdominal wall defects are generally associated
with malrotation

Management
Acute
• If require resuscitation at birth, try to avoid bag mask ventilation, rather intubate
for ventilation during resuscitation.
• Decompress the stomach with oro- or naso-gastric tube
• Cover the intestine with sterile warm saline soaked gauze or surgical swab and
with a clear plastic wrap.
• Keep the infant warm and check glucose
• Keep NPO and put on intravenous fluids
• Start on antibiotics (penicillin and gentamicin)
• Examine baby for other abnormalities
• Call surgeons
• Admit infant with gastroschisis to NICU, will require silo placement or reduction or
closure (according to surgeons)
• If reduction is done in stages, prescribe analgesia and sedation (morphine) and
muscle relaxant (Pavulon).
• Fluids of 80-100 mLs/kg/day of non-potassium neonatalyte or 5% dextrose water.
• Immediately postoperative, send blood for electrolytes and Hb, and may require
to increase fluids up to 100-120 mLs/kg/ day.
• Strict monitoring of intake and output of fluids.
• Replace gastric drainage every 8-12 hours with normal saline if the fluid loss over
24 hours is predicted to be >10% of total fluid intake per day.
• Start on TPN by day 2

Long term management

• Infants with gastroschisis might require contrast study before feeding to exclude
obstruction, this will depend on surgeons.
• More likely to have problems of gut motility, resulting in feeding intolerance
including reflux. Therefore, one may consider giving prokinetic agents, like

68
 Erythromycin, Chlorpropamide (Maxolon) and Antacid (Zantac) when starting
feeds.
Reference
1. Weber TR, Aug-Fliegner M, Downard CD, et al. Abdominal wall defects. Curr
Opin Pediatr 2002;14:491-7
2. Marven S, Owen A. Contemporary postnatal surgical management strategies for
congenital abdominal wall defects. Semin Pediatr Surg 2008;17:222-35

69
 NECROTISING ENTEROCOLITIS
Introduction: Risk factors include prematurity, hypoxia/ischaemia, infection and
formula feeding. Feeding breast milk reduces risk of developing NEC by 6-10 folds.
Therefore to prevent this disease we need to aim that every neonate is fed
mother’s own milk or donated human milk at all times.

Presentation: Early diagnosis may impact outcome and depends on awareness of

which infants are at risk, and careful observation of these infants for signs suggestive
of NEC. The signs of NEC are variable ranging from feeding intolerance to fulminant
presentation with sepsis, shock, peritonitis with or without perforation and death.
Usual presentation includes vomiting, bloody stools, gastric aspirates and abdominal
distension.

Management
Investigations:
• FBC (Wbc, Hb) + Diff + Platelets, CRP, U&E, creatinine, Blood culture, Lumbar
puncture
• Abdominal X-ray (AXR) (supine and lateral shoot through- cross table)
• Arterial blood gas if acutely ill (Stage IIB and greater)

Treatment:
Immediate
• Bowel rest- Keep NPO, free nasogastric drainage
• Start intravenous fluids and monitor glucose (HGTs) 3 hourly
• Start on second line antibiotics, e.g. Cefepime. If haemodynamically unstable
and/ or requiring to be put on respiratory support or an increase in respiratory
support , may need to add Meropenem and Vancomycin but this must be done in
consultation with consultant covering the ward or on call.
• If acutely ill (Stage II and greater) admit to TC or NICU, put on cardio-respiratory
monitor and monitor BP.
• Consult surgeons if infant has stage II and greater.
• Infants with intestinal perforation (Stage IIIB) need to go for laparatomy as soon
as possible if stable, or insertion of penrose drain if unstable; therefore call
surgeons immediately.
• Other indications for which surgery should be considered include abdominal
mass, sentinel loop, pneumobilia, abdominal wall erythema, metabolic acidosis
not responding to medical treatment. These are relative indications, so discuss
with surgeons.
• Strict monitoring of fluids and electrolytes, if hyponatraemic during acute phase it
is most likely from intravascular sodium deficit from third spacing; therefore
replace sodium, if serum sodium is <125 mmols/L.
• If develops hyponatraemia after the acute phase of NEC consider reducing total
fluid intake as hyponatraemia is most likely dilutional.
• FFP may be used during resuscitation if there signs suggestive of DIC, e.g.
bleeding from puncture sites. After resuscitation, volume of 160-180 mLs/kg/day
should be adequate.

70
Treatment:
Subsequent
Further management should be according to Modified Bell’s Staging Criteria of NEC
• Stage I - Bowel rest for 3 days and stop antibiotics in 48-72 hours if FBC and
CRP are normal, and blood culture negative. Consider starting on TPN.
• Stage II- Bowel rest and Antibiotics for 5-7 days, Start on TPN.
• Stage III- Bowel rest for 7-10 days, Antibiotics 7 – 10 days, Start on TPN,

Long term management

• Starting of feeds should be considered as soon as fluid from free drainage is
clear in colour and small in volume; no vomiting; abdomen- soft, not distended
and non-tender and bowel sounds are present and normal.
• Otherwise, restart feeds after completion of treatment, starting at 20 mL/kg/d and
increasing daily by the same volume and weaning TPN by the same volume.
• May stop TPN if oral feeds are at 80-100mLs/kg and being tolerated.

Prevention
• Antenatal steroids
• Breast milk feeding unless contra-indicated
• Slow increase of feeds in preterm infants by 20ml/kg daily
• Early identification and treatment of infections

References:
1. Patole S. Prevention and treatment of necrotising enterocolitis in preterm neonates. Early
Hum Dev 2007, doi:10.1016/j.earlhumdev.2007.07.007
2. Thompson AM, Bizzarro MJ. Necrotizing enterocolitis in newborns: pathogenesis,
prevention and management. Drugs 2008;68:1227-38
3. Blakely ML, Gupta H, Lally KP. Surgical management of necrotizing enterocolitis and
isolated intestinal perforation in premature neonates. Semin Perinatol 2008;32:122-6

71
 ENTERAL FEEDING OF PRETERM INFANTS

Introduction: To promote growth of preterm infants of 15-20 g/kg/day, one must

provide 110-140 kcal/kg/day. Infants with BPD or congenital heart disease have
higher caloric requirements due to a higher resting energy expenditure.

Type of Feeds: Breast milk is the best feed for the preterm as well as term infants.
Therefore, all infants should be fed breast milk unless there are medical reasons not
to feed breast milk. Preterm formula is indicated for infants less than 1800g, should
breast milk not be an option.

Initiation of enteral feeding: The ability to digest and absorb nutritional substrates
and to tolerate enteral volumes relates to gestational age and postnatal age.
Initiation of feeds should be delayed for 24-48 hours in infants with severe asphyxia
(HIE II or III) who are having seizures or are comatose. Infants with severe
respiratory distress should not be fed for the first 12-24 hours of life. Infants with mild
to moderate respiratory distress should be fed preferably with feeding tube.
Well near term and term neonates (>34 weeks or weight ≥ 1800g) should be fed ad
lib (as much as they want) with volumes of at least 50-60 mls/kg on day 1. Infants
weighing 1501-1800g can be fed at birth if well; but feeds should start at 30-40
mLs/kg/day, the rest being intravenous fluids. Infants weighing <1500g should be fed
at birth starting at feeds of 20 mLs/kg/day, and rest being iv fluids. If an infant is not
fed at birth feeds should be started by 12-24 hours of life unless there are contra-
indications.

Route of feeding: Well near-term and term infants should be breast fed. Infants less
than 34 weeks may not be able to suck well; therefore, they might need tube or cup
feeding. Tube feeding can be used for ill infants irrespective of gestational age.

Rate of increase: It is recommended that a single change in the feeding rate be

made each day. Recommended rates of increase are cautious and often preclude
the provision of adequate calories for growth. Therefore if there is a delay in increase
of feeds or feeds are not initiated by day 2-3 of life, TPN must be provided. Feeds
must be increased by i). 20 mls/kg/day for infants at gestation <32 weeks or
weighing ≤ 1500g; ii). 30-40 mls/kg/day for infants at 32-34 weeks or weighing 1501 -
1800g, and increased by 40 mls/kg/day for infants weighing >1800 or gestational
age >34 weeks (see suggested feeding guidelines on the next page). The
maximum feed volume to achieve is 160-180 mls/kg/d for preterm infants and 150
mls/kg/d for term infants.

Monitoring tolerance: Intolerance in feeds may be associated with vomiting, gastric

residuals, abdominal distension and watery diarrhoea. These signs may also be
seen in infants with NEC, therefore it can be difficult to differentiate NEC from
feeding intolerance.
• Vomiting is fairly common in neonates. Therefore, it should only be considered
significant if persistent, bilious or associated with abnormal clinical examination
e.g. lethargy, abdominal distension, apnoea and respiratory distress.
• Any gastric residual >20% feed for more than 2 feeds should be considered
significant, therefore feeds must be omitted and infant be assessed.

72
• Gastric aspirates ≤2ml are generally insignificant.
• So called “coffee-ground” aspirates usually require no intervention.
• Any gastric aspirate requires attention if bile stained and/ or associated with
abdominal signs, therefore feeds must be discontinued immediately.

References
1. Ziegler EE, Thureen PJ, Carlson SJ. Aggressive nutrition of the very low birthweight infant.
Clin Perinatol 2002;29:225-244.
2. Chauhan M, Henderson G, McGuire W. Enteral feeding for very low birth weight infants:
reducing the risk of necrotizing enterocolitis. Arch Dis Child Fetal Neonatal Ed 2008;93:F162-
F166
3. Sharon Groh-Wargo, Sapsford A. Enteral nutrition support of the preterm infant in the
neonatal intensive care unit. Nutr Clin Pract 2009;24:363-376

73
 SUGGESTED GUIDELINES OF FEEDING WELL NEONATES

Birth Weight/ Frequency of Step Step Step Step Step Step Step Step Step Step
Gestational feeds & 1 2 3 4 5 6 7 8 9 10
age Feeding
Method
Composition of Feeding
Daily Intake Volume (mls/ kg/ day)
≤1500g 3 hourly, Feed breast milk, only if not available that preterm formula (e.g. Pre-
OGT/ NGT Nan) can be given
20 40 60 80 100 120 140 160 180

1501 – 1800g 3 hourly, Feed breast milk, only if not available that preterm formula (e.g. Pre-
OGT/ NGT Nan) can be given. Infants >1500g and are not expected to stay longer
Breast/ Cup (>10days) in hospital they must be given term formula (e.g. Nan).
30 60 90 120 150 180

1801 – 2500g 3 hourly, Feed breast milk, only if not available that term formula (e.g. Nan) can
Breast/ Cup/ be given
OGT/ NGT 40 80 120 150

> 2500g Adlib or 3 Feed breast milk, only if not available that term formula (e.g. Nan) can
hourly, Breast/ be given
Cup / OGT/ 40 80 120 150
NGT

74
 NUTRITIONAL SUPPLEMENTATION

Start oral supplements when infants are on full enteral feeds

Insert Table

A. Supplements for term infants

• Term infants generally do not require supplements except for the following:
• Vitamin K – 1 mg imi at birth 1
• Vitamin D It is now recommended that all exclusively breastfed infants
and infants receiving less than 1L of fortified formula a day should be given
a daily intake of 400 IU of vitamin D beginning soon after birth2 .
• Vitamin B12 – 0.3 µg/kg/day to infants of strict vegans
• Iron- 1mg/kg, for infants who are exclusively breast fed beyond 6 months

B. Supplements for preterm infants

Current AAP guidelines to achieve serum 25-hydroxyvitamin D [25(OH)D] status of at
least 50 nmol/L and to receive at least 400 IU/day are safe and possibly adequate 3
• Multivitamins- Vidaylin drops- 0.6 mLs/day until 1 year of age
0.6 mLs of Vidaylin contain Vitamin A- 5000iu; Vitamin D- 400iu; Vitamin B1- 1.5mg;
Vitamin B2- 1.2mg; Vitamin B6- 0.5mg; Vitamin C- 50mg; Nicotinamide- 10mg
• Folate- 0.1 mg/day p.o.
• Iron:
a. Start when on full feeds at an age of 2-4 weeks
b. Dose
i. <1000g- 4mg/kg/day
ii. 1000-1500g- 3mg/kg/day
iii. 1500-2500g- 2mg/kg/day
c. Duration: continue until 1 year of age
Iron should be given in a form of ferrous gluconate, current available form is
Kiddivite- contains 30 mg/5mL of elemental iron

• Vitamin K - currently using 0.5 mg imi

Footnote:
New evidence supports a potential role for vitamin D in maintaining innate immunity
and preventing diseases such as diabetes and cancer. Pediatrics 2008;122:1142–
1152

References:
1. Puckett RM, Offringa M. Prophylactic vitamin K for vitamin K deficiency bleeding in neonates.
Cochrane Database of Systematic Reviews 2000, Issue 4.
2. Ardell S, Offringa M, Soll R. Prophylactic vitamin K for the prevention of vitamin K
deficiency bleeding in preterm neonates (Protocol). Cochrane Database of Systematic
Reviews 2010
3. Wagner CL, Greer FR. Prevention of Rickets and Vitamin D Deficiency in Infants, Children,
and Adolescents. Pediatrics 2008;122:1142–1152.
4. Taylor SN. Vitamin D Needs of Preterm Infants NeoReviews 2009;10:e590

75
 ONGOING CARE OF WELL VERY LOW BIRTH WEIGHT INFANTS

Growth/ Nutrition Monitoring

Weight
All babies are weighed on Mondays and Thursdays. Please plot the weight on the
postnatal growth chart found in the back cover of the bed-letter. If weight gain is not
adequate (<15g/kg/day) check that the infant is getting the recommended amount of
calories. If calories are adequate exclude any illnesses that can contribute to poor
weight gain. After excluding illnesses call the dietician to supplement feeds. Amount
of calories that the baby is getting should be calculated and recorded everyday.

Head Circumference
Measure the head circumference weekly and plot it in the growth charts at the back
of the bedletter. For those with suspected hydrocephalus or diagnosed with
hydrocephalus measure the head circumference twice a week on Mondays and
Thursdays and record it on the bedletter.

Laboratory Monitoring
Do bed-side Haemoglobin weekly.
Do serum Urea and Electrolytes weekly if weighing ≤1200 grams and every 2 nd week
if weighing >1200 grams.
Do serum Albumin, Calcium, Phosphate, Phosphate and Alkaline Phosphatase in
VLBW infants every 2nd week after they are a month of age.

Vitamin supplementation:-
All preterm infants must be put on daily vitamin supplementation once on full feeds.

Kangaroo Mother Care and use of incubators

Infants weighing more that 1000 grams are eligible to be considered for transfer to
ward 40 for 24 hour KMC.
All preterm infants should be put on intermittent KMC while in ward 66 or TC. Please
put this as part of your daily orders to the nurses.
Try the patients off the incubator if weighing ≥1400 grams.

All teenage mothers/ scholars should be referred to the social worker as soon
as possible.

76
 PARENTERAL NUTRITION

Introduction: The current gold standard for growth in neonates is to mimic in utero
weight gain rates. TPN provides calories in the form of protein, carbohydrates and
lipids and also provides electrolytes and trace minerals. In general, protein is
essential for growth and to counteract negative nitrogen balance. At least 1.5 to 2
g/kg/d of protein is required to avoid catabolism, and perhaps as low as 1 to 1.5
g/kg/d in those weighing <1000g. Glucose is the main energy substrate for the
neonate in early life or days. Essential fatty acid deficiency can develop within 72
hours if exogenous fat is not given. At least 0.5-1 g/kg/day of intravenous lipid is
required to prevent essential fatty acid deficiency.

Indications for TPN

• Infants with definite NEC (Stage II and above)
• Infants who cannot be fed for surgical reasons e.g. bowel atresias, gastroschisis,
TOF etc
• Critically ill infants (e.g. severe respiratory distress, severe hypotension) and
cannot be fed by day 2-3 of life, or of admission
• Low birth weight infants who are not tolerating feeds for more than 2 days
• All infants < 1200g should be started on TPN within the 1 st 48 hours of life.

Aim
• To deliver adequate and appropriate nutrients for homeostasis and growth
• Calories- 90-100 kcal/kg/day in VLBW babies; 100-115kcal/kg/day in ELBW
babies
• Protein- 2.5-3.5 g/kg/day; Fat- 2-4g/kg/day;
• Glucose- 4-6 mg/kg/min in term infants and 6-8 mg/kg/min in preterms, can go to
a maximum of 10-12mg/kg/min if tolerated.

Starting infant on TPN

TPN is currently provided by Fresenius Kabi, with fixed combination of nutrients; thus
can order TPN within certain restrictions in terms of nutrients or electrolytes.
Types of TPN available from FB:

ITN Baby 100 ITN Baby 101 ITN Baby 102 ITN Baby 103
(5% dextrose, (10% dextrose, (10% dextrose (10% dextrose
no fat) no fat) with fat) with fat)
Volume 150 mLs 150 mLs 150 mLs 235 mLs
Kcals 34.46 57.43 93.48 148.30
Protein (grams) 2.68 2.68 2.875 4.94
Lipids (grams) 0 0 3.12 4.94
Glucose (grams) 8.61 14.36 15.58 24.72

• In Infants ≤1000 grams use ITN Baby 102

• In infants >1000 grams use ITN Baby 103
• Start infants on ITN with aim of providing at least 1g of fat and 2 grams of protein.

77
• Using ITN,starting at a volume of 75-100 mLs/kg will provide the above amount of
fat and protein.
• Therefore, start ITN at this volume in all preterm infants. May start term infants at
100mLs/kg if not having respiratory problems or septic.
• Increase protein and fat by 1g/kg/day until get to a protein and fat of 3g/kg/d. This
will be provided by 150mLs/kg of ITN..
• Therefore, infants should be on full ITN within 2-3 days of starting ITN.

Monitoring of infants on TPN

• Urea and electrolytes to be done on initiation of TPN; then on alternate days
while increasing TPN and then at least once weekly once on full TPN.
• Do triglycerides once when on full TPN
• Calcium and phosphate and liver function tests weekly while on TPN
• If infant septic or in moderate to severe respiratory distress, do triglycerides daily
during build-up of TPN and then weekly.
• Infants should be weighed daily in NICU or twice a week if TICU. Weekly length
and head circumference measurements should be taken.

When to reduce or stop TPN

• Start feeds as soon as possible, and if feeds tolerated reduce TPN as you
increase feeds and stop TPN when oral feeds can provide ⅔ to ¾ of required
calories.
• Reduce fat to 0.5g/kg/day if serum bilirubin levels approach exchange levels.
• If a patient develops cholestasis, reduce TPN intake to provide 1-1.5g/kg of
protein and 0.5-1g of fat and start small enteral feeds

References:

1. Ziegler EE, Thureen PJ, Carlson SJ. Aggressive nutrition of the very low birthweight infant.
Clin Perinatol 2002;29:225-244.
2. Uhing M, Das UG. Optimizing growth in the preterm infant. Clin Perinatol 2009;36:165-176.
3. Thureen PJ, Melara D, et al. Effect of low versus high amino acid intake in very low birth
weight infants in the early neonatal period. Pediatr Res 2003;53:24-32

78
 FLUID THERAPY

Introduction
The goal of fluid therapy in newborns over the first week of life is to allow a gradual
weight loss and maintain urine output (≥ 1mL/ kg/hr).
• Term infants can lose 5-10% of birth weight and preterm infants lose 10-15% in
the first 5-7 days of life.
• It is estimated that the non-growing term neonate requires 60 mLs/kg/d, this
accounts mainly for insensible water losses, maintaining basal metabolic rate and
urine output.
• Insensible water losses increase as birth weight and gestational age decreases.
Therefore, preterm infants will require more fluids than term infants.

Near term and term infants (>34 weeks, or weight >1800 kg)
• Start fluids at 60mLs/kg.
• If an infant has good urine output & appropriate weight loss, fluids can be
gradually increased by 20 mLs/kg/day aiming for 150 mLs/kg/day by day 5-7
• At 7 days, most infants should be receiving about 150 mLs/kg/day.

Preterm infants
• Gestational age 30-34 weeks or weight 1000-1800g:
o Start fluids at 70-80 mLs/ kg/ day.
• Gestational age <30 weeks or weight <1000g:
o Start fluids at 80-100 mLs/kg/day.
• The infants in the lower range of birth weight or gestational age will need fluids in
the higher range.
• The changes in fluid rates should be based on urine output, weight loss and/or
serum electrolytes.
• Therefore, these infants should have serum electrolytes done within 24 hours
after birth, especially infants at the lower range of birth weight or gestational age.
o For infants weighing <1000 grams do U&E within the first 8-12 hours of
life, thereafter every 12-24 hours during the first week depending on
presence or absence of electrolyte abnormalities.
o For infants weighing 1000-1500 grams do U&E within first 12-24 hours
of life.
• If urine output is normal, with appropriate weight loss and normal electrolytes,
fluids may be increased by 15-20mLs/ kg/ day.
• If there is no weight loss or there is weight gain keep fluids the same.
• If have weight loss >3% per day, hypernatraemia or poor urine output increase
fluids by 20-40 mLs/kg and repeat electrolytes within 24 hours.
• Continue monitoring HGT as you increase the fluids.
• In infants with HMD, it is advisable not to increase fluids in the first 48-72 hours
unless have hypernatraemia or excessive weight loss or urine output
<1mL/kg/hr.
• At 10-14 days, most infants should be receiving 160-180 mLs/kg/day.

79
Fluid management in some special cases
1. Asphyxia
• Asphyxia may result in increased secretion of ADH (SIADH) and asphyxiated
infants are at increased risk to develop cerebral oedema and renal failure.
• Therefore, infants with hyponatraemia (SIADH) or decreased urine output or
stage II-III HIE, fluid intake should be kept at 40-60 mLs/kg/day for the first 48-
72 hours.
• These infants require close monitoring of serum sodium and weight.
• Treatment of hyponatraemia due to SIADH is fluid restriction.
• Treatment of renal failure due to acute tubular necrosis is fluid restriction

2. Postoperative abdominal surgery

• Fluid requirements are high in this group of infants. The more extensive the
procedure the greater the third spacing and therefore the fluid needs.
• Even on day 1 these infants may require 100-120 mLs/kg/d immediately
postoperative with subsequent increase as determined by capillary refill time,
BP measurements and urine output. Sodium supplementation may be
required because of third spacing.
• Therefore, hyponatraemia immediately post-surgery is most likely due to third
spacing and should be treated by sodium supplementation if sodium is <130
mmols/L.
• Might need reduction of fluids during the recovery phase, especially if have
hyponatraemia or fluid overloaded.

References
1. Baumgart S, Costarino. Water and electrolyte metabolism of the micropremie. Clin Perinatol
2000;27:131-146
2. N. Modi. Management of fluid balance in the very immature neonate. Arch Dis Child Fetal
Neonatal Ed 2004;89:F108-F111
3. Bhatia J. Fluid and electrolyte management in the very low birth weight neonate. J Perinatol
2006;26:S19-S21

80
 HYPONATRAEMIA

Definition: Serum sodium less than 130 mmoL/L.

Daily sodium requirements are 2-3 mmol/kg/day. In growing preterm infants this
requirements increase to 3-6 mmols/kg/day.

Causes
1. Low intake
2. Dilutional or fluid retention (common in sick neonates)
a. SIADH (2° to asphyxia, IVH, pneumothorax, PPV, pain/ narcotics)
b. Water overload
i. Sepsis
ii. Congestive heart failure
iii. Recovering from NEC
iv. Paralysis
3. Losses
i. Gastrointestinal losses
1. Postoperative abdominal surgery
2. Early NEC
3. Vomiting and diarrhoea
ii. Post acute tubular injury
iii. Diuretics
iv. Osmotic diuresis (glycosuria)
v. Adrenal insufficiency/Congenital Adrenal hyperplasia

Work up
• Check sodium intake (normal requirements- 2-3mmoLs/kg/d, in growing preterm
infants requirements may increase to 3-6 mmoLs/kg/d).
• Check weight, if recent increase suggests fluid retention
• Check urine sodium losses by doing FeNa
• Do urinalysis, serum electrolytes and creatinine

Treatment
1. If fluid retention, treatment is fluid restriction.
2. If fluid retention, consider sodium replacement only if sodium is <120mmoL/L,
correcting sodium to 130mmoL/L.
3. If due to sodium losses, for replacement, correct sodium to 135mmoL/L using
the formula = 0.7 x weight (kg) x sodium deficit. Correct sodium over 24
hours. The supplementation should be added to the fluids the infant is
currently getting. Note: You must not infuse hypertonic solution, therefore
sodium content of the intravenous fluid you administer should not be >150
mmoL/L.
4. Do not forget to add normal sodium requirements as part of the fluid and
electrolyte calculations.

Note: If need to use 5% sodium chloride to add to the fluids, the concentration is
0.85 mmoL in 1 mL of 5% sodium chloride.

81
References
1. Haycock GB. Management of acute and chronic renal failure in the newborn. Semin Neonatal
2003;8:325-34
2. Gregory JA. Fluids and electrolytes. In the Harriet Lane Handbook, A manual for paediatric house
officers, 18th edition 2009, p301-311
3. Coulthard MG. Will changing maintenance intravenous fluid from 0.18% to 0.45% saline do more
harm than good? 2008;93:335-340

82
 HYPERNATRAEMIA

Cause
• Common cause of hypernatraemia in neonates is insensible water losses.
• Very low birth weight infants are at increased risk of hypernatraemia because
they have increased insensible water losses.
• Skin sloughing can accelerate water losses.
• Excessive administration of isotonic or hypertonic fluids such as sodium
bicarbonate can result in hypernatraemia.
• ADH deficiency or diabetes insipidus can present with hypernatraemia.

Management
• Ensure that the total sodium intake does not exceed 3 mmols/kg/day.
• Frequent monitoring of serum sodium especially in ELBW infants is critically.
• Check sodium in the first 12-24 hours then daily if weight loss is excessive.
• After the 2nd week of life sodium requirements are estimated at 3– 6 mmol/kg/day.
• If hypernatraemia is due to insensible water losses increase fluids by 20-40
mls/kg/day or increase fluids by calculating the free water deficit in mls: 600 X
weight (kg) X [1-140/Current Na] mls over 24 hours. (Add the calculated water
deficit to the maintenance).
o Decrease intake of sodium if more than the maintenance requirements
o Repeat Na after 8-12 hours after making changes on fluids.

References
1. Gregory JA. Fluids and electrolytes. In the Harriet Lane Handbook: a manual for paediatric house
officers, 18th edition 2009, editors, Jason W. Custer, Rachel E. Rau, Elsevier publishers, p301-
311
2. Haycock GB. Management of acute and chronic renal failure in the newborn. Semin Neonatal
2003;8:325-34
3. Coulthard MG. Will changing maintenance intravenous fluid from 0.18% to 0.45% saline do more
harm than good? 2008;93:335-340
4. Greenbaum LA. Electrolyte and acid-base disorders. In Nelson textbook of paediatrics, 17 th
edition, 2004, editors Richard E. Behrman, Robert M. Kliegman, Hal B. Jenson, Saunders
publishers, Ch 45, p196-199,.
5. Frank Shann, Intensive Care Unit, Royal Children’s Hospital, Australia, 14 th Edition, 2008

83
 HYPOKALAEMIA

Introduction: Hypokalaemia is defined as potassium <3 mmols/L.

It can lead to arrhythmias, ileus and renal concentrating defects.
Daily potassium requirements are 1-3 mmol/kg/day.

Causes: Nasogastric or ileostomy drainage, diuretic use and renal tubular defects

Treatment
• Intravenous- use 15% KCL added in maintenance fluid other than TPN.
• 1 mL of 15% KCL has 2 mmoL of K+.
• The concentration of K+ in any solution infused to patient should not exceed 40
mmol/L. For example, if you add 2 mLs of 15% KCL in 200mLs of Neonatalyte,
the potassium concentration will be 40 mmoLs/L, therefore you cannot add more
than 2mls of 15% KCL to Neonatalyte.
• The rate of potassium infusion should not exceed 0.3 mmol/kg/hr.
• Because of the risk of hyperkalaemia, i.v. potassium should be used cautiously,
and levels monitored regularly while on i.v. potassium replacements
• If patient is on feeds give oral potassium if serum K+ is between 2.5 and 3.0
mmols/kg otherwise give it intravenously.
• Oral- You can use Mist KCL infans= which has 3.5 mmoL/ 5 mL
• Remove the cause of hypokalaemia if identifiable e.g. stopping lasix

References

1. Haycock GB. Management of acute and chronic renal failure in the newborn. Semin Neonatal
2003;8:325-34
2. Greenbaum LA. Electrolyte and acid-base disorders. In Nelson textbook of paediatrics, 17 th
edition, 2004, editors Richard E. Behrman, Robert M. Kliegman, Hal B. Jenson, Saunders
publishers, Ch 45, p196-199

84
 HYPERKALAEMIA
Introduction: Normal potassium levels are higher in neonates. Hyperkalaemia is
defined as potassium level >6 mmoL/L.
• Elevated potassium occurs relatively often in preterm infants especially among
VLBW infants.
• Before diagnosing hyperkalaemia make sure that the specimen is not from a
capillary or heel stick, to exclude haemolysis.
• Hyperkalaemia can result in arrhythmias; therefore, can be lethal.
• It is a common complication of acute renal failure resulting from decreased
tubular secretion and increased release of K from cells.

Management
Treatment has three goals:
1. Decrease myocardial excitability
a. Calcium gluconate 10%- 0.5 to 1mmols/kg or
b. Calcium chloride- 0.25 to 0.5 mmols/kg, once
2. Enhance potassium uptake by cells
a. Sodium bicarbonate 1mmol/kg
b. Salbutamol 4µg/kg iv over 30 minutes
c. Combined administration of glucose with insulin at a ratio of 5:1 -10:1
by starting continuous infusion of 5-10mls/kg/hour of 5% dextrose
water and separate continuous infusion of actrapid (insulin) at 0.1-0.2
units/kg/hour. Monitor glucose every 30 minutes.
3. Enhance potassium excretion
a. Kayexelate 0.5-1g/kg, 4-6 hourly
b. Lasix 1-2mg/kg as a stat dose
c. Dialysis if hyperkalaemia is not improving on full medical treatment.
This must be done in consultation with nephrologists.

Treatment of hyperkalaemia according to serum levels

• Central K: 6-7 mmol/l
Remove K from all solutions
Check pH, if acidotic correct pH and give bicarbonate if metabolic acidotic
• Central K >7.0 mmol/l
• Remove K from all solutions
• Obtain ECG
• Give calcium gluconate if have ECG changes or calcium low
• Check pH, if acidotic correct pH and give bicarbonate if metabolic acidosis
• Give salbutamol if no response after correcting pH, can be repeated 4 hourly.
• Insulin + glucose: Calculation similar as to when giving insulin for
hyperglycaemia.
• Give rectal kayexelate if no response.
• If no response, consider Lasix and dialysis
References
1. Haycock GB. Management of acute and chronic renal failure in the newborn. Semin Neonatal
2003;8:325-34
2. Vemgal P, Ohlsson A. Interventions for non-oliguric hyperkalaemia in preterm neonates.
Cochrane Database Sys Rev 2007;1:CD005257

85
 HYPOCALCAEMIA
Introduction: Neonatal hypocalcaemia may be defined as serum total calcium <2
mmol/L in term infants and <1.75 in preterm infants, and ionized calcium <0.75.
At risk of developing hypocalcaemia are infants who are premature, asphyxiated,
born to diabetic mothers and postoperative. Significant decreases in ionized calcium
may occur during acute alkalosis and following exchange transfusion with citrated
blood. Clinical signs include muscle twitching, jitteriness, seizures and a prolonged
QT interval.

Treatment for neonatal hypocalcaemia

• Acute treatment
o Elemental calcium- 10-20 mg/kg/dose
o Calcium gluconate 10%: 100-200mg/kg/dose or 1-2 mLs/kg/dose or
o Calcium chloride 10%: 35-70mg/kg/day or 0.35-0.7mLs/kg/dose
o Infuse over 10-30 minutes, do not give intra-arterial
o Mix it in at least 1:2 with sterile water
o Monitor heart rate
• Maintenance treatment
o Elemental calcium- 20-80 mg/kg/day
 Calcium gluconate 10%: 200-800mg/kg/day or 2-8 mLs/kg/d iv or
PO 6hr
 Calcium chloride 10%: 75 – 300mg/kg/day or 0.75– 3mLs/kg/d iv
 Infusion over 24 hours is preferred because of less renal losses
• Calcium gluconate is preferred.
• Calcium gluconate10% has elemental calcium of 9.3mg or 0.23 mmol/ mL.
• Calcium chloride 10% has elemental calcium of 27 mg or 0.68 mmol/mL.
• Emergency calcium therapy for infants with seizures: administer 1-2 mls/kg of
calcium gluconate 10% over 5-10 minutes, and repeat dose in 10 minutes if no
response.
• Prolonged use of calcium chloride must be avoided as it may be associated with
acidosis.
• Oral calcium supplements are hypertonic therefore may precipitate NEC.
• Vitamin D supplementation does not offer any advantage in acute
hypocalcaemia.
• Points to note when treating hypocalcaemia:
o Sudden elevation of serum calcium may result in bradycardia and
arrhythmias.
o Drip infiltration may result in severe tissue necrosis.
o If umbilical vein catheter gets into one of the branches of the portal vein
this may result in hepatic necrosis.
o Infusion through umbilical artery may result in arterial spasm, therefore
should be avoided.
o Calcium is incompatible with sodium bicarbonate.
• Hypocalcaemia generally accompanies hypomagnesaemia since
hypomagnesaemia impairs PTH secretion and peripheral PTH action.
Hypocalcaemia may not be corrected unless hypomagnesaemia is corrected.

86
References
1. Greenbaum LA. Electrolyte and acid-base disorders. In Nelson textbook of paediatrics, 17 th
edition, 2004, editors Richard E. Behrman, Robert M. Kliegman, Hal B. Jenson, Saunders
publishers, Ch 45, p208-214

87
 HYPOMAGNESAEMIA

Introduction: Hypomagnesaemia occurs when serum Mg is <0.65 mmol/L.

It is associated with maternal diabetes, intrauterine growth retardation, neonatal
hypoparathyroidism, malabsorption and renal tubular defects.

Treatment for hypomagnesaemia

• Magnesium sulphate 50%, 25-50 mg/kg/dose, intramuscularly or intravenously.
• Intramuscular injections may cause intramuscular necrosis.
• Therefore use intravenous route, infuse slowly over 2 to 4 hours
• Maximum concentration for infusion is 30mg/mL or less, therefore dilute it in
sterile water
• Monitor heart rate
• May repeat the dose every 6 hours
• When given iv be aware of hypotension, respiratory depression, complete heart
block and hyperglycaemia. Calcium gluconate should be given as an antidode.
• Daily maintenance is 30-60 mg/kg/day.

References
1. Greenbaum LA. Electrolyte and acid-base disorders. In Nelson textbook of paediatrics, 17 th
edition, 2004, editors Richard E. Behrman, Robert M. Kliegman, Hal B. Jenson, Saunders
publishers, Ch 45, p217-219.
2. Gregory JA. Fluids and electrolytes. In the Harriet Lane Handbook: a manual for paediatric house
officers, 18th edition 2009, editors, Jason W. Custer, Rachel E. Rau, Elsevier publishers, p319-
320

88
 HYPOPHOSPHATAEMIA

Introduction: Approximately 85 to 90% of total phosphorus is in the bone.

Phosphorus absorption depends on the absolute amount of dietary phosphorus and
on relative concentrations of calcium and phosphorus. Serum Ca is inversely
proportional to serum phosphorus.
VLBW infants fed mineral unsupplemented human milk or on TPN may develop
hypophosphotaemia associated with hypercalcaemia.

Treatment
• Start treatment if phosphate is <1.5 mmols/L
• Give maintenance dose of phosphate 0.5 – 2 mmoL/kg/day iv or p.o.
• Maximum concentration should be 1mmol/20 mL peripheral line and 1mmol/8 mL
for central line.
• Infuse over 24 hours, unless is acute hypophosphataemia where it can be
infused over 6 hours at 0.2 – 0.3 mmols/kg/dose
• Do not run through arterial line
• Can use potassium or sodium phosphate for intravenous dose
• Potassium phosphate 10% has 1.4 mmols of phosphate and 2 mmols of
potassium per ml. Avoid to mix or run it in a solution that contains calcium.
• For oral replacement give 30-90mg/kg/day divided 3-4 times a day
• Oral replacement can be given in a form of Phosphate Sandoz- Tablet which has
500 mg of phosphate (equivalent to 16 mmols of phosphate; conversion: 31mg
phosphate = 1mmol). It should be made into a solution of 10 mls with sterile
water. Then give appropriate dose according to weight.

References
1. Greenbaum LA. Electrolyte and acid-base disorders. In Nelson textbook of paediatrics, 17 th
edition, 2004, editors Richard E. Behrman, Robert M. Kliegman, Hal B. Jenson, Saunders
publishers, Ch 45, p220-222
2. Gregory JA. Fluids and electrolytes. In the Harriet Lane Handbook: a manual for paediatric house
officers, 18th edition 2009, editors, Jason W. Custer, Rachel E. Rau, Elsevier publishers, p948-
949

89
 HYPOGLYCAEMIA
Introduction: Hypoglycaemia is defined as blood glucose less than 2.6 mmol/L or
47 mg/dl. Arterial values are usually higher than venous blood glucose levels.
Plasma glucose (lab glucose) is usually 10-18% higher than whole blood glucose
(reagent strips-glucose oxidase/ haemoglucotest). The glucose requirement for a
term infant is 4-6 mg/kg/min, and 6-8mg/kg/min for preterm infants.

Presentation: Clinical manifestations of hypoglycaemia are non-specific and are

similar to other disorders in neonates. Symptoms include apnoea or cyanotic spells,
convulsions, irritability, jitteriness, lethargy and tachypnoea. Ensure that disorders
such as sepsis and asphyxia which have similar presentation are not missed.
Symptoms of hypoglycaemia should improve with correction of hypoglycaemia.

Causes:
• Diminished production/ stores
o SGA, Preterm
• Increased utilization
o Infant of diabetic mother, Beckwith-Wiedemann syndrome,
nesidioblastosis, post-exchange transfusion.
• Increased utilization and/ or decreased production
o Sepsis, asphyxia, hypothermia, glycogen storage disease, inborn
errors of metabolism, endocrine deficiencies e.g. adrenal insufficiency,
and polycythaemia.
Management
Management should include:
1. Anticipation in the high risk or sick infant
a. High risk infants: e.g. Birth weight <2500g, Preterm (<37 weeks),
Macrosomia (Birth weight >4000g, infant of a diabetic mother, midline
defect, post-exchange
b. Sick infant: e.g. respiratory distress, temperature instability,
encephalopathic, jittery, seizures, not tolerating feeds/ poor suck,
apnoea, jittery/ irritability,
• Do 3 hourly dextrostix in the first 24 hours.
• Start feeds early or use intravenous fluids if NPO

2. Correction of hypoglycaemia (always confirm hypoglycaemia by sending

serum glucose to the laboratory)
• Asymptomatic infant, clinically well and on feeds only
• Give feeds and measure glucose in 30 minutes.
• If glucose is normal, continue monitoring hourly for 3 hours then 3
hourly for 24 h.
• If glucose is still low, put up a drip and start on 10% dextrose solution
e.g. neonatalyte to run at a rate that will deliver glucose at 6 mg/kg/min
in term infants and 8 mg/kg/min in preterm infants, admit infant if not
admitted already.

• Calculating glucose delivery:

Glucose delivery (mg/kg/min) = % dextrose of solution/ drip x drip rate(ml/hr)

wt(kg) x 6
90
Asymptomatic infant, not on feeds therefore on a drip (iv fluids)
• Ensure that the drip/ intravenous line is working
• Ensure that the infant is getting adequate glucose delivery 6 mg/kg/min
for term infants and 8mg/kg/min in preterm infants.
• If above are cleared or already done, give 10% dextrose 2-5 mLs/kg
intravenously. If do not have 10% dextrose, can mix 50% dextrose with
sterile water in a ratio of 1:4 to make 10% dextrose. For example mix
0.5 mls/kg of 50% dextrose with 2 mls/kg of sterile water and give the
mix as bolus.
• Repeat the glucose check (HGT) 30 minutes after the bolus and then
hourly until HGTs have remained within a normal range for 3 hours,
then 3 hourly.
• If glucose levels do not increase to normal after the bolus, send serum
glucose to the laboratory for confirmation and increase glucose delivery
by 1-2mg/kg/min every 2-3 hours, as you give boluses in between to a
maximum of 12-15 mg/kg/min. If need more than this consider other
medication to treat hypoglycaemia.
• May need to stop feeds to deliver large amounts of glucose with less
fluids and to reduce stimulation of insulin release.
• Might need to increase dextrose concentration to increase glucose
delivery. If need to increase dextrose concentration to >12.5%, must
insert umbilical venous catheter or central line.

Symptomatic
• Put up a drip/ iv line, if does not have one already, if has one check
that is working
• Give 10% dextrose 2-5 mLs/kg intravenously as a bolus. If do not have
10% dextrose, can mix 50% dextrose with sterile water in a ratio of 1:4
to make 10% dextrose. For example mix 0.5 mls/kg of 50% dextrose
with 2 mls/kg of sterile water and give the mix as bolus.
• Ensure that the infant is getting adequate glucose delivery 6 mg/kg/min
for term infants and 8mg/kg/min in preterm infants.
• Repeat glucose check (HGT) 30 minutes after the bolus and then
hourly until HGTs have remained within a normal range for 3 hours,
then 3 hourly.
• If glucose levels do not increase to normal after the bolus, send serum
glucose to the laboratory for confirmation and increase glucose delivery
by 1-2mg/kg/min every 2-3 hours, as you give boluses in between to a
maximum of 12-15 mg/kg/min. If need more than this consider other
medication to treat hypoglycaemia.
• May need to stop feeds to deliver large amounts of glucose with less
fluids and to reduce stimulation of insulin release.
• Might need to increase dextrose concentration to increase glucose
delivery. If need to increase dextrose concentration to >12.5%, must
insert umbilical venous catheter or central line.

91
 Weaning glucose delivery
• Tapering can begin once you have 2 or more consecutive values
>50mg/dl =2.8mmol/L, taper by 1-2mg/kg/min 6hrly. Start increasing
oral feeds once glucose is maintained with delivery of 4-6 mg/kg/min in
term infants and 6-8 mg/kg/min in preterm infants

Resistant hypoglycaemia:
• This is failure to maintain adequate glucose levels despite a glucose
infusion of 12 -15 mg/kg/min or stabilization by day 7 of life, consider
other causes of hypoglycaemia and workup needs to be taken at the
time of the hypoglycaemic episode.
• The workup should include the following tests:
i. Bloods- Glucose, Insulin, C-peptide, Cortisol, Growth hormone,
Lactate, Pyruvate, and Amino acids
ii. Urine- Ketones, Organic acids, Amino acids and Reducing
substances
• Drugs to be considered in persistent hypoglycaemia
i. Hydrocortisone- 5 mg/kg/day i.v. or p.o. 8-12 hourly
ii. Glucagon- 0.2-0.3 mg/kg/dose i.m. (maximum dose 1mg)
(enhances gluconeogenesis, promotes ketogenesis, mobilises
hepatic glycogen stores, side-effects includes- hypokalaemia,
vomiting and diarrhoea).
iii. Diazoxide- 10-15 mg/kg/day 8 hourly i.v. or p.o. (reduces
secretion of insulin)
iv. Octreotide (synthetic somatostatin)- 2-10 ug/kg/day
subcutaneous 6-8 hourly
NB. Diazoxide and glucagon are not recommended in preterm
infants

3. General guide on management of hypoglycaemia.

• For most infants intravenous 10% dextrose at daily maintenance rates will
provide adequate glucose.
• If hypoglycaemia is due to decreased stores increasing basal rate of
infusion should correct the problem
• Sepsis should always be considered as a possible cause of
hypoglycaemia.
• If secondary to hyperinsulinaemia, may need increased glucose
requirements for several days.
• Some infants with hyperinsulinaemia and infants with IUGR may require
12-15mg/kg/min of glucose to control hypoglycaemia
• If hypoglycaemia is not responding to high glucose delivery (>15
mg/kg/min) a short course of steroids may be considered- hydrocortisone
5mg/kg/day 8-12 hourly, and glucagon 0.2-0.3 mg/kg intramuscularly.
• In cases of hypoglycaemia not responding to high glucose delivery or
persistent (more than 3 days) secondary to hyperinsulinism, e.g.
nesidioblastosis, diazoxide 10-15 mg/kg/day 8hrly iv or p.o. or
somatostatin 3.5-4 µg/kg/min may be tried. Surgery may be necessary.

92
 HYPOGLYCAEMIA

Ketotic Non Ketotic

High Lactate Normal Lactate Reducing Substances

PC Deficiency Type 3 GSD

PEPCK Deficiency Type 6 GSD Negative Positive
G-6-P Deficiency Hormonal Deficiency
F-1,6-P Deficiency Ketotic Hypoglycaemia

Hyperinsulinism HFI
Fatty Oxidation Defect Galactosaemia
Drugs

(Abbreviations: PC- pyruvate carboxylase; PEPCK- phosphoenolpyruvate carboxykinase; G-6-P

glucose-6- phosphatase; F-1,6-P- fructose 1,6 diphosphatase; GSD- glycogen storage disease; HFI-
hereditary fructose intolerance)

Figure: Approach to Causes of Persistent Hypoglycaemia 3

References:
1. Srinivasan G et al. Plasma glucose values in normal neonates: A new look. Pediatrics 1986
2. Koh THHG et al. Neural dysfunction during hypoglycaemia. Arch Dis Child 1988;63:1353-8.
3. Lteif AN et al. Hypoglycaemia in infants and children. Endocrine and metabolism clinics vol
28, no 3 ,1999.

93
 HYPERGLYCAEMIA

Introduction: Defined as whole blood glucose >125mg/dL (6.9 mmol/L) or

plasma glucose level 145 mg/dL (8 mmol/L).

Clinical Effects: Hyperosmolarity, osmotic diuresis, dehydration, contraction of

intravascular volume and potential IVH

Causes
o Parenteral glucose infusion above the normal glucose requirements;
o Parenteral lipid infusions- infants on TPN;
o Drugs- Steroids, caffeine and theophyllines;
o VLBW infants- variable insulin response/ resistance/high fluid
requirements;
o Sepsis;
o Stressed/ hypoxic infants;
o Neonates undergoing surgical procedure;
o Neonatal diabetes mellitus-usually transient

Treatment
1. Primary goal is early detection by monitoring HGTs and urine for glycosuria

2. Treat the underlying cause e.g. Pain control, check medication etc.

3. Check urine output, glycosuria, plasma glucose and U+E- monitor for
dehydration

4. If HGT is >8 mmol/L (145 mg/dL),

• Reduce parenteral glucose intake to 3-4 mg/kg/min, by changing to 5%

dextrose or reducing fluid rate, decrease gradually by 1-2mg/kg/min every
2-4hrs. Hypotonic fluids (solution which is <5% dextrose water) should be
avoided

• If still hyperglycaemic on 5% dextrose, please send serum glucose to the

laboratory for confirmation.

5. Start on insulin if glucose level is 16.7 mmols/L (300 mg/dL) despite lowering
glucose delivery

• Give intermittent dose of subcutaneous insulin (actrapid) - 0.1-0.2 units/kg

every 6 hours for 2-3 doses and monitor HGTs hourly.

• If no response to subcutaneous insulin start on continuous insulin infusion

dose 0.02 – 0.05 units/kg/hour or ratio of 1 unit of insulin to 5-10 grams of
glucose.

• Monitor HGTs hourly if the patient is getting insulin infusion

94
 6. Calculation of insulin infusion

Step 1: Insulin/ glucose (ratio) x grams of glucose per day/24 hours = units of
insulin/hour

Step 2: How to mix insulin: units/hr ÷ desired rate (mls/hr) = units/ mL

Start at a rate of 0.4 mLs/hour

Example: you have a 2kg infant on 5% dextrose running at 5 mLs/hr, you want to
start on insulin infusion running at 0.4mls/hour, at a ratio of 1:10 to glucose

Calculation: 1/10 (ratio of 1:10) x 6 (grams of glucose per day if giving 5% at

5mls/hr)/24hr =
0.025 units/ hour

(Over a day infant will get 6g of glucose= 120mls/day x5g (5%) /100 mls)

Mixing = 0.025 units/hr divided by / 0.4 mls/hr (chosen rate) = 0.06u/ml = 0.6u/10ml
= 1.2u/20 ml

It is difficult to measure 1.2 units, therefore take 10units (0.1ml) of actrapid and mix
with 9.9mLs of normal saline and from this solution take 1.2 mls and mix with 18.8
mLs of normal saline- this will give you 1.2u/20 mls. Run this at 0.4mls/hr

• Monitor HGTs hourly while on insulin infusion, if no response increase the rate of
infusion until blood glucose levels start decreasing.
• Wean insulin once levels are less than 18 mmols/L, or are decreasing rapidly.
• Stop insulin, once levels are <12 mmols/L and continue to monitor HGTs hourly
for 3 hours after stopping insulin.

Reference:
1. Hemachandra AH, Cowett RM. Neonatal hyperglycemia. Pediatr. Rev 1999:20:16

95
 METABOLIC ACIDOSIS

Introduction: Metabolic acidosis is defined as a fall in pH with low bicarbonate or a

rise in base deficit. It is a common problem in critically ill neonates. The normal pH is
7.35 – 7.45

The normal anion gap= (Na+ + K+ - Cl- - HCO3-) is 8-15mmol/L in general and 8-
18mmol/L in ELBW infants. Calculation of the anion gap allows for differentiating the
causes of acidosis into two groups; increased and normal anion gap acidosis.
Increased anion gap results from unmeasured acidic anions due to increased
production or retention of acid. A normal anion gap is due to elevated chloride
secondary to bicarbonate loss.

Increased Anion Gap Normal Anion Gap

1. Lactic acidosis due to tissue
hypoxia or inadequate perfusion:
-Shock
-Sepsis
-Hypoxia-Asphyxia
-Hypothermia
2. Renal Failure
3. Inborn errors of metabolism:
- Ketoacidosis,
- Organic aciduria
1. Gastrointestinal bicarbonate losses:
- Acute diarrhoea or ileal drainage
2. Renal bicarbonate loss:
-Renal tubular acidosis or bicarbonate
wasting due to immaturity of the renal tubules.
3. Excessive chloride in IV fluids
4. Hypoaldosteronism

Effects of metabolic acidosis:

• Pulmonary vasoconstriction ( with risk of PPHN)
• Decreased myocardial contractility
• Shift of O2-Hb dissociation curve to right (decreased saturation at given PO 2)
• CNS damage with severe acidosis
• Increased work of breathing as compensation for acidosis

Treatment
• The most effective treatment of acidosis is to establish and correct the
cause of acidosis.
• Avoid volume expansion unless there are signs of poor perfusion or shock
(a volume load is poorly tolerated in severe acidosis because of the
decreased contractility of the myocardium).
• Give sodium bicarbonate only if pH is <7.15 or if pH <7.25 with poor
oxygenation or acidosis due to base or bicarbonate losses ideally the infant
should be receiving assisted ventilation that is adequate to avoid worsening
the acidosis due to liberation of CO2.
• Base deficit of >10 needs to be corrected.
• The dose of bicarbonate is 1-2 mmols/kg of 4.25% sodium bicarbonate. If do
not have 4.25%, use 8.5% but dilute it with sterile water at a ratio of 1:1 to
make it 4.25%. Give sodium bicarbonate as infusion over 30 minutes.
• If multiple doses of sodium bicarbonate are required consider starting
infusion of bicarbonate. Remember that sodium bicarbonate cocktail mixed

96
 at 200mls 5% dextrose and 8 mls of 8.5% sodium bicarbonate will give you
0.04mmols/ml of bicarbonate and 0.04 mmols/ml of sodium.
• Alternatively the dose of alkali required (mmol/L)= base deficit x 0.3 x body
weight, administration should not exceed a rate of 1mmol/kg/min
• With severe acidosis and CO2 retention and high Na despite assisted
ventilation consider use of the organic buffer tromethamine THAM TM
( 0.3mmol/mL) initial dose 1-2mmol/kg IV, rate of administration not
exceeding 1ml/kg/min, once a blood gas available dose required to correct
pH can be estimated using dose in Ml= base deficit (mmol/L) x weight(kg) –
(THAM currently not available in our unit).

Risks of alkali administration:

• Acute hyperosmolality with rapid shift of water from intracellular to
extracellular space
• The intracellular dehydration increases the risk of intracranial haemorrhage
• Acute expansion of intravascular volume
• Decreased ionized calcium
• Shift of O2 –Hb dissociation curve to left
• Paradoxical CNS acidosis (H+ + HCO3- ↔ H2CO3↔ H2O +CO2)
• Increased sodium load and increased CO2
• With THAMTM ,risk of apnoea and hypoglycaemia

Approach to diagnosis of an infant with persistent metabolic acidosis with

increased anion-gap

97
.

References:
Taeuch HW, Ballard RA, Gleason CA, Avery MA. Avery’s diseases of Newborn textbook 2005, p 389-
393

98
 SEPSIS
Introduction:
• The signs and symptoms of sepsis may suggest respiratory (e.g. tachypnoea and
cyanosis) or gastrointestinal disease (e.g. vomiting and abdominal distension).
Sepsis must be included as differential diagnosis when evaluating infants with
these problems.
• Infants with sepsis present with non-specific signs and symptoms such as
apnoea, feeding intolerance, abdominal distension, increasing respiratory
support, lethargy, temperature instability, unexplained metabolic acidosis and
hyperglycaemia.
• Though it is tempting to recommend workup for sepsis in all infants with these
non-specific signs and symptoms, this is impractical and unnecessary in many
cases.
• A complete history and examination with clinical experience are the best guides.
Persistence and/or severity of signs and symptoms should persuade one to do
sepsis work up.

Causative organisms: Neonatal sepsis is classified into two groups according to

postnatal age at onset of illness: early-onset (<72 hours of life) and late-onset (≥
72hours of life).
The organisms causing early-onset sepsis are maternal acquired whereas those
causing late onset are hospital-acquired. The predominant organisms causing early-
onset sepsis are group B streptococci and enteric bacilli especially E. coli. The
organisms causing late-onset sepsis in our unit include Klebsiella, E. coli,
Acinetobacter, Enterobacter, MRSA and Candida. Some of the gram negatives are
producing extended spectrum β-lactamases (ESBL’s).

A. Evaluation and empiric treatment of neonates with suspected sepsis

1. Early-onset sepsis:
• FBC + Platelets + Diff count, Blood culture.
• Start on empiric treatment using Ampicillin and Gentamicin.
• Do CRP 12 to 24 hours after the initial work-up except in infants whose
problem was only respiratory distress which settled (off oxygen) within 12-
24 hours of life.
2. Late-onset sepsis:
• FBC + Platelets + Diff count, Blood culture, CRP, Lumbar puncture
(always do blood glucose for comparison when doing LP) and urine culture
(do suprapubic or send catheter specimen)
• Start on empiric treatment with Cefepime.
• May need repeat FBC and CRP after 24-48 hours to assess response to
treatment or to pickup delayed changes.
• A blood culture must always be repeated prior to the commencement/
addition of new antibiotic/ s

Restricted Antibiotics: In the absence of positive culture the decision to use

restricted antibiotics should be taken in consultation with the consultant. Restricted
antibiotics are only used under specific conditions as stated below:

99
 1. Meropenem
a. Positive culture due to ESBL-producing gram-negative e.g. Klebsiella
b. If infant was on Cefepime at the time of work-up or has been on
Cefepime within the last 3 days of the work-up.
c. Infants with cardiorespiratory decompensation, e.g. hypotension
requiring inotropes, increasing respiratory support.
d. If infant has been in hospital for >72 hours and has a culture negative
abnormal CSF in keeping with bacterial meningitis (abnormal white cell
count and biochemistry).

2. Vancomycin/ Linezolid
a. Positive MRSA culture
b. Two positive cultures due to Coagulase-Negative Staphylococcus
(CONS) within 48 hours of each other.
c. One positive culture due to CONS, with worsening clinical condition on
antibiotics, especially when infant has central venous line.
d. Use of vancomycin for CONS positive culture must be discussed with
the consultant.

3. Fluconazole/ Amphotericin B/ Voriconazole

a. Positive fungal culture
b. Elevated β-D Glucan (>80)
c. Persistent, acquired thrombocytopaenia especially if associated with
hepatosplenomegaly and negative blood cultures (send β-D Glucan
prior to starting an antifungal empirically). Note β-D Glucan should
only be done in those at high risk namely VLBW with persistent
thrombocytopaenia with or without hepatosplenomegaly

4. Third generation cephalosporins e.g. Cefotaxime

a. Gram-negative meningitis due to organism sensitive to cephalosporins.
b. Persistent gram-negative bacteremia on aminoglycosides.

5. Colimycin/ Colistan/ Polymixin B

a. For multi-drug resistant (MDR) Acinetobacter species.
b. Needs approval by the Medicines Control Council (MCC).
Approval forms with parental consent are given to senior pharmacist
to fax to the MCC with R200.00 payment (for 2010), might change
with time.

B. Definite Sepsis (Culture-proven sepsis): Clinical signs and Blood/ CSF

Culture positive
• Repeat culture and continue or change to appropriate antibiotic depending on
sensitivity results.
• If repeat culture is negative, complete 7 days of treatment.
• If repeat culture is still positive, ensure that the patient is getting the
appropriate drug and appropriate dose, repeat culture and evaluation every
48 to 72 hours until culture is negative and antibiotics should be continued for
7 days from the last negative culture.

100
 • The usual duration of treatment for uncomplicated bacterial infection is 7-10
days. For meningitis, a minimum of 14 days for gram-positive infection;
minimum of 21 days for gram-negatives.
• Antibiotic dosages must be calculated on the infant’s most recent weight.
• For cultures which remain positive despite adequate/ appropriate therapy,
look for a focus (eg. echocardiograph, ultrasound, bone scan etc.).
• Bacillus, Micrococcus and Corynebacteria are almost always contaminants in
neonates.
• CONS is often a contaminant, but if is positive on consecutive cultures done
within 72 hours of each other or patient is not improving clinically it should be
considered as a pathogen especially if they have a central line..

C. Probable Sepsis: Clinical signs and Abnormal Laboratory tests but Culture
negative
• Clinically septic or abnormal FBC+Plt+Diff or abnormal CRP treat for 5-7days,
consider other organisms e.g. Viruses like Herpes simplex and CMV,
Ureaplasma/ Mycoplasma, and Fungi.
• Infants with severe sepsis or septic shock, should be commenced empirically
on Meropenem and Vancomycin if is hospital acquired sepsis, in discussion
with consultant. Consider changing antibiotics to Cefotaxime, Vancomycin
and Ampicillin for early-onset sepsis.
• Repeat LP in 72 hours to exclude or confirm meningitis if the CSF was a
bloody tap with high white cell count before stopping treatment.

D. No Sepsis
• Clinically not septic (signs resolved within 24 hours), FBC+Plt+Diff count and
CRP normal, and blood culture negative discontinue treatment after 48 hours.

Note:
• All blood cultures and differential counts must be checked and documented in
patients file on a daily basis.

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 USE OF INDIVIDUAL ANTIBIOTICS

Antibiotic When to start When to stop When to continue When to change

Ampicillin • Respiratory • Clinical • Culture +ve • Resistant
distress improvemnt • Inadequate organism
• Asphyxia • FBC- N improvement • Significant
• Suspected • CRP ≤10 • Platelet <100 Clinical
sepsis within 72 • Culture -ve • Wcc<4 or >30 worsening after
hours of life or • CRP >10 24-48 hours on
hospital • Abnormal CXR treatment
admission
Gentamicin • Respiratory • Clinical • Culture +ve • Resistant
distress improvement • Inadequate organism
• Asphyxia • FBC- Ń improvement • Clinical
• Suspected • CRP ≤10 • Platelet <100 worsening
sepsis within 72 • Culture -ve • Wbc <4 or >30 despite 24-48
hours of life or • CRP >10 hours on
hospital • Abnormal CXR treatment
admission
Cefepime • Suspected • FBC Ń • Culture +ve • Resistant
nosocomial • Culture -ve • CRP > 10 organism
sepsis • CRP < 10 • Inadequate • Clinical
• Clinically improvement worsening
improvement • Platelet <100 despite 48 hrs
• Falling platelets on treatment
• Wbc >25
• Wbc <4
Meropenem • Suspected • FBC Ń • Culture +ve • Resistant
nosocomial • Culture -ve • CRP > 10 organism
sepsis following • CRP ≤ 10 • Inadequate • Clinical
recent (<48 hrs) • Clinical improvement worsening
use of Cefepime improvement • Platelet <100 despite 48 hrs
• Suspected • Falling platelets on treatment
meningitis • WBC >25
• Clinical • WBC <4
worsening
despite 24-48
hours of
Cefepime
• Cardiorespiratory
compromise
Vancomycin • Persistent sigs
sepsis when esp.
having a central
line
• MRSA
• 2 positive CONS
within 48 hours
of each other
Clindamycin/ • Perforated NEC
Flagyl
Amphotericin B/ • Positive fungal

102
Fluconazole cultures
• Persistent low
platelets esp., if
is VLBW with or
without HSM
hepatosplenome
galy
Cefotaxime or • Meningitis due to
Ceftriaxone sensitive Gram
negative
Colimycin/ • Organism
Colistan or resistant to
Ciprofloxacin above antibiotics
eg.Acinetobacter

Clinical condition while on antibiotics (definitions of terms used above)

Clinical Resp BP Temp Feeds CNS

classificatio
n
Improvement ↓↓ O2 N N ↑ Vigorous
Hungry
Stable ↓ O2 N N Tolerating Alert, responsive
Inadequate = O2 Inotropes Spikes Not Reduced activity,
improvement needed tolerating Irritable, Floppy,
Lethargic
Significant ↑ O2 ↑ <36 Aspirates Extreme lethargy,
worsening Apnoea inotropes >39 (green, Convulsions,
large) Unconscious
Vomiting

Suspected clinical sepsis

Indications for a septic work-up

• Cardiorespiratory instability (increasing respiratory distress or oxygen need,
tachycardia, low BP, poor perfusion)
• Persistent hypoglycaemia (>3 low dextrostix in absence of any other explanation)
• Persistent vomiting (> 3 episodes in 24 hours)
• Abdominal distention associated with large or green aspirates
• Bleeding (bloody stools, pulmonary haemorrhage, etc.)
• Convulsions

Septic work-up not indicated

A single:
- large aspirate
- vomit
- temperature spike (>38°C) (if in incubator)

103
- low dextrostix

104
Clinical sepsis conditions

Condition 1st Antibiotic Duration

Respiratory distress within first Ampicillin & Gentamicin 48-72 hours
72 hours of life.
Pneumonia- congenital Ampicillin & Gentamicin 5 days
Pneumonia- nosocomial Cefepime 5-7 days
Perinatal Asphyxia Ampicillin & Gentamicin 48-72 hours
Suspected sepsis (<72 hours) Ampicillin 48-72 hours
Gentamicin
Suspected sepsis (≥72 hours) Cefepime 48-72 hours
Suspected meningitis Ampicillin & Gentamicin 48-72 hours
Confirmed meningitis Ampicillin or Cefotaxime 14-21 days
or Cefepime or
Meropenem (depending
on organism)
NEC- suspected Cefepime 48-72 hours
NEC- confirmed Cefepime 5-7 days

NEC- perforation Cefepime 7 days

Umbilical/skin infection Cloxacillin 5 days
Cellulitis Cloxacillin 5 days
Skin abscess Cloxacillin 5 days
Note: Penicillin G can be used as a substitute, if Ampicillin is not available.

105
 ASYMPTOMATIC TERM INFANTS WITH OBSTETRIC RISK FACTORS FOR
SEPSIS

Introduction
The following are obstetric risk factors for sepsis:
• Chorioamnionitis (Maternal fever >38°, purulent/offensive liquor, fetal
tachycardia)
• Mother with a previous infant diagnosed with GBS infection
• Mother with GBS bacteriuria
• Preterm labour/ delivery
• Prolonged (>18 hours) rupture of membranes (PROM)
• Foul smelling placenta or infant

Risk factor: Chorioamnionitis

1. Do FBC+Diff+Plat and blood culture
2. Start on Ampicillin hourly imi and Gentamicin imi daily.
3. Infant to stay with the mother and for review daily
4. Discharge after 48 hours if remains well and blood results are normal. If becomes
symptomatic or blood results are suggestive of sepsis admit the child and change
to iv antibiotics.

Risk factor: History of GBS infant or GBS bacteriuria and no intrapartum

antibiotics given to mother
1. Do FBC+Diff+Plat and blood culture
2. Start on Ampicillin imi 12 hourly, for 48 hours and stop if FBC and blood cultures
are normal after 48 hours (stays with the mother if weight >1800g).
3. If mother was treated during labour, no blood tests and no treatment but observe
for 48 hours (see parenthesis above).

Other Risk factor/ s present:

a) Term or near term infant (Weight ≥1800g or ≥35 weeks):
i) No blood tests/ antibiotics
ii) Consider observing infant in hospital for 24-48 hours (stays with mother).
b) Preterm infant (Weight <1800g or <35 weeks):
i) Do FBC+Diff+Plat and blood culture,
ii) Admit and Start ivi antibiotics (Ampicillin and Gentamicin)

References
1. Ungerer RLS, Lincetto O, McGuire W, Saloojee H, Gulmezoglu AM. Prophylactic
versus selective antibiotics for term newborn infants of mothers with risk factors for
neonatal infection. The Cochrane Database of Systemic Reviews 2004; 3.

2. Schrag S, Schuchat A. Prevention of Neonatal Sepsis. Clin Perinatol 2005; 32:601-15.

3. Maragakis LL, Perl TM. Acinetobacter baumannii: Epidemiology, Antimicrobial

Resistance &Treatment Options. Clin Infect Dis 2008;46:1254-63.

4. Venkatesh MP, Placencia F, Weisman LE. Coagulase-Negative Staphyloccocal

Infections in the Neonate & Child: Update. Sem Pediatric Infect Dis 2006;17:120-27.

106
 5. Wynn JL, Neu J, Moldawer LL, et al. Potential of immunomodulatory agents for
prevention & treatment of neonatal sepsis. J Perinatol 2009;29:79-88.

FUNGAL INFECTION
Introduction: Candida is the common cause of fungal infections in our unit. The
most common Candida species are Candida Parapsillosis and Candida Albicans.

Risk factors for development fungal sepsis

- Post abdominal surgery
- Very low birth weight infants
- Prolonged use of antibiotics
- Central lines
- Parenteral nutrition

When to suspect fungal infection

In a patient with one of the above risk factors and signs of infection with one of the
following
• Hepatosplenomegaly/ Splenomegaly
• Persistent acquired thrombocytopaenia
• No response to antibiotics

Investigation
- Bloods similar to those done in a patient with suspected sepsis
(FBC+Plat+Diff, CRP, LP, Blood culture)
- Beta-D-Glucan

Treatment
Oral candidiasis (oral thrush):- Mycostatin suspension p.o. 1ml 6hourly until
Candida dermatitis:- Mycostatin ointment to apply to affected areas 6-8hourly
Suspected Systemic Candida infections:-
- Empiric treatment only done if no response to antibiotics and has persistent
thrombocytopaenia, and/ or critically ill and not responding to 48-72 hours of
antibiotics.
o Start Amphotericin B at 1mg/kg to be infused IVI over 6hours daily
(common cause of fungal infection is Candida Parapsillosis and some
of the species are intermediate sensitive or resistant to fluconazole)
o Change to Fluconazole after blood culture results if organism is
sensitive to Fluconazole
o If empiric treatment is started and blood cultures are negative for fungal
and Beta-D-Glucan is normal, stop antifungal treatment by day 7.

Culture proven or Beta-D-glucan Fungal Sepsis

- Start on Amphotericin while awaiting ID and sensitivity results and change to
appropriate antifungal agent once get the complete results
- Repeat fungal culture after 5-7 days of Amphotericin
- Duration of therapy is 14 days after the first negative culture if is septicaemia
- For Meningitis-
- For Osteomyelitis-

107
 - For Endocarditis-
- For Pneumonia-
- For Arthritis-

What to do if culture is not clearing

- Fungal sepsis might take time to respond to antifungals up to two weeks (ref)
- If culture is still positive after 2 weeks of treatment look for the focus
- Echocardiograph to exclude endocarditis
- Abdominal sonar to exclude intra-abdominal collections, fungal balls in the
bladder and micro-abscesss in the liver
- Cranial ultrasound to exclude intracranial abscesses
- CT-scan brain to exclude intracranial abscesses
- Ophthalmology consult to exclude fungal endophthalmitis
- Bone scan to exclude osteomyelitis

108
 CONGENITAL SYPHILIS

Introduction:
• Management of infants born to mothers with positive RPR/ WR depends on
whether infant has symptoms or not.

• Therefore, it is important to do a complete clinical examination of the infant.

• If mother is fully treated (Bicillin, ≥3 doses, more than a month before delivery),
the infant does not require treatment if follow up visits can be guaranteed.

• Because of difficulties in guaranteeing follow up of these infants and poor

documentation of completed treatment and decrease in titres, we manage infants
whose mothers are reportedly fully treated similar to those whose mothers are
not fully treated.

• To ensure that no infant born to mother who is infected with syphilis goes home
without getting treatment, the infants born to mothers with unknown RPR results
should not be discharged until one gets mother’s RPR results.

Management of asymptomatic infant

• No workup or evaluation/ investigation needed.

• A single dose of Bicillin 50 000u/ kg IM. (maximum 150 000u)

Management of symptomatic infant

• Signs and symptoms of congenital syphilis include pallor, rashes,
hepatosplenomegaly, oedema (nephrotic syndrome) and snuffles.

• Investigations: FBC+Plat+Diff; LP for cell count, biochemistry and VDRL; X-ray

long bones, LFTs and U&E, as indicated by clinical findings.

• Admit and treat with Penicillin G- 50 000u/ kg iv 12 hourly for 10 days and Notify
soon after admission.

Follow-up
• All sero-reactive infants should have a physical examination and repeat WR/
RPR titre at 3-monthly intervals until test becomes non-reactive or titre decreases
4-fold.
 If titre increases or remains reactive at 6-12 months, the infant should be
re-evaluated for congenital syphilis and re-treatment should be
considered.
• Infants with neurosyphilis should undergo repeat CSF examination at 6-monthly
intervals until CSF is normal.
 If CSF VDRL remains positive at any 6-monthly interval, re-treatment is
recommended.

109
References

1. J.P. Cloherty, Eric C. Eichenwald, Ann R. Stark. Manual of Neonatal Care. 2004; 5:321-27.

2. H. Saloojee, S. Velaphi, Y. Goga, N. Afadapa, R. Steen. O. Lincetto. The prevention and

management of congenital syphilis: overview & recommendations. Bulletin of the World Health
Organization. 2004; 82(6): 424-30.

110
 TUBERCULOSIS

Guidelines on management of an infant born to a mother with TB

• Prophylaxis must be given where mother is considered infectious, i.e. poor
compliance with anti-TB treatment, positive sputum/smear at delivery and/or start
of anti-TB treatment only within 3 months of delivery.
• For infants born to mothers who are HIV positive and infected with TB during
pregnancy it might be safer to give prophylaxis to all babies, irrespective of
duration of anti-TB treatment.
• Complete examination of infant is critical, as infants with signs suggestive of TB
infection require treatment rather than prophylaxis.
• For a mother who is sputum positive at delivery, separation of the mother and
child for ± 2 weeks or until mother is non-contagious is recommended, though
not always possible. Mother can still breastfeed, but should wear a mask while
feeding.
• Consider TB in infants with severe persistent pneumonia unresponsive to
antibiotics

Evaluation and management of asymptomatic infant exposed to TB

• Do not give BCG vaccine at birth.
• Do CXR, gastric/ tracheal aspirates for AFBs & TB culture and start
prophylaxis while awaiting gastric washing results.
• Ensure normal baseline liver function prior to starting prophylaxis.
• Start infant on INH- 5-10mg/kg/day and rifampicin 10 mg/kg/day for 3 months.
• Review at 3 months: Do PPD, repeat CXR and check previous aspirate
cultures. If well, CXR normal, TB cultures negative & PPD negative, stop
prophylaxis & give BCG. If unwell or poor weight gain or one or more
abnormal investigations, consider notification and anti-TB treatment.

Evaluation and management of symptomatic infant

• Do not give BCG vaccine at birth.
• Check CXR, gastric washings for AFBs, send other samples according to clinical
findings e.g. liver biopsy if has hepatomegaly.
• If infant HIV-exposed, exclude other co-infections such as CMV, congenital
syphilis and HIV. If infant HIV-PCR positive, refer to HIV unit for initiation of
HAART.
• Notify & start on treatment once diagnosis is made using 4 drugs (Isoniazid,
Rifampicin, Pyrazinamide and Ethionamide) for 2 months & 2 drugs (Isoniazid,
Rifampicin) for 4-10 months.
• May consider empiric anti-TB treatment in sick infant after investigating &
notifying.
• Ensure normal baseline liver function prior to starting treatment & repeat after 1-2
weeks.

Management of infant exposed to mother with multi drug resistant-TB (MDR-

TB)
• Manage infants in consultation with TB expert/ s

111
 • High dose INH can still be used (15-20 mg/kg/day) in combination other drugs

Asymptomatic infant:
• Treat with at least two drugs to which MTB is not resistant to for 6 months.

Symptomatic infant:
• Treat with at least 4-5 drugs (PZA, Ethambutol, Ethionamide, Ofloxacin,
Streptomycin, Kanamycin), 3 of which MTB not resistant to, for Duration: 18-24
months.

References for TB:

1. Adhikari M. Tuberculosis and tuberculosis/ HIV co-infection in pregnancy. Seminars in Fetal &
Neonatal Medicine. 2009; 1-7.

2. Whittaker E, Kampmann B. Perinatal tuberculosis. New challenges in the diagnosis and

treatment of tuberculosis in infants and the newborn. 2008;84:795-99.

3. Hassan G, Qureshi W, Kadri SM. Congenital Tuberculosis. JK Science. 2006;8:4193-94.

112
 CHICKEN POX/ VARICELLA

Introduction: Certain neonates need varicella zoster immunoglobulin (VZIG) if they

get exposed to a person with chicken pox infection. They include the following:
• Infants born to mothers whose varicella began between 5 days before and 2 days
after delivery.
• Premature infants <28 weeks gestation or birth weight <1000g
• Hospitalised preterm infants (<36 weeks) with no maternal history of chicken pox.

Management
Asymptomatic infant

A. Maternal Chicken pox Onset 5d • Isolate mother from other mothers.

before delivery to 2 days after •
delivery.
B. Maternal Chicken pox Onset >5 •
days before delivery.
C. Maternal Chicken pox
Onset > 2days after delivery.
Encourage hand-washing.
• The infant should be isolated from other
babies in a negatively vented room
• Alternatively infant can room-in with the
mother in a negatively-vented room.
• Infant has to receive Varicella Zoster
Immunoglobulin (VZIG)
• Other infants exposed to infected mother
should receive VZIG if:
their birth-weight is <1000g or <28 wks
gestation
or
if their mothers are non-immune (from
history)
or
history unavailable
• Infants exposed to asymptomatic infant
(infant of infected mother): no precautions.
• Non-immune hospital personnel should not
make contact with infected mother.
Mother no isolation
• Isolate exposed infant from other infants up
to 16d
• Other mothers and infants no special
precautions
• Isolate the mother
• For full term infants VZIG is not indicated
• Exposed preterm infants to receive VZIG

• Dose for VZIG is 1 vial (125U) intramuscular injection, to be given within

72 hours of development of rash. VZIG available through pharmacy.

• Symptomatic infants
• Isolate/ separate from other infant and encourage hand-washing.

113
 • Admit & investigate using skin scrapings for microscopy and direct
fluorescent antigen staining (serologic tests have a high false-
negative rate) and, treat with intravenous acyclovir therapy (45-
60mg/kg/day X 7 days).
• Exposed infants to get VZIG as in point A above.
• No antiviral therapy indicated for congenital infection/ congenital
varicella syndrome.

References
1. Smith CK, Arvin AM. Varicella in the fetus and newborn. Seminars in Fetal & Neonatal Medicine.
2009; 14:209–17.

2. Cloherty JP, Eichenwald EC, Stark AR. Manual of Neonatal Care. 2004; 5:279-81.

114
 HUMAN IMMUNODEFICIENCY VIRUS

 Introduction: The best modalities to reduce Mother to child transmission of

HIV is treating the mother with HAART. In 2010, updated guidelines on the
Prevention of Mother to Child Transmission were released by the National
Department of Health.

The principles of the new guidelines in summary are:

 1. To further reduce MTCT by providing AZT from 14 weeks of pregnancy or
lifelong ART as soon as possible, depending on the mother’s clinical
indications
 2. To reduce maternal nevirapine resistance
 3.To initiate neonates born to HIV-positive mothers with antiretroviral
prophylaxis immediately at birth
 4. To make breastfeeding safer by the use of daily Nevirapine to infants for a
minimum of 6 weeks depending on the feeding option chosen by the mother
and whether the mother of the infant is on lifelong ART or not.


Management of infants
• Ensure that all mothers who have delivered at CHBH have HIV results; if not
ensure that mothers are referred for counselling and testing.
• If mother is positive: prescribe nevirapine,2mg/kg p.o. in the treatment chart
• If mother is unbooked or HIV status unknown refer her to counsellors, and order
nevirapine for the child once results are known to be positive.
• Counselling, testing and treatment of the neonate must be done within 72 hours
of delivery (ideally within 24 hours).

Current guidelines depend on the health of the mother as measured by her CD-4
count and the feeding option chosen by the mother following appropriate and
thorough feeding counselling.

115
Notes: TDF+FTC = Truvada

The following algorithms should be used to guide the appropriate use of infant
nevirapine.

116
Feeding choices
The risk of transmission of HIV through breastfeeding is between 10% and 20%.
Formula feeding is recommended for all infants born to mothers who are HIV
positiveif the mother can safely and sustainably formula feed. If the mother cannot
safely formula feed or chooses to breastfeed after she has been counselled, she

117
must be advised to exclusively breastfeed her infant until the infant is 6 months old.
Nevirapine must be given to the infant throughout the period of breastfeeding.
Another option is to pasteurise her breast milk.

Infant Nevirapine dosing

Footnote: The nevirapine dose for premature infants or infants weighing less than
2.5kg has not been well studied. Pharmacological studies are urgently required.

In the absence of strong evidence, infants weighing less than 1800g will receive
AZT (Zidovudine).

Revised protocol for CH Baragwanath

Birth weight Drug Dose Duration
<1800g Single dose NVP 2mg/kg stat po Stat dose
AZT 2mg/kg 12 hourly 6 weeks if formula
po fed or until the
weight is >1800g
for breastfed infants
1800 -2499g NVP 10mg (1ml) daily ≥ 6 weeks
po
≥2500g NVP 15mg (1.5ml) daily ≥ 6 weeks
po

Note: Intravenous AZT dose: 1.5mg/kg (for infants nil per mouth)
Follow up management
• At 6 weeks follow up, do PCR in all infants born to mothers who are HIV positive.
• Do PCR earlier than 6 weeks if there are clinical signs suggestive of HIV infection
in the baby.
• If PCR is positive, refer to Harriet Shezi Clinic.
• If infant has respiratory problems and born to mother with HIV consider TB,
pneumocysti carinii pneumonitis (PCP) as possible diagnoses.
• Infant with hepatosplenomegaly, consider CMV especially if associated with
thrombocytopaenia and consider TB too.

118
References
National Department of Health Clinical Guidelines: PMTCT (Prevention of Mother to Child
Transmission) 2010

119
 CYTOMEGALOVIRUS
Introduction: Infants who are HIV-exposed / infected have a high rate of CMV
infection. CMV can be acquired in-utero, perinatally or postnatally. Congenital CMV
is defined as CMV diagnosed within the first three weeks of life.

Consider CMV infection when:

• Petechiae/ purpura
• “Blue-berry muffin” spots
• Hepatomegaly or splenomegaly or hepatosplenomegaly
• Prolonged jaundice; usually conjugated (direct bilirubin >3mg/dL) with
transaminitis
• Severe persistent thrombocytopenia (platelet count <100 X 10 9/ L)
• Severe persistent pneumonia not responding to conventional antibiotics
• Microcephaly (with periventricular intracranial calcifications)
• Hearing or visual impairment
• Severe persistent haematochezia (CMV-colitis)
• Infant with congenital TB, congenital syphilis or HIV infection

Management
• If infant HIV-exposed exclude other co-infections such as HIV, TB and
syphilis.
• Do CMV serology (IgG & IgM). CMV serology has limited clinical implications.
• Send urine for CMV (shell-vial) culture.
 Urine CMV positive within the first 3 weeks of life implies congenital
infection.
• Serum pp65 antigen should also be done (to be sent with messenger for
transport to central lab before 12h00).
• Infant with suspected pulmonary infection, send tracheal aspirates for CMV-
PCR.
• If liver involvement is suspected a liver biopsy specimen should be sent for
CMV-PCR (in consultation with gastroenterology unit).
• Infant with culture negative CSF with predominant lymphocytosis, should send
CSF for CMV-PCR.
• Whole blood can also be sent for CMV-PCR.
• If urine, blood or CSF positive for CMV, refer to ophthalmologist to look for
CMV retinitis. A hearing assessment must also be done by speech therapist)
• Consider treatment with Ganciclovir in neonates/ infants (in consultation with
microbiology team and newborn consultant/ s) at dose 6mg/kg/daily ivi for 6
weeks with twice weekly monitoring of neutrophil counts:
 with CNS involvement (including confirmed CMV retinitis)
 with CMV-colitis
 empirically in ill ventilated infant with suspected CMV-pneumonitis
(after being investigated)
• Postpone/ suspend Ganciclovir therapy if:
 absolute neutrophil count <500 cells/ µL, or,
 platelet count <25 X 109/ L

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 • Follow-up
 Hearing assessment to be done at 3-4 monthly intervals up to the age
of 24 months
 Visual assessment to be done at 6-12-monthly intervals up to age of 3
years
 Developmental assessment at each visit.

REFERENCES
1. R.S. Gandhi, J.R. Fernandez-Alvarez. H. Rabe. Management of congenital cytomegalovirus
infection: an evidence-based approach. Acta Paediatrica. 2010; 99: 509-15.

2. S.P. Adler, G. Nigro, L. Pereira. Recent advances in the prevention and treatment of
Congenital Cytomegalovirus Infections. Seminars in Perinatology. 2007; 31:10-18.

3. G. Malm, M. L. Engman. Congenital cytomegalovirus infections. Seminars in Fetal & Neonatal

Medicine. 2007; 12:154-59.

4. J.P. Cloherty, Eric C. Eichenwald, Ann R. Stark. Manual of Neonatal Care. 2004; 5:255-59.

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 HERPES SIMPLEX VIRUS

Introduction:
HSV 2 is the predominant cause of neonatal disease. Disseminated HSV disease
usually presents by day 10-12 of life, with vesicular lesions in 20% of infants. CNS
disease usually presents by 16-19 of life with vesicular skin lesions in 60-70% of
infants. Disease limited to skin, eyes and / or mouth usually presents by day 6-9 of
life with vesicular skin lesions in 80-85% of infants

Consider HSV infection in an ill infant if:

• Vesicular skin lesions
• Unexplained seizures refractory to treatment with conventional
anticonvulsants.
• CSF with predominant lymphocytosis
• Shock and DIC (with associated transaminitis)
• HIV infected infants
• Hepatomegaly

Management
Symptomatic infants
• If infant HIV-exposed exclude other co-infections such as HIV, TB, CMV and
syphilis.
• HSV serology (IgM) is of limit value if negative.
• Consult dermatologist/ microbiologist for scraping of skin or mucous
membrane lesions (vesicular lesion/ s have the highest sensitivity).
 Send for cytology and direct fluorescent antibody testing and culture
• A normal CSF does not exclude HSV encephalitis (may need serial CSF
examinations)
• Send CSF or whole blood for HSV-PCR.
• If liver involvement is suspected, a liver biopsy specimen should be sent for
HSV-PCR (in consultation with gastroenterology unit).
• Consult ophthalmologist to look for keratoconjunctivitis, cataracts or retinitis.
• Consider treatment with Acyclovir (in consultation with microbiology team and
newborn consultant/ s) at dose 60mg/kg/daily given at 8-hourly intervals for 21
days (CNS/ Disseminated) or 14 days (skin, eyes and/ or mouth) with weekly
monitoring of neutrophil counts:
 if culture-confirmed
 HSV eye disease
 empirically in ill infant with systemic or CNS infection (after being
investigated)

Asymptomatic infants
• With maternal active lesions and infant delivered vaginally, opt to treat infants
empirically with acyclovir after swabbing conjunctivae and nasopharynx. If
results negative, stop acyclovir.

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 • With maternal active lesions and infant delivered by caesarean section, opt to
investigate & watch infant.

REFERENCES
1. G. Malm. Neonatal herpes simplex virus infection. Seminars in Fetal & Neonatal Medicine.
2009; 14: 204-8.

2. L. Corey, A. Wald. Maternal & Neonatal Herpes Simplex Virus infections. NEJM. 2009; 361(1):
1376-85.

3. J.P. Cloherty, Eric C. Eichenwald, Ann R. Stark. Manual of Neonatal Care. 2004; 5: 259-63.

4. D. W. Kimberlin. Herpes Simplex Virus infections of the Newborn. Seminars in Perinatology.

2007; 31: 19-25.

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 RESPIRATORY SYNCYTIAL VIRUS (RSV)

Introduction:
RSV is usually spread by respiratory secretions as droplets or fomites which can
survive on environmental surfaces for up to 12 hours. Aerosol transmission is rare.
Diagnosis is usually made by immunofluorescent antigen testing of respiratory
secretions either obtained by anterior nasal swabbing or nasopharyngeal or tracheal
aspirates or by viral culture in specialised medium.

Management
Symptomatic infants
• Infants confirmed to be infected should be isolated/ cohorted.
• Routine use of Ribavarin or systemic corticosteroids is not recommended.
• Short-term use of inhaled bronchodilators may be of benefit.
• Empiric use of antibiotic therapy in ventilated infants is usually indicated due
to the high likelihood of bacterial co-infection.
• Health-care workers should also be cohorted.
• Health-care workers must decontaminate their hands after contact with
infected patient or infected secretions.
 Use soap and water if hands visibly contaminated and alcohol-based
rubs when contact with infected infant.
• Limiting visits by family members and siblings.

Prevention
The South African guideline 1 recommends Palivizumab (Synagis) prophylaxis in the
following infants:
• All infants born <32 weeks’ gestation
o continue until 6 months chronological age or end of RSV season (last
dose in July), whichever comes first.
• All Infants born 32-36 weeks’ gestation
o continue until 3 months chronological age or end of RSV season (last
dose in July), whichever comes first.
• Infants of any gestation who are <24 months of age at the start of the RSV
season, with any of the following:
o chronic lung disease
o primary immunodeficiency
o cyanotic congenital heart disease.
• Prophylaxis should be used for duration of 5 months, beginning in February
• High risk premature infants should ideally commence their prophylaxis while
still in hospital.

REFERENCES for RSV:

1. R.J. Green, H.J. Zar, P. M. Jeena, S.A. Madhi, H. Lewis. South African guideline for the
diagnosis, management and prevention of acute viral bronchiolitis in children. South African
Medical Journal. May 2010; 100(5): 320-25.

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2. Louis Bont. Insights from the Sixth Global Experts’ Meeting on Respiratory Viruses.
Nosocomial RSV infection control & outbreak management. Paediatric Respiratory Reviews.
2009; 10(1):16-17.

3. Shaun K. Morris, Biljana Dzolganovski, Joseph Beyene, Lillian Sung. Meta-analysis of the
effect of antibody therapy for the prevention of severe respiratory syncytial virus infection.
BMC Infectious Diseases. 2009; 9:106-115.

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 HEPATITIS B VIRUS

Introduction
Transmission of Hepatitis B virus (HBV) from infected mothers to their newborns
results primarily from exposure to maternal blood during labour and delivery.
Intrauterine infection occurs rarely (<5%). Hepatitis B virus infection may run an
acute course with complete recovery or a fulminant course due to hepatic failure with
a high mortality. The virus may also persist for more than 6 months to become a
chronic infection. All health-care workers must receive hepatitis B vaccination.

Diagnosis
Maternal hepatitis B surface antigen (HBsAg) positive with or without hepatitis B ‘e’
antigen (HBeAg) positive.

Management

Asymptomatic infants
• Newborn (either term or preterm) to receive immunoprophylaxis in the form of
hepatitis B immunoglobulin (HBIG: 0.5 mLs IM) and hepatitis B vaccine (0.5
mLs IM) at a different anatomical site, within 12-24 hours of birth.
• Repeat hepatitis B vaccination at 6, 10 and 14 weeks as per EPI.
• Breastfeeding can continue once immunoprophylaxis has been administered
(risk of transmission of HBV negligible).
• These infants need to will need ongoing follow-up post-discharge and
serological testing to exclude carrier state 9-18 months of age.

Symptomatic infants
• Care of HBV infected infants involves strict infection control measures
(handwashing, use of gowns and gloves)
• In the event of exposure (either close contact or contaminated needle) in a
non-immunised person, send blood for HBV serology and administer HBIG.

References for HBV:

1. Chang MH. Hepatitis B Infection. Seminars in Fetal & Neonatal Medicine. 2007; 12:160-67.

2. Shi Z, Li X, Ma L, Yang Y. Hepatitis B immunoglobulin injection in pregnancy to interrupt

hepatitis B virus mother-to-child transmission–a meta-analysis. International Journal of
Infectious Diseases. 2010; e1-13.

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 INFLUENZA VIRUS

(with specific reference to Pandemic Influenza; H1N1)

Introduction: Influenza is rapidly and easily spread by aerosol droplet or by contact

with contaminated secretions. Type A influenza is further classified on the basis of
two main surface antigens, haemaglutinin (H) and neuraminidase (N).
Infected patients are contagious from one day prior to onset of symptoms until either
the resolution of fever or until seven (7) days have elapsed since symptom onset.
All persons who live with or provide care for infants younger than 6 months of age
(e.g., parents, guardians, siblings, and day care providers) should be vaccinated
against 2009 H1N1 as well as seasonal influenza.

Diagnosis
• Samples collected from the upper respiratory tract (nasal swabs,
nasopharyneal secretions and/ or throat swabs) or the lower respiratory tract
(tracheal aspirates in intubated patients) should be sent for influenza specific
RNA by real time-polymerase chain reaction (rRT-PCR).
• For intubated patients, initial testing for pandemic (H1N1) 2009 infection
should consist of paired nasopharyngeal and tracheal aspirate specimens for
rRT-PCR.
• If initial tests are negative, they should be repeated within 48-72 hours in
patients with a high likelihood of the infection on clinical or epidemiological
grounds.
• The sensitivity of rapid antigen testing is low (10-70%).
• Viral culture has limited clinical application due to the long turnaround time.

Management

A. Pregnancy
• It is recommended that all pregnant women who are or will be pregnant during
the influenza season be immunized with inactivated influenza vaccine,
preferably in their second or third trimester of pregnancy.
• Maternal fever should be adequately treated during pregnancy/ labour
• In order to protect the infant from exposure to respiratory secretions during
delivery the mother should use a facemask throughout labor, as tolerated.

B. Asymptomatic infant
• During the immediate recovery/postpartum period, consider temporarily
separating the infant from the mother until ALL of the following criteria are
met:
o The mother has received antiviral medications for at least 48 hours
and;
o The mother is without fever for 24 hours without antipyretics and;
o The mother can control cough and respiratory secretions.
• Prior to feeding and caring for the infant the mother should:

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 o Wash her hands with soap and water;
o Put on a face mask;
o Observe all respiratory hygiene/ cough etiquette guidelines.
• These precautions to be followed for 7 days after onset of symptoms or 24
hours after resolution of symptoms, whichever is longer. Instead of the mother
visiting the newborn nursery, the infant can be brought to the mother’s room
for feeding and care.
• Infants can stay with their mothers and should breastfeed if both are well
enough and there are no other contraindications to breastfeeding.
• If either the mother or the infant is too ill they should be separated but the
infant to continue receiving expressed breastmilk.
• The infant needs close monitoring for evidence of influenza-like illness and,
should symptoms develop, infant needs to be tested for influenza virus
infection.
• Antiviral chemoprophylaxis only to be given to newborn infants
o born within 48 hours of mother’s symptoms
o who remain with their mothers
o who are not breastfeeding during the first seven (7) days after onset of
maternal symptoms.
• Parental consent must be obtained prior to starting prophylaxis.
• Prophylaxis dose:
o Oseltamivir (Tamiflu) suspension 3 mg/kg (maximum total dose of 12
mg) po daily X 10 days.
• Potentially infected family members should not be allowed to visit.
• Both infant and mother should be discharged as soon as possible.

C. Symptomatic infants
• Neonates born to mothers with suspected or proven H1N1 at or after delivery
are to be treated if they develop signs of influenza-like illness.
• Treatment should be stopped if mother or infant test negative for H1N1.
• Parental consent must be obtained prior to starting treatment.
• Treatment Dose:
o Oseltamivir (Tamiflu) suspension 3 mg/kg (maximum total dose of 12
mg) PO twice daily x 5 days.
• The decision to treat preterm infants should be individualized and specialist
advice should be sought.

References
1.United South African Neonatal Association. Pandemic influenza (H1N1): management of neonatal
contacts and cases. 28 Aug 2009.

2.Clinical management of human infection with pandemic (H1N1) 2009: revised guidance by World
Health Organisation. November 2009.
http://www.who.int/csr/disease/swineflu/guidance/surveillance/WHO_case_definition_s

wine_flu_2009_04_29.pdf
3.Influenza outbreak (swine flu) a/ H1N1. Clinical information for health care professionals 03 may
2009. swineflu_info_healthworkers DOH SA.pdf

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4.CDC H1N1 Flu; Interim Guidance: Considerations regarding 2009 H1N1 Influenza in Intrapartum
and postpartaum hospital settings.

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 ACCIDENTAL EXPOSURE: NEEDLE STICK INJURIES

INTRODUCTION
If you have accidentally pricked yourself with a needle, cut yourself with a blade, or
come into contact with the body fluids of a confirmed or likely HIV infected patient,
then you are probably worried that you may get infected with HIV as a result of the
accident.

MANAGEMENT
1. No matter what you have been exposed to, immediate cleaning of the
exposure site is the first priority.
• Wash the wound with soap and water.
• Flush splashes to the nose, mouth, or skin with water.
• Irrigate eyes with one litre of sterile (or clean) water.

2. Start post-exposure prophylaxis immediately to prevent HIV infection.

• You can get this treatment urgently at any time from Neonatal ICU (NICU)
• Try to start the treatment within an hour of the accident.
• Post-exposure starter packs contain combination AZT and 3TC (take one
tablet twice-a-day/ 12-hourly) for 3 days.

3. Try to speak to one of the advisors below as soon as possible, as depending

on the level of risk of the exposure, you may need a third medication called
Alluvia (lopinavir/ ritonavir) or Efavirenz.

4. List of advisors in the Department of Paediatrics

NAME # NUMBER/SMS CELL. NUMBER

Dr. Lee Fairlie (Harriet Shezi) #6153 082 780 9997
Dr. H. Diar (Neonatal ICU) #6690 083 231 2679
Dr. David Moore (Ward17/ Unit 3) #6391 083 297 2468
Sr. E.N. Motsoaledi (Maternity Infection Control) #6772 --------------------

5. There is a 24-hour call-list in ward 20, NICU, casualty, and at switchboard.

6. The person on call will offer advice to you as to what to do and arrange a
follow up.
7. A hospital outpatient file (from casualty) will be required for the prescription to
collect the remainder of the 28-day course.
8. Wits students should report incident to CHSE and get follow-up at Campus
Health after starter-pack and counselling.

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 THROMBOCYTOPAENIA

Definition: Platelet count less than 150 000/ mm3 in both term and premature
infants. Platelet count 100–150 borderline significance. Platelet count <100
considered significant.

Causes
• Decreased production, e.g. congenital megakaryocytic hypoplasia,
thrombocytopaenia absent radius syndrome.
• Increased destruction, e.g., neonatal alloimmune thrombocytopaenia (NAIT),
autoimmune thromocytopaenia (ITP), giant haemangioma, DIC, maternal PIH
• Both decreased production and increased destruction e.g. Infection- congenital
and acquired

Evaluation
• Review smear report to ensure not spurious (from platelets clumping)
• Repeat platelet count
• History- Maternal bleeding e.g. nose bleeds (ITP), previous siblings with bleeding
(NAIT), drugs, maternal rash (infections), maternal PIH
• Maternal blood results- platelets, WR results and HIV results
• Physical examination- Congenital abnormalities e.g. signs of rubella, absent radii,
hepatosplenomegaly
• Blood tests- FBC and a smear, platelet; blood culture and CRP, RPR, HIV PCR if
mother HIV positive, urine CMV (if indicated),
• If the above are negative consider other tests e.g. herpes, rubella, toxoplasmosis
and platelet antigens.

Platelet count
<100

Sick Infant Well Infant: Perform Physical Examination

Sepsis (Congenital,
Acquired)
DIC Normal Abnormal
Hepatosplenomegaly Alloimmune TAR
Congenital Infection Autoimmune Giant
Malignancy Drugs haemangioma
Haemolytic disease of the
newborn

Management
• Transfuse with platelets if count is less than 20.
• Transfuse with platelets if platelet count is <50 and needing invasive procedure.
• Transfuse with platelets if count is <100 with active bleeding
• Platelet transfusion volume is 15mLs/kg

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• In confirmed alloimmune thrombocytopaenia (NAIT):
i) Transfuse with Human Platelet Antigen (HPA)-compatible platelets if count
is less than 30
ii) If compatible platelets not available, transfuse with random donor platelets
iii) Consider the use of IVIG at 1g/kg/day X 2 days
iv) Transfuse with HPA 1a and 5b negative platelets

References:
1. Roberts I, Murray NA. Neonatal thrombocytopenia: causes and management. Arch Dis Child
Fetal Neonatal Ed 2003;88:F359–F364
2. British Committee for Standards for Haematology transfusion task force. Transfusion
guidelines for neonates and older children. British Journal of Haematology, 2004,:24:
433–453

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 ANAEMIA

Definition: Defined by a haemoglobin (Hb) value that is more than 2 standard

deviations (SD) below the mean for age. At birth normal Hb values for newborns >36
weeks are 16.5± 1.5 g/dL (mean ± 1SD). In premature infants it varies according to
gestational age. Therefore, an Hb of <13 at birth in term infants should be
considered abnormal.

Physiologic anaemia and anaemia of prematurity: After birth there is a transient

increase in Hb, thereafter it gradually falls to reach levels of 11.4± 0.9 g/dL in term
infants by 8 to 12 weeks of age and 7 to 10 g/dL in premature infants by 6 weeks of
age. The reasons for this decrease include decreased erythropoietin production,
short lifespan of erythrocytes and rapid growth.

Causes of anaemia
A. Blood loss
Note: With acute blood loss, the initial Hb may not reflect the true extent of blood
loss as equilibration leading to anaemia usually takes 3-6 hours to occur.
• Obstetrical, e.g. placenta abruption or praevia;
• Occult, e.g. feto-maternal haemorrhage, feto-fetal transfusion
• Postnatal, e.g. Umbilical bleeding, subaponeurotic haemorrhage,
cephalhaematoma, internal bleed

B. Haemolysis
• Isoimmune e.g. Rh, ABO incompatibility
• Other immune haemolytic anaemias e.g. congenital infections
• Hereditary e.g. hereditary spherocytosis, G6PD deficiency
• Acquired e.g. DIC

C. Decreased red blood cell production e.g. physiological anaemia, congenital,

infection, iron deficiency

Evaluation
• History and physical examination
• Reticulocyte count, blood types and Coombs test
• Examination of peripheral smear
• Examine maternal blood for fetal cells (Kleihauer-Betke test)

Guidelines as to when transfuse neonates

It is impossible to produce clear evidence-based criteria for the administration of red
cells in the neonatal period but the use of guidelines has been shown to reduce
transfusions.

• The absolute indications for rapid blood transfusion are to restore tissue
oxygenation and to expand blood volume after severe acute blood loss.
• Shock secondary to blood loss
• Haemoglobin less than 13g/dL at birth

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 • Haemoglobin less than 12g/dL in infants with severe lung disease (on ventilator),
cyanotic heart disease, heart failure or for surgery
• Haemoglobin less than 10 g/dL if infant on supplemental oxygen but not
ventilated
• Haemoglobin less than 8g/dL if the infant has the following: unexplained
tachycardia, recurrent apnoea, poor weight gain unexplained by other causes.
• Haemoglobin less than 7g/dL if infant has no symptoms and reticulocyte count is
≤3%. If reticulocyte count is >3, do not transfuse and repeat Hb in 3-5 days.
Transfuse if Hb continues to drop.
• Volume for transfusion of packed cells is 10-20ml/kg over 4 hours

Always make sure that the blood is compatible with infant’s blood group
Criteria for ABO and Rh Compatibility of Blood Components

Guidelines for ABO-Compatible Blood Components

ABO Group (Infant) ABO Group (Packed RBC’s) ABO Group (Platelets/ FFP)
O O O, A, B, or AB
A A or O A or AB
B B or O B or AB
AB AB, A, B or O AB
Guidelines for Rh-Compatible Blood Components
Rh Type (Infant) Rh Type (Packed RBC’s) Rh Type (Platelets/ FFP)
Positive Positive or Negative Positive or Negative
Negative Negative Negative (FFP- also Positive)

Prevention of anaemia
• Minimise phlebotomy losses
• Erythropoietin is not recommended for routine use in preterm infants but it
may be considered in sick preterm infants requiring ventilation whose parents
might refuse blood transfusion for example those who might refuse on
religious grounds. Dose is 200-400U/ kg given three times a week
subcutaneously or intravenously.

References:
1. Ohlsson A, Aher SM. Early erythropoietin for preventing red blood cell transfusion in preterm
and/or low birth weight infants. Cochrane Database of Systematic Reviews 2006, Issue 3. Art.
No.: CD004863
2. British Committee for Standards in Haematology Transfusion Task Force. Transfusion
guidelines for neonates and older children. British Journal of Haematology, 2004,:24:
433–453

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 POLYCYTHAEMIA

Definition: Polycythaemia refers to an increase in red cell mass with a haematocrit

of 65% (0.65) or greater. It may result in hyperviscosity. Blood viscosity is dependent
on haematocrit, red cell characteristics, platelets, plasma components and their
interaction with vessel wall.

Factors predisposing to development of polycythaemia

• Intrauterine hypoxia, e.g. IUGR, maternal diabetes, maternal smoking
• Placental transfusion, e.g. twin-twin transfusion, delayed cord clamping
• Fetal risk factors, e.g. Trisomy 21, hyper-or hypothyroidism.

Management: Haematocrit >0.65

Symptomatic Asymptomatic
e.g. seizures, jitteriness, resp. distress,
hypoglycaemia, oliguria or anuria
Hct 0.65-0.70 Hct >0.7

PET Consider hydration PET

Partial exchange transfusion (PET)

The goal is to reduce the infant’s haematocrit and viscosity while maintaining
circulatory volume.
Preparation: Maintain normal temperature during procedure; monitor vital signs
before and during the procedure- use pulse oximeter saturation and/ or cardiac
monitor. Resuscitation equipment should be readily available.
Techniques: Use umbilical venous-peripheral venous exchange- Remove blood from
umbilical venous catheter and infuse normal saline via peripheral vein (good running
peripheral venous line).
Blood volume to exchange:
Total exchange volume= Blood volume x (current Hct – desired Hct) ÷ current Hct
(Blood volume is estimated to be 80-90 ml/kg). Desired haematocrit is 0.5 to 0.55.
Procedure: Calculate the blood volume to be exchanged. Ensure good running
peripheral intravenous line. Insert umbilical venous catheter under sterile conditions.
Infuse the calculated volume as normal saline over an hour as you withdraw the
same volume at the same rate as you infuse the normal saline. Infusion and
withdrawal must occur at the same time so that the infant does not get into shock or
gets overloaded. If unable to insert peripheral intravenous line, can use umbilical
venous exchange technique (as for jaundice) - using aliquots of 5-10 ml.
Example: 3 kg infant requires exchange blood transfusion for haematocrit of 0.7; desired haematocrit
is 0.5 and blood volume of 90 ml/kg. Volume to exchange is 77mls. Will infuse 77 mls over an hour
(drip at 77 mls/hr) as you withdraw 77 mls over the same period. To convert to minutes- 77mls/hr ÷
60 = 1.3mls/min. This means you will withdraw 1.3 mls of blood per minute as you run the drip rate at
77 mls/hour.

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Monitoring post procedure: Withhold feeds for 3 hours (omit next feed). Leave written
instructions to monitor the baby ¼ hourly for the first hour, ½ hourly for the 2 nd hour,
then hourly for next 4 hours then 3 hourly, monitoring the heart rate, respiration and
O2 saturation. Do dextrostix 3 hourly.

References:
1. De Waal KA, Baerts W, Offringa M. Systematic review of the optimal fluid for dilutional
exchange transfusion in neonatal polycythaemia. Arch Dis Child Fetal Neonatal Ed.
2006;91:F7-F10.
2. Dempsey EM, Barrington K. Short and long term outcomes following partial exchange
transfusion in the polycythaemic newborn: a systematic review. Arch Dis Child Fetal
Neonatal Ed. 2006 Jan;91(1):F2-F6.

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 ANTI-COAGULATION GUIDELINES IN NEONATES AND INFANTS

General
• Before the initiation of antithrombotic therapy, baseline testing of aPTT, PT/
INR, and platelet count should be performed.
• Intracranial bleeding should be excluded, especially in premature infants, by
cranial ultrasound.
• Therapeutic options include supportive care through maintaining blood
pressure and vital organ perfusion and non-specific measures such as
warming the involved or contralateral limb by the mechanism of reflex
warming.
• Avoid other antiplatelet drugs, intramuscular injections and arterial punctures
during anticoagulation and avoid sampling from indwelling lines.
• Monitor clinically and platelet counts (Plats) for bleeding and heparin-induced
thrombocytopaenia (Plats <100X109/ L), respectively.
• Avoid physical manipulation in the form of chest physiotherapy on patients on
anticoagulant therapy.
• Consultation with paediatric haematologist is recommended for any infant with
thrombotic disease especially where long-term anticoagulation is needed.

Indications
• Acute large venous thrombosis, related to a central venous catheter e.g.
Renal vein thrombosis or pulmonary embolism
• Acute large arterial thrombosis related to either a central arterial catheter (e.g.
aortic thrombosis) or a peripheral arterial catheter (e.g. peripheral gangrene)
• Inherited thrombophillia’s eg. Deficiencies of Protein C, Protein S and
Antithrombin.

Low-molecular-weight heparin (LMWH)

• Clexane (Enoxaparin) is presently the only LMWH that is available in South
Africa for neonates, infants and children. The recommended dosages for
Clexane cannot be extrapolated to other LMWH’s.
• Data in neonates on the use of LMWH is limited, with safety and efficacy data
being extrapolated from small neonatal case series and paediatric/ adult
studies.
• The advantages of LMWH over standard heparin make it the preferred agent
for anticoagulation.
o These include;
 Decreased need for laboratory monitoring
 Twice daily subcutaneous dosing (half-life: 3 - 6 hours)
 Reduced risk of heparin-induced thrombocytopaenia
 Reduced risk of bleeding at recommended dosages.
• Mechanism of action: Potentiates antithrombin’s inactivation mainly of
Factor Xa.
• Avoid use in severe renal insufficiency.

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• Dosing guidelines for treating neonates and infants aiming for an anti-factor
Xa level of between 0.5 - 1.0 U/ mL
o Initiation dose for:
 Term neonates: 1.7 mg/ kg/ dose s/c given twice daily
 Preterm neonates age <2 months: 2.0 mg/ kg/ dose s/c given
twice daily
 Infants age >2 months: 1.0 mg/ kg/ dose s/c given twice daily
• To avoid wastage a 20mg (0.2ml) or multidose vial enoxaparin injection
should be used.
• For doses of <10mg (0.1ml), it is recommended that the dose be diluted 1:2
with sterile water.
• The syringe must be kept in the refrigerator after opening.
• Do anti-factor Xa level (5ml citrate tube or 1ml paediatric citrate tubes x2), 4
hours after first or second dose.
o If anti-factor Xa level:
 <0.35 U/ mL; increase dose by 25%
 0.35 - 0.49 U/ mL; increase dose by 10%
 0.5 - 1.0 U/ mL; hold dose and monitor 2-weekly, however, more
frequent monitoring needed with renal/ hepatic dysfunction.
 1.1 - 1.5 U/ mL; decrease dose by 20%
 1.6 - 2.0 U/ mL; decrease dose by 30%
 >2.0 U/ mL; stop LMWH and measure anti-Xa 12-hourly until
<0.5U/ mL, thereafter recommence Clexane at 40% of original
dose.
• Duration of therapy
o Minimum of 7 – 10 days.
• Reversal of anticoagulation
o As for heparin above
• Anti-factor Xa levels are still not being done at the Chris Hani Baragwanath
Laboratory (CHB-Lab).
• Samples are to be dropped off at the CHB-Receiving-Office within an hour of
collection.
• The samples are then sent to CHB-Haematology for spinning and thereafter
sent back to CHB-Receiving-Office to be sent off to Charlotte Maxeke
Johannesburg Academic Hospital (CMJAH).
• Alternatively, the collection times for samples from CHB-Lab are either 09h00,
11h00, 13h00 and 15h00 or 09h00 and 11h00, on Weekdays and Saturdays,
respectively.
• Transport is arranged through the CHB-Lab, and there is normally a collection
for CMJAH three times a day with a call-out option, if required or after-hours.
However, there is normally no transport to CMJH over weekends.
• For queries at the CHBara-Lab, contact Sakina on 011-489-8749.
• Anti-factor Xa levels can be requested on Saturdays and Sundays by special
arrangement.
o Contact Bongiwe/ Megan at the CMJAH Lab on 011-489-8471/ 8534.

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Heparin
• Term infants have increased clearance of heparin in comparison to adults and
therefore require a relatively higher heparin dosage (half-life: 25 minutes). In
contrast, the clearance of heparin is significantly diminished in premature
neonates.
• Mechanism of action: Potentiates antithrombin’s inactivation of Factors IIa
and Xa.
• As far as possible, heparin should be infused through a dedicated intravenous
line that is not used for any other medications or fluids.
• Adjustment of heparin infusion rate is based on clinical response, serial
evaluation of thrombus (usually by ultrasound) and monitoring of laboratory
parameters.
• In neonates, the use of PTT to monitor heparin effect is unreliable due to the
variable coagulation factor concentrations and prolonged baseline PTT levels.
Heparin activity level is a more reliable marker (anti-factor Xa level: 0.3 - 0.7
U/ mL).
• Since heparin activity is dependent on the presence of antithrombin, consider
giving Fresh Frozen Plasma (FFP),10 mL/ kg, in any patient when
anticoagulation with heparin is difficult to achieve.
• Dosing guidelines for neonates:
o <28 weeks loading dose: 25 U/kg; continuous infusion: 15 U/kg/hour.
o 28 - 37 weeks loading dose: 50 U/kg; continuous infusion: 15
U/kg/hour.
o ≥37 weeks loading dose: 75 - 100 U/kg; continuous infusion: 28
U/kg/hour.
• Dosing guidelines for Infants and children >1 month:
o loading dose: 75 U/kg; continuous infusion: 20 U/kg/hour.
o Do PTT/ anti-factor Xa level (5ml citrate tube or 1ml paediatric citrate
tubes x2)
 4 hours after the loading dose, and
 4 hours after each change in infusion dose, and
 24-hourly once therapeutic infusion dose is achieved
o aim for PTT: 2 - 3 x baseline:
 if PTT <40 seconds or anti-factor Xa: 0 - 0.15 U/ mL
• increase infusion rate by 20%
 if PTT 40-60 seconds or anti-factor Xa: 0.15 - 0.29 U/ mL
• increase infusion rate by 10%
 if PTT 60-80 seconds or anti-factor Xa: 0.3 - 0.7 U/ mL
• hold infusion rate
 If PTT >80 seconds or anti-factor Xa >0.7 U/ mL
• decrease infusion rate by 10-15%
• Duration of therapy
o Minimum of 10-14 days.
• Reversal of anticoagulation
o Termination of heparin is sufficient to reverse the anticoagulation effect
of heparin therapy.

139
 o Alternative:
 Protamine sulphate 10 mg/ m at a maximum dosage of 50 mg
and at a rate not exceeding 5 mg/ min
o Dosing based on total amount of heparin received in last 2 hours
Time since last heparin dose Protamine dose
(min) (mg/ 100 mL heparin received)
<30 1.0
30 - 60 0.5 - 0.75
60 - 120 0.375 - 0.5
>120 0.25 - 0.375

Indications for thrombophillia testing in neonates/ infants

o Consider testing in neonates and infants with:
 Non-catheter-related thrombosis
 Recurrent catheter-related thrombosis

Recommended first line thrombophilia tests (EDTA x1, plain tube x1 and 5ml
citrate tubes x2 are required for testing)
• Testing is best done at least 6 weeks after discontinuation of
anticoagulation therapy.
• Alternatively, both parents can undergo a thrombotic workup.
 Factor V Leiden mutation in Caucasians
 Prothrombin 20210 mutation
 Antithrombin deficiency
 Protein C deficiency
 Protein S deficiency
 Lupus Anticoagulant

References
1. Martin RJ, Fanaroff AA, Walsh MC. Neonatal-Perinatal Medicine. Diseases of the Fetus and
Infant. 2006. 8(2):1333-1336.

2. Monagle P, Chalmers E, Chan A et al. Antithrombotic therapy in neonates and children:

American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest.
2008. 8:133: 887S-968S.

140
 NEONATAL JAUNDICE

Introduction
• Jaundice (hyperbilirubinaemia) is a sign, not a diagnosis. The main aim is to
exclude pathological causes of jaundice and to initiate treatment to prevent
bilirubin neurotoxicity.
• Jaundice within the first 24 hours of life is pathological and needs to be
urgently investigated.
• Prolonged jaundice (>14 days in term infants and >21 days in preterm infants)
needs to be investigated.
• If mother is Rh-negative, cord blood/ serum bilirubin must be sent in labour
ward for Coombs test and Rh-grouping (send blood samples to the laboratory-
NHLS). Serum bilirubin must be done within 12 hours in all infants born to Rh-
negative mothers.
• All infants admitted from home or clinic for phototherapy to Ward 40/ General
wards must be discussed with neonatal consultant (covering ward 66 during
hours and on-call after hours).

Trancutaneous Bilirubin Measurements (TcB)

• A doctor or a professional or an enrolled nurse shall perform a TcB
measurement between 06h00 and 08h00 on a daily basis on all babies in the
lying wards, using the Jaundice-meter.
• In addition to the above, a total serum bilirubin (TSB) should be done routinely
and sent to the laboratory in the morning (before 8am) following delivery or
anytime if jaundiced, on all babies weighing <2000g at birth in lying-in wards
before discharge. The order must be made by the doctor who is clerking the
patient in labour ward nursery, or the doctor covering the lying-in wards.
• Do not use the Jaundice-meter on infants:
o in the labour-ward nursery
o after the initiation of phototherapy
o after an exchange transfusion
o with jaundice as a result of an incompatible blood type or haemolytic
jaundice. Due to the rapid rise of bilirubin with ABO and Rh incompatibility
do serum bilirubin.
Total serum bilirubin (TSB) level shall be performed when:
• TcB level >8 mg/ dL on infants < 24 hours of age.
• TcB level >15 mg/ dL on infants > 24 hours of age.
• Nursing personnel who identify jaundice of the newborn regardless of the TcB
measurement may obtain a TSB based upon nursing judgement.

Management of Jaundice in the Term neonate

Age (hours) Total serum bilirubin (TSB) level, mg/ dL (µmol/ L)
Exchange
Consider Observe & Phototherapy transfusion, if Exchange
stopping repeat TSB intensive transfusion
TSB within 24 phototherapy and intensive
hours fails/ unwell phototherapy
infant

141
 ≤ 24 Infants who are clinically jaundiced at ≤ 24 hours require further
evaluation
25 - 48 <7 ≥ 12 (210) ≥ 15 (260) ≥ 20 (340) ≥ 25 (430)
49 - 72 <9 ≥ 15 (260) ≥ 18 (310) ≥ 25 (430) ≥ 30 (510)
>72 <10 ≥ 17 (290) ≥ 20 (340) ≥ 25 (430) ≥ 30 (510)
• Note:
o Intensive phototherapy should produce a decline of TSB of 1-2 mg/ dL
within 4-6 hours.
o Consider interrupting breastfeeding temporarily if TSB is >24 mg/ dL and
persistently elevated despite adequate phototherapy.
o An unwell/ sick infant has risk factors such as; haemolysis,
hypoglycaemia, hypoalbuminaenia, hypoxia, sepsis or meningitis,
asphyxia, and metabolic acidosis, for developing acute bilirubin
encephalopathy at lower thresholds and therefore an exchange
transfusion must be done at a lower SBR level.

Risk Assessment for Significant Hyperbilirubnaemia Term/ Near Term newborn

infants based on hour-specific bilirubin.

Risk zone Percentile Risk Action

High ≥95 57% Repeat within 4 - 8 hours
Intermediate
High 75th - 90th 13% Repeat within 8 - 12 hours
Low 40th - 75th 2.1% Repeat within 48 hours
Low ≤40th 0% Follow-up at age 3 - 5 days

142
Management of jaundice in low-birth-weight infants
TSB mg/ dL (µmol/ L)
Recent weight (grams) Phototherapy Exchange transfusion
< 1000 ≥5 (≥85) ≥14 (≥240)
1001- 1499 7 - 10 (120 - 170) 15 - 18 (255 - 310)
1500 – 1999 10 - 12 (170 - 205) 18 - 20 (310 - 340)
2000 – 2499 12 - 14 (205 - 240) ≥20 (≥340)
• Note:
o An exchange transfusion must be done at a lower SBR level in an unwell/
sick infant with risk factors as mentioned above for term infants.
o Rough guide for starting phototherapy in LBW infants (1000 - 2000g) after
24 hrs of life: Weight (kg) x 7.

Guidelines on management of infants under phototherapy

• All babies on phototherapy must be examined on a daily basis by a doctor.
• Infants should be nursed with only their eyes covered (no napkins).
• Phototherapy units must be checked on a regular basis to ensure that all
lights are working.
• Phototherapy lights should be as close to the baby as possible (without
overwarming the baby).
• Maintain adequate hydration, i.e. frequent feeding.

Intravenous immune globulin (IVIG)

• IVIG been shown to reduce the need for exchange transfusion in patients with
isoimmune haemolytic jaundice.
• Use of IVIG must be considered in infants with haemolysis due to Rh or ABO
incompatibility when Serum Bilirubin is within 75 % of Exchange SB level (a
consultant must make the decision to use it) at a dose of 500-1000 mg/ kg.
• The routine use of IVIG is not recommended.

References for Neonatal Jaundice:

1. Maisels MJ, Baltz RD, Bhutani VK, et al. American Academy of Pediatrics. Subcommittee on
Hyperbilirubinemia. Clinical Practice Guideline: Management of Hyperbilirubinemia in the
Newborn Infant 35 or More Weeks of Gestation. Pediatrics. 2004; 114:297-316.

2. Western Cape Consensus Guidelines for Phototherapy & Blood Exchange Transfusions in
Neonates. South African Medical Journal. 2006; 96(9):820-24.

3. Smitherman H, Stark AR, Butani VK. Early recognition of neonatal hyperbilirubinaemia and its
emergent management. Seminars in Fetal & Neonatal Medicine. 2006; 11:214-24.

4. Keren R, Luan X, Friedman S, Bhutani VK. A Comparison of Alternative Risk-Assessment

Strategies for Predicting Significant Neonatal Hyperbilirubinaemia in Term & Near-Term
Infants. Pediatrics. 2008; 121(1):e170-79.

5. Carceller-Blanchard A, Cousineau J, Delvin EE. Point of care testing: Transcutaneous

bilirubinometry in neonates. Clinical Biochemistry. 2008.

143
144
 EXCHANGE TRANSFUSION

Introduction: An exchange transfusion is a medical emergency, and any infant that

may require an exchange transfusion must be fast-tracked with regard to admission,
blood samples and intensive phototherapy. All infants that may require or need an
exchange transfusion, must be discussed with neonatal consultant (covering Ward
66 during hours or the consultant on-call after hours).

Preparing for an exchange:

• An exchange transfusion is a medical emergency, and any infant that may
require an exchange transfusion must be fast-tracked with regard to admission,
blood samples and intensive phototherapy.
• All infants that may require or need an exchange transfusion, must be discussed
with neonatal consultant (covering Ward 66 during hours or on-call after hours).
• Obtain consent from parent/s
• Ensure that the baby is not fed for at least 2 hours before the procedure.
• Order fresh whole blood (<72 hours old), if not available you can use blood that is
up to 7 days old, volume 160-180mLs/kg
• Always examine the infant, check dextrostix and temperature before starting the
procedure
• Get an assistant who well help with monitoring of infant and recording of blood
volume given and removed from infant during the exchange.
• Restrain baby’s limbs and monitor heart rate, respiration, colour and O 2
saturation.
• Each unit of blood must be heparinized with 400u of heparin and mix well,
thereafter add 4mLs of 10% calcium gluconate in each unit and mix well.
• A double volume exchange (160- 180 mLs/kg) is done in 10-20 mL aliquots.
• Do not rush the procedure as it may compromise the infant, can be done over 45-
60 minutes
• Connect 2 two-way taps in series to the feeding tube or umbilical catheter at one
end and to the syringe at the other end.

Procedure
• Catheterise the umbilical vein with feeding tube or umbilical catheter under sterile
conditions and advance catheter until get back flow of blood, usually few
centimeters
• Attach the tubing from the blood pack to the side hole of one of the two-way taps
and connect a second tubing from the disposal bag to the other side hole of the
second two-way pack for disposal of blood from the infant.
• Blood must be warmed throughout the exchange either using a warmer or a coil
put in a bucket of water with a temperature maintained at 37ºC (not higher as will
cause haemolysis).
• Start the exchange by pulling blood from the patient first, and send this blood for
FBC, U&E, calcium, magnesium, phosphate and bilirubin.
• Send blood for the same tests at the end of exchange
• Once the exchange is complete, remove the catheter and put on a gauze with
pressure bandage to ensure homeostasis or the catheter can be left in-situ and

145
 infuse maintenance intravenous fluids through it if the infant is likely to need a
second exchange
• Recheck dextrostix and temperature at the end of an exchange, leave written
instructions to monitor the baby ¼ hourly for the first hour, ½ hourly for the 2 nd
hour, then hourly for next 4 hours then 3 hourly, monitoring the heart rate,
respiration and O2 saturation. Do dextrostix 3 hourly.
• Put the infant back on intensive phototherapy immediately after the exchange
• Inform the mother about how the procedure went.
• Document summary of the procedure in the bedletter including indications for the
procedure, how the procedure went, any complications or difficulties during the
procedure.

References
1. Thayyil S, Milligan DWA. Single versus double volume exchange transfusion in
jaundiced newborn infants. The Cochrane Database of Systemic Reviews 2006:4.

2. Alcock GS, Liley H. Immunoglobulin infusion for isoimmune haemolytic jaundice in

neonates. The Cochrane Database of Systemic Reviews 2002; 3.

3. Maisels MJ, Baltz RD, Bhutani VK, et al. American Academy of Pediatrics.
Subcommittee on Hyperbilirubinemia. Clinical Practice Guideline: Management of
Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics.
2004; 114:297-316.

4. Western Cape Consensus Guidelines for Phototherapy & Blood Exchange

Transfusions in Neonates. South African Medical Journal. 2006; 96(9):820-24.

146
 PROLONGED NEONATAL JAUNDICE

Introduction
• Prolonged Neonatal jaundice is defined as hyperbilirubinaemia, either
conjugated or unconjugated;
o beyond 2 weeks of life in a term infant.
o beyond 3 weeks of life in a preterm infant.
• Causes include:
o Infections (viral/ bacterial/ fungal),
o Prolonged TPN use,
o Biliary atresia or choledochal cyst,
o Galactosaemia,
o Intestinal obstruction,
o Haemolysis due to ABO incompatibility,
o Hypothyroidism
o Idiopathic neonatal hepatitis and
o Breastmilk jaundice

Investigation and Management

1) Check fractionated SBR (conjugated and unconjugated fraction)

a) Baby is term, well and breastfeeding, continue monitoring SBR if

predominantly unconjugated, provided SBR’s declining. Breastfeeding should
not be discontinued/ discouraged.
b) If SBR’s not declining or increasing and infant is anaemic, check both for
blood group incompatibility between infant and mother and the infant’s FBC
smear. An abnormal FBC smear (eg. spherocytes, target cells) may suggest
red cell/ haemoglobin abnormality.
c) If conjugated fraction >20% of total SBR, see point 2-7.

2) Check liver function tests (LFT) if the infant is term or preterm and is unwell

a) Predominantly elevated hepatic enzymes (ALT and AST) suggest infective

aetiology; exclude:
i) Bacterial/ fungal sepsis
ii) Urinary tract infection (preferably suprapubic or catheter specimen)
iii) Viral infection (CMV, syphilis, Rubella, HSV, Hepatitis B and Hepatitis C).

3) Check infant’s urine and stools. If these are dark/ bilirubin present and/or pale
respectively, exclude obstructive jaundice.

a) Check LFT and abdominal ultrasound with the infant starved for at least 4-6
hours.
b) Elevated ALP and GGT on LFT with dilated bile duct/ s and/ or absent
gallbladder suggest an obstructive aetiology.
c) A suspicious abdominal ultrasound warrants both a radionuclide scan (HIDA
scan) to assess biliary tract excretion and a Paediatric Surgical opinion.

147
4) If LFT abnormal and infection (viral/ bacterial/ fungal/ UTI) has been excluded,
a) Consider reducing/ temporarily stopping TPN, if being infused for >2weeks.
b) Check urine for reducing substances which if positive, send serum for
galactose-1-PO4-uridyl-transferase enzyme (GALT),
c) Send for thyroid function tests (TSH, T4) and α1-antitrypsin levels.
d) Check clotting (INR) and serum ammonia, and, if these are abnormal;
(1) Give vitamin K and FFP.
(2) Monitor HGT’s for hypoglycaemia.
(3) Manage as liver failure in consultation liver specialist.
e) Send urine and blood as per metabolic screening protocol.

5) If infant syndromic, consider:

a) Skeletal survey.
b) Chromosomal analysis (trisomy 21, 13, 18).
c) St John’s eye clinic assessment (posterior embyotoxon for Allagille’s
syndrome).
d) Geneticist referral.
e) Endocrinologist referral (if concerned about hypopituitarism and/ or abnormal
thyroid function).

6) A liver biopsy may be considered as an aid to a diagnosis in consultation with

liver specialist.
7) The diagnosis of an idiopathic neonatal hepatitis is one of exclusion.

References
1. Maisels MJ, Baltz RD, Bhutani VK, et al. American Academy of Pediatrics. Subcommittee
on Hyperbilirubinemia. Clinical Practice Guideline: Management of Hyperbilirubinemia in
the Newborn Infant 35 or More Weeks of Gestation. Pediatrics. 2004; 114:297-316.

2. N. Ratnavel, N.K.Ives. Investigation of prolonged neonatal jaundice. Current Paediatrics.

2005. 15:85-91.

3. Gupte G. Conjugated hyperbilirubinamia. Pediatrics and child heath. 2008.18:10:474-76.

4. Martin RJ, Fanaroff AA, Walsh MC. Neonatal-Perinatal Medicine. Neonatal Jaundice and
Liver Disease. 2:8:1450-60.

148
 SEDATION AND ANALGESIA
Introduction: The goals of sedation in NICU include analgesia for painful diseases,
procedures and compliance with mechanical ventilation. Opioids are widely used
because of their relatively high toxic-to-therapeutic ratio and their potent analgesic
properties.

Newborns routinely experience pain associated with care in the nursery. These
include ventilation, blood sampling, injections and invasive monitoring. Evidence
suggests increase sensitivity to pain in neonates compared to older groups.

The following procedures are associated with pain.

Diagnostic Therapeutic Surgical

Arterial puncture Bladder Mechanical

catheterisation ventilation
Bronchoscopy Surgical
Central line Postural drainage procedures
insertion and
removal
Endoscopy Removal of adhesive
Chest tube tape
insertion and
removal
Heel lancing Suture removal
Chest
physiotherapy
Lumbar puncture Tracheal
Dressing change intubation/extubation
ROP exam
Feeding tube Tracheal suctioning
insertion
Suprapubic Ventricular tap
bladder tap Intramuscular
injection
Venipuncture
Peripheral venous
catheterisation

Prevention and Management of pain in the newborn

• Prevention
o Avoiding painful stimuli.
o If procedure needs to be done- plan for it.
o Limit environmental interventions to reduce stress in NICU.
• Management of pain can be divided into pharmacological and non-
pharmacological strategies.
o Non-pharmacological:

149
 Behavioural methods sucrose/glucose pacifiers and non-

nutritive suck.
 Pacifier or dummy with sucrose 12-24% given 2min before can
be repeated during the procedure.
 Non-nutritive sucking (using pacifier or dummy on its own).
 Swaddling, containment or facilitated tucking.
o Pharmacological strategies:
 Pharmacological agents as preemptive analgesia.
 Pharmacological therapy for ongoing pain.
 EMLA cream (when available) to proposed site.
 Subcutaneous lignocaine infiltration at site of procedure e.g.
insertion of chest drain.
 Use opoids if performing more invasive procedures e.g. central
venous catheters, percutaneous venous/arterial catheter
insertion, arterial/venous cutdowns, chest tube insertion or
removal, suctioning.
 Low dose opioid infusion if patient is on a ventilator

Guidelines on use of analgesia/ sedation in neonates for specific conditions

• Infants who are post-operative- use Morphine only
• NEC with tense abdomen before surgery- Morphine only
• Before any painful procedure- Morphine combined with Dormicum
• All neonates in the first 3 days of mechanical ventilation (excl. CPAP)- Morphine
• Neonates older than 3 days requiring improvement in efficacy of mechanical
ventilation- Dormicum, if no response add Morphine
• Insertion of chest drain- Local Anaesthesia (Lignocaine) and Morphine or
Fentanyl
• Chest drain in situ- Morphine
• Tachycardia of unknown cause, consider pain as a cause- Morphine
• On HFOV- Morphine
• Use Morphine for all invasive procedures e.g. insertion of intercostal drain,
central line.
• Endotracheal intubation in active babies: Atropine, Fentanyl and Suxamethonium

Note
• There is no benefit in giving both Dormicum and Morphine simultaneously, as
a routine.
• In presence of hypotension use Fentanyl 1-2 µg/kg/dose as it has less effect
on BP than Morpine does.
• Fentanyl does not have sedative effect, therefore both sedation and analgesia
are required then give a combination of Fentanyl and Dormicum

150
 Recommended analgesics for neonates

Agent Intermittent dose Infusion dose Local/Topical

Opoid analgesics
Morphine sulfate 0.05-0.1mg/kg IVI 0.01-0.03mg/kg/hr
Fentanyl citrate 0.5-3ug/kg IVI 0.5-2ug/kg/hr
Anaesthetic agents
Lignocaine (local) 2-5 mg/kg subcut
EMLA (topical) 0.5-2 g under
occlusive dressing 1
Ketamine hydroCl 0.5 – 2 mg/kg IVI
hr before procedure
Thiopental sodium 2-5 mg/kg IVI 0.5-1 mg/kg/hr
Other agents
Paracetamol 10-15 mg/kg orally; 20-
30 mg/kg rectally*

Sucrose 12-24% solution orally

2 min before the
procedure, 2 ml for
term neonates and 0.1-
0.4 ml for preterms.

*Paracetamol: maximum daily dose preterm infants (28-32 weeks)= 40mg/kg;

preterm (32-36wks) and term infants (<10 d)= 60mg/kg; term
infants(>10 d) =90mg/kg

It is important to know the side effects of the drugs that you are prescribing.

Paralysis
• Fighting ventilator and on pressures >30 or rate >60/ minute
• Post tracheo-oesophageal repair.
• Reduction of abdominal wall defect
• Drugs: Pancuronium (Pavulon) (currently available at CHBH) or Vecuronium
• Dose: 0.1 – 0.2 mg/kg
• Generalized oedema and a gasless abdomen may result from absent muscular
activity and swallowing.
• Pavulon may induce hypertension - mechanism unknown, possible mediated
through release of catecholamines. Vecuronium has minimal cardiovascular
effects.

References:
1. Lago P, Garetti E, Merazzi D, et al. Guidelines for procedural pain in the newborn. Acta Paediatr
2009;98:932-939.
2. Anand KJS, international Evidence-based group for neonatal pain. Arch Pediatr Adolesc Med
2001;155:173-180.

151
3. Carbajal R, Nguyen-Bourgain C, Armengaud JB. How can we improve pain relief in neonates?
Expert Rev. Neurother 2008;8(11):1617-20.

152
GUIDELINES ON ASSESSING WHETHER THE PATIENT NEEDS SEDATION OR ANALGESIA

Assessment for pain should be done every 3-6 hours. The pain and agitation
assessment portion of the N-PASS is scored from 0→+2 for each behavioural and
physiological criterion, and then summed for infants 36 weeks gestational
age/corrected age:
 Additional points are added to the premature infant’s pain score
based on their gestational age/ corrected age to compensate for
their limited ability to behaviourally or physiologically communicate
pain:

 Add 3 pts to total score for infants < 28 weeks gestation/

corrected age.
 Add 2 pts to total score for infants 28-31 week’s gestation/
corrected age.
 Add 1 pt to total score for infants 32-35 week’s gestation/
corrected age.

 Total pain/agitation score is documented as a positive number 0→

+10 plus the additional points added for the gestational
age/corrected age of the infant.

 Treatment/interventions are indicated for scores > 3

 Interventions for known pain/painful stimuli are indicated before the

score reaches 3

 The goal of pain treatment/intervention is a score ≤3

The sedation assessment portion of the N-PASS is scored from 0→ -2 for each
behavioural and physiological criterion, and then summed:
 The sedation assessment is scored with stimulation to evaluate the
infant’s response to stimuli.

 A score of 0 is given if the infant’s response to stimuli is normal

for their gestational age.

 Desired levels of sedation vary according to the situation. For deep

sedation a score of -10 to -5 is the goal. For light sedation a score
of -5 to -2 is the goal.

 Deep sedation should be considered in extremely medically

compromised infants.

 A negative score without the administration of opioids/sedatives

may indicate the premature infant’s response to prolonged or

153
 persistent pain/stress, neurological depression, sepsis, or other
pathology.
Neonatal Pain, Agitation & Sedation Scale (N-PASS)

Assessment Sedation Normal Pain / Agitation

Criteria -2 -1 0 1 2
Appropriate Irritable or High-pitched or
Moans or cries
Crying No cry with crying crying at silent-continuous
minimally with
Irritability painful stimuli intervals cry
painful stimuli Not irritable
Consolable Inconsolable
Arching, kicking
Arouses
No arousal to minimally to Restless, Constantly awake
Behaviour any stimuli stimuli Appropriate for squirming or
No spontaneous Little gestational age Awakens Arouses
State
movement spontaneous frequently minimally / no
movement movement (not
sedated)
Facial Minimal Relaxed Any pain Any pain
Mouth is lax
expression with expression expression
Expression No expression Appropriate
stimuli intermittent continual
Intermittent Continual
Weak grasp Relaxed hands clenched toes, clenched toes,
Extremities No grasp reflex
reflex and feet fists or finger fists, or finger
Tone Flaccid tone splay splay
↓ muscle tone Normal tone
Body is not tense Body is tense

10-20% from > 20% from

baseline baseline
No variability
Vital Signs < 10% variability Within baseline SaO2 ≤ 75% with
with stimuli SaO2 76-85%
HR, RR, BP, from baseline or normal for stimulation –
Hypoventilation with stimuli gestational age with stimulation
SaO2 slow recovery
or apnoea –
quick recovery Out of sync with
vent

154
 RECOMMENDED DOSAGE SCHEDULE FOR ANTIMICROBIAL AGENTS AND OTHER
MEDICATIONS FREQUENTLY USED IN THE NEONATAL UNIT AT CHB HOSPITAL.
DOSAGE (mg/kg/day) AND INTERVAL ADMINISTRATION
BODY WEIGHT ≤2000 g BODY WEIGHT >2000 g
ANTIBIOTIC Routes of 0-7 DAYS 8-28 DAYS 0-7 DAYS 8-28 DAYS >28 DAYS
Administration OLD OLD OLD OLD OLD
Ampicillin IV, IM 100 div 12hrly 150 div 8hrly 150 div 8hrly 200 div 6hrly 200 div 6hrly
Amphotericin B IV 1 once daily 1 once daily 1 once daily 1 once daily 1 once daily
Cefotaxime IV, IM 100 div 12hrly 150 div 8hrly 100 div 12hrly 150 div 8hrly 200 div 6hrly
Ceftazidime IV, IM 100 div 12hrly 150 div 8hrly 100 div 12hrly 150 div 8hrly 150 div 8hrly
Ceftriaxone IV, IM 50 once daily 50 once daily 50 once daily 75 once daily 100 once daily
Cefuroxime IV, IM 100 div 12hrly 150 div 8hrly 150 div 8hrly 150 div 8hrly 150 div 8hrly
Clindamycin IV, IM, PO 10 div 12hrly 15 div 8hrly 15 div 8hrly 20 div 6hrly 30 div 6hrly
Erythromycin IV, PO 20 div 12hrly 30 div 8hrly 20 div 12h 40 div 8hrly 40 div 6hrly
Flucloxacillin PO 12.5-25 div 6hrl 12.5-25 div 6hrl 12.5-25 div 6hrl 12.5-25 div 6hrl 12.5-25 div 6hrl
Isoniazid PO 10-20 daily 10-20 daily 10-20 daily 10-20 daily 10-20 daily
Metronidazole IV, PO 7.5 once daily 15 div 12hrly 15 div 12hrly 30 div 12hrly 30 div 6hrly
Cloxacillin IV, IM 50-100 div 12hr 75-150 div 8hr 50-100 div 12hr 75-150 div 8h 100-200 div 6hrly
Penicillin G IV 200 000 U 225 000 U 200 000 U 200 000 U 200 000 U
div 12hrly div 8hrly div 12hrly div 6hrly div 6hrly
Penicillin G for IV 100 000 U 150 000 U 100 000 U div 150 000 U 200 000 U
Cong. Syphilis div 12hrly div 8hrly 12hrly div 8hrly div 6hrly
Benzathine IM 50 000 U 50 000 U 50 000 U 50 000 U 50 000 U
Penicillin G (one dose) (one dose) (one dose) (one dose) (one dose)
Procaine IM 50 000 U 50 000 U 50 000 U 50 000 U 50 000 U
Penicillin G once daily once daily once daily once daily once daily
Rifampicin PO 10-20 daily 10-20 daily 10-20 daily 10-20 daily 10-20 daily
Tazocin IV 300 div 8hrly 300 div 8hrly 300 div 8hrly 300 div 8hrly 300 div 8hrly
DOSAGE RECOMMENDED DOSAGE (BASED ON GESTATIONAL AGE PLUS WEEKS OF LIFE)
(mg/kg/dose) <30 WK 30-35 WK >35-43 WK >43 WK
Acyclovir IV 20mg/ kg 12hrly 20mg/ kg 12hrly 20mg/ kg 8hrly 20mg/ kg 8hrly
Amikacin* IV, IM 7.5mg/kg 24hrly 10mg/kg 24hrly 15mg/kg 24hrly 15mg/kg 24hrly
Gentamicin** IV, IM 2.5mg/kg 24hrly 3.5mg/kg 24hrly 5mg/kg 24hrly 5mg/kg 24hrly
Vancomycin*** IV 15mg/kg 24hrly 15mg/kg 12hrly 15mg/kg 12hrly 15mg/kg 8hrly
Ciprofloxacin IV 5-10mg/kg 12hrly 5-10mg/kg 12hrly 5-10mg/kg 12hrly 5-10mg/kg 12hrly
Ciprofloxacin PO 10-20mg/kg 12hrly 10-20mg/kg 12hrly 10-20mg/kg 12hrly 10-20mg/kg 12hrly
Fluconazole IV, PO 10-12mg/kg- loading dose, and then 5-6mg/kg/dose daily; for all age groups
MEROPENEM Sepsis: 20mg/kg/dose 8hrly Meningitis: 40mg/kg/dose 8hrly

PO PROPHYLACTIC DOSING
Amoxicillin 25mg/kg/day UTI Prophylaxis
Nitrofurantoin 1-2mg/kg/day UTI Prophylaxis
Bactrim 1-2mg/kg/day UTI Prophylaxis
Nevirapine 2mg/kg/dose HIV Exposed Infant
Zidovudine (AZT) 1.5mg/kg 12hrly <35wks, 2.0mg/kg 6hrly >34 wks HIV Exposed Infant
Bactrim 5mg/kg/day PCP Prophylaxis in HIV exposed/ infected infants
OTHER DRUGS/ MEDICATIONS
Aminophylline 5–6mg/kg/dose iv over 30 minutes (as a loading dose only) For Apnoea
Neulin 2mg/kg/dose 8hrly (maintenance dose) For Apnoea/ Chronic lung dis.
Hyrochlorothiazide 1-2mg/kg/dose 12hrly p.o. For chronic lung disease
Spironolactone 1-2mg/kg/dose 12 hrly p.o. For chronic lung disease
Ranitidine 2-4mg/kg/dose 8-12hrly p.o. ; 1.5 mg/kg (Term), 0.5 mg/kg (Preterm) i.v. Antacid
8hrly
Cimetidine 5-10mg/kg/dose 6hrly p.o., 10-15mg/kg 12hrly iv Antacid
Maxolon 0.03-0.1mg/kg/dose 8hrly i.v. or p.o. Facilitate GI motility

155
Salbutamol 5-10 mcg/kg/min for 1hr, then 1-2mcg/kg/min Bronchodilator
Sildenafil 0.3 mg/kg 3-6hrly, until effective or low BP occurs, max 2-3mg/kg Vasodilator
Clexane 1.5mg/kg 12hrly SC (<2mo), 1mg/kg 12hrly SC (≥2mo), do anti-Xa 4h pd Anti-coagulant
Elemental Iron 2 – 3 mg/kg daily p.o. Nutritional
Abidec 0.6mls daily p.o. Nutritional
Vitamin D 400 U daily p.o. Nutritional
Folate 0.1mg daily p.o. Nutritional
*Desired levels: Peak 20-30 mcg/mL, Trough <5mcg/ mL
** Desired levels: Peak 6-12 mcg/mL, Trough <2mcg/ mL
*** Desired levels: Peak 20-40 mcg/mL, Trough 5-10mcg/ mL

(Adapted from Nelson JD. Antibiotic Therapy for Newborns. In: Pocket Book of Pediatric Antimicrobial Tharapy: Williams &
Wilking, 2000-2001
Young TE. Mangum B. A manual of Drugs Used in Neonatal Care. Neofax, Fifteenth Edition, 2002
Shann F. Drug doses, Intensive Care Unit, Royal Children’s Hospital , Parkville, Victoria 3052, Australia, Fourteenth edition 2008)

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 GUIDELINES FOR REFERRAL TO NEURODEVELOPMENT TEAM, DIETICIAN
AND SOCIAL WORKER
Physiotherapist/ Occupational therapist
• Lung collapse
• Asphyxia with HIE II, and HIE III
• Generalised hypotonia
• Generalised hypertonia
• Contractures
• Hand pathology
• Branchial plexus injury

Speech therapist/ Audiologist

• Term or near term infants with suspected sucking and/ or swallowing difficulties
• Cleft palate
• External ear abnormalities e.g. Treacher Collins
• Asphyxia with HIE II, and HIE III
• Considering gastrostomy
• Refer infants with the following problems before they are discharged
• Meningitis
• Jaundice requiring exchange transfusion
• Prolonged (>2 weeks) on the mechanical ventilator
(Note: Audiologist have a protocol on screening of high risk newborns who
have been admitted to our unit)

Nutritionists/ Dieticians
• Inadequate weight gain on maximum volume of feeds or excessive weight gain
• Persistent passage of loose stools or diarrhoea (esp. those with colostomy)
• Considering gastrostomy
• Chronic lung disease
• Inborn error of metabolism
• Problems of breastfeeding

Social Workers
• Mothers with social problems making them unable to visit their babies
• Mothers refusing to be transferred to ward 40
• Mothers less than 18 years old
• Babies given up for adoption
• Abandoned babies
• Mother has demised

Contact Numbers
• Physiotherapists- 933-8309, or page - 23581
• Occupational therapists- 933-9014, or page - 23456
• Speech therapists- 933-9263/4, or page - 23441
• Nutritionist- 933-9233, or page - 23555
• Social workers- 933-8288

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 FORMULAE/ CALCULATIONS/NORMAL VALUES

Respiratory

aA ratio (mmHg) = PaO2(mmHg) ÷ (

Aa gradient
Oxygen index(OI)= MAP x FiO2 x 100/ PaO2(mmHg)
Mean airway pressure= (PIPX Ti)+(PEEPX Te) or (PIP-PEEP)X Ti
+PEEP
(TI+ Te) (Ti+ Te)
Ventilation index(VI)= PaCO2(mmHg) x RR x PIP/ 1000

Blood
Blood volume: term 80ml/kg preterm 90ml/kg
Osmolality of serum= 2xNa + glucose + urea(mmol/L) (N=275-295mosmol/kg)

Metabolic
Anion gap = Na+ + K+- Cl-- HCO3- Normal 8-15 term and preterm 8-18
Dextrose infusion rate : mg/kg/min= %dextrose x rate÷(weight x 6)

Renal
Sodium
FeNa(%)= 100 X UNa(mmol/L) X PCr(mmol/L)
PNa(mmol/L) X UCr(mmol/L)

(NB first convert PCr from µmol/L to mmol/L by ÷ 100)

Na deficit(mmol)=(135- Na) x 0.7 x weight(kg)

GFR
GFR estimate <1 week= 72/ serum creatinine(µmol/L)
>1 week= 66/ serum creatinine(µmol/L)

Phosphate (P):
Tubular reabsorption of P= 1 - {urine P(mmol/L) x plasma creatinine(mmol/L)} x
100%
(Normal>80%) {urine creatinine (mmol/l) x plasma P(mmol/L)}

( First convert plasma Cr from µmol/L to mmol/L by ÷ 1000)

Umbilical Catheter
Measurement
Umbilical catheter lengths/ placement can be calculated according to the following:
UVC length tip at T8-T10 = 2/3 vertical shoulder- umbilicus length
UAC length tip at L3-L4 (Low line) = 2/3 vertical shoulder-umbilicus length - 0.5 cm
UAC length tip at T8-T10 (High line)= full vertical shoulder-umbilicus length + 1.5 cm

Calculated for UVC and high UAC

UAC = 3 X Weight (kg) + 9 +length of remaining stump
UVC= (3 X Weight (kg) + 9)/ 2

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Body Surface Area
Body Surface area(BSA) m2= weight(kg) x 0.05) + 0.05

Biochemistry
Albumin(g/L) GA(wks) 0-7d 7-14d 14-21d 21-28d
27 21-33
29-33 22-35
35 22-36
>36 28-43 30-43 27-44 32-44
ALP (IU/L) >36wks 36wks 34-35wks 32-33wks 30-31wks 28-
29wks
28-300 88-326 113-320 110-398 112-450 119-
465
Ammonia(µmol/L) Up to 100 if well, up to 200 if sick/preterm
AST (IU/L) Up to 100
Ca total(mmol/L) 1-3d 4-5d 6-12d 21-28d
Term 2.14-2.6 2.2-2.6 2,25-2.69
Preterm 2.14-2.65
Ca ionized(mmol/L) 1d 3d 5d
Term 1.05-1.37 1.1-1.44 1.2-1.48
Preterm 0.81-1.41 0.72-1.44 1.04-1.52
Cortisol(mmol/L) >1day 200-400
CRP(mg/L) <10
Creatinine(µmol/L) Gest age(wks) Birth Peak(hr) 48hr 7d 14d
27-29 77±12 179±21(39h) 116±40 84±32
72±32
30-32 65±4 139±19(33h) 104± 38 83±41
69±32
33-35 73±6 120±20(15h) 93±39 68±44
55±36
>36 65±5 75±38 50±36
38±20
Growth Term: <2wks 15-40 >2wks <20
hormone(ng/ml=µg/L) Preterm <2months 15-40 >2months <20
17- Term 2-10 days
hydroxyprogesterone(nmol/ 0.7-12.4 (2-3x higher if sick/preterm)
L)
Iron(µmol/L) Term 10-33
Preterm 1.6-22
Ketone bodies(mmol/L) Preterm 0.01-0.51 Term 0.01-2.06
Lactate( mmol/L) Term 1hr: 0.9-2.7 24hr:0.8-1.2 7d: 0.5-1.4
LDH(U/L) 357-953
Magnesium(mmol/L) Preterm(0-28d): 0.62-1.24
Term (0-28d): 0.72-1.05
Osmolality(mosm/kg) Term: 275-295
Phosphate(mmol/L) Term: 1-3d: 1.9-2.9 4-6d: 1.7-2.7 7-12d: 1.5-2.9
Potassium(mmol/L) Preterm: 0-7d: 4.6-6.6 8-21d : 4.6-7.0
Term; <1wk: 3.5-6 1-4wk: 3.7-6.6
Protein (g/L) Term: 54-70
Sodium(mmol/L) Preterm: 0-7d: 133-146
Term: <1wk: 133-146 1-4wks: 134-144
Thyroxine (pmol/L) Preterm 4-10d: 10-30
Term 4-10d: 13.7-28
TSH (nmol/L) >7d: 0.3-5
TG (fasting) (mmol/L) Term 3wks; 0.24-1.55
Urea(mmol/L) Birth 48hrs 1wk
Preterm: 3-3.8 4-9 0.5-4.2

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 Term: 0.7-6.7
Urine
Nephrotic range protein: >200mg/mmol
creatinine ratio
Sodium excretion(mmol/kg/24h) Preterm <28wk <7d <22
Preterm 29-32wk <7d <12
Term <1
Tubular phosphate reabsorption >80%, higher in prems
CSF NORMAL VALUES
WBC/mm3 % polys Protein g/L CSF/ blood
glucose
Term <7d 0-30 0-66 0.3-2.5 At least 50% of
Term >7d 0-10 0.2-0.8 serum, low levels
Preterm <7d 0-30 0-28 0.5-2.9 may persist for
Preterm >7d 2-70 0-60 0.5-2.6 weeks after IVH

Haematological values- term infants

cord 12hr 24hr 3d 7d 4wk
Hb(g/dl) 14-20 19.3±2.2 18.8±2 17.9±2.5 12.7±1.6
Hct(%) 43-63 61±7.4 62±9.3 56±9.4 36±4.8
RBC(x10/L) 4.2-5.8 5.14±0.7 5.11±0.7 4.86±0.6 3.6±0.4
Retics (%rbc) 3-7 3.2±1.4 2.8±1.7 0.5±0.4 0.9±0.8
Nucleated 200-600 200-500 0-5 0 0
rbc/mm3/(100wbc) (2.9-8.7) (2.9-7.3) (<0.1)

MCV (fl) 100-120 119±9.4 116±5.3 118±11.2 101±8.1

MCHC (g/dL) 32-40 31.6±1.9 31.1±2.8 32±1.6 34.9±1.6
Platelets (x109/L) 150-350 150-350 150-350 150-350 150-350
WBC (x109/L) 9-30 13-38 9.4-34 5-21 5-19.5
Total neutrophil 1.8-6.2 7.5-14.4 7.2-12.6 1.8-7 1.8-5.4 1.8-5.4
Immature 0-1.1 0-1.4 0-1.3 0-0.6 0-0.5 0-0.5
neutrophils
I/T ratio 0-0.16 0-0.16 0-0.16 0-0.14 0-0.12 0-0.12
I/T ratio>0.2 suggests sepsis
Lymphocyte 3.5-8.5 3-8 3-6 2-5 3.5-7 5.5-9
Monocyte 0.5-1.6 0.9-2 0.8-2 0.3-1 0.5-1.7 0.7-1.7
Eosinophil 0.2-2.2 0.1-2 0.1-2.2 0.2-1 0.2-1 0.3-0.8
PTT (s) 42.9±5.8 40.4±7.4
PT (s) 13±1.43 11.8±1.2

Haematological values –Preterm infants<1500g

Day 1 Day3 D12-14 D24-26 D40-42
Hb (g/dL) 16.5-21.7 11.6-19.3 10.8-18.4 8.9-16.5 7.9-14.9
Hct (%) 52-69 36-59 32-55 27-50 24-47
Rbc (x1012/L) 3.87-5.76 3.3-4.9 3-5.2 2.6-4.8 2.5-4.6
MCV (fl) 112-144.5
Platelets (x109/L) 112-380 75-400 110-543 128-600 133-619
WBC (X109/L) 5-19 4-33.8 7.5-22.1 6.4-15.8 6.1-14.1
Total neutrophil 2-9 1-23.1 1.8-12.4 0.8-6.1 0.9-5.8
Neutropaenia in infants <1500g is<1.1x109/L
Immature neutrophil 0-1.1 0-1.4 0-1.3 0-0.6 0-0.5
I/T ratio 0-0.16 0-0.16 0-0.16 0-0.14 0-0.12
Lymphocyte 2-5 1.5-4.5 4-8 4-8
Monocyte 0.4-1.5 0.3-1.3 0.8-1.8 0.7-1.5
Eosinophil 0.1-1.1 0.1-0.9 0.3-1.7 0.3-2.8
PTT (s) 27.5-79.4 26.9-62.5

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PI (s) 10.6-16.2 10-13.6

161