Aukland Newborn Guideline PDF

Home | Contact Us | Phone Directory | Search
● Clinical Guidelines are listed alphabetically.

❍ Titles without an underline are not yet available online, or have been withdrawn.
● If you are looking for a specific topic and cannot find it in the list below, click here to open the search page.
● Paediatric Resources (Starship)

● aA Ratio ● Gestation-Based Flow Sheet (intranet only)
● AaDO2 calculator (now only available via NICU ● Parenteral nutrition
database) ● Parenteral nutrition worksheet
● Abbreviations in use in Newborn ● Gestational Age Calculator
for individualised solutions
Services ● Glucose calculator
Granulocyte transfusion
● Parent Infant Nursery
● Acute Fatty Liver of Pregnancy - ●
● Parvovirus
Investigation of Infants
● Patent ductus arteriosus
● Admission Rates to NICU and
● Percutaneous Central Venous
Respiratory Support
Catheter Insertion
Requirements
● Perinatal asphyxia
● Admissions & Discharges from
(links to the Neonatal
NICU/SCBU encephalopathy guideline)
● Admissions from Home ● Periventricular leukomalacia
● Adoption procedure ● Persistent Pulmonary Hypertension
(intranet link to ADHB policy) of the Newborn (PPHN)
● Albumin ● Phototherapy
❍ Albumex TM4
● Chest physiotherapy
❍ Albumex TM20
● Haematological Disorders in the ● Physiotherapy
● Alcohol in Pregnancy ● Plasma
Neonate
● Ambiguous Genitalia ● Plastic wrap of babies <30 weeks
● Haematology values
● Anaesthetic and Self Inflating Bags ● Platelets
- Laerdal ● Handling small babies
❍ Platelet concentrates
● Analgesia for Simple Procedures ● Head Cooling following ● Pneumothorax and Underwater
● Ankyloglossia Perinatal Asphyxia Sealed Drainage
● Antenatal Doppler ● Head ultrasound scans
● Postnatal ward care
● Antenatally Diagnosed Congenital ● HELLP Syndrome - ● Postnatal ward obstetric care
Heart Disease Investigation of Infants ● Prevention of hypothermia in infants
● Antenatally Diagnosed Renal Tract Hepatitis B Vaccination
● <30 weeks gestation
Anomalies Hepatitis C
● ● Prolonged and Late-Onset Jaundice
● Anticonvulsant use in pregnancy
❍ Hepatitis C - Nursing
● Antimicrobial therapy
Care
● Apnoea monitoring (Home)
● Apnoea monitoring and caffeine
● High Frequency Ventilation
● Assignment of Consultant in Charge ● High Risk Deliveries
of Infants ● Human Immunodeficiency Virus
● Auditory testing ❍ HIV - Nursing Care of
Babies
● Humidification
● Hydrops
● Hyperglycaemia
● Hyperkalaemia
● Hypertension
● Hypoglycaemia ● Radiology Requirements in
● Hypospadias NICU
● Baby Safety ● Hypotension ● Red Blood Cell Transfusions
● Back to Sleep ● Hypotonia ● Renal Tract Anomalies
(intranet only) ● Hypoxic Ischaemic ● Respiratory Indices Calculator
● Bilious vomiting Encephalopathy ● Reticulocytes
● Blood Products ● Retinopathy of Prematurity
❍ Red Cells ● ROP Screening Form
❍ Immunoglobulin (Intranet only)
❍ Platelets ● Rotavirus
❍ Albumin (TM4 and TM20)
❍ FFP
❍ Buffy Coat
❍ Cryoprecipitate
● Blood Pressure
❍ Hypotension ● Immunisations
❍ Hypertension Immunisation of Preterm Infants
Immunoglobulin ● SARS
● Blood sampling ●
Infant of Diabetic Mothers (Severe Acute Respiratory

● Borderline viability ●
INIS Study Syndrome)

● Breast milk additives and ●
Intracranial Haemorrhage ● Seizures

handling of formula ●
Intravascular catheters ● Sepsis

● BRM2 Monitor ●
Intravenous cannulation ● Single Umbilical Artery

● Budesonide ●
● Buffy Coat Concentrates ● Intravenous and Medication ● Skeletal Surveys

Certification ● Skin Care ELBW (<1000g)
● Intravenous Drug Compatibility and VLBW (<1500g) Babies
● Small-for-Gestational Age
● Intravenous Nutrition
Infants
● Intravenous nutrition -
● Solid foods for Premature Infants
individualised prescription
(58KB pdf file)
worksheet
● Caloric Calculator ● Specialist Responsibilities
● Intraventricular haemorrhage
● Capillary Blood Sampling ● Spina bifida and
● Intubation
● Care map for infants <32 weeks meningomyelocoele
● Isolation
gestation ● Sucrose Analgesia
● Chickenpox ● Suctioning
● Child Development Services ● Surfactant
❍ Surfactant on Level 2
(Community)
This link opens the fax referral ● Surgical Guidelines
form. For information on criteria for ● Surgical Neonates
referral, click here ● Survival statistics
● Child Development Unit (borderline viability guideline)
● Cleft Lip and Palate
● CLD review
Chronic Lung Disease Discharge ● Jaundice
❍ Jaundice on the
● Collapsed ventilated baby
● Complementary and alternative Postnatal Ward
medicine (CAM) ● Jehovah's Witnesses and Blood
● Congenital Heart Disease
(Antenatally Diagnosed)
● Congenital Heart Disease -
Screening of First Degree
Relatives
● Congenital infection
● Conjugated hyperbilirubinaemia ● Laboratory tests ● Thermal environment
● Conjunctivitis ● Large-for-Gestational Age ● Thrombocytopenia
● Consent Infants (see also Neonatal Alloimmune
● Continuous Positive Airway ● Life Support Withdrawal Thrombocytopenia)
Pressure (CPAP) ● Longline Insertion ● Thyroid disorders (maternal)
● Coroner's Act 1951 ● Tongue-Tie
● Cranial ultrasound scans ● Top up transfusion readmissions
● CRP (C-Reactive Protein) ● TORCH infections
● Cryoprecipitate ● Trainee interns
● Cytogenetics ● Transfer of Infants to the
● Cytomegalovirus ● Meconium stained liquor Postnatal Ward after Brief
● Metoclopramide (Maxolon) and Admission to NICU
Breastfeeding ● Transfers
● Metabolic Bone Disease ● Transfusion Handbook
● Metabolic disorders ● Transport and retrieval
● Metabolic screening Transports
● Milk - Drugs in Breast milk
(links to MedSafe website)
● Multiple Birth Association
● Death on NICU
● Ultrasound scans (cranial)
● Delivery attendance
● Umbilical Catheter Insertion
● Developmental care
● Urinary Catheterisation of the
● Developmental paediatric
Newborn
service
● Urine Measurement & Urinalysis
● Developmental Therapists
● Urine sampling
● Dexamethasone for CLD
● Dietitian referral
● Discharge summaries
● Documentation on NICU
● Domperidone as a Galactogogue
(Domperidone and
Breastfeeding)
● Down Syndrome
● Drug dependant mothers
● Narcotic depression ● Vaccinations

● Nappy rash ● Vascular Malformation Clinic
● Neonatal Alloimmune ● Ventricular Reservoirs
Thrombocytopenia ● Visiting therapy
(NAIT) ● Vitamin K
● Neonatal Encephalopathy
● Neonatal Nutrition
(links to ADHB Nutrition Services
● ECG
Intranet site)
● ECMO
● Nephrocalcinosis
(Extracorporeal Membrane
● Neural Tube Defects
Oxygenation)
● Newborn Examination ● Weighing Babies
● Environmental and
● NICU Nutrition Guidelines ● Weight Conversion Calculator
Developmental Care
● Nitric Oxide (Kilos-to-Pounds and Pounds-to-
● Exchange transfusion
Kilos)
● Withholding feeds
● Feeding
● Feeding and Nutritional
guidelines ● Operating Room Issues for
Neonatal Staff ● Zinc deficiency
● Feeding on postnatal wards
● Fetal Alcohol Syndrome ● Orthopaedic problems
Alcohol in Pregnancy ● Osteopenia of prematurity
● Fluid and electrolytes ● Oxygen therapy and monitoring
● Fluid and electrolyte calculator ● Oxygen therapy standing orders
● Follow-up ● Oxygen Saturation Targets
● Forms (intranet only) ● Oxygen - low flow calculator
❍ Exchange transfusion results ● Home oxygen
❍ Exchange transfusion record ● Oxygenation Index Calculator
❍ Telephone advice sheet
● Formula Handling and Breast
Milk Additives
● Fractional Excretion of Sodium
● Fresh Frozen Plasma
● Drugs are indexed alphabetically by their generic name. Trade names are included for user reference.
● Some of the drugs listed below do not have protocols available. This is either because they have been withdrawn (in
which case, hard copies are available through Carl Kuschel) or because protocols are currently under construction.
Those without protocols are not underlined.
Generic Trade Generic Trade Generic Trade
Acyclovir Zovirax IV Erythromycin EES Pancuronium Pancuronium

sodium ethylsuccinate bromide bromide
Adenosine Adenocor Erythromycin Erythromycin DBL Paracetamol Panadol,
lactobionate Pamol
Adrenaline Adrenaline Erythropoietin Recormon , Paraldehyde Paraldehyde
hydrochloride (Recombinant Exprex, Epoetin
Human)
Amikacin Amikin Phenobarbitone Gardenal
sulphate sodium sodium
Amiloride Midamor Fentanyl citrate Sublimaze Phenylephrine Metaoxedrine
hydrochloride
Aminophylline Aminophylline Ferrous gluconate Fergon Phenytoin sodium Dilantin
Amiodarone Cordarone X Ferrous sulphate Ferro-liquid Phytomenadione Vitamin K,
hydrochloride Konakion
Amoxycillin Ibiamox Flucloxacillin Floxapen, Piperacillin sodium Pipril
sodium Flucloxin
Amphotericin B Fungizone Fluconazole Diflucan Poractant alpha Curosurf
Atropine Atropine Flucytosine Alcobon Potassium chloride Potassium
sulphate
Frusemide Frusemide DBL, Propranolol Inderal
Lasix hydrochloride
Benzylpenicillin Crystapen, Prostaglandin E1 Paediatric
Penicillin (Alprostadil) Prostin VR
Sodium
Biochemie
Beractant Survanta Gaviscon Gaviscon Pyridoxine Vitamin B6
hydrochloride
Budesonide Pulmicort Gentamicin Gentamicin DBL
sulphate
Glucagon Glucagen hypokit Ranitidine Zantac
hydrochloride
Caffeine Caffeine Rifampicin Rifampin
Calcium Calcium Heparin sodium Heparin
gluconate gluconate
Carbamazepine Tegretol Hydrochlorothiazide Hydrochlorothiazide Salbutamol Ventolin,
Respax
Cefaclor Ceclor Hydrocortisone Solu-cortef Sodium bicarbonate Sodium
sodium succinate bicarbonate
Cefotaxime Claforan Sodium Chloride Sodium
sodium Infusion Chloride
(links to fluid
guideline)
Cefoxitin Mefoxin Ibuprofen Brufen Sodium Intal
sodium cromoglycate
Ceftazadime Fortum Imipenem / Primaxin Sodium nitroprusside Nipride
pentahydrate Cilastatin sodium dihydrate (DBL)
Ceftriaxone Rocephin Indomethacin Indocid Sodium polystyrene Resonium A
disodium sulphonate
Cefuroxime Zinacef Insulin (neutral) Actrapid penfill Sotalol hydrochloride Sotacor
sodium
Cephalothin Keflin Intralipid 20% Intralipid Spironolactone Aldactone
Chloral Hydrate Ipratropium Atrovent Sucrose 66.7% Syrup BP
bromide (Medical Guideline)
Chloramphenicol Chloromycetin Isoprenaline Isoproterenol, Suxamethonium Ethicholine
sodium hydrochloride Isuprel chloride
succinate
Chlorothiazide Chlorothiazide
Chlorpromazine Largactil Lignocaine Xylocaine Thiopentone sodium Pentothal
hydrochloride
Cisapride Prepulsid Ticarcillin disodium Tarcil
Clonazepam Rivotril Magnesium Magnesium Tolazoline Priscoline
sulphate hydrochloride
Cotrimoxazole Meropenem Merrem Trichloroacetaldehyde Chloral hydrate
(links to HIV hydrate
guideline)
Cyclopentolate Cyclogyl Metoclopramide Maxolon Tromethamine THAM
hydrochloride hydrochloride
Metronidazole Metronidazole
(Baxter)
Dexamethasone Dexamethasone Miconazole Daktarin Urokinase Ukidan
sodium DBL,
phosphate Decadron
Diazepam Valium Midazolam Hypnovel
Diazoxide Hyperstat Morphine Morphine Vancomycin Vancocin CP
(Oral)
Digoxin Lanoxin Morphine sulphate Morphine Vitadol C Vitadol C
(IV)
Dobutamine Dobutrex Vitamin K Konakion
hydrochloride (Phytomenadione)
Dopamine Dopamin Naloxone Narcan
Doxapram Dopram Neostigmine Neostigmine
methylsulphate
Nestargel Nestargel
Netilmicin sulphate Netromycin
Nitric oxide Nitric oxide
Nitroprusside Nipride
Noradrenaline Levophed
Nystatin Mycostatin, Nilstat
Last edited Monday, 09 January 2006
Newborn Services Clinical Guideline
Note: The electronic version of this guideline is the version currently in use.
Any printed version can not be assumed to be current. Printed copies of this document are valid for Sunday, May 21,
2006.
The general disclaimer regarding use of Newborn Services Guidelines and Protocols applies to this guideline.
Respiratory Indices Calculator

Reviewed by Carl Kuschel
Oxygenation Index (OI)

Ventilation Index (VI)
September
Arterial Alveolar Ratio (aA Ratio) 2005
Alveolar Arterial Oxygen Difference (AaDO2)
Respiratory indices have two main uses:
● Eligibility for determining a eligibility for a treatment (for example, OI for ECMO) or research
intervention (for example, AaDO2 for the LessMAS trial)
● Research or audit purposes when evaluating the amount of respiratory support required for
individual babies, particularly when making comparisons between differing levels of support
that an infant may require.
● All calculations are performed using mmHg.

Blood If you choose kPa, the values will be converted to
gas units: -Choose- mmHg
% 100
%
inspired
oxygen
PaO2
PaCO2
Ventilation Choose ventilation

mode
Calculate Reset
Any printed version can not be assumed to be current. Printed copies of this document are valid for Sunday,
May 21, 2006.
The general disclaimer regarding use of Newborn Services Guidelines and Protocols applies to this
guideline.
Abbreviations in Use in Newborn Services Reviewed by Charge Nurse -

Newborn and Carl Kuschel
July
2004
Introduction
● The following list is an accepted list of abbreviations that can be used in

documentation within the Newborn Service at National Women’s Health.
A-M N-Z
A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
AB Apex beat N10 Newborn intravenous

nutrition 10% dextrose
ABG Arterial blood gas Na+ Sodium

AGA Appropriate for gestational NaHCO3 Sodium bicarbonate
age
AMSIS Auckland Maternity Service NBF Neville Barnes forceps
Information System
APH Antepartum haemorrhage NBM Nil by mouth
ARM Artificial rupture of NEC Necrotising enterocolitis
membranes
ASD Atrial septal defect NG Nasogastric
AXR Abdominal x-ray NICU Newborn intensive care unit
BE Base excess NIF National Women’s infant
formula
BP Blood pressure NO Nitric oxide
BPD Bronchopulmonary dysplasia NO2 Nitrogen dioxide
BW Birthweight NND Neonatal death
Ca++ Calcium NP Nasophargyneal
CCN Clinical Charge Nurse N.PR Nasal prongs
CDH Congenital diahragmatic NSA Normal serum albumin
hernia
CHD Congenital heart disease NVD Normal vaginal delivery
CLD Chronic lung disease OA On admission
CMV Cytomegalovirus OG Orogastric
CNC Clinical Nurse Consultant OT Operating theatre
CO2 Carbon dioxide OTT Orotracheal tube
CPAP Continuous positive airway P5 Premature baby intravenous
pressure nutrition 5% dextrose
CVL Central venous line P7.5 Premature baby intravenous
nutrition 7.5% dextrose
CVP Central venous pressure P10 Premature baby intravenous
nutrition 10% dextrose
CXR Chest x-ray PaCO2 Partial pressure arterial
carbon dioxide
D5W Dextrose 5% in water PaO2 Partial pressure arterial
oxygen
D10W Dextrose 10% in water Paw Mean airway pressure
DDH Developmental dysplasia of PDA Patent ductus arteriosus
the hips
DIC Disseminated intravascular PEEP Positive end expiratory
coagulation pressure
DU Delivery unit PIE Pulmonary interstitial
emphysema
EBM Expressed Breast Milk PIN Parent Infant Nursery
ECG Electrocardiogram PIP Peak inspiratory pressure
EDD Estimated date of delivery PINSP Peak inspiratory pressure
EEG Electro-encephalogram PPH Postpartum haemorrhage
ELBW Extremely low birthweight PPHN Persistent pulmonary
hypertension of the newborn
ET Expiratory time PPROM Prelabour premature rupture
of the membranes
ETA Estimated time of arrival PROM Prolonged rupture of

membranes
ETT Endotracheal tube PSV Pressure support ventilation
FAS Fetal alcohol syndrome PTU Phototherapy unit
FEBM Fortified expressed breast PVH Periventricular haemorrhage
milk
FDP Freeze dried plasma PVL or Periventricular leucomalacia
PVLM
FFP Fresh frozen plasma RDS Respiratory distress
syndrome
FH Fetal heart Resp Respiration
FiO2 Fraction of inspired oxygen RHT Radiant heat table
FLN Family Liaison Nurse ROP Retinopathy of prematurity
FLP Fresh lyophilised plasma RSV Respiratory synctival virus
FRC Functional residual capacity RV Residual volume
GPH Gestational proteinuria & SpO2 Oxygen saturation
hypertension
HFOV High frequency oscillatory SBR Serum bilirubin
ventilation
HIE Hypoxic ischaemic SGA Small for gestational age
encephalopathy
HMD Hyaline membrane disease SIMV Synchronised IMV
HPU Has passed urine SIPPV Synchronised IPPV

HR Heart rate SFD Small for dates
IA Intra-arterial SLE Systemic lupus erythematosis
ICP Intracranial pressure SRM Spontaneous rupture of
membranes
IDM Infant of diabetic mother SVD Spontaneous vaginal delivery
IDDM Insulin dependent diabetes T or Temp Temperature
mellitus
IE Ratio Inspiratory/expiratory ratio TAPVD Total anomalous pulmonary
venous drainage
IFD Intermediate fetal death TBW Total body water
IMV Intermittent mandatory TCM Transcutaneous monitoring
ventilation
Inc Incubator TE Expiratory Time
IPPV Intermittent positive pressure TGA Transposition of the great
ventilation vessels
IT Inspiratory time TI Inspiratory Time
IUCD Intrauterine contraceptive TLC Total lung capacity
device
IUD Intrauterine death Tet Tetralogy of Fallot
IUGR Intrauterine growth restriction TOF Tracheal oesophageal fistula
IV Intravenous TTN Transient tachypnoea of the
newborn
IVH Intraventricular haemorrhage TV Tidal volume
IVN Intravenous nutrition UAC Umbilical arterial catheter
IWL Insensible water loss UVC Umbilical venous catheter
K+ Potassium VC Vital capacity
KCL Potassium chloride VG Volume Guarantee
LBW Low birthweight VLBW Very low birthweight
LFT Liver function test V/Q Ventilation perfusion
LGA Large for gestational age VSD Ventricular septal defect
LMP Last menstrual period VT Tidal Volume
LP Lumbar puncture Vx Vertex
LSCS Lower segment caesarean ZIG Zoster immune globulin
section
MAP Mean arterial pressure
MAS Meconium aspiration
syndrome
Mec Meconium
Mv Minute volume
May 21, 2006.
guideline.
Investigation of Infants born to Mothers with HELLP Reviewed by Carl Kuschel,

Syndrome and Acute Fatty Liver of Pregnancy Callum Wilson (Metabolic
Paediatrician), and Dianne
Webster (National Testing Centre)
August
2001
Introduction
An association has been demonstrated between long chain 3-hydroxyacyl-CoA-

dehydrogenase (LCHAD) deficiency and maternal HELLP (Haemolysis, Elevated Liver
enzymes, Low Platelets) and AFLP (Acute Fatty Liver of Pregnancy). This inherited,
autosomal recessive abnormality of fatty acid oxidation can result in significant morbidity
and mortality in infants if untreated. Treatment with dietary manipulation is possible.
Approximately 80% of infants with LCHAD diagnosed in childhood have been born after
pregnancies complicated by AFLP or HELLP. However, what is not known is how many
pregnancies complicated by AFLP or HELLP result in infants with LCHAD deficiency.
In view of the association, and the implications of detecting this condition early and
providing appropriate dietary and genetic advice, we recommend the following:
Guidelines for Screening
In pregnancies complicated by the HELLP syndrome or AFLP,
● Take the Newborn Screening Card at the usual time

● Send a specific lab form request with the screening card requesting Acylcarnitine
levels for detection of possible LCHAD deficiency.
● This will be processed by the National Testing Centre laboratory
A thorough family history is important. Infants should be observed for hypoglycaemia in

the early newborn period.
● If babies are symptomatic and LCHAD is considered a likely diagnosis, requests

should be marked as urgent.
Discuss with Dr Callum Wilson, Metabolic Paediatrician, if there are any clinical concerns.
References
1 Ibdah JA, Yang Z, Bennett MJ. Liver disease in pregnancy and fetal fatty acid oxidation defects. Molecular
Genetics and Metabolism 2000; 71:182-9.
2 Ibdah JA, Bennett MJ, Rinaldo P, et al. A fetal fatty-acid oxidation disorder as a cause of liver disease in
pregnant women. N Engl J Med 1999; 340:1723-31.
Any printed version can not be assumed to be current. Printed copies of this document are valid for Sunday, May 21, 2006.
Admission Rates to NICU and Type of Respiratory Support Reviewed by David Knight and Carl
Required Kuschel
April
2003
Admission Rates and Support for all Babies Admission Rates and Support for babies 35-42 weeks
This guideline provides some data regarding admission rates by gestation, as well as the level of
respiratory support required.
● This information may be valuable when discussing anticipated neonatal care with parents who are
expecting a baby.
● Note that the figures include all babies, including those known before birth to have problems.
● Refer also to the Borderline Viability Guideline for information on infants 30 weeks gestation and
below.
Summary data are presented for the years 1999 and 2000. Further data will be added as available.
NICU Admission Rates and Respiratory Support for All Babies Born at NWH
NICU Admission Rates and Respiratory Support for Infants 35-42 weeks
May 21, 2006.
guideline.
Guidelines for Admissions to NICU, and Discharges Reviewed by Carl Kuschel

and Transfers from NICU
December
2005
Discharge of Low Transfers to and from Level

Admissions Discharge Documentation
Birthweight Infants 2 and PIN
Admissions
Guidelines for Admission to 1. Birthweight less than 1250g.

Level 3 2. Gestation less than 30 weeks. Some infants born
at 30-32 weeks may be admitted to Level 3
because of staffing acuity.
3. Requirement for intermittent positive pressure
ventilation.
4. Requirement for an exchange transfusion.
5. Any other baby whose clinical condition is such
that they cannot be appropriately cared for in
Level 2.
Guidelines for Admission to 1. Low Birthweight - under 2500g.

Level 2 Some babies between 2000 and 2500g may be
able to go directly to the postnatal ward.
This will depend upon the clinical assessment of
the baby and whether the postnatal ward is
deemed likely to provide an appropriate level of
care or not.
2. Prematurity - 36 weeks gestation or less.
For babies between 35 and 36 weeks gestation,
criteria as in (1) apply.
3. Infection - suspicion of infection together with
clinical concern.
4. Respiratory problems
(a) Apnoea or cyanotic episodes.
(b) Any respiratory distress causing concern.
(c) Persisting signs of respiratory distress for more
than one hour.
5. Gastrointestinal problems
(a) Feeding problems severe enough to cause
clinical concern.
(b) Bile stained vomiting, or other signs
suggesting bowel obstruction.
6. Metabolic problems
Inability to maintain a serum glucose
concentration greater than or equal to 2.6mmol/L
despite adequate feeding.
7. CNS problems
(a) Convulsion.
(b) Moderate birth asphyxia, which may require
monitoring for an initial period to ensure problems
do not ensue.
8. Malformations
Congenital anomalies that may require
intervention unavailable on the postnatal wards, or
an initial period of observation, eg Pierre Robin
Syndrome.
9. Cardiovascular
Problems requiring monitoring or intervention
unavailable on the postnatal wards.
10. Miscellaneous
Any baby that is causing concern to such a
degree that the attending doctor or NS-ANP feels
that the baby requires observation or treatment in
Level 2. It is better for a baby to be admitted
unnecessarily than for a baby requiring admission
to be left on the ward.
11. Social issues/terminal care
Such babies ideally be nursed on the ward with
parents, or at home. On occasions (after
multidisciplinary consultation) circumstances
dictate that these babies require a period of care
on Level 2.
Discharge of Low Birthweight Infants
Infants that have been born at very low birthweight or low birthweight, represent an at risk
group of children. Increasingly they are being discharged home at a weight less than
2.5kg. The following guidelines are suggested when considering discharge of such infants.
1. The baby has to be gaining weight - it doesn't have to have reached any
particular weight, however, as long as there is weight gain.
2. The baby has to be sucking all feeds.
If breast feeding is being established, it is not a prerequisite that the baby is on full
breast feeding prior to discharge, provided we are happy that the baby is able to
suck strongly.
However we must be sure that the mothers are aware of the need to continue to
monitor progress once further feeding changes are made at home, i.e. a switch
from complementing to fully breast feeding etc.
3. The baby must be able to maintain his or her temperature in a cot in a normal
household environmental temperature.
This is particularly important when discharging low birthweight babies home in the
winter.
4. Parents must be willing and happy to take the baby home and to have
demonstrated that they have adequate parenting skills.
This may be self-evident, particularly when there have been other children in the
family, although not always.
5. Some basic information should be known about the home environment and the
community to which the infant is going, i.e. if they are living in a remote area in a
caravan, then one would be less likely to effect a discharge home at a low
birthweight.
6. There should be adequate community follow up services available.
It may be appropriate to contact the general practitioner by telephone to discuss
follow up.
In remote areas details should be known about the availability of a Well Child
Service visiting.
The neonatal home care nurses will be able to provide some initial support and
follow up and to provide liaison for ongoing community follow up.
Transfers & Discharges from NICU and PIN
Transfers from Level 3
● For transfers from Level 3 to Level 2 or PIN a formal transfer should occur
between Level 3 Registrar or NS-ANP and the appropriate registrar or NS-ANP.
● Ideally the parents would have been told a few days in advance to accustom to the
transfer and possibly have looked around Level 2 or PIN.
● A transfer letter should be in the notes (and should also be sent to the LMC/GP).
● The problem list should be up-to-date (as should happen when a discharge/
transfer summary is prepared)
For infants discharged from Level 2
● Babies transferred to PIN need a formal letter if they have had a complicated
course whilst in Level 2. If they have had a recent transfer summary from Level 3
to Level 2, this may not be necessary.
❍ Babies who are transferred to PIN should have an up-to-date problem
summary in the notes.

● Babies transferred to other hospitals must not go without a registrar or NS-ANP
letter.
● Babies being transferred to towns outside the Auckland area should have a formal
letter prior to discharge.
Discharge Documentation
All patients discharged from hospital must have:
● A full examination record on the appropriate form (include age in days, weight,
length, head circumference).
● A plan for follow up clearly documented in the case notes.
● A record of any prescribed therapy.
Discharge Letters
● No baby is to be discharged from Level 3, Level 2, or PIN without a letter.

● For babies who are being discharged to the postnatal wards and where there are
going to be delays in generating a discharge letter, the baby can be discharged
with out a letter being available. However, it is the responsibility of the resident
team (registrar or NS-ANP) to ensure that a letter is completed as soon as
possible and is filed in the notes of the baby.
● PLEASE ENSURE that the discharge letter contains the correct information.
❍ The database can only use the information available within it.
❍ It provides a structure for the letter, and makes an attempt at providing a
letter that is nearly complete. You need to check the letter you have
produced and edit it in Word.
● The quality of the letters you sign your name to reflects on your abilities as well as
the quality of the care that the baby has received in NICU. PLEASE CHECK AND
EDIT THE LETTERS BEFORE YOU SIGN THEM AND SEND THEM OFF.
May 21, 2006.
guideline.
Guidelines on Admission to NICU from Home Reviewed by Simon Rowley

(Home Delivery or Early Discharge)
December
2000
The following guidelines cover admissions to the Neonatal Unit for babies who have been
delivered at home, have been discharged early or recently from NICU/PIN, and in whom
problems arise.
The general principles are:
1 Ideally babies admitted should be isolated, nursed in incubators or single room.

2 All home births under 48 hours of age can be considered for admission.
3 Some home births, early discharges and recent NICU/PIN discharges between
48 hours and 1 week, can be considered.
4 Few babies over 1 week of age, or discharged home > 1 week, would qualify for
admission.
a: Those needing specific neonatal expertise, e.g.:
● Low birthweight (including recent NICU/PIN discharge).

● Birth asphyxia, or convulsions in first 48 hours.
● Early onset respiratory distress (48 hours).
● Meconium aspiration syndrome.
● Jaundice requiring phototherapy or exchange transfusion.
b: Those infants requiring expertise likely to be more appropriately managed at

other institutions, should be referred accordingly, eg:
● Congenital heart disease or severe cyanosis in the absence of other

respiratory symptoms – Green Lane Hospital.
● Congenital malformations requiring assessment – Starship Hospital.
● Obvious surgical problems – Starship Hospital.
c: Infants with problems that appear infectious and particularly in which isolation
will be a priority, should be directed to Starship Hospital, e.g. respiratory viral
infections, apnoea – bronchiolitis, gastro-enteritis and Herpes virus infection.
d: Infants less than 1 week of age with feeding difficulties. In this situation having
mother and baby together is a priority and therefore the options should be:
● Mother and baby admitted to a postnatal ward at National Women’s

Hospital (baby sounds well).
● Admission to Starship Hospital where mothercraft can be facilitated
(sounds like sepsis or other pathology likely)
A yellow card (detailing perinatal history) is preferred.

May 21, 2006.
guideline.
Albumex TM4 Authorised by Charge Nurse -

Newborn
April
2006
Albumex TM4 Parental Consent Prescribing Dose

Checking, Administration,
Ordering Storage Monitoring and Adverse Reactions
Documentation
Albumex TM4
● Available in two sizes - 500ml and 50ml.

❍ In NICU we usually use the 50ml size.
● 4% albumin is free of risk of transmission of known viral diseases (heat

inactivated).
Parental Consent
● Informed consent required.

● Parent signs on Agreement to Treatment Forms (CR0111).
Prescribing of Albumex TM4
● Prescribed on the blood transfusion/IV fluid chart (CR5541).
Dose
● 10-20mls/kg.
Ordering
● On NZBS requisition form (111F01802)
Storage
● Once opened use immediately as the product contains no antimicrobial
agent.
● Should be straw colour. Should not be cloudy.
Checking, Administration, Monitoring, and Documentation
● As for blood and blood products.

● Checking
● Administration
● Monitoring
● Documentation
Adverse Reactions
● See Transfusion Reactions.

May 21, 2006.
guideline.
Albumex TM20 Authorised by Charge Nurse -

Newborn
April
2006
Albumex TM20 Parental Consent Prescribing Ordering

Monitoring and Adverse Reactions
Documentation
Albumex TM20
● Albumex TM20 is free of the risk of infectious disease as it is heat inactivated.

● Albumex TM20 comes in two sizes - 10ml and 100ml and is made from large pools
of New Zealand donor plasma. It is used for babies with low protein and oedema.
● Request 100ml volume as 10ml ampoule is too small to filter using blood filter
giving set.
● Can be utilised 2 ways:
❍ As a volume expander like TM4.
Must be diluted - 1 part to 4 parts of 0.9% sodium chloride.

❍ To draw fluid out of the tissues.
Albumex TM20 draws 4 volumes of fluid from the extra cellular fluid into the
circulation.
Thus, 20ml of Albumex TM20 results in approximately 80ml increase in the
circulating volume.
This can cause volume overload, particularly in the presence of renal failure.
It should be given undiluted over 1 hour (approximately). 2gm in 10ml is
equal to 40ml Albumex TM4.
● Once the bottle is opened it must be used straight away.
Parental Consent

Prescribing of Albumex TM20

● Prescribed on the blood transfusion/IV fluid cart (CR5541).
Ordering
● On NZBS requisition form (111F01802).
Checking, Administration, Monitoring and Documentation

● Checking
● Administration
● Monitoring
● Documentation
Adverse Reactions
● See Transfusion Reactions

May 21, 2006.
guideline.
Alcohol in Pregnancy Reviewed by Simon Rowley
December
2000
Management of the Neonate whose Mother has been Using or Abusing

Alcohol During Pregnancy
1. These infants are at risk of Fetal Alcohol Syndrome or Fetal Alcohol Effect.
Fetal Alcohol Syndrome is difficult to diagnose in the newborn period.
2. They are also at risk of withdrawal particularly if the mothers are drinking alcohol
during labour and delivery.
3. There is also the risk of respiratory depression in these circumstances.
● Paediatric attendance is recommended at delivery. The initial assessment should

include careful head, length and body weight measurements and any dysmorphic
features should be noted. The baby would normally be able to go to the postnatal
ward with the mother.
● Urine toxicology is recommended (there may be polydrug abuse).
● Consider using a drug withdrawal nursing chart as for narcotic withdrawal.
● Paediatric Consultant review should be arranged non-urgently.
❍ Drs Simon Rowley and Carl Kuschel are the specialists who primarily
evaluate these infants in the newborn period.
Follow Up Arrangements
These may need to be in conjunction with Social Services if already involved. Social work
evaluation is usually required to look at child protection issues. Referral of mother to a
detoxification programme may be appropriate.
● Paediatric Clinic at four months of age and at one year.

● Parents should be made aware of potential late effects of alcohol, e.g. attention
difficulties and where to seek help if concerned.
More protracted follow up although desirable, is probably not practical.
If neurodevelopmental problems are evident, then appropriate referral to Child

Development Services should be made.
May 21, 2006.
guideline.
Ambiguous Genitalia in the Newborn Reviewed by Carl Kuschel and

Initial Assessment and Investigation Wayne Cutfield (Paediatric
Endocrinology)
July
2003
Aetiology History Physical Examination Investigations Management
The neonate presenting with ambiguous genitalia should be treated as an emergency as

underlying causes, such as Congenital Adrenal Hyperplasia (CAH) can be life-
threatening. In addition, determination of gender is a primary concern for parents.
Aetiology
Virilised Females Feminised Males

Congenital Adrenal Hyperplasia Congenital Adrenal Hyperplasia
● 21-hydroxylase deficiency ● 3β-hydroxylase deficiency

● 11-hydroxylase deficiency
● 3β-hydroxylase deficiency
Chromosomal Abnormalities Partial Androgen Resistance

Syndromes
● XO/XY
● XX/XY ● 5 α-reductase deficiency
● Variants ● Partial androgen receptor
defects
Maternal Virilisation Defect in Testicular
Development
● Drug-induced
● Excessive androgen
production by mother
True Hermaphroditism True Hermaphroditism

Idiopathic Idiopathic
● Isolated ● Isolated
● Associated with midline ● Associated with midline
congenital anomalies congenital anomalies
History
● Drug ingestion during pregnancy?

● Any recent androgenic changes in the mother suggesting androgen excess?
● Are there few (or no) male offspring in families on mother's side?
● Any siblings dying in the newborn period?
● Any siblings with over-virilisation or precocious puberty?
● Any history of infection or exposure to teratogens?
Physical Examination
Although physical examination is useful, a diagnosis should not be made solely on

examination findings. However, the following information is useful in determining what
investigations are required.
● Are gonads palpable?

❍ 25% of infants with undescending testes and hypospadias have an intersex
disorder
❍ Gonads palpable in the perineum almost always indicate a male karyotype
● Is the penile length normal?

❍ Measure stretched length with a spatula from the symphysis pubis to the
stretched tip (not foreskin) of the penis

❍ Normal stretched length >3cm at term
❍ <2.5cm at term indicates a microphallus
❍ Is there reasonable penile girth on palpation?
❍ Is the phallus straight or is there chordee present?
● Where is the urethral opening?

● How fused are the labioscrotal folds?
● Is the scrotum hypoplastic?
● Is the anus normally sited?
● Are there any other physical abnormalities?
Investigations
● Chromosome analysis
● Pelvic/abdominal ultrasound scan to determine pelvic structures and the presence

or absence of gonads.
Uterine tissue excludes the presence of any testicular tissue in early gestation.
● 17-hydroxyprogesterone (newborn screening card for urgent 17OHP)
● Serum for Testosterone
● Serum electrolytes and glucose
Management
● Be careful with discussions with parents. Discuss with the specialist on call before
discussing specifics with parents.
❍ It is important to say that the baby has "unfinished genitalia" rather than to
talk about a penis or clitoris.

❍ Parents should be advised not to name the baby until the gender is known.
❍ Parents may choose to delay a birth notice and may wish to restrict visitors
until the gender has been assigned.

❍ Gender assignment is not dependent on what structures are present alone,
nor the karyotypic gender.

● Early referral to the Paediatric Endocrine Service after initial clinical evaluation.
❍ Surgical service involvement will be at the discretion of the Paediatric
Endocrine Service.
● Specific investigations and management will depend on the underlying cause.
May 21, 2006.
guideline.
Sucrose Analgesia for Simple Neonatal Procedures Created by Dr Mike Fernando

Reviewed by Dr Karen Munro,
Karen Anderson-Hawke, Bronwyn
Jones, Diane Saint, and Brenda
Hughes
Amended March 2004
(Consent guidelines changed)
Aim Criteria Administration Contraindications

Supporting Information Storage References
Aim
Neonates feel pain as intensely as adults. Oral Sucrose has been shown to be an
effective and safe treatment for reducing the pain response of neonates. A neonatal
admission will typically involve between 2 and several hundred painful procedures. The
aim is to reduce the discomfort caused by these procedures.
Criteria
Prior to any invasive procedure consideration should be made on how to minimize any
resulting pain. Painful procedures include but are not limited to venepuncture, peripheral
venous line placement, heel prick, arterial stab, and peripheral arterial line placement.
Ways to reduce pain can be through the use of pharmacological and non-
pharmacological measures. Non pharmacological measures include ensuring, where
possible, that the baby is calm, relaxed, warm, fed and that all necessary equipment for
the procedure is at hand. Once non-pharmacological measures have been implemented,
oral sucrose analgesia may be used in babies in Level II NICU and the Parent Infant
Nursery. Oral sucrose will not always eliminate all crying, but is known to significantly
reduce the physiological stress of pain.
Administration
● Dose: 0.2ml of a 66.7% Sucrose Solution (Syrup BP, 0.667g/ml).

● No more than 4 oral sucrose doses are to be administered in any 24 hour period.
● There is no minimum interval time between doses of oral sucrose.
Contraindications
● Neonates with known fructose intolerance.
● Neonates <1500g and <31 weeks postconceptional age.
● Lack of parental consent.
Supporting Information
● Parents should be advised that this procedure is to be used in hospital only. An

information leaflet is available.
● Consent is no longer required but information should be given to parents about the
use of sucrose, and this should be documented on the nursing care map.
Storage
● Oral Sucrose Solution (Syrup BP) should be stored in the refrigerator and
discarded one week after the bottle has been opened.
References
1 Stevens B, Yamada J, Ohlsson A. Sucrose analgesia in newborn infants undergoing painful procedures.
Cochrane Database of Systematic Reviews Issue 2, 2002.
2 Haouari N, Wood C, Griffiths G, Levene M.. The analgesic effect of sucrose in full term infants: a
randomized controlled trial. BMJ 1995; 310: 1498-1500.
3 Johnston CC, Filion F, Snider L,et al. Routine sucrose analgesia during the first week of life in neonates
younger than 31 weeks’ postconceptional age. Pediatrics 2002;110:523-528.
May 21, 2006.
guideline.
Ankyloglossia (Tongue-Tie) Reviewed by Simon Rowley, Carl

Kuschel, Lynley Nichols (Lactation
Consultant NICU), and Stuart
Ferguson (Paediatric Surgery)
December
2005
Diagnosis of Clinically Significant

Definition Incidence
Tongue-Tie
Assessment Management References
Definition
● The bottom of the tongue is tethered to the floor of the mouth by a membrane
(frenulum).
● This restricts the range of movements of the tongue.
● If the frenulum is too restrictive (tongue-tie, ankyloglossia), it may impact feeding,
speech, swallowing, and associated oral development problems.
Incidence
● Most reports give an incidence of 3-5%, although an incidence of up to 10% has

also been cited.
❍ Males are more commonly reported to be affected than females (1.5:1 to
2.6:1 ratio)
● Fewer than half of those infants identified as having a tongue-tie will require
intervention for symptoms.
Diagnosis of Clinically Significant Tongue-Tie
● Based on a combination of anatomical appearance and functional disturbance
Anatomical ● Type 1: Frenulum attaches to tip of

tongue in front of alveolar ridge in
low lip sulcus
● Type 2: Attaches 2-4mm behind
tongue tip and attaches on alveolar
ridge
● Type 3: Attaches to mid-tongue and

middle of floor of the mouth, usually
tighter and less elastic. The tip of
the tongue may appear “heart-
shaped”
● Type 4: Attaches against base of

tongue, is shiny, and is very inelastic
Functional disturbance ● Feeding difficulties

● Cannot initiate tongue grooving, cupping or depression
❍ Interferes with front-to-back peristalsis as well
as tongue palate synchronisation in breast

feeding
❍ May also adversely affect bottle feeding (rare)
● Older children may have difficulties with feeding (for

example, licking ice creams) or speech
Assessment
● There is no single reliable tool for assessment that adequately predicts the degree
of problems an individual infant will have. Staff familiar with the Hazelbaker
Assessment Tool For Lingual Frenulum Function (ATLFF) may wish to use this.
Physical examination ● Rule out thrush, clefts, and other defects including
neuromuscular conditions
● Range of motion of tongue and degree of extension
beyond lower dental ridge and lip
● Elevation to palate with mouth wide open
● Transverse movement of tongue without twisting of
the tongue
Maternal assessment ● Document degree of maternal nipple pain and nipple
skin erosion
● Painful breasts
● Low milk supply
● Plugged ducts
● Mastitis
● Untimely weaning
● Candida
Infant assessment ● Adequacy of latch and milk transfer

● Efficiency of bolus handling
● “Clicking” during feed due to loss of latch
● Sliding off breast
● Fatigue
● Irritability during/after feeding
● Poor weight gain (serial test weighs, supervised by a
senior team member, may be helpful)
Management
● Not all infants with tongue-tie will need any intervention other than good lactation
support.
● Assessment should be performed by a lactation consultant and/or speech
language therapist. If it is determined that the baby is likely to benefit from a
frenulotomy, this should be discussed with the specialist looking after the baby.
● Frenulotomy has been shown in prospective studies to improve feeding outcomes
and maternal symptoms in infants with significant ankyloglossia.
❍ Whilst some institutions undertake frenulotomy using sucrose analgesia,
local practice is to refer to a paediatric surgeon. Other institutions may

instead refer to ORL or plastic surgical services.
❍ Contact the paediatric surgical registrar on call and indicate that the infant
has a significant tongue-tie that is interfering with feeding.

❍ Frenulotomy should be performed within a few days of the referral being
made. The procedure will usually be performed under a light general
anaesthetic, using diathermy.
● All babies should have had Vitamin K administered at birth or at least 1 day prior to
the procedure.
● Post-operatively, babies will require a period of observation for at least 4 hours.
❍ Ex-premature infants should have a longer observation period in view of the
increased risk of apnoea.

● Paracetamol may be given as needed.
● If mothers are Hepatitis C positive, breast feeding should be postponed until the
wound has healed.
● Complications (such as excessive bleeding) are rare and should be documented
carefully.
References
1 Hall DMB, Renfrew MJ. Tongue tie. Arch Dis Child 2005;90;1211-5.
2 Messner AH. Lalakea ML. Aby J. Macmahon J. Bair E. Ankyloglossia: incidence and associated feeding
difficulties. Archives of Otolaryngology -- Head & Neck Surgery 2000;126:36-9.
3 Ballard JL, Auer CE, Khoury JC. Ankyloglossia: assessment, incidence, and effect of frenuloplasty on the
breastfeeding dyad. Pediatrics 2002;110:e63.
4 Ricke LA, Baker NJ, Madlon-Kay DJ, DeFor TA. Newborn tongue-tie: prevalence and effect on breast-
feeding. J Am Board of Family Practice 2005;18:1-7.
5 Hazelbaker AK. The assessment tool for lingual frenulum function (ATLFF): use in a lactation consultant
private practice [thesis]. Pasadena (CA): Pacific Oaks College; 1993
6 Amir LH, James JP, Beatty J. Review of tongue-tie release at a tertiary maternity hospital. J Paediatr Child
Health 2005;41:243-5.
7 Hogan M, Westcott C, Griffiths M. Randomized, controlled trial of division of tongue-tie in infants with
feeding problems. J Paediatr Child Health 2005;41:246-50.
8 Maternity and Neonatal Services, Women's Health Division, Canterbury DHB. Recognition, assessment
and ankyloglossia release and its impact on breastfeeding outcome: a quality-team initiative.
Doppler Studies in High Risk Pregnancies Reviewed by Associate Professor Lesley

McCowan (High Risk Maternity Service,
NWH)
February
2001
Background
Doppler ultrasound detects frequency shifts from moving targets (red blood cells). The flow velocity waveform
(FVW) which is produced is unique to the vessel being studied.
Flow velocity waveforms are analysed mathematically by creating a ratio of the systolic to diastolic frequencies.
The most common index in use at NWH is the resistance index (see figure 1).
Figure 1: Maximum frequency envelope of Doppler flow velocity waveform showing peak systolic frequency shift
(S) and end-diastolic frequency shift (D).
Umbilical Artery
In normal pregnancy, there is a progressive increase in end-diastolic velocity due to growth and dilatation of the
umbilical circulation. The resistance index therefore falls. A resistance index > 0.72 is outside the normal limits
from 26 weeks gestation onwards. In some pregnancies with fetal growth restriction and/or preeclampsia, there is
a reduction in the diastolic velocity and in severe cases as in c) and d) below, there is absent or reversed end
diastolic velocity.
Figure 2: Umbilical Doppler waveforms in healthy pregnancy and in pregnancies with fetal growth restriction.
These abnormal waveforms are associated with histological evidence of reduced numbers of small placental blood
vessels and therefore reflect "placental insufficiency". In pregnancies with reduced, absent or reversed end-
diastolic velocity, there is an increased risk of stillbirth, asphyxia, chromosomal and congenital abnormality.
Abnormal umbilical Doppler waveforms can be present for weeks before there is evidence of fetal compromise
and therefore are a marker of a high risk situation and should not normally be used in isolation as an indication for
delivery. However, most obstetricians would consider delivering a fetus with absent end-diastolic velocity from
about thirty two weeks gestation following administration of corticosteroids. In many instances, fetuses with absent
end-diastolic velocity would present much earlier in pregnancy and may require extremely preterm delivery.
Umbilical artery Doppler studies have been well evaluated in randomised controlled trials and use of umbilical
artery Doppler studies in small for gestation age pregnancies and in pregnancies with the preeclampsia is
associated with a 30% reduction in perinatal mortality (Cochrane Library 2000). The likely reason for the reduced
perinatal mortality is that the abnormal Doppler waveform highlights the at risk fetus who is then subject to more
frequent surveillance ultimately resulting in timely preterm delivery.
About two thirds of small gestational age fetuses have normal umbilical artery Doppler studies and are unlikely to
have histologic evidence of abnormal placental vascular development . These fetuses have a very low risk of
antenatal fetal compromise, have a low perinatal mortality, and do not normally require preterm delivery.
Uterine Artery Doppler Studies
Uterine artery Doppler studies reflect the resistance in the utero-placental circulation and have not been proven to
reduce perinatal morbidity or mortality. In conditions such as preeclampsia and fetal growth restriction abnormal
uterine artery Doppler studies indicate inadequate placentation and have been correlated with histological
evidence of defective replacement of spiral arteries by maternal trophoblast.
Figure 3:
Normal Uterine Artery Doppler Abnormal Uterine Artery Doppler
Abnormal uterine artery Doppler studies in the context of a growth restricted pregnancy suggest a maternal cause
for the growth restriction where as normal uterine artery Doppler studies suggest that a fetal cause of growth
restriction needs to be considered.
May 21, 2006.
guideline.
Antenatally Diagnosed Major Congenital Heart

Reviewed by Carl Kuschel, Tom
Disease Gentles (PCCS), and John Beca
Management at Delivery and in NICU (PICU)
May
2004
Immediate Delivery Room

Management in Labour Immediate Management in NICU
Management
Duct-dependent for Systemic Blood
Duct-dependent Cyanotic Lesions Rhythm Disturbances
Flow
See also the guideline on screening First Degree Relatives

See also the S.T.A.B.L.E. Cardiac module
National Women's Health acts as the primary delivery unit nationally for infants with an
antenatal diagnosis of major congenital heart disease who are likely to need surgical
intervention in the newborn period. A fetal cardiology service is provided by the Starship
Paediatric and Congenital Cardiology Service and in most instances the anatomical and
physiological lesion is able to be identified accurately prior to delivery.
The major cardiac lesions diagnosed antenatally can be generally divided into three
groups:
● Duct-dependent for systemic blood flow (e.g. Hypoplastic Left Heart Syndrome,
critical aortic stenosis, interrupted aortic arch).
● Duct-dependent cyanotic lesions (e.g. pulmonary atresia, transposition of the great
arteries)
● Rhythm disturbances (e.g. congenital heart block, fetal supraventricular
tachycardia)
Management in Labour
● A copy of the fetal echocardiography report(s), and Fetal Medicine Panel report if
applicable, should be obtained so accurate information is available.
● The obstetric service should notify the Level 3 neonatal registrar or NS-ANP
(pager 93-5535) that delivery is anticipated. The registrar or NS-ANP should
inform the neonatal unit clinical charge nurse and the neonatal specialist on duty
or on call.
● The paediatric cardiologist on call should be informed during normal working hours
if the mother is in labour or is going to be induced or electively delivered by
caesarean section.
● The paediatric cardiologist has usually already met with the parents to explain
what is planned post-delivery.
Immediate Delivery Room Management
● Most infants with major congenital heart disease will not require additional
resuscitation at birth and will be asymptomatic of their cardiac disease for hours or
days postnatally.
❍ An infant who is cyanosed and bradycardic at birth requires effective
resuscitation, and the cause of the cyanosis and bradycardia should

be assumed to be respiratory and not cardiac.
❍ Resuscitation measures may include the administration of oxygen and
positive pressure ventilation.

● Cardiac lesions that are responsible for an infant being in poor condition at birth
are rare (e.g. severe Ebstein's anomaly, or other cardiac conditions such as
arrhythmia, particularly if accompanied by fetal hydrops).
● Following resuscitation and assessment, the infant should be transferred to NICU
as soon as practical. The parents should be given the opportunity to hold their
baby if the baby's condition allows this.
Initial Management in NICU
Initial management will depend on the underlying cardiac lesion and the anticipated
neonatal problems.
● Infants should be admitted to Level 3 NICU.

● Cardiorespiratory and oxygen saturation monitoring should be commenced as
soon as possible.
● If the infant is unwell or requiring significant support, take blood cultures and
commence antibiotics.
● Intravenous access
❍ If the infant requires significant ventilatory support, arterial and venous
access should be obtained.

❍ Infants with lesions dependent on the duct for systemic blood flow, a double
lumen umbilical venous cather should be inserted.

❍ For infants with other lesions it is not necessary to insert umbilical catheters
if the baby is otherwise well.
Duct-dependent for Systemic Blood Flow
With severe left-sided obstructive lesions systemic blood flow is dependent on right-to-left
flow through a patent ductus arteriosus, so these babies are duct-dependent. Examples:
Hypoplastic Left Heart Syndrome, critical aortic stenosis, interrupted aortic arch.
● Insert a double lumen umbilical venous catheter
● Commence a prostaglandin infusion at an initial dose of 10 nanograms/kg/min.
● Do not over-oxygenate the infant (over-oxygenation will result in increased
pulmonary blood flow and reduced systemic blood flow).
● Accept oxygen saturations of 75% or above. Reduce inspired oxygen if
saturations >85%.
● Contact the paediatric cardiologist on call.
● The baby is to remain nil by mouth.
● If the infant requires assisted ventilation, ensure that the baby is not over-
ventilated. The aim should be to initially ventilate to keep a low-normal arterial
pH. Sedation, muscle relaxation, and controlled hypoventilation to further reduce
arterial pH may be necessary if there is excessive pulmonary blood flow and
reduced systemic blood flow (oxygen saturations >85%, low MAP, tachycardia,
cool peripheries).
Duct-dependent Cyanotic Lesions
These lesions are duct-dependent either to ensure adequate pulmonary blood flow (e.g.
pulmonary atresia, critical pulmonary stenosis) or to ensure adequate mixing between the
systemic and pulmonary circulations (transposition of the great arteries).
● Commence a prostaglandin infusion at an initial dose of 10 nanograms/kg/min.

● Ensure that at least one extra IV leur is available in the event that the PGE1
infusion tissues.
● If the systemic oxygen saturation is below 75%, call the paediatric cardiologist on
call.
● If the infant develops apnoea or the systemic oxygen saturation is below 75%
despite prostaglandin, they should be ventilated.
● If the infant develops apnoea but has a systemic oxygen saturation of 75% or
above, the dose of prostaglandin can be reduced (but not below 5 nanograms/kg/
min). If apnoea continues, the infant should be ventilated.
● If the infant is delivered after midnight but is stable, the paediatric cardiologist
should be contacted in the morning by 0700 hours. If unstable, contact the
paediatric cardiologist on call.
Rhythm Disturbances
Many infants are asymptomatic despite rhythm disturbances which have been detected
antenatally or postnatally. Some infants may require significant resuscitation, particularly
if they are hydropic. Hydropic infants require the attendance of a neonatal specialist.
Severely hydropic infants may require emergency insertion of intercostal and/or
abdominal drains at delivery.
Congenital Heart Block
● In the case of complete heart block with fetal hydrops, delivery should be planned
in consultation with the paediatric cardiologist and/or paediatric cardiac surgeon on
call as urgent pacing may be necessary.
● Transfer to NICU as quickly as possible.
● Intravenous access should be obtained.
● It is preferable but not essential to obtain a 12-lead ECG soon after admission to
NICU.
● If the heart rate is above 55bpm and the infant is stable, contact the paediatric
cardiologist non-urgently.
● If the heart rate is below 55bpm, contact the paediatric cardiologist on call.
● Do not commence chronotropic agents (e.g. isoprenaline) without first discussing
management with the paediatric cardiologist.
Tachyarrhythmias
● Be aware that some pregnant mothers are treated with one or more anti-
arrhythmic medications when the fetus has SVT, in order to treat the fetus, thus
the baby may have anti-arrhythmic medication(s) on board at delivery.
● If the tachycardia is still present after delivery, transfer to NICU as quickly as
possible
● Intravenous access should be obtained.
● Obtain a 12-lead ECG soon after admission to NICU. During normal working hours
contact the ECG technicians; after-hours, medical or nursing staff will need to
perform the ECG.
● Contact the paediatric cardiologist on call to discuss further management.
● If the tachycardia has resolved by delivery and the infant is stable, the baby can be
admitted to the postnatal ward under paediatric care. The baby should have Q4H
observations initially. Arrange review by the neonatal specialist on call the
following morning with a 12 lead ECG available.
Postnatal Management of Antenatally Diagnosed Renal Disorders Reviewed by Rita Teele, Carl Kuschel,
William Wong (Paediatric Nephrologist),
Max Morris (Paediatric Nephrologist), and
Vipul Upadhyay (Paediatric Surgeon)
October
2004
Background Information Indications for Scans References
Background
● Kidneys in the fetus can usually be identified on ultrasonography after 16 weeks gestational age.
● Single umbilical artery may be associated with anomalies, among them renal.
● Oligohydramnios may be a consequence of renal abnormality and poor urinary output by the fetus.
● Many of the aneuploidies and syndromes are associated with renal anomaly.
● Dilatation of the collecting system can involve calyces, renal pelvis and ureter(s).
● Dilatation may be due to obstruction, reflux, dysplasia.
● The definition of hydronephrosis varies between authors of publications.
● A normal antenatal scan rules out neither reflux nor the possibility of obstruction.
Information
Anatomy does not equal physiology; it is common for the fetal renal collecting system to fluctuate in size during an
antenatal scan. We also know that most babies and children ‘outgrow’ reflux. However it would be prudent to
identify those newborns who are at risk of renal infection because of reflux and those who have significant
obstruction. Because screening ultrasonography is generally done at 18 weeks, a ‘normal’ scan at this gestational
age does not rule out subsequent, severe dilatation associated with obstruction. Therefore, any comment as to
normal or abnormal prenatal ultrasonography has to include the gestational age at which the scans were obtained.
If one uses a transverse pelvic measurement of ≥ 4mm at any time during intrauterine life, as a definition of
dilatation, 13% of those neonates would be expected to have primary vesicoureteric reflux in neonatal life (based
on Christchurch study of primarily Caucasian babies). There is no difference in the prevalence of reflux between
fetuses who have anywhere from 4-9mm of measured renal pelvic diameter. Although unproven, it is likely that this
same prevalence of reflux also occurs amongst those with 0-3mm pelvic measurement. As mentioned, obstructive
hydronephrosis (e.g pelviureteric junction obstruction), may become apparent only later in pregnancy or after birth.
A ‘normal’ scan rules out neither future obstruction nor ongoing reflux.
Because of the difficulties of screening for urinary tract abnormality in the prenatal population, the following
guidelines are given as a compromise solution.
Indications for Scan
1. Remember: Any antenatally detected renal tract abnormality needs to be confirmed with postnatal imaging.
2. Postnatal renal ultrasonography can be requested at any time if there is concern regarding pulmonary
hypoplasia, other anomalies, a renal mass etc.
Antenatal Findings
The table below is to guide referral patterns rather than to state definitive neonatal clinical management.
Note: PUT clinic = Paediatric Urinary Tract Clinic. This is a multidisciplinary clinic with paediatric nephrologists,
urology, and paediatric surgical services. There is close liaison with the Radiology service.
Antenatal Ultrasound Postnatal Prophylactic Other Comments Refer to:
Findings Imaging Antibiotics Investigations
Bilateral renal pelvis Postnatal scan Ceclor from ● Blood In a male, ● Surgeon
dilatation ≥10mm Day 1 (or as birth pressure admit to on call
soon as ● Creatinine - NICU and ● If the baby
● Bilateral PUJ possible after repeat Day catheterise does not
obstruction delivery) 5 if abnormal after delivery have
● Bilateral VUJ (i.e. this posterior
obstruction represents urethral
● Posterior urethral posterior valves,
valves (in males) urethral refer to
● Prune Belly valves till PUT clinic.
Syndrome (in proven
males) otherwise).
If normal, repeat None if Refer to PUT
Day 5-7 normal clinic
Unilateral renal pelvis Renal Ceclor from See
dilatation ≥10mm ultrasound scan birth comments
Day 5 below about
● Unilateral PUJ If abnormal Continue VUR Refer to PUT
obstruction prophylactic clinic for further
● Unilateral VUJ ceclor investigation
obstruction Refer to PUT clinic
If normal Stop Celcor
● VUR
● Follow-
up USS
at 2-3
months
Unilateral or bilateral Renal Do not start See

renal pelvis transverse ultrasound scan at birth - wait comments
diameter ≥4mm and Day 5 for USS below about
VUR
<10mm If abnormal Prophylactic Refer to PUT
ceclor clinic for further
● PUJ obstruction investigation
● VUJ obstruction
If normal No ceclor Refer to PUT
● VUR
clinic or arrange
● Follow- GP follow-up
up USS
at 2-3
months
Unilateral "Cystic" Renal Ceclor if Refer to PUT

Kidney ultrasound scan confirmed as clinic
Day 5 obstruction
● Multicystic
Dysplastic Kidney
● Severe
hydronephrosis
Single Kidney Renal None May have Refer to Renal
ultrasound scan further Clinic, Starship
Day 5 investigations
as indicated
by
ultrasound
and
arranged by
the renal
service
Obstructed Ureterocoele Renal Ceclor from Refer to surgeon
ultrasound scan birth on call if
Day 1 obstruction
confirmed
Family history of Renal Ceclor if The Refer to PUT
Vesicoureteric Reflux ultrasound scan abnormal incidence of clinic for
Day 5 if family VUR is consideration of
wish higher (20- further
investigations 40%) in investigations
siblings of
children with
known VUR
than in the
general
population.
The
incidence is
also higher
(40-60%) in
offspring
born to
mothers with
VUR.
Horseshoe Kidney Renal Ceclor if May not be Refer to PUT
ultrasound scan evidence of detected clinic
Day 5 dilatation antenatally
References
1 Chertin B, Puri P. Familial vesicoureteral reflux. Journal of Urology 2003; 169(5):1804-8.

May 21, 2006.
guideline.
Guidelines for Babies of Mothers on Anticonvulsants

Reviewed by Salim Aftimos
October 2002
Most studies have shown a 2-4 fold increase in the incidence of malformations and /or
developmental disorders in infants of epileptic mothers on anticonvulsants as compared
to epileptic mothers not taking drugs. Some malformations are more common in
association with certain drugs.( Neural tube defects with valproate and carbamazepine.
Oral clefts with phenytoin. Skeletal defects with valproate). As well, dysmorphic findings
particularly midface hypoplasia may be seen in some infants. The incidence of
developmental delay as well as behavioural problems varies in between studies as well
as between the type of drug or combination of drugs used.
There is insufficient information at present on the teratogenicity of the newer

anticonvulsant drugs (gabapentin, lamotrigine, topiramate)
Neonatal withdrawal symptoms such as irritability, jitteriness, hypertonia, tachypnoea,

exaggerated startle reflex and vomiting have been reported in some infants, particularly in
infants of mothers on valproate, phenytoin, or polytherapy. Asymptomatic neonatal
hypoglycaemia has also been reported in infants of mothers on valproate.
In view of the above, infants of mothers on anticonvulsants should:
a. be admitted to the postnatal ward (or NICU, if appropriate for other reasons) under
paediatric care and observed for symptoms of withdrawal. For infants of mothers
on valproate, ensure early and adequate feeding. Monitor glucose as per the
infants at risk for hypoglycaemia guidelines.
b. receive a thorough physical examination by a paediatric registrar / consultant.
Assess facial dysmorphism particularly evidence of mid-facial hypoplasia. Look for
hypoplastic nails or distal phalangeal hypoplasia
c. be reviewed by the consultant at an outpatient clinic in 6-9 months to check for
developmental problems. It is possible that such problems may not emerge until a
later date. The parents could be informed and encouraged to seek medical
attention should such problems emerge.
● Please ensure that the baby has received the standard dose of Vitamin K at birth.
If an infant is identified with a problem secondary to maternal anticonvulsant, then the

parents should be informed of an increased risk of recurrence with subsequent
pregnancies. Quantification of the risk is difficult and advice could be obtained from the
genetic service. Periconceptual folic acid supplementation may be offered to the mother
keeping in mind that there is no good evidence for protection at least with the standard
0.4 mg dose.
Infants of mothers who received anticonvulsants in the first /second trimester then had
their medication stopped should still be admitted under paediatric care.
References
Ardinger H. et al; Verification of the fetal valproate syndrome phenotype. Am J Med Genet 1988;29:171-
1
185.
Jones K. et al; Pattern of malformations in the children of women treated with carbamazepine during
2
pregnancy. NEJM 1989;230:1661-1666
Thisted E. & Ebbesen F; Malformations, withdrawal manifestations and hypoglycemia after exposure to
3
valproate in utero. Arch Dis Child 1993;69:288-291
Nulman I et al; Findings in children exposed in utero to phenytoin and carbamazepine monotherapy:
4
Independent effects of epilepsy and medications. Am J Med Genet 1997;68:18-24.
Ebbesen F et al; Neonatal hypoglycemia and withdrawal symptoms after exposure in utero to valproate.
5
Arch Dis Child Fet Neonat Ed 2000. 83:F124-F129.
Moore S et al; A clinical study of 57 children with fetal anticonvulsant syndromes. J Med Genet
6
2000;37:489-497.
Dean J et al; Long term health and neurodevelopment in children exposed to antiepileptic drugs before
7
birth; J Med Genet 2001;39:251-259
May 21, 2006.
guideline.
Antibiotics for Neonatal Sepsis Reviewed by Carl Kuschel
August
2003
Classification Indications for Antibiotics Risk factors for Sepsis Signs of Sepsis
Antibiotic Use Duration of Treatment References
● Bacterial sepsis is a major problem in the newborn unit. Approximately 10% of all
neonates admitted to NICU are treated with antibiotics for suspected sepsis.
● A bacterial cause is found in less than 10% of these infants (1-5 per 1000 live
births).
● The incidence of sepsis is higher in preterm infants, especially the very low
birthweight infant (<1500g).
● Common organisms identified are Coagulase negative Staphylococci (28%*),
Staphylococcus aureus (19%*), Streptococcus agalactiae (10%*) and Escherichia
coli (5%*).
● Other important pathogens include Listeria monocytogenes, Streptococcus
pneumoniae, Haemophilus influenza and other gram-negative organisms (total of
20%*).
● The clinical presentation of sepsis in the newborn is often non-specific; there may
however be an acute deterioration.
* Figures for blood stream infections within NICU at NWH 1998.
Classification of Neonatal Sepsis
Early Onset Sepsis Late onset sepsis

(infection occurring in the first 5 (infection occurring after 5 days of
days of life) age)
Exposure to bacteria can occur: Usually due to
● Before delivery due to ● Nosocomial infection,

infected amniotic fluid or organisms acquired from
occasionally following the environment
maternal sepsis ● Coagulase negative
● During delivery when staphylococci are the most
contact with organisms in common causative
the vagina can occur organisms
● After delivery following ● VLBW infants with
exposure to organisms in indwelling catheters,
the infants environment. central lines, chest drains
etc are at particular risk.
When should Antibiotics be Given?
● Antibiotics should be considered in any baby with signs of sepsis, particularly in

the presence of risk factors.
● Risk factors may be an indication for investigation - particularly a full blood count -
but are not in themselves an indication for antibiotics if the baby is born at term
and is clinically well.
● This is not a complete list and if there are any doubts a more senior member of
staff should be consulted.
Risk Factors for Sepsis
● Prolonged rupture of membranes (>24 hours).

● Prematurity (especially in association with PROM).
● Preterm labour with no adequate explanation
● Fetal distress without adequate explanation (fetal heart rate abnormalities
especially fetal tachycardia, passage of meconium).
● Maternal fever or other evidence of infection.
● Foul smelling amniotic fluid or malodorous baby
● Indwelling vascular catheter
Signs of Sepsis in the Newborn
● Fever, hypothermia and/or temperature instability.

● Respiratory distress.
● Apnoea and bradycardia
● Cyanotic episodes
● Lethargy, irritability, poor feeding.
● Unexplained high/low or unstable blood sugars
● Abdominal distension and bile stained aspirates
● Unexplained jaundice
● Umbilical flare, skin rashes
What Investigations should be Perfomed?
● Full blood count.

● Differential white cell count (Normal WBC 10-30,000 x 109/L) and percentage left
shift (immature neutrophils/total neutrophil count).
❍ If >20% this is moderately predictive of sepsis.
❍ A low WCC especially with neutropenia is also suspicious of sepsis.
● Blood cultures.
● Chest radiograph
● A C-Reactive Protein may be indicated.
● On occasion skin/wound swabs and gastric aspirate (at birth only).
● CSF may be needed in some cases - discuss with specialist.
The following investigations may need to be considered depending on the

organism isolated.
Late onset sepsis: In addition to the above consider
● Blood culture taken through central line.

● Lumbar puncture and CSF for microbiology/biochemistry.
● Urine by suprapubic aspirate (preferable) or catheter.
Antibiotic Use in Suspected Sepsis
First five days After first five days

Start amoxycillin and gentamicin Start flucloxacillin and amikacin
for all VLBW neonates and any in all babies
infant who
● Almost all Coag negative
● Appears septic or is sicker Staphylococcus is
than would be usually sensitive to amikacin but
anticipated. resistant to gentamicin.
● Has any vascular catheter ● Flucloxacillin being used
(UVC/UAC, percutaneous at present because of an
long lines or surgically increased number of
placed central venous lines) Staphylococcus aureus
isolates within the unit.
Start amoxycillin and cefoxitin in all
other babies. Add amoxycillin if specific cover
for Enterococci, Strep fecaelis
(suspected NEC), Listeria or
Group B Streptococcus is
needed.
● Review clinical progress and microbiology results at 48 hours.

❍ If cultures negative consider stopping therapy.
❍ Cultures positive/sepsis very likely or confirmed continue therapy.
● Add metronidazole if suspicion of anaerobic infection.
● Consider vancomycin for coagulase negative Staphylococci sepsis, especially if
infant unwell or central line infection with line staying in. Discuss with specialist
first.
● Change to cefotaxime if neonatal meningitis. Discuss with specialist first.
Duration of Treatment
Infection type Duration (days) of

therapy
Pneumonia 5-7
Septicaemia 7-10
Urinary Tract Infection 7-10
Meningitis 14-21
(depending on organism
isolated)
Skin conditions 5
Conjunctivitis 5-7
Oral thrush 7-10
References
1 Neonatal sepsis and meningitis. Philip AGS. GK Hall Medical Publishers. Boston 1985. ISBN 0-8161-2253-
9.
2 Neonatal Sepsis; progress in diagnosis and management. St Geme III JW. Polin RA. New Ethicals 1989;
25(6); 133-41(part 1) and 25(7); 109-31(part 2).
May 21, 2006.
guideline.
Apnoea Monitoring on Discharge from NICU Reviewed by Carolyn Dakin and

Simon Rowley
December
2001
The following are practical guidelines for apnoea monitoring of neonates being
discharged from National Women’s Hospital.
1. There is no evidence that monitoring of infants is of value in saving lives.

2. Apnoea monitors are not designed to detect obstructive apnoea, and will fail to
detect obstructive apnoea.
Infants with respiratory obstruction (e.g. Pierre-Robin sequence, upper airway
anomalies, and infants with abnormalities of tone contributing to feeding and
swallowing difficulties) should be treated appropriately as indicated by the
underlying problem.
3. Low birthweight (LBW, VLBW, ELBW) in itself is not an indication for home
monitoring.
4. It is not clear that polygraphic studies identify infants at particularly high risk of
SIDS. However, they may be useful in individual cases.
5. Monitoring does not preclude the need in may cases to fully investigate and treat
causes of apnoea.
6. Some weeks prior to discharge all infants should be nursed in the supine position
unless clinical condition indicates otherwise.
7. Reduction of risk factors for SIDS should be emphasised:
❍ supine sleep position
❍ no bedding around the head (including no cot bumpers)
❍ no overwrapping
❍ avoidance of cigarette smoke
❍ it is preferable that co-bedding is avoided and the infant is breastfed.
With these points in mind, the following infants should be considered for home apnoea
monitoring:
1. Preterm infants with chronic lung disease discharged on home oxygen, or having
recently (within the last two weeks) come off oxygen.
2. Where practicable, preterm infants of narcotic and polydrug abusers. Infants
exposed to opioids in utero have a higher risk of SIDS. Preterm infants may be at
increased risk and should be considered for home apnoea monitoring. Reduction
of risk factors for SIDS should be emphasised (that is, supine sleep position,
breast feeding, avoidance of cigarette smoke and co-bedding).
3. Infants who have an Apparent Life Threatening Event (ALTE) in Hospital, with no
remediable cause identified.
4. Infants with respiratory obstruction, e.g, infants with Pierre Robin Syndrome, other
upper airways anomalies and with abnormalities of tone contributing to feeding
and swallowing difficulties.
5. Some infants with apnoea continuing beyond the normal period of prematurity, e.g
beyond 36 weeks gestation. These infants should be considered for further
investigation (e.g polygraphic and EEG studies) to determine the cause of apnoea,
and some will require monitoring.
6. Siblings of infants with SIDS who have additional risk factors such as prematurity,
apnoeas, or chronic lung disease.
❍ Parents of a previous SIDS victim should be referred, preferably in early
pregnancy to the Cot Death Society for counselling. Infants when born can
be referred for polygraphic studies but monitoring would not routinely be
indicated for these infants.
7. Infants of parents in a state of extreme anxiety where there are contributory
factors, e.g. poor obstetric history.
These recommendations are according to the NIH Consensus Development

Statement (1986) that monitoring is medically indicated for symptomatic but
not asymptomatic preterm infants. This was reiterated by the CHIME study
(JAMA 2001; 285:2199).
Practical Points
1. Polygraphic monitoring may be provided by consultation with Starship Respiratory

Team, Dr Carolyn Dakin, in response to Consultant referral. A referral sheet
should be completed and placed in the infant’s notes at the same time as the
phone call. The monitoring will usually be done at the Starship. The Respiratory
Department anticipates having full sleep monitoring available in the future but
currently performs Edentrace respiratory monitoring.
2. The Neonatal Homecare Nursing Service supervise the supply and use of the
monitors available for infants discharged from the Neonatal Unit who fit the above
criteria. Referral should be made after discussion with the Consultant and parents.
The Cot Death Society also has monitors, most of which are supplied to infants
who have had an ALTE after discharge home. For some anxious parents whose
infant does not fit the above criteria and for whom a Hospital monitor cannot be
made available, hiring of a monitor from certain Pharmacies may be a satisfactory
alternative.
3. All parents should attend the cardio-pulmonary resuscitation talks given by
Neonatal Homecare Nurses on the unit prior to discharge.
Click here to read the Information Sheet for Parents of infants on home
apnoea monitoring
May 21, 2006.
guideline.
Caffeine Treatment and Apnoea Monitoring Reviewed by David Knight
January
2001
A baby having apnoea needs a full assessment. The various causes of apnoea
need to be considered and excluded.
● Initial treatment is usually by caffeine.

● CPAP is sometimes necessary (the baby may already be on this if weaned from
ventilation or recovering from respiratory distress).
● If the baby remains unstable on CPAP and caffeine, consider IMV.
● There are no fixed guidelines on the initiation of any of these treatments, as the
assessment of apnoea tends to be subjective, and each baby needs individual
assessment.
● In general, exercise caution in giving caffeine to babies with acute respiratory
problems; apnoea often indicates respiratory deterioration needing respiratory
support, not caffeine.
Monitoring the Baby
● Babies with apnoea severe enough to consider treatment should be monitored by

a cardio-respiratory monitor and pulse oximeter.
● Once the baby becomes more stable, discuss changing to an apnoea mattress on
the ward round.
❍ Usually this is at >32 weeks gestation.
❍ Apnoea mattresses are less sensitive at picking up apnoeas and do not
detect bradycardias or desaturations.
Monitoring Caffeine
● It is not necessary to do routine levels on stable babies.

● Serum concentrations should be obtained either if toxicity is suspected or if a baby
continues to have apnoea and has not previously had an optimal level
documented.
❍ Note that the assay is not very accurate and has a coefficient of variation of
15%, so that a reported level of 165 mmol/L has a 95% chance of being
between 115 and 215 mmol/L.
❍ Levels should not be checked within 6 hours of previous dose.
❍ Order levels the day before assay is to be done (clearly dated with the next
day’s date). Levels to be done at 0830 hours.
❍ Therapeutic range is: 135-200 m mol/L, toxicity is unlikely at <400 m mol/L.
Discontinuing
When
● In most babies, caffeine can be stopped between 32 and 34 weeks gestation, as

apnoea ceases to be an ongoing problem. At the latest, it should be discontinued
several days before the baby goes home.
How
● Continue apnoea monitoring for several days after stopping caffeine. Depending
on the clinical situation, this can be either by an apnoea mattress or cardio-
respiratory monitor plus pulse oximetry.
● For babies about to go home, monitoring is usually for 4 days, with a further day
off an apnoea monitor before discharge.
May 21, 2006.
guideline.
Assignment of Consultants In Charge of Infants Reviewed by Simon Rowley
December
2000
● Infants admitted to NICU are generally admitted under the Consultant on service
rostered for that day's admissions.
● All infants admitted to NICU are automatically under public care regardless of
whether they have been seen or assessed privately.
● If the delivery or baby being admitted has been attended by a private Consultant,
then the infant will be assigned to the Consultant who arranged the admission, but
looked after by the Team of the day. As such the Resident/Consultant on call
assumes responsibility for acute problems.
● All day to day management is directed by the Team and Consultant on service that
the infant is currently under, NOT by the private admitting Consultant (unless that
Consultant is also on service).
● The parents are informed by the private Consultant admitting their infant, that their
baby is under the Team Care for daily decisions and management, but that at
discharge follow up will be by the private Paediatrician who admitted them.
● Babies seen at North Shore and Waitakere Hospitals by Paediatricians are always
admitted under the Team Consultant on service.
May 21, 2006.
guideline.
Auditory Testing Reviewed by Simon Rowley
December
2000
Identifying Infants at Risk of Hearing Loss
Generally speaking all those infants admitted to Level 3 and some in Level 2 are at high
risk of future hearing impairment. The Newborn Hearing Screening Committee of United
States of America, which includes a panel of Otolaryngologists, Audiologists and
Paediatricians suggest that 9 groups of high risk should be followed up with hearing tests.
These are as follows:
1. Familial (member of family deaf. In Auckland this comprises the largest group of
children with hearing defects).
2. CMV, rubella (or other congenital infections).
3. Immaturity (birthweight <1500g).
4. Malformation (of cranium or face, e.g. cleft palate, auricular deformity, not pre-
auricular tags alone).
5. Hyperbilirubinaemia (>340μmol/L).
6. Meningitis.
7. Asphyxia.
8. Therapy with ototoxic drugs (where toxic levels reached, particularly loop diuretics
and aminoglycosides in combination).
9. Prolonged mechanical ventilation (> 5 days).
Follow up of the above children will detect 50% of all deaf children in any community and
give a greater yield of abnormal hearing testing. Therefore in New Zealand it is general
strategy to screen all the above children within the first few months of life. A newborn
hearing screening programme is being developed at National Women's Hospital.
Practically speaking this is accomplished as follows:
Referral BEFORE or AT discharge to:

1. Starship Hospital Audiology
2. Middlemore Hospital if the family are in the South Auckland
catchment area (south of Otahuhu, east of Panmure)
or
3. National Audiology Centre
98 Remuera Road
Auckland
Ph: 520 4009 Fax: 522 1622
● Please include parent's telephone number with referral as the appointments are
frequently phoned.
● The testing in neonates is generally using auditory brain stem response
audiometry which is an EEG based test. It does, however, have a relatively high
false positive rate and re-testing will be needed in some cases.
● Otoacoustic emissions may be added to testing. A pilot otoacoustic emission
screening programme is being developed at National Women's Hospital.
Suggested Plan for National Women's Health
Babies admitted to NICU are at high risk of hearing impairment.
● All infants under 1500g, those who have suffered birth asphyxia or any of the other
risk factors mentioned above, should be referred AT or PRIOR to discharge.
● In cases of hyperbilirubinaemia, referral is suggested if the serum bilirubin was
>340μmol /L.
❍ Premature babies will be at greater risk with lower levels, but will be
included under other categories, e.g. <1500g).
Once follow up has been organised, this fact should be recorded
● in the front sheet of the notes,

● on the discharge letter to the General Practitioner, and
● at an appropriate place in the Health and Development Book, which is given to the
parents and in which details are supervised by Plunket Society personnel.
May 21, 2006.
guideline.
Withholding Feeds in the NICU

Carl Kuschel, Barbara Cormack
Assessment of Bilious Aspirates and Vomiting (Dietitian), and Phil Morreau
(Paediatric Surgery)
July 2005
Background Indications to Withhold Feeds Indicative Colour Chart of Aspirates

Investigation of Bilious Aspirates or
Management References
Vomiting
Background
Withholding feeds is a significant decision for infants in the NICU, particularly extremely
low birth weight infants. An audit of practice in NICU identified that withholding feeds was
1
a significant contributor to poor growth in infants. Calories and nutrients can be more
safely and more easily delivered by enteral feeds than by intravenous nutrition, without
increased cost and increased risks of complications.
However, some infants with feed intolerance may have significant intra-abdominal or
other problems.
Indications to Withhold Feeds
Absolute indications to ● Clear abdominal pathology

withhold feeds ❍ Suspected or proven NEC
❍ Significant abdominal distension or
discolouration
❍ Other suspected or proven bowel
pathologies
❍ Blood in stool
● Heavily bile-stained or large gastric residuals or

vomiting ("avocado" or "spinach" in the reference
chart below)
Relative indications to ● Feed intolerance
withhold feeds ❍ If <25% of 6-hour total feed volume - return
aspirate and give full feed

❍ 25-50% of 6-hour total feed volume - return
aspirate and miss feed

■ Check aspirate next feed. If
significant aspirate next feed, then

withhold feed and notify registrar or
NS-ANP
❍ >50% of 6-hour total feed volume - withhold
feed and notify registrar or NS-ANP

● Unstable condition causing clinical concern
❍ This may include infants with significant
cardiorespiratory instability or presumed

sepsis
● Infants about to undergo surgical or anaesthetic
procedures
❍ Refer to the preoperative surgical guideline
Indicative Colour Chart for Assessing Aspirate Colour
Milk Lemon Mustard Wasabi Lime Avocado Spinach
● Note that colostrum may appear yellow in colour.

● Some infants will have bilious aspirates that are bright yellow in colour in the initial
phases.
Investigation of Bilious Aspirates or Vomiting
Feed intolerance is common in preterm infants. However, it is less common in term

infants. In term infants, especially those with bile-stained vomiting or bilious aspirates,
gastrointestinal pathology needs to be investigated and early surgical consultation
should be considered.
Causes of bilious aspirates/vomiting include (but are not limited to):
● Proximal bowel obstruction (yet distal to the duodenum).

2
❍ It is particularly important to consider intestinal malrotation. Radiographs
and abdominal examination may be normal in infants with malrotation,
particularly in the early stage of the condition or if the obstruction is
intermittent. If malrotation is considered a possible diagnosis, an upper GI
contrast study should be considered. A recent report of infants presenting
to a surgical NICU with bilious vomiting demonstrated that 22% had an
3
intestinal malrotation.
● Other bowel obstruction
❍ Distal obstruction may result in bilious vomiting or aspirates.
❍ An abdominal radiograph may indicate intra-abdominal pathology, with air-
fluid levels
● Necrotising enterocolitis
● Paralytic ileus associated with generalised sepsis
❍ This usually presents with a silent abdomen in an infant with signs of
generalised sepsis.
● In some infants, no cause will be found despite thorough investigation.3
Management
1. The baby should be examined for signs of generalised sepsis or instability. Close
attention should be paid to the abdomen, paying particular attention to signs of
tenderness, erythema, or guarding.
2. The baby should be placed nil by mouth.
3. An abdominal series (AP supine and lateral decubitus with the left side down)
should be ordered.
❍ It may be appropriate to repeat the radiographs in 4-8 hours to evaluate any
change in bowel gas pattern or any evolution in radiographic features.

4. Antibiotics after an appropriate sepsis screen should be considered.
❍ If intra-abdominal pathology is suspected, the antibiotics of first choice are
amikacin, amoxycillin, and metronidazole.

❍ If sepsis is considered likely but an intra-abdominal source is not thought to
be the primary source, then the antibiotics of first choice are amikacin and
flucloxacillin.
5. Surgical consultation should be considered early.
6. Reintroduction of feeding will depend on the underlying condition and the
individual preferences of the supervising specialist.
References
1 Cormack BE, Bloomfield FH. An audit of feeding practices in babies <1200g or 30 weeks gestation during
the first month of life. Perinatal Society of Australia and New Zealand 9th Annual Congress, Adelaide,
2005. A42.
2 Strouse PJ. Disorders of intestinal rotation and fixation ("malrotation"). Pediatr Radiol 2004;34:837-51.
3 Foster JK, Mills JF. Neonatal bilious emesis: when does it matter? Perinatal Society of Australia and New
Zealand 9th Annual Congress, Adelaide, 2005. P61.
May 21, 2006.
guideline.
Guidelines for Red Cell Transfusion Reviewed by Jane Harding
December
2003
Causes of Anaemia Indications for Transfusion Consent Ordering Multipacks

Transfusion Volume Other Related Documents References
Common Causes of Neonatal Anaemia
● Preterm delivery before establishment of normal red cell and iron stores in last
trimester.
● Blood loss for Laboratory testing.
● Expansion of blood volume with growth.
● Physiological cessation of red cell synthesis in the first 6 weeks after birth.
Although these factors combine to result in the ‘normal’ fall in haemoglobin concentration
in the first 6-9 weeks after birth, this is accompanied by improved oxygen unloading
capacity as 2,3-DPG levels rise, so that tissue oxygen delivery may improve despite
reduced oxygen carrying capacity. Thus the possible benefits of transfusion need to be
balanced against the known (and unknown) risks for each individual baby.
Indications for Transfusion
1. Shock due to blood loss.

2. Babies with cardiorespiratory disease.
Transfuse if haematocrit:
❍ <40 if unwell (ventilated, <1000g, ongoing problems)
❍ < 35 if moderate lung disease (O requirement > 30%, significant apnoeas

2
and bradycardia)
❍ < 30 if mild residual lung disease (CPAP or low rate ventilation in ≤ 30%
O2).
3. Stable growing babies < 6 weeks old.
❍ Transfuse if haematocrit < 30 and baby symptomatic (recurrent apnoea and
bradycardia, failure of weight gain).

❍ Baby for surgery.
4. Stable growing babies > 6 weeks old.
❍ Transfuse only if haematocrit < 25 and baby symptomatic. Transfusion at
this age will inhibit the normal onset of erythropoiesis and should usually be
discussed with a Specialist. Oral iron supplements should be started at 4
weeks of age.
Consent
● Informed consent must be obtained unless the situation is life threatening.

● Consent is documented on a consent form (Agreement to Treatment CR111).
● However, verbal consent by a parent is acceptable provided it is documented in
baby’s chart, until written consent is obtained.
Ordering Multipacks
● For infants who are under 1000g and less than 10 days old, or infants who are
likely to need multiple transfusions within the first few weeks, order a mulitpack.
This will provide 4 paediatric packs of red cells from a single donor, thereby
reducing donor exposure.
Transfusion Volume
● Small babies (<1500g) in the first week of life: 10ml/kg over 2h.
● Larger babies and older babies: 15ml/kg over 2h to maximise haemoglobin rise
while minimising numbers of transfusions required. Consider frusemide 1mg/kg
half way through the transfusion to minimise volume load.
References
1 Stefano JL and Bhutani VK. Role of furosemide therapy after booster-packed erythrocyte transfusions in
infants with bronchopulmonary dysplasia. J Pediatr 1990;117, 965-8.
2 Stute H, Greiner B, Linderkamp O. Effect of blood transfusion on cardiorespiratory abnormalities in preterm
infants. Arch Dis Child 1995; 72: F194-6.
3 Yu VYH and Gan TE. Red cell transfusion in the preterm infant. J Pediatr Child Health 1994; 30;301-9.
4 Fetus & Newborn Committee, Canadian Paediatric Society. Guidelines for transfusion of erythrocytes to
neonates and premature infants. Can Med Assoc J 1992; 147: 1781-6.
May 21, 2006.
guideline.
Administration of Immunoglobulin (IVIG)

Reviewed by
Complications/
IVIG Indications Ordering
Problems
Other Related Documents References
The Product
● IVIG 3g in 50ml (6% solution) l0ml aliquots available for neonatal use.
● Contains antibodies to normal range of infections in New Zealand.
● Prepared by cold ethanol fractionation and is free of HIV, and Hepatitis B and C
virus transmission risks.
● pH 4 for IV use only.
Complications/Problems
● Adults sometime react to IVIG with fall in blood pressure. Baby should be watched
carefully particularly at the start of the infusion.
● Most patients have no side effects at all.
● Low pH should be considered in sick babies with acid/base problems. Undiluted it
is hyperosmolar. Should be given over 1 hour or longer.
❍ If high osmolarity or low pH are a potential problem may be given diluted
with equal volumes of saline, ½ normal saline or 5% dextrose.
Indications
1. Sepsis in Compromised Neonates

❍ IVIG 750mg/kg = 12.5ml/kg infused over 2 -3 hours.
❍ May be repeated after 3 -5 days if inadequate response./li>
2. Treatment of Immune Thrombocytopenia

❍ IVIG 2g/kg in divided doses over 4 days, i.e, 0.5g/kg/day = 8.3ml/kg given
over a 3 hour period each day.

Ordering
● After consultation with ARBC Medical Officer, write Blood Products request form
with patient's name, number, date of birth, birthweight and present weight.
References
1 Muratt et at, Vox Sang 51: suppl 2, 22-29 (1986).
2 Sidiropoulos et at: Peds, 109:3; 505-508 (1986)
3 Hill. Pediatr Infect Dis J, 1993, 12:549-59
For further details see the Big Blue Blood Bank Book.
May 21, 2006.
guideline.
Platelet Concentrates Authorised by Charge Nurse -

Newborn
April
2006
Platelet Concentrates Indications Consent Prescribing

Ordering Dose Shelf Life
Monitoring, and Adverse Reactions
Documentation
Platelet Concentrates
● Single random platelet concentrates are made from individual units of CMV
negative whole blood.
● These platelet concentrates are resuspended in 50 - 60mls of plasma with each
concentrate containing at least 5.5 x 1010 platelets, 1-2 x 108 lymphocytes and
some granulocytes and a small number of red cells.
Indications
Vary for individuals but below are guidelines:
● Thrombocytopenia (platelets reduced)

● Thrombasthaenia (platelets not functioning)
Click here to link to the Thrombocytopenia guideline for guidelines on what levels to
transfuse at.
Parental Consent

Prescribing of Platelets
Ordering
● One unit of platelet concentrate can be ordered over 24 hours for one baby without
contacting the NZBS Medical Officer. However, for longer, or daily concentrates,
please discuss with the NZBS Medical Officer.
● Remembering that every effort must be made to reduce exposure of neonatal
patients to blood products and separate blood donations.
Dose
● Usually 10-15ml/kg.
● Usually given 30-60 minutes.
Shelf Life
● Shelf Life of 5 days only.

● Checking
● Administration
● Monitoring
● Documentation
Adverse Reactions

May 21, 2006.
guideline.
Plasma Authorised by Charge Nurse -

Fresh Frozen Plasma (FFP) Newborn
April
2006
Fresh Frozen Plasma (FFP) Consent Prescribing Ordering

Storage Monitoring and Adverse Reactions
Documentation
Fresh Frozen Plasma
● Fresh frozen plasma (FFP) is processed from a single donor blood donation either
prepared from a whole blood unit or from a plasmapheresis donor.
● It is prepared within 8 hours of collection. This method ensures the preservation of
labile coagulation factors.
● The plasma is stored at -30°C and thawed under controlled conditions at the
Bloodbank.
● Neonatal packs take 15-20 minutes to thaw in the Bloodbank.
Parental Consent

● Parent signs Agreement to Treatment form (CR0111).
Prescribing of Fresh Frozen Plasma
Ordering
● On NZBS requisition form (111F01802).
Storage
● Shelf life once thawed is 4 hours, when stored in blood fridge.
● FFP pack will have a yellow expiratory sticker, stating ‘date’ and ‘time’ of expiry.
● When pack arrives in Newborn Services it must be used within 2 hours.
● Once plasma is partially transfused it should never be returned to the fridge for
reuse at a later time because of the risk of contamination.
● For neonatal transfusions AB Plasma is used (compatible to all blood
groups).

● Checking
● Administration
● Monitoring
● Documentation
Adverse Reactions
● See Transfusion Reactions

May 21, 2006.
guideline.
Buffy Coat Concentrate Authorised by Charge Nurse -

Newborn
February
2003
Buffy Coat Concentrate Ordering Indications

Checking, Administration, Monitoring,
Adverse Reactions Other related documents
and Documentation
Buffy Coat Concentrate
● This is a concentrate of the white cells and platelets obtained from a freshly
centrifuged unit of whole blood. The buffy coat separates out as a layer which can
then be removed and if necessary buffy coats from different donors can be pooled
for the treatment of a single patient. The blood unit must be fresh and the buffy
coat separated under sterile conditions. Buffy coats must be used within 12 hours
of preparation to get maximal effect of the leucocytes.
● Buffy coat preparations are sometimes used in the treatment of overwhelming
gram negative septicaemia in young neonates. Multiple doses of buffy coats are
required to produce a clinical effect. Because of the relatively small dose of
leucocytes obtained by this method the procedure is not suitable for treatment of
adults who require granulocytes. Buffy coat preparations are not often used as
leucopheresis is the preferred option.
● Caution: Hyperviscosity Syndrome may be induced by transfusing babies to a
haemoglobin of greater than 160g/L. Partial exchange transfusion may be
needed. Red cell compatibility is needed for granulocyte transfusion.
● Neonates are given granulocytes from an O Rh(D) negative, usually CMV negative
donor. If granulocytes from an O Rh(D) negative donor are not available, they
may be made from a donor of a different group compatible with the baby.
● ‘Buffy coat’ one unit blood collected in the morning is spun hard and the buffy coat
and upper layer of red cells harvested into a variable volume of 20-50ml.
● This will have perhaps 80% of the total white blood cells in that 450ml of donor
blood and is also a packed red cell preparation. Should ideally be irradiated prior
to use.
● N.B.: This is prepared only on special request.
Ordering
● Prior to ordering buffy coat concentrate it must be discussed with Medical
Officer of NZBS.
● Granulocytes last only 12 hours once made up.
● Kept at room temperature. Should not be refrigerated.
Indications
1. Septic neutropenic baby with neutrophils 0.5 or less.

2. Septic baby with poorly functioning neutrophils, e.g. chronic Granulomatous
Disease.

● Checking
● Administration
● Monitoring
● Documentation
Adverse Reactions

May 21, 2006.
guideline.
Cryoprecipitate Authorised by Charge Nurse -

Newborn
February
2003
Cryoprecipitate Indications Dosage Storage

Monitoring, and Adverse Reactions
Documentation
Cryoprecipitate
● Cryoprecipitate is prepared by freezing and then thawing plasma at which time a

cryoprecipitate occurs which contains a high concentration of factor VIII fibrinogen,
fibronectin and factor XIII.
● Cryoprecipitate (Lyophilised) is prepared from a single donation of apheresis
plasma obtained from NZ volunteer donors. It is processed within 6 hours of
collection. It is suspended in buffer under sterile conditions and then lyophilised
and heat treated.
● Cryoprecipitate should be ABO compatible wherever possible.
Indications
● Cryoprecipitate is now mainly used as a source of fibrinogen.

● Cryoprecipitate is sometimes used for the treatment of haemophilia A, where there
is a demonstrated deficiency of activity of the plasma clotting factor (AHF Factor
VIII). However the product of choice is Recombinant Factor 8 (synthetic derived
product).
● Can be used for the treatment of patients with fibrin stabilising factor (Factor XIII
deficiency).
The reconstituted product will contain approximately 200 units of Factor XIII).
● Von-Willebrands Syndrome.
Dosage
● 10 – 20ml/kg.
● Cryoprecipitate does not contain an antimicrobial preservative and is therefore
readily susceptible to contamination.
Storage
● Frozen cryoprecipitate is stable for one year at -30

● Shelf life is 6 hours when stored in Blood Fridge. When unit arrives in Newborn
Services it must be used within 2 hours.
● Must be transfused within 6 hours of thawing. It will have a yellow
expiratory sticker on stating date and time of expiry. Do not refrigerate after
thawing as otherwise insoluble cryoprecipitate may reform.

● Checking
● Administration
● Monitoring
● Documentation
Adverse Reactions

May 21, 2006.
guideline.
Hypotension Reviewed by David Knight
December
2000
Importance of Low Blood Fluctuation in Blood

Normal Blood Pressure Blood Pressure to Aim For
Pressure Pressure
Treatment of Low Blood
Blood Pressure in PPHN References
Pressure
Normal Blood Pressure
Blood pressure increases over the first hours, then days after birth. Very low birth weight
babies often have a low blood pressure, especially on the first day. Infants with low Apgar
scores or requiring assisted ventilation tend to have lower BPs, while those whose
mothers were hypertensive or who received antenatal steroids have higher BPs. There
are poor relationships between blood pressure and either cardiac output or blood volume
1 2
in preterm infants , . Systemic vascular resistance is of great importance.
In very low birth weight infants, patent ductus arteriosus may contribute to low blood
3 4 5
pressure, even in the first few days, and its closure may result in an increase in BP , , .
Importance of Low Blood Pressure
There is controversy as to how active to be in treating a low blood pressure in a small sick
baby. There are several publications linking low BP with poor outcome. There may be
reporting bias in these publications. No-one has shown that treating low blood pressure
improves outcome.
6 7
Some have found a correlation between periods of hypotension and IVH , . Miall-Allen
8
also showed an association between MBP <30 and IVH, ischaemic lesions or death .
Low found a relationship between low BP and hypoxaemia and a poor neuro-
9
developmental outcome . The association between a low BP and IVH was not
10
supported by D’Souza .
Blood Pressure to Aim For
8
Miall-Allen used a mean BP of 30mm as her cut off irrespective of size or gestational
6
age. Watkins used his 10th centiles, which were:
For very low birth weight infants, a good rule of thumb is to aim for the baby’s gestational
age as the desired minimum mean blood pressure.
Fluctuation in blood pressure
Blood pressure fluctuation may be as important as its absolute value in the development
of cerebral lesions and the long term outcome of infants. Blood pressure variability should
be minimised as much as possible in the first days of life in very preterm infants. This
involves strategies of minimal handling, careful and gradual management changes and
avoiding interventions that can cause changes in catecholamine levels and blood
pressure.
Blood pressure in Persistent Pulmonary Hypertension
PPHN is associated with poor cardiac function. The ductus arteriosus is often patent so
that, with supra-systemic pulmonary artery pressure there is R-L ductal shunting. If
systemic pressure can be increased without a corresponding increase in pulmonary
pressure, the shunt will lessen and oxygenation improve. There is not much information
on the effect of inotropes on pulmonary vascular resistance in sick newborn infants. What
there is suggests that dopamine does not produce a selective increase in systemic
11
pressure.
However,
● Attempt to keep systemic blood pressure high.

● Treat initially with volume (judicious) and then with inotropic support.
● See the PPHN guidelines.
Treatment of low blood pressure
Normal Saline ● Give one to two boluses of 10-15ml/kg over 20 minutes.

● Equal response to 5% albumin infusion but fewer repeat doses
of volume were needed and a lower weight gain was seen over
12
48 hours, with no difference in serum [Na+] in the one trial .
13
● Saline similar to albumin/FFP in effect .
● Volume (albumin in the published paper) is less consistent at
increasing BP than dopamine and starting dopamine should not
14
be delayed if hypotension persists .
Dopamine ● Start at 5mcg/kg/min and increase incrementally to a maximum

of 20mcg/kg/min.
● Increases BP. More consistent response, at a lower dose with a
15, 16
bigger increase in BP than dobutamine .
Dobutamine ● Start at 5mcg/kg/min and increase incrementally to a maximum

of 20mcg/kg/min.
● Dobutamine is added to dopamine in persistently hypotensive
infants, when the dopamine dose has been increased to 10-
20mcg/kg/min.
4% Albumin ● This is an alternative to Normal saline.

● There is no data on the relative merits of each in babies outside
the immediate newborn period (first couple of days) so use
albumin rather than saline in these babies as it is the ‘more
established’ treatment.
Blood ● Use ‘whole’ blood as volume support if the baby is also

relatively anaemic.
● If volume expansion is desired, do not give frusemide with the
blood.
Hydrocortisone ● 2.5mg/kg IV 4hrly x 2 then 6hrly x 48 hrs then 0.125mg/kg 6hrly

x 48 hrs, then 0.0625 mg/kg 6hrly x 48 hrs.
● Increases BP a little less consistently but to a greater extent
1
than with dopamine 7 .
Dexamethasone ● 0.1-0.25mg/kg/dose. Studies of dexamethasone for ventilator

dependence shows a fairly rapid increase in BP and ability to
1
wean off inotropes 18, 9 .
Noradrenaline ● 0.05-0.5mcg/kg/min, incrementally.
● Primarily raises systemic vascular resistance.
● It may produce a reflex reduction in cardiac output and can
produce coronary artery changes.
● Very little (if anything) published on its use in the newborn. Use
with caution and only after a decision by a specialist 20 .
References
1 Bauer. Arch Dis Child 1993; 69:521-2
2 Kluckow J Pediatr 1996;129:506-12
3 Knight Early Hum Dev 1992;29:287-92
4 Evans Arch Dis Child 1992; 67:1169-73
5 Evans Arch Dis Child 1993; 68:584-7
6 Watkins. Early Hum Dev 1989;19:103-10
7 Moise Pediatrics 1995;95:845-50
8 Miall-Allen Arch Dis Child 1987;62:1068-9
9 Low Acta Paediatr 1993; 82:433-7)
10 D’Souza (Arch Dis Child 1995; 72:162-7).
11 Feltes. Pediatr Pharmacol.1986;5:261-71
12 So. Arch Dis Child 1997;76:43-7
13 Wright. unpublished
14 Gill. Arch Dis Child 1993;69:284-7
15 Klarr. J Pediatr 1994;125:117-22,
16 Greenough Eur J Pediatr 1993;152:925-7
17 Bourchier Arch Dis Child 1997;76:174-8
18 Fauser. Eur J Pediatr. 1992;152:354-6.
19 Yeh. J Pediatr 1990;117:273-82
20 Martinez. J Dev Physiol. 1990;13:141-6.
21 Bolande. Exp Mol Pathol. 1996;63:87-100

May 21, 2006.
guideline.
Neonatal Hypertension Reviewed by Carl Kuschel, Jon

Skinner (Cardiology, Starship
Hospital), and William Wong
(Nephrology, Starship)
February
2003
Definition Normal Data Causes

Investigations Treatment References
Definition
Hypertension is not commonly diagnosed in newborn infants. The incidence in infants

discharged from neonatal units ranges from 0.7% to 2.0%
Hypertension is defined by a systolic blood pressure in a neonate which is ≥95th

percentile for age and sex on 3 separate occasions.
The gold standard for blood pressure measurement is an appropriately calibrated intra-
arterial catheter. However, for babies who do not have or require invasive monitoring, the
most frequently used technique is via an oscillometric manometer (e.g Dinamap). Blood
pressure should be taken when babies are quiet and not feeding (systolic BP is 5mmHg
lower in sleeping babies) with an appropriate sized cuff.
Hypertension detected on oscillometry (Dinamap) must be confirmed with another

modality such as Doppler sphygmomanometry
1
Normal Data
Gestation Age Systolic Blood Pressure

95th % 97th%
Term Day 1 96
Day 8-30 104
Term Day 4 95
6 weeks 113 (awake)
Term Day 1 82
Day 10 111
24 weeks Day 1 57
Day 10 71
28 weeks Day 1 62
Day 10 83
32 weeks Day 1 67
Day 10 94
36 weeks Day 1 74
Day 10 104
Causes
1. Renal
❍ Renal artery thrombosis (particularly if a UAC has been in place)
❍ Renal vein thrombosis
❍ Renal artery stenosis or compression (e.g. from tumour)
❍ Parenchymal renal disease
❍ Severely obstructed urinary tract
2. Cardiovascular
❍ Coarctation of the aorta
❍ Interrupted aortic arch
❍ Distal aortic thrombosis (particularly if a UAC has been in place)
❍ Fluid overload
3. Endocrine
❍ Congenital Adrenal Hyperplasia
❍ Hyperaldosteronism
❍ Hyperthyroidism
❍ Adrenal haemorrhage
❍ Hypercalcaemia
4. Neonatal Chronic Lung Disease

❍ May manifest late after discharge from NICU
5. Drugs
❍ Dexamethasone
❍ Adrenergic agents
❍ Caffeine
6. Neurological
❍ Pain
❍ Seizures
❍ Intracranial hypertension
❍ Drug Withdrawal
Investigations
First Line Investigations:

1. Repeat your clinical examination:
❍ Are there any abdominal masses? Can you feel the kidneys?
❍ Feel the pulses! Are the femoral pulses the same as the brachial pulses?
❍ Are the fontanelle and sutures normal?
2. 4-limb blood pressures

❍ Note: Dinamap BP can be normal in the lower limbs in a baby with
coarctation in.
❍ Do not rely on four limb Dinamap BP measurement to exclude coarctation -
use fingers or ideally Doppler sphygmomanometry

3. Electrolytes, urea, and creatinine
4. Urinalysis
5. Renal ultrasound scan
6. Chest radiograph (if cardiac murmur or signs of congestive cardiac failure)
Second Line Investigations (when history suggests):
1. Echocardiogram to exclude coarctation or interrupted aortic arch.

❍ Also useful to assess cardiovascular function and complications in long-
standing or severe hypertension.

2. Plasma renin activity
❍ Renin levels are higher in newborn infants than in older children and adults
and an elevated PRA may not indicate underlying renal disease

3. Plasma cortisol, aldosterone, or thyroxine (as indicated)
4. Cranial ultrasound or MRI if any suspicion of an intracranial cause
5. Renal radionucleotide study
Treatment
1. Treatment will depend on the underlying cause and should be commenced only
after discussion with either a paediatric nephrologist or a paediatric cardiologist
(depending on underlying cause).
❍ In general, Labetalol is the first-line treatment of hypertension severe
enough to require treatment (once coarctation is excluded).

❍ Second line agents include calcium channel blockers (however, not
Nifedipine) or Hydrallazine.
References
1 Watkinson M. Hypertension in the newborn baby. Arch Dis Child Fetal Neonatal Ed 2002; 86:F78-F81
Task force on blood pressure control in children. Report of the Second Task Force on Blood Pressure
2
Control in Children - 1987. Pediatrics, 1987; 79:1-25
3 Flynn JT. Neonatal hypertension: diagnosis and management. Pediatr Nephrol 2000;14(4):332-4.
May 21, 2006.
guideline.
Blood Sampling in NICU Reviewed by Joy Reilly (RN)

Laboratory Specimen Requirements
November
2005
NICU Radiometer Gas

Arterial gas Biochemistry Haematology
Machine
Drug Levels Blood Bank Other Tests Capillary Sampling Devices
Tests Volume Container

Arterial gas 0.3ml BD A-line
syringe
● Includes:Na, K, Glucose, Hb, Hct, MetHb.
● NICU Radiometer machine also measures
bilirubin and lactate
NICU Radiometer Gas Machine
● Capillary gas - includes: 95 uL Gaslyte

Na, K, Glucose, Bilirubin, Hb, Hct, MetHb,
lactate
● Glucose only 35 uL Small capillary

tube
● Bilirubin only 35 uL Small capillary
tube
Laboratory Gas
● Capillary gas - includes: 0.2 ml A full capillary

Na, K, Glucose gas tube
Biochemistry Laboratory
● SBR (total) only 0.3 ml Green top
(heparinised)
● Total & Direct SBR 0.4ml Green top
(heparinised)
N.B.: Full Biochemistry including all or any 0.7ml Green top
combination (heparinised)
● Electrolytes, Ca, Gluc, Creat, Urea, LFT,

SBR, Mg, PO4
● When collecting 3 – 4 tests 0.5-0.6ml
● LFT – Liver Function Tests

Medical Staff required to complete laboratory form stating specific tests required –
as this determines the amount of blood required. Routine tests will be bilirubin,
AST, ALT, GGT, and ALP.
Thyroid Function Tests

● TSH, Free T3 & T4 - use 2 tubes 860 uL blood Yellow top
(‘plain tube’ = no
anticoagulant)
● Free T3 & T4 500 uL
● Free T4 & TSH 600 uL
● These are minimum amounts, if the PCV is higher than 0.5, then more blood is
required
● When the laboratory requests SERUM approximately double the amount of
BLOOD is needed to obtain adequate serum for processing.
● Consult Medical Staff re tests required as this determines the amount of blood
required
CRP (C-Reactive Protein) 0.3 – 0.5 ml Green top

(depending on (heparinised)
PCV)
Haematology
Full Blood Count 0.3 ml Purple top

(EDTA)
Coagulation Screen 1.0 ml Blue top micro-
Venous / Arterial container
● N.B. – NICU stock – if not available obtain
from PICU – ( not Lab. incorrect size tube for
neonates, larger volume required)
Ferritin – (NOT routinely processed on Public Hols. 0.3 ml Green or Yellow

or Weekends) top
Whole Blood PR/INR &/or APTT Contact Lab Special container
G6PD 0.3 ml Purple top
(EDTA)
Drug Levels
● Amikacin All of these Green top

● Gentamicin drug levels container
● Vancomycin require 0.3ml
● Phenobarbitone
● Phenytoin
● Theophylline
● Caffeine (Lab. to be notified by medical staff 0.4 ml Yellow or Green

24 hours prior to collect) top
Vitamin A ● All samples taken 0.3 ml Yellow top

for vitamin levels (plain tube = no
Vitamin D must be wrapped 0.2 ml anticoagulant)
in tinfoil
Vitamin E 0.4 ml
Blood Bank
Will only accept ‘REQUEST FOR BLOOD COMPONENTS OR PRODUCTS’ Form for
blood samples – not Laboratory Form – complete ‘TESTS REQUIRED’ section
Blood Bank require their BLOOD SAMPLES to be legibly HAND LABELLED using the
specific labels, with:
● patient’s first & last names

● NHI number
● DOB
● date & time of collection
● signature/initials of collector
Group & Coombs 0.3 ml Purple top

(EDTA)
Neonatal Crossmatch 0.7 ml Purple top
(EDTA)
Other Tests
Neonatal Zinc Level 1.5 ml 2 x green top

Arterial or containers AND
● Samples to lab Monday to Friday, but not Venous sample 1 x empty
weekends or public holidays. container
● Samples are processed Monday,
Wednesday, and Friday.
● 1 empty container is required for control test
to detect zinc level in the containers.
Therefore THEY MUST BE THE SAME
BATCH NUMBERS - USE CONTAINERS
FROM AN INTACT PACKET FROM the
Cupboard in the RADIOMETER ROOM (or
use NAVY BLUE TOP container – adult
trace metal tube – obtain from lab.)
Lactate 0.6 ml Yellow top

Albumin 0.5 ml Green top
Cholesterol
● Level only 0.3 ml Yellow or Green
top
● Hg/etc 1.0 ml Yellow top
TORCH Screen 0.6ml Yellow top

Hepatitis screen 0.6ml Yellow top
Karyotype 1-2ml arterial or Green top
venous
Note:
● Other tests requested which are not routinely required for NICU infants –
PLEASE consult the Laboratory staff for information on the amount of blood
required and the appropriate container to use for the particular MICRO-
COLLECT, also state for NEONATE.
● For infants with a high PCV (often new admissions) when the blood clots
easily causing difficulty in obtaining a result via the Radiometer Gas
Machine, we have a supply of 55uL glass capillary tubes containing extra
Heparin which may ensure you obtain a result – please ask the CCN for
these capillary tubes when required.
Capillary Blood Sampling Devices

Tenderfoot– Micro- Blue
preemie For infants up to 1000
grams
Quikheel - Preemie Mauve ● Depth 0.85mm
Lancet For infants 1005-1500 ● Length 1.75mm
grams ● May also be used for a
small collect of 35mL
ONLY = glucose only or
bilirubin only via
Radiometer Gas Machine.
Quikheel - Infant Lancet Teal ● Depth 1.00mm

For infants >1500 grams ● Length 2.50mm
Management of Pregnancies at Borderline Viability

Reviewed by Jane Harding
December 2005
Less than 23 weeks 23+0 to 23+6 weeks 24 weeks and more

Survival Rates Long-term Disability
All discussions regarding management of such pregnancies should involve the parents and members of both
Neonatal and Obstetric services. Members of these services are available to discuss cases by telephone at any
time.
● Click here to open the guideline on Admission Rates to NICU and the degree of Respiratory Support
required.
≤23 weeks 0 days
Standard Practice ● Do not refer to National Women’s Health.

● No fetal monitoring.
● No Paediatrician present at delivery.
● Obstetric staff will usually provide antenatal counselling regarding
outcomes.
23 weeks 0 days to 23 weeks 6 days
Usual Practice ● No fetal monitoring and therefore no caesarean section for fetal distress.
● Consider referral to National Women’s Health<.
● No attendance by paediatric staff.
If parents make a ● Consider steroids if delivery thought to be imminent or gestation of 23

decision for active weeks, 5 days plus.
treatment after informed ● Paediatrician called for delivery.
discussion with ● If birthweight >500g and gestation appears appropriate start resuscitation.
neonatal and obstetric ❍ Stop early if response poor.
specialists
≥24 weeks 0 days
Standard Practice ● Definite referral to National Women’s Health.

● Antenatal steroids.
● Fetal monitoring, consider caesarean section for fetal distress.
● Paediatrician called for delivery.
❍ If birthweight <500g discontinue resuscitation.
At parental discretion ● If <26 weeks, parents may elect after discussion for no fetal monitoring, no
caesarean section and no Paediatrician at delivery.
Survival Rates of Extremely Preterm Infants
● Survival for preterm infants has been increasing steadily over time. National Women's survival data by
birthweight are shown below. These birthweight data are only for infants admitted to the NICU.
Data collated by Associate Professor Ross Howie and Dr David Knight.
● Although birthweight is easy to measure and is an important determinant of survival, gestation is a better
predictor of outcome. The gestation-based survival figures of all infants born at National Women's
Health are:
● The outcomes above include all infants presenting in utero at National Women's
❍ It includes intrauterine deaths, stillbirths, and infants who were born alive but were
unable to be resuscitated.
❍ Admission to the neonatal unit results in higher survival rates as this is a more
selected group of infants.

● For the graphs below, subgroups are shown for gestations 30 weeks and below.
❍ Note that the numbers of infants in some gestational groups (for example, 23 and
24 week infants) or by some analyses (for example, outborn infants) are relatively
small.
Click on the link to the left to look at survival figures for all infants between 22 and 30 weeks gestation who were born
alive at National Women's 1996-2004.
Click on the link to the left to look at survival figures for all admissions to NICU for inborn infants at National Women's
1996-2004.
Click on the link to the left to look at survival figures for all admissions (inborn and outborn) to NICU 1996-2004.
Click on the link to the left to look at survival figures for outborn infants (infants born in other institutions) admitted to
NICU 1996-2004.
Click on the link to the left to look at overall survival for liveborn infants 24-30 weeks gestation at National Women's
Health between 1996 and 2004. Infants born at 23 weeks have been excluded, due to the relatively low numbers of
infants.
These data have largely been collected by Dr David Knight as part of ongoing audit for the Annual Report.
Long-Term Outcomes
● Disability rates are approximately 20% in extremely low birthweight (<1000g) survivors at any gestation.
❍ The rate of cerebral palsy is relatively constant at around 10%.
❍ Severe disability rates are approximately 10%.
❍ Disability rates are higher in infants below 25 weeks.
❍ Around 50% of surviving infants at 23 weeks have moderate or severe disability.
❍ At 24 weeks, approximately 40% of surviving infants have moderate or severe disability.
● Disability includes cerebral palsy, developmental delay, visual and hearing impairment.
May 21, 2006.
guideline.
Handling Powdered Formula and Breast Milk with Reviewed by Barbara Cormack
Additives (Dietitian) and Carl Kuschel
May
2005
Recommendations for Handling of

Background References
Enteral Nutrition Preparations
Background
This guideline should apply to all infants in a neonatal unit, maternity ward, or children's
hospital ward. It should also be applied to all healthy term infants for the first two months
of life.
There has been recent concern about the role of powdered formula preparations in the
development of Enterobacter sakazakii infection in neonates. Previously known as "yellow
pigmented" Enterobacter cloacae, it was renamed Enterobacter sakazakii in 1980. It has
been known to cause meningitis, septicaemia, and necrotising enterocolitis in neonates,
with reported mortality rates of up to 80%.
The incidence of E.sakazakii infection is low. In a report describing infection rates from
over 10,000 VLBW infants, only one case was identified from over 6,000 blood cultures
1
taken after the third day of life. Case reports and outbreaks of E.sakazakii infection
2-9
have variably been associated with the use of powdered formula. In 2002, the FDA
released a statement indicating that neonatal units should take steps to minimise the risk
10,11
associated with powdered formula and additives. In New Zealand, an investigation
into a case of E.sakazakii from a New Zealand neonatal unit led to local
12
recommendations from the Ministry of Health.
It is important to appreciate that powdered formulas and milk preparations are not sterile
and can provide a medium for bacteria to proliferate. Appropriate preparation and
handling of nutritional products is necessary to reduce the risk of milk becoming a source
13
of nosocomial infection. Breast feeding - apart from providing immunity through other
means - reduces the risk of infection associated with formula preparation and storage,
although care needs to be taken with breast milk which has been modified with additives.
Recommendations for Handling of Enteral Nutrition Preparations
Recommendation Comments
Encourage the use of sterile liquid "ready to ● Liquid formula is sterile.

feed" formula for both healthy newborn infants ● Although powdered formula is
in maternity wards, infants in NICU, and infants pasteurised, it is not sterile. Bacteria
in the wards of Starship Children's Health present in the formula, the preparation
equipment or the containers may
contaminate the preparation.
If formula needs to be prepared in advance, it ● Refrigerate feeds on delivery to the

should be prepared on a daily basis and should patient care room.
be kept at 4°C or below for not more than 30 ● Ensure that fridges are kept at ≤4°C
hours and are monitored.
● New feeds are to be delivered by every
24 hours.
❍ Only enough feed for 24 hours
should be delivered at one time.

● A “use by” date and time is to be visible
on every feed label.
Prepare only a small amount of reconstituted ● This is not practical for most areas in
formula for each feed to reduce the quantity the hospitals, hence the move to a
and time that formula is held at room liquid formula.
temperature for consumption ● This does apply to human milk fortifier
and other food additives.
❍ Make up no more than 50ml
(unless the infant's feed is a

greater volume than this)
Minimise the "hang-time" of formula feeds (or ● "Hang-times" should be recorded and
breast milk with additives) monitored.
● No "hang-time" should exceed 4 hours.
There should be surveillance of formula for ● ADHB Nutrition Services undertakes

possible contamination random sampling with specimens
analysed by an external laboratory.
Health professionals should investigate and ● The Ministry of Health has indicated
report sources and vehicles (including that Enterobacter sakazakii is a
powdered infant formula) of infection by E. notifiable disease.
sakazakii and other Enterobacteriaceae
References
1 Stoll BJ, Hansen N, Fanaroff AA, et al. Enterobacter sakazakii is a rare cause of neonatal septicaemia or
meningitis in VLBW infants. J Pediatr 2004;133:821-3.
2 Muytjens HL, Zanen HC, Sonderkamp HJ, Kollée LA, Wachsmuth IK, Farmer JJ 3rd. Analysis of eight
cases of neonatal meningitis and sepsis due to Enterobacter sakazakii. J Clin Microbiol 1983;18:115-20.
3 Biering G, Karlsson S, Clark NC, Jónsdóttir KE, Lúdvígsson P, Steingrímsson O. Three cases of neonatal
meningitis caused by Enterobacter sakazakii in powdered milk. J Clin Microbiol 1989;27:2054-56.
4 Muytjens HL. Kollee LA. Enterobacter sakazakii meningitis in neonates: causative role of formula? Pediatr
Infect Dis J 1990;9:372-3.
5 Jaspar AH. Muytjens HL. Kollee LA. Neonatal meningitis caused by Enterobacter sakazakii: milk powder is
not sterile and bacteria like milk too! Tijdschr Kindergeneeskd 1990;58:151-5.
6 Clark NC, Hill BC, O'Hara CM, Steingrimsson O, Cooksey RC. Epidemiologic typing of Enterobacter
sakazakii in two neonatal nosocomial outbreaks. Diagn Microbiol Infect Dis 1990;13:467-72.
7 Bar-Oz B, Preminger A, Peleg O, Block C, Arad I. Enterobacter sakazakii infection in the newborn. Acta
Paediatr 2001;90:356-8
8 Block C, Peleg O, Minster N, et al. Cluster of neonatal infections in Jerusalem due to unusual biochemical
variant of Enterobacter sakazakii. Eur J Clin Microbiol Infect Dis 2002;21:613-6.
9 van Acker J, de Smet F, Muyldermans G, Bougatef A, Naessens A, Lauwers S. Outbreak of necrotizing
enterocolitis associated with Enterobacter sakazakii in powdered milk formula. J Clinical Microbiology
2001;39:293-7
10 Anonymous. Enterobacter sakazakii infections associated with the use of powdered infant formula--
Tennessee, 2001. MMWR - Morbidity & Mortality Weekly Report Apr 12 2002;51(14):297-300
11 Anonymous. From the Centers for Disease Control and Prevention. Enterobacter sakazakii infections
associated with the use of powdered infant formula--Tennessee, 2001. JAMA. 2002;287:2204-5.
12 Ministry of Health, New Zealand. Inquiry into Actions of Sector Agencies in Relation to Contamination of
Infant Formula with Enterobacter Sakazakii. March 2005. Available online at http://www.moh.govt.nz
13 Agostoni C, Axelsson I, Goulet O, et al. Preparation and Handling of Powdered Infant Formula: A
Commentary by the ESPGHAN Committee on Nutrition. J Pediatr Gastroenterol Nutr. 2004;39:320-2.
May 21, 2006.
guideline.
BRM2 Monitor Reviewed by Angela Warren

(CCN), Robin Gardner (CCN),
Malcolm Battin and Carl Kuschel
September
2005
Indications Application Start the Monitor Log on

Enter Patient Details Check Contact Quality Mark Events Turn Off
The following policy/recommended best practice outlines practice applies to all Medical
and Nursing staff working in Newborn Services.
Indications
The following infants should be considered for Brainz BRM2 monitoring.
Infants ≥34/40 with:
● Definite or questionable seizures

● Muscle relaxed infants at risk of seizures that may not be clinically apparent
● Moderate perinatal asphyxia (neonatal encephalopathy)
● Unexplained apnoea
Monitoring should not be commenced unless directed by a specialist.
Application
Electrodes to be applied by newborn Medical and Nursing staff who have undertaken
BrainZ BRM2 training.
Equipment required:
● BrainZ sensor set

● BrainZ sensor positioning strip
● Marker pen
● Skin prep gel (NuPrep®)
● Wrap hat
● Water / gauze/ cotton tips
Step Action
1 Position infant supine
2 Using sensor positioning strip,
measure from the sagittal suture to the
tragus of the ear. Align so each end
point has the same letter (A,B etc)
3 Mark the site for electrode placement.
4 Clean the marked areas with water and gauze, parting the hair in a line towards
the top of the head
5 Gently pat dry with gauze maintaining the part in the hair
6 Using cotton tips clean the area with a
very small amount of NuPrep®
7 Using gauze and water clean off the NuPrep®, continuing to maintain the
parting.
8 Pat dry the area.
9 Site electrodes in the following manner.
● All leads to be directed to the

top of the head
● Black electrode placed at the
back
● White electrode placed in front
● Ensure electrodes do not touch
10 Gently turn infants head over and

repeat process.
11 Apply head wrap with adequate tension to support electrodes.

12 Site the green reference electrode,
either on the neck, shoulder, or back.
13 Plug blue connector into the data

acquisition unit (DAU)
14 Note: If electrodes lift, reapply using a small drop of sterile water. Do Not stop
the machine. Continue monitoring, making a note on the trace, of the event.
Start the Monitor
Step Action
1 Plug monitor into wall power supply.
2 Ensure power cable and serial cable is connected from monitor to the isolation
unit.
3 Connect the data cable from the isolation unit to the DAU.
4 Turn on the AC power switch (at back of monitor).
5 Check that the green light on the DAU comes on.
Log on
Step Action
1 Touch the white field next to ‘user name’ to display the onscreen keypad.
2 Type in the word NICU, press enter.
3 Touch the white field next to ‘password’ to display the onscreen keypad.
4 Type in the word NICU, press enter.
5 Once both user and password are entered touch the ‘login button’ to display
the main menu screen.
Enter Patient Details
Data must be entered before monitoring commences. Once monitoring, patient data can
not be altered.
Step Action
1 On main menu screen touch the ‘assess patient’ button to display the new
patient screen.
2 Touch the first white field to display the on-screen keypad.
3 Typing the appropriate data, touch enter at the end of each entry.
4 Touch the appropriate check box to select the gender.
5 Use arrows to adjust birth weight / current weight.
6 Touch appropriate date on calendar to enter birth date.
Check Contact Quality
Contact impedance is displayed on the ‘signal status screen’.
Step Action
1 On main menu screen touch the ‘check signal’ button.
2 All 4 dots displayed on the graphics should be green.
3 If dots are yellow or red check the corresponding electrode.
4 Once all dots are green press the ‘OK’ button.
Mark Events
During monitoring Mark events i.e. suctioning, cares, observation of seizure-like

movements, administration of anticonvulsants
Step Action
1 Touch ‘mark events’ button.
2 Touch white description area to display the onscreen keypad.
3 Enter a brief note
4 Touch enter, then OK
5 A green line and number will appear on the aEEG graphics. To recall the event
data touch the green line on the screen.
Turn Monitor Off
Step Action
1 On main menu screen touch ‘shutdown’ button.
2 On confirmation screen touch yes.
3 Once screen says shutdown complete, turn AC power off.
4 Remove sensors by dampening the gel with water.
References
1 BrainZ BRM2 Brain monitor reference manual

May 21, 2006.
guideline.
Caloric Calculator © Carl Kuschel
February
2006
● This calculator provides an estimate of caloric intake.

● This may be useful when considering caloric intakes in infants who are
hyperglycaemic, where the use of insulin may be considered.
● It may also be used in those infants in whom referral to a dietitian for ongoing
nutritional management is being considered.
Working Weight: g
Current Fluid and Nutritional Intakes
Enteral Feeds
0 ml per hour
● Please
divide the 2- 0 ml/kg/day
or 3-hourly
feed amount
to work out
the hourly
0 kcal/kg/day
amount
Intravenous Nutrition
Amino Acid
0 ml per hour 0 ml/kg/day
Solution:
20% Intralipid: 0 ml per hour 0 ml/kg/day
0 g/kg/day 0 kcal/kg/day
Other Intravenous Fluids

● Do not count solutions in saline or half-normal saline (for example, arterial line fluids or infusions that
are not in dextrose).
● Do not count insulin infusions.
Infusion 1: 0 ml/hour 10 % dextrose 0 ml/kg/day

Calculate Reset
May 21, 2006.
guideline.
Care Map for Infants <32 Weeks Gestation Reviewed by Jean Bertram, Frank
Bloomfield, Robyn Wilkinson,
Bronwyn Jones, and Carl Kuschel.
March
2006
Prior to Admission On Admission Ongoing Care
Prior to Admission
● CPAP incubator to DU/OT for delivery.
Admission
● Appropriate respiratory support (optimal CPAP).

● Baseline observations / monitor
❍ HR
❍ Respirations
❍ SaO as per oxygen saturation targets (range 85 – 92% with O2

2
requirement / alarm limits set appropriately)
❍ BP (mean blood pressure ≥ gestational age)
❍ Temperature (monitor skin temperature initially)
● Commence incubator humidity 50% (discontinue 3 weeks of age or 32 weeks

gestation, whichever comes first)
● IV 10% Dextrose 60-90mls/kg per day.
● FBC.
● Blood cultures if risk factors for sepsis or baby unwell.
❍ Commence antibiotics if indicated.
● Blood glucose.
● Capillary gas.
● Commence urine weighs.
Ongoing Care
● May need 1-2 hourly cuff BP measurement initially,

then 4 hourly,
then minimum 8 hourly till stable.
❍ Discuss frequency on ward round.
❍ Report hypotension or fluctuations in blood pressure to medical staff.
● Continue:
❍ urine weighs.
❍ urine testing for glucose, blood, and protein.
Test 8-hourly initially then discuss frequency on ward round.

❍ blood glucoses as indicated.
❍ capillary gases/electrolytes/SBR as indicated.
● Careful observation / assessment / documentation of respiratory status

❍ Report changes to medical staff.
❍ Have a low threshold for restarting babies back on CPAP if they are being
trialled off and become symptomatic with increasing tachypnoea,

desaturations, oxygen requirement, or apnoea.
● Discuss and assist mother with expressing.
● Demonstrate and encourage parents’ safe handling of baby
❍ nappy changes
❍ top and tail
❍ positioning / settling
❍ Kangaroo care
■ <30 weeks not in first 5 days
■ ≥30 weeks consider stability
■ Monitor infant's physiological status carefully.
■ Discuss on ward round if unsure.
NB: Read appropriate parts of Developmental Care Protocol

May 21, 2006.
guideline.
Chickenpox Exposure in NICU

Reviewed by Dr Liz Wilson and
Judy Gilmour (Infection Control)
May 2005
● An individual with chickenpox (varicella) is infectious from 2 days prior to the

appearance of lesions to 5 days after or until the lesions are dry and crusted
(whichever is longer).
● Determine true diagnosis in index case / call infection control
● Susceptible contacts will require VZIG. VZIG needs to be given within 72 hours of
exposure and no later than 96 hours. See VZIG information.
● Note that VZIG costs $360 per vial and must be approved by the Medical Officer or
the "on call" transfusion specialist.
● Exposed individuals that are non-immune become potentially infectious from 8
days following initial contact until 21 days following the last contact with the index
case. See Chickenpox information.
● For isolation see Chickenpox - Infectious precautions.
May 21, 2006.
guideline.
The Child Development Unit (CDU)

Reviewed by Anne Dezoete
Information for Parents
December
2000
See also CDU site
This follow up programme is available for children in the groups listed below who received
special care in the Neonatal Intensive Care Unit at National Women's Health. It is
provided as a service to parents and children, and to the hospital to give information on
how some of the children cared for progress in the years after they go home.
The Developmental Psychologist will check you child's development (mental, motor and
behavioural). This service is in addition to periodic medical checks by your Paediatrician.
At present the Child Development Unit service is offered to the following groups of children
1. BABIES WHO WEIGHED LESS THAN 1000 GRAMS AT BIRTH:

These are seen at the ages of nine and eighteen months and thereafter as
considered necessary.
2. BABIES OF 1000-1500 GRAMS:
These are seen ordinarily at eighteen months, earlier on special request, and later
as considered necessary.
3. OTHER INFANTS REFERRED BY THE CONSULTANT PAEDIATRICIAN:
These are seen as considered necessary.
This service is intended to benefit parents, children and the hospital. Parents and children
have the advantage of regular assessments, so that any problem may be identified at an
early age and appropriate help arranged. The hospital needs to know how infants from its
neonatal care units are progressing, which will help the staff of the Unit to take better care
of babies who need special care in the future.
Telephone contact: (09) 3074949 Ext.25364

See also CDU site
May 21, 2006.
guideline.
Cleft Lip and Palate Guidelines Reviewed by Maeve Morrison

(SLT, Middlemore Hospital) and
Carl Kuschel
November
2003
Incidence Immediate Management Feeding Guidelines

Timing of Surgery Other Issues Followup
Incidence
● Bifid uvula 2%. This may indicate underlying submucous cleft.

● 1:800-1,000 cleft lip and palate.
● 1:2,000 isolated cleft palate.
Immediate Management
1. Paediatric assessment (SHO, NS-ANP, Registrar, or Consultant). In particular

examination for other abnormalities, airway and breathing difficulties.
2. Paediatric staff will refer to the Middlemore Hospital Plastics Team Clinic.
❍ Fax: 276 0004
Referral will be acknowledged by Clinic Manager by return fax Monday

to Friday
❍ Plastic Surgical Registrar can be contacted after hours or on the weekend if
urgent acknowledgement is required.

3. Referral to the Lactation Consultant, National Women’s Hospital.
4. Referral to the Speech Language Therapist, Middlemore Hospital
❍ Phone 263 0792 Ext.3245
❍ Locator 93 8155
❍ Plus written referral by fax 263 0539 to SLT.
5. Cleft Lip and Palate Support: The information pack is the Blue Book which is
available on NICU and is given to and discussed with the parents (available from
the Cleft Lip & Palate Support Group and available online (downloadable in Adobe
Acrobat format)). A visit can be arranged if parents request via the email address
in the Blue Book.
Feeding Guidelines
● Click here to open the Feeding Guidelines
Timing of Surgery
Surgical priorities are:
● speech
● appearances
● dental occlusion
● Lip and primary palate is usually repaired at around 5 months of age.

● Soft palate repair is usually around nine months of age.
Other Issues
● Children with Pierre Robin Syndrome or severe micrognathia are at high risk of
airway obstruction and may need to be nursed prone so that the tongue falls
forward and they may need tube feeding and saturation monitoring. The relative
mandibular under-development and glossoptosis usually disappears by early teens.
● Cleft lip and palate may be part of dysmorphic syndromes. Up to 40% will have
associated malformations. Investigations may include:
❍ A detailed family history is important.
❍ Chromosomes.
❍ Consider velocardiofacial syndrome, chromosome 22q syndrome or Di
George Syndrome – cytogenetics.

❍ Ultrasound scans of head, heart and kidneys. Radiographs of spine.
❍ Referral to the Geneticist for counselling.
Follow Up
The Middlemore Hospital Cleft Lip and Palate Team Plastic Surgeon and Speech-
Language Therapist try to see the newborn baby within a few days after birth. The team
will then assess the child in clinic within 6 weeks. The surgeon will outline and
individualise management for that child. The team includes:
● Plastic surgeon
● Orthodontist
● Speech-Language Therapist
● Plastic Surgery Nurse
● ENT Surgeon
If other anomalies are present then the Specialist will need to follow up as appropriate, e.
g. Paediatric Cardiology at Starship Hospital. A National Women’s newborn service
appointment may be offered for three months to ensure that all is progressing normally in
terms of follow up arrangements, feeding, growth and early development.
Parents are not always aware that the management of cleft lip and palate is long term and
follow up may be into the child’s twenties before orthodontics is completed. Rhinoplasty,
jaw and further lip surgery may also need to be scheduled at this late stage. We should
endeavour to inform the parents with the help of literature that the immediate repair is
only the beginning of a long term relationship with the Plastic Surgical Team.
May 21, 2006.
guideline.
Paediatric Respiratory Service Review of Infants on Reviewed by Innes Asher

NICU
May
1992
Dr Innes Asher, the Respiratory Registrar and Rhonda Akroyd, Dietitian, Auckland
Children's Hospital.
Visit starts 8.50am, NICU (or SCBU if previously notified) and lasts until l0am, on the
designated Monday.
Recommended information available on each patient:
To be received ONE WEEK before visit:
● Written medical summary, and copy of growth charts
Available on the Day:
● Problem list (up to date).

● Drug list.
Investigations:
● All chest radiographs displayed on viewing boxes. Chest radiograph within last four weeks.
First, worst, best and latest are of greatest interest.
● All ECGs including one within last four weeks. Reports available if possible.
● Blood gases, especially those within last two weeks.
● Any other relevant investigations if done, e.g. barium swallow, immunoglobulins,
echocardiograph, viral titres.
● Records of pulse oximetry in the last week including print out of oximetry over 24 hours.
Note duration of feeding, sleeping, activity etc on the printout.
Nutrition
● Charts up to date (up to the day of visit) for: weight, length, head circumference.
● Calculated 24 hour ml/kg and cal/kg intake
● Information on feeding methods and any problems.
Very important to have access to a nurse who currently knows the child well, and the Paediatric
Registrar who knows the child best.
May 21, 2006.
guideline.
The Collapsed Ventilated Infant Reviewed by Simon Rowley

Aids to Diagnosis and Treatment
December
2000
Situation
You are called to see the small ventilated premature baby with RDS. The baby has
suddenly collapsed, is cyanosed, pale, with a falling BP, falling HR. How does one deal
with this situation?
Strategy
● Have a systematic checklist to rapidly ascertain the problem and then treat it
appropriately.
● Aim to achieve adequate oxygenation. If any delay in diagnosis or management
remember to maintain CPR basics.
● Don't hesitate in calling the consultant if you anticipate major problems that require
expertise beyond your abilities.
PROBLEM ACTION
● Delivery System fault, i.e. ● Reconnect or change to
interruption of gas adequate gas supply.
supply to ventilator.
Loss of desired ● Check ventilator settings and
ventilation from tubing circuit integrity.
machine to ETT.
● ET Tube Extubation ● Remove ETT, bag, reintubate.
Problems
● poor chest
movement, poor
air entry
‘blowing
bubbles’.
Tube Placement ● Directly visualise ET tube and

check position.
● e.g. right main ● Withdraw 0.5-1cm.
bronchus ● Check CXR.
Blockage ● Remove ETT, bag, reintubate.
● poor chest
movement, poor
air entry,
copious
secretions,
difficulty passing
suction catheter.
● Ectopic Air Pneumothorax ● Aspirate with fine gauge

butterfly needle, 3-way tap and
● decreased chest syringe.
movement and/ ● If free air proceed to insertion
or decreased air of intercostal drain.
entry, that may
transilluminate
with a cold light.
Pneumopericardium ● Aspirate with fine gauge

butterfly needle, 3-way tap and
● present on syringe via subxiphisternal
previous CXR space.
● signs of ● If air recollects consider drain
tamponade – insertion.
loss of cardiac
output with no
heart sounds
heard but
normal
complexes on
ECG.
● In both situations, consider obtaining a chest
radiograph if time allows to confirm diagnosis
● Acute Blood Revealed ● Control bleeding if possible.

Loss ● Give volume, FFP, blood
● From arterial promptly.
line, umbilical ● Check clotting.
vessels, GI
tract, renal tract
or up ETT.
Concealed ● Give volume , FFP, blood

promptly.
● Pulmonary, GI ● Check clotting.
tract bleeds and ● Arrange CXRs, cerebral USS.
also IVH/PVH.
● Neurological Convulsions ● Administer anticonvulsant –

Phenobarbitone 20-25 mg/kg
● associated load is usual.
abnormal limb ● Correct any predisposing
truncal, facial factors.
movements ● Arrange cerebral USS.
● Other Septicaemia ● Maintain optimal

occasional cardiovascular support with
causes of colloid and inotropic agents.
acute cardio- ● Obtain microbiological samples
respiratory if stable.
collapse. ● Check FBC, clotting.
● Commence on antibiotics.
Metabolic disturbances ● Administer 2ml/kg of 10%

e.g. Hypoglycaemia Dextrose as bolus, increase
rate of maintenance Dextrose
infusion and recheck blood
glucose in 30 minutes.
Hypocalcaemia ● Administer 1ml/kg of 10%

Calcium Gluconate, increase
maintenance infusion and
recheck serum calcium in 30
minutes.
Hyperkalaemia ● Administer 1ml/kg of 10%
Calcium Gluconate and
consider further treatment
depending on degree of
hyperkalaemia. e.g. Resonium,
Dextrose and Insulin.
Congenital Cardiac ● Maintain optimal oxygenation

Disease and cardiac output.
● Arrange urgent CXR, ECG and
With heart failure ECHO.
commonest lesions ● Treatment dependent on
presenting in first week diagnosis and in consultation
of life: with Paediatric Cardiologist.
● In the absence of a rapidly
accessible Echocardiogram or
● Hypoplasia of
Cardiology assessment, a
the left heart
prostaglandin infusion may be
● Coarctation of
the aorta life-saving.
syndrome.
With severe cyanosis:
● Transposition of
the great
arteries.
● Pulmonary
atresia or
severe
pulmonary valve
stenosis.
Pulmonary ● Keep optimal oxygenation.

Hypertension: ● Keep pH high using base +/-
hyperventilation.
● Maintain adequate systemic
● Commonly a
blood pressure with colloid and
problem in
inotropes.
known term
● Consider inhaled Nitric Oxide.
baby with PPHN.
● However,
significant R to L
shunting may
cause acute
collapse in the
ventilated
premature baby.
● Pulmonary
vasculature is
PO2 and pH
sensitive.
May 21, 2006.
guideline.
The Use of Complementary and Alternative Medicine Reviewed by Carl Kuschel

(CAM) in NICU with advice from ADHB Legal
Services
March
2005
Background Summary References
Background
Having a baby in the NICU is a stressful experience for parents. For some parents,
conventional medicine may not fit well with their framework of personal, health, and
spiritual beliefs. Occasionally, parents will request that their infant receives
complementary and alternative medicine (CAM) care (for example, naturopathy,
osteopathy, or homeopathy).
1
The prevalence of CAM in NICUs is not widely reported. Some interventions that have
previously been regarded as “complementary” 2 (for example, kangaroo care, and music
therapy) have moved more into mainstream “conventional” care within the bounds of
some developmental care practices. For older children, there is evidence that CAM use
3
is relatively prevalent. In an Australian paediatric gastroenterology outpatient setting,
36% of children were using or had recently used CAM, and 78% of their parents indicated
4
that they would use CAM if they thought it would be beneficial. Similarly, 18% of
children were receiving CAM treatments at the time of hospitalisation for acute illness in a
New Zealand paediatric inpatient unit. 5 Many parents of children in a paediatric ICU
suggested that they would appreciate the opportunity to provide CAM therapies, and
those that were using CAM were reluctant to discuss this with conventional medicine
6
providers.
The Health and Disability Code of Rights states that “every consumer has the right to be
provided with services that take into account the needs, values, and beliefs of different
7
cultural, religious, social, and ethnic groups”. Whilst the code is geared more for adults
who are able to make autonomous decisions, there is potential conflict where parental
beliefs may conceivably place their infant at risk by not providing appropriate conventional
care or by exposing the infant to risk from untested or dangerous therapies (particularly
medications that may interact with conventional medicines). The legal position of the
Auckland District Health Board is that Newborn Services is responsible for the care of
infants in NICU and under paediatric care in the postnatal wards.
Summary
● If parents wish their infant to receive homeopathic or naturopathic treatments, or

treatments specific to a particular cultural or religious background, this needs to be
fully discussed with the specialist who is looking after the baby.
❍ The safety of the infant is paramount, although the needs of the family to
make a contribution to the health of their child should be considered.

❍ The use of CAM should not be a substitute for nor interfere with effective
conventional medical care.

❍ If CAM is used within NICU, it is the choice of the infant’s guardian and it is
not prescribed by, recommended or endorsed by Newborn Service staff.

❍ Any treatment which involves ingestion or topical application needs to be
considered in the context of possible interactions with conventional

medicines and the potential for significant absorption of the constituents of
complementary medicines through skin. However, information may not be
available pharmacology and interactions for complementary medicines.
● External health care providers are not able to administer complementary or
alternative care which involves direct patient contact within ADHB facilities, without
the approval of the NICU specialist and ADHB management. This is only an
option in exceptional circumstances.
References
1 Mark JD, Barton LL. Integrating complementary and alternative medicine with allopathic care in the
neonatal intensive care unit. Alternative Therapies in Health and Medicine;2001;7:134-6.
2 Jones JE, Kassity N. Varieties of alternative experience: complementary care in the neonatal intensive
care unit. Clin Obstetr Gynecol 2001;44:750-68.
3 Ernst E. Prevalence of complementary/alternative medicine for children: a systematic review. Eur J
Pediatr 1999;158:7-11.
4 Day AS. Use of complementary and alternative therapies and probiotic agents by children attending
gastroenterology outpatient clinics. J Paediatr Child Health 2002;38:343-6
5 Armishaw J, Grant CC. Use of complementary treatment by those hospitalised with acute illness. Arch Dis
Child 1999;81:133-7.
6 Moenkhoff M. Baenziger O, Fischer J, Fonconi S. Parental attitude towards alternative medicine in the
paediatric intensive care unit. Eur J Pediatr 1999;158:12-7.
7 The HDC Code of Health and Disability Services Consumers' Rights Regulation 1996.Clause 2, Code 1.
Available online at http://www.hdc.org.nz
8 Cohen MH, Kemper KJ. Complementary therapies in pediatrics: a legal perspective. Pediatrics 2005;115
(3):774-80.
9 Anonymous. Guidelines on complementary, alternative or unconventional Medicine. Medical Council of
New Zealand.April 1999. Available online at http://www.mcnz.org.nz/portals/1/Guidance/guidelines%20on
%20complmentary%20medicine.pdf
May 21, 2006.
guideline.
Screening for Congenital Heart Disease in First Reviewed by Salim Aftimos and
Degree Relatives Tom Gentles (PCCS)
February
2004
The baseline prevalence of congenital heart disease (excluding PDA in preterm infants,
mitral valve prolapse, and biscuspid aortic valves) is approximately 0.5-0.8% of all live-
births.
The recurrence risk for siblings of children with congenital cardiac malformations have
been variably estimated in the region between 1% and 4%, provided there is no strong
family history of that particular malformation. The risk is higher in first degree relative
where the lesion is Hypoplastic Left Heart Syndrome (HLHS, 19.3%) and coarctation of
1
the aorta (9.4%). The most common finding in relatives was of a bicuspid aortic valve,
but some individuals had significant left-sided obstructive lesions including HLHS and
coarctation.
If a neonate is born who has a first degree relative (parent or sibling) who has been
diagnosed with these conditions:
● The baby requires a complete cardiovascular examination, ideally on the first day
but also later in the first week.
● Infants with symptoms or signs of congenital heart disease should be assessed as
indicated.
● Those infants with a normal examination should be referred to the Paediatric and
Congenital Cardiac Service outpatient clinic at Starship Hospital for assessment,
preferably within the first few weeks of life when sedation for an echocardiogram
should not be necessary.
See also the management of antentally diagnosed congenital heart disease
1 Loffredo CA, Chokkalingam A, Sill AM, Boughman JA, Clark EB, Scheel J, Brenner JI. Prevalence of
congenital cardiovascular malformations among relatives of infants with hypoplastic left heart, coarctation
of the aorta, and d-transposition of the great arteries. Am J Med Genet 2004 Jan 30;124A(3):225-30.
May 21, 2006.
guideline.
Congenital Infection Reviewed by Dr Liz Wilson and Dr

Guidelines for Investigation of Suspected Cases MC Croxson
December
2000
Infection of the fetus can result in embryonic death, stillbirth, prematurity, intrauterine
growth retardation, developmental abnormalities or congenital disease.
Clinical findings are rarely disease specific but include:
● Low birthweight for ● Purpura ● Jaundice

gestational age. ● Chronic rash ● Anaemia
● Prematurity. ● Cerebral calcification ● Hepatosplenomegaly
● Seizures ● Micro-ophthalmia ● Pneumonitis
● Chorio-retinitis
● Cataracts
Toxoplasmosis Rubella Cytomegalovirus Herpes Simplex Virus Syphilis
See also: Hepatitis C and HIV
Toxoplasmosis
● 85% of congenitally infected infants appear normal at birth.

● Only 75% of congenitally infected children will produce detectable specific IgM.
● Maternal infection in first trimester less likely to infect fetus (10%) but if it does the
damage is more severe. Mid or late trimester infection more likely to infect fetus
(30-50%) but the effects are milder.
Investigation of babies born to Toxoplasma IgM positive mothers
The following samples will enable search for toxoplasma DNA (by PCR) in baby's blood,
placenta and amniotic fluid.
The newborn blood and maternal blood will allow direct comparison of maternal/fetal
antibody levels, i.e, is there any evidence of fetal infection as revealed by fetal antibody
production? Cord blood is proving unreliable for antibody titration.
● Cord blood - label clearly 'cord blood'.

● Plain (red top) blood 5ml.
● CPD (yellow top) blood 5ml.
● Placenta - 100g placenta (fetal side near umbilical cord): place sterilely in sterile
disposable plastic container. Keep chilled.
● Amniotic fluid - please collect where available as this may be very informative -
10ml in sterile plastic container.
● Newborn serum - 1ml plain blood (red top) for toxoplasma IgG and IgM. Label
clearly 'newborn serum - not cord blood'.
All these samples should be sent to:
● Department of Virology & Immunology

● Level 2, Building 31
● LabPlus
If suspected after delivery:
● Maternal serum for toxoplasma IgG and IgM

● Infant serum (red top) for toxoplasma IgG, IgM and infant blood (CPD or EDTA
tube) for PCR
● Head ultrasound
● CSF for M, C and S, protein, glucose and toxoplasma PCR
Refer to Paediatric Infectious Diseases Team for treatment and follow up.
Rubella
● Infection of the fetus is CHRONIC, so congenitally infected infants will shed virus
at high titre for many months.
Investigations
● Mother
❍ Check antenatal serology and perform if result not available (mother may
have IgG from infection very early in pregnancy, so documented

seropositivity from a previous pregnancy is more reliable)
● Baby: • Urine +/- CSF for rubella virus PCR.
❍ • White blood cells (cord blood or infant blood) for rubella PCR (EDTA or
CPD tube).
❍ • Serum (cord or infant blood) for rubella IgM.
Isolation
● Contact isolation required: consider infectious for first year of life

● Only those known to be immune should care for the baby in hospital and pregnant
visitors at home should be warned.
Cytomegalovirus
● There may be a history of maternal 'mono'-like illness.

● Most infected infants are asymptomatic but may have later deafness or learning
disability.
● Approximately 15% of infants born after primary infection of mothers will have one
or more sequelae of intrauterine infection.
● CMV infection may show marked liver involvement than congenital toxoplasmosis
with hepatosplenomegaly and jaundice.
Investigations
● Urine culture for CMV (must be in first two weeks of life to confirm congenital
infection). Urine must be chilled and transported immediately to the lab on melting
ice.
● Cord or infant blood for CMV PCR (EDTA or CPD tube).
● Head ultrasound.
● Long term: serial audiology and developmental assessment, head circumference,
ophthalmology.
Click here to link to Nursing Care of Infants who are CMV positive
Herpes Simplex Virus
● Only 30% of mothers whose infants have neonatal herpes have a history of
symptomatic genital herpes.
● Most infections are acquired at birth. Intrapartum/post natal infection can become
manifested up to 4-6 weeks, disseminated infection usually in first two weeks,
localised CNS or SEM (skin, eye, mucous membrane) during second and third
week.
● The risk of HSV infection in an infant born vaginally to a mother with a first episode
or primary genital infection is 33-50% (hence caesarean section usually
performed) and such infants may warrant Acyclovir treatment once cultures have
been taken. Alternatively cultures can be taken at 24-48 hours if the infant is
asymptomatic and acyclovir only initiated if HSV is identified.
● The risk from recurrent genital HSV infection is 3-5% at most and empiric therapy
is not recommended.
● Scalp electrodes must be avoided wherever there is suspicion of active HSV in the
mother.
Investigations
● Skin vesicles: swab for viral culture and HSV PCR.
● Swabs from eyes, mouth/nasopharynx for HSV culture.
● WBCs (CPD or EDTA tube) for HSV PCR.
● CSF - cells, protein, glucose, culture, viral culture and HSV PCR.
● Head CT/EEG may localise disease but not essential.
● Subtype specific (HSV1 and 2) serology may be useful on mother and baby.
● Ophthalmic consultation.
Consult Paediatric Infectious Disease Team
Isolation
● Contact isolation required, especially if skin lesions present.

● Isolate infants born vaginally to mothers with active genital infection for four weeks.
Room-in with mother in isolation if possible. Advise mother re handwashing.
Observation/Surveillance
● Known exposed infants require careful observation.

● Take eye, mouth, nasopharyngeal +/- skin swabs at 24-48 hours
● The family must be educated regarding the symptoms and signs of neonatal HSV.
Syphilis
● Trans-placental infection can occur at any stage of pregnancy, during any stage of
maternal disease.
● NB: Testing of cord blood/infant serum is not adequate for screening because
these tests may be non-reactive when mother is positive. Therefore mother's
serology must be reviewed/performed in all suspected cases.
Evaluation of newborn for syphilis is indicated if:
● Maternal syphilis not or inadequately treated or treated with inadequate follow up.
● Syphilis in pregnancy treated with non-penicillin regime (e.g. erythromycin).
● Syphilis treated within one month prior to delivery.
Or if any of the following clinical features present:
● Osteochondritis/periostitis.
● Snuffles, haemorrhagic rhinitis.
● Condylomata lata.
● Bullous lesions, palmar/plantar rash.
● Mucous patches.
● Hepatomegaly/splenomegaly.
● Jaundice.
● Non immune hydrops fetalis (NB: check for parvovirus).
● Generalised lymph adenopathy.
● CNS signs, elevated cell count or protein in CSF.
● Haemolytic anaemia, DIC, thrombocytopenia.
● Pneumonitis.
● Nephrotic syndrome.
● Unexplained enlarged placenta.
● IUGR; failure to thrive.
Investigations
● FBC, LFTs and syphilis serology on infant blood.

● Maternal syphilis serology.
● CSF for VDRL, cells protein and glucose.
● Long bone radiographs.
● Darkfield microscopy of skin lesions, nasal discharge, placental tissue or amniotic
fluid may show spirochaetes (but majority of cases have none of these).
Refer to Paediatric Infectious Disease Team for treatment and follow up.
May 21, 2006.
guideline.
Conjugated Hyperbilirubinaemia Reviewed by Carl Kuschel and

Simon Chin
January
2001
Background 1st Line Investigations 2nd Line Investigations Other Investigations
Background
Conjugated hyperbilirubinaemia is relatively common occurrence in neonates. Generally,

the direct (conjugated) fraction of bilirubin should not be greater than 20mcmol/L, or more
than 10% of the total bilirubin if the bilirubin is greater than 200mcmol/L. Most commonly
it is seen in extremely immature infants who are recovering from their immediate neonatal
illnesses, and who have had prolonged parenteral nutrition.
The list of possible causes is extensive and a decision to investigate will depend on the
clinical circumstances. Investigations should be targeted towards either
a. confirming a clinically suspected diagnosis, or

b. excluding a condition for which there is an available treatment.
Therefore, the form below is a template for investigation - this is not an exhaustive list and
other investigations may be warranted. In general, first line investigations should be
performed prior to discussing the case with the Paediatric Gastroenterology Service.
Other investigations should be performed as indicated.
Referral to the Paediatric Gastroenterology service should be considered early if:
a. there is progression of liver disease or liver failure

b. no clear cause is identified
● This page can be printed out by clicking on the "Print" button on the toolbar at the
top of the browser window, or by clicking on the print icon on the banner at the
bottom of the page. This page can be filed in the baby's notes and filled out
according to which investigations are ordered.
Remember: Identifying one possible cause does not exclude co-existent pathology. For
example, it is entirely possible to have both CMV and biliary atresia as dual pathologies.
First Line Investigations
● These should be done prior to consulting the Gastroenterology Service.
Test Date taken Result

Full Blood Count
and film
Total
and conjugated
bilirubin
Liver function tests -
specify:
AST
ALT
GGT
ALP
Blood gas
Albumin
Often low in preterm
infants.
If assessing synthetic
function, consider a
coagulation screen
Blood group and

Coombs
Liver ultrasound
scan
Ferritin
Thyroid function
tests
α1 Antitrypsin
(including phenotype)
Urine CMV
Maternal
toxoplasma serology
Maternal/congenital
infection Maternal Syphilis
(can be obtained from the
obstetric record as
status
necessary)
Maternal Rubella
status
Maternal Hepatitis B
status
bacterial culture
Urine sample
reducing substances
Second Line Investigations
● Second line investigations that are relatively easy to obtain and may be considered
early are:
Test Date taken Result

Coagulation screen
HIDA scan
Urine organic acids
Urine amino acids
Serum amino acids
Plasma ammonia
Plasma Lactate and
Pyruvate
Herpes simplex PCR
(if clinically suspected)
Other Investigations
● These should only be ordered after discussion with a specialist from the Paediatric
Gastroenterology service and include:
Test Date Taken Result

Hepatitis A Virus IgM
Adenovirus serology
Epstein Barr Virus
serology
Other acquired and Stool Enterovirus
congenital infections (ECHO, coxsackie)
Parvovirus PCR
HHV6 PCR
HCV
(very uncommon cause in
the initial perinatal period)
HIV
Triglycerides and
Cholesterol
Carnitine
Urine bile acids
(bile acid synthetic defects)
Very long chain fatty

acids
(peroxisomal disorders)
White Blood Cell

enzymes or
Bone Marrow
aspirate
(storage disorders)
Karyotype
Neonatal Conjunctivitis Reviewed by Simon Rowley and Lesley

Voss
December
2000
Demographics Diagnosis Causes References Antibiotics
Incidence
● 2-12% of newborns develop conjunctivitis in the first 28 days of life.
Presentation
● Conjunctival erythema
● Purulent discharge
● Lid oedema
● Look for involvement of any other system, e.g. herpes vesicles, infected scalp pH site.
History
Maternal history
● sexually transmitted diseases or exposure.

● results of high vaginal, cervical and urethral swabs in pregnancy
● length of labour and duration of membrane rupture.
Diagnosis
Bacterial culture ● dry swab for gram stain.

● wet swab for culture (eye swabs received on
● Do this first unless Chlamydia is strongly an infant <4 weeks of age routinely cultured
suspected for N. gonorrhoeae).
● if Gram stain finds Gram -ve bacilli, seriously
consider Pseudomonas and consider sepsis
screen and parenteral anti-Pseudomonal
antibiotics
Chlamydia ● Conjunctival scrapping - done with cotton-
tipped wire swab applied vigorously to the
lower palpebral conjunctiva.
● Purple swab.
● detection of C.trachomatis by EIA
(processed 5 days/week), PCR available on
request (more expensive, performed 3x/
week).
● Generally don’t look for this earlier than 5
days of age.
HSV ● Green viral culture swab (processed 5 days/

week).
NB: Transport all specimens ASAP to Microbiology Laboratory, LabPlus.
Causes
Non- ● Silver Nitrate drops

Infectious ● Corneal abrasion following trauma at delivery.
● Glaucoma (watch for corneal clouding or proptosis, is associated with portwine
stains in the ophthalmic region).
● Foreign body.
● Nasolacrimal duct obstruction may cause ‘sticky’ eyes.
Infectious Organism Age of Onset Clinical Therapy

Features
Staphylococcus 2-5 days Unilateral, Topical
aureus crusted purulent soframycin
discharge drops
Neisseria 3 days to 3 Bilateral, Ceftriaxone
# weeks hyperaemic, 50mg/kg IV/IM
gonorrhoeae
chemosis, as a single
copious thick dose
white discharge (maximum
125mg),
Saline
irrigations
hourly until
exudate
resolves.
Streptococcus 2 days Mild purulent Topical

pneumoniae, conjunctivitis soframycin
Haemophilus drops
spp, Enterococci
Pseudomonas 5-18 days Oedema and IV anti-
+ erthyema of lid, pseudomonal
aeruginosa
purulent antibiotics.
discharge.
Topical
polymyxin.
Chlamydia 2-20 weeks Unilateral or PO
* bilateral, mild erythromycin
trachomatis
conjunctivitis, 50mg/kg/day x
copious purulent 14d (bid or qid).
discharge.
Herpes simplex Conjunctivitis Acyclovir 30mg/
with vesicles kg/day IV tid x
elsewhere 14-21d.
Topical
acyclovir.
Isolation.
# Uncommon, potential for serious consequences - severe keratitis and endophthalmitis.

Requires early recognition and treatment. Needs blood and CSF culture. Consider
concomitant chlamydial infection if poor response to cephalosporin. Parents require
investigation and screening.
+ Risk of rapid progression from purulent discharge to denuding of corneal epithelium, and
perforation of cornea. The anterior chamber can fill with fibrinous exudate, iris can adhere to
cornea and later blood vessel invasion. The late ophthalmic complications can be followed by
bacteraemia and septic foci.
* Most common pathogen, 20-50% of exposed infants will develop chlamydia conjunctivitis,
10-20% will develop pneumonia. If relapse occurs repeat course of erythromycin for further
14 days. Parents require treatment.
NB: Chloramphenicol in topical therapy can obscure results of tests for chlamydia.
References
1 Tsang B, Infectious conjunctivitis in childhood. New Ethics Nov 1994, 1-8.
2 Remington and Klein. Infectious diseases of the fetus and newborn. 4th Ed. 1995.
Antibiotic Eye Preparations
Generic Name Trade Name Usual susceptibility Potential

and Staphylococci Steptococci Gram Pseudomonas Adverse
Preparation negative Effects
bacilli
Chloramphenicol Chlomin + + + - May obscure
drops, results of
ointment tests for
Chloromycetin Chlamydia;
drops, rarely
ointment marrow
Chloroptic aplasia.
drops,
ointment
Chlorsig
drops,
ointment
Minims drops
Chloramphenicol/ Chloromyxin + + + + May obscure
polymyxin B drops, results of
ointment tests for
Chlamydia;
rarely
ototoxicity or
marrow
aplasia.
Framycetin Soframycin + - + - Sensitisation;

drops, development
ointment of resistant
organisms.
Fusidic acid Fucithalmic + + - - Rarely

drops transient
stinging.
Gentamicin Genoptic + - + + Sensitisation;

drops development
Minims drops of resistant
organisms.
Gramicidin/ Neosporin + + + + Sensitisation;

neomycin drops development
polymyxin B of resistant
organisms;
rarely
ototoxicity.
Sulphacetamide Acetopt drops + + + - Inactivated

Bleph by pus and
Liquifilm drops tissue
Minims drops breakdown
products.
Tetracycline Achromycin + + + -
ointment
Tobramycin Tobrex drops, + - + + Sensitisation;
ointment development
of resistant
organisms.
May 21, 2006.
guideline.
Guidelines for Consent in Newborn Care Reviewed by David Knight and

Sarah Devine
April
2002
National and ADHB

Written or Signed Consent Verbal Consent Procedures
Guidelines
National and ADHB Guidelines
1. The national guidelines are the Code of Health and Disability Services Consumer’s
Rights (http://www.hdc.org.nz/keyword/codetop.html ). The code states:
‘Services may be provided to a consumer only if that consumer (the parent or

guardian on NICU) makes an informed choice and gives informed consent (Right
7.1).’
‘Where a consumer is not competent … and no person entitled to consent on

behalf of the consumer is available, the provider may provide services where (a) it
is in the best interest of the consumer; and (b) reasonable steps have been taken
to ascertain the views of the consumer; and (c) either, - (i) If the consumer’s views
have been ascertained, … that the provider believes that the provision of services
in consistent with (those views); or (ii) if the consumer’s views have not been
ascertained, the views of other persons who are interested in the welfare of the
consumer are taken into account. (Right 7.4)’
Right 4 states that every consumer has the right to have services provided with
reasonable care and skill. The services must comply with legal, professional,
ethical, and other relevant standards. They must be provided in a manner
consistent with his or her needs. They must be provided in a manner that
minimises the potential harm to, and optimises the quality of life of, that consumer.
2. The Crimes Act (1961) Section 151 states that everyone who has charge of any
other person unable by reason of age, sickness or any other cause to provide
himself with the necessities of life, is under a legal duty to supply that person with
the necessities of life, and is criminally responsible for omitting without lawful
excuse to perform such a duty if the death of that person is caused, or if his life is
endangered or his health permanently injured, by such omission.
3. The ADHB generic guidelines on Informed Consent are available via the intranet.
Written or Signed Consent must be obtained for:
1. All surgical procedures i.e. those requiring a general anaesthetic. Use standard
Hospital Agreement to Treat form (CR0111). Usually the surgeon and anaesthetist
get this consent, unless they are unable to meet the parents pre-operatively.
2. Blood products e.g. red cells, platelets, plasma, granulocytes, immunoglobulin.
See the Blood and Blood Products folder for further information. Use the standard
hospital Agreement to Treat form (CR0111).
3. Exchange transfusion (may be combined with consent for other blood products).
Use the standard Hospital Agreement to Treat form (CR0111).
4. Immunisation:
For hepatitis B at birth i.e. carrier mother, use the special form (HNN2). For routine
6 week and 3 month vaccinations (DTP and hepatitis B) prescribe on the ordinary
drug chart and ask the parents to countersign the prescription.
5. Autopsy:
Use the ADHB form ‘Consent for autopsy’. Specific consent must be obtained for
any organs that are to be retained. Coroner’s autopsies are not subject to consent,
but provide a general explanation of the procedure. See separate ADHB
guidelines.
6. Special radiological procedures requiring use of intravenous contrast e.g. IVP, CT
& MR scan. Use the standard Hospital Agreement to Treat form (CR0111).
7. Guthrie card: Record on the Blue Card the parent’s consent (their signature is not
required) for the blood test and to retain the blood-spot card.
8. Vitamin K: Record the parent’s consent on the Blue Card (their signature not
required).
9. Any procedure or treatment that is considered to be innovative.
10. All research. Use the consent form approved by the Ethics Committee for that
project.
Verbal consent and information for parents:
Neonatal intensive care often involves a prolonged stay with the parents not present for
much of the time. However, we encourage parents to be involved in both the care of their
baby and the decisions on treatment.
Parents must be informed of the condition of their infant and the treatment that is to be/
being used. Such information sharing is usually considered to be adequate consent for
ongoing intensive care.
If possible, parents should be seen before delivery and likely treatment explained. This is
usually only possible for parents of some very low birth weight infants.
At delivery, the baby’s condition and the initial treatment that is necessary should be
explained. Often the father accompanies the baby to NICU, and can receive further
explanation and information.
For ongoing problems and treatment, the parents should be informed as the baby’s
condition changes and the new treatments are introduced. Ideally this can be done before
the treatment. However, on some occasions this is not possible (parents may not be
readily available, the treatment may be urgent or there may not be time because the unit
is busy). In such situations the doctor or nurse should inform the parents as soon as is
practicable.
Some treatments and investigations can be anticipated, and discussed before they occur.
Examples are ultrasounds, long lines, phototherapy, treatment of PDA etc.
Discussions with parents on treatment are done by all staff. The FLNs have an important
role in keeping parents informed of ongoing treatment. Written information (pamphlets
and the ‘baby book’ etc) is particularly useful. Medical staff and NS-ANPs need to ensure
that parents are adequately informed on the specifics for their baby.
Discussions with parents should be recorded in the clinical record. It is not practical to
record every discussion with parents, but those involving significant new or changes in
treatment should be.
Occasionally, parents have very little involvement in the care of their baby on NICU and
are difficult to contact. The need for ongoing changes in treatment should be discussed
with such parents when they are present or are in contact.
Postnatal dexamethasone should be discussed in detail and consent obtained, because

of the uncertainties surrounding its use. Such discussion should be recorded in the
clinical record.
Note: Urgent treatment should never be withheld or delayed until the parents have
been informed. However the treatment must be discussed with the parents
afterwards.
Procedures that parents should be informed about include:
Blood samples Oxygen and CPAP Phototherapy

Antibiotics Ventilation Type of feeding
Other drugs X-rays Milk used
IV fluids Ultrasounds Tube feeds
IVN PDA treatment LPs
Umbilical lines Vitamin K Guthrie card
Long lines
May 21, 2006.
guideline.
Continuous Positive Airway Pressure Reviewed by Charge Nurse

Overview Newborn
May
2004
Overview Other Related Documents
● Bubble CPAP delivered

by binasal prongs is the
preferred mode of initial
ventilatory support in
infants with respiratory
distress.
● It was initially introduced
into the NICU at
National Women's
Hospital in 1997.
May 21, 2006.
guideline.
Coroner's Act 1951 Reviewed by David Knight
December
2000
Back to Guideline on Deaths in NICU
How to contact the Coroner
5. WHEN CORONER TO HOLD INQUEST
1. A Coroner shall hold an inquest in each case where he is informed that a person is
dead and there is reasonable cause to suspect that the person:
a) Has died either a violent or an unnatural death or
b) Has died while [in the legal custody of the Superintendent of a penal
institution]; or
c) Has died in such a place or under such circumstances that, in

accordance with the provisions of any enactment other than this Act, an
Inquest is required to be held.
2. A Coroner shall hold an Inquest where he is informed that any person has died a
sudden death of which the cause is unknown;
Provided that in any such case the Coroner may decide, in

accordance with section 6 of this Act, not to hold an Inquest.
3. Where a Coroner is informed that a person has died while (a committed patient or a
special patient within the meaning of the Mental Health Act 1969), or while committed to
the care of the Superintendent of Child Welfare under the Child Welfare Act 1925, or
while an inmate of a children's home under Part 1 of the Child Welfare Amendment Act
1927, or while an inmate of an Intebrates Home or a Reformatory Home under the
Reformatory Institutions Act 1909, or while in such a place or in such circumstances that,
in accordance with the provisions of any enactment other than this Act, notice of the
death is required to be given to a Coroner, the Coroner shall hold an Inquest if he
considers an inquest to be necessary or desirable:
Provided that nothing in this subsection shall be deemed to authorise a

Coroner to dispense with an Inquest in any case to which subsection (1) or
subsection (2) of this section applies.
4. It shall be the duty of any person finding a person lying dead, or having knowledge of
the death of any person in any of the circumstances set forth in the foregoing provisions
of this section, to report the death to a constable, who shall thereupon report the death to
a Coroner.
5. After a constable has reported the death to a Coroner in accordance with subsection
(4) of this section, the police shall make such inquiries as may be necessary for the
purposes of this Act or as may be directed by the Coroner.
Head Ultrasound Scans

Detection of Germinal Matrix-Intraventricular Haemorrhage Reviewed by Carl Kuschel
and Periventricular Leukomalacia

June
2005
Associated Risk Factors Timing of IVH Diagnosis

Indications for USS Grading System Other Information
Intracranial
haemorrhage
(ICH) can
affect
newborns of
all gestational
ages and
often is
clinically
‘silent’.
Germinal
matrix
haemorrhage
and
intraventricular
haemorrhage
(GM-IVH) is
most common
in the
premature
population.
Estimates of
frequency
have
changed over
the last 20
years.
Currently,
large series
report a 15%
prevalence in
infants <32
weeks.
National
Women's
data for the
period 2001-
2003
indicates an
incidence of
10.0% for GM-
IVH in
infants<32
weeks.
Those most
at risk were
infants <28
weeks
gestation.
Grade 3 and
4 GM-IVH
was seen in
2.9% of
infants<32
weeks, with a
higher
incidence
(15.5%) in
infants <26
weeks
gestation.
The incidence
of
periventricular
leukomalacia
(PVLM) in
infants <32
weeks at
National
Women's
over the
same period
of time was
1%.
Routine
screening for
GM-IVH is
performed in
infants <30
weeks or
<1250g at
birth.
Associated Risk Factors
● SGA status of newborn ● Outborn infant

● Maternal pre-eclampsia ● Antepartum haemorrhage
● Asphyxia ● Base deficit >10
● Male gender
Timing of IVH
● Most haemorrhage occurs within the first three days of life.

● "Late" haemorrhage (i.e., after three days of age) may be associated with pneumothorax and its
restriction of venous return to the heart.
Diagnosis
● GM-IVH is reliably diagnosed with ultrasonography.

● Parenchymal injury (ischaemia, petechial haemorrhage, haemorrhagic infarct) can be diagnosed
with ultrasonography, but with less sensitivity.
● Parenchymal ischaemia, without haemorrhage, may not be evident even with transducers of high
frequency and very good equipment.
● MRI is more sensitive but currently impractical as a routine investigation in preterm infants.
● CT scanning is more sensitive than ultrasonography in cases where extra axial (subdural,
subarachnoid) or posterior fossa haemorrhage is suspected.
Indications for Cerebral Ultrasound Scan
● Routine screening for GM-IVH should be performed in infants <30 weeks or <1250g at birth.
❍ Some more mature or larger infants will have cranial ultrasound scans performed because
of clinical suspicion of GM-IVH.

❍ The first scan should be performed at 4-5 days of age, by which time most cases of GM-
IVH will have occurred.

❍ Discussion with parent(s) regarding prognosis/follow up can be conducted by the admitting
team.
● Ultrasonograms can always be obtained when clinical signs and/or symptoms suggest that
intracranial haemorrhage has occurred, regardless of the baby’s age.
● A second ultrasound scan should be done at one month of age, looking at resolution of previous
GM-IVH, evidence of parenchymal injury, and for evidence of periventricular leukomalacia (PVLM).
● A "discharge" head ultrasound scan should be done at "term" (36 weeks is often chosen as the
most appropriate time) or at discharge from the nursery.
❍ In infants <30 weeks, this should be done at the same time as the screening renal
ultrasound scan for nephrocalcinosis.

● Be aware that ultrasound is not a sensitive method of detecting cortical or brainstem injury as
seen with neonatal encephalopathy, or for detecting evidence of cerebrovascular events or
collections outside the brain.
❍ In infants suspected of other pathologies, MRI or CT should be considered.
Grading Systems
GM-IVH
I Germinal layer (subependymal haemorrhage)

II Intraventricular haemorrhage - no dilatation (<97th percentile)
III Intraventricular haemorrhage with dilatation
IV Intraparenchymal haemorrhage
Periventricular Leucomalacia
without cysts echogenic periventricular margins (flare)

cystic multiple small periventricular cysts
porencephaly large intraparenchymal cysts
Other Information
● Research protocols may require variations on a grading system; grading should follow the
requirement of the protocols.
● The ultrasonographers describe abnormalities in detail on their reports.
● Be aware that transverse measurements of lateral ventricles from the midline will be influenced by
the size of the cavum septum pellucidum, a normal midline structure in preterm infants. Scans
should be reviewed with the Radiologist at conferences in NICU.
May 21, 2006.
guideline.
C-Reactive Protein (CRP) Reviewed by Alan Groves

Indications and Interpretation
February
2003
● C-Reactive protein should NOT be checked as a routine part of a septic screen in

neonates.
● It may be helpful in excluding infection in some cases of sepsis if normal levels are
obtained 24-48 hours after the onset of symptoms. It should therefore be
considered in cases in which diagnosis of sepsis is unclear, and where negative
cultures may not give sufficient reassurance to discontinue antibiotics. Common
examples may include when maternal intrapartum IV antibiotics were given, and in
late onset sepsis where lumbar puncture specimens were unobtainable or blood-
stained.
● A level of greater than 10mg/litre is abnormal
❍ Less than 10 is normal and makes sepsis much less likely (see Background
and Applications).
● Judicious use of CRP to enable earlier discontinuation of antibiotics in some
instances may be cost-effective, decrease the possibility of resistance and in some
cases may decrease duration of hospital stay.
Sample
● The laboratory requires 0.10-0.15 ml of SERUM, therefore 0.3-0.5ml (depending

on haematocrit) of whole blood will be required, in a lithium heparin (green top)
tube.
Background
● CRP is an acute phase protein synthesised in the liver in response to inflammatory

cytokines. Its levels may increase up to a thousand-fold during an acute phase
response. Its short half-life (19hours) means levels should fall rapidly after
1
elimination of the (often microbial) source.
● There is generally a delay of up to 24 hours between onset of symptoms of
infection and a rise in serum CRP. Sensitivity of the test at presentation is only
40% - that is, 60% of subsequently proven sepsis episodes will have a normal
2
initial CRP (compared to 80% sensitivity of immature to total neutrophil ratio).
● With this in mind CRP level should not be checked at birth or at initial presentation
with symptoms suggestive of sepsis.
Applications
● The value of CRP is in its reliability in the 24-48 hours after birth/onset of infection.
● In early onset sepsis (before 72 hours old), a single CRP 24 hours into illness has
3
a 93% sensitivity for "probable" sepsis. 2 measures 24 hours apart are even
better. A more intuitive measure is the Bayesian ratio (likelihood ratio) - for a single
normal CRP the ratio for probable sepsis was 0.10. In effect this means that
having obtained a normal CRP one can assume probable sepsis to be 10 times
less likely. For 2 measures the ratios is 0.03, making probable sepsis 30 times less
likely.
● In late onset sepsis the reliability of the test is similarly high. A single CRP has a
sensitivity of 85%, with likelihood ratio of 0.19 (sepsis 5 times less likely given
normal result), and 2 separate measures have a likelihood ratio 0.07 (sepsis 14
times less likely).
● The positive predictive value for a raised CRP is poor so a positive test is poorly
predictive of sepsis. False positives arise from intraventricular haemorrhage,
meconium aspiration, NEC, pneumothorax, surgery and immunisation.
● Reassuringly, false positives don’t tend to occur with birth asphyxia, prolonged
rupture of membranes, respiratory distress syndrome and viral illnesses (except
invasive HSV).
● False negative results generally only occur early in infective episodes, though also
in UTI. False negatives don’t appear to occur in either infection with coagulase
2
negative staphylococcus or childhood meningitis, though there have been few
45
studies focussed on neonatal meningitis. ,
● A level of 10mg/litre has consistently been shown to be the most reliable cut-off to
indicate sepsis. There is a link between the level of elevation of the CRP and the
risk of sepsis, with positive predictive value steadily increasing up to CRP >100.
● Judicious use of CRP to enable earlier discontinuation of antibiotics in such
instances would be cost-effective, decrease the possibility of resistance and in
some cases may decrease duration of stay.
References
1 Ehl, S., et al. C-reactive protein is a useful marker for guiding duration of antibiotic therapy in suspected
neonatal bacterial infection. Pediatrics, 1997; 99:216-21.
2 Franz, A.R., et al. Reduction of unnecessary antibiotic therapy in newborn infants using interleukin-8 and
C-reactive protein as markers of bacterial infections. Pediatrics 1999. 104:447-53.
3 Benitz, W.E., et al., Serial serum C-reactive protein levels in the diagnosis of neonatal infection. Pediatrics
1998;102:E41.
4 Gerdes, L.U., et al., C-reactive protein and bacterial meningitis: a meta-analysis. Scand J Clin Lab Invest
1998; 58:383-93.
5 Tatara, R. and H. Imai, Serum C-reactive protein in the differential diagnosis of childhood meningitis.
Pediatr Int 2000; 42:541-6.
May 21, 2006.
guideline.
Chronic Lung Disease Discharge Planning

Reviewed by Simon Rowley and
Lynley Nichols
June 2003
Criteria for Referral to

Pre-referral assessment Discharge Planning Follow-Up
Respiratory Service
Recommended Saturations
Weaning
at Home
Criteria for Referral to the Respiratory Service
The Respiratory Service are keen to be involved where at discharge:
a. Severe clinical disease (marked respiratory effort, indraw etc).

b. Severe chronic lung disease on chest radiograph.
c. Requiring more than 250ml/min of oxygen.
d. Right ventricular hypertrophy on ECG
❍ R wave in V1 and V2 >20mm
❍ RSR’ pattern in V1 with R > R’
❍ Positive T wave in V1
❍ Right axis deviation
e. Babies without these criteria and who are expected to require home O2 briefly,
need not be referred.
Pre-referral Assessment For Infants Going Home on Oxygen
a. Overnight oximetry with printout, preferably current but also two weeks prior to
establish trend.
b. ECG.
c. Early morning capillary gas.
d. Current chest radiograph.
e. Growth chart.
f. Social Work/Homecare or Family Liaison Nurse assessment, usually including a
home visit.
g. Interim summary of neonatal course.
Discharge Planning
a. There will usually be a pre-discharge planning meeting approximately two weeks

prior to discharge in order to set a discharge date.
b. This meeting should include an invitation to the Respiratory Nurse Specialist,
General Practitioner, the Consultant Respiratory Paediatrician, Dietitian, other
NICU staff including the Neonatal Consultant, Family Liaison Nurse, Visiting
Therapist, Social Worker etc as appropriate.
c. The Respiratory Consultant may choose not to attend or become involved at this
stage if the risk factors for severity are not present (that is, if we anticipate the
baby will have minimal problems and come off oxygen relatively quickly following
discharge).
d. Infants will be not be considered for discharge if they have poor feeding, poor
growth, frequent desaturations, instability with feeding.
e. Infants being considered for discharge should have had 10 days stability on NICU
or PIN.
f. Infants who have just come off oxygen should also fulfil these criteria if being
discharged.
Outpatient Follow-Up for the Infant on Oxygen
a. Neonatal paediatrician
b. Respiratory Paediatrician for severely affected infants or other infants whose
progress is not as expected once discharged
c. The Homecare Nurses will visit weekly or according to need.
Recommended Best Practice For Home Oxygen
Saturation Level Proportion of Study

96-100% 80-90%
90-95% 10-20%
<90% None
This is different from the inpatient NICU Oxygen Saturation Targets, which are lower at
around 90-95%. Babies at home are not continuously monitored, and therefore their
discharge and home saturations are targeted higher.
Weaning
a. No changes should be made for the first two weeks on home oxygen.
b. If 90% of the time saturations are >95%, weaning can be initiated.
c. Minimum flow rate at home 0.1L/min.
d. Weaning should consist of periods during the day off oxygen initially 2-4 hours,
then 8 hours, finally off oxygen at night.
e. Following each change, day-time oximetry ± overnight oximetry should be carried
out.
f. Overnight oximetry needs to be carried out following discontinuing oxygen.
May 21, 2006.
guideline.
Cytogenetic Studies in the Neonatal Period Reviewed by Julie McGaughran
January
2001
Note: Given the increasing concerns around genetic testing without informed consent,
only tests for diagnostic or management reasons should be carried out in the neonatal
period.
● Consultation with the Northern Regional Genetic Service is recommended when

further advice is needed (Ext. 5530 AKH)
Cord Blood ● Confirmation of suspected chromosomal disorder following

abnormal antenatal ultrasound undertaken late in pregnancy or
where further investigation declined during in the pregnancy.
● Chromosome mosaicism found at CVS, amniocentesis or
cordocentesis (where indicated)
● DNA studies. Cord blood confirmation of single gene disorder
suspected on ultrasound findings eg achondroplasia
Testing for late onset disorders should not be undertaken
● Confirmation of biochemistry where prenatal diagnosis of a
known condition undertaken (requested by testing lab)
Neonatal ● Blood
Testing
i. Clinical features consistent with known
chromosomal abnormality.
ii. Multiple congenital anomalies consistent with
possible chromosomal abnormality
iii. FISH; where range of clinical features suggests a
specific microdeletion syndrome, specific FISH
test should be requested.
iv. Ambiguous genitalia.
● Solid Tissues
i. Products of conception.
ii. Post mortem - (1) - (4) as above.
Guidelines for ● Features of a single gene disorder/syndrome (for diagnostic

DNA Studies in purposes) e.g. hypotonia
the Neonatal ● Mitochondrial myopathy syndrome.
Period ● Features of possible single gene disorder where infant may die
and genetic testing may later become available (DNA storage)
Blood Collection Tubes
● DNA studies - EDTA (1 tube)

● Chromosomes + FISH - Lithium heparin (2ml)
May 21, 2006.
guideline.
Death of an Infant on NICU Reviewed by Simon Rowley and

Jane Harding
March
1998
See also ADHB guidelines on referral to the Coroner
See also Deceased Baby Forms (intranet only)
These guidelines are not necessarily to be followed exactly. Each situation will be
different and will need to be handled accordingly.
On intensive care usually the death of a child will be anticipated and there will be time for
both parents to be present. Where possible they should have the situation clearly outlined
and the likely course of events (and mode of death) explained. This is especially
important in the event of' turning off the ventilator support so that the parents are not
unduly frightened by the prospect of an imagined horrible spectacle.
Parents should be encouraged but not forced to be present and to ask any family,
including the child's siblings or close friends to come in for support. Opportunities for
photography should be offered and efforts should be made to enable them to cuddle and
hold the child before, during and after death. One needs to gauge their feelings about this
at the time and not force them to do anything against their inclination. Similarly after
death, time should be allowed for the parents to be alone with the child if they wish but
someone should be popping in and out of the room to provide support if necessary .Once
the child has been laid out peacefully and if possible with some flowers, a photograph can
be taken which can be given to the parents. This may be more comforting than previous
photographs which have included intensive care apparatus etc. They may also wish to
return to see the child several times.
The parents are seen as soon as possible afterwards by a Paediatrician who must have
enough time to fully discuss the cause of death. Post mortem is offered as a final
examination to reveal any other factors relevant to counselling, genetic or otherwise.
Although most parents are keen to know about whether the same circumstances might
occur with the next child, a few parents may not initially see the relevance of post mortem
results and it is therefore the doctor's (preferably the registrar's) duty to impart this
information. One can usually explain that not only will it help other children in the future
with similar problems if we know as much as possible about the particular condition
causing death, but also that it is important from their own point of view if they wish to have
children in the future. (It is our experience that in the past when parents have been
several weeks afterwards who have not consented to a post mortem, invariably express
regret for having made that decision at the time). If the parents object to a post-mortem it
should be assumed that further discussion would be best carried out by another doctor
and that one should not persevere to get consent. At this point the Consultant should be
approached to decide whether further discussions with the parents is appropriate.
Post-mortem consent should always be requested in a proper manner and should be fully
informed. In Maori families particularly and with young parents, it should be suggested
that the parents ask their elders or relatives to participate in the discussion and have
more family involvement if this is appropriate. This may avoid the distress which can
occur when young Maori parents consent to post mortem but the grandparents and Maori
elders object for spiritual and cultural reasons.
In cases which are to be referred to the Coroner (if in doubt the Coroner is happy to be
telephoned at any time, day or night to discuss the desirability of a Coroner's autopsy),
the consent of the parents is not sought. It is important to explain to the parents the
reasons for the need for a Coroner's autopsy. The attached Coronial Autopsy Clinical
Summary form must be completed. Please note that all IV lines, catheters, NG tubes are
to be left in-situ but if being viewed by the parents before autopsy, tubes, lines etc, can be
cut short and covered with a dressing.
Many people need to be informed as soon as possible and the following check list should
be completed:
1.Paediatrician.
2.Obstetrician or other Consultant involved.
3.General Practitioner and Plunket Nurse.
4.Referring Consultant if applicable.
5.Social Worker if applicable.
6.Death certificate.
7.Post mortem consent.
8.A note for Pathologist if there are any specific questions to be answered at post
mortem.
9. The Perinatal Mortality Summary sheet should be completed at the same time as
the Death Certificate.
10. A clinical discharge letter should be dictated before the notes leave the nursery if
at all possible, even if final arrangements, post-mortem results etc are not known.
These can always be added later.
11. A follow up appointment should be made after discussion with the specialist
involved. This is initially 6 -8 weeks after the death and preferably after the
relevant Perinatal Morbidity Meeting discussion. An appropriate appointment letter
is available with the Secretaries if desired.
NB: There is also a booklet 'Neonatal Death' in NICU which can be used as a reference
relating to responsibilities of nursing and medical staff after an infant dies.
May 21, 2006.
guideline.
Guidelines for Paediatric Presence at Delivery Reviewed by Carl Kuschel
April
2004
See also Attendance at High Risk Deliveries
Paediatric resident medical staff and NS-ANP’s are available to attend at risk deliveries
and compromised fetuses. Referrals should be made by the LMC attending the mother. In
emergencies or situations of urgency, messages can be relayed through clerical staff.
Paediatric staff often have to prioritise calls, so accurate information is needed.
In most situations the 1st call locator (usually a paediatric SHO, registrar, or NS-ANP)
should be called. Except in the situations set out below when 2nd call registrar or NS-ANP
should attend, the 1st call person is responsible for informing other paediatric staff if he/
she wants them to attend as well. The registrar/NS-ANP will attend deliveries with a
house surgeon at the beginning of a run, until the house surgeon is competent at
resuscitation.
The paediatric registrar/NS-ANP will contact the specialist if his/her presence is indicated,
unless there is a prior arrangement.
The paediatric service should be informed of labours likely to produce babies needing
paediatric care. This communication would normally be to Paediatric Medical Staff.
Referrals requesting paediatric input to the management of pregnancy/labour should be
to specialists.
1st Call
Level 2 Level 3
Registrar-
Registrar- Registrar-
NS-ANP-
NS-ANP NS-ANP Specialist
SHO
Locator Locator
Locator
93 5536 93 5535
93 5537
Meconium staining No
light, no fetal distress
light + fetal distress Yes
Thick Yes
Fetal distress Yes if severe
Preterm 34-36 weeks Yes
Preterm < 34 weeks Yes
Preterm < 31 weeks Yes Yes Discuss

prior to
labour/
delivery
Severe IUGR Yes
IUGR Post
delivery
Suspected fetal infection Yes
Maternal diabetes mellitus Post

delivery
Multiple pregnancy Yes Yes
LSCS Yes
Immediate LSCS Yes Yes
Low forceps No
High forceps Yes
Low ventouse delivery, no No
fetal concerns
Ventouse delivery with Yes
fetal distress, meconium,
or obstetric concerns
Breech delivery Yes
Drug dependent mother Post
delivery
Fetal abnormality likely to No Yes Possibly Discuss
affect condition at delivery prior to
labour/
delivery
Fetal abnormality other After Discuss
than above delivery prior to
labour/
delivery
Haemolytic disease Pre/post Discuss Possibly Discuss
delivery prior to prior to
labour/ labour/
delivery delivery
There may be other situations when a paediatric resident should be called. Any baby who
has problems or is unwell should be referred to the paediatric service. Private doctors
(GP or specialist) or independent midwives should either refer to the paediatric service
when appropriate, or to a private paediatric specialist.
All three resident paediatric staff answer 777 emergency calls. The 777 call does not go
to the specialist on call - a request for specialist attendance will need to be directed
through the operator. If a specialist is required urgently, then contact them via their pager
(and append with "*777") or their cell phone.
May 21, 2006.
guideline.
Developmental Care
Reviewed by Charge Nurse -
Newborn
December 2004
Scope Background Related Documents References
Scope
● Applies to all nurses employed in the Newborn Service.
Background
● Developmental support integrates the developmental needs of the infant in NICU

within the framework of medical care.
● Key concepts for delivery of developmental care include promoting organised
infant neurobehavioral and physiological function and tailoring the physical
environment, such as light and sound, to protect vulnerable developing sensory
systems, all within a context of family centred care.
● When providing developmental care for infants two overriding principles need to be
considered:
❍ First, that infants are unique and can display a wide variety of behaviours.
❍ Second, that the physiological condition of infants differs widely. For
example, a baby born at term who becomes critically ill will have different
developmental needs to an infant who is term but born prematurely.
● Hence these recommendations are a guide not a rigid prescription for every baby.
Assessment of infant cues remains central in the provision of developmental care.
May 21, 2006.
guideline.
Referral to Community-Based Child Development Reviewed by Carl Kuschel and

Services Rosemary Marks
April
2002
Many infants admitted to NICU are at risk of developmental problems in childhood. For
many infants, developmental problems do not surface until after discharge. However,
some infants require referral for developmental follow-up prior to discharge.
Note: National Women’s Newborn Services have a Child Development Unit (CDU) which
is distinct from the community-based Child Development Services (CDS). Please do not
confuse the two when making a referral.
● All infants <1500g are automatically referred to NWH CDU to have

their developmental progress assessed at the age of 18 months and
4 years (infants <1000g are also seen at 9 months). See also the
CDU guideline.
● Infants referred to the community-based Child Developmental
Services (CDS) generally require ongoing surveillance and/or
intervention for developmental concerns (e.g. motor delay, feeding
problems). Click here to open a referral form.
In addition, NICU has a developmental therapist service that performs inpatient

developmental assessments and intervention. A referral should be made for infants who
are going to require community developmental follow-up and who will be in-patients in
NICU for more than a few days.
Generally, there are two situations where developmental follow-up should be arranged
prior to discharge.
Infants expected to ● Early referral to the appropriate Developmental
have developmental Paediatrician within the family’s catchment area.
problems ● The referring doctor needs to provide sufficient
information about the baby’s condition, what clinical
● This includes course is expected, and what information the parents
infants with have been given.
severe birth ❍ It may be most appropriate for this to be done
asphyxia with at a specialist-to-specialist level.

persisting ● It is important to specify if a referral has already been
neurological made to the appropriate CDS.
abnormalities, ● Early referral (2-3 week prior to discharge) to the
infants with appropriate Child Developmental Service within the
significant brain family’s catchment area.
lesions (e.g. major ● It is important to specify which paediatricians are
intracranial involved or to whom referrals have been sent.
haemorrhage, ● Need to provide sufficient information (including social
periventricular circumstances, if appropriate) for the CDS to be able
leukomalacia), to prioritise the needs of the baby and family.
and infants with ● Provide a name and contact number so further
syndromes known information can be provided if necessary.
to involve
developmental
delay (e.g. Down
Syndrome).
Infants at risk of ● An early referral (2-3 weeks prior to discharge) to the

developmental appropriate Child Development Service is preferred
problems but is not always possible.
● Staff need to specify what follow-up arrangements
● This may include have been made (for example, NWH Paediatrician vs.
preterm or term Starship Paediatrician vs. other paediatrician).
infants where ● Sufficient information needs to be provided for the
developmental CDS to be able to prioritise the needs of the baby and
concerns are family.
raised prior to ● Provide a name and contact number so further
discharge, but information can be provided if necessary
referral to a
Developmental
Paediatrician is
not indicated at
this point
May 21, 2006.
guideline.
Referral to NICU Developmental Therapists

Reviewed by Gaela Kilgour,
Inpatient Neurodevelopmental Assessment and Lynette Eaton, and Simon Rowley
Intervention
May
2002
● Designated time for this service is Wednesday morning each week with capacity to
respond to urgent referrals within 48 hours as necessary.
● A developmental assessment and intervention service is provided by an
occupational therapist and physiotherapist for infants who meet the following
criteria:
● Less than 1000 gms birthweight

These referrals are automatic via FLN
The following four criteria are via medical team referral:

● Infants with clearly defined special needs e.g. neuromuscular disease and
chromosomal abnormalities
● Infants having suffered perinatal asphyxia with HIE
● Preterm infants with extra risk factors e.g. grade IV IVH, PVL, difficult or
complex course
● Long stay infants e.g. 3 months or more with developmental needs
● This service may apply to infants described in the "expected" and "at risk" groups
outlined in the Community Child Development Service guideline.
● Other specific interventions such as splinting or strapping with known diagnoses
will occur following discussion with the medical team.
● If a child is referred to Community Child Development Services, the developmental
therapists will liaise with the appropriate agency and will forward appropriate
reports.
May 21, 2006.
guideline.
Referral to Dietitian - Neonatal Nutritional Risk Reviewed by Barbara Cormack

Screening Criteria (Dietitian) and Carl Kuschel
November
2005
● Children meeting these criteria may have special nutritional requirements and
should be considered for referral to a dietitian.
Over 2 weeks of age ● <2/3 expected caloric requirement

❍ Fluid restriction ≤160 ml/kg/day
❍ <100ml/kg/day P10 or N10 after Day 4 of life
❍ <180ml/kg/day enteral feeds in a preterm infant
❍ <150ml/kg/day enteral feeds in a term infant
● <10 g/kg/day weight gain for >5days (<38 weeks CGA)

<20 g per day weight gain for >7days (>38 weeks CGA)
● Significant obstructive jaundice
● Serum phosphorus <1.3mmol/L
● Intolerance to preterm formula or breast milk fortifier
● Intake >200ml/kg/day of preterm formula or breast milk
fortifier
Any infant with ● NEC where elemental formula is being considered

● Short bowel syndrome
● Malabsorption
● Chronic lung disease where growth impairment is likely
● Congenital heart disease where growth impairment is likely
● Gastrointestinal anomaly
● Metabolic disorder
● Chylothorax
● Renal failure
● Osteopenia requiring additional calcium and phosphate
● Possible zinc deficiency
● Breastfed baby where there are concerns about maternal nutrition
Note: All infants with a birth weight of <1.8 kg should be receiving fortified breast
milk or preterm formula until 2.5kg or they reach term or are fully breast fed.
Any printed version can not be assumed to be current. Printed copies of this document are valid for
Monday, May 22, 2006.
guideline.
Review and Recording Notes on NICU Babies Reviewed by David Knight
January
2001
New or Unstable Babies More Stable Babies Very Stable Babies Review
Procedures Weekly Plan Weekend Plan
This gives a guideline for reviewing and writing notes on NICU babies to ensure that
babies are appropriately assessed and residents use their time efficiently.
New/Unstable Babies
● Assess twice daily.

● Write notes twice daily
● Examine Acute problem list
● Assessment Progress in last day
● Observations and assessment
● Plan, reasons and interpretation
More Stable Babies
● Once in detail (as above). During the day except at weekends.

● Once in brief: Either in the day or at night. At weekends, split these assessments
between day and night staff.
Very Stable Babies
● Review daily during the week.

● At weekends, review daily in brief, often on the ward round. Write in notes.
Review
● If asked to review a baby, record appropriate observations and interpretations at

the time. Do not wait until the next routine review
Procedures
It is important to document significant procedures undertaken, whether successful or

unsuccessful. Procedures which should be clearly documented (with date and time)
include:
● Intubation/reintubation
● Extubation
● Intercostal drain insertion
● Umbilical venous and arterial catheterisation
● Peripheral artery catheterisation
● Longline insertion
● Urinary catheterisation
● Lumbar puncture
● Ventricular tap
● Exchange transfusion
● Institution of non-routine medications should also be clearly documented.
Weekly Plan
For stable babies, ensure that there is a weekly plan. Avoid duplication (of full
assessments and of tests etc.).
● Investigations: Blood tests: day, tick when ordered

● Scans/X-rays/Other
● Drugs: List once weekly or if changed.
● Record levels, date, change, plan.
● Growth/Nutrition: Measure at least weekly.
● Plot growth weekly.
● Respiratory: Part of daily review. Summarise overall course weekly.
Weekend Plan
● Write a weekend plan including blood tests.

guideline.
Domperidone (Motilium) as a Galactogogue Reviewed by Carol Thomas and
(Domperidone and Breast Feeding) Carl Kuschel
October
2002
Rationale Efficacy Dosage Precautions Recommendations References
● Domperidone has replaced Metoclopramide as the Galactogogue of choice
in NICU
Rationale
Domperidone is a peripheral dopamine-receptor antagonist used in the treatment of
dyspepsia, reflux oesophagitis, and nausea and vomiting. One of its side effects is an
1 2
increase in prolactin levels , .
Unlike metoclopramide that works centrally, domperidone works on peripheral dopamine
1
receptors in the GI wall and CTZ centre of the brainstem . Its effects on prolactin
secretion occurs at the pituitary level (outside the blood-brain barrier) 2. Domperidone is
less lipid soluble, has a larger molecular weight (426), and is highly protein bound (93%)
1, as compared to metochlopramide. Combined with the peripheral action this results in
2
fewer central side effects such as anxiety, depression and extrapyramidal symptoms
and less medication crossing through into breastmilk. Because domperidone crosses less
freely into breastmilk (compared with metoclopramide) the possible risks to the infant are
also reduced 3. There has been some concern of the possible effect of dopamine
antagonists on the functional maturation of central dopamine mechanisms in newborns
4
(identified in experiments on rats) .
Da Silva showed a milk domperidone concentration of 1.2ng/ml, after a dose of 10mg
2
three times per day, measured on day 5 from randomly selected samples . This is
compared with 125.7ng/ml of maxalon from milk samples taken 2 hours after a dose of
10mg of metoclopramide 4
Efficacy
Domperidone has been approved by the American Academy of Pediatrics (AAP) for use
in breastfeeding 1 and is currently the only galactogogue that has been scientifically
evaluated through a randomised, double-blind placebo-controlled trial 3. This trial by da
Silva et al 2 showed milk volume increased by 44.5% in the domperidone group
compared with 16% in the placebo group (p<0.05). There was a steady increase in milk
volume commencing 48 hours after initiation of treatment up until day 7, which was the
last day of medication. This correlated with a rise in serum prolactin in the domperidone
group, rising from 12.9 trial μ /L [SD7.7], measured as baseline, to 119.3 [SD97.3] μ/L
of a randomly sampled blood test on day 5. The serum prolactin levels returned to
baseline 3 days after treatment was ceased.
Dosage
● 10-20mgs, orally, 3-4 times per day
● A prescription for 2 weeks should be given initially and may be repeated if
necessary. The medication may need to be continued for up to 8 weeks, however
the long-term use of domeperidone has not been studied 1.
● There is little evidence to guide practice as regard to when to start, how long to
continue and how to wean from domperidone.
Precautions, Interactions, and Adverse Effects
● Prescribers should be aware of maternal conditions or medications that may be
affected by Domperidone
● Dosage should be reduced if there are underlying maternal renal or hepatic
conditions.
● Domperidone use should be avoided with antacids and antisecretory agents.
● Medications that inhibit the Cytochrome P450 enzyme system (e.g. azole
antifungals, macrolide antibiotics, HIV protease inhibitors, and nefazodone) may
increase Domperidone levels.
● Rare adverse effects include headache, dizziness, abdominal cramps, dry mouth,
drowsiness, and allergic reactions.
Recommendations
● Domperidone therapy to enhance lactation does not replace expressing and may
not work in some cases. It should only be given if the mother has been expressing
at least 6 times in 24 hours for at least 3 days. She must have had specific
teaching in effective expressing techniques and positioning of the baby at the
breast if possible.
● If the mother is still under obstetric or medical care, she should discuss the
possible use of domperidone with her medical adviser(s).
● To ensure that adequate assistance is given to the mother, it is advisable that the
mother is referred to a Lactation Consultant and or the charge nurse, or her LMC
before therapy is commenced.
References
1 Hale. Domperidone. Medications and Mothers’ Milk 2002: 10th Edition;230-231
2 da Silva et al. Effect of domperidone on milk production in mothers of premature newborns: a randomized,
double-blind, placebo-controlled trial. CMJ 2001;164(1):17-21.
3 Gabay. Galactogogues: Medications that induce lactation. J Hum Lact 2002;18(3):274-279.
4 Hofmeyr et al. Domperidone: secretion in breast milk and effect on puerperal prolactin levels. Br J Obs
Gynae 1985; 92:141-144.
5 New Ethicals Catalogue. Adis International. May-Nov 2002; 256

guideline.
Management of Down Syndrome Babies at NWH Reviewed by Salim Aftimos
November
2002
1. A Specialist Paediatrician discusses the diagnosis with the parents. He/she may
ask the Family Liason Nurse, NICU Charge Nurse, or the involved midwife on the
ward to attend this meeting. The meeting should normally be held in a private
place with both parents present.
2. The Specialist Paediatrician will notify the GP and/or Obstetrician and obtain
information or advice that may help with the counselling of parents.
3. The parents should be given the time they need to absorb the news. Repeat visits
may be necessary to deal with questions and distress.
4. In consultation with the Family Liaison Nurse, Charge Nurse/or Midwife and
parents, a decision is made on the need and timing of referral to the Hospital
Social Worker, Home Care Nurse, Physiotherapist, Chaplain etc.
5. The Paediatrician will consult with the parents and Family Liaison Nurse/Charge
Nurse/Midwife/Social Worker on the timing of introduction of books/pamphlets on
Down Syndrome and referral to the Down Syndrome Association.
6. A referral is made to the Developmental Therapist and a separate referral is made
to the Early Intervention Team. If the baby resides in Central Auckland or the North
Shore, Dr Rosie Marks should be contacted to offer her the chance of meeting the
parents before discharge.
7. Cardiac assessment -ECG, CXR. Echo at GLH.
8. Thyroid function testing. Ensure the Guthrie card has been sent.
9. Obtain an FBC as a screen for polycythemia and transient myeloproliferative
disorder.
10. Anticipate feeding difficulties and if required arrange for Lactation Consultant and/
or Speech-Language Therapist input
guideline.
Infants Born to Drug Dependent Mothers Reviewed by Carl Kuschel
July
2004
Medical and Nursing Treatment of The Unsettled Irritable

Universal Precautions Points of Interest
Care on the Ward Withdrawal Baby
Guidelines
● The pregnancy will be managed by a Specialist Obstetric Team with the Midwife
being the key person. The aim is to ensure continuity of care for mother and her
partner. The Team meets regularly.
The team is as follows:

❍ Obstetrician: Dr Harilal.
❍ Midwives: Marian Cornwell (Midwife), and midwifery staff of Ward 32.
❍ Paediatricians: Dr Carl Kuschel and Dr Simon Rowley.
❍ Social Workers: ADAPT team social workers, or NICU Social Workers if
baby in NICU.
● The baby is expected to be normal in all respects other than smaller than average
for gestation.
● Maternal drug use alone is not an indication for delivery attendance - delivery will
be attended by neonatal staff only if there are other fetal or maternal reasons for
attendance. If NICU admission is necessary and there are no complications (e.g
asphyxia, LBW) the baby may spend time with the parents before transfer.
Naloxone should be avoided if possible because of the likelihood of precipitating
and intensifying withdrawal symptoms.
● The baby will be admitted to Ward 32 for observation. This will generally be for a
minimum of 7-10 days but may be for several weeks if medication is needed
because of drug withdrawal.
● Breastfeeding is encouraged, regardless of the drugs that have been taken by the
mother.
● Parents are expected and will be encouraged to spend as much time as possible
with their baby.
● Drug dependency care may include:

❍ Methadone maintenance during pregnancy.
❍ Methadone detoxification /benzodiazepine detoxification.
❍ Attendance at counselling agencies or therapeutic communities.
❍ Alcohol use.
❍ Other drugs including antipsychotic tranquillisers (prescribed or not).
● A file will be kept on Ward 32, including care plans and letters from Paediatricians
which will also be filed in the maternal notes. These files are kept in strict
confidence in the Charge Midwife office.
● Exclusions from the plan to send babies direct to Ward 32 (i.e. indications for
being nursed on the Newborn Intensive Care Unit)
❍ Low birthweight, premature or unwell as for normal indications for
admission to NICU.
❍ Polydrug abuse should be considered, particularly if there are confounding
social factors but the methadone dose alone is not an exclusion criteria.
❍ Maternal and other social complicating factors.
● There is a need to ensure confidentiality for parents. A single room should be

allocated if possible. The baby's history must not be discussed in front of other
parents. The case notes and drug charts are to be kept in the office at all times.
The baby's condition or reason for admission or length of stay is not to be
discussed with anyone other than the parents. This includes grandparents.
● Visiting is the same as for all postnatal wards.
Medical and Nursing Care on the Ward
● There are a small group of primary midwives that will be dealing with the mother
and baby.
● It is important during the baby's stay in hospital that the mother has consistency in
management, deals with as few staff as possible, i.e., one consultant or delegated
junior staff member and one senior nursing staff member to be the information
providers.
● Score sheets are to be kept in the office and maintained regularly.
● It is not routine to send a urine sample for toxicology if the mother is well known to
the ADAPT team and drug use is well documented.
❍ If a toxicology screen is required, the first urine from the baby is to be sent
for toxicology.
❍ Meconium samples (which will give an indication of drug use over recent
weeks rather than days) can be sent if indicated but need to be negotiated
on an individual basis with Toxicology at LabPlus.
● The Paediatric Consultant on service for the ADAPT team will visit as indicated
and communicate with the parents and nursing staff. If the baby is on medication,
then this will be daily.
● The Paediatric House Surgeon or Registrar should be called for any fever,
vomiting, feeding problems or unstable temperature which may be the signs of a
sick baby other than drug withdrawal.
● If the baby scores 8 or higher on the score chart then the Paediatric Registrar
should be informed.
● 75% of mothers on the methadone programme are Hepatitis C positive. The infant
will need antibody and RNA virus testing at 4-6 months, 12 months and 2 years. A
cord sample should be sent at birth for PCR, although there is a risk that this may
be falsely positive if contaminated by maternal blood in which case a repeat
sample should be taken on the baby.
Universal Precautions
● Gloves should be used for all nappy changes or for nursing staff changing the
babies - and handling baby before initial bath.
Treatment of Withdrawal
● This is managed by the Paediatric Consultant in conjunction with the Registrar and
Charge Midwife and parents. Medications are started when the baby has several
scores of >8 and after adequate consultation.
● The medication may only be changed by a Paediatric Consultant or Registrar.
● The drug used is neonatal morphine solution 1mg/ml.
❍ Start at 0.5mg/kg/day in 4 divided doses (that is, 6-hourly) and reduce by
10-15% of the original dose every 2-3 days if possible. The infant may need
increasing doses for stabilisation in the first few days.
● Medication must be given strictly as charted given directly into baby's mouth by
syringe. The drug must be given by a Registered Nurse/Midwife who checks the
drug - not a parent.
● Medication times are not to be changed to fit in with baby's feeds times. This
interferes with the withdrawal regime. Do not draw up milk into the syringe
because dead space can lead to overdose of morphine.
● If the medication time falls between feeds it is not necessary to wake the infant
completely. It has been noted on past experience that babies take the medication
well if the syringe is slipped into the mouth and medication is taken without any
problems. The baby is then tucked back to sleep.
● It is always a help if identification is on the left as this disturbs the baby less when
noting identification.
● An alternative treatment is chlorpromazine 2.2mg/kg/24 hours given in four divided
doses either orally or by injection. Full dosage should be given for two to four days
then tried to decrease at two day intervals if baby's condition, according to the
clinical score, permits.
Management of an Unsettled, Irritable Baby
● Check baby has dry napkin.

● Baby may be hungry. These babies will often take extra feeds but may be difficult
or sloppy feeders. They should not be tube fed unless there are other indications
such as hypoglycaemia or scores are approaching treatment levels and being
unduly influenced by symptoms of hunger. Dummies are very useful. Deep water
bathing and massage often help relax the baby if needed. Many babies will settle
well in the swinging cradle sling. A disposable napkin or incontinent pad must be
used when nursing baby in the sling to protect the sling cover.
● Frequent cuddling, walking with front pack, may be soothing music or quietness
rather than loud music (individual variation).
● When baby is stable, mother may take baby for a walk within the unit, if on NICU,
or outside the ward if on Ward 32. This is arranged between mother/charge
midwife/nurse - times to be specific so that all staff are aware. The day nursery
may be used. Later on, following negotiation with charge midwife, mother may take
baby for a walk in the grounds. This is subject to permission on each occasion and
excludes the Nurses Home.
● Midwives and nurses need to know the routine lines of communication when:
❍ threatened with violence
❍ parents are uplifting baby against medical advice
❍ there is inappropriate behaviour from parents and/or visitors
Discharge Planning
● A meeting may be organised prior to discharge. The following people may be

asked to attend:
❍ Paediatrician
❍ Charge Midwife/Nurse
❍ Public Health Nurse or Plunket Nurse,
❍ GP (if possible)
❍ Parents
❍ Liaison Midwife
❍ Counsellor Methadone Services/CADS Unit
❍ ADAPT S/W.
● For short stay infants who have not had withdrawal symptoms, e.g. less than 10
days there should be adequate communication between GP, Paediatrician,
Charge Midwife/Nurse with phone contact with other parties.
● Babies are not followed up by Neonatal Homecare unless they have other
problems such as prematurity or low birthweight, that would normally be referred.
● Medical follow up will be by the Paediatrician at clinic in 3-4 months or as
necessary and we will offer a follow up appointment at one year. This is
particularly important if mothers are Hepatitis C positive.
● These infants have a higher incidence of Sudden Infant Death Syndrome and
although this does not justify the use of monitors, the various community support
networks must be alerted. Advice about reduction of risk factors (supine sleeping
position, breast feeding, discouraging smoking, discouraging co-bedding) should
be given. Monitors may be indicated for preterm infants.
● Mother should attend teaching sessions for:
❍ Home environment/clothing/when baby is sick.
❍ Infant resuscitation classes.
❍ Deep warm bathing.
❍ Car seat needed.
❍ The Ward Clerk makes Paediatric appointment at 3-4 months for Outpatient
follow up. For infants discharged home from NICU, the Paediatric
Registrar will dictate a discharge letter with a copy to the General
Practitioner. Include follow up of HCV testing. NB: Note the privacy act and
confidentiality.
Points of Interest
● 70% of babies born to mothers taking heroin or methadone will manifest signs of
withdrawal. Some are only mildly affected. Babies born to methadone addicts
show more frequent and severe signs than heroin addicted mothers.
● The likelihood of the baby being affected is related to maternal consumption and
the length of time addicted. However some babies born to heavily affected
mothers may show no signs, while those born to 'light' users may show significant
signs of withdrawal.
● Although 70% will show signs of withdrawal, only about half of these will have
signs severe enough to require treatment. 90% of these showing signs will start to
have them within 48 hours. Initial signs of withdrawal are rare after 10 days of age.
● About half of affected infants requiring treatment need it for 10 - 20 days and one
third for up to 49 days after birth.
● Mortality is said to be about 3% but with treatment should be virtually nil.
guideline.
The Neonatal Electrocardiograph Reviewed by David Knight and

Clare O'Donnell
October
1998
Normal Values Interpretation Conditions with Specific ECGs
● Report the rate, rhythm, conduction, p waves, frontal plane axis, QRS complex.
● Comment on T waves over R chest. Look at QT interval
● Rate = 1500 / number of little squares or
= 300 / number of big squares
● Frontal plane QRS axis
Normal Values
SV1+ R+S
Ht QRS PR QIII RSV RV RV6 V4
QV6 RV1 SV1 1 6 SV6 R/S V6
Rate vector interval
Age
mm
o mm mm mm mm sec mm mm
/min sec sec mm
+59 to 4.5 2 5-26 0-23 0.1- ? 0-11 0-9.5 0.1 - ? 28 52.5

93- -163 0.08-.16 (14) (8) (2.2) (4) (3) (2.0)
<1
154 (137)
day (0.11)
(123)
91- +64 to 6.5 2.5 5-27 0-21 0.1 - ? 0-12 0-9.5 0.1 - ? 29 52
0.08-.14
1-2 159 -161 (14) (9) (2.0) (4.5) (3) (2.5)
(0.11)
days (123) (134)
91- +77 to 0.07-.14 5.5 3 3-24 0-17 0.2 - ? 0.5-12 0-10 0.1 -? 24.5 49
3-6 166 -163 (0.10) (13) (7) (2.7) (5) (3.5) (2.2)
days (129) (132)
107- +65 to 0.07-.14 6 3 3-21 0-11 1.0- ? 2.5- 0-10 0.1 - ? 21 49

1-3 182 -161 (0.01) (11) (4) (2.9) 16.5 (3.5) (3.3)
weeks (148) (110) (7.5)
(mean), ? = undefined
Interpretation
P waves Peaked (>3mm) = RA hypertrophy
Broad or biphasic = LA hypertrophy
Right Ventricular Pure RV1 >10mm (no SV1)

Hypertrophy
RV1 >25 (SV1 present)
Upright TV1 after 3 days (RV strain)
Right axis deviation >+180°
Left Ventricular RV6 >17mm in 1st week (>25mm in 1st month)
Hypertrophy
SV1 >20mm
SV1 + RV6 >45mm
QV5 or V6 >5mm with tall symmetric T
Asymmetric T inversion = LV strain
ST depression = LV strain
Biventricular Hypertrophy Abnormal voltages over R and L chest leads
Prominent mid-precordial voltages
AV Block 1° Prolonged P-R interval
2° Mobitz Type 1 Progressive increase in P-R
(Wenkebach) then dropped beat
2° Mobitz Type 2 Dropped beats without P-R
prolongation
3° Complete heart block
Tachycardias Atrial flutter - atrial rate 300-400, and regular saw-tooth
pattern of P waves in LI and LIII.
Ventricular rate depends on degree of A-V block.
Atrial fibrillation (rare in newborn). Often associated with
cardiac abnormalities, especialy if LA enlargement.
Atrial tachycardia.
AV re-entry tachycardia.
WPW: Short P-R paroxysmal tachycardias. Wide QRS
with ∆ wave re-entry through accessory pathway.
AV Nodal re-entry tachycardia
Sinus tachycardia
Ventricular Tachycardia >5 ventricular ectopics in rapid succession
Identify independent atrial activity
Direct
Indirect (Capture, atrial capture
beats with narrow complexes
(Fusion, supraventricular
beat with ventricular
complex)
Regular, broad complex tachycardia
Concordant pattern over chest leads
Ventricular Fibrillation
Prolonged Q-T
Ectopic Beats Common: 21-31% of healthy preterm and up to 23% of

term infants
Conditions with Specific ECGs
Preterm Infant Shorter QRS duration, shorter PR and QT interval

Less RV dominance than term infant at birth
AV Canal QRS -30 to -90°
RA enlargement
Prolonged PR
Ebstein's Anomaly QRS low voltage or RBBB or ventricular pre-excitation
PR prolonged, RA enlargement
Hypoplastic Right Heart Variable.
Absent or diminished RV voltages
Transposition of the Often normal
Great Arteries
Tricuspid atresia RA hypertrophy

Left axis deviation
guideline.
Guidelines for Consideration of ECMO Reviewed by John Beca (PICU)

(ExtraCorporeal Membrane Oxygenation) and Carl Kuschel
July
2002
Eligibility Criteria Contraindications Pre-ECMO Investigations

Optimal Pre-ECMO Tubes and Lines Consideration of ECMO
ECMO is proven treatment for life-threatening respiratory and/or cardiac failure in

neonates. Overall survival rates are approximately 80% in infants with a predicted survival
of 20%.
Eligibility Criteria
ANY of the following AND underlying disease process which is likely to be reversible
1. OI ≥30 - 60 for 0.5 - OI = (MAP x FiO2 x 100) / PaO2 (mmHg) (click here to open
6 hours the OI calculator)
Standard criteria: OI ≥40 on conventional ventilation
OI ≥50-60 for HFOV
2. PaO2 <5.3kPa Despite maximal ventilatory support
(40mmHg) for >2
hours
3. Acidosis and Shock pH <7.25 due to metabolic acidosis
Raised lactate
Intractable hypotension
Contraindications to ECMO
Absolute
● Gestational age <34 weeks

● Birth weight <2kg
● >Grade 1 intracranial haemorrhage
● Severe and irreversible brain injury (as best as can be judged by
consultant neonatologist)
Lethal malformations or congenital anomalies
● Significant non-treatable congenital heart disease

● Severe and irreversible lung, liver or kidney disease
Relative
● > 10-14 days of mechanical ventilation

● Uncontrolled bleeding or coagulopathy
● IVH Grade 1
● Congenital Diaphragmatic Hernia if PaO2 never > 9.3kPa (70mmHg)
or PaCO2 never < 10.7–13.3kPa (80–100mmHg)
Pre ECMO Investigations
Investigation Responsibility
CXR NICU
FBC and Differential NICU
INR, APPT, Fibrinogen NICU
Electrolytes NICU
Urea and Creatinine
LFTs
Head Ultrasound Scan NICU
Cardiac Echo NICU but should have repeat
study performed by Paediatric
Cardiologist prior to cannulation
Crossmatch (2 adult units) NICU
Optimal Pre ECMO Tubes and Lines
Item Responsibility Comments

Nasal ETT NICU ● If very unstable, the
risks of electively
changing an oral ETT
to a nasal ETT need to
be considered carefully.
● Otherwise change to
nasal ETT after
cannulation
Peripheral arterial line NICU ● Ideally, this should be

pre-ductal (right radial
or brachial) but if
unsuccessful a
functioning UAC is
satisfactory.
Double lumen femoral PICU

venous catheter
Urinary catheter NICU
Consideration of ECMO
With the advent of HFOV and nitric oxide, patients being referred for ECMO will generally
be sicker than previously with little or no reserve. As a treatment with a proven survival
benefit, ECMO should be considered for any neonate with severe cardio-respiratory
failure and discussed early to facilitate timely transfers.
As many as possible of the pre-ECMO investigations, tubes and lines should be done
prior to transfer to allow for rapid initiation of ECMO if it is required.
Consider and discuss ECMO in any near-term neonate with:
● PaO2 <6.7kPa (50 mmHg)

● FiO2 1.0
● PIP >35cm H2O
● OI >30 on conventional ventilation

● OI >40 on HFOV
● Failure to improve with HFOV over 2-12 hours is also a very poor prognostic sign
● In the first instance discussion should be with either Dr John Beca or Dr David
Buckley
❍ If neither is available, contact the PICU Specialist on call with the
switchboard.
If a decision is made to transfer to PICU:
1. Ensure that 2 adult units of red cells have been cross matched
2. The transfer will be performed by either a Consultant Neonatologist or Senior
Fellow
3. PICU nursing staff will liaise with NICU nursing staff to determine current drug
infusions and doses
4. Initial ventilator settings and drug infusions at PICU will be as per the most recent
NICU settings
guideline.
Exchange Transfusion Reviewed by David Knight
March
2004
Technique Procedure Partial Exchange Transfusion

Other Related Documents References
Technique
● There are a variety of techniques for exchange transfusion. That chosen will
depend on the vascular access available and the choice of the specialist
supervising the exchange.
● The exchange equipment is usually set up by nursing staff, but the specialist
responsible for the exchange must check the set-up prior to commencing the
exchange.
❍ This set-up is a joint responsibility between medical and nursing staff, but
the specialist doing the exchange has overall responsibility for the
procedure.
1. Isovolumetric Exchange
● Remove blood from an artery while infusing through a vein at the same rate.
In Out
Umbilical vein Peripheral artery
or Umbilical vein 2
Umbilical artery
1
or Peripheral vein Peripheral artery
or Peripheral vein Umbilical artery
2. Push-pull
● This can be done through an umbilical venous catheter. 3 Exceptionally, an

umbilical artery catheter can be used.
● Ideally, the tip of the UVC should be in the IVC/right atrium (at or just above the
diaphragm) but can be used if it is in the portal sinus. For ‘high’ UVC placement,
position should be checked by an X-ray. This is not always necessary for a low
position. A low positioned catheter is usually removed after each exchange.
<1000gms Use 5ml aliquots

1000-2000gm 10ml
3 15ml
>2000gm
● Withdraw blood over 2 minutes, infuse slightly faster. Aim to exchange 180 ml/kg
over 1½ -2 hours.
● If using a 2-catheter push-pull method, withdraw the blood at the same time that
blood is given.
3. Infusion Method
● The choice of method is that of the specialist supervising.

● The choice of infusion method is a syringe or an infusion pump.
● Blood removal is by syringe.
● With the isovolumetric method and syringes, the doctors/NS-ANPs involved infuse
and withdraw at the same rate.
● REFER TO THE OTHER RELATED DOCUMENTS FOR LINKS TO THE
DIAGRAMS OF THE SET-UPS.
Volume
● Usually use two blood volumes (180 ml/kg).

❍ One blood volume removes 65% of baby’s red cells.
❍ Two blood volumes removes 88%.
3
● Thereafter the gain is small.
Procedure
● There must be at least one doctor/NS-ANP and one nurse exclusively involved in
the exchange throughout its progress.
● Meticulous care must be taken throughout, especially with volume balance, the
rate of the exchange, the vital signs and any signs of air in the lines.
● A doctor/NS-ANP must be present throughout the exchange. He/she may leave
the room briefly to get blood results, but if called away, the exchange is stopped
and the lines flushed.
● All exchanges are to be conducted in NICU Level 3.
● It may be necessary for another doctor/NS-ANP to cover the rest of the unit during
the exchange.
● IF THERE ARE ANY DOUBTS ABOUT THE SET-UP OR THE METHOD OF
DOING THE EXCHANGE TRANSFUSION, THEY MUST BE IMMEDIATELY
REFERRED TO SENIOR MEDICAL OR NURSING STAFF AND THE EXCHANGE
INTERRUPTED UNTIL THEY ARE ANSWERED SATISFACTORILY.
3
Partial Exchange Transfusion
● To correct severe anaemia without hypovolaemia or polycythaemia.
Polycythaemia
Blood Volume x (PCV initial - PCV desired)

Volume exchanged (ml) =
PCV initial
Anaemia
Blood Volume (ml) x (Hb desired - Hb

Volume exchanged (ml) = initial)
(Hb Donor - Hb Initial)
● Blood volume = 70-90 ml/kg for term and 85-110 ml/kg for preterm infants.
References
1 Fok TF. So LY. Leung KW. Wong W. Feng CS. Tsang SS. Use of peripheral vessels for exchange
transfusion. Arch Dis Child. 1990 65(7 Spec No):676-8
2 Martin JR. A double catheter technique for exchange transfusion in the newborn infant. NZMJ 1973; 77
(490):167-9
3 Edwards. chapter 41 in Atlas of procedures in neonatology. 2nd ed. Lippincott. 1993
4 Ramirez AM. Woodfield DG. Scott R. McLachlan J. High potassium levels in stored irradiated blood.
Transfusion 1987; 27(5):444-5
5 Ramirez. Unpublished. Potassium in blood for exchange transfusion. 1986.
6 Schuerger G. Robertson A. Ertel I. Effects of agitation of donor blood on neonatal exchange transfusions.
Clinical Pediatrics 1970; 9(12):715-8
7 Peterec SM. Management of Neonatal Rh Disease. Clinics in Perinatology 1995;22:561-92
Newborn Services Feeding Policy Reviewed by Charge Nurse -
Newborn
December
2004
Introduction Purpose Scope Associated Documents

Breastfeeding Policy Artificial Feeding Policy Other Related Documents
Introduction
The Newborn Service at National Women’s Health promotes breast milk and
breastfeeding as the optimum nutrition for infants as it provides many benefits. Benefits
apply to both the mother and the infant and include nutritional, immunological, psycho-
social and financial components.
The cultural, personal and/or physical factors affecting infant feeding are to be respected
and staff are to support and assist women in their choice of infant feeding.
This document details the policies and recommended best practices to support
breastfeeding the preterm or sick infant within the Newborn Service. It also provides
policies and recommended best practice for alternative methods of infant feeding
including bottle feeding and gastric tube feeding.
Purpose
The purpose of this policy is to ensure that Newborn Service health professionals protect,
promote and support breastfeeding during all stages of the infants association with the
service. This policy also seeks to provide information and skills on safe infant feeding
regardless of the method used.
Scope
This policy applies to all Newborn Service health professionals and employees who
provide care for, or have contact with, women and infants within Newborn Services. This
also applies to both inpatient and outpatient services.
The policies reflect the Global Criteria of WHO/UNICEF to meet accreditation for a Baby
Friendly Hospital.
Associated Documents
The table below indicates other documents associated with this policy.
Type Document Title(s)
Infection Control Manual ● Decontamination. Standard Precautions
Board Policy ● Informed Consent
NW Policy & Procedure ● Infant Feeding
Supporting ● Global Strategy for Infant and Young

literature regarding Child Feeding. WHO/UNICEF 2003
breastfeeding: ● Breastfeeding: A Guide to Action. MOH
2002.
● Baby Friendly Hospital NZ
Breastfeeding Authority 2000
● Food and Nutrition Guidelines for
Healthy Infants and Toddlers (aged 0-
2years) MOH 1999 PHC
● Interim Statement on HIV and
Breastfeeding WHO Sept. 1999.
● Infant Feeding – Guidelines for NZ
Health Workers MOH 1997 PHC
● Ten Steps To Successful
Breastfeeding WHO/UNICEF 1989
Pamphlets ● Breast Massage and Hand Expressing

regarding breastfeeding Breastmilk.
● Mastitis/plugged Ducts 2004 NW
Lactation Consultant
● Guidelines for Expressing Breastmilk
2004
● Storage and Transport of Expressed
Breast Milk 2003
● Use of Breast Pumps in Newborn
Services 2003
● Breastfeeding the Preterm infant: Hints
for Going Home 2004 (Newborn
Services Lactation Consultant)
Publications ● Global Strategy for Infant and Young
Regarding Artificial Feeding Child Feeding. WHO/UNICEF 2003
● Food and Nutrition Guidelines for
Healthy Infants and Toddlers (aged 0-
2years). MOH 1999 PHC
● Infant Feeding – Guidelines for NZ
Health Workers. MOH 1997 PHC
● Guidelines for Interpretation of the
WHO International Code of Marketing
of Breastmilk Substitutes in N.Z. MOH
PHC 1995.
● International Code of Marketing of
Breastmilk Substitutes. WHO 1981.
Pamphlet regarding artificial ● Information about Bottle feeding Your

feeding Baby (NW Lactation Consultant &
Nutrition Services 2000)
Breastfeeding Policy
Responsibility of the Health Professional
Health professionals are to give current, accurate and consistent, non-judgmental

breastfeeding information and supportive encouragement to enhance successful
breastfeeding. It is essential that feeding of preterm or sick infants is managed in a safe
and professional manner that enhances success for the infant, whatever the feeding
method.
The respect of, and sensitivity to each woman’s personal and psychosexual dignity is to
be upheld when assisting her to breastfeed. It is expected that touching the woman’s
breast will be minimised and the health professional will seek each woman’s permission
before touching and/or gentle handling of her breasts.
The health professionals breastfeeding practice will be in accordance with the WHO/
UNICEF Ten Steps to Successful Breastfeeding (1989), New Zealand College of
Midwives Handbook (1992), and the NZ Breastfeeding Authority Incorporated Baby
Friendly Hospital Initiative, particularly Part Two: Hospital Level Implementation for
Aotearoa New Zealand (2002), and the NWH Breastfeeding Policy (2003).
In order to maintain health professionals’ breastfeeding knowledge and skills, ongoing

review of practice is expected and will include annual updates of breastfeeding
knowledge in accordance with BFHI Aotearoa, 2002.
Feeding challenges and /or difficulties identified

Breastfeeding challenges and/or difficulties are to be identified early and documented in
the clinical records with a management plan.
● If breastfeeding difficulties are unresolved consult with the Clinical Charge Nurse
or Nurse Specialist. Appropriate referral will be made to the Speech and Language
Therapist or Lactation Consultant, Newborn Services.
● The Newborn Services Lactation Consultant is available to provide education to
both staff and mothers.
Discharge Planning
Discharge planning is to incorporate written breastfeeding information and referral to

appropriate services in the community resources to support continued breastfeeding
success.
Artificial Feeding Policy
Responsibility of the Health Professional
The health professional has a responsibility to meet the WHO Recommendations for
Infant Feeding, Article 4:2.
The health professional's responsibilities to women who choose to artificially feed their
babies are to:
● Ensure they have made an informed choice and are aware of the benefits of
breastmilk/breastfeeding.
● Ensure they are aware of the financial costs for providing feeding equipment and
providing formula until the infant is 12 months old.
● Document in the infant’s clinical records the feeding choice of the mother.
● Initiate a documented feeding plan that includes the appropriate volume and
frequency of feeds for age and weight of the baby.
● Provide one on one education on the safe administration of artificial feeding
including the correct preparation of formula, safe storage, sterilisation techniques,
and how to bottle-feed.
● The opportunity exists for the mother to provide her own feeding equipment for the
infant.
● No feeding equipment or formula is to be given to a mother or family unless it is
specialised and or prescribed.
Feeding challenges and/or difficulties identified
● Bottle feeding challenges and/or difficulties are to be identified early and

documented in the clinical records with a management plan.
● Consult with the Clinical Charge Nurse or Family Liaison Nurse. Appropriate
referral will be made to the Speech and Language Therapist or Lactation
Consultant, Newborn Services.
● Ongoing bottle feeding challenges will require referral to appropriate community
resources including Community Speech and Language Therapist.
guideline.
Neonatal Nutrition Guideline Reviewed by Barbara Cormack

(Dietitian) and Carl Kuschel
February
2006
Born at less than 32 weeks OR Born at 32+ weeks AND birthweight

Additional Notes
birthweight <1800g 1800+g
● These guidelines have been developed based on the current RDIs

(Recommended Daily Intakes) for low birthweight infants and the specific nutrient
composition of Nutricia low birthweight feeds and fortifier.
● The guidelines do not apply to other feeds, which may have different nutrient
levels.
● If at any time growth is inadequate, consider referral to a dietitian.
Born at At any time if

growth is Preparation
<32 weeks Transition Stable At
inadequate, for
OR consider referral to Oral Feed Growing Discharge
Discharge
birthweight to dietitian
<1800g IVN then, When full feeds Stop Breast Milk Breast milk or
Breast milk or reached add Fortifier or term formula
term formula Breast Milk change from
Fortifier preterm formula
Karicare BMF 1 to term formula
pkt per 50ml when
Feed breast milk approaching
or discharge
change to or
Preterm approximately 40
Formula weeks or 2500g,
(Nutriprem) whichever occurs
earliest.
Begin at 1ml 2- Grade up to 3- Beginning 3- to 4-hourly or
hourly or as hourly feeds as sucking feeds. on demand
tolerated tolerated
Grade up as (approximately
tolerated 1500g) If the baby is
Usually increase going to be
Frequency feed volume by breast fed, then
1ml, every 12 to the first feeds
24 hours. offered should be
Increase more breast feeds.
rapidly once
tolerated.
Increase to 180ml/kg/day Usual volume is Demand volumes

180ml/kg/day 180ml/kg/day.
Increase to
Feed Volume Increase to 200ml/kg/day if
200ml/kg/day if poor growth.
poor growth.
Start Vitadol C Continue Vitadol Start Vitadol C Prescribe 0.3ml

0.30ml per day C only until 0.3ml per day. (10 drops) per
when tolerating tolerating 180ml/ day Vitadol C and
1/3 enteral feeds kg/day, then stop. 0.5ml/kg/day
or >50ml/kg/day Start 0.5ml/kg/ Ferrous sulphate
Supplements day Ferrous
elixir once 4
If volume taken sulphate elixir weeks of age or
is <180ml/kg/ once 4 weeks of on discharge,
day, add Vitadol age. whichever comes
C 0.15ml per day
earlier.
Note:
● The recommended daily neonatal intake of Vitamin D is 10μg or

400iU. This is provided by ≥180ml/kg/day of fortified EBM or
preterm formula because breastmilk fortifier and preterm formula
have higher levels of vitamins and minerals.
● Babies having lower volumes of FEBM or preterm formula need
Vitadol C 0.15ml daily to meet the recommended Vitamin D intake.
● Babies on all other feeds (e.g. unfortified EBM, term or hydrolysed
formula, which have much lower levels of vitamins and minerals)
need Vitamin D 0.3ml daily.
Born at 32 At any time if

growth is Preparation
+ weeks Transition Stable At
inadequate, for
AND consider referral to Oral Feed Growing Discharge
Discharge
birthweight to dietitian
1800+g Breast milk or Breast milk or Breast milk or Breast milk or
Feed term formula term formula term formula term formula
3-hourly unless 3-hourly feeds 3-hourly feeds or Demand
risk of on demand
hypoglycaemia
If the baby is
Frequency going to be
breast fed, then
the first feeds
offered should be
breast feeds.
Day 1 60-90 ml/ 180 ml/kg/day Increase to 200 Demand volumes

kg/day ml/kg/day if poor
Day 2 90-120 ml/ growth or on
kg/day Increase to demand
Feed Volume Day 3 120-150 200ml/kg/day or
ml/kg/day more if poor
Up to 180 ml/kg/ growth
day
Nil Nil Nil Nil

Supplements (see notes
below)
Additional ● Some infants with a gestation at birth ≥32 weeks and

Notes: birthweight ≥1800g may require fortifier or preterm formula for
growth.
● Some infants who are demand feeding will take volumes in
excess of 200ml/kg/day of expressed breast milk or term
formula.
● Iron (ferrous sulphate) should be commenced at 4 weeks of age
in eligible infants.
❍ Usual starting dose 3mg/kg/day of elemental iron (0.5ml/
kg/day) but increase dose to 6mg/kg/day in iron-deficient

infants.
❍ Infants receiving treatment with erythropoietin require
iron supplementation on commencement.

● Vitamin and iron supplements should be continued till the infant
is well established on a balanced diet of solids.
❍ Some groups recommend that infants should be
supplemented until 12 months of age.

● Iron and/or vitamins may be commenced in some infants who
do not fit the above criteria. These may include:
❍ Infants at risk of nutritional deficiency, for example –
malabsorptive diseases, long term parenteral nutrition,

fluid restriction (<160ml/kg/day), gastrointestinal tract
losses, and infants of mothers who are known to have or
are at risk of nutritional deficiencies.
❍ Babies at high-risk of iron deficiency.
● Note that a small number of infants who do not fulfil the criteria
above for iron supplementation may nevertheless develop iron
deficiency anaemia within the first few months of life. A FBC
and iron studies should be undertaken to confirm the diagnosis,
and supplementation should be instituted.
References
1 Franz AR, Mihatsch WA, Sander S, Kron M, Pohlandt F. Prospective randomized trial of early versus late
enteral iron supplementation in infants with a birth weight of less than 1301 grams. Pediatrics 2000;106
(4):700-6.
2 Klein CJ. Nutrient requirements for preterm infant formulas. J Nutr 2002;132(6 Suppl 1):1395S-577S.
3 Hay WW Jr, Lucas A, Heird WC, et al. Workshop summary: nutrition of the extremely low birth weight
infant. Pediatrics 1999;104;1360-1368.
4 Rao R, Georgieff MK. Neonatal iron nutrition. Semin Neonatol 2001;6:425-35.
guideline.
Feeding Newborn Babies on Postnatal Wards Reviewed by Salim Aftimos and

Carol Thomas
January
2001
1. The main aim of these guidelines is promotion of successful breastfeeding.

2. Mothers should be encouraged to breastfeed their babies soon after birth.
❍ Newborns should be nursed whenever they show signs of hunger, such as
increased alertness or activity, mouthing or rooting.

❍ Ideally, they should be nursed frequently, 8-12 times per 24 hours until
baby is satisfied, usually 10-15 minutes of effective sucking on each breast.

❍ Milk delivery time varies between mothers. Some babies may be satisfied
with less frequent feeds.

❍ When breastfeeding is well established, feeding frequency gradually
decreases and most babies will be satisfied with around 6 feeds per day.
3. Healthy term babies do not require supplements (water/formula). See section on
indications for supplementation of breastfeeding.
4. Premature Babies
❍ Well premature babies usually at 35-36 gestation are often admitted to
postnatal wards with their mothers.

❍ These babies should be offered the breast as soon as possible after birth
and then demand up to 3 hourly.

❍ For those who latch and suck well on the breast, there is no need for
supplementation.
❍ Serum glucose may be checked if there is uncertainty about feeding
success or if there are risk factors (e.g., hypothermia).

❍ On the other hand if the baby does not show interest in feeding, is having
difficulties latching, or does not suckle for long, a supplementary feed will
be required.
❍ A feeding plan needs to be individualised.
❍ Feeding volumes should follow the recommended standards.
❍ Expressed breast milk is the food of choice, but if this is not available in
sufficient quantity, infant formula may be offered. Advice may be sought

from a Lactation Consultant.
5. Supplementation
❍ Supplementation of breastfeeding is usually requested when there is
concern that baby is at risk for hypoglycaemia. In that context consider the
following:
❍ Expressed breast milk is preferable to formula.
❍ Birth asphyxia
■ Significant birth asphyxia may be a risk factor for hypoglycaemia.
■ Such babies remain unwell after the initial resuscitation and are
admitted to NICU.
■ Term babies, depressed at birth, but responding quickly and fully to
resuscitation and are judged well enough to go to the postnatal

ward, should be considered well babies and encouraged to proceed
with normal breastfeeding.
❍ Small for gestational age babies.
■ Keep in mind that babies below the 10th centile in birthweight are
not necessarily SGA.

■ Consider such factors as ethnic background, parity and maternal
height which may influence birthweight.

■ Asymmetrically small babies with disparity between head
circumference and weight are more at risk for hypoglycaemia.

❍ Infants of Diabetic Mothers
■ These babies who are clinically macrosomic are at a greater risk for
hypoglycaemia.
■ Babies with adequate weight for gestational age are at a lower risk.
■ Should these babies require supplementation for initial
hypoglycaemia, attempt to expedite transfer to full breastfeeding.

(See nursing management of infants of diabetic mothers of postnatal
wards separate guideline).
❍ Large for Gestational Age Infants
■ Currently the NWH guidelines advise checking glucose levels in
babies above 4500g.

■ Hypoglycaemia is typically early in such babies and is rare beyond 8
hours of age.
■ Early feeding should be stressed again and any supplementation
should be limited to the initial few feeds, with attempts to expedite

full breastfeeding.
❍ Occasionally babies are seen on postnatal wards who may have been
receiving suboptimal quantity of breast milk, appear clinically dehydrated,
may have had significant weight loss from birthweight (7-10% below
birthweight), may have elevated temperature and show excessive sucking
activity.
■ These babies need to be supplemented with EBM/formula until they
are clinically well.

■ To support breast feeding, always offer breast feeds first and
supplement after this.

❍ Phototherapy
■ Phototherapy causes an increase in insensible water loss and in
stool water contents, equivalent to 15-25ml/kg/day.

■ This should be balanced by increased demand for breast milk in a
well term baby who has established breastfeeding.

■ Thus routine supplementation of babies under phototherapy is not
recommended.
■ If breastfeeding is not well established or baby appears clinically
under-hydrated, then formula supplementation is advised.
References
1 Breastfeeding and the use of Human Milk. American Academy of Pediatrics Policy Statement. Pediatrics
100; 1035-1039, 1997.
2 Hypoglycaemia of the Newborn. WHO Report 1997.
guideline.
Fluid and Electrolyte Requirements Reviewed by Carl Kuschel
July
2004
Volume Recommended Electrolytes Arterial Line Fluids Glucose Intake

Insensible Water Loss GI Obstruction Chest and Peritoneal Drains Renal Impairment
Hyponatraemia Hypernatraemia References
Click here to link to the fluid and electrolytes calculator
Volume (ml/kg/day) Recommended
Day1 Day 2-3 Day 4-5 Day 6-7 Day >7
<1000g 60-90 120 140 150 180

>1000g 60 90 120 150 180
1. Start on 10% dextrose. Monitor blood glucose.

2. If under a radiant warmer, add 20 (mature) to 40 (immature) ml/kg/day.
3. If under phototherapy, add 20 ml/kg/day
Volume given will depend on the clinical condition of the infant, with fluid restriction
indicated with asphyxia, renal impairment or PDA.
Very preterm infants with immature skins can lose large amounts of fluid transcutaneously
over the first few days. This is monitored by serial serum Na+ measurements and by
change in weight. Fluid intake may have to increase to 200 ml/kg/day.
Electrolytes
Day 1 None routinely

Add electrolytes:
Na+ 3 mmol/kg/day (very preterm

infants may need more)
K+ 2 mmol/kg/day
Ca ++ 1 mmol/kg/day
Day 2 onwards
● Do not add Ca++ routinely in relatively well

infants only likely to be on short term IV
fluids. (This is most babies as the sicker,
longer term babies will be on IVN)
Additive Concentration Requirement Formula

4 Molar 3 mmol/kg/day 500 x weight x 0.75
Na+
(4mmol/ml) (0.75ml/kg/day) 24 hour total fluids
1 Molar 2 mmol/kg/day 500 x weight x 2
K+
(1mmol/ml) (2ml/kg/day) 24 hour total fluids
10% Ca
1 mmol/kg/day 500 x weight x 4.5
Ca2+ gluconate
(4.5ml/kg/day) 24 hour total fluids
(0.22mmol/ml)
Notes:
● Assumes that additives are added to a 500ml bag of fluid

● Add Heparin 250units/500ml to central venous (including long) line fluids.
● If daily requirements are increased or decreased, these formulations need to be
recalculated
● This system does not take into account the amount of sodium in arterial fluids or
other infusions and calculations need to be adjusted accordingly.
Arterial Line Fluids
<1000gms ● Initially 0.5ml/hr of 0.45% NaCl (= 0.9 mmol/

day Na+)
● Change to 0.9% NaCl as soon as Serum [Na
+] is stable. (= 1.8 mmol/day Na+)
>1000 gms ● Initially 0.5 ml/hr of 0.9% NaCl (= 1.8 mmol/

day Na+)
● Increase to 1 ml/hr as fluid intake increases.
(= 3.6 mmol/day Na+)
● Add Heparin 250units/500 ml to arterial fluids
Glucose Intake
● The neonatal liver normally puts out 6 - 8 mg/kg/min of glucose. This is

approximately the basal requirement of a newborn infant. Hypoglycaemia is severe
if it persists despite an intake of >10 mg/kg/min. Calculate the glucose intake:
% Dextrose x Volume (ml/

Glucose intake (mg/kg/min)
kg/day)
=
144
See also the Glucose
or
Calculator
Glucose intake (mg/kg/min) % Dextrose x Hourly Rate
= Weight (Kg) x 6
Intake 5% Dextrose 10% Dextrose 12.5% Dextrose

(ml/kg/day) mg/kg/min of dextrose
60 2.1 4.2 5.2
90 3.1 6.25 7.8
120 4.2 8.3 10.4
150 5.2 10.4 13.0
180 6.25 12.5 15.6
To get concentrated glucose solutions: See also the Fluid and Electrolytes calculator
Solution 10% Dextrose 50% Dextrose

12.5% 450 ml 30 ml
15 % 420 ml 60 ml
20 % 400 ml 135 ml
Solution 5% Dextrose 50% Dextrose
7.5% 450ml 30ml
● Dextrose solutions of >10% are best administered through central venous lines.
❍ Peripheral IVs do not last long, and extravasation can result in tissue
damage.
Insensible Water Loss
● This varies greatly with gestation and depends on the thermal environment. It
decreases markedly over the first few days.
❍ A 26 week baby under a radiant warmer on day 1 may lose over 150ml/kg/
day. Mature babies will lose <30ml/kg/day.
● Very preterm infants should be placed in humidified incubators in a neutral
thermal environment as soon as practical after birth.
IWL ml/kg/day
750-1000gm 64-82
1001-1250 56
1251-1500 38-46
>1500 20-26
GI Obstruction
● If there are significant gastric aspirates, replace these ml for ml with 0.9% NaCl
plus 10mmolKCl/500ml.
Chest and/or Peritoneal Drains
● If there are significant fluid losses from these, measure the volume and replace
with 4% albumin as indicated.
● Monitor serum albumin concentrations.
● Monitor the composition of the fluid being lost as this may assist with calculating
requirements
Renal Impairment
● Restrict intake to insensible water loss + urine output.

● Monitor fluid balance, serum electrolytes and weight carefully.
● In early Acute Tubular Necrosis, consider a pre-renal cause. Fractional Excretion

of Sodium will help sort this out.
❍ FE Na ≥2.5% in term infants suggests renal failure.
+
+
❍ FE Na <2.5% in term infants suggests pre-renal failure.
+
❍ FE Na is high in preterm infants because of tubular immaturity.
Urine [Na] x Serum

Creatinine
FE Na+ = x 100%
Serum [Na+] x Urine
Creatinine
Hyponatraemia
● Commonest Causes
❍ Prematurity
+
■ Renal Na loss from glomerulo-tubular imbalance
❍ Inadequate Na+ intake
❍ Excessive water intake.
❍ Diuretic therapy, especially loop diuretics.
❍ Acute tubular necrosis (tubular Na+ loss)
❍ Indomethacin
■ Reduces free water clearance and fractional excretion of sodium,
with the lower free water clearance leading to hyponatraemia.

❍ SIADH
■ ADH has a limited ability to concentrate the urine in the newborn,
and acts primarily as a vasopressor.

❍ Excess Na+ loss
■ Diarrhoea, Gastric, pleural, CSF, 17-OH progesterone deficiency.
If a concentrated solution of Sodium chloride is required for treatment of

hyponatraemia due to increased losses, refer to the sodium infusion calculator.
Hypernatraemia
● Commonest causes
❍ Excessive water loss
■ Very preterm insensible loss
■ Diarrhoea
■ Polyuria
+
❍ Excess Na intake.
References
1 Cloherty JP and Stark AR. (Ed) Manual of Neonatal Care. 3rd Ed. Little Brown. 1991.
2 Gomella TL (Ed). Neonatology 2nd Ed. Appleton & Lange. 1992.
3 Roberton NCR. A manual of Neonatal Intensive Care. 2nd Ed. Churchill Livingston. 1986
Any printed version can not be assumed to be current. Printed copies of this document are valid for Monday, May 22, 2006.
Fluid and Electrolyte Calculator

© Carl Kuschel
August 2004
Click here to open the Glucose calculator to determine glucose intake
● Do not add electrolytes on Day 1.

● Do not add Ca++ routinely in relatively well infants only likely to be on short term IV fluids.
(This is most babies as the sicker, longer term babies will be on IVN)
Weight grams
Total Fluid Intake ml/kg/day
Dextrose concentration 10 %
● Usual requirement 3mmol/kg/day
Sodium 3 mmol/kg/day
● Usual requirement 2mmol/kg/day
Potassium 2 mmol/kg/day
● Add 1mmol/kg/day if required
Calcium 0 mmol/kg/day
Calculate Reset
Home | Contact Us | Careers | Phone Directory | Search
The Paediatricians at National Women's Health Newborn Services provide a follow-up service for babies
who have been cared for by the service. A timetable is included below. Registrars and house officers are
welcome to sit in with the specialists during their clinic sessions.
The focus of the clinic is surveillance. If problems are identified, babies will generally be referred to
another service (such as general paediatrics).
Infants who have been back-transferred to another neonatal unit - even in Auckland - will be followed by
paediatric services at that hospital, rather than at National Women's Health.
Criteria for Follow-Up at National Women's Health
● Preterm infants
❍ All infants with a birthweight <1500g
Ministry of Health ❍ Infants <32 weeks
NZ Government ● Infants <3rd% for birthweight who have been admitted to NICU
● Infants with at risk of neurological or developmental problems
❍ Infants who were ventilated in the newborn period and where there are concerns about the
degree of illness and the risk of subsequent growth or developmental problems

©Copyright ❍ Infants with seizures in the newborn period, unless referred to another follow-up service
Published: 11/01/2006 ❍ Infants who had meningitis, unless referred to another follow-up service
❍ Infants who were neurologically abnormal on discharge and who are not being followed by
other services
❍ Note that most term infants who have identified neurological problems at discharge will be
followed by their local developmental paediatric or neurology services

● Infants in research studies (e.g. selective head cooling). These may be followed up by the
researcher involved
● Infants born to mothers on the methadone programme or mothers using significant quantities of
alcohol in their pregnancy (these infants will generally see Dr Kuschel or Dr Rowley)
● Some infants with congenital anomalies or other problems (for example, infants with an Erb's palsy)
who are not being followed by another service
● Families of infants who have died whilst on NICU will be offered an appointment to discuss events
surrounding the baby's admission and death
● Some infants who do not qualify for routine neonatal follow-up but are being followed by neonatal
home care services may be referred following discharge if there are clinical concerns
Timing of Follow-Up
● The need for and time of follow-up should be discussed with the specialist concerned or the
specialist on service responsible for the care of the infant in NICU
● The timing of the first follow-up is for 3 months following discharge
❍ Professor Harding and Dr Bloomfield prefer to see the infants 4 months after going home
● Infants are generally seen intermittently until the age of around 18 months
● Appointments can be requested by neonatal staff via the request an appointment link
Timetable
Specialist Day and Time

Battin Every Wednesday at 1:30pm
Bloomfield 3rd Tuesday of the month at 1:30pm
Harding 1st Tuesday of the month at 1:30pm
Knight 2nd and 4th Tuesdays of the month at 1:30pm
Kuschel Every Tuesday at 1:30pm
Rowley Every Friday at 10:00am
Revised May 2005
David Knight and Carl Kuschel
guideline.
Fractional Excretion of Sodium (FENa

+) © Carl Kuschel
August 2003
Serum Sodium mmol/L

Urine Sodium mmol/L
Serum Creatinine mmol/L
Urine Creatinine mmol/L
Reset
The Fractional Excretion of Sodium is %.

FENa+ >2.5% in term infants suggests renal failure. FENa+ <2.5% in term infants suggests pre-renal failure.
This value in a term infant suggests .

● The Fractional Excretion of Sodium is higher in preterm infants because of renal
immaturity.
Gestation Calculator
© Carl Kuschel
May 2004
First day of - -Choose-

LMP -Choose-
EDD by - -Choose-
scan or
dates -Choose-
Calculate 1 January
the
gestation at 2000
Calculate Reset
Used with permission from www.nicutools.

Glucose Calculator org
with subsequent modifications by Carl

Kuschel
Enter infant Weight: kg
Rate Fluid Volume Sugar Load

Enter infant nutrition: Dextrose
(ml/hour) (ml/kg/day) (mg/kg/min)
IV fluid #1: %
IV fluid #2: %
Milk: - Select an option -
Polycal: %
Reset Totals --- ---
This calculator determines how much sugar (in mg/kg/min) an infant is receiving.
Enter the infant’s weight, then specify the various inputs – dextrose percentage and flow rate for one or two
infusions, and type of milk and hourly milk volumes, and use of polycal (a sugar) in terms of specifying how
many grams are added to each 100 ml of milk.
Assumptions:
● Breast milk sugar content 7.1 g / 100 ml
● Term formula sugar content 7.1 g / 100 ml
● Pre-term formula sugar content 8.5 g / 100 ml
● Assumption made that all enteral feeds are absorbed
● Any infant requiring a glucose load of 10 mg/kg/minute to maintain normoglycaemia should be

investigated for hyperinsulinism.
Contact this calculator's developers

guideline.
Granulocyte Concentrate
Reviewed by
The Product
● "Buffy Coat" 1 unit blood collected in the morning is spun hard and the buffy coat
and upper layer of red cells harvested into a variable volume of 20-50 ml.
● This will have perhaps 80% of the total white blood cells in that 450ml of donor
blood and is also a packed red cell preparation.
● Should ideally be irradiated prior to use.
Indications
● Septic neutropenic baby (neutrophils <3 x 109/L in first week or <1 x 109/L
subsequently).
● Septic baby with poorly functioning neutrophils (e.g chronic granulomatous
disease).
Complications
● As for other blood cell products -infections, allergy, leucocyte antibodies, red cell
antibody problems and volume overload.
● Raising red cell count too much causing hyperviscosity syndrome.
● Potential GVH (Graft versus Host) disease if not irradiated.
● Potential source of CMV infection UNLESS from Anti-CMV negative donor -
Please Request.
Administration
● Granulocytes last only a few hours and survive best at room temperature.
❍ The preparation should be infused as soon as received and should NOT be
refrigerated.
● Draw up via a 170u blood filter.
● Transfuse over 2-3 hours maximum.
● It would be hard to give too many granulocytes to a septic neutropenic baby by
infusing even a whole buffy coat preparation.
❍ Volume that can be given is usually dictated by volume that baby can
receive.
● NOTE the high Hb content of the product. Be very careful not to raise the baby's
Hb too high or hyperviscosity problems and serious consequences may occur.
For further details, see the Big Blue Blood Bank Book
guideline.
Investigation of Possible Haematological Disorders Reviewed by Carl Kuschel,

in Neonates George Chan (Haematology) and
Paul Harper (Haematology)
February
2004
Introduction Thrombocytopenia Haemophilia and Comments von Willebrand Disease

Protein C/S/Antithrombin
Factor V Leiden Mutation Thalassaemia Intravascular Haemolysis
DeficiencyI
Vitamin K Deficiency
G6PD References
Bleeding
Introduction
"Bleeding problems" or a tendency to bruise or bleed are common problems. There may
be a family history of specific haematological diagnoses, or there may be more general
notes about bleeding tendencies in the maternal history.
Thrombocytopenia
See the Thrombocytopenia guideline.
Haemophilia
There are a number of coagulation factor defects that fall under the general heading of
haemophilia. The two most common are Factor VIII Deficiency and Factor IX Deficiency.
von Willebrand Disease is also classified as a haemophilia although it is clinically less
severe than Factor VIII and IX Deficiencies.
Factor VIII Deficiency (Haemophilia A)
This is the "classical" haemophilia, inherited as an X-linked recessive gene (affecting

males), and causes approximately 75% of all significant inborn coagulopathies. There
may be a family history of affected males on the maternal side. The incidence is
approximately 1:10,000 male births. The underlying abnormality is a defect in factor VIII.
It may present as severe bleeding after procedures (including intramuscular injection of
vitamin K), or even intracranial bleeding.
Investigations ● If male infant, urgent (<3 hours) Factor VIII assay from
cord blood or the baby (avoid heel prick samples)
❍ Normal neonatal ranges are the same as adult
ranges, so low values are pathologic

● If urgent factor VIII assay is not available, do a coagulation
screen (avoid heel prick samples)
❍ Activated Partial Thromboplastin Time will be
prolonged (neonatal upper limit of normal 36

seconds)
Newborn ● Avoid intramuscular injections

Management ● Discuss with a paediatric haematologist
● See other comments
Factor IX Deficiency (Haemophilia B, Christmas Disease)
This accounts for about 12% of all patients with haemophilia, is sex-linked (affecting
males), and is clinically indistinguishable from Factor VIII Deficiency (that is, it may
present with significant bleeding in the newborn period)
Investigations ● If male infant, urgent (<3 hours) Factor IX assay from cord
blood or the baby (avoid heel prick samples)
❍ The normal neonatal ranges are decreased
compared with adults, so diagnosis of a mild

deficiency can be difficult
● If urgent factor IX assay is not available, do a coagulation
screen (avoid heel prick samples)
❍ Activated Partial Thromboplastin Time will be
prolonged (neonatal upper limit of normal 36

seconds)
Newborn ● Avoid intramuscular injections

Management ● Discuss with a paediatric haematologist
● See other comments
Other comments about Haemophilia A and B
If factor assay indicates a severe (<1%) or moderate (1-4%) factor VIII or IX deficiency,
● The result should be sensitively communicated to the parents by experienced staff

● Take a further factor VIII/IX level
● Follow the neonate closely for a minimum of 7 days after birth through daily phone
contact from the Haemophilia Centre or GP, and frequent midwife visits.
● Educate parents regarding the symptoms and signs of intracranial haemorrhage
(poor feeding, irritability, listlessness, full fontanelle, pallor, convulsions)
❍ Do a CT (In preference to ultrasound) if there is suspicion of an intracranial
haemorrhage.
● Suggest that Factor VIII/IX levels are done on females born to carrier mothers to
detect the occasional carrier female with low levels at risk of symptomatic bleeding.
von Willebrand Disease (VWD)
This is most commonly inherited as an autosomal dominant trait with a mild to moderate
bleeding tendency. There is variable clinical and laboratory expression of platelet
dysfunction and factor VIII deficiency. The basic defect in vWD is an abnormality of von
Willebrand factor (vWF) which promotes platelet adhesion and transports factor VIII by
the factor VIII-vWF complex. There are different recognised types of vWD, depending on
qualitative or quantitative abnormalities of vWF.
There are very few reports of newborn infants with bleeding secondary to vWD. The most
common manifestations in children and adults are nosebleeds and easy bruising, with
more severe bleeding problems being rare. Bleeding after dental extractions can be
serious in some individuals. The diagnosis is made by platelet function analysis (PFA)
and specific tests for vW antigen and activity. Bleeding times are rarely performed.
Investigations ● No investigations are necessary

● Levels of vWF are physiologically increased in the neonatal
period
Newborn ● No special precautions unless clinically significant bleeding

Management ● Referral to paediatric haematology
Factor V Leiden Mutation
This may be found because of investigations performed on mothers with a history or pre-
eclampsia or recurrent miscarraige. It is generally associated with an increased lifetime
risk of thrombosis, although most individuals with Factor V Leiden mutation will remain
well. A severe neonatal form has been described.
Investigations ● No investigations are indicated at birth or in the neonatal

period.
Newborn ● No specific investigations

Management
Protein C, Protein S, and Antithrombin Deficiency
These are conditions which predispose to thrombosis. The classic presentation of Protein
C deficiency is purpura fulminans occurring within hours or days of birth. Infants with
homozygous Protein C deficiency often have significant in utero thrombotic events
(cerebral or ophthalmic) and severe DIC and large vein thromboses . Heterozygous
Protein C deficiency has been associated with neonatal thrombotic events. Coagulation
screens are usually normal but may show an elevated platelet count and increased fibrin
degradation products. Protein S deficiency has been very rarely reported in neonates.
Antithrombin deficiency most commonly presents in adulthood, although there are reports
of neonates with significant thromboses.
The ranges for protein C and protein S in normal neonates may be as low as 20-30% of
the normal adult value.
Investigations ● Discuss with a paediatric haematologist
Newborn ● Avoid indwelling central intravenous or intra-arterial

Management catheters
● Fresh frozen plasma or replacement products (Protein C or
Antithrombin concentrates) as symptomatically indicated
after discussion with a paediatric haematologist.
Thalassaemias
These are hereditary conditions with decreased or absent synthesis of at least one globin
chain. α- and β- thalassaemia refer to deficiencies of the α and β chains, respectively.
α-thalassaemia conditions are usually due to deletion of the α-globin gene. There are 4
copies of the α-globin gene. Deletion of one or two α-globin genes leads to α-
thalassaemia trait. The red cell changes are mild and may not be detected clinically or
may present with mild microcytic anaemia that should be differentiated from iron
deficiency. Deletion of three α-globin genes results in HbH Disease with chronic mild to
moderate anaemia but the patient is not transfusion dependent. The most severe form of
α-thalassaemia condition is Hb Bart's hydrops foetalis. All the four α-globin genes are
absent, and the condition is lethal with the affected baby dying in utero or soon after birth.
β-globin production is controlled by a pair of β-globin gene. β-thalassaemia conditions

arise from different genetic defects not limited to deletion. Defect of one β-globin gene
leads to β-thalassemia trait, which can be asymptomatic or more usually associated with
mild microcytic anaemia. When both β-globin genes are defective then there is no or very
little β-globin produced. This leads to β-thalassaemia major. Usually this presents as a
transfusion dependent chronic anaemia, but the severity of disease is dependent on the
interaction of a number of complex genetic factors, and some patients are not transfusion
dependent even though they have a moderate anaemia.
At birth the predominant circulating haemoglobin is Hb F (α2γ2). Adult haemoglobin, Hb A
(α2β2), becomes the predominant haemoglobin after birth. Therefore, infants with α-chain
abnormalities tend to be symptomatic at birth (or before) whereas those with β-chain
problems develop symptoms usually after 4-6 months. The cord blood red cells from
infants with either α-thalassaemia trait or HbH Disease are microcytic, and the level of Hb
Bart's (an abnormal haemoglobin composed of only γ-chains) in the cord blood is raised.
Investigations ● Cord blood for haemoglobin electrophoresis, particularly Hb

Bart's quantitation if α-thalassaemia is suspected
● Venous blood for haemoglobinopathy study.
❍ If β-globin defect is suspected the specimen should
usually be taken at 3 months at the earliest.

● FBC (may be normal in thalassaemia traits)
Newborn ● Haematology follow-up as indicated by particular

Management haemoglobinopathy
Intravascular Haemolysis
This is relatively common in neonates. It may be due to a variety of causes including

infection, AV malformations, alloimmune haemolysis (such as ABO incompatibility),
exposure to toxins (including bacterial toxins) and oxidant drugs, haemoglobinopathies,
red cell enzyme and membrane abnormalities. Often, no specific underlying cause is
found, as in the transient Infantile Pyknocytosis often seen 4-6 weeks after birth. Vitamin
E deficiency should be rare nowadays but also needs to be considered in some cases,
particularly very premature infants. It is important to look at the blood film for evidence of
haemolysis (spherocytes, cell fragment, polychromatic cells) or infection. There may be
prolonged or exaggerated jaundice.
Investigations ● Group and Direct Antiglobulin test

● Reticulocyte count
● Pyruvate Kinase screen
● Glucose-6-Phosphate Dehydrogenase screen
● Haemoglobinopathy study
● Vitamin E level
● Blood from both parents for Haemoglobin and blood film (to
evaluate red cell morphology)
● Exclude infection
Newborn ● Red Cell Transfusions as required to maintain a normal

Management haemoglobin
● Monitor and treat neonatal jaundice as indicated
● Discuss with a paediatric haematologist.
If no apparent cause is found, then further testing (such as investigations for red cell
membrane defects or unusual haemoglobinopathies) should be discussed with the on-call
paediatric haematologist.
Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD)
This is a relatively common abnormality of red cell metabolic enzymes, inherited as a sex-
linked disorder in males (although females can sometimes also be affected). G6PD is
required to protect the haemoglobin and the red cell membrane from oxidative damage.
The clinical presentation of G6PD deficiency varies. The severe forms can lead to severe
haemolysis, which can be spontaneous or after exposure to drugs or chemicals (including
fava bean and moth balls or naphthalene used as insect repellents in closets). Infection
can also precipitate haemolysis. It commonly manifests as severe jaundice in affected
male babies. G6PD is ubiquitous but is most common in South East Asia, the Indian
subcontinent, the Mediterranean area, and in tropical and subtropical Africa. Infants from
these ethnic groups who develop jaundice severe enough to require phototherapy should
be investigated.
Investigations ● G6PD screen and/or G6PD assay

❍ As red cell G6PD levels depend on the age of the
red cell, the result of the G6PD assay can be

equivocal or even normal during acute haemolysis.
If clinically appropriate, consider repeating the
G6PD study when the acute haemolysis has settled.
● FBC may show evidence of haemolysis with red cell
fragments, spherocytes, and "bite" cells
Newborn ● If confirmed to be affected, advise regarding medications

Management and other factors which may precipitate acute haemolysis
including foods.
● Advise parents of early recognition of symptoms and signs
of acute haemolysis, which can be a haematological
emergency.
Vitamin K Deficiency Bleeding (VKDB, Haemorrhagic Disease of the

Newborn)
See the Vitamin K Guideline.
This diagnosis should be considered in infants who appear to bleed excessively easily,
particularly if there is major evidence of haemorrhage (e.g. gastrointestinal or cerebral)
and it is not clear that the baby received adequate vitamin K supplementation at birth.
Investigations ● INR (Prothrombin Ratio)
❍ This is prolonged and corrects with the
administration of vitamin K.
Newborn ● Intramuscular Vitamin K 1mg.

Management
References
1 Christensen RD (Ed). Hematological problems of the neonate (1st ed). WB Saunders Co, Philadelphia. 2000
Any printed version can not be assumed to be current. Printed copies of this document are valid for Monday, May 22,
2006.
Normal Haematological Values

Reviewed by
Normal Haematologic Values During the First Two Weeks of Life in the Term Infant
Value Cord Blood Day 1 Day 3 Day 7 Day 14

Hb (gm/100ml) 16.8 18.4 17.8 17.0 16.8
Haematocrit (%) 53.0 58.0 55.0 54.0 52.0
Red cells (cu.mm. x 106) 5.25 5.8 5.6 5.2 5.1
MCV (m 3) 107 108 99.0 98.0 96.0
MCH (yy) 34 35 33 32.5 31.5
MCHC (%) 31.7 32.5 33 33 33
Reticulocytes (%) 3-7 3-7 1-3 0-1 0-1
Nuc RBC (cu.mm) 500 200 0-5 0 0
Platelets (1000’s/cu.mm) 290 192 213 248 252
● MCV = mean corpuscular volume

MCH = mean corpuscular haemoglobin
MCHC = mean corpuscular haemoglobin concentration
The White Blood Cell Count and the Differential Count During the First Two Weeks of
1
Life
Age Leukocytes Neutrophils Eosinophils Basophils Lymphyocytes Monocytes

Total Seg Band
Birth
Mean 18.100 11,000 9,400 1,600 400 100 5,500 1,050
Range 9.0-30.0 6.0-26 20-850 0-640 2.0-11.0 0.4-3.1
Mean - 61 52 9 2.2 0.6 31 5.8
%
7 Days
Mean 12,200 5,500 4,700 830 500 50 5,000 1,100
Range 5.0-21.0 1.5- 70-1100 0-250 2.0-17.0 0.3-2.7
10.0
Mean - 45 39 6 4.1 0.4 41 9.1
%
14 Days
Mean 11,400 4,500 3,900 630 350 50 5,500 1,000
Range 5.0-20.0 1.0-0.5 70-1000 0-230 2.0-17.0 0.2-2.4
Mean - 40 34 5.5 3.1 0.4 48 8.8
%
Haematologic Values in Low Birthweight Infants
Age of Infant
Determination 1-3 Days 4-7 Days 2 Weeks 4 Weeks 6 Weeks 8 Weeks
Birthweight less than 1200g
Haemoglobin 15.6 16.4 15.5 11.3 8.5 7.8
Reticulocytes as % of 8.4 3.9 1.9 4.1 5.4 6.1
RBC
Platelets 148,000 163,000 162,000 158,000 210,000 212,000
± 61,000 ± 69,000
Leukocytes 14,800 12,200 15,800 13,200 10,800 9,900
± 10,200 ± 7,000
Segmented 46 32 41 28 23 23
neutrophils
Band neutrophils 10.7 9.7 8.0 5.9 5.8 4.4
Juvenile neutrophils 2.0 3.9 5.3 3.6 2.6 2.0
Lymphocytes 32 43 39 55 61 65
Monocytes 5 7 5 4 6 3
Eosinophils 0.4 6.2 1.0 3.7 2.0 3.8
Nucleated RBC as % 16.7 1.1 0.1 1.0 2.7 2.0
of total RBC
Birthweight 1200-1500g
Haemoglobin 20.0 18.0 17.1 12.0 9.1 8.3
Reticulocytes as % of 2.7 1.2 0.9 1.0 2.2 2.7
RBC
Platelets 151,000 134,000 153,000 189,000 212,000 244,000
± 35,000 ± 49,000
Leukocytes 10,800 8,900 14,300 11,000 10,500 9,100
± 4,000 ± 2,900
Segmented 47 31 33 26 20 25
neutrophils
Band neutrophils 11.9 10.5 5.9 3.0 1.4 2.1
Juvenile neutrophils 5.1 2.4 2.7 1.8 1.7 1.6
Lymphocytes 34 48 52 59 69 64
Monocytes 3 6 3 4 5 5
Eosinophils 1.3 2.2 2.5 5.1 2.6 2.3
Nucleated RBC as % 19.8 0.8 0 0.4 1.4 1.0
of total RBC
References
1 From Altman, P.L and Dittmer, D.S: Blood and Other Body Fluids. Federation of American Societies for Experimental
Biology, Washington, D.C, 1961.
guideline.
Handling of Small Babies Reviewed by Bronwyn Jones (NS-

ANP), Angela Warren (CCN), and
Carl Kuschel
April 2005
Introduction Scope Babies Most at Risk

Timing of IVH Haemodynamic Instability Kangaroo Care
Infant Postioning, Weighing and
Blood Pressure Management Related Documents
Optimal Haemodynamic Stability
Introduction
● Germinal Matrix - Intraventricular Haemorrhage (GM-IVH) is one of the most

frequently encountered neurological problems of the premature neonate. This
document outlines information and recommended best practice for assessing the
risks and subsequent nursing care of the infant <30 weeks gestation.
Scope
● Applies to all Nurses caring for ELBW and VLBW babies in the Newborn Service.
Babies Most At Risk
● Infants between 23 and 32 week gestation are at risk, with infants under 30 weeks
gestation being most at risk. There are, however, exceptions to this.
Timing of GM-IVH
● 0-90% of bleeds in the first 3 days.

● 7-20% in the next 4 days until <5% after 7 days.
Haemodynamic Instability
● All haemorrhages seem to start in the germinal matrix as the thin walled blood
vessels are vulnerable to damage due to disturbances in perfusion, caused by an
increase, decrease or fluctuating blood pressure. Changes in blood pressure may
occur as a result of handling, for example movement, crying, feeding, intubation,
suctioning and stimulation.
● Hypotension/hypertension is often a recurring and difficult problem exacerbated by
the fact that normal ranges for blood pressure in infants that are VLBW/ELBW has
not been firmly established.
● In very low birthweight infants during the first 48-96 hours blood pressure is
influenced by birthweight and gestational age.
Kangaroo Care
● Infants <30 weeks should not be offered cuddles or kangaroo care in the first 5
days of life.
❍ Discuss at ward round if appropriate for family to be offered cuddles to
infant >3 days old, stable and over 30 weeks gestational age.
❍ Infants that are 30 weeks and over should have their stability and disease
process considered prior to offering cuddles.

● An infant that is not expected to survive may also be an exception to these
guidelines.
Infant Positioning, Weighing and Optimal Haemodynamic Stability
Try to cluster cares to allow long rest periods particularly between stressful interventions.
The frequency and duration of handling during intensive care have been shown to
influence the occurrence and severity of hypoxaemia which can increase the risk of GM-
IVH in VLBW/ELBW infants. Disruptive tactile stimulation can precipitate a negative
physiologic chain of events and lead to intracranial pressure or cause haemodynamic
fluctuations. Excessive handling can also initiate hypoxaemia.
When changing nappies care can be taken by sliding the nappy under to avoid raising
legs as increase to intracranial pressure occurs when infants legs are lifted, especially if
above the head. Position with the head midline and the head of the bed slightly elevated.
Intracranial pressure is lowest when the head of the bed is elevated. Side lying with head
in midline to avoid twisting of the infants body also reduces the risk of increasing
intracranial pressure.
Blood Pressure Management
Monitor blood pressure diligently
1. Infants <32/40 with arterial lines have their BP monitored continuously and
recorded hourly on observation sheet.
2. VLBW/ELBW babies and sick infants i.e. <32/40 weeks ventilated, Hudson CPAP,
O2 requirement, without arterial lines may need 1-2 hourly cuff BP measurement
initially. Discuss frequency with NS-ANP/medical staff.
3. The optimal mean is decided by NS-ANP/medical staff. BP should be equal to or
greater than the gestational age in the first 24 hours.
4. Alarm limits on HP monitors should always be on and set at appropriate levels i.e.
upper level slightly above recommended mean BP and lower alarm level set at
slightly lower than desired mean BP.
5. Report fluctuations in BP, hypotension and hypertension to medical staff/NS-ANP.
6. Consider allowing recovery periods to avoid rapid BP fluctuations during handling.
Reduce fluctuations in blood pressure
1. Minimal handling and cluster cares to allow rest periods. Handle gently.
2. Refer to Suction Policy regarding babies on Hudson CPAP and IPPV. Pre-
oxygenate as indicated and allow time for SpO2 to recover between suctions.
3. ELBW infants ideally should only be warm weighed with two people to facilitate
procedure.
❍ Infants <30 weeks are not to be weighed in the first 5 days unless
requested by the medical staff or NS-ANP.

4. To avoid fluid overload, use accurate checking under RBP of rate of IV pumps.
❍ Rate of intermittent infusions e.g. blood plasma, via Graseby or IVAC pump
is also checked by two RNs and signed.

❍ Volume limit on IV pumps to be set within 10% of limit.
5. Nurse infant flat or head of bed slightly raised, not head down. Head needs to be
in line with body, not twisted so as not to increase intracranial blood flow and
pressure.
guideline.
Hepatitis B Vaccination
Authorised by:
Charge Nurse Newborn
July 2002
Positive Mothers and those Hib-HepB (Comvax) 2-in-1

Information Other Related Documents
with Unknown Status Vaccine
Hepatitis B - Information
Information ● Spread through close physical contact with body fluids of

an infected person.
● The most infectious period is from several weeks before
symptoms appear until several weeks or months later.
● Carriers have the virus in their blood and can remain
infectious for many years.
● The younger a person is when Hep B infection occurs the
more likely they are to become a chronic carrier.
● Babies born to carrier mothers are at greater risk of
catching Hep B virus during birth. Baby can be protected
from Hepatitis B by having extra injections of Hep B
vaccine and Immunoglobulin (HBIG) at birth. If the
recommended immunisations are completed the baby’s risk
of becoming infected is reduced by about 95%.
Hepatitis B ● Is prepared from plasmas that contain high levels of

Immunoglobulin antibody to the surface antigen of the Hepatitis B virus. It
(HBIg) is given to all babies (including premature infants) whose
mothers are Hepatitis B antigen positive.
Storage of ● See Cold Chain Management

vaccine-
Hepatitis B - Mothers Antigen Positive and Status Unknown

Parental consent/ ● See flow chart for parental consent and vaccinations to
prescribing of give.
Hep B vaccine.
Mothers Hepatitis ● See flow chart for process – consent vaccinations and
B antigen Hep B Immunoglobulin (HBIG).
(HBsAg) status
unknown
Efficacy ● 85-95% and virtually complete protection in those who

develop antibody levels of greater than or equal to 10mlU/
ml (the protection level). At least 95% in children after 3
doses.
● The red form HNN2 then goes into the multidisciplinary
notes. Later one copy goes to the Medical Officer of
Health, Community Health.
Ordering of Hep B ● On the request form for Human Plasma Protein Products
Immunoglobulin (S405). Send to Blood Bank by chute plus a phone call.
Hepatitis B - Nursing Care of Baby whose Mother is Hep B Antigen Positive or

Status Unknown
Nursing care of ● The Nurse will ensure the following steps are carried out
baby in the nursing care for baby whose mother is Hepatitis B
antigen positive or status unknown.
Step Action
1 Strict handwashing.
2 Gloves for all cares, where contact with body fluid is anticipated.
3 Baby may have breast milk.
4 Babies greater than 32 weeks gestation bath as soon as possible, if condition
stable, using chlorhexidine surgical scrub 4%:
● Have bath water and towels on hand.

● Nurse wears long sleeve gown and gloves.
● Nurse wets hands, pours some chlorhexidine surgical

scrub 4% into hands, lathers up solution. Then using
hands cover all of baby's skin-hair (avoiding eyes and
ears)
● Place baby in bath water and rinse off the chlorhexidine.
● Dry baby.
Hib-Hep B (Comvax) 2 in 1 Vaccine - Information
This is a 2 in 1 vaccine for Haemophilus Influenza Type B (Hib) and Hepatitis B.

Haemophilus ● Haemophilus Influenzae Type B bacterium is a gram
Influenzae Type B negative coccobacillus.
(Hib) ● Hib causes meningitis, pneumonia, epiglottitis, septic,
arthritis, bacteraemia, cellulitis and empyema in infants and
young children. Mortality rate is 5% despite antibiotics and
medical care. Survivors of Hib meningitis may have a 30-
40% risk of long term neurological development impairment.
guideline.
Hepatitis C Virus Reviewed by Kitty Croxson

Maternal Infection and Vertical Transmission (Virology), Lesley Voss (Paediatric
ID), Simon Rowley, and Carl
Kuschel
September
2003
Hepatitis C Virus Epidemiology Vertical Transmission Tests

Management of Pregnant Management of Infants born
Other related Documents References
Women to HCV Positive Mothers
Hepatitis C Virus
● Single-stranded negative sense RNA virus.

● Cytopathic virus, replicating in liver cells and spilling over into blood stream during
active infection.
● Damage to liver leads to steatosis, fibrosis, cirrhosis and in some cases
hepatocellular carcinoma.
● Major reason for liver transplantation world-wide.
● USA – 0.2% seroprevalence of HCV for children under 12 years of age.
Epidemiology
● Currently no tissue culture infectivity assay, so information on distribution of virus

based largely on detection of viral RNA.
● Transmission still incompletely understood. Up to 40% of infected individuals may
have no identifiable risk factors.
● >95% of infections thought to be parenteral, with injection of infectious blood the
most at risk procedure eg injecting drug users, and (pre-transfusion service
screening), haemophiliacs, transfusion recipients.
● In Western communities, < 5% of infections linked to sexual transmission or
household exposure.
● Antibodies not protective against re-infection.
● Currently no vaccine available.
Vertical Transmission
● Infrequent (as opposed to vertical transmission of Hepatitis B in the pre-vaccine

era).
● Rate approximately 6% in HCV viraemic, non-HIV infected mothers. May increase
to ~ 15% in HIV positive mothers.
● Majority of infant infections probably acquired during exposure to infectious blood
at delivery (infants not viraemic until several weeks post-delivery). However, there
are no convincing studies at this time demonstrating that Caesarean section
should be recommended.
● Transmission from breast milk has not been documented, although virus RNA can
be found in breast milk. Currently there are no recommendations concerning
breast feeding by HCV positive mothers. This should be discussed with the women
but breast feeding is not contraindicated.
Tests
● Antibody to HCV. Indicates past infection, or passive acquisition of maternal

antibody (infants).
● HCV RNA. Detects specific HCV genetic sequences by RT-PCV. Usually applied
to blood (serum). If positive, indicates ongoing active infection.
● Currently there is no reliable HCV antigen test.
Management of Pregnant Women
● Offer testing to all pregnant women at risk of HCV (eg on the methadone
programme or attending clinic for substance abuse).
● Ensure that the laboratory request is annotated " HCV screening in pregnancy."
● All antibody positive women must have HCV RNA tested.
● If positive, HIV testing must be offered also. (Note. This may become redundant
with the introduction of widespread screening for HIV in pregnancy).
Management of Infants Born to HCV Positive Women
● Since essentially no infected infants have been found viraemic at birth, testing of
cord blood is not necessary.
At 4-6 months:-
● Test for HCV RNA (HCV PCR), HCV antibody plus liver function
tests.
❍ Note: in many instances, maternal antibody will be detectable
for >12 months.
● If HCV RNA positive, refer to Paediatric Gastroenterology Clinic.

● If HCV RNA negative and HCV antibody positive, repeat antibody
test at 18 months to document clearance of antibody (and therefore
absence of infection).
● If HCV RNA and HCV antibody negative, no further follow-up is
required.
Index of ● Nursing Care of Infants Born to Hepatitis C Positive Mothers
Other
Related
Documents
References
1 Croxson M et al. Vertical transmission of Hepatitis C virus in New Zealand. NZMJ, 9 May 1997, Vol 110,
No 1043:165-7.
guideline.
Hepatitis C
Nursing Care of a Baby whose Mother is HCV Authorised by:
Positive Charge Nurse Newborn
February 2006
Nursing Care of Baby
Step Action
1 Strict hand-washing and universal precautions.
2 Gloves worn for all cares where contact with body fluid is anticipated.
3 Babies greater than 32 weeks gestation if condition stable, are to be bathed
on admission (using baby soap).
4 Baby can have mother's breast milk provided the mother does not have co-
infection (e.g. with HIV) or severe liver failure but Doctor/NS-ANP need to
discuss with mother the theoretical risks.
guideline.
High Frequency Ventilation Reviewed by Malcolm Battin

(HFV)
January
2001
Making Adjustments once

Background Terminology Initial Settings on HFV
Established on HFV
Chest Radiographs Weaning Other Related Documents References
Background
High frequency ventilation (HFV) is defined by the ‘high frequency’ (2.5-15 Hz) and low
tidal volume (0.5-5 mL/kg). The tidal volume is barely greater than the dead space hence
1
alternative mechanisms of gas transport are required to explain the effect of HFV .
Indications for high frequency ventilation include
23
1. Rescue following failure of conventional ventilation (PPHN, Meconium). ,
4
2. Air leak syndromes (pneumothorax, pulmonary interstitial emphysema)
3. To reduce barotrauma when conventional ventilator settings are high.
HFV is not as yet proven to be of benefit in the elective treatment of respiratory distress
5
syndrome . Furthermore, caution is needed when HFV is used as high airway pressures
may result in impaired cardiac output causing a low BP requiring inotropic support or
volume expansion. Also some infants poorly tolerate the extra handling involved in
switching ventilators or may not respond to HFV. If no improvement with HFV consider
reverting to conventional ventilation.
Terminology
Frequency ● High frequency ventilation rate (Hz, cycles per second)

MAP ● Mean airway pressure (cmH2O)
Amplitude ● delta P or power is the variation around the MAP
Oxygenation is ● MAP provides a constant distending pressure equivalent to

dependent on MAP CPAP. This inflates the lung to a constant and optimal lung
and FiO2 volume maximising the area for gas exchange and
preventing alveolar collapse in the expiratory phase.
● Ventilation is dependent on amplitude and to lesser degree
frequency. Thus when using HFV CO2 elimination and
oxygenation are independent.
Initial settings on HFV
If you are using HFOV on the Babylog 8000plus, click here.
Optimal lung ● Set MAP 2-3 cmH2O above the MAP on conventional
volume strategy ventilation
(aim to maximise ● MAP in 1-2 cmH2O steps until oxygenation improves
recruitment of
alveoli). ● Set frequency to 10 Hz
Low volume ● Set MAP equal to the MAP on conventional ventilation

strategy ● Set frequency to 10 Hz
(aim to minimise lung ● Adjust amplitude to get an adequate chest wall vibration.
trauma)
● Obtain an early blood gas and adjust settings as appropriate.
● Changes in frequency should only be made in discussion with attending

Neonatologist.
Making adjustments once established on HFV
Poor Over
Under Ventilation Over Ventilation
Oxygenation Oxygenation
Increase FiO2 Decrease FiO2 Increase Decrease

Amplitude Amplitude
Decrease Increase
Increase MAP Decrease MAP Frequency Frequency
(1-2cmH2O) (1-2cmH2O) (1-2Hz) (1-2Hz)
if Amplitude if Amplitude
Maximal Minimal
Chest Radiograph
● Initial x-ray at 1-2 hrs to determine the baseline lung volume on HFV (aim for 7-8
ribs).
● A follow-up chest x-ray in 4-6 hours is recommended to assess the expansion.
● Thereafter repeat chest x-ray with acute changes in patient condition.
Weaning
● Reduce FiO2 to <40% before weaning MAP (except when over-inflation is evident).
● Reduce MAP when chest x-ray shows evidence of over-inflation (>9 ribs).
● Reduce MAP in 1-2cm increments to 8-9.
● In air leak syndromes (low volume strategy), reducing MAP takes priority over
weaning the FiO2.
● Wean the amplitude in 4cm H2O increments.
● Do not wean the frequency
● Consider switching to conventional ventilation when MAP <10cm H2O, Amplitude

20-25 and blood gases satisfactory.
● Suction is indicated for diminished chest wall movement indicating airway or ET

tube obstruction or if there are visible/audible secretions in the airway.
● Avoid in the first 24 hours of HFV, unless clinically indicated.
● Avoid hand-bagging during the suctioning procedure
❍ use PEEP protector and continue with patient on the ventilator.
❍ increase FiO following the suctioning procedure.

2
❍ MAP may be temporarily increased 2-3cm H2O until oxygenation improves.
References
1 Chang H K. Mechanisms of gas transport during ventilation by HFO. J Appl Physiol 1984 ; 56: 553-63
2 Clark RH et al. Prospective, randomized comparison of HFO and conventional ventilation in candidates for
ECMO. J Pediatr.1994;124: 447-54
3 Kohe et D, et al. High-frequency oscillation in the rescue of infants with persistent pulmonary hypertension.
Crit Care Med. 1988; 16: 510-6
4 Clark RH et al. Pulmonary interstitial emphysema treated by HFOV. Crit Care Med 1986; 14: 926-30
5 Bhuta T, Henderson-Smart D. Elective high frequency oscillatory ventilation vs conventional ventilation in

preterm infants with acute pulmonary dysfunction. (Cochrane Review) In: The Cochrane Library, Issue 2.
Oxford: Update Software; 1998. Updated quarterly
guideline.
Guideline for Attendance at High Risk Deliveries by a Reviewed by Carl Kuschel

Specialist Neonatologist
April
2004
The need for a specialist Neonatologist to attend a delivery depends on:
1. The experience of the registrar, fellow, or NS-ANP "on call".

2. The level of concern of the obstetric staff.
3. The clinical scenario.
There should be good communication between the neonatologist and both the resident
neonatal staff and the obstetric service. During office hours a "high risk" case should be
discussed with the neonatologist "on duty" for level 3 and out of hours with the
neonatologist "on call".
If an obstetrician has concerns regarding a potential delivery and wishes a specialist

neonatologist to attend that delivery the specialist obstetrician should speak directly to
the neonatologist.
It is envisaged that:
a. Deliveries <28/40 should be discussed so the neonatologist has the option of

attending the delivery.
b. Deliveries of infants <26 weeks must be attended by a staff member with
appropriate neonatal expertise (that is, an experienced senior registrar, NS-ANP,
or specialist). This should be discussed with the neonatologist in advance. If in
doubt, the neonatologist should always be called.
c. Deliveries of infants with fetal hydrops or life-threatening congenital anomalies (e.
g. diaphragmatic hernia or other conditions) requiring immediate decisions
regarding resuscitation should be attended by a neonatologist.
d. For any case in which the infant resuscitation was unexpectedly complex or where
there is a poor response to resuscitation the attending neonatologist should be
called urgently.
The attending neonatologist should be notified shortly before or as soon as
practicable following the admission of infants to level 3 care who are:
1. <28/40, or <1000 g or ventilated or have significant respiratory disease.

2. Any sick baby causing concern for medical or senior nursing staff.
3. Any circumstance where the resident staff are inexperienced or not confident in
undertaking a treatment or procedure required.
guideline.
Guidelines for Paediatric Management of Infants Reviewed by Simon Rowley,

Born to HIV+ Pregnant Women Lesley Voss (Paediatric ID), and
Kitty Croxson (Lab Plus)
October
2004
Prenatal Period Post-Delivery Testing Treatment

Follow Up People to Contact Other Related Documents References
Prenatal Period
1. A paediatric consultant (Dr Rowley or Dr Kuschel) should aim to see the parent
and discuss the postnatal management of the infant with her. A Blue team
obstetrician and Obstetric Physician will usually monitor the pregnancy.
2. Maternal blood specimen should be taken for HIV PCR prior to AZT being
commenced.
If not an established patient here, send to be processed by Auckland City Hospital
Department of Virology and Immunology, LabPlus, Building 31, Auckland Hospital
(3x EDTA tubes). This will confirm that the mother's virus is detectable by PCR in
the Auckland system.
3. Confirm that AZT syrup is available at the Auckland City Hospital Pharmacy. This
will ensure availability if there is premature delivery. Liaise with paediatric
pharmacist (Brenda Hughes) 93-4136.
4. Obtain details of maternal antiretroviral treatment during pregnancy and current
HIV viral load prior to delivery.
Post Delivery
1. Vitamin K should be given intramuscularly once the baby has been bathed. The
baby is to be admitted to the postnatal ward, and the number of paediatric staff
involved in the care of the baby should be kept to a minimum.
2. Breastfeeding is contraindicated (as there is an increased risk of HIV transmission
to babies)
Testing
● Code for all lab forms: 4 letter, 6 number code - first 2 letters of the last name, first
letter of the Christian name (B if the baby is unnamed) and sex (M or F), followed
by the 6 figure birth date.
Tests
HIV Clinical
Time T Cell Antibody FBC
PCR Review
Subsets (Western
Blot)
Day 1 No longer required from cord + +
(Cord blood) blood (Pre-AZT)
Week 1 + + + + +
Week 4-8 + + + + +
(Post-AZT)
4-6 months + + +
12 months + +
18 months + +
(if still seropositive at
12 months)
● Any positive PCR test must be confirmed by repeat test to confirm

infection.
Treatment
Antiretrovirals
1. Zidovudine: start within 8 hours of delivery, and give for 6 weeks.

Term Infants 4mg/kg/dose q12h
There is no need to adjust the dose with

increasing weight.
Preterm Infants <30 1.5mg/kg/dose q12h IV

weeks GA at birth
1 or
2mg/kg/dose q12h orally
After 4 weeks, reduce dosing interval to

8-hourly
Preterm Infants ≥30 1.5mg/kg/dose q12h IV
weeks GA at birth
1 or
2mg/kg/dose q12h orally
After 2 weeks, reduce dosing interval to

8-hourly
❍ Recommend FBC prior to starting AZT and repeat at 6 weeks, if abnormal
at 6 weeks repeat at 12 weeks.

❍ Indications to stop AZT treatment include jaundice requiring phototherapy, a
neutrophil count of <750/mm3, Hb <80g/L or a platelet count <50,000/mm3.

❍ Zidovudine has special exemption under Pharmac CEC regulations to allow
the Auckland City Hospital pharmacy to dispense the discharge

medications.
2. Nevirapine if indicated 2mg/kg, single dose to be given ASAP within 3 days of
birth.
3. Lamivudine (3TC, 10mg/ml) 2mg/kg/dose b.d to start within 8 hours of delivery.
Use will be decided on by Paediatric ID team along with Neonatologist.
Prophylaxis
● If the initial PCR is positive, start Co-Trimoxazole 0.5mls/kg, daily at 6 weeks.

Stop when testing at 4 months confirms absence of HIV infection
Immunisations
● No BCG vaccination or other live vaccines should be given until it is clear that the
infant is HIV negative.
Follow Up
● Dr Rowley or Dr Kuschel will follow these babies at the Neonatal Outpatient Clinic
until 18 months, unless they are infected when care will be transferred to Dr L
Voss, Starship Children’s Hospital.
People to be contacted
● Neonatologists – Dr Simon Rowley, Dr Carl Kuschel

● Paediatric Infectious Disease Team (Dr L Voss, 93-4636 if available).
Phone as well as written consultation form should be sent.
● Virologist - Dr K Croxson, Department of Virology and Immunology, LabPlus
Building 31, Auckland Hospital, ext 6130, loc 93-4197, should be informed that the
bloods are being sent.
Index of ● Nursing Care of Infants born to HIV Positive Mothers
Related
Documents
References
1 Capparelli EV, Mirochnick M, Dankner WM, et al. Pharmacokinetics and tolerance of zidovudine in
preterm infants. J Pediatr 2003; 142:47-52.
guideline.
Human Immunodeficiency Virus (HIV)

Nursing Care of Infants born to HIV Positive Mothers Authorised by:
July 2002
Nursing Care of Baby whose Mother is HIV Positive
Step Action
1 Use standard precautions.
2 Babies greater than 32 weeks gestation if condition stable, after birth bath
using chlorhexidine surgical scrub 4%:
● Have bath water and towels on hand.

● Nurse wears long sleeve gown and gloves.
● Nurse wets hands, pours some

chlorhexidine surgical scrub 4% into
hands, lathers up solution. Then using
hands cover all of baby's skin-hair
(avoiding eyes and ears) with the
chlorhexidine surgical scrub 4%.
● Place baby in bath water and rinse off the
chlorhexidine.
● Dry baby.
3 After baby bathed Vitamin K given IM in right leg (Parent consent needed).
4 Baby is not given breast milk or breastfed (as there is increased risk of HIV
transmission to baby).
5 Sample of baby’s urine sent to laboratory to test for cytomegalovirus (CMV).
6 No BCG vaccination or other live vaccines should be given until baby’s
status is clear.
Non-Immune Hydrops Reviewed by David Knight
December
2000
Fluid in two body cavities or one cavity plus oedema at birth. The prognosis depends on associated prematurity, the
underlying cause, the severity of any associated pulmonary hypoplasia and the severity of the ongoing post-natal
1
fluid accumulation (with problems of infection and malnutrition). Mortality is still up to 70%.
Resuscitation
Resuscitation and stabilisation is often difficult. It may be necessary to drain pleural effusions in the delivery room,
at the same time as resuscitating the baby. Find out about the size of pleural effusions and severity of the hydrops
2-3
from obstetric staff before delivery. It is important to prepare equipment before delivery .
Click here to see images of hydropic infants.
● The level III specialist should be informed and may well need to attend the delivery. A senior neonatal nurse
should also attend.
Associations with Non-Immune Hydrops
Cardiovascular Gastrointestinal Lymphatic Skeletal

● SVT ● Jejunal atresia ● Chylothorax ● Osteogenesis
● Heart block ● Midgut volvolus ● Congenital imperfecta
● Truncus arteriosus ● Meconium lymphangectasia ● Asphyxiating thoracic
● Coxsackie peritonitis ● Cystic hygroma of dystrophy
myocarditis ● Hepatitic fibrosis neck ● Thanatophoric
● Hypoplastic Left ● Hepatic vascular ● Noonan's dwarfism
Heart Syndrome malformations Syndrome ● Achondrogenesis
● Endocardial ● Familial cirrhosis ● Hyperphosphatasia
fibroelastosis and portal ● Saldino-Noonan
● VSD/AV canal hypertension Infective dwarfism
● Premature closure ● Parvovirus
of foramen ovale ● CMV
● Premature closure ● Toxoplasma Tumours
of PDA ● Syphilis ● Teratoma
● Tumours ● Leptospirosis ● Neuroblastoma
(rhabdomyomas) ● Chagas Disease ● Haemangioma
● Arterial calcification Genitourinary ● Congenital hepatitis
● Cardiomyopathy (e. ● Rubella
g. carnitine ● Herpes simplex Placental/Umbilical
deficiency) ● Varicella ● True knot
● AV malformations ● UV thrombosis
● Any cause of heart ● Placental
failure chorioangioma
Respiratory ● UA aneurysm
Maternal
● Congenital ● Diaphragmatic ● Diabetes
nephrotic hernia ● Preeclampsia
Chromosomal
syndrome ● Cystic ● Drugs (i.e.
● Trisomy 21 ● Urethral adenomatoid indomethacin)
● Triploidy obstruction and malformation
● 45XO (Turner's) renal dysplasia ● Hamartoma
● Many others ● Polycystic kidneys ● Tracheo- Metabolic
reported ● Renal vein oesophageal fistula ● Gaucher's Disease
obstruction ● Atresia of right ● GM1 gangliosidosis
● Vaginal and main bronchus ● Hurler's Syndrome
Dysmorphic Syndromes
uterine ● Sequestration (MP 1H)
abnormalities ● Pulmonary ● Morquio (MP IVb)
Neurological lymphangiectasia ● MP type VII
● Mediastinal ● Mucolipidosis type I
● Encephalocoele teratoma and II
● Agenesis of the Haematological ● Sialic acid storage
corpus callosum ● Twin-twin disease
● Tuberous sclerosis transfusion Other ● Galactosialidosis
● Vein of Galen ● Rhesus ● Retroperitoneal
aneurysm isoimmunisation fibrosis
● Arthrogryposis ● Feto-maternal
haemorrhage
● α-thalassaemia
(homozygous)
● Fetal anaemia or
blood loss
● G6PD deficiency
● Pyruvate kinase
deficiency
This list is not comprehensive! Also it does not give an idea of how common conditions may be.
Investigations
Many of these may have been done antenatally. Particular clinical findings may indicate other investigations for
aetiology. Target investigations at clinical features. Collect cord blood EDTA and clotted samples. Up to 50% of non-
immune hydrops remain unexplained after full investigation.
Anaemia ● Evidence of fetal anaemia.

● Maternal blood group and antibodies.
● Baby blood group and Coombs.
● Early haemoglobin/PCV.
● Maternal Kleihauer
Biochemistry ● Liver function including albumin/protein

● Renal function.
Cardiac rhythm in ● Evidence from ultrasound scans and CTGs.

utero ● Post-natal ECG + monitoring.
Fluid examination ● Protein and albumin

● Cell cytology (commonly finding marked lymphocytosis).
● Triglyceride levels after feeding started.
Placenta ● Macroscopic examination, histology and Toxoplasma PCR.

Ultrasound ● Head, heart, chest, abdomen.
X-rays ● Chest, abdomen and long bones (skeletal abnormalities and congenital infection).
● Further CT/MRI as indicated by clinical course and other results.
Infections ● Maternal or baby evidence of infections listed above.
Chromosomes
Hb electrophoresis
Metabolic testing ● Use family history as a guide.
● Look for features of possible conditions before launching into investigations for
specific conditions.
Infective causes
Parvovirus ● Fetal anaemia that may have recovered

● PCR, IgG and IgM titres
● Send baby/cord serum.
CMV ● Urine culture/PCR.

● Serum for CMV PCR.
Toxoplasma ● Maternal and baby blood, placenta and amniotic fluid PCR
● Baby/cord IgM.
Syphilis ● Maternal serology (VDRL)

● Baby/cord serology.
Congenital hepatitis ● Maternal hepatitis B serology

● Baby LFTs and liver US.
Rubella ● Maternal serology before pregnancy

● Urine ± CSF PCR.
● WBC for rubella PCR
● Serum IgM.
Herpes simplex ● WBC PCR.
Varicella ● Other features of congenital varicella.
Look for supportive evidence with long bone X-rays, cerebral US/CT and ophthalmic exam.
References
1 Fraser SH. Non-immune hydrops: no longer an automatic death sentence. Australia and NZ Perinatal Society. Perth 1997.
2 Stephenson T et al. Diagnosis and management of non-immune hydrops. Arch Dis Child 1994; 70: F151-4
3 Jones DC. Diagnosis and management of nonimmune hydrops. P452-61
guideline.
Hyperglycaemia Reviewed by Jane Harding
January
2001
Complications Criteria for Insulin Exceptions to Insulin Management of Insulin References
Complications of Hyperglycaemia
1. Undernutrition leading to growth failure

2. Osmotic diuresis leading to dehydration
3. Association with periventricular haemorrhage
4. Exacerbation of hypoxic ischemic brain injury
Criteria for use of Insulin
Link to Insulin protocol
Persistent glycosuria ≥ 2+
Tolerating <100 calories/kg/day
AND or
(see below for caloric calculations)
Blood glucose ≥ 10mmols
Exceptions to Insulin Use
i. First 72 hours of life

ii. Acute transient stress e.g. post surgery, acute sepsis etc.
Management of Insulin Infusion
i. Administer in same line as intravenous fluids, so if there are any interruptions, both
are interrupted together
ii. Starting dose usually 0.05units/kg/hr, then adjusted according to requirements
iii. Do not include insulin in the total daily fluid intake - it should be titrated on top of
the prescribed fluid intake
iv. Monitor blood glucose, initially 2 hourly, and once stable at least 8 hourly
v. Aim for blood glucose ≥4mmol with glycosuria ≤1+
Calorie Intakes
● 150ml/kg of P10 with 1g lipid gives 81 calories/kg/day

Thus a baby who is not tolerating 150ml/kg of P10 with 3g lipid, or 180ml/kg of P10 with
1g lipid would qualify for insulin infusion.
References
1 Binder ND, Raschko PK, Benda GI, Reynolds JW. Insulin infusion with parenteral nutrition in extremely low
birth weight infants with hyperglycemia. J Pediatr 1989; 114: 273-80.
2 Collins JW, Hoppe M, Brown K, Edidin DV, Padbury J, Ogata ES. A controlled trial of insulin infusion and
parenteral nutrition in extremely low birth weight infants with glucose intolerance. J Pediatr 1991; 118: 921-
7.
3 Pildes RS. Neonatal hyperglycaemia. J Pediatr 1986; 109: 905-7
guideline.
Hyperkalaemia Reviewed by Carl Kuschel
May
2003
Definition and
Aetiology Complications Treatment References
Diagnosis
Definition and Diagnosis
● Hyperkalaemia is defined as a serum potassium concentration greater than 7mmol/

l.
● Unfortunately, this is relatively common when capillary blood samples are
haemolysed. The first step should be to confirm a high serum potassium with a
non-haemolysed venous or arterial sample.
● ECG changes (peaked T waves, or arrhythmias) indicate severe hyperkalaemia
and require urgent treatment.
Aetiology
● The most important cause to investigate is oliguric renal failure.

● However, extremely premature babies may develop hyperkalaemia without
significant renal impairment due to release of potassium from catabolised cells, as
well as shift of intracellular potassium to the extracellular spaces. This may be
exacerbated by dehydration.
Complications
● In general, elevated potassium levels even above 7mmol/l are tolerated well by
neonates.
● The main complication is arrhythmia, with the most common arrhythmias being
ventricular tachycardia and sinus bradycardia.
Treatment
1. Remove K from IV (i.e. hang 10% dextrose with Na+)

2. 10% Calcium Gluconate 0.5ml/kg IV (0.1mmol/kg)
3. Sodium bicarbonate 2mmols/kg IV given over 30 minutes.
4. IV 20% - 50% dextrose so blood glucose >12mmol/L.
Then Insulin 0.3 unit/gram of glucose.
5. Resonium 0.5 - 1g/kg rectally.
3
6. Salbutamol 4micrograms/kg IV over 10 minutes . May be repeated after 2 hours.
7. Peritoneal dialysis.
References
1 Avery GB, Fletcher MA, MacDonald MG (eds). Neonatology: pathophysiology and management of the
newborn. 4th Ed. JB Lippincott Co, 1994.
2 Mildenberger E. Versmold HT. Pathogenesis and therapy of non-oliguric hyperkalaemia of the premature
infant. Eur J Pediatr, 2002; 161:415-22
3 The Northern Neonatal Network. Neonatal Formulary (3rd Ed), BMJ Publishing 2000.
guideline.
Guidelines for the Management of Hypoglycaemia Reviewed by Jane Harding
July
2004
Definition Diagnosis Treatment

Continuing Therapy References
Also see guideline on investigation of severe hypoglycaemia
Click here for the Glucose calculator
Hypoglycaemia is important because:
1. It is a common, readily diagnosed and readily treated problem.

2. If untreated, it may cause permanent brain damage.
Definition
Serum glucose <2.6mM. This is based on the following:
1. Glucose levels within the ‘normal’ range are not necessarily optimal.
2. There is no physiological reason why brain glucose requirements should differ
between term and preterm infants, or between the first and subsequent days of life.
3. The aim is to define a level which is safe for all babies, rather than is adequate for
most.
4. Altered electrophysiological measurements and poor long-term neurological
outcome have been reported in infants with recurrent serum glucose levels
<2.6mM.
Diagnosis
1. Monitor at-risk infants

❍ All infants <10th centile or >95th centile on customised centile charts
❍ If customised centiles are not available, all infants or birthweight < 2.5kg or
>4.5kg.
Infants of diabetic mothers
❍
❍ Stressed infants - i.e. those with birth asphyxia, sepsis, haemolytic disease,
respiratory distress or congenital heart disease

❍ Infants with possible symptoms
2. When to monitor
❍ Measure plasma glucose at 1-2 hours of age, 4 hours, and then 4 hourly,
preferably before feeds.

3. How long to monitor
❍ If feeding well At least 12 hours
❍ Any recorded hypoglycaemia At least 12 hours after last low level
Click here to link to the flowchart for management of infants at risk of hypoglycaemia
Treatment
1. All at risk infants (see above) should receive milk feedings (either breastfeed or
formula - maternal preference) or intravenous dextrose as soon as feasible, and
always within the first 2 hours of life.
2. If glucose below 2.2mM on first testing (1-2 hours)
or 2.2-2.6mM after first 2 hours
feed immediately and recheck glucose within 1 hour.
3. If glucose below 2.2mM after first 2 hours
or below 2.6mM on more than 2 occasions
or feeds not tolerated
❍ start IV dextrose 10% at 60ml/kg/day (= 4.2mg/kg/min glucose)
❍ continue feeds if possible
❍ consider a bolus of 1-2ml/kg 10% dextrose IV
❍ recheck glucose within 1 hour
4. Recurrent or persistent hypoglycaemia not responding to above measures -

increase IV dextrose concentration or volume e.g. 12.5 or 15% dextrose and
continue feeding if tolerated.
5. For small- or large-for-gestational age infants or infants of diabetic mothers on
postnatal wards, see separate guidelines.
Continuing Therapy
Continue to monitor glucoses while IV dextrose is being gradually reduced. Rapid

reductions in glucose infusion are likely to cause rebound hypoglycaemia.
● Click here to link to the flowchart for weaning of infants receiving dextrose for
hypoglycaemia
Persistent or severe hypoglycaemia (requiring more than 10mg/kg/min of glucose or

lasting longer than 1 week) may require further investigation and management, e.g. with
glucagon, diazoxide, steroids or surgery.
Click here for the Glucose calculator
In an emergency, particularly if there is difficulty in starting intravenous glucose infusion,
glucagon 100 to 300ug/kg intramuscularly will stabilise blood glucose in most babies for
one to two hours. The dose can be repeated, but subsequent doses are much less likely
to be effective. (Glucagon mobilises glycogen stores. After the first dose, stores will
probably be depleted).
References
1 Koh THHG, Aynsley-Green A, Tarbit M, Eyre JA; Neural dysfunction during hypoglycaemia. Arch Dis Child
1988; 63: 1353-1358.
2 Koh THHG, Eyre JA, Aynsley-Green A; Neonatal hypoglycaemia - the controversy regarding definition.
Arch Dis Child 1988; 63:1386-1398
3 LaFranchi S; Hypoglycaemia of infancy and childhood. Pediatric Clin N Amer 1987; 34(4): 961-80.
4 Lubchenco LO, Bard H; Incidence of hypoglycemia in newborn infants classified by birth weight and
gestational age. Pediatrics 1971; 47: 831-8.
5 Lucas A, Morley R, Cole TJ; Adverse neurodevelopmental outcome of moderate neonatal hypoglycaemia.
Br Med J 1971; 297: 1304-8.
6 Senior B, Sadeghi-Nejad A; Hypoglycemia: A pathophysiologic approach. Acta Paediatr Scand Suppl
1989; 352: 1-27.
7 Glaser B, Thornton P, Otonkoski T, Junien C. Genetics of neonatal hyperinsulinism. Arch Dis Child Fetal
Neonatal Ed 2000; 82:F79-F86.
8 Shepherd RM, Cosgrove KE, O'Brien RE, et al. Hyperinsulinism of infancy: towards an understanding of
unregulated insulin release. Arch Dis Child Fetal Neonatal Ed 2000; 82:F87-F97.
9 Aynsley-Green A, Hussain K, Hall J, et al. Practical management of hyperinsulinism in infancy. Arch Dis
Child Fetal Neonatal Ed 2000; 82:F98-F107.
10 Rahier J, Guiot Y, Sempoux C. Persistent hyperinsulinaemic hypoglycaemia of infancy: a heterogenous
syndrome unrelated to nesidioblastosis. Arch Dis Child Fetal Neonatal Ed 2000; 82:F108-F112.
Any printed version can not be assumed to be current. Printed copies of this document are valid for Monday,
May 22, 2006.
Hypospadias Reviewed by Carl Kuschel and

James Hamill (Paediatric Surgery,
Starship Hospital)
May
2005
Incidence Definition and Description Investigations

Surgical Management Referrals References
Incidence
● Hypospadias is a very common congenital anomaly (1 in 300 male births). It is most

1
often an isolated finding but may be associated with other abnormalities.
● The incidence is increased if first degree relatives are affected. Up to 26% of male
offspring of an affected father may have hypospadias, and the risk in subsequent
2
siblings is 12%.
● It is more common in male infants who are growth restricted and premature. Other
3
risk factors include parental subfertility.
Definition and Description
Hypospadias (hypo =
below; spadon = a
fissure or a ‘hole’)
consists of some or all
of the following
features:
● Ventral
displacement of
the urethral
meatus
(hypospadias).
● Incomplete
formation of the
prepuce (dorsal
'hooding')
● Ventral
curvature
(chordee).
Urethral meatal
openings are generally
described as being:
● Anterior – where
the meatus is
near the tip of
the penis
● Middle – where
the meatus is
along the shaft
of the penis
● Posterior –
where the
meatus is near
the base of the
penis or in the
scrotum
● Early
recognition and
paediatric
urological
referral is useful
for counselling
and planning
timing of
surgery
Investigations
● The baby requires a complete examination to determine whether other external

abnormalities are present.
● Penile length should be determined
❍ Normal stretched penile length at term >2.5cm
❍ If penile length <2.5cm, refer to the Paediatric Endocrinology service for
assessment. Testosterone may be indicated.

● Renal ultrasound is not indicated for simple anterior or middle hypospadias unless
there are other features of concern (for example, dysmorphic features).
❍ Other conditions, such as an enlarged utricle, may be present particularly with
posterior hypospadias
❍ Renal abnormalities are more common with more posterior hypospadias.
Renal ultrasound is the investigation of choice initially.

● Posterior hypospadias – particularly in the absence of palpable gonads – should be
regarded as an intersex disorder and investigated appropriately.
Surgical Management
● Parents should be reassured that hypospadias is a common condition which can be

corrected with surgery.
● Surgery is performed by the Paediatric Urologists at Starship Children’s Hospital.
● Surgery is usually undertaken between 6 and 18 months, although timing will depend
on the surgeon and other factors. Often more than one procedure is required and it is
preferable to complete all stages in early childhood.
● It is critical that parents are told that circumcision should not be performed as the
foreskin remnant is required for surgical repair.
● The surgical principles are:
❍ To reposition the meatus on to the head of the penis (meatoplasty and
glanduloplasty)
❍ To straighten the chordee (othoplasty)
❍ To correct the hooded foreskin (by circumcision)
❍ To achieve all of this with an aesthetically acceptable result
Referrals
● Babies should be referred on discharge to the paediatric surgical service at Starship

Children’s Hospital.
● Send referrals to the Department of Paediatric Surgery – Fax 307 8952
● Alternatively contact a paediatric urologist directly.
References
1 Kulkarni BK, Oak SN, Patel MP, Merchant S, Borwankar SS. Developmental anomalies associated with
hypospadias. J Postgrad Med 1991;37:140-3
2 Bauer SB, Retik AB, Colodny AH. Genetic aspects of hypospadias. Urol Clin North Am 1981;8:559-64.
3 Manson JM, Carr MC. Molecular Epidemiology of Hypospadias: Review of Genetic and Environmental Risk
Factors. Birth Defects Research 2003;67(Part A):825– 36.
4 Smith EP, Wacksman J. Evaluation of severe hypospadias. J Pediatr 1997;131:344-6.
5 Shukla AR, Patel RP, Canning DA. Hypospadias. Urol Clin North Am 2004 Aug;31(3):445-60. (This entire
issue is devoted to hypospadias)
6 Anonymous. Timing of elective surgery on the genitalia of male children with particular reference to the risks,
benefits and psychological effects of surgery and anesthesia. Pediatics 1996;97(4):590-4.
guideline.
Reviewed by Nicky Webster, Carl

Neonatal Hypotonia Kuschel, Salim Aftimos
(Genetics), and Melinda Nolan
(Neurology)
December
2004
Aetiology History Physical Examination Investigations References
Congenital hypotonia is a relatively common diagnosis in the newborn period. It is defined

as a subjective decrease of resistance to passive range of motion in a newborn and can
be due to a defect at any level of the nervous system.
Aetiology
Causes include (but are not limited to):
Central ● Hypoxic ischaemic encephalopathy

(most common) ● Intracranial haemorrhage
● Cerebral malformations
● Chromosomal abnormalities (e.g.
Trisomy 21, Prader-Willi syndrome)
● Congenital infections (TORCH)
● Acquired infections
● Peroxisomal disorders
● Drug effects (e.g. benzodiazepines)
Spinal cord ● Birth trauma (especially Breech

delivery)
● Syringomyelia
Anterior Horn Cell ● Spinal Muscular Atrophy

● Pompe’s disease (acid maltase
deficiency)
Neuromuscular ● Myasthenia gravis (transient/
junction congenital)
● Infantile botulism
Muscle ● Muscular dystrophies (inc. congenital

myotonic dystrophy)
● Congenital myopathies (e.g. central
core disease)
Peripheral nerves ● Hereditary motor and sensory

neuropathies
Metabolic ● Acid maltase deficiency

myopathies ● Carnitine deficiency
● Cytochrome-c-oxidase deficiency
The first goal in diagnosing the source of neonatal hypotonia is to ascertain if it is central
(upper motor neuron) or peripheral (lower motor neuron). Central causes are the most
common. This delineation will determine the investigations most likely to yield a
diagnosis.
History
● Any significant family history – affected parents or siblings, consanguinity,

stillbirths, childhood deaths
● Maternal disease – diabetes, epilepsy, myotonic dystrophy (may not be
recognised)
● Pregnancy and delivery history – drug or teratogen exposure
● Decreased fetal movements
● Abnormal presentation
● Polyhydramnios/ oligohydramnios
● Apgar scores
● Resuscitation requirements
● Cord gases
● History since delivery
❍ Respiratory effort
❍ Ability to feed
❍ Level of alertness
❍ Level of spontaneous activity
❍ Character of cry
Physical Examination
A detailed physical examination should be performed, assessing muscle tone, any

asymmetry, the infant’s strength, deep tendon reflexes (DTR), and any dysmorphic or
unusual features.
Anterior Neuromuscular
Central Nerve Muscle
Horn Cell Junction
weakness,
normal generalised weakness, weakness,
face/ eyes/
strength weakness distal>proximal proximal>distal
bulbar
normal/
decreased/ decreased/ decreased
increased normal DTRs
absent DTRs absent DTRs DTRs
DTRs +
+/-
+/-seizures fasciculations no fasciculations
fasciculations
+/- often
dysmorphic described as
features alert
+ At times babies with profound central hypotonia may have absent DTR,
therefore absent DTR at least in the first few days of life would not rule out
a central cause for the hypotonia
* Note that the presence of profound weakness as well as hypotonia

suggests a disorder of the lower motor neuron. A sign of this may be a
weak cry. Weakness is uncommon in central hypotonia except in the acute
stages.
Arthrogryposis (the fixation of joints at birth) may be associated with neonatal hypotonia,
more commonly with lower motor neuron unit or multisystem abnormalities.
Additional clues which may direct to a specific diagnosis:
● Hepatosplenomegaly – storage disorders, congenital infections

● Renal cysts, high forehead, wide fontanelles – Zellweger’s syndrome
● Hepatomegaly, retinitis pigmentosa – neonatal adrenoleukodystrophy
● Congenital cataracts, glaucoma – oculocerebrorenal (Lowe) syndrome
● Abnormal odour – metabolic disorders
● Hypopigmentation, undesceded testes – Prader Willi
Examination of the mother is also important in suspected cases of congenital myotonic

dystrophy or myasthenia gravis.
Most studies have found that central causes account for 60-80% of cases and that the
diagnosis can usually be made by a careful history and examination. However, there may
be a mixed picture. Infants with a peripheral cause for their hypotonia may be at
increased risk for problems during labour, delivery and resuscitation and develop hypoxic
ischaemic encephalopathy.
Investigations
Further investigation needs to be guided by history and examination.
● If the infant is hypotonic but has a degree of strength, a central cause is most
likely and investigations should be directed toward this.
● If the infant is hypotonic and weak a peripheral cause is possible and an early
review by the neurology service is warranted.
Central causes ● Neuroimaging

❍ Ultrasound scan in the first instance.
❍ MRI may be indicated if a structural abnormality
of brain development is suspected and to

exclude other abnormalities (for example,
evidence of HIE)
● EEG: prognostic information as to brain function, useful
clinically if seizures suspected
● Genetics review if any dysmorphic features present
● Karyotype (if dysmorphic features)
● TORCH screen
● DNA methylation studies or FISH for Prader-Willi
syndrome (if clinically indicated after a genetics review)
● Metabolic workup
Peripheral causes ● Neurology services review

● Cervical myelopathies are an infrequent cause of
hypotonia. The diagnosis is made by history and
examination. Diagnostic studies are of limited value.
● Molecular genetics – CTG repeats, deletions in SMN
gene
● Creatine kinase (levels need to be interpreted with
caution in the newborn, as levels tend to be high at
birth and increase in the first 24 hours, they also
increase with acidosis). If elevated in an early sample,
repeat after a few days.
● Nerve conduction studies and muscle biopsy
(Depending on clinical situation, may be delayed until
around 6 months of age as neonatal results are difficult
to interpret)
References
1 Fenichel GM. Neonatal Neurology 3rd edition. Churchill Livingston Inc. 1990
2 Paro-Panjan D, Neubauer D. Congenital hypotonia: is there an algorithm? Journal of Child Neurology;

Jun2004, Vol.19 (6): 439-43
3 Prasad AN, Prasad C. The floppy infant: contribution of genetic and metabolic disorders. Brain and
Development; Oct 2003, Vol.25(7): 457-76
guideline.
Neonatal Encephalopathy Reviewed by Malcolm Battin

(NE)
November
2004
Long Term Follow-Up

Background Initial Management Ongoing Management References
and NWH Audit
See also: Seizure guideline Head cooling Metabolic Disease
Background
Neonatal Encephalopathy (NE) is “a clinically defined syndrome of disturbed neurological

function in the earliest days of life in the term infant, manifested by difficulty with initiating
and maintaining respiration, depression of tone and reflexes, sub normal level of
consciousness and often seizures” 1. NE occurs in approximately 3.5 - 6/1000 live births
and usually affects the full term infant. The terminology NE is preferred to Hypoxic
Ischemic Encephalopathy (HIE) as it is not always possible to document a significant
hypoxic-ischemic insult 2and there are potentially several other aetiologies 3, 4.
Specifically, it is important to exclude metabolic disease, infection, drug exposure,
nervous system malformation and neonatal stroke as possible causes of the
encephalopathy. The requirement for investigation to exclude these possibilities will
depend on the presentation, history and clinical features of the individual case.
Three clinical stages of encephalopathy are described.
Stage 1 ● Duration < 24 hours with hyperalertness

● Uninhibited Moro and stretch reflexes
● Sympathetic effects
● Normal electroencephalogram.
Stage 2 ● Obtundation
● Hypotonia
● Decreased spontaneous movements with or
without seizures.
Stage 3 ● Stupor
● Flaccidity
● Seizures
● Suppressed brain stem and autonomic functions
● The EEG may be isopotential or have infrequent
periodic discharges.
● Stage 3 or persistence of stage 2 for more than seven days or failure of the EEG
to revert to normal is associated with neurodevelopmental impairment or death 5.
● Full-term infants who develop long-term neurologic sequelae from intrapartum
asphyxia may not have low Apgar scores but will demonstrate neurological
dysfunction within 48 hours.
Initial Management
1. Adequate resuscitation should be promptly instituted at birth. Aim to keep oxygen

saturation > 95% in term infants.
2. Cord gases should be collected
3. Apgar scores : a low Apgar score indicates an abnormal condition at birth but it is
not exclusive to asphyxia and drug exposure, trauma, hypovolemia, infection, or
congenital anomalies should be excluded.
4. A note should be made of
❍ the time for respiration to be established, and
❍ the return of tone as this may help indicate the severity of the insult.
❍ Also slow recovery of the heart rate despite adequate resuscitation may
indicate a severe insult and meconium staining of umbilical cord and skin
suggests prolonged exposure to meconium (> 3 hrs).
Ongoing Management
Once oxygenation is established management is supportive.

Note: If the clincal course is not typical of a hypoxic-ischaemic insult, consider other
causes (possible other causes include [but are not limited to] metabolic disease, infection,
drug exposure, CNS malformation, or neonatal stroke)
1. Monitor blood gases, glucose, urea & electrolytes, creatinine and fluid balance.
2. If metabolic acidosis is severe or persistent then sodium bicarbonate may be used
but caution is advised as rapid infusion increases serum osmolality and
alkalisation may decrease cerebral blood flow.
3. Inotropes and volume expansion may be cautiously used to maintain blood
pressure and renal blood flow. Hypotension and low cerebral flow may be
associated with adverse neurologic outcome but the loss of cerebral
autoregulation makes hypertension equally hazardous.
4. Acute tubular necrosis or the presence of inappropriate ADH secretion affect fluid
output and thus fluid overload is a distinct but avoidable hazard. Urine output must
be carefully measured and urinary cateterisation should be considered.
5. Other organ impairments such as persistent fetal circulation require specific
measures. Echocardiogram will help to rule out structural cardiac disease and will
assist with assessment of cardiac function.
6. Seizures require prompt treatment as cerebral oxygen use is increased almost
fivefold during a seizure.
7. The use of mannitol or steroids for either the early cerebral oedema or increased
intracerebral pressure is not supported by any controlled studies.
8. All infants should have serial clinical neurologic assessment.
9. For infants with Stage 2 or Stage 3 NE, further investigations should be performed
to assist with prognosis. Every attempt should be made to co-ordinate
appointments.
❍ Where possible an EEG should be performed at approximately 7 days of
age (Auckland Hospital ext. 7524).

❍ Imaging
6 should be performed to assist with exclusion of haemorrhage
and other intracerebral abnormalities.
❍ Cerebral ultrasound scans provide little additional information regarding
prognosis. Doppler studies suggest that a resistive index of less than 0.5-
0.6 is consistent with the diagnosis of HIE.
❍ CT scanning may be useful to exclude haemorrhage and may assist with
prognosis. Ring Starship Hospital CT scanning on ext. 25132.

❍ MRI may provide prognostic information. Abnormalities of the thalami and
basal ganglia are associated with an increased risk of subsequent abnormal

developmental outcome. Discuss with the on-duty paediatric radiologist
at Starship Hospital.
■ Because MR demonstrates findings similar to CT and has greater
inter-observer agreement, it appears that MR is a superior test to CT

in determining brain abnormalities in the term neonate 7.
■ Furthermore, since MR eliminates the use of ionizing radiation, a
putative cause of malignancy, it should be the standard in neonatal

brain imaging.
10. Recruitment to the Selective Head Cooling Study has now been completed and
results are awaited.
Long term follow up and audit of Perinatal Asphyxia outcome of at NWH
Full term infants who suffer from Grade 2 or 3 encephalopathy are known to have a high
incidence of neurologic damage. A systematic follow up of these infants born at NWH is
necessary to feed back to those involved with the initial care. In order to obtain this
information ALL TERM AND POST TERM INFANTS WITH CLINICAL SEIZURES OR
STAGE 3 encephalopathy should have a psychometric assessment at 18 months in the
Child Development Unit at NWH.
This definition is clear cut and has the advantage of simplicity. Most of the infants with
seizures will have had moderate-to-severe NE. Seizures due to metabolic problems or
meningitis are rare - but these infants also frequently have an adverse outcome.
The parents of all term infants who have had clinical seizures should have a follow up
process defined, preferably at a discharge planning meeting. Dependent on the clinical
state and consultant decision these infants should have a psychometric assessment at 18
months of age, in the Child Development Unit at NWH. Referrals should be sent to Dr A
Dezoete after the discharge planning meeting, with the name, address and telephone
number of the infant's parents and a contact person (usually grandparent). If the
paediatrician following these infants is not from NWH they should be notified of the
provision of such an assessment and be told that this is done for audit purposes.
A neurological examination should be done at 12 months of age, either by the

paediatrician who provided care in the neonatal period or the paediatrician providing care
at 12 months of age. A copy of this neurologic examination should be sent to the Director
of the Child Development Unit for inclusion in the annual report.
References
1 Nelson KB, Leviton A. How much of neonatal encephalopathy is due to birth asphyxia? Am J Dis Child
1991;145(11):1325-31.
2 Edwards AD, Nelson KB. Neonatal encephalopathies. Time to reconsider the cause of encephalopathies.
[comment]. BMJ 1998;317(7172):1537-8.
3 Badawi N, Kurinczuk JJ, et al. Antepartum risk factors for newborn encephalopathy: the Western
Australian case-control study.[comment]. BMJ 1998;317(7172):1549-53.
4 Badawi N, Kurinczuk JJ, et al. Intrapartum risk factors for newborn encephalopathy: the Western
Australian case-control study.[comment]. BMJ 1998;317(7172):1554-8.
5 Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress. A clinical and
electroencephalographic study. Arch Neurol 1976;33:696-705
6 Ment LR, Bada HS, Barnes P, et al. Report of the Quality Standards Subcommittee of the American
Acedemy of Neurology and the Practice Committee of the Child Neurology Society. Practice Parameter:
Neuroimaging of the neonate. Neurology 2002; 58:1726-38.
7 Robertson RL, Robson CD, Zurakowski D, Antiles S, Strauss K, Mulkern RV. CT versus MR in neonatal
brain imaging at term. Pediatr Radiol 2003 Jul;33(7):442-9. Epub 2003 May 13
8 JJ Volpe. Hypoxic-ischemic encephalopathy. In Volpe Neurology of the Newborn.
9 Levene MI. Management of the asphyxiated full term infant. Arch Dis Child 1993;68:612-6
guideline.
Vaccinations
Authorised by:
July 2002
Introduction Index of Related Documents
This Document
● This document covers the following topics relating to the administration of

immunisations and nursing care for baby’s exposed to infections.
Introduction
Purpose The following policy/recommended best practices outline the way

in which immunisations are administered to ensure safety and
best outcome.
Scope Applies to all Nurses who:
1. Are required to administer Hepatitis B vaccination and Hep

B Immunoglobulin after birth.
2. Have completed the Vaccination Programme Training to
administer immunisations to infants at six weeks and three
months in Newborn Services.
3. BCG immunisations can only be given by gazetted nurse.
See page 24.
4. Care for infants with infections (or contact with infections in
Newborn Services).
Parental consent As outlined in each individual RBP.

and prescribing
guideline.
Vaccination Schedule Authorised by Charge Nurse

Newborn and Dr Liz Wilson,
Paediatric Infectious Diseases
August 2005
Hepatitis B Vaccine and Hepatitis B Vaccine Routine Vaccination BCG

Hepatitis B Immunoglobulin Schedule
at Birth
Guideline for GPs - Infants Infants with Chronic Lung Siblings References
<1000g or <29 weeks Disease or Congenital Heart
Disease
Hepatitis B Vaccine and Hep B Immunoglobulin (HBIG) at Birth

Hepatitis B Vaccine
a. Mother HbsAg positive

i. Infant should receive HBIG (<12 hours but some effect up to 72 hours),
dose 100iU (0.5ml) IM given in right leg.
ii. Vaccinate as soon as possible after birth.
Dose 5.0mcg = 0.5ml IM in left leg.
iii. Recommend follow up serology in 3-6 months to confirm status as vaccine/
HBIG only 95% effective at preventing transmission.
iv. Need consent signed in two places on the National Hepatitis B
immunisation programme form
(a) for the Hep B vaccine
(b) for the Hep B immunoglobulin
then chart on drug sheet.
b. Mother's status unknown
i. Infant should receive HBIG (<12 hours but some effect up to 72 hours),
dose 100iU (0.5ml) IM given in right leg.
ii. Vaccinate as soon as possible after birth
Dose 5.0mcg = 0.5ml IM in left leg.
iii. Need consent signed in two places on the National Hepatitis B
immunisation programme form
(a) for the Hep B vaccine
(b) for the Hep B immunoglobulin
then chart on drug sheet.
c. Mother HbsAg negative
i. Vaccinate at 6 weeks, 3 months, 5 months if weight >= 2000g at time of
dose, 2.5mcg = 0.25ml IM.
d. Follow-up doses for infants who are born to mothers who are Hepatitis B positive
or of unknown status
i. At 6 weeks - Hib-HepB (Convax) 0.5ml IM given in left leg

ii. At 3 months - Hib-HepB (Convax) 0.5ml IM given in left leg
iii. At 5 months - HepB II 2.5mcg IM given in left leg.
Routine Schedule for All Infants
Age Vaccine Dose Site

DTaP - IPV 0.5ml Right Leg
Hib - Hep B 0.5ml Left Leg
6 Weeks
2 days after above
MeNZB 0.5ml
vaccines
DTaP - IPV 0.5ml Right Leg
Hib - Hep B 0.5ml Left Leg
3 Months
2 days after above
MeNZB 0.5ml
vaccines
● After discussion with Registrar/NS-ANP, Parent to countersign on Stat page of
Medication Chart
● The 6 week and 3 month vaccinations are only administered by a Vaccination
Team member and ideally checked by another Vaccination Team member.
Vaccinations will be done ideally Mon – Fri between 1000 and 1530 hours.
● Paracetamol will not be given routinely. However, if the baby develops a
temperature >37.5° C, inform the Registrar/NS-ANP and a stat dose of
paracetamol may be charted. Dose 10mgs/kg.
BCG ● If the baby meets criteria and is over 2000grams, BCG

consent form is signed by parent
● Doctor charts on stat page of medication chart – BCG
0.05mls Intradermally.
● Will be given by Gazetted Nurse.
● Current recommendation is that neonatal BCG will be

offered to those infants at increased risk of tuberculosis, i.e:
a. Will be living in a household containing a

person who has arrived in New Zealand
within the previous five years from any
country with a high incidence of tuberculosis
(this includes most countries outside North
America, Australia and Western Europe or
where there will be visitors to the household
from high risk countries).
b. Will be living in a household containing a
person with either current TB or history of TB.
c. Will be living in a high incidence area of NZ
where all neonates are offered BCG.
● These infants need to be identified prior to discharge and

ideally vaccination given in hospital or arrangements made
for referral to a Public Health Nurse Community BCG clinic.
● * Contraindications
❍ Sick infants.
❍ Infants < 2000g.
❍ Infants where an immuno-deficiency is suspected.
● Baby must weigh ≥2000g.

● Dose 0.05ml intradermally
NOTE: 1. See below Guidelines for GPs Immunisation Schedule for
Babies <1000 grams or <29 weeks.
2. See further information – Individual Policy – Nurses
Immunisation/Infection Policy.
3. For further information see MOH Immunisation Handbook.
Guidelines for General Practitioners - Immunisation Schedule for Babies

<1000 grams or <29 weeks
● If babies are >1000 grams AND ≥29 weeks routine schedules apply.
Age Vaccine Dose Due Date Date Given

DTaP – IPV 0.5mls IM Right Leg
6 Weeks
Hib – Hep B 0.5mls IM Left Leg
3 Months
5 Months
And Blood test (micro red top tube) to check sero conversion antibody levels of Hep B
>10mIU/ml (the protective level)
If sero conversion is not found give the following

6 Months Hepatitis B 5mcg IM Left Leg
7 Months Hepatitis B 5mcg IM Left Leg
8 Months Repeat blood test on baby and advise parents of result.
For Babies with Chronic Lung Disease or Cardiac Anomalies
At least 6
months
old and
Influenza Vaccine
prior to the
Influenza
season
1 month
Influenza Vaccine
later
Then annually
N.B.: This differs from routine schedule in offering an extra Hib dose at 5 months
to allow for poorer sero conversion to Hib in premature babies.
Siblings
● Note that the vaccination status of siblings should be checked.

● Siblings should be fully vaccinated, particularly for pertussis.
● For infants with Chronic Lung Disease who are receiving the Influenza vaccination,
siblings should also be considered for Influenza vaccination (although the family
may have to pay for this unless the siblings have a chronic medical condition)
References
1 NZ Immunisation Handbook, Ministry of Health 1996
2 1997 Red Book, Report of the Committee on Infectious Diseases

guideline.
Management of Infants of Diabetic Mothers on the Reviewed by Simon Rowley

Postnatal Ward
July
2004
See also Guideline on Management of Hypoglycaemia
See also Hypoglycaemia on the Postnatal Ward
● These babies are at risk of hypoglycaemia.

● Routine blood glucose measurement should have been requested by the LMC or
paediatrician within the first hour following birth and 4-hourly or pre-feed thereafter
(whichever comes first).
● All blood glucose measurements should be performed by the Laboratory.
● Bedside testing methods (BM-stix, Precision-G monitors) are not reliable at
detecting hypoglycaemia.
● Baby should be closely observed for signs of hypoglycaemia, e.g. jitteriness.
● Feeding should be commenced early; first feed within one hour of delivery and
thereafter at least 3 hourly.
● Either breast or formula feeds (maternal preference) can be given.
● Complementary feeds are not necessary unless the baby's blood glucose falls to
<2.6mmol/L.
guideline.
INIS (International Neonatal Immunotherapy Study) Reviewed by Ana Kennedy and

Study Information Malcolm Battin
February
2006
Eligibility Consent Prescribing Pre-administration Checks

Administration of the Study
Monitoring Complications or Problems Storage
Drug
Eligibility
Proven, or suspected, serious infection
AND
<1500grams
OR
Positive Blood Culture, CSF or usually sterile body
fluid
OR
on a ventilator
AND
On Antibiotics
Consent

● Parent signs Agreement for INIS Study.
Prescribing of INIS Study Drug
● Order INIS Study Drug 8.3 ml/kg over 4 hours (may be slowed to 6 hours if
reactions occur).
❍ Weight should be written on the drug chart so that the dose can be checked.
● Second dose is to be given 48 hours after start of 1st dose (can be as early as 36
hours if required).
● After consultation with New Zealand Blood Service (
Cellphone and Fax Details ), fax a copy of Drug Administration
Record to NZBS.
● With larger babies and older babies consider Frusemide 1 mg/kg half way through
transfusion.
● INIS Study Drug is prescribed on the drug administration record on the single dose
section. Both doses are to be charted at the same time.
● It is also recorded in patient’s multidisciplinary clinical records.
Preadministration Checking
● INIS Study Drug for INIS patient comes in pre-primed BD syringe and
infusion set, the entire amount is to be given.
Step Action
1 The study drug must be checked by two Registered Nurses with current IV
certificates.
2 Check consent for INIS Study is signed by parent.
3 Baby’s identity - the baby’s identification band is checked against study drug
syringe label.
4 Check prescription order and amount to be given.
Administration of Study Drug
For specific information on the immunoglobulin preparation which may be used, click here.
Step Action
1 Should not be filtered.
2 Needs dedicated line; double lumen UVC OK.
Do not put through a long line as it may clot line.
3 Syringe pump to be lower than level of baby
4 If baby is charted Frusemide give via the injection port. (Flush with saline
before and after giving Frusemide.)
Monitoring
Step Action
1 Before commencement of study drug, baseline recordings of temperature,
heart rate, respirations and blood pressure will be taken and then repeated 15
minutes after commencement of study drug.
2 Temperature, heart rate and BP will be recorded hourly.
3 Record on normal observation chart if space allows. If not enough space then
record on blood transfusion record and make a note on the bedside
observation chart that you have recorded the vital signs on the blood
transfusion record.
Complications/Problems
● Adults sometime react to IVIG with fall in blood pressure. Baby should be watched
carefully particularly at the start of the infusion.
● Most patients have no side effects at all.
● Low pH should be considered in sick babies with acid/base problems.
Adverse Most patients have no side effects.

Reactions
Symptoms The following symptoms may occur.
● Hypotension, facial flushing or pallor, dyspnoea, non-urticarial

skin rash, itching, vomiting.
● May get delayed adverse reactions to Intragam P after the
infusion has stopped but usually within 24 hours.
● The low pH of IVIG should be considered in any sick babies
with acid/base problems.
● Undiluted, it is hyperosmolar. If the baby has high osmolarity or
low pH, there is a potential problem.
Follow the steps below to ensure best outcome for the infant.
Step Action
1 If any reaction to INIS study drug, it tends to be related to the infusion rate and
is most likely to occur in the first hour of infusion.
2 Stop the infusion temporarily.
3 Inform Doctor/NS-ANP.
4 Wait until infant has improved clinically (5-10 minutes).
5 Doctor/NS-ANP orders INIS Study Drug to be recommenced at a slower rate.
6 All adverse reactions should be reported to Dr Malcolm Battin, Prof. Jane
Harding, Dr Frank Bloomfield, or Ana Kennedy.
Storage
● In medication refrigerator in NICU for 24 hours (syringe will have expiration date
and time).
● Protect from light.
● Refrigerate at 2° to 8°C. Do not freeze.
guideline.
Intravascular Catheters
Authorised by:
Charge Nurse - Newborn
November 2003
Purpose Scope Other Related Documents Associated Documents
Purpose
To ensure the best outcome for babies in the Newborn Service.
● The insertion and use of all lines

● Standard fluid regimes and practices
● Standard infusion lines
● Drug administration
● Monitoring procedures
● Blood sampling, including blood gases
● Possible complications of fluid/line therapies
Scope
Applies to all nurses working in Newborn Services.

NW Nursing & ● Skin Care of the VLBW Infant
Midwifery Practice ● Baby Safety RBP
Manual
References ● Skinner J, Milligan C, Hunter S, Hey E (1992). Central
venous pressure in the ventilated neonate. Arch Dis
Child. Vol 67, Pages 374-377.
● Chair H, Kuhn M, Baum V (1994). Inferior vena caval
pressure reliability predicts right atrial pressure in
paediatric surgical patients. Critical Care Medicine. Vol
22, No 2, Page 219.
guideline.
Intravenous Cannulation
Overview Authorised by:
April 2006
Purpose Scope Criteria for Certification Maintenance of Certification
Purpose
● The following policy/RBP outlines the criteria for certification of nurses undertaking
IV cannulation within Newborn Services to ensure safety and best outcome.
Scope
● Applies to all Nurses applying to do IV cannulation within Newborn Services
Criteria for Certification
1. Must have worked within the newborn service at least 12 months and have
completed the Level III Care Competency booklet.
2. View DVD/video on ‘Intravenous Cannulation Insertion’.
3. Read teaching package and pass written test.
4. IV insertion to be demonstrated by a staff member on the IV Certification list.
5. Nurse is to be supervised/instructed for IV insertions by a certified IV cannulation
nurse. Three successful IV insertions are to be witnessed and signed off by the
supervising nurse.
6. IV cannulation certificate issued.
Maintenance of Certification
On a 2 yearly basis
1. Show proof of attendance at an education session on IV therapy.

2. Complete a competency review test.
3. Show documentation of recent IV insertion signed off by IV certified nurse.
guideline.
Intravenous/Medication Certification
Authorised by:
July 2004
Purpose IV Update Process Associated Documents
Purpose
● To ensure all staff have attained competency for checking/giving IV fluids and
medications and have an understanding of medications commonly used in the
service.
IV Update Process
Stage Description
1 Clinical Nurse Educators ensure all nursing staff have an understanding of
common medication (IV and oral) and IV therapy use in the Newborn service.
2 Coaching is provided for all new staff on IV and oral medications and IV
therapy.
3 Extra coaching and support is provided for staff having problems or when
errors are made with IV therapy or medication.
4 Staff must complete and pass successfully:
● an IV/medication level II test within four weeks of starting in Newborn

Service.
● a level III IV/medication test within four weeks of completing level III part
1 orientation.
● an annual IV/medication update test.
5 ● Clinical Nurse Educators and Senior Nursing staff assist with updates of
the Drug Protocols as required.
● IV/Medication tests are updated as required to ensure all staff are skilled
in current drugs or therapies used in the Newborn Service.

Board Policy ● IV Medication Information
● Newborn Drug Protocols
● IV/Medication Test
Hospital Policy ● N/A

Newborn Services Drug Protocol
Compatibilities for IV Y-site Administration Prepared by Brenda Hughes

Clinical Pharmacist,
Dept. Of Pharmacy, Auckland Healthcare
May 1999
● The compatibility data in the chart apply to drug concentrations as used in the protocols of Newborn
Services, National Women's Hospital.
● Where greater concentrations are used, contact the Pharmacy for compatibility advice
Compatible (at Y-site only) X Incompatible ? Unknown
Numbers below refer to references. Symbols are explained immediately below the table.
Caffeine Fentanyl Heparin Morphine NaHCO3 IVN

Aminophylline Dobutamine Dopamine Indomethacin Prostaglandin Intralipid
pH 2.0- pH 4.0- pH 5.5- pH 2.5- pH 7.0- pH
pH 8.8-10.0 pH 2.5-5.5 pH 2.5-4.5 pH 6.0-7.5 E1 pH 5.5
3.0 7.55 8.0 6.0 8.5 5.5-6.5
Aminophylline X X X
pH 8.8-10.0
? ? ? ?
1 1 +++ 1 12 ++ 10 + 21 13
Caffeine X X
pH 2.0-3.0
? ? ? ? ? ? ? ? X
2 4
Dobutamine X ? X X
pH 2.5-5.5
? ? ? ?
1 1 *** 11 5 1 20
Dopamine X X
pH 2.5-4.5
? ? ?
1 1 1 11 1 + 10 1, 3 20
Fentanyl
pH 4.0-7.55
? ? ? ? ? ? ? ? ?
1 20
Heparin
pH 5.5-8.0
? ? ? ? ?
+++ 1 1 1 *6 + 10 #1
Indomethacin X X X X X X X
pH 6.0-7.5
? ? ? ?
2 11 11 8, 9 11 11 8, 9
Morphine X ?
pH 2.5-6.0
? ?
12 5 1 *6 8, 9 + 10 1, 18 20 **15
Prostaglandin X
E1
? ? ? ? ? ?
++ 10 + + 10 + 10 + 10 7
NaHCO3 X X X
? ? ? ? ? ? X
pH 7.0-8.5 1 1, 3 11 1, 18
IVN X X X
pH 5.5-6.5
? ? ? ?
21 4 20 20 20 11 20
Intralipid X X ? X
pH 5.5
X ? ? ? X ?
13 #1 8, 9 ** 15 7
IVN = Intravenous Nutrition
+ = these drugs have a negligible effect on alprostadil (PGE 1), but the reverse not studied.
++ = in sodium chloride 0.9%
+++ = in glucose 5%
* = morphine ≤5mg/ml
** No conclusive data
*** conflicting results in studies (16, 19)
# destabilisation of fat emulsion has been noted at heparin 5 iU/ml (14) & 0.5 iU./ml (17) when co-infused
with TPN containing Ca++
Concentrations of Drugs used in NICU
Drug Concentration Used in NICU

Aminophylline 5mg per mL
Caffeine base 10mg per ml (Caffeine citrate 20mg per
mL)
Dobutamine 0.05 to 3.5 mg per mL
Dopamine 0.05 to 3.5 mg per mL
Fentanyl 1.0 to 15.0 mcg per mL
Heparin 0.5 to 2.0 units per mL
Indomethacin 0.5 to 1.0 mg per mL
Morphine 0.01 to 2.0 mg per mL
Prostaglandin (PGE1) 3.0 to 6.0 mcg per mL
Sodium bicarbonate 0.5 mmol per mL
Parenteral Nutrition
Intralipid 20%
References
1 Trissel LA, (ed). Handbook on Injectable Drugs (7th ed.). Bethesda: American Society of Hospital Pharmacists,1992.
2 Indocid P.D.A. Data Sheet. Auckland: Merck Sharp & Dohme (NZ) Ltd., 1997.
3 Dopamine data sheet. Victoria: F.H.Faulding & Co.Ltd,1992.
4 Roiall V. (Personal Correspondence). McGaw Biomed, August 1997.
5 Hasegawa G, Eder J. Visual compatibility of dobutamine HCl with other injectable drugs. Am J Hosp Pharm 1984;41: 949-51.
6 Baker DE,Yost GS et al. Compatibility of heparin sodium & morphine sulphate. Am J Hosp Pharm 1985;42:1352-5.
7 Little H. (Personal correspondence). Baxter Healthcare Ltd. 17 July 1996.
8 Indomethacin data sheet. West Point: Merck&Co.Inc,1994.
9 Reynolds JF, (ed). Martindale - The Extra Pharmacopoeia(30th ed). London: The Pharmaceutical Press,1993 .
10 Saunders J. (Personal correspondence) .Pharmacia & Upjohn.Aug.1996
11 Ishisaka D, Van Vleet J, et al. Visual compatibility of indomethacin sodium trihydrate with drugs given to neonates by
continuous infusion. Am J Hosp Pharm 1991; 48: 2442-3
12 Dasta JF, Hale KN et al. Comparison of visual and turbidimetric methods for determining short-term compatibility of
intravenous critical -care drugs. Am J Hosp Pharm.1988; 45:2361-6.
13 Gillies IR. Physical stability of Intralipid following drug addition. Aust J Hosp Pharm 1980; 10(3):118-120.
14 Johnson O, Washington C, et al. The destabilization of parenteral feeding emulsions by heparin. Int. J of Pharmaceutics.
1989;53: 237-240.
15 Little H. (Personal correspondence). Baxter Healthcare Ltd. June 1996.
16 Schilling CG. (Correspondence). Compatibility of drugs with a heparin-containing neonatal total parenteral nutrient solution. Am
J Hosp Pharm 1988; 45:313-4
17 Raup P, Von Kries R. et al. Incompatibility between fat emulsion and calcium plus heparin in parenteral nutrition of premature
babies. Lancet 1988; 1:700.
18 Zenk KE. Y-Site compatibility of drugs commonly used in the NICU. Neonatal Pharmacology Quarterly 1992; 1(2): 13-22.
19 Hasegawa GR, Eder JF. Dobutamine-heparin mixture inadvisable. Am J Hosp Pharm 1984; 41:2590-1.
20 Veltri M, Lee C. Compatibility of neonatal parenteral nutrient solutions with selected intravenous drugs. Am J Health-Syst
Pharm 1996; 53:2611-3.
guideline.
Parenteral Nutrition Guidelines Reviewed by Carl Kuschel
July
2004
Composition of
Indications Lipid Emulsions Parenteral Vitamins References
Solutions
See also the Individualised Solution Worksheet for calculating individualised IVN
solutions.
● When enteral feedings are not possible, the use of parenteral nutrition is essential
for the care of the sick newborn.
● The goals of parenteral nutrition are several-fold:
1. to promote nitrogen retention and protein sparing,

2. to provide energy for metabolic processes, and
3. to establish growth and maturation during the critical postnatal
period.
● The premature newborn has limited glycogen and fat stores, which become rapidly
depleted with starvation.
● Sick premature and term newborns generally require more than 70kcal/kg/day and
2.5 to 3.5g/kg/day of amino acids to support growth and nitrogen retention as
compared with the intrauterine rate.
Indications for Parenteral Nutrition
● The premature infant who weighs less than 1500g and who has respiratory
distress or other contraindications to enteral feedings should be started on
intravenous glucose during the first hours of life.
● Electrolyte and calcium supplementation should begin by 12 to 24 hours after birth
and amino acids should be started by 2 days of age.
● Trace elements are automatically added to all standard solutions (P10, N10,
P7.5) but need to be specifically requested for individualised solutions ("special"
solutions).
● Heparin is added to all intravenous nutrition solutions but can be omitted on
specialist orders if felt to be contraindicated.
● Larger premature and sick term newborns may be maintained on only glucose and
electrolyte solutions, if is anticipated that full enteral feedings will be tolerated by 5
to 7 days of age.
Parenteral Lipid Emulsion
● Since VLBW prematures develop biochemical evidence of essential fatty acid

insufficiency within 3 days of fat-free nutrition, low doses (1g/kg/day) of
intravenous lipid should be started within 3 days of starting parenteral nutrition,
even if hyperbilirubinaemia requiring phototherapy is present.
❍ If the serum bilirubin is >50% of the level requiring exchange transfusion,
lipid should be restricted to 1g/kg/day.

● Intralipid is highly susceptible to oxidation causing lipid hydroperoxides which are
cytotoxic. Elevated levels can be formed during clinical use in ambient light,
especially when intralipid infusion is combined with phototherapy.
❍ This may be prevented by covering the intralipid by aluminium foil during
1
light exposure.
● 20% Intralipid emulsion 1 to 3g/kg/day - over 24 hours (1g provides 10Kcal)
● Syringes of intralipid will be stored in the fridge in NICU.
Parenteral Vitamins
● To maintain vitamin A and E levels near to recommended values, multivitamin

Paediatric solution 2ml/kg/day, is added to the intralipid and infused over the 24
hour period. 2
● Consultant advice should be obtained as to when oral multivitamins may be given
instead of parenteral. In most cases this should be done when the baby is
tolerating at least 30% of the feed orally.
Composition of Standard IVN Solutions
Reformulated as of Preterm Infants Term

November 2004 Infants
P5 P7.5 P10 N10
Protein g/L 10 15 20 20
Nitrogen g/L 1.6 2.4 3.3 3.3
Amino acid g/L 11 16 21 21
Glucose g/L 50 75 100 100
Sodium mmol/L 15 20 29 15
Potassium mmol/L 15 20 30 15
Chloride mmol/L 14 19 30 14
Gluconate mmol/L 20 24 28 24
Acetate mmol/L 15 23 20 24
Calcium mmol/L 10 12 14 12
Magnesium mmol/L 1.0 1.0 1.2 1.2
Phosphate mmol/L 10 12 14 12
Trace elements ml/L 6.7 6.7 6.7 6.7
Heparin U/L 500 500 500 500
Non protein energy 170 255 340 340
kcal/L
Non protein energy 714 1071 1428 1428
kJ/L
Total energy kcal/L 211 315 422 421
Total energy kJ/L 885 1324 1771 1770
Osmolality mOsm/kg 429 623 817 779
● In exceptional circumstances special solutions may be necessary.

❍ See also the Individualised Solution Worksheet for calculating and
prescribing individualised IVN solutions.

❍ Special solutions require prospective approval by a specialist and
should be countersigned by them each day.

❍ They cost substantially more than standard solutions and have not been
shown to have any advantage over appropriately formulated standard

solutions in the majority of infants . 3
❍ There may be alternative methods of changing nutrient and electrolyte
intake, such as a simultaneous infusion of sodium, potassium, or glucose.
References
1 Neuzil J, Darlow BA, Inder TE, et al. Oxidation of parenteral lipid emulsion by ambient and phototherapy
lights: potential toxicity of routine parenteral feeding. J Pediatr 1995; 126:785-90.
2 Inder TE, Carr AC, Winterbourn CC, Austin NC, Darlow BA. Vitamin A and E status in very low birthweight
infants: development of an improved parenteral delivery system. J Pediatr 1995;126:128-31.
3 Yeung MY, Smyth JP, Maheshwari R, Shah S. Evaluation of standardized versus individualized total
parenteral nutrition regime for neonates less than 33 weeks gestation. J Paediatr Child Health 2003;39:613-
7.
Parenteral Nutrition
Individual Solution Worksheet © Carl Kuschel
October 2005
Note: ● Individualised IVN is not to be ordered without approval from the specialist on duty.
● Standardised solutions should be used in preference to individualised solutions, except in
circumstances where nutritional needs cannot be met with the available IVN preparations.
❍ If the only difference between a standard solution and the requested individualised solution is
that more sodium is required, consider using a standardised solution and run in a separate
infusion of sodium chloride.
● This worksheet is designed to provide a prescription for individually prescribed IVN.
● Some features are built in to the calculator including a limit on protein, glucose and lipid intakes, and
limits on sodium, potassium, calcium and phosphate.
● The prescriber takes responsibility for the IVN prescription.
● Press the button at the bottom of the page to view and print out your prescription
Patient Details
Surname Hospital Prescriber

Number Name
Weight for Date of Default values have been assigned to protein,
calculations g Day Month Year
lipid and fluid intakes on the basis of this baby's
Birth age.
Default values will change when you alter the
age of the baby until you choose to alter or
accept any one of these 3 values.
Fluid Calculations
Fluid Volumes Lipid Prescription
Total Daily Fluid Lipid

g/kg/day
Intake intake
(This includes all fluids - ml/kg/day ml/day
Recommended maximum 3g/kg/day
IVN, lipid, infusions, and
feeds)
Current Infusions
Arterial fluids 0.0 ml/hour ml/day
ml/kg/day
Drug infusions 0.0 ml/hour ml/day
(do not count lipid)
ml/kg/day
Feeds 0 ml/day ml/kg/day
Amino Acid and Glucose Solution

Amino Acid and ml/day Caloric Calculations
Glucose Solution
ml/kg/
day Protein
ml/hour Glucose
Protein g/kg/day g/day Lipid
Recommended 2.5-3.5g/kg/day
g/L Enteral
g/kg/
Glucose 10 % dextrose
day
Recommended 12-18g/kg/day
Total
mg/kg/ Non-nitrogenous calories per gram of protein

min
g/L This ratio is calculated as if no enteral nutrition is
mmol/ being given
Sodium 3 mmol/kg/day A ratio of 24-32 is thought to optimise anabolism
day
Recommended 2-3mmol/kg/day
Preterm infants may need more mmol/L
mmol/
Potassium 2 mmol/kg/day
day
Recommended 1-2mmol/kg/day
Preterm infants may need more
mmol/L
Anion -Choose anion-
mmol/
Calcium 1.5 mmol/kg/day
day
Recommended 1.5-2.5mmol/kg/day
The maximum you can give is 2.5mmol/kg/day mmol/L
mmol/
Phosphate 1.5 mmol/kg/day
day
This will give the same amount as for calcium
mmol/L
mmol/
Magnesium 0.20 mmol/kg/day
day
Recommended 0.15-0.25mmol/kg/day
mmol/L
Trace will be added at a concentration of 1ml/150ml to all
elements solutions
Heparin will be added at a concentration of 500U/L to all solutions
Days to Days Volume to supply
Supply ml
Clicking on this button will perform a check of all data.
Click Here to Produce Your IVN Prescription
If all calculations are correct, a window will open with your IVN prescription
Reset All Values

guideline.
Premedication for Intubation Reviewed by Carl Kuschel
December
2000
Most intubations occur at the time of delivery in the process of resuscitation, or semi-
electively in infants with either poor respiratory effort or with severe immediate respiratory
distress in the immediate newborn period. Intubation medications are therefore not
usually given. However, once the infant is in the NICU environment and IV access is
obtained, the use of intubation agents for elective or semi-elective intubations should be
considered, particularly in large vigorous infants.
Contraindications and Precautions
1. Intubation drugs should not be used ● if there is a known allergy to any of

the agents
2. Suxamethonium should not be used ● if there is a family history of

malignant hyperthermia
● if there is a suspicion of muscular
dystrophy, or
● if there is significant hyperkalaemia
3.Suxamethonium should be used with ● if there is concern that the infant has
caution abnormal upper airway anatomy (for
example, severe micrognathia) and
that intubation may be technically
extremely difficult.
❍ In this situation, a consultant
(and potentially an ENT

surgeon) should also be
present.
Preparation and Equipment

1. Consider intubation drug use in all elective or semi-elective intubations where IV
access is available or can easily be obtained.
2. Premedication should be strongly considered for all vigorous term infants.
3. Equipment must be ready, especially the bag-mask circuit and laryngoscope. The
infant will have no spontaneous respiratory effort once muscle relaxing agents (or
Fentanyl) have been given.
4. Suxamethonium should not be given if there is significant hyperkalaemia.
5. If Fentanyl is given, Suxamethonium should be ready to be given if chest-wall
rigidity occurs.
6. Medications should be administered in the order of:
See Intubation Quick Reference Guide.

Atropine 20mcg/kg IV
Anticholinergic
(if given)
Give slowly (30 seconds)

Fentanyl 4mcg/kg IV to avoid muscle rigidity
Sedation
Allow at least 30 seconds
for sedation
Suxamethonium 2mg/kg
Muscle relaxation IV
(if given)
If Morphine is used instead of Fentanyl, drugs should be administered in the order

of
Morphine, then Atropine, then Suxamethonium
7. The infant should have bag-mask ventilation during the administration of Fentanyl
and Suxamethonium, or prior to this if respiratory effort is poor.
8. Laryngoscopy should commence once spontaneous respiratory movements have
ceased.
9. Muscle fasciculation from Suxamethonium administration does not occur in
neonates and should not be relied upon as a sign of successful neuromuscular
blockade.
10. If bradycardia occurs in the presence of hypoxaemia, a second dose of Atropine
should not be given. The bradycardia is due to inadequate oxygenation and/or
ventilation.
11. If the intubation is unsuccessful, Suxamethonium can be re-administered but
Atropine and Fentanyl should not be repeated.
To view a literature review and rationale for this protocol, click here
guideline.
Isolation Guidelines
Reviewed by
Antibiotic resistant ● Until cleared

organisms
+ contacts
CMV * ● ubiquitious but pregnant staff not asked to nurse -
not a danger to other infants.
Diarrhoea ● until cultures negative and asymptomatic.

+ contacts
Enterovirus + contacts ● until asymptomatic and cultures negative.
Gonococcal ophthalmia ● until treated ? 24 hours.
Hepatitis A ● mother: 3 weeks from onset of jaundice.

● baby remain with mother in isolation - no treatment.
Hepatitis B ● clinical - mother isolated in hospital.

● carrier mother - syringe needle isolation
● infant - see immunisation schedule
Herpes simplex* ● until proven negative.

+ contacts
Outborn infants except ● until cultures negative.
from other delivery suites ● Infants from home -postnatal ward
Staphylococcal sepsis ● until negative and/or treated.
+ contacts
Necrotising enterocolitis * ● desirable to isolate.
Rubella * ● single room only because of danger to pregnant

nurses
Toxoplasmosis ● isolation not necessary.
Varicella-Zoster ● mother and infant -until lesions crusted.
* Isolation may not be possible except for known highly contagious disease, but barrier
nursing with gloves is indicated.
guideline.
Management of Neonatal Jaundice Reviewed by Peter Nobbs
May
2001
Assessment Management (including Atypical Jaundice Related Documents

graphs)
See also Neonatal Jaundice on the Postnatal Ward.
● Jaundice (SBR >50 μmol /L) is one of the most common physical signs observed
during the neonatal period.
● Approximately 50-60% of newborn infants will become jaundiced during the first
week of life.
● For many newborn infants the jaundice may be regarded as a manifestation of
their ongoing adaptation to the extra uterine environment.
● Although most jaundice is mild and physiological in origin, it cannot safely be
automatically assumed to be either.
● Jaundice may be a sign of pathology and demands evaluation and rational
management.
● Atypical presentation of jaundice (early onset, rapid rise in SBR, prolonged
jaundice, and/or late onset jaundice) is likely to reflect pathology.
● Furthermore, it is important to appreciate that an infant's symptoms may be
attributed to its jaundice when in fact they are due to other pathology.
Assessment
The evaluation of the jaundiced newborn infant must include a thorough history and
physical examination, with particular emphasis on the state of hydration and consideration
of the possibility of an acute haemolytic process and/or infection.
● The following approach to the evaluation of neonatal jaundice is recommended:-
1. Review maternal blood group.

2. Request infant's blood group and Coomb’s test if mother's blood
group is O.
3. Check SBR (note that a direct SBR very rarely indicated within the
first 5 days of life).
4. Haemoglobin, WBC and differential, and reticulocytes if suspicion/
evidence of haemolysis.
5. Urine for microscopy and a culture only if clinical suspicion of a
urinary tract infection.
6. If galactosaemia is suspected, then discuss an urgent serum assay
through the National Testing Laboratory. Urine samples for reducing
substances are not reliable nor specific.
● Other investigations may be necessary depending upon the specific clinical

situation.
● The significance of any SBR estimation depends upon the maturity and postnatal
age of the infant, the clinical status of the infant (hypoxaemia, acidaemia,
hypoalbuminaemia, and/or hypothermia) and the aetiology of the jaundice.
● Serial SBR estimations are an essential component of the continuing assessment
and management of the jaundiced newborn infant. Graphs are available to aid the
interpretation of SBR estimations.
Management
● Treatment Guidelines for Term

Infants without Haemolysis
❍ Click on the picture on the right
● Treatment Guidelines for Preterm

Infants or Infants with Haemolysis
❍ Click on the picture on the right
● It is important to maintain normal hydration and nutrition of the jaundiced newborn

infant. This may be achieved by the encouragement of breastfeeding, the provision
of additional oral fluids or may require the intravenous administration of fluid.
There is no evidence to support the administration of excessive quantities of fluid
and most infants will not need extra fluids.
● Phototherapy causes photodegradation of bilirubin in the infant's skin.
❍ This form of physical therapy has been shown to be an efficient method of
lowering the SBR and is usually effective.

❍ Complications of phototherapy are generally mild and include increased
insensible water losses, loose green stools, skin rashes, overheating and/or
chilling.
❍ The levels of SBR at which phototherapy is recommended in various
situations are indicated in the accompanying graphs.

2
❍ An inadequate quantum of phototherapy (<4 mcw/nm/cm ) is ineffective.
Recommended range for phototherapy is 5-10 mcw/nm/cm2. Increasing

phototherapy about 9-10 mcw/nm/cm2 is unlikely to provide any additional
benefit.
● Infants receiving phototherapy should be under paediatric supervision.
● An exchange transfusion is indicated for any infant in whom the degree of
hyperbilirubinaemia cannot be adequately controlled by phototherapy alone.
❍ Discuss the indications for exchange transfusion with the appropriate
specialist.
❍ Note that infants with jaundice due to a haemolytic disorder usually benefit
from phototherapy but may also require an exchange transfusion.

❍ With appropriate management, exchange transfusion should rarely be
required.
Atypical Jaundice
● Separate guidelines are available for the evaluation and management of late onset
jaundice (7-10 days or later) and prolonged jaundice (SBR >200 μmol /L after 7-
10 days of age).
guideline.
Neonatal Jaundice on the Postnatal Ward Reviewed by Peter Nobbs
May
2001
Significance of Jaundice Indications for Paediatric Referral Management
See also Neonatal Jaundice, which contains graphs indicating treatment levels.
The Significance of Jaundice
● Although 50-60% of newborn infants develop jaundice it cannot be assumed it is

either mild or "physiological" unless conscious evaluation, examination and
investigation has taken place.
● The significance of any serum bilirubin estimation depends upon the maturity and
postnatal age of the infant, the clinical status of the infant and the aetiology of the
jaundice.
● Jaundice is important because in itself it may cause kernicterus and because it
may be a presenting sign of an apparently unrelated condition. For example,
Chinese boys with jaundice may have G6PD deficiency.
Indications for Paediatric Referral
● Jaundice requires paediatric evaluation in the following situations and whenever

there is a possibility that hyperbilirubinaemia may indicate or cause pathology.
1. Clinically present before 24hrs of age.

2. Whenever other symptoms and/or signs of illness are present. When
SBR >200 μmol/L on the second day of life.
3. When SBR >250 μmol/L
4. When jaundice is of late onset (7-10 days or later) or is prolonged
with SBR >200 μmol/L after 7-10 days of life.
Management of Neonatal Jaundice
● Management is dictated both by the bilirubin level and by the underlying condition.
For example, a significant haemolytic condition may indicate earlier or longer
treatment.
● Treatment may consist of both ensuring adequate hydration, and encouraging

photo-degradation of unconjugated bilirubin in the skin by the provision of
phototherapy. This may prevent serum bilirubin levels rising to levels where
exchange transfusion would be necessary. Phototherapy is very effective at
preventing the need for an exchange transfusion.
guideline.
Blood Product Transfusion for Jehovah's Witnesses Reviewed by David Knight
March
2004
Urgent Transfusions Less Urgent Transfusions The Law in NZ Court Wardship
Jehovah's witnesses do not agree with blood transfusions. Our policy is to try to avoid
transfusion, but always to have the best interests of the infant as the foremost aim. Blood
tests should be kept to the safe minimum. Erythropoietin is used early and should be
considered even if the baby has received a transfusion.
Transfusion needs to be discussed with the parents. Consider inviting a Jehovah's

Witness Elder to such meetings, with the parent's consent. We have had a lot of contact
with Elders of the Church over the years and, although they disagree with transfusion,
these discussions have been helpful, particularly for the Witness parents.
Click here to open the contact details for the Witness's Hospital Liaison Committee
(intranet only)
For Urgent Transfusions
● We need to ask for consent.

● If consent is withheld, we can transfuse if it is thought that the transfusion is
needed to save life or prevent permanent injury or prolonged and avoidable pain
and suffering.
● This decision is made by a specialist and must be recorded in the clinical record.
● Unless impracticable the specialist should consult with a colleague before
proceeding.
● If further transfusions are likely to be needed, there should be discussion with
ADHB legal counsel.
For Less Urgent Transfusions (or if the need for transfusion is anticipated)
● We need to discuss with the parents.

● If consent is withheld, tell them that we will be consulting legal counsel and
seeking guardianship.
● In these circumstances, guardianship will only apply to blood transfusion.
Anticipated transfusion need: Unwell ELBW infants, babies <26 weeks, anaemic VLBW
infants, significant haemolytic disease, very sick term infants (although many of these
would fit the urgent transfusion criteria).
The law in New Zealand
The law in New Zealand covering transfusion to minors is as follows:
'Section 126B of the Health Act 1956: This section protects medical practitioners from
civil or criminal proceedings for administering blood transfusions without consent to any
person under the age of 20 years as long as the judge is satisfied that:
1. The transfusion was (in the reasonable opinion of the person administering the
transfusion) necessary to save life, or to prevent permanent injury or prolonged
and avoidable pain and suffering; and
2. There were reasonable attempts to obtain consent, or it was impracticable to
obtain consent given urgency; and
3. In all the circumstances, administering the transfusion is reasonable
Note: 16 to 19 year olds have the right to consent to medical treatment and their informed
refusal of blood products should be respected.
Court Wardship
In Re J [1996] 2 NZLR 134 Ellis J had made a three-year-old boy, whom doctors
considered in need of a blood transfusion after a severe nose bleed, a ward of the Court
and appointed a medical specialist to act as agent of the court to consent to any medical
treatment involving blood transfusion, over the objection of the boy's Jehovah’s Witness
parents. The Court of Appeal dismissed the parents’ appeal, noting that the parents’ right
to practise their religion cannot extend to imperil the life or health of the child.
The Court confirmed that S126B of the Health Act 1956 does not provide an exclusive
statutory mechanism, and that an application to place the child under the guardianship of
the Court and seek prior consent to a blood transfusion, may be brought where time and
circumstances permit. Before the Court, as guardian, authorises a transfusion to a child in
the face of parental opposition: there must be real or substantial risk that the patient's
condition will in the course of medical care be such as, on accepted medical practice,
would call for blood transfusion and that in the event that condition develops a blood
transfusion will be necessary.
guideline.
Laboratory Testing Reviewed by Carl Kuschel
May
2002
Collecting Ordering Tests New Admissions Babies on the Neonatal Unit

Jaundice Respiratory Distress Infection Screen Drug Monitoring
Collecting
On NICU and PIN nurses do capillary and arterial line collects. Doctors and NS-ANPs do
the venous collects. These can be ordered at any time although it is better to stick to
‘standard times’.
On Postnatal Wards, there is collecting round at 0900. At other times inform the
laboratory (3051) that a collect is necessary. Group the collections at 1300, 1600 or 1700,
2100, 0100 and 0500. For serial glucoses, write the times on the first glucose form and
the rest will be done.
Ordering tests
● Order laboratory tests when clinically indicated. Think of the use the test will be
and what information you will get from the result.
● Avoid unnecessary tests: they are unpleasant for the baby and expensive.
● Do not order tests more that a day ahead as clinical situations change at old
orders may no longer be relevant.
What tests to order
● This list is a guide. It is not exhaustive or exclusive.
New Admissions
● No routine tests. Admitting doctor or NS-ANP to decide what is warranted for that
baby.
Preterm, IUGR, ● Blood glucose monitoring 2, 4, 8, 12 hours and after that as
Unwell, >4kg, IDM indicated
● See hypoglycaemia guideline
● FBC
Respiratory ● Surface swabs and gastric aspirate

distress or ● Blood culture
possible infection ● FBC
● Glucose monitoring
● Consider LP
● Urine if >24 hours old
Unwell, asphyxia, ● Consider blood gas (arterial or capillary)

respiratory distress ● FBC
IUGR ● Consider congenital infection screen:

● Urine CMV, rubella/toxo serology ± IgM.
● Get maternal information
Babies on the Neonatal Units
<1000gms for 1st ● Regular blood gases include Na+, K+, ICa++ and glucoses.
few days These do not need to be done separately.
● Blood gases as indicated by baby’s condition.
● Daily FBC, urea and creatinine.
● SBR in first day and as indicated thereafter.
● If no regular gases, glucoses 4 hourly initially, decreasing
frequenct if stable. Electrolytes 8-12 hourly initially
<1500gms for 1st ● Very dependant on clinical condition

few days ● Glucoses serially initially.
● Electrolytes daily. Urea and creatinine daily initially.
● FBC initially and daily if unwell.
● Gases as indicated.
● SBR if any sign of jaundice.
Babies on IV ● Glucoses 4-8 hourly until stable then daily.

therapy ● Electrolytes, urea and creatinine daily initially.
Babies on IVN ● Initially daily urea, electrolytes, blood gas, glucose, FBC.
● When stable, 2 x weekly bloods. More frequent glucoses.
Preterm babies ● Weekly electrolytes if indicated.
after first few days ● FBC if symptoms and/or signs of anaemia.
Babies <1000gms, ● Ca2+, PO43-, and ALP as indicated clinically.

or on IVN for >2
weeks, or diuretics/
steroids for chronic
lung disease
Jaundice
● SBR regularly. Frequency a severity, age, rate of change. Rarely >1 daily in well
term infants.
● Direct SBR if prolonged (>2 weeks term or >3 weeks preterm) or if atypical, or
unwell baby or before an exchange.
● Group & Coombs, FBC (look at film result). Consider reducing substances, urgent
Guthrie, Consider the cause and investigate if indicated.
Respiratory Distress
● Blood gases (capillary or arterial). Individualise frequency. Are repeated gases

clinically useful in that baby?
● FBC as indicated.
● If chest drain, regular protein and albumin.
Infection screen
● FBC, blood culture

● Urine (SPA or catheter if possible) if > 24 hours old.
● CSF in 1st 24 hours if baby unwell and may be septicaemic, provided baby stable
enough for an LP.
● CSF after 24 hours of age unless treating respiratory deterioration only.
● CXR if chest infection likely.
Drug monitoring
● Gentamicin/netilmicin/vancomycin: Trough and peak after 1st dose or after change

in dose and repeat every 3-5 days.
● Caffeine: In a baby with no signs of toxicity and controlled apnoeas, NO DRUG
LEVELS ARE NEEDED.
Any suspicions of toxicity: check level
Persisting apnoea: check level.
DISCUSS WITH THE LABORATORY PRIOR TO SENDING AS CAFFEINE
SAMPLES ARE FORWARDED TO EXTERNAL LABORATORIES
● Phenobarbitone/phenytoin: 12-24 hours after 1st dose and thereafter at intervals.
● Digoxin: 10-12 hours after last loading dose and repeat at intervals, including after
change in dose.
10-12 hours post dose.
guideline.
Management of Small- or Large-for Gestational Age Reviewed by Jane Harding

Infants on the Postnatal Ward
July
2004
See also Guideline on Management of Hypoglycaemia
See also Hypoglycaemia on the Postnatal Ward
This guideline refers to term or near-term babies who are:
● <10th or >95th centile by customised centile charts, or

● <2.5kg or >4.5kg if customised centiles are not available
These babies are at risk of:
● hypoglycaemia
● hypothermia
● jaundice secondary to polycythaemia
1. Temperature should be monitored before feeds for 12 hours or until stable

2. Baby should be closely observed for signs of hypoglycaemia or hypothermia (e.g
jitteriness, pallor, lethargy).
3. Routine blood glucose measurement should have been requested by the LMC or
Paediatrician within the first hour following birth and 4-hourly or pre-feed thereafter
(whichever comes first).
❍ All blood glucose measurements should be performed by the Laboratory.
❍ That is, bedside testing methods (BM-stix, Precision-G monitors) are not
reliable at detecting hypoglycaemia.

4. Feeding should be commenced early; first feed within one hour of delivery and
thereafter at least 3 hourly.
❍ Either breast or formula feeds (maternal preference) can be given.
❍ Complement feeds are not necessary unless the babies blood glucose falls
to <2.6mmol/L.
5. The baby should be watched for jaundice and bilirubin levels measured as
indicated.
guideline.
Withdrawal of Life Support Treatment

Refusal to Consent
Ethical Issues
1. The Welfare of the Child and best interests of the Child are Paramount
Interpreted with respect to what a reasonable adult would choose for themselves.
2. The Role of the Parent; its Scope and Limitations
The Guardianship Act: parent's ability to consent to treatment of a child.
(a) Parents cannot choose against the best interests of the child where these are clear e.
g. refusal of blood transfusion by Jehovah Witness parents.
(b) Discretionary role where parents are competent and the best interests of the child are
in doubt.
(c) Parents cannot insist on treatment that is not in the child's best interests
(i) Futile treatment: where it would not produce an outcome beneficial to

the child.
(ii) Treatment contrary to the child's best interests e.g. epidermolysis

bullosa (Lethalis).
3. The Role of Medical Practitioners
Whether providing for or withholding treatment is in child's "best interests: physicians

have a responsibility to prevent undue suffering including that from inhumane treatments
and in the case of a dying child, allow "death with dignity" .
(a) There is no legal duty to provide futile treatment.
(b) Courts will not order treatment against clinical judgement if there is medical diagnostic
and prognostic certainty.
(c) Courts will not lightly overrule parents.
(d) Family, clinical and ethical consensus is desirable.
(e) Clinicians/parental disagreement equals "alarm". In these cases, review legal issues
by legal advisers and ethical issues by the Hospital Ethics Committee is recommended. It
may be appropriate to obtain a Court Order approving the decision to withdraw.
References
1 Annas GJ. Asking the Courts to set the standards of emergency are -the case of Baby K. N Engl J Med
1994; 330: 1542-5.
2 Biachi DW, van Mater LJ. An approach to ventilator dependent neonates with arthrogryposis. Paediatrics
1994; 94: 682-6.
These guidelines were initially developed by Dr Andrew Howie, Ms Jane Bowden, and Associate Professor Tania Gunn
- September 1997
guideline.
Percutaneous Central Venous Catheter (Longline) Reviewed by Malcolm Battin,

Insertion Bernadette Page, and David Odd
February
2002
Indications Contraindications Sites

Procedure Other Related Documents
Indications
● The insertion of a longline

should not be considered a routine. However, infants who are VLBW, likely to be
slow to reach full enteral feeds, have IV access problems or long term IV nutrition
needs (NEC, major surgical problems etc.) may require line placement.
● Infants to have longlines inserted should be discussed on ward round and/or with a
Specialist at the time of presentation.
● In babies <1000g insertion of an umbilical venous catheter on admission is the
preferred option. In those who are very small, sick or have respiratory distress an
umbilical artery catheter should be considered at the same time. In sick term
babies a double lumen UVC should be used as they may require several infusions.
● Where ever possible discuss the risks of the procedure with the family.
Contraindications
● Skin sepsis at insertion site

● Bacteraemia or septicaemia
Sites
● Large vein in antecubital fossa, long saphenous vein or posterior tibial vein
Procedure
Important: Use a full sterile technique.
DO NOT ATTEMPT THIS PROCEDURE THROUGH THE PORTHOLES
Insertion ● For longlines inserted via the leg, measure from insertion site
Distance to xiphisternum.
● For longlines inserted via the arm, measure from insertion site
to the sternal notch.
Equipment ● Open longline

Required pack onto trolley and add:
❍ 20 gauge cannula
❍ Longline
set
❍ Scalpel blade
❍ 5ml syringe
❍ 0.9% NaCl 5ml ampoule
❍ Heparinised saline 10 unit/ml
❍ Skin wash
■ Either Chlorhexidine 0.5% in 70% alcohol or
0.2% for infants <1000gms. <2 weeks old.

❍ Steristrips
❍ Duoderm dressing
❍ Tegaderm or Opsite dressing
Procedure ● Don mask, gown, and gloves.

● Flush the longline
with 0.9% NaCl leaving syringe attached
● Cut round the IV cannula at the hub leaving cannula on the
introducer
● Position the infant maximising access i.e. open the incubator
door, slide tray out and use overhead heater. Secure limbs if
necessary
● If an assistant is required they must wear a gown and sterile

gloves
● Clean the skin with the chlorhexidine solution appropriate for
the infant’s gestation.
❍ Wait about 1 minute until it dries otherwise it will
not be an effective skin prep.
● Create a sterile field with sterile guards

● Apply tourniquet above site
● Position line, syringe and forceps on sterile field

● Insert cannula, advance cannula off the introducer and
withdraw introducer
● Insert longline
with forceps and feed to premeasured distance releasing
tourniquet when catheter is through the cannula
● Withdraw cannula over the longline ensuring the longline is
stable by using pressure on the limb above the cannula
● Detach longline at blue connection, remove cannula and
reattach connection, ensuring air is not introduced. The black
marker that lies over the metal insert must not be visible.
● Flush longline with 0.5ml of heparinised saline (10U/ml)
Securing the ● Coil longline next to site without crossing longline.

Line ❍ Steristrips should be used to anchor the line preventing
inward movement and may also help to keep the

longline coiled.
● Place a small piece of Duoderm on skin under connection and
secure everything with Tegaderm.
Confirm the ● Wrap syringe in sterile guard until position confirmed by x-ray
position ❍ The Department of Health (UK) has recently reviewed
four cases of neonatal death due to pericardial

tamponade associated with the presence of a central
venous percutaneous line. The recommendation from
this group was that the line tip is placed OUTSIDE the
heart.
● X-ray with contrast medium prior to connecting fluids. This
must be done using sterile technique
● Record in the clinical notes the date, insertion site and length of
catheter. Enter the procedure in the neonatal database.
❍ It is also important that we note the catheter tip position

in the clinical record
guideline.
Meconium-stained Liquor and Meconium Aspiration Reviewed by David Knight
October
2004
Delivery Room Management Further Management Criteria for Admission to NICU

Management of the Symptomatic
Complications of Meconium Aspiration References
Infant
Delivery Room Management
1. The Paediatric Resident (SHO, Registrar, or NS-ANP) should be called if there is

thick meconium staining or light meconium plus fetal distress.
2. There is no advantage in oral and pharyngeal suction as the head delivers and this
1
is no longer indicated.
Suctioning does not alter the chance of developing respiratory distress or
symptomatic meconium aspiration syndrome, even in sub-groups with thick
meconium, fetal distress or delivered by Caesarean section.
3. If the baby is apparently vigorous at birth (heart rate >100, spontaneous
respiration, reasonable tone), intubation and tracheal suction is not indicated,
unless the baby subsequently has poor respiratory effort or early respiratory
distress. 2
Intubation of vigorous babies does not improve respiratory outcomes and can
result in trauma to the infant.
4. Intubation and tracheal suction should be performed if the baby has moderate or
thick meconium and depression at birth.
● Laryngoscope and suction the pharynx under direct vision. Intubate

and suction the trachea with a meconium aspirator tube, applying
suction as it is withdrawn. Use a pressure of -100mm Hg or -13Kpa
2
for 1-5 seconds, with withdrawal of the tube .
● If meconium is present in the trachea, consider repeating ET suction.
● Resuscitate infant appropriately. If the heart rate is low, the infant
should be ventilated after the first intubation (bag and mask) or on
the second intubation.
5. Assess the infant.
Arrange for cord blood gas (arterial if possible) to be taken from a double clamped
section of cord.
Further Management
● All infants with meconium stained liquor must be well observed. For most babies
this is with their mothers.
● If there is thick meconium or any worrying clinical features, the paediatric resident
staff should review the baby at an hour of age.
● All babies should have AC temperature and respiration recordings with instructions
to call the paediatric resident if there is any respiratory distress. 3
Criteria for Admission to NICU
● Symptomatic meconium aspiration syndrome.

● Meconium in trachea with significant asphyxia
(> 10 minutes to establish spontaneous ventilation or cord pH < 7.2).
● Other significant risk factors for infection.
Management of the Symptomatic Infant
● Assess the infant.

● Give enough oxygen to maintain SpO2 >95% initially. Put on CPAP to deliver
oxygen.
● CXR if significant respiratory distress or tachypnoea persists.
● Consider antibiotics:
I. if unwell
II. if persistent symptoms
III. if other risk factors for infection
● Take blood culture if treating with antibiotics.
Complications of Meconium Aspiration
1. Infection: Uncommon unless sepsis was the stimulus to make the infant pass
meconium. Consider LISTERIA, especially if preterm. Meconium is a good culture
medium so secondary infection may occur.
2. Pneumothorax: May occur at any stage (MAS is an air-trapping disease). So
consider this any time from resuscitation onwards if there is unexpected
deterioration or significant disease.
3. Respiratory Failure: Can occur because of respiratory obstruction, inflammation,
infection or shunting.
4. Persistent Pulmonary Hypertension: Is common in severe MAS and can be very
difficult to treat. Early assessment and avoidance of hypoxaemia, hypothermia,
hypoglycaemia are important to avert PPHN.
References
1 Oropharyngeal and nasopharyngeal suctioning of meconium-stained neonates before delivery of their
shoulders: multicentre, randomised controlled trial. Vane NE, Szyld EG, et al. Lancet 2004: 364: 597-602
2 Delivery room management of the apparently vigorous meconium-stained neonate: results of the
multicenter, international collaborative trial. Wiswell TE, Gannon CM, Jacob J, et al. Pediatrics 2000;
105:1-7.
3 Clinical audit of babies delivered through meconium stained liquor. Ashton M. NWH 2001
guideline.
Metoclopramide (Maxolon) and Breastfeeding Reviewed by Carl Kuschel
October
2002
Rationale Recommendations References
● Domperidone has replaced Metoclopramide as the galactogogue of choice in

NICU.
Rationale
Metoclopramide (Maxolon) is an anti-dopaminergic agent which has been shown to

significantly increase milk yields in mothers with lactational deficiency.
A placebo controlled double blind study of metoclopramide started on the first day post
partum and continued for eight days, showed a 50% greater milk yield in the
1
metoclopramide treated group .
In a placebo controlled study of mothers 4-20 weeks post partum metoclopramide 10mg
tds for three weeks caused a significant increase in milk yield and in serum prolactin
levels. There was no change in the serum concentration of TSH or free thyroxine of either
mothers or infants and there was no rise in the prolactin levels in the infants in either
group. This study showed no effect on the hypothalamo-hypophyseal axis of the neonate
2
.
Metoclopramide taken orally by the mother is transferred to the breast milk. However it
3
was detected in the plasma from only one of the five neonates studied . Exposure of the
infant to metoclopramide was 6-24mcg/kg/day compared to the therapeutic dose of
500mcg/kg/day, i.e, less than 5%. Metoclopramide has been used successfully to treat
preterm infants with persistent functional feeding intolerance in a dose of 300mcg/kg/day
4
and no side effects were noted .
Maternal side effects are mild, uncommon and non-specific, e.g. tiredness. Extra
pyramidal dystonia has been reported and parents need to be aware of the possibility.
Recommendations
● Maxolon (metoclopramide) should only be given after the mother has been
expressing at least six times in 24 hours for three days. She must have had
teaching in effective expressing techniques and positioning of the baby at the
breast if possible.
● If the mother is still under obstetric or medical care, she should discuss the
possible use of metoclopramide with her medical adviser(s). The RMO may then
give the mother a prescription for Maxolon 10mg tds orally for two weeks. This
prescription may be repeated as necessary.
● Discuss with the Paediatric Consultant or Lactation Consultant and/or primary
charge nurse before starting therapy, to ensure that adequate assistance is in
place.
References
1 De Gezelle et al. Metoclopramide and breast milk. Euro J Obst Gynec Reprod Biol 1983; 15:31-6.
2 Kauppila et al. Metoclopramide and breastfeeding: Efficacy and anterior pituitary responses of the mother
and child. Euro J Obstet Gynec Reprod biol 1985; 19: 19-22.
3 Kauppila et al. Metoclopramide and breastfeeding: Transfer into milk and the newborn. Euro J Clin Pharm
1983; 25: 819-23.
4 Sankaran K et al. Use of metoclopramide in preterm infants. Devel Pharm & Therap 1982; 5: 114-9.
guideline.
Metabolic Bone Disease/Osteopenia of Prematurity Reviewed by Barbara Cormack

(Dietitian)
June
2005
Risk Factors Treatment References
Risk Factors
● <30 weeks gestation.

● <1000g birthweight.
● Delayed establishment of full enteral feeds/prolonged parenteral nutrition.
● Enteral feeds with low mineral content or bioavailability (unfortified EBM, standard
term formula).
● Chronic use of medications that increase mineral excretion (diuretics,
dexamethasone, sodium bicarbonate).
● Cholestatic jaundice.
When an infant is identified to be at risk of osteopenia, measurement of urinary

mineral excretion and serum 25-OH D should be considered.
Guidelines for the Treatment of Osteopenia of Prematurity
1. Prescribe elemental calcium 2.5mmol/kg/day and elemental phosphate 1.6mmol/

kg/day to be given in divided doses, four times daily.
Calcium and phosphate must not be given at the same time, so in practice
should be given at alternate feeds.
For example,
0600hr Calcium 1.25mmol/kg/dose
Phosphate 0.8mmol/kg/
1200hr
dose
1800hr Calcium 1.25mmol/kg/dose
Phosphate 0.8mmol/kg/
2400hr
dose
As intestinal obstruction has been associated with calcium supplementation of

enteral feeds, incremental advancement of calcium and phosphate supplements is
recommended starting at 50% of the target dose recommended above.
Contact the Newborn Unit Pharmacist for directions.
2. Ensure an adequate intake of calcium and phosphate from feeds:

❍ If <3.5kg Fortified EBM or Preterm formula
❍ If >3.5kg Unfortified EBM or Term formula (not Soy)
❍ N.B. This is different from the usual recommendation of 2.5kg.
3. Ensure a daily intake of 400IU Vitamin D per day.

❍ If on Fortified EBM or Preterm formula - Vitadol C 0.15ml/day (note this is
different to usual recommendations)

❍ If on Unfortified EBM or term formula - Vitadol C 0.3ml/day
4. Weekly monitoring in infants being treated with additional calcium, phosphate, or

vitamin D:
❍ serum calcium.
❍ serum phosphate.
❍ sodium.
❍ potassium.
❍ creatinine.
❍ acid/base balance.
5. Treatment is continued until biochemical indices are normal and radiographic

evidence of healing is present.
6. Consider other nutritional deficiencies (for example zinc) in an infant who is failing
to thrive with evidence of significant bone disease.
Caution: ● Infants on chronic diuretic therapy with loop diuretics (frusemide) are at
risk of increased urinary calcium excretion. High urinary calcium
increases the risk of nephrocalcinosis.
References
1 Groh-Wargo S, Thompson M, Hovasi Cox J, Hartline J. Nutritional Care for High-Risk Newborns, 3rd
Edition, Illinois, Precept Press, 2000
guideline.
Investigation and Treatment of Suspected Metabolic Reviewed by Callum Wilson

Disease
January
2001
General Guidelines Post-Mortem Samples and Analysis Emergency Management
General Guidelines
● Any sick baby where metabolic disease is part of the differential diagnosis. Please
discuss with the consultant acutely - many of the presentations can present rapid
demise.
● Important - you will get the best out of these tests if you contact the laboratory
when you suspect metabolic disease. Some of these tests have long turn-around
times - if you don’t tell the lab you have a problem they can’t do the tests urgently
for you.
❍ Auckland site - Claire de Luen (Biochemical Genetics, LabPlus, can be
contacted for all the tests re sample and destination Ext 6678).
Blood
● Glucose
● Gases
● U&E
● LFT’s
● Ketones (β-Hydroxybutyrate, acetoacetate)
● Lactate
● Acylcarnitine profile (plasma or blood spot on Guthrie card)
● Ammonia
● Alanine
● Free Fatty Acids
Urine
● Ketones - β-Hydroxybutyrate, acetoacetate)

● Organic acids screen
● Amino acid screen
● Glycoaminoglycan screen (if lysosomal disorder suspected)
General Notes
● Ask the lab not to discard specimens until you have an alternative diagnosis.
1. Obtain bloods BEFORE treatment is commenced.

2. Lactate: fluoride tube, grey top 0.5ml minimum
All other tests need green top (Li. Heparin) 2-5 mls.
3. If hypoglycaemia a prominent feature check growth hormone, insulin and cortisol.
4. If serum ammonia high check urinary orotic acid and plasma amino acids.
Any child who dies without a diagnosis, SIDS:
Information for post-mortem studies
● Blood (cardiac if not otherwise available) on filter paper

● Blood (separate if possible and freeze red cells and plasma separately) as soon as
possible post-mortem.
● Bile - freeze
● Urine - freeze
● Skin biopsy -fibroblast line
● Liver/kidney/muscle (small sugar cube size wrap in tinfoil, and snap frozen, -70°C,
use liquid nitrogen or dry ice if possible. Samples are best taken as soon after
death as possible. Consider a needle biopsy if it might take some time to get the
post-mortem samples).
● Hold samples. Await histology. Remember to ask for fat stains as important
indicators of metabolic disease (e.g.. fatty acid oxidation defects).
Remember Guthrie cards are kept by National Testing Centre for organic acid analysis
etc. (via Tandem Mass Spec. Also possible to do DNA studies [e.g.. MCAD] when a likely
diagnosis is found).
Emergency protocol for presumed metabolic disease
General
Contact expert help - Dr Callum Wilson is the local metabolic paediatrician. He can be
contacted through the Starship Operator.
● Treat hypoxia, infection, dehydration vigorously

● Fluids: 150-175%of maintenance
● Carbohydrate: maintenance of at 10-16% dextrose (pyruvate dehydrogenase
deficiency or electron transport chain defect patients worsen with high
carbohydrate load)
● Lipid: 2-3 g/kg per day (not in suspected fatty acid oxidation defects)
● Amino acids: to meet minimal RDA requirements (monitor amino acids)
Acidosis
● Severe metabolic acidosis in neonatal period is often fatal.

● Consider sodium bicarbonate when HCO3 <15. May need huge amounts to
correct acidosis in organic acidaemias (beware hyperammonaemia)
● Megadoses of vitamin co-factors are recommended by some authors.
❍ Thiamine B1 50-150mg/day (MSUD,PDH)
❍ Cobalamin B12 1-2mg/day (MMA)
❍ Biotin 10-20mg/day (Propionic aciduria, multiple carboxylase)
❍ Riboflavin 20-40mg/kg
❍ Coenzyme Q 4mg/kg (Resp. chain)
❍ Carnitine 100-200mg/kg (FAOD’s organic acidemias, urea cycle)
❍ Vitamin C 250-1000mg/kg
❍ Vitamin B6(pyridoxine dependent convulsions)
Hyperammonaemia
● Sodium benzoate, Sodium phenylacetate or sodium phenylbutyrate: 250mg/kg

loading dose (over 90 minutes) then 250mg/kg /day slow infusion.
● IV L-carnitine 100-200mg/kg /day
● L-arginine 400mg/kg /day (or citrulline)
● Consider testosterone/growth hormone/insulin infusion (0.2-0.3u/kg/hr) (decrease
catabolism)
● Early consideration of peritoneal dialysis or haemodialysis. Peritoneal dialysis: 40-
50ml/kg dialysate via peritoneal catheter, one hour cycles for 24-36 hrs. Careful
fluid balance, blood glucose, electrolyte measurements, All neonatal patients with
severe hyperammonaemia (plasma levels greater than 10 times normal) should be
haemodialysed.
● Contact expert help early
guideline.
Guidelines for Metabolic Screening of Newborn Reviewed by Callum Wilson and

Infants Dianne Webster
January
2001
The National Testing Centre (NTC) performs approximately 60,000 screening tests per
year for the following conditions (NZ incidence noted). Diagnostic tests are available for
the conditions marked "*", and therapeutic monitoring is available for PKU and MSUD.
● Cystic Fibrosis
1:3,500
● Congenital Hypothyroidism
1:4,800
● Phenylketonuria *
1:20,500
● Congenital Adrenal
Hyperplasia 1:25,000
● Biotinidase Deficiency *
1:83,000
● Galactosemia *
1:128,000
● Maple Syrup Urine Disease *

1:189,500
Diagnostic tests are also offered in conditions where the diagnosis can be made on the
basis of abnormal amino acid levels in physiological samples. About 30 such samples are
tested annually. Colleagues, primarily those in Australia provide invaluable support for
this service.
For infants with suspected metabolic problems, Dr Callum Wilson should be contacted via
Starship Hospital.
● Newborn screening samples on the Guthrie card should be collected after at least
48 hours of protein feeding in all newborn infants. The Ward Clerk should label a
Guthrie card for each infant born in another Hospital.
● For babies in NICU and PIN a Guthrie card should be put on the incubator by the
Ward Clerk and blood collected 4 days after birth on all infants regardless of
feeding regime and health status. If this is not done conditions such as congenital
hypothyroidism will have a delayed diagnosis and treatment. If the baby is not
tolerating full feeds, this first sample should be labelled stating, "Baby is not fully
orally feed".
● The Nurse (or laboratory staff) are responsible for documenting the collection of
the blood sample in the chart of the baby.
● The National Testing Centre will send a report of the original sample with a further
sample card and reminder for the retest. This is important because they are then
able to link subsequent samples with the original one.
● When these infants are taking full oral feeds for 48 hours, this further sample
should be taken and sent to the National Testing Centre.
Prescriber Update Articles
Drug Safety in Lactation
Website: May 2001
Prescriber Update No.21:10-23
Sharon Gardiner, Drug Information Pharmacist, Christchurch Hospital and Evan

Begg, Clinical Pharmacologist, Christchurch School of Medicine.
Many mothers are required to use drugs during breastfeeding. Almost all drugs transfer into
breast milk and this may carry a risk to a breastfed infant. Factors such as the dose received
via breast milk, and the pharmacokinetics and effect of the drug in the infant need to be taken
into consideration. Problems should not be overstated however, as many drugs are considered
'safe' during breastfeeding.
Transfer of drugs into breast milk is influenced by protein binding, lipid solubility and ionisation
Calculation of infant exposure to drugs can be used to help guide safe use
Infants have lower drug clearance than adults
Minimise risk to the breastfed infant by reducing drug exposure
Safety assessment of some frequently used drugs
Tabulated summary of drug distribution into breast milk
Primary sources
Transfer of drugs into breast milk is influenced by protein binding, lipid solubility and
ionisation<//h4>
Nearly all drugs transfer into breast milk to some extent. Notable exceptions are heparin and insulin
which are too large to cross biological membranes. The infant almost invariably receives no benefit
from this form of exposure and is considered to be an 'innocent bystander'. Drug transfer from
maternal plasma to milk is, with rare exceptions, by passive diffusion across biological membranes.
Transfer is greatest in the presence of low maternal plasma protein binding and high lipid solubility.
In addition, milk is slightly more acidic than plasma (pH of milk is approximately 7.2 and plasma is
7.4) allowing weakly basic drugs to transfer more readily into breast milk and become trapped
secondary to ionisation. Milk composition varies within and between feeds and this may also affect
transfer of drugs into breast milk. For example, milk at the end of a feed (hindmilk) contains
considerably more fat than foremilk and may concentrate fat-soluble drugs.
Transfer of drugs into breast milk is most commonly described quantitatively using the milk to
plasma (M/P) concentration ratio. The accuracy of this value is improved if it is based on the area
under the concentration-time curves (AUC) of the drug in maternal milk and plasma (M/PAUC).
Calculation of infant exposure to drugs can be used to help guide safe use
The infant's dose (Dinfant) received via milk can be calculated using the maternal plasma
concentration (Cmaternal), M/PAUC ratio and the volume of milk ingested by the infant (Vinfant):
Dinfant (mg/kg/day) = Cmaternal (mg/L) x M/PAUC x Vinfant (L/kg/day)
The volume of milk ingested by infants is commonly estimated as 0.15L/kg/day. The infant dose (mg/
kg) can then be expressed as a percentage of the maternal dose (mg/kg). An arbitrary cut-off of 10%
has been selected as a guide to the safe use of drugs during lactation. Drugs such as lithium (infant
dose as high as 80% of the weight-adjusted maternal dose) and amiodarone (infant dose up to 50%)
should be avoided due to high infant exposure and potential for significant toxicity. For drugs with
greater inherent toxicity such as cytotoxic agents, ergotamine, gold salts, immunosuppressives and
isotretinoin, the cut-off of 10% is too high and breastfeeding is contraindicated.
As a general rule, maternal use of topical preparations such as creams, nasal sprays or inhalers would
be expected to carry less risk to a breastfed infant than systemically administered drugs. This is due
to lower maternal concentrations and therefore lower transfer into breast milk. However, the risk to
the infant must be considered in relation to the toxicity of the drug used, the dosage regimen and the
area of application. For example, use of corticosteroids nasal sprays or inhalers in standard doses
would be considered compatible with breastfeeding.
Other factors to consider in conjunction with the infant's dose include the pharmacokinetics of the
drug in the infant. Generally, drugs that are poorly absorbed or have high first-pass metabolism are
less likely to be problematical during breastfeeding. For example, gentamicin is highly hydrophilic
and is very poorly absorbed when administered orally. Should any gentamicin be ingested via breast
milk, it is unlikely to be absorbed.
Infants have lower drug clearance than adults
Drug clearance in the infant is a particularly important consideration and premature infants have a
severely limited ability to clear drugs. Within a few days of delivery, term infants have glomerular
filtration rates approximately one-third of adult values after adjusting for difference in body surface
area, and premature infants have even more impaired clearance (see Table 1). Generally, adult
glomerular filtration rates (adjusted for the difference in surface area) are attained by five to six
months of age. Metabolic processes such as phase 1 oxidation and phase 2 glucuronidation are also
impaired in the neonate. Drugs subject to high first-pass metabolism may have higher oral availability
in premature or term infants due to impaired ability to metabolise on first-pass. Adult metabolic
capacity is attained towards the latter part of the infant's first year of life. The following table is
useful for estimating infant clearance.
Table 1: Approximate clearance values at different ages
Clearance of drug
Post-conceptual age
(compared with adults)
24-28 weeks 5%
28-34 weeks 10%
34-40 weeks 33%
40-44 weeks 50%
44-68 weeks 66%
> 68 weeks 100%
Minimise risk to the breastfed infant by reducing drug exposure
The overall risk of a drug to a breastfed infant depends on the concentration in the infant's blood and
the effects of the drug in the infant. If, after assessment of the risks and benefits, the decision is made
to breastfeed while the mother is using a drug, the infant should be monitored for adverse effects such
as failure to thrive, irritability and sedation. However, it is difficult to identify adverse reactions
occurring in neonates. Feeding immediately prior to a dose may help to minimise infant exposure as
concentrations in milk are likely to be lowest towards the end of a dosing interval. However, for some
drugs, milk concentrations lag behind plasma concentrations.
For drugs that have an infant dose greater than the arbitrary cut-off of 10% of the weight-adjusted
maternal dose, it may be reasonable to reduce infant exposure by alternating breast and bottle-
feeding. For drugs that are not considered safe in breastfeeding, breast milk may be expressed and
discarded for the treatment duration. Breastfeeding may be resumed after the drug has been
eliminated from the maternal blood stream. A period of approximately four half-lives will reduce
maternal concentrations to around 10% of steady-state concentrations.
Safety assessment of some frequently used drugs
A discussion of the safety of the more commonly used drugs is provided below. The data must be
assessed in conjunction with information on the maternal dose and therefore probable maternal
concentrations, the age of the infant and their likely ability to eliminate the drug. In general, if the
infant dose as a percentage of the maternal dose (corrected for weight) is close to 1%, the drug can be
considered 'safe' regardless of infant age. For drugs where the weight-adjusted dose is closer to 10%,
the infant clearance should also be taken into account (see Table 1). For example, if the weight-
adjusted infant dose is 10% but the infant is premature, the lower clearance will mean that the infant
concentrations may be well above those expected.
Analgesics:
Analgesics such as paracetamol, ibuprofen, naproxen and codeine are considered to be 'safe', due to
low transfer into breast milk and few problems with extensive usage. Transfer of aspirin into breast
milk appears to be low but it is best avoided due to the theoretical risk of Reye's syndrome.
Sumatriptan has a short half-life of approximately two hours and infant exposure can be almost
completely avoided by expressing and discarding breast milk for approximately eight hours after
dosing. Limited data on tramadol suggest low transfer into breast milk although where possible, it
would be preferable to use agents which are more established such as codeine and paracetamol.
Morphine is usually considered 'safe' because of low transfer into milk, and high first-pass
metabolism.
Anthelminthics:
There does not appear to be any data on the transfer of mebendazole or pyrantel embonate into
human breast milk although these agents are generally considered to be 'safe' due to poor absorption
from the gastrointestinal tract.
Antibiotics:
Antibiotics such as penicillins, cephalosporins and macrolides are considered to be compatible with
breastfeeding although there are theoretical risks of alterations to infant bowel flora and allergic
sensitisation.
The safety of metronidazole is controversial due to the possibility of high transfer into breast milk.
The weight-adjusted infant dose may be as high as 36% of the maternal dose indicating that infant
exposure may be higher than the arbitrary cut-off of 10%. Techniques that may be considered for
minimising infant exposure include choosing an alternative antibiotic such as amoxycillin/clavulanic
acid (if appropriate), alternating breast and bottle feeding, or withholding breastfeeding during the
treatment course. If breastfeeding is to be withheld, the mother should be encouraged to continue to
express breast milk while on the antibiotic course but to discard the milk. This will help to maintain
lactation and enable the mother to resume breastfeeding at the end of the course.
The transfer of tetracyclines into breast milk is low but they are usually avoided due to the possible
risks of inhibiting bone growth or causing dental staining. Fluoroquinolones should also be avoided
in breastfeeding as they have been reported to cause arthropathies in immature animals.
Sulphonamides such as sulphamethoxazole are unlikely to be problematical in most situations but are
best avoided in infants with hyperbilirubinaemia or glucose-6-phosphate dehydrogenase deficiency.
Anticoagulants:
Heparins (unfractionated and low molecular weight) are considered 'safe' since these agents have a
large molecular weight and do not cross into breast milk to a significant extent. They are also poorly
absorbed. Warfarin is also considered to be compatible with breastfeeding as transfer is low, and
adverse effects and changes in prothrombin time have not been detected in breastfed infants.
However, it would be prudent to monitor the infant's prothrombin time during treatment.
Anticonvulsants:
Carbamazepine, phenytoin and sodium valproate are generally considered to be compatible with
breastfeeding although the infant should be observed for evidence of central nervous system
depression. Available data on the safety of lamotrigine in breastfeeding suggest that transfer into
breast milk may be considerable and therapeutic concentrations have been detected in breastfed
infants. There are insufficient published data to comment on the safety of gabapentin in breastfeeding.
Antidepressants:
Selective serotonin reuptake inhibitors (SSRIs) transfer into breast milk to varying extents.
Paroxetine is reported to have the lowest transfer into breast milk (weight-adjusted infant dose 1-3%).
Fluoxetine transfers to a greater extent (weight-adjusted infant dose ≤ 14%) and its active metabolite,
norfluoxetine, has a long half-life of one to two weeks and may accumulate in a breastfed infant. Data
on citalopram (weight-adjusted infant dose approximately 5%) suggest that the relative infant dose of
citalopram is intermediate between paroxetine and fluoxetine. Based on these data, paroxetine is the
preferred SSRI in breastfeeding women.
Most tricyclic antidepressants are considered to be compatible with breastfeeding due to low transfer
into breast milk and this is supported by extensive usage data. Moclobemide has low-transfer into
breast milk and is considered compatible with breastfeeding.
Antihistamines:
Agents such as promethazine, dexchlorpheniramine and diphenhydramine are considered to be safe
through extensive usage, although it would be prudent to monitor for evidence of sedation or
irritability in the infant. There is less data on the non-sedating antihistamines, although loratadine and
fexofenadine are likely to be safe due to low transfer into milk.
Benzodiazepines:
Sporadic use of benzodiazepines with a short plasma half-life such as midazolam and temazepam is
unlikely to be problematical due to low quantities transferred into breast milk. Agents with a long
half-life such as diazepam may accumulate in the infant with prolonged exposure and may be
associated with lethargy, poor suckling and reduced weight gain.
Decongestants:
A short course of pseudoephedrine (weight-adjusted dose < 4%) is unlikely to be problematical.
However, topical decongestant nasal sprays or drops are usually preferred due to lower infant
exposure.
Social drugs:
These have particular problems because the dose and pattern of usage are uncontrolled. In addition
most have relatively high infant doses. Infant exposure following maternal ethanol ingestion may be
as high as 20% and has been associated with impaired psychomotor development. Alcohol
consumption should be minimised during lactation (e.g. by withholding breastfeeding for about two
hours after ingestion of a standard alcoholic drink).
Caffeine exposure may be as high as 34% of the weight-adjusted maternal dose and side effects such
as restlessness and irritability have been reported in infants exposed via breast milk.
Nicotine has been detected in the plasma of breastfed infants, and smoking is best avoided by
breastfeeding mothers. The use of nicotine replacement therapy (e.g. transdermal delivery systems) in
breastfeeding mothers should be considered in terms of risks and benefits. However, as a general
rule, the short-term use of nicotine replacement therapy is far preferable than continued smoking.
Drugs affecting milk:

Drugs can affect milk secretion or composition by affecting factors such as mammary gland
development, milk secretion and hormonal regulation of lactation. Prolactin is necessary for human
milk secretion and may be affected by drug use. Dopamine agonists such as cabergoline reduce
prolactin and are sometimes used therapeutically to stop lactation. Dopamine antagonists such as
metoclopramide and most antipsychotics may increase prolactin (see article on Hyperprolactinaemia
With Antipsychotics) and milk production. Other drugs that have been associated with causing
hyperprolactinaemia include SSRIs and opioids.
Tabulated summary of drug distribution into breast milk
Table 2 shows published M/P ratios from the literature and provides an estimate of the weight-
adjusted infant dose. Interpretation of these requires an understanding of the limitations associated
with published data, such as the availability of only single pairs of plasma and milk concentrations.
Infant clearance (related to post-conceptual age) should always be considered.
Table 2: Summary of distribution of drugs into breast milk
ID = insufficient data
Drug M/PAUC % maternal dose Comments

Acid-suppressants:
Avoid in favour of safer alternatives with
Cimetidine 1.7-5.8 5.4-6.7 lower potential for side effects. May
accumulate in milk due to active transport.
Famotidine 1.5 1.6 Probably safe.
Probably safe when restricted to sporadic
Ranitidine 2.8 5.0-7.8 doses or a single dose at night-time. May
accumulate in milk due to active transport.
Analgesics:
Avoid due to possible association with
Aspirin 0.06 3.2
Reye’s syndrome.
Codeine 2.16 6.8 Considered safe.
Ibuprofen 0 < 0.6 Considered safe. Not detected in milk.
Considered safe. One case of seizures
Indomethacin 0.37 < 1.0
(causality questionable).
Mefenamic acid ID 0.3 Probably safe.
Considered safe in methadone maintenance
as 60% of infants born to mothers in
Methadone 0.47 2.2
maintenance programmes develop
symptoms of withdrawal.
Morphine 2.46 0.4 Considered safe.
Probably safe.
Naproxen ID 1.1
Nefopam ID 0.4 Probably safe.

Use a NSAID with a shorter half-life where
Piroxicam ID 5-10
possible.
Paracetamol 0.8 2.9-7.9 Considered safe.
Exposure limited by low oral availability in
Sumatriptan 4.1-5.7 0.3-6.7 term infants. Expressing for 8 hours post-
dose will almost completely avoid exposure.
Antibiotics:
Aminoglycosides
Considered compatible with breastfeeding
Gentamicin 0.17 2.2
due to low transfer and low oral availability.
Cephalosporins
Cefaclor ID 0.7
Considered safe. Low transfer into
milk. Third generation cephalosporins
Cefalexin 0.09 0.5-1.2
have greater potential to alter bowel
flora.
Cefotaxime ID 0.3
Ceftriaxone 0.04 0.7-4.7
Fluoroquinolones
Avoid fluoroquinolones due to theoretical
Ciprofloxacin 2.17 4.8
risk of arthropathies.
Macrolides
Clarithromycin 0.25 1.8 Considered safe. May alter bowel flora.
Erythromycin 0.41 2.1
Penicillins
Considered safe. Note: although
Amoxycillin ID 0.7 amoxycillin/clavulanic acid combination
is used extensively in lactation, there are
Benzylpenicillin 0.37 0.8 no published data on the safety of
clavulanic acid.
Phenoxymethyl-penicillin ID 0.25
Tetracyclines
Avoid tetracyclines where feasible due
to the possible risks of dental staining
Minocycline ID 3.6
and adverse effects on bone
development.
Tetracycline 0.58 4.8
Others
Considered safe. No adverse effects noted
Aciclovir ID 1.1-1.2
in breastfed infants.
Potential for accumulation particularly in
Fluconazole 0.75 11
premature infants.
Controversial as exposure may be high.
Metronidazole 0.9-1.1 0.1-36.0 With high doses consider expressing and
discarding milk.
Avoid in G6PD-deficient infants (due to
Nitrofurantoin ID 0.6-6.0
the risk of haemolysis).
Sulphamethoxazole &
0.1 2-2.5 Avoid suphaemethoxazole in infants with
Trimethoprim
1.26 3.8-5.5 hyperbilirubinaemia and G6PD deficiency.
(i.e. co-trimoxazole)
Anticoagulants
Probably safe. No changes in prothrombin
Warfarin 0 < 4.4 times detected in breastfeeding infants.
Monitor prothrombin time.
Anticonvulsants:
Considered safe. Monitor for sedation,
Carbamazepine 0.36-0.39 2.8-7.3
poor suckling.
Concentrations in breastfed infants have
Lamotrigine ID 10-22 been consistent with those expected to
produce clinical effect. Best to avoid.
Phenobarbitone ID 23-156 Avoid due to high infant exposure.
Considered safe. Observe for sedation, poor
suckling. One report of
Pheyntoin 0.13-0.18 3.0-7.2
methaemoglobinaemia, poor suckling and
sedation.
Considered safe at low doses. High doses
Sodium valproate 0.05 1.8
may increase the risk of hepatitis.
Vigabatrin ID <1% Avoid until further data are available.
Antidepressants:
Tricyclics:
Amitriptyline 0.83 0.6-0.9
Desipramine ID 0.5-1.0
Probably safe. Negligible or no

Dothiepin 0.8-1.6 0.2-1.5 concentrations detected in breastfed
infants.
Doxepin ID 0.01
Imipramine ID 0.13
Nortriptyline ID 0.53
SSRIs
See text
Others
Moclobemide 0.72 1.6 Probably safe.
Antiemetics:
Domperidone ID 0.05 Probably safe. May increase milk secretion.
Low dose or sporadic use probably safe.
Metoclopramide ID 4.7-11.3
May increase milk secretion.
Antihistamines:
Probably safe. No adverse effects reported
Loratadine 1.2 0.7
in infants.
Triprolidine 0.53 0.9 Considered safe.
Antipsychotics:
Chlorpromazine ID 0.2 Probably safe. May increase milk

secretion. Monitor infant for sedation,
Flupenthixol ID 0.5-0.8 irritability etc.
Haloperidol ID 0.15-2.0
Cardiovascular:
Amiodarone ID 37 Avoid in breastfeeding.
Avoid in favour of antihypertensives with
Atenolol 2.3-4.5 5.7-19.2
lower infant exposure.
Captopril 0.03 0.014 Considered safe.
Digoxin 0.6-0.9 2.3-5.6 Considered safe.
Unlikely to be problematical in
Diltiazem 0.98 0.9
breastfeeding.
Enalapril 0.02 < 0.1 Considered safe.
Metoprolol 2.8-3.6 1.7-3.3 Probably safe.
Consider choosing a beta-blocker with a
Nadolol 4.6 5.1
lower infant dose, if feasible.
Propranolol 0.32-0.76 0.2-0.9 Probably safe.
Quinapril 0.12 1.6 Considered safe.
Verapamil 0.6 0.14-0.84 Considered safe.
Sedatives/hypnotics:
Short-term use of low doses is probably
Clonazepam ID 1.5-3.0
safe.
Reasonable to breastfeed after a low single
dose but potential for accumulation with
Diazepam 0.16 2.0-2.3
prolonged use. Sedation has been reported
in breastfed infants.
Lorazepam ID 2.2
safe.
Midazolam 0.16 0.7
safe.
Nitrazepam ID ID safe. Potential for accumulation with
prolonged administration.
Zopiclone 0.5 4.1
safe.
Social Drugs:
Cannabis (THC) ID ID Avoid as long-term effects are unknown.
Low intake probably safe. Restlessness
Caffeine 0.5-0.8 0.6-21.0 and irritability documented. Prolonged
half-life (80-100 hours) in neonates.
Occasional low usage probably safe.
Chronic intake may be associated with
Ethanol 0.9 3-4 impairment of psychomotor development.
Consider withholding breastfeeding for 1-2
hours per standard drink.
Cigarette smoking should be avoided due
to health hazards associated with smoking.
Use of nicotine patches may be considered
Nicotine 2.92 ID
compatible with breastfeeding and is
favoured over smoking.
Miscellaneous:
Ethinyloestradiol ID 0.3 May suppress lactation.
Levonorgestrel ID 1.1 Considered safe.
Medroxyprogesterone ID-0.72 3.4-5.0 Considered safe.
Norethisterone ID-0.26 0.02-1.9 Considered safe.
Short courses of low doses (≤ 20mg daily)
are probably safe. Note: there are
Prednisone ID 0.26 insufficient data on other systemic
corticosteroids (e.g. betamethasone,
dexamethasone).
Pseudoephedrine 2.5 4.0 Low doses or sporadic use probably safe.
Avoid in infants with hyperbilirubinaemia
Sulphasalazine ID 1.2-7.0
or G6PD deficiency.
Correspondence to Sharon Gardiner, Department of Clinical Pharmacology, Christchurch Hospital,

Private Bag 4710, Christchurch. E-mail: sharon.gardiner@cdhb.govt.nz
Primary sources
Atkinson HC, Begg EJ, Darlow BA. Drugs in human milk. Clinical pharmacokinetic considerations.
Clinical Pharmacokinetics 1988;14:217-40.
Bennett PN and the WHO Working Group, editors. Drugs and human lactation. 2nd edition.
Amsterdam: Elsevier, 1997.
Ilett KF, Kristensen JH, Begg EJ. Drug distribution in human milk. Australian Prescriber 1997;20
(2):35-40.
Speight TM, Holford NHG, editors. Avery's Drug Treatment. 4th edition. Auckland: Adis
International Ltd, 1997.
guideline.
Narcotic Depression in the Newborn Infant Reviewed by David Knight
January
2001
Treatment of Narcotic Depression Observation and Documentation References
● This is manifest either at delivery when a baby needs resuscitation, or following

delivery with behavioural changes in the infant.
● Narcotics given to the mother in labour can contribute to depression in an
asphyxiated infant, or can result in depression without asphyxia. In this latter case,
the baby usually has a normal heart rate initially, but depressed respiration.
Treatment of Narcotic Depression
1. When indicated, resuscitation must be instituted without delay, usually before

naloxone administration.
2. Treat narcotic depression with naloxone (Narcan) intramuscularly.
a. Dose 0.1-0.2mg/kg per dose, IM.

b. Naloxone comes in ampoules containing 0.4mg/ml.
c. Intramuscular administration is preferable. The onset
of action is almost as rapid as with IV administration,
but the duration of action is much longer.
See Naloxone Drug Protocol for more details.
● DO NOT GIVE NALOXONE TO INFANTS AT RISK OF DRUG WITHDRAWAL,

WHOSE MOTHERS HAVE BEEN TAKING OPIOID DRUGS.
Observation and Documentation
● The half life of intravenous naloxone is very short, and there is the potential its
action will wear off before that of the opioid causing the depression. This appears
not to be a problem with large intramuscular doses of naloxone (as recommended
here).
● There appears to be a depot effect of the IM injection. Measurable effects of
naloxone have been seen up to 48 hours after the dose.
● Babies needing resuscitation and/or naloxone at birth need observation
afterwards. This need not necessarily be on NICU but can be with the mother in
the delivery unit or post natal ward.
● When administered in the delivery room, naloxone will often be given on the verbal
order of the doctor or NS-ANP. This order should be written on the ‘blue card’ by
the doctor/NS-ANP after the resuscitation.
References
1 Committee on Drugs. American Academy of Pediatrics. Pediatrics 1989;83:803.
2 Wiener PC et al. Br Med J 1977;2:228-31.
3 Brice JEH et al. Arch Dis Child. 1979;54:356-61

guideline.
Nappy Rash
Reviewed by Robyn Wilkinson,
Brenda Hughes, and Carl Kuschel
December 2003
Treatment of an Excoriated
Prevention Candida Nappy Rash Severe Nappy Rash
Bottom
Prevention
● Wash bottom with water/soap free solution and dry thoroughly.

● Apply petroleum jelly -a must for infants on Nutriprem or fortified milk.
❍ Petroleum jelly does not need to be prescribed on the drug chart.
Treatment of an Excoriated Bottom
● If Candida is not suspected, apply zinc oxide ointment (Karicare ointment) at

nappy changes.
❍ Zinc oxide ointment does not need to be prescribed on the drug chart.
● If bowel motions are frequent

❍ Change nappies and apply zinc oxide ointment more often.
❍ Exposing buttocks to air may not be effective.
❍ There is no evidence to suggest any benefit from using heat lamps.
● If there is no improvement after 2 days of treatment

❍ Consider sending a skin swab for Candida (Candida may not always
display a typical appearance).
Treatment of Candidiasis
● Take a skin swab

❍ It is a clinical decision as to whether you await the result or commence
treatment immediately.
● Apply nystatin (Mycostatin, Nilstat ) cream four times a day (prescribed on drug
chart).
● Continue to apply zinc ointment (after Nystatin application) to treat
excoriation.
● Treatment should extend for at least 3 days after rash has healed.
● Infant should also be treated with Oral Nystatin 0.5ml-1.0ml QID.
Severe Nappy Rash
● For example, in Short Bowel Syndrome, malabsorption, opiate withdrawal,

infectious diarrhoea, or Cystic Fibrosis.
● SECURA Extra Protective Cream cream (prescribed on drug chart) must be
applied to prevent excoriation after each nappy change.
References
1 Lund C, Kuller J, Lane A, Lott JW, Raines DA. Neonatal skin care: the scientific basis for practice. J Obstet
Gynecol Neonatal Nurs 1999; 28(3):241-54.
2 Lund CH, Osborne JW, Kuller J, Lane AT, Lott JW, Raines DA. Neonatal skin care: clinical outcomes of the
AWHONN/NANN evidence-based clinical practice guideline. Association of Women's Health, Obstetric and
Neonatal Nurses and the National Association of Neonatal Nurses. J Obstet Gynecol Neonatal Nurs 2001;
30(1):41-51.
3 Bowring AR, Mackay D, Taylor FR. The treatment of napkin dermatitis: a double-blind comparison of two
steroid-antibiotic combinations. Pharmatherapeutica 1984; 3(9):613-7
guideline.
Neonatal Alloimmune Thrombocytopenia Reviewed by Alan Groves and

(NAIT) Carl Kuschel
April
2003
Background Presentation Differential Diagnosis Investigation

Management References Index of Related Documents
● Low platelet count in an otherwise healthy term newborn is due to NAIT

until proven otherwise.
● Urgent matched platelet transfusion should be discussed with specialist
on call at all times.
Background
● Neonatal Alloimmune Thrombocytopenia (NAIT) is a disorder caused by

fetomaternal platelet incompatibility analogous to that in Rhesus Haemolytic
Disease, with maternal anti-platelet antibodies crossing the placenta and
destroying fetal platelets.
● The majority of cases are caused by antibodies directed against Human Platelet
Antigen-1a (HPA-1a) and HPA-5b, but many rarer reactions have been reported.
1
● Prospective studies have shown incidence to be 1:1,100 live births, but the
2
condition is under-reported.
● Mortality is around 10% of presenting cases, with neurological sequelae, including
intracranial haemorrhage and subsequent neurodevelopmental delay in up to
3
25%.
Presentation
The commonest mode of presentation is probably the well neonate with bruises or
petechiae. However the spectrum of disease ranges from sub-clinical moderate
thrombocytopenia to catastrophic intracranial hemorrhage (ICH) and death. A high index
of suspicion is essential in all cases of active bleeding, but also in asymptomatic
laboratory diagnosed thrombocytopenia. A history of thrombocytopenia in a previous
sibling makes the diagnosis almost certain.
Modes of ● Previously affected sibling

presentation ● Recurrent fetal loss
● Antenatal ICH/hydrocephalus
● Stillbirth
● Bruising/bleeding neonate
● Excessive haematoma at injection site
● Disseminated intravascular coagulopathy
● Postnatal ICH (silent or presenting with seizures, etc)
Differential Diagnosis
Also see Neonatal Thrombocytopenia protocol
● Sepsis
● NEC
● DIC
● Placental insufficiency
● Congenital infection
● Asphyxia
● Artefact - clotted FBC sample
● Autoimmune thrombocytopenia (maternal ITP)
Investigation
FBC to confirm platelet count

Maternal FBC likely to have been performed during pregnancy. Maternal platelet
count is normal in NAIT.
● Definitive diagnosis of NAIT depends on parental testing.
● In most cases the lab prefers to do this prior to platelet transfusion, but discussion
with haematologist on call is necessary to arrange urgent testing.
● FURTHER TESTING SHOULD NOT DELAY PLATELET TRANSFUSION IF

REQUIRED URGENTLY
Maternal blood 3 x CPD (yellow) and 1x plain (red) tubes for anti-platelet antibodies
samples and genotyping.
Paternal blood 3 x CPD (yellow) tubes for genotyping.
samples If no paternal blood available, send 1 x infant plain tube for platelet
grouping.
● Direct crossmatch between parents will also be performed.

● Maternal antibody levels fall towards term, so repeat testing 6 weeks post-partum
is required in some cases.
● Phone laboratory with specimen queries (523 5731).
Management
Platelet Count
Action
(x109)
<30 Transfuse
30-49 Transfuse if any bleeding
50-99 Transfuse if major bleeding
>99 Do not transfuse
● If the infant’s platelet count is <30x109/L and the maternal count is normal, the
treatment of choice is urgent transfusion of 10ml/kg of matched platelets.
● In most cases these will be HPA-1a negative, but Maori and Asian mothers are
more likely to have antibodies other than anti HPA-1a.
● Infuse platelets over 30-60 minutes (see platelet protocol), and recheck platelet
count after one hour.
● Antigen-negative platelets should be given urgently, as infants are at significant
risk of ICH in the first days of life
● If antigen negative platelets are not available, intravenous immunoglobulin (IVIG)
1g/kg/day for 2 days may be effective.
❍ There is often a delay of 24-48 hours prior to response, leaving a window of
risk for ICH.

● If the platelet count fails to rise in response to matched platelets consider
alternative diagnoses, and check for rarer maternal antibody types.
● Affected infants should have a FBC checked daily until platelet count is stable over
100x109/L. Need for platelet transfusion at moderately low platelet counts (30-100
x 109/L) is not clear.
● It is essential that parental investigation is initiated prior to discharge and adequate
follow up arrangements made.
❍ The risk of a subsequent pregnancy being affected is 100% if the father is
4
homozygous for the reacting antigen, and 50% if heterozygous.
❍ In general, subsequent pregnancies are at least as severely affected as the
first.
❍ Antenatal therapy in subsequent pregnancies remains contentious, but
options include intrauterine platelet transfusion, maternal immunoglobulin
5
and steroids.
References
1 Williamson, L.M., et al., The natural history of fetomaternal alloimmunization to the platelet-specific antigen
HPA-1a (PlA1, Zwa) as determined by antenatal screening. Blood, 1998. 92(7): p. 2280-7.
2 Murphy, M.F., S. Verjee, and M. Greaves, Inadequacies in the postnatal management of fetomaternal
alloimmune thrombocytopenia (FMAIT). Br J Haematol, 1999. 105(1): p. 123-6.
3 Management of alloimmune neonatal thrombocytopenia. Lancet, 1989. 1(8630): p. 137-8.
4 Bussel, J.B., et al., Fetal alloimmune thrombocytopenia. N Engl J Med, 1997. 337(1): p. 22-6.
5 Roberts, I.A. and N.A. Murray, Thrombocytopenia in the newborn. Curr Opin Pediatr, 2003. 15(1): p. 17-23.
Screening for Nephrocalcinosis Reviewed by Carl Kuschel, Rita Teele

(Paediatric Radiology), and William Wong
(Paediatric Nephrology)
April
2005
Background Screening Policy Ultrasound Appearances

Follow-Up References
Background
The incidence of nephrocalcinosis (NC) in ex-premature infants is reported to be high. Although the overall
incidence of NC in VLBW infants is reported to be around 20%, 1 the incidence may approach 50% in infants
<750g at birth. 1 Local data from a group of infants who received dexamethasone for treatment of evolving
chronic lung disease showed an incidence of 83%. 2
NC may be a consequence of neonatal treatments such as diuretics and steroids, 1 or may just be a marker
of neonatal illness. Nutritional factors are thought to contribute, particularly high intakes of calcium in the diet
which may not necessarily be absorbed and instead are excreted in urine.
Although the natural history of NC is that 66% of infants will have resolution by 15 months of age and 85% by
30 months, 3 some infants will develop renal calculi. Renal function does not appear to be adversely affected
into childhood. 3
Screening Policy
● In view of the potential clinical significance of NC, infants who are <30 weeks at birth should be
screened for NC.
● These infants should have a renal ultrasound scan at the same time as their pre-discharge head
ultrasound scans (that is, around 36 weeks corrected gestational age, or earlier if ready for discharge
prior to this time).
Ultrasound Appearances of Nephrocalcinosis

More marked changes may be seen, with significant calcium deposition in the collecting systems, as below.
Follow-Up
● If significant NC is demonstrated, a referral should be sent to Dr William Wong for follow-up in the
Renal Clinic at Starship Hospital
References
1 Saarela T, Vaarala A, Lanning P, Koivisto M. Incidence, ultrasonic patterns and resolution of nephrocalcinosis in very low
birthweight infants. Acta Pædiatr 1999; 88: 655–60.
2 Cranefield DF, Odd D, Harding JE, Teele RL. The high incidence of nephrocalcinosis in a preterm neonatal population receiving
steroids. European Society for Pediatric Radiology, Genoa, 2003.
3 Schell-Feith EA, Kist-van Holthe·JE, van Zwieten PHT, et al. Preterm neonates with nephrocalcinosis: natural course and renal
function. Pediatr Nephrol 2003;18:1102–8.
guideline.
Management of Infants with Myelomeningocoele Reviewed by Colette Muir, Carl

Kuschel, Andrew Law (Paediatric
Neurosurgery, Starship Hospital),
Raewyn Gavin (General
Paediatrics, Starship Hospital),
Bobby Tsang (General
Paediatrician, Waitemata District
Health Board)
October 2005
Definition Aetiology Incidence Antenatal Issues

Place and Mode of Delivery Postnatal Management Postoperative Care Prognosis
Definition
● The neural tube usually closes between 15 and 28 days post-conception. Failure
of normal closure results in a neural tube defect (NTD). 90% of NTDs are spina
bifida or anencephaly.
❍ Anencephaly is caused by a defect in the closure of the anterior portion of
the neural groove. This results in an unfused partially developed forebrain

and incompletely developed calvarium. This condition is always lethal.
❍ Spina bifida is caused by failure of closure of the posterior portion of the
neural tube.
❍ A meningomyelocoele (MM), the most common type of spina bifida, is a sac
like structure which protrudes through a defect in the vertebral arches,

containing meninges, CSF and spinal cord and /or nerve roots.
❍ Meningocoeles are rare. The structure contains meninges and CSF only.
❍ Spina bifida occulta is a common anomaly consisting of a midline defect of
the vertebral bodies without protrusion of spinal cord or meninges. The

incidence is reported to be between 5% and 40%. Most often it is
asymptomatic and of no consequence, but it can be associated with
developmental abnormalities or tethering of the spinal cord.
● Both meningomyelocoeles and meningocoeles may occur anywhere along the
spinal cord but are most common in the lumbar and sacral area.
Thoracolumbar junction 45%

Lumbar 20%
Lumbosacral 20%
Sacral 10%
Other (high) lesions 5%
● The degree of neurological impairment depends on the position and extent of the
lesion. There will usually be loss of sensation in corresponding dermatome,
complete or partial paralysis of skeletal muscles and often bladder and/or anal
sphincter paralysis.
● The Chiari II malformation (herniation of the cerebellar vermis through the foramen
Magnum, with dislocation of the fourth ventricle towards the neural canal, and
downward displacement of the tentorium) is present in 95% of children with
myelomeningocoele. This is associated with obstructive hydrocephalus.
❍ Other abnormalities of CNS development (e.g. polymicrogyria, heterotopias,
aqueduct stenosis) may co-exist.

● Orthopaedic abnormalities related to disrupted innervation of muscles (i.e.
dislocated hips, club feet) are common.
● There may be an associated spinal deformity (scoliosis or kyphosis).
● Other major abnormalities of other organ systems are unusual.
Aetiology
● The aetiology is felt to be multifactorial. However, risk factors include:

❍ previous pregnancies have been affected with NTDs
❍ some anticonvulsants such as carbamazepine and sodium valproate
❍ pregnancies complicated by diabetes at conception
● 10% of infants may have an associated chromosomal defect (e.g. trisomy 18,
triploidy, or single gene disorders). A referral to the genetic service should be
arranged, and karyotype considered as indicated.
Incidence
● The true incidence of NTDs appears to be decreasing in most parts of the world.
● Estimates of rate approximate 0.2-0.4 per 1000 livebirths.
● In 1999 in New Zealand, the prevalence of neural tube defects was 0.5 per 1000
live births. Many pregnancies complicated by NTDs result in termination –
therefore the incidence increases to 0.91 per 1,000 total births and terminations.
Antenatal Issues
● Periconceptional folate supplementation has been shown to reduce the incidence

of NTDs, with data suggesting that a daily intake of 0.4mg of folic acid reduces the
risk of 1st neural tube defects by up to 70%.
● Current New Zealand recomendations are for women to take 800 micrograms of
folic acid 4 weeks prior to and 12 weeks after conception. Women at high risk
require 5mg daily.
● Problems exist in that a real proportion of NZ pregnancies are not planned and
preconceptual folate is not taken.
Screening and Detection
● Alpha feto protein (AFP) from amniotic fluid is very reliable except when the defect
is closed.
● Maternal serum AFP is less reliable, detecting between 50-90% of open
anomalies, but is falsely positive in 5%.
● USS: Diagnosis often made at 16-18 week Coronal view of

USS. Often seen as lateral displacement of
the spinal pedicles, but the sac may also be
visualised.
❍ An axial cross section through the fetal
skull may demonstrate a “lemon head” spine

shape, with a depression of the
metopic suture in the frontal region.
❍ Visualisation of the posterior fossa
may demonstrate a “banana sign”,

observed at the level of the cerebellum
and cistern magna. It is caused by
herniation of the cerebellar vermis Sagittal view of spine
through the foramen magnum, giving
the cerebellum the appearance of a
banana.
❍ USS should evaluate for other
structural abnormalities of limbs, brain,

kidneys, and other organs.
"Lemon" shaped skull
Counselling
● Parents will usually have seen the neurosurgeon prior to delivery to discuss
treatment options and prognosis.
● Genetic counselling – 2-4% recurrence risk.
Place and mode of delivery
● Tertiary institution with access to neurosurgical services.

❍ Delivery by elective lower segment Caesarean section (LSCS) prior to the
onset of labour may result in better motor function than vaginal delivery or
LSCS after a trial of labour.
Postnatal Management
● The goal is for neurosurgical closure within 24 hours.

● Some parents may opt, after discussions with the neurosurgeon, for palliative care
or conservative management.
General Cares 1. Avoid latex products (use latex-free gloves for all
handling).
Clinical 1. Careful clinical assessment.

Assessment ❍ It is unusual, however, for other abnormalities to be
present.
2. Place the infant prone and evaluate the size, position, and
appearance of the lesion.
3. Palpate the fontanelle and sutures for evidence of raised
intracranial pressure.
4. Measure the head circumference.
5. Evaluate spontaneous movements (note that any
stimulation to promote movements should be confined to
the upper body, as reflex movements may occur in
response to stimulation of paralysed lower limbs and trunk).
6. Evaluate the level of sensation. This can be determined
using an open nappy pin (not a hypodermic needle).
7. Assess anal tone.
8. Urine output.
❍ Is there dribbling of urine?
❍ Is the bladder palpable?
Infection Risk 1. Antibiotics should be administered as per the Newborn

Services policy.
2. Blood and other cultures are not required unless the baby
is clinically unwell.
Fluids/Electrolytes 1. Remain NBM.

2. 10% dextrose as per Newborn Services Fluids and
Electrolytes policy.
3. Infants with urinary retention will require urinary
catheterisation.
Neurosurgical 1. Inform the neurosurgical team at the Starship Hospital.

Referral They will arrange for early transfer and repair of the lesion.
Imaging 1. Cranial ultrasound scan of brain to evaluate ventricular

size and to assess other malformations.
2. A CT scan or MRI is commonly obtained peri-operatively
but will be organised by or on the instruction of the
neurosurgical team.
3. Renal imaging (renal ultrasound scan and MCUG) should
be performed in the postoperative period.
Dressings 1. The baby should be nursed in the prone position.
2. The sac must be kept covered and moist prior to closure.
3. Exposure of the tissue to trauma or drying out can lead to
a “shock-like” state of the spinal cord.
4. This needs to be a strictly aseptic technique.
a. Apply saline soaked Telfa over the sac.
b. Obtain a Butterfly infusion needle, and remove the
needle.
c. Insert the Butterfly tubing on the layers of Telfa with
a second Telfa.
d. Seal the entire dressing with Tegaderm.
e. The wound can be irrigated hourly using the fine
Butterfly tubing, with small amounts of warmed
saline.
Parental Support 1. Referral to Paediatric Neurosurgical Social Worker will be

arranged following surgery.
2. A Child Disability Allowance form should be filled out.
3. Useful information for parents can be accessed from the
Australian Spina Bifida and Hydrocephalus Association
(www.asbha.org.au)
Postoperative Care
1. Will usually be undertaken on the Neurosurgical and Neurology ward (26A) at

Starship Hospital.
2. A urinary catheter usually remains in situ postoperatively (preferably until renal
imaging has been undertaken).
Prognosis
● Children require multidisciplinary follow-up including the neurosurgical team, a

developmental or general paediatrician, urologists, orthopaedic surgeons, and
physiotherapists. There should be a supervising “overviewing” paediatrician.
❍ Children with spina bifida from West and North are seen by Dr Bobby
Tsang, Paediatrician at Wilson Centre. Those from Central and South are
seen by Dr Raewyn Gavin, Paediatrician at Greenlane Clinical Centre.
● Hydrocephalus is a common occurrence after surgery but may not develop for
some weeks. However most become evident in the first 10 days post closure.
❍ The baby should be watched with serial head circumference measures and
ultrasound imaging.
❍ A shunt should be inserted if there is clear evidence of progressive
ventriculomegaly or increasing head circumference.

❍ Shunt infections and revisions are common throughout childhood.
● In the absence of treatment, the mortality of myelomeningocoele is approximately

50%.
● Normal intellect should be assumed in the absence of significant hydrocephalus or
dysmorphism.
● Children with MM have a lifetime increased risk of latex sensitivity and therefore
need to be cared for in a latex-free environment.
● Urological and orthopaedic referral will be organised by the neurology/
neurosurgery services.
References
1 Improving folate intake in New Zealand: Policy Implications: Ministry Of Health, 2003.
Folic acid and neural tube defects: the current evidence and implications for prevention. Ciba foundation
2
Symposium 181:192-208
3 Volpe JJ. Neurology of the newborn 4th ed. WB Saunders Co, Philadelphia 2001
Levene MI, Chervanek FA, Whittle MJ (eds). Fetal and neonatal neurology and neurosurgery, 3rd Ed.
4
Churchill Livingstone, London 2001.
guideline.
Recommendations for Newborn Examination of All Reviewed by David Knight

Babies
December
2000
Early Examination
On the first day, all babies should have a full clinical examination.
The examiner should have full knowledge of the perinatal history and relevant family and
social history. No baby should be left in the sole care of its parents before having a full
clinical examination. The examination should include:
● Weight + percentile
● Length + percentile
● Head circumference + percentile
A general examination including looking for dysmorphic features, checking for cardio-
respiratory problems and checking the palate, hips, genitalia and anus. Eyes can be
difficult to see soon after birth; if so, this should be noted for the later examination.
Late Examination
At the end of the first week (4-10 days) the check should include the following:
● Weight (relate to birth weight)

● Head circumference (relate to birth head circumference)
● Length (relate to birth length)
● Feeding
● Meconium passage in first day
● Vomiting (especially bile stained)
● Colour, especially Cyanosis & Jaundice
● Respiratory distress (including respiratory rate)
● Heart murmur. Femoral pulses
● Eye check: Eyes open; Pupil size, shape, equal and Cornea clear, Red Reflex.
● Hips
● Cord
● Tone and activity
● Newborn screening done
guideline.
Nitric Oxide
Authorised by:
October 2003
Introduction Purpose Scope Prescribing of Nitric Oxide

Dose Index of Related Documents
Introduction
● Nitric oxide is a colourless, odourless toxic and non-inflammable gas that can be
administered via the ventilator circuit as an additional therapy in Newborn Services.
● Nitric oxide is used to treat persistent pulmonary hypertension.
Purpose
● The following policy outlines the way in which Nitric Oxide is administered in
Newborn Services to ensure safety and best outcome.
Scope
● Applies to Level 3/Level 4 nurses in Newborn Services who have completed a NO

training session and are involved in the administration of Nitric Oxide.
Prescribing of Nitric Oxide
● Treatment initiated only on Consultant's orders.

● Charted and signed by Registrar/Nurse Specialist - Advanced Neonatal Practice
(NS-ANP) on Level 3 Nursing Chart in parts per million (ppm) including all changes
in concentration.
Dose
● Refer to the Nitric Oxide drug protocol

guideline.
Process Issues for Neonatal Staff Attending Reviewed by Anne Wroe, CNE,
Deliveries in Operating Rooms Operating Rooms
May
2004
Welcome to NWH Caesarean Section Theatres
The theatres that deal with all Obstetric cases are Theatres 1 & 2, although occasionally
Theatres 3 or 4 may be used for an emergency case. Theatre 1 is dedicated to all acutes
and multiple births and Theatre 2 is used for elective cases, but sometimes it is also used
in the event of an emergency.
When you are required to come to the OR, in most cases you will not be required to
scrub. However, as you are entering a sterile field it is important that you maintain a level
of sterility and be absolutely aware of the sterile field.
The recommendations are:
● All persons receiving the baby from the surgeon must wear a mask. These masks
are located on the wall outside the scrub bay door (in the theatre corridor).
● All persons receiving the baby from the surgeon must wash their hands before
donning a pair of sterile gloves. It is not acceptable to wear unsterile gloves when
receiving the baby.
● Once you have put your sterile gloves on, you are not permitted to touch anything
else. Please stand with your hands clasped together out in front of you and wait
until the scrub nurse can drape a sterile guard over your arms and chest.
● Please ensure that you don’t stand too close to the sterile instrument trolley when
the nurse does drape you with the guard; sterile instrument trolley’s have been
contaminated during this process.
● All persons receiving the baby must be draped in a sterile guard, which the scrub
nurse will drape you with.
● It is not acceptable to reach onto the sterile scrub trolley and lift this guard up
yourself, even though you are wearing sterile gloves.
❍ The reason for this is that more often that not, your arms are uncovered and
you skin will shed onto the sterile field.

● You are only permitted to touch the sterile field if you have performed the correct
surgical scrub, & are wearing sterile gloves and a sterile gown.
As neonatal staff, the need to scrub and don sterile gloves & gowns is not usually a
requirement, but there are some instances where this may be necessary:
● In the event of multiple births. It is preferable if both neonatal staff members

present scrub and don sterile gloves and gowns.
● If there is evidence of meconium and the baby will require suctioning on the
operating field.
● If any baby suctioning is required in the acute case (placenta previa, placental
abruption etc) it is preferable for the neonatal staff member to scrub.
❍ The scrub nurse’s priority will be to deal with the mothers bleeding,
instruments etc and will not be able to tend to any needs of the baby on the
sterile field.
● Please consider a complete sterile scrub for all acute cases where it may be
necessary for the baby to require immediate suctioning.
There is an ADHB policy governing the practices of the surgical scrub, as well as a policy
governing the practice of donning surgical gloves and gowns. These policies are available
to read and is the responsibility of all staff who work for the ADHB to become familiar with
them. Please be aware that not all hospitals have the same policies and scrubbing
practices, but it is important that you become familiar with each hospitals different policy.
The ADHB requires you to follow their Recommended Best practices and Policies whilst
working here.
● There is also a Nurse Educator available to assist you and teach you with
scrubbing, gowning & gloving. The Nurse educator is available on Locator 93 4390
should you need help. Please call up in advance to set up a time to teach you
these practices.
If you are bringing a Trainee Intern with you to the OR to assist, please ensure that they
adopt the appropriate practices.
If you have any problems at all, please don’t hesitate to contact the Nurse Educator.
guideline.
Orthopaedic Problems Reviewed by Starship

Orthopaedic Service
March
2003
Talipes
Congenital Dislocation Abnormalities of
Talipes Equinovarus Calcaneovalgus and Arthrogryposes
of the Hips Hands, Feet and Digits
Vertical Talus
There is a Paediatric Orthopaedic Team at Starship Hospital. Referral to an Orthopaedic

Surgeon should not be carried out before a baby has been seen by a Consultant
Paediatrician.
● Referral is done by faxing a referral consultation sheet to the Paediatric

Orthopaedic Clinic (internal 5906, External 307 8906) and phoning through to
extension 6116 as well.
❍ More urgent referrals should also be telephone through to the on-call
Orthopaedic Registrar at Starship Hospital.
They will either visit National Women's Hospital within the first week to 10 days of life, or
request that the infant be given an appointment to their weekly outpatient clinic at
Starship Children's Hospital.
Congenital Dislocation of the Hips
The term encompasses a spectrum of abnormalities ranging from severely dysplastic or

teratogenic hip to one which is barely subluxatable. The treatment modality is according
to the classification (e.g. frankly dislocatable hips need treatment from the first week,
whereas subluxable hips may only need to be seen with radiographs at 4 months by an
Orthopaedic Surgeon).
The Starship Orthopaedic Surgeons would like to have referred:
1. Babies who fall into the at risk category

a. breech deliveries
b. family history of hip problems, particularly congenital
dislocation
c. babies where there are other orthopaedic abnormalities or
neuromuscular problems
2. Any baby in whom, at any stage, there has been a query about their
hips regardless of the experience of the examiner.
It is not generally useful to see babies with unstable hips before the age of 5- 7 days of
life, so that they would normally be seen at the end of the first week and then again at the
age of 4 months with radiographs. The question of using double nappies as an interim
measure for subluxable hips depends upon the individual Orthopaedic Consultant
Note: If a baby has not been assessed by an Orthopaedic Surgeon at the time of
discharge from hospital it must be quite clear from the details given on the referral form
whether the hip is one which needs to be seen urgently or at 4 months of age. In addition
adequate arrangements must be made to maximise the probability of families with
transport or financial problems being able to attend.
Talipes Equinovarus
Talipes equinovarus referrals should be sent to the Paediatric Orthopaedic Department at

Starship Hospital as soon as possible.
Talipes Calcaneovalgus and Vertical Talus
These may need to be x-rayed and it is recommended that specialist Orthopaedic

Radiology be performed at Starship Hospital. This would normally be arranged after
consultation with the Orthopaedic Surgeon.
Abnormalities of Hands, Feet and Digits (Syndactyly, Amputations, and

Duplications)
Although this is in the field of both plastic and orthopaedic surgery it has been our
practise to refer cases to the orthopaedic team at Starship Hospital. However an
alternative source of referral for hand anomalies would be Middlemore Hospital.
Arthrogryposes
This is a complex group of disorders which may result from intrauterine compression or
underlying neuromuscular disorder. This should be considered when making assessment
and referral, particularly where neurological problems are suspected.
guideline.
Oxygen Therapy and Monitoring Reviewed by David Knight
August
2002
● Supplemental oxygen must always be monitored.

● There are risks of too little or too much oxygen.
❍ Preterm infants are at risk of ROP with high levels.
❍ Term infants are at risk of pulmonary hypertension if hypoxaemic.
❍ Babies with chronic lung disease are at risk of pulmonary vascular disease
if hypoxic.
See the list of related documents
Monitoring
Pulse Oximetry (SpO2)
● Any baby receiving oxygen therapy (except chronic babies prior to discharge)
should have continuous pulse oximeter monitoring. These are very useful and
easy to use.
● Accuracy is about ± 2%. The therapeutic range is small. Remember the oxygen
dissociation curve in interpreting the result.
Moves to the Left Moves to the Right

● Fetal Hb ● Adult Hb
(SpO2 higher for given (SaO2 lower for a
PaO2) given PaO2)
● Alkalosis ● Acidosis
● Low temperature ● High temperature
● Low PaCO2 ● High PaCO2
● Low 2-3 DPG ● Low 2-3 DPG
Umbilical Artery Catheter
● Use in preference to peripheral in VLBW or babies likely to have prolonged or

difficult course.
❍ Use size 3.5 FG <1000 gms, 5 FG >1000 gms.
● Preferably, use a high catheter position (T6-T10) rather than the low position (L3-
L4).
Peripheral Artery (Radial, Ulnar or Posterior Tibial)
● For Radial/Ulnar, check patency of other artery by transillumination. (Allen test is

unreliable.)
● Do not use if other artery is not patent.
Arterial Stabs
● These are seldom necessary as oxygenation can be determined by SpO2 and CO2
is often inaccurate with a stab on an unsettled baby.
Transcutaneous Monitor (TcPO2 and TcPCO2)
● These may be useful in complementing SpO2 monitoring, but are less reliable and
more difficult to use.
Capillary Blood Gas
● This gives an indication of pH and PCO2 only and is not accurate.

● They are NOT useful for PO2 assessment.
● Interpret results with caution.
● Check with an arterial blood gas if necessary.
● Interpret in the whole clinical context (i.e. look at the baby).
● The result tells you that the true pH and PCO2 are probably no worse (well not
much) than the capillary result.
● Do not repeat an imprecise and not very useful test too often!
Tissue Oxygenation
● This is dependent on the tissues need (utilisation or uptake) and oxygen delivery.
● O2 delivery varies with blood flow and O2 content, in turn a product of haemoglobin
and saturation.
guideline.
Oxygen Therapy: Standing Orders for Nursing Staff Reviewed by David Knight
July
2001
● Oxygenation and oxygen therapy must be closely monitored.

● Appropriate use is life saving but inappropriate use has dangers: i.e. high levels
contributing to retinopathy of prematurity and low levels to pulmonary hypertension.
● In unwell infants, oxygen needs are continually changing and the nurse should
vary the inspired oxygen concentration within these guidelines.
1. A cyanosed baby or one with a low saturation (SpO2) should be given enough
oxygen to become pink or saturated. It may be necessary to initiate other
resuscitative procedures. Call medical staff for urgent assistance.
2. Babies receiving supplemental oxygen, or those likely to need it should be
monitored by continuous pulse oximetry, (with the exception of babies close to
being discharged on oxygen). If an arterial line is in situ, regular blood gases
should be done. The frequency of these varies with the clinical situation (discuss
this with medical staff or NS-ANPs).
3. The following are the recommended values. Any different range for an individual
baby should be noted and signed on the nursing chart by Dr/NS-ANP.
Click here to open the saturation targets
4. The nurse should alter the inspired oxygen to maintain the appropriate SpO2/
PaO2. Remember that babies having apnoeas need to breath to oxygenate: it may
be more appropriate to stimulate, bag or change ventilation settings rather than
increase FiO2.
5. If there is a sustained change in FiO2 of more than 0.1 (10%), inform medical staff.
6. Be careful to decrease FiO2 after a desaturation and avoid overshooting to
high SpO2 levels.
7. With Persistent Pulmonary Hypertension of the Newborn, FiO2 is not to be
decreased except on (signed) medical orders.
8. In some babies with complex cardiac conditions, a low saturation is desirable to
help prevent ductus closure and excessive pulmonary blood flow. In these babies,
the medical staff will determine the desired saturation range.
guideline.
Oxygen Saturations and Targeting Reviewed by David Knight, Simon

Rowley, and Carl Kuschel
May
2004
Oxygen Saturation Targeting in Infants
Infants PaO2 (kPa) Saturation Range

VLBW (<1500g) 6.5-9.0 85-92%
VLBW >4 weeks old 8.0-10.0 90-95%
LBW 8.0-10.0 90-95%
90-100%
Term/post-term 8.0-12.0 In the first 24
hours, 95-100%
CLD AND 36 weeks
8.0-10.0 90-95%
PMA
Overnight Saturation Run Guidelines
● For infants who are in air and do no need supplemental oxygen,

saturations which are mostly above 90% are regarded as
satisfactory.
● For babies who are in oxygen, saturations should be targeting the
following values:
Saturation Level Proportion of Study

90-95% 80-90%
<90% 10-20%
Reference: Askie LM, Henderson-Smart DJ, Irwig L, Simpson JM. Oxygen-saturation targets and outcomes in
extremely preterm infants. N Engl J Med 2003;349:959-67.
Low Flow Oxygen FiO2 Calculator

Page developer: http://www.nicutools.org/ with
modifications by Dr Michael Hewson, NICU, Wellington
Hospital
● Use this calculator to estimate the effective FiO2 that low flow oxygen delivers.
Weight: Kg
Respiratory rate: breaths/min
Gas flow: ml/Min
Blender Oxygen: 100 %
Actual Inspired O2:
● Simply input the child's weight (in kg), his or her respiratory rate, the current O2 flow rate and percent O2 at the blender.
● The algorithm uses a method validated by Finer et al, Pediatr Pulmonol 1996;21(1):48-51. Finer’s formula has been modified to allow for the
use of an O2 blender. A tidal volume of 5.5mL/kg is assumed.
guideline.
Guidelines for the Parent-Infant Nursery Reviewed by Moira Malarkey, Carl

(PIN) Kuschel, and Simon Rowley
April
2006
Medical and Nursing

Purpose Admission Criteria Handover Discharge
Staffing
Back to the Parent-Infant Nursery (PIN)

See also the PIN Registrar Guideline
Purpose
● The PIN environment should be quiet, intimate, and provide privacy and comfort
but also provide company for parents to support each other.
● There is an expectation that parents will actively participate in the discharge
planning process.
● Staff in the Newborn Service are there to support parenting with the emphasis on
encouraging the family/whanau to stay and carry out many of the baby’s cares.
● An important aim is to be able to "demedicalise" the baby before discharge home
in an environment that is safe.
Admission Criteria
● PIN is not an observation unit for acute babies. Babies will not be admitted
directly to the Neonatal Service via PIN, unless transferred in from another
neonatal unit and requiring only the level of care provided in PIN.
Absolute Admission Criteria:
● >1200g (and preferably >1400g)

● ≥32 weeks gestation (corrected)
● on full oral feeds
Relative Criteria for Admission to PIN:

Infants who have "greater than usual" medical needs can still be considered for PIN (if
staffing allows):
● On low flow oxygen

● On antibiotics
● Long line antibiotics (if staffing appropriate)
● Top up transfusions (if staffing appropriate)
Contraindications to Admission to PIN:
● ADAPT babies. These babies should either be nursed on the postnatal wards with
the mother, or on NICU.
● Babies who are expected to be in PIN for less than 48 hours and whose mother is
still on the postnatal ward should not be admitted as they may directly to the ward
Medical and Nursing Staffing
● The infants will be under the Level 2 Specialist Team.

● A Registrar will be assigned to spend one week on PIN.
● Click here to access the PIN Registrar guidelines

● The specialist is available to review babies or meet with parents as
requested by the Registrar/FLN or family/whanau on other days.
● There will be a Family Liaison Nurse in PIN Monday to Friday. The FLN will co-
ordinate discharge planning with the multidisciplinary team.
● When patient numbers are high it is important to try to maintain the special
purpose and ambience of PIN.
Handover
● There will be a list on the whiteboard in NICU of babies coming up to readiness for
transfer to PIN. The decision is made by the Specialist, FLN and CCN each day.
● It is expected that all babies being transferred will have a handover written in the
case notes pending the letter.
❍ Complicated infants who are transferred directly from Level 3 require a
formal transfer letter and a consultant handover.

❍ Infants who have been in Level 2 following an admission to Level 3 do not
require a further letter if they have had an uncomplicated course and a

letter of transfer from Level 3 to Level 2.
❍ Complicated infants who have been cared for primarily in Level 2 also
require a formal transfer letter.
Discharge Criteria
In general, an infant is ready for discharge when

● They are able to maintain their temperature in a cot,
● They have had 24 hours of full sucking feeds OR 3-4 breast feeds during the day,
● They are medically stable, and
● The family/whanau are adequately prepared for discharge and follow-up through
Newborn Home Care Nursing service or transfer to a well health provider has been
arranged.
● Most babies will achieve these criteria at 36 weeks corrected gestational age or
greater.
guideline.
Parvovirus Infection and the Fetus

Availability of Testing in Auckland Reviewed by
One available test involves using a DNA probe to identify the virus. This means that this
test needs to be done during the acute phase as basically one is looking for virus particles
in the blood.
IgM, IgG and DNA testing for parvovirus are available in Auckland. Thus active parvovirus
infection can be identified locally by the IgM/IgG (just need 1-2ml plain serum) and
parvovirus viraemia can also be identified if this is an issue, also (2ml plain serum). In
many instances the viraemia will have cleared by the time the rash is apparent, so
serology is a useful option for the acute (as well as the not quite so acute) diagnosis.
In regard to fetal hydrops, there is little data on finding parvovirus in the amniotic fluid
when the fetus is infected, but it would seem reasonable to assume it would be there. We
could certainly assay for parvovirus DNA in amniotic fluid. The same goes for any/all
tissues, including placenta – direct assay for parvovirus DNA would be the most useful
thing to do. A small quantity of tissue (not in formalin) in a sterile disposable plastic
container, put on ice and sent to the Virology Laboratory.
If parvovirus is suspected in a fetus or young infant, examination of mother’s serology

may be helpful diagnostically.
guideline.
Patent Ductus Arteriosus Reviewed by David Knight
December
2000
Incidence Diagnosis Investigations

Management Other Related Documents
Incidence
● PDA is a problem in ventilated very low birth weight infants. About 40% of these
will have a large PDA at 3 days of age.
Diagnosis
● Early: Mostly silent, with no murmur. BP may be low (systolic, diastolic and mean)
with normal pulse pressure.
● Late: Murmur. Hyperactive precordium.
● Increased pulses. Wide pulse pressure. These are not reliable signs in the first
few days.
● Congestive Heart Failure
❍ Cardiomegaly.
❍ Hepatomegaly.
❍ Pulmonary congestion/oedema/plethora.
● Clinical respiratory deterioration.

● Rising PaCO2.
Usually diagnosed late. Most babies treated before this stage.
Investigations
Echocardiogram ● Rules out (most) congenital heart disease. Important to rule
out duct dependent lesions.
Click here to see some still ● Establishes duct patency and size.
images of ducts ● Indicates size of shunt. (ductus shunt best assessed by its
physical size, then by descending aortic flow pattern, then
by LA and LV size).
● Assesses atrial shunt and size.
Chest X-ray ● To look at heart size and lung fields.
ECG ● Usually normal. Do if ‘atypical’, PDA persists or suspicion

on congenital heart disease.
Management
<1000gms and ● Echocardiogram at 3 days.

on IPPV or ● Significant PDA: Consider indomethacin.
CPAP
Other babies ● Investigate if clinical suspicion.
on IPPV
Indomethacin ● See drug protocol.
● Monitor creatinine, electrolytes, urine output & platelets before
and at least daily.
● Review baby and results before each dose.
● Contraindications:
Thrombocytopenia
NEC
Bleeding diathesis
Poor renal function
Pulmonary haemorrhage (note: may occur because there
is a PDA)
Fluid restriction ● While on indomethacin, reduce by 20-40ml/kg/day.

● There is no evidence that fluid restriction per se results in
closure of the duct but there are studies suggesting that early,
liberal fluid intakes are associated with a higher incidence of
PDA.
Surgery ● If PDA is still clinically significant after indomethacin, or if

indomethacin is contraindicated. Surgery will usually be
performed on NICU.
● Note that a increase in respiratory support is often required
immediately after surgery.
guideline.
Persistent Pulmonary Hypertension of the Newborn Reviewed by Simon Rowley and

(PPHN) Carl Kuschel
January
2001
Pathogenesis Diagnosis Investigations

Management Aims Specific Therapies References
Infants with Persistent Pulmonary Hypertension of the Newborn (PPHN) are exceptionally
unstable and difficult to manage. After initial resuscitation the management should always
be discussed with the consultant on call.
Pulmonary hypertension of the newborn with right to left shunt occurs in a variety of
clinical situations. These include Meconium Aspiration Syndrome, hypoplastic lungs,
transient tachypnoea of the newborn, congenital pneumonia and hyaline membrane
disease. Secondary disturbances such as polycythaemia and myocardial failure are
contributory. There is frequently a history of chronic in utero hypoxia, but some cases
remain idiopathic.
Pathogenesis
● Pulmonary vasoconstriction is exacerbated by hypoxia, acidosis, and

hypercapnia (?secondary to changes in pH). Meconium may trigger vasoactive
process to exacerbate this.
● Anatomic abnormality of the pulmonary vascular bed (e.g. pulmonary hypoplasia
with pulmonary arteriolar smooth muscle hypertrophy) or chronic in-utero
hypotension following chronic intrauterine hypoxia may also play a role.
● Birth asphyxia with hypoxia, acidosis and shock is clinically associated with
increased responsivity of the pulmonary vascular bed.
● Group B streptococcal sepsis via Strep polysaccharide toxins.
● Polycythaemia, hyaline membrane disease, hypocalcaemia and hypoglycaemia
may contribute similarly.
● Structural lung abnormalities (e.g. congenital diaphragmatic hernia, CCAM, ...) are
frequently associated with PPHN.
Diagnosis
● This is essentially one of exclusion of significant cyanotic congenital heart disease
and severe parenchymal lung disease. However, PPHN may coexist with
significant parenchymal lung disease.
● Have a high index of suspicion for the 'at risk' group in a term baby with respiratory
distress and cyanosis, particularly if there has been a history of intrauterine
hypoxia and meconium exposure or birth asphyxia.
Investigations
Necessary investigations include
● chest radiograph
● serial arterial blood gases (simultaneous pre- and post-ductal samples may be
helpful)
● full blood count
● blood cultures
● blood glucose
● calcium
● Echocardiogram.
This is crucial to exclude cyanotic congenital heart disease (particularly
transposition of the great arteries, and totally anomalous pulmonary venous
return). In the presence of significant parenchymal lung disease, cardiac
assessment is less urgent.
Echocardiography is also useful to
1. assess myocardial function, which is often severely affected
2. assess the severity of PPHN, and assess responses to treatment.
■ Tricuspid regurgitation - allows indirect measurement of the RV
pressure and therefore severity

■ Ductual shunting
■ Shunting through the foramen ovale
3. Click here to see echocardiographic images of PPHN

● The hyperoxic test may play a role in diagnosis if 2D echocardiography is not
available. However, severe PPHN is likely to produce a similar result to cyanotic
CHD.
Aims of Management
1. Lower pulmonary vascular resistance.

2. Maintain systemic blood pressure.
3. Reverse right-to-left shunting.
4. Improve arteriolar oxygen saturation and oxygen delivery to the tissues.
5. Minimise barotrauma.
Specific Therapies
1. Oxygen and a. 100% O2
ventilation Always start with 100% oxygen and reduce the FiO2, rather
than starting on 25% and increasing. In the short term
there is no risk to a term baby using such measures.
b. Normo-ventilation i.e. pO2 7-12 kpa is acceptable if baby
stable
c. pCO2 5-7 kpa if this can be achieved
d. Use of HFOV, particularly in combination with inhaled Nitric
Oxide, has been shown to reduce the need for ECMO.
2. Normotension a. Myocardial function is frequently poor, despite reasonable

blood pressures.
b. Aim to keep the mean arterial pressures above 50mm Hg
in term infants
c. Use volume (initially normal saline) and dopamine -starting
with 5-10 mcg/kg/min and/or dobutamine 5-10 mcg/kg/min
if systemic pressure raises and pulmonary pressure stays
the same, R-L shunt will diminish .
d. Adrenaline infusions may be indicated if there is severe
myocardial dysfunction
3. Avoid a. Aim to keep the PCV between 0.40 and 0.45.

polycythaemia
4. Alkalosis a. Establish the critical pH- preferably 7.45 but may be

higher. If there is no dramatic improvement in PaO2 at a
pH >7.6, the infant can be deemed to be "pH
unresponsive".
b. Use small boluses of bicarbonate (1-2 mmol/kg) or a
continuous infusion (0.5mmol/kg/hour initially). Liberal
bicarbonate use may result in hypernatraemia and
hypokalaemia.
5. Sedation a. Many babies are very unstable.

b. Consider early use of narcotic infusions.
6. Muscle a. This may be necessary to gain initial control in very

Relaxation vigorous babies who are not adequately sedated with
narcotics and are fighting the ventilator to their detriment.
b. Use pancuronium 100micrograms/kg/dose PRN preferably
for 24 hours or less.
7. Pulmonary a. Inhaled nitric oxide (iNO) is the vasodilator of choice.
vasodilators iNO should be started at 20ppm and reduced to 5ppm as
able, according to response and to stability.
Methaemoglobin levels should be monitored (these are
measured automatically on blood gases).
Nitrogen dioxide (NO2) levels should be monitored and
kept below 1ppm.
b. Magnesium sulphate may be used in refractory cases. The
use of MgSO4 is controversial but may be indicated in
selected instances.
c. Prostacyclin may also be used in severe and refractory
cases, although it is difficult to obtain and its use is
controversial.
d. Tolazoline is no longer used at NWH. It is a non-registered
medication. It has an unpredictable effect and frequently
results in systemic hypotension and collapse.
8. Hyperventilation a. Inducing alkalosis by hyperventilation often creates as

many problems as it solves and is best avoided. There can
be an improvement in PO2.
9. ECMO a. This is essentially prolonged cardio-pulmonary bypass and is provided via

PICU at Starship Hospital.
b. Usual criteria are infants who have an Oxygenation Index (OI) >40 but it may
be appropriate to discuss infants who may potentially require ECMO with the
PICU specialist early rather than when ECMO or death are imminent. This will
be done specialist-to-specialist. The neurological status of the infant may be
an important factor in determining if ECMO is offered.
Click here to open the OI

OI = MAP x100 x FiO2
calculator
PaO2 (mmHg)
where MAP is Mean Airway Pressure,

PaO2 is the arterial oxygen tension in mmHg (1kPa
= 7.5mmHg), and
FiO2 is the fraction of inspired oxygen (100% = 1.0,
air = 0.21)
10. Weaning a. Weaning such babies is invariably difficult. Steps should be

taken one at a time and by small increments once lability
appears to have stabilised.
Other
● Pay careful attention to maintaining normal electrolytes, blood glucose, calcium

and nutrition.
● In babies on long term ventilation, particularly if they are growth retarded from the
outset, intravenous nutrition may be required.
References
1 Drummond WH. Persistent pulmonary hypertension of the neonate (Persistent fetal circulation syndrome).
1984, Year Book Medical Publishers, In. pg 61-85.
2 Fox WW, Duara S. Persistent pulmonary hypertension in the neonate: Diagnosis and management. J
Pediatr 1983; Vol 103:4 pg 505-514.
3 Drummond WH, Gregory GA, et al. The independent effects of hyperventilation, tolazoline, and dopamine
on infants with persistent pulmonary hypertension. J Pediatr 1981; 9(4): 603-611
4 Wung J, James LS, et al. Management of infants with severe respiratory failure and persistence of the fetal
circulation, without hyperventilation. Pediatrics 1985; 76:4, pg488-494.
5 Hansen and Corlet from "Diseases of the Newborn" : Disorders of the transition. Taeusch Ballard Avery 6th
edition -Chapter VIII.
6 Finer NN, Barrington KJ. Nitric oxide for respiratory failure in infants born at or near term. Cochrane
Database of Systematic Reviews 2000; Issue 2. Update Software.
7 UK Collaborative ECMO Trial Group. UK collaborative randomised trial of neonatal extracorporeal
membrane oxygenation. Lancet 1996; 348:75-82.
guideline.
Administration and Monitoring of Phototherapy Reviewed by Charge Nurse -

Newborn
June
2005
Purpose Medela Phototherapy Lamp Ohmeda Biliblanket Phototherapy Lite Meter
Purpose The following policy/recommended best practice outlines the use of

phototherapy lights and the Ohmeda Biliblanket to ensure the best
outcomes for babies in the Newborn Service.
Scope Applies to all Nurses who work in Newborn Services
Associated Operating manuals for:

Documents
● Medela Phototherapy Lamp (Instructions for Use)
● Minolta/Airshields Fluoro-Lite Meter (Model 451)
● Biliblanket Plus Phototherapy System (Operation, Maintenance
and Service Manual)
Medela Phototherapy Lamp
● Follow the steps below to ensure that phototherapy is delivered safely
Step Action
1 Position phototherapy unit 25-30cm from baby in a cot or 2cm above the top of
the incubator.
2 Baby is nursed naked.
3 Use appropriate sized eye shields to protect eyes.
4 Use the phototherapy lite meter to check the unit’s light output each duty.
Output should be over 10mcw/nm/cm2.
5 To avoid the possibility of burns do not use baby lotions or creams on baby’s
skin.
Ohmeda Biliblanket
● Follow the steps below for using the biliblanket.

● Use in conjunction with Medela Phototherapy lamp when SBR level high/rising.
Step Action
1 Insert the fibreoptic pad into, disposable cover.
Secure the cover around the protruding cable with the self-adhesive tabs.
Do not use without disposable cover.
2 Set the brightness selector switch to high.
3 Place covered pad directly under baby with the white illuminating side facing up.
4 Use appropriate sized eye shields to protect eyes.
5 Ensure the air circulation vents on the top and bottom of the illuminator are
unobstructed at all times and that the blocked air circulation indicator is not on
Minolta/Airshields Fluoro-Lite Meter 451
● Follow the steps below.
Step Action
1 Place cap firmly over the receptor head dome.
2 Set the on/off switch to on. The letters ‘Cal’ should appear in the display
window.
3 The ‘Cal’ display will be followed by a zero level display. This indicates that the
meter is calibrated.
If the display window is blank, or three decimal points (…) appear, this indicates
a weak battery.
4 Hold receptor level with the upper surface of baby. Read the digits displayed. If
<10mcw/nm/cm2 remove the phototherapy unit and send to electronics for
evaluation
5 If no measurement is recording, press the hold/run measuring switch. This will
allow the measurement to be displayed
guideline.
Guidelines for the Use of Chest Physiotherapy

Reviewed by David Knight
November 2000
1. Chest physiotherapy is no longer used at National Women’s Hospital on newborn

babies. It is not available. However, it is possible that a baby with a particular
problem may need chest physiotherapy at some time in the future and that this
may be organised with paediatric physiotherapists in another Auckland Hospital.
Therefore, this guideline is still in the file.
2. Babies under 1500g, less than a month of age should not be treated with chest
physiotherapy.
3. Chest physiotherapy should only be commenced when specifically ordered by the
Specialist.
4. Chest physiotherapy should be discussed by a doctor/NS-ANP with the parents
before starting.
5. The physiotherapist will decide on the method of physiotherapy to be given. For
percussion, the baby’s head must be held during physiotherapy.
6. Chest physiotherapy is given by physiotherapists only.
7. The need for ongoing chest physiotherapy should be reviewed daily and recorded
in the medical notes, unless an order for long term chest physiotherapy is made
and recorded.
8. Head ultrasounds should be done at least two weeks after ceasing physiotherapy.
guideline.
Plasma Administration
Reviewed by
FDP Complications Administration Volume to Transfuse Ordering
Fresh Lyophilised (Freeze dried) Plasma (FDP)
Platelet poor plasma separated from single unit of donor blood within 6 hours of its
collection and therefore rich in all coagulation factors, freeze dried in 50ml volume. This
contains approximately 80% of clotting factors present in fresh normal plasma.
Fresh frozen plasma is also available, but is usually only indicated for:
1. Cl esterase inhibitor deficiency.

2. Some cases of Von Willebrand's for factor deficiency
Complications
1. Infections with HBV, HIV, bacterial contamination etc. as for red cell transfusion.
2. Volume overload.
3. Allergic reactions.
4. Antibody mediated reactions, e.g. if group A plasma (containing Anti-B) is given to
a group B baby, haemolysis may occur. Leucocyte antibodies may be present in
donor blood and could cause reactions.
5. May contribute to rise in blood viscosity.
Administration
1. Reconstitute over 10 minutes swirling gently. Use immediately.

2. As for red cells, draw into syringe through a new 170u blood group filter and infuse
generally over not more than 2 hours.
Volume to Transfuse
● FDP contains around 80% of clotting factors found in fresh normal plasma.
● Bleeding and abnormal clotting may occur when one or more clotting factors fall
below 30%.
● Baby's plasma volume will be approximately 50ml/kg
Therefore: 50 x 0.3 = 18.75ml/kg of FDP containing 80% clotting factors

should correct bleeding if clotting factor levels are 0%.
● Where volume overload is a problem, double or triple strength plasma can be

made by reducing the volume of reconstituting fluid to 1/2 or 1/3 - this solution will
be hypertonic and should be infused SLOWLY over at least 1 hour if possible.
Ordering
For individual patients order on green blood product request form (S407) through Blood
Bank.
Any printed version can not be assumed to be current. Printed copies of this document are valid for Monday, May
22, 2006.
Prevention of Hypothermia in Infants <30 weeks Reviewed by Bronwyn Jones (NNP)

Gestation and Malcom Battin
August
2005
Introduction Which Babies When and How to Apply In the Operating Theatre
In Delivery Unit When CPAP is Required When to Remove the Wrap References
Introduction
● Hypothermia in the premature newborn is associated with increased mortality and

morbidity. 1
● In infants <1500g, temperatures on admission to the neonatal unit are on average <35.5°
C.
● Polyethylene wraps have been shown to be an effective intervention in improving core
temperature on admission to neonatal units. 2
Which Babies
● This guideline applies to infants born at <30 weeks gestation at National Women’s Health
in either delivery unit or theatre and - if practical - elsewhere in Auckland City Hospital (e.
g. antenatal wards, WAU or ED).
When and How to Apply
● Plastic wrap should be pre-warmed.

● Note that the infant is not dried prior to being placed in the wrap.
a. Baby wrapped
without drying
wrapping the
head first.
b. Sides
wrapped in
similar fashion
as one would
when using a
towel.
c. Infant is
resuscitated in
plastic wrap.
d. Heart-rate can
be
auscultated
through
plastic.
e. A SaO2 probe should be applied to the right arm/hand as soon as possible following
delivery via the bottom of the wrapped infant.
f. Vitamin K should be given in the Newborn Unit. (Note this should be prescribed on the
stat dose side of the drug sheet).
g. Temperature should be taken immediately on arrival in the NICU and again at 1 hour.
In the Operating Theatre
● In theatre the infant is transferred to the radiant warmer and placed on a plastic wrap that
has been pre-warmed.
● Plastic wrap pre-
warmed on heat
table.
In Delivery Unit
● In the Delivery Unit the infant is wrapped in warmed plastic wrap directly at mother’s
bedside in the same manner as outlined above.
● The infant is then transferred to the radiant warmer for immediate management.
When CPAP is Required
● If CPAP is required the babies head should be dried and CPAP bonnet applied in the
usual way keeping the babies body wrapped in plastic.
When to Remove Wrap
● When the infant is stabilised in the neonatal unit in either a humidified incubator or heat
table the plastic can be removed.
● Drying the infant is not necessary.
● Admission temperature and temperature at 1 hour should be recorded and care must be
taken not to overheat the infant.
References
1 Costeloe K, Hennessy E, Gibson A, Marlow N, Wilkinson A. The EPICure Study: Outcomes to discharge from
hospital for infants born at the threshold of viability. Pediatrics 2000;106(4):659
2 McCall E, Alderdice F, Halliday H, Jenkins J, Vohra S. Interventions to prevent hypothermia at birth in preterm and/
or low birthweight babies. The Cochrane Database of Systematic Reviews 2005.
guideline.
Pneumothorax Reviewed by Charge Nurse

Overview Newborn
April
2004
See also the radiology pages on air leak syndromes
Overview
Purpose ● This document details the policies and recommended best practices
of air leak syndromes and chest drain management in Newborn
Services.
Scope ● Applies to all Nurses in Newborn Services caring for baby requiring
chest drain management.
Associated Type Document Title(s)

Documents
Newborn ● All policies/RBP associated with the care/treatment
Services of baby while in Newborn Services
References ● Askin D (1997). Acute respiratory care of the
neonate. Complications of positive pressure
ventilation (6, p139-143).
● Wyatt TH (1995). Pneumothorax in the neonate.
JOGGN March/April (p211-216)
● Literature Research 1998 ® GLH Librarian.
CINAHL & Medline 0-18 months – no relevant
journal articles located.
● Deacon J, O' Neil P (1999). Core curriculum for
neonatal intensive care nursing. (p144-5. P682-3).
2nd edition.
guideline.
Babies under the Care of the Newborn Service on the Reviewed by Carl Kuschel
Postnatal Wards
November
2005
Referrals
● Referrals during normal working hours should be directed to the Neonatal SHO
(pager 93 5815).
❍ If the LMC is not the hospital team, please ensure that the private LMC is
aware of the referral. Some LMCs may choose to assess the baby
themselves or refer the baby to a private practitioner.
● After hours referrals should be made to the 1st on call neonatal staff member
(pager 93 5537). If appropriate, please inform the LMC that the referral has been
made.
● Note that babies should not be referred to the neonatal SHO solely for neonatal
examination (for example, for a hip or eye check, or to listen for heart sounds).
However, referral should be made for those babies where the examination
demonstrates an abnormality or the practitioner is uncertain about their
examination findings.
Care on the Postnatal Ward
● Babies who are under the care of the neonatal paediatric service will be reviewed
daily by the neonatal SHO (or registrar or NS-ANP on weekends and public
holidays).
❍ The SHO will liase with the PIN registrar in the first instance during the
normal working week. The Registrar should see that appropriate

supervision and investigations are in place.
❍ The Level 2 specialist on service will be available to see those infants who
need specialist review.

● Infants under the ADAPT team will primarily be reviewed in normal hours either by
Dr Kuschel or Dr Rowley. After hours and on weekends, these babies will be
reviewed by the 1st call neonatal staff member (pager 93 5537).
guideline.
Management of Paediatric Problems on Postnatal Reviewed by Salim Aftimos

Wards by Obstetric House Staff and LMCs
January
2001
Tachypnoea Meconium Exposure Infants of Diabetic Mothers Low Birth Weight and IUGR
Prematurity Temperature Control Risk Factors for Sepsis Risk Factors for GBS Sepsis
Heart Murmurs Jaundice Cord Flare
The following are some guidelines and list of conditions which may be managed by
obstetric house staff and Lead Maternity Carers on postnatal wards.
Please note that all referrals are to be directed to the Paediatric Registrar or Paediatric
House Surgeon who with Dr Aftimos is on for the postnatal wards. All signatures must be
clear, printed if necessary so that we can audit problems when they occur.
Tachypnoea
● The normal respiratory rate is between 40-50/minutes.

● Some normal healthy infants will breathe at 50-60.
● If the respiratory rate is consistently above 60/minute, babies should be referred to
the Paediatric Registrar.
Meconium Exposure
● Where the Paediatric house staff have attended the delivery and there are no
problems, care should be handed over to the obstetric staff.
● Most of these babies will present within the first 6 hours. AC temperature and
respiratory recordings should be for 24 hours on the postnatal ward. If respiratory
rates >60/minute and/or temperature >37.5°C, the infant should be examined and
then referred to the Paediatric Registrar.
NB If the infant is feeding well and pink on examination, and seems normal
despite the presence of a fever or tachypnoea, then a chest x-ray and full
blood count could be organised before being seen by the Paediatric
Registrar.
Infants of Diabetic Mothers
● These babies are at risk of hypoglycaemia.

● Blood glucose measurement should be requested for one hour and 4 hourly for 12
hours.
● Feeding should be 3 hourly.
● If blood glucose (preferably pre-feed) is <2.6mmol/L repeat feed (either
complement NIF or BF) should be given and the glucose repeated in one hour. If
the repeat is <2.6mmol/L refer to the Paediatric Registrar.
● If a blood glucose is <2.2mmol/L, immediate referral is necessary.
● The volume of complement feed will vary according to size of infant - usually 15-
30ml.
See the guideline for management of infants of diabetic mothers on the

postnatal ward.
Low Birthweight (<2.5kg) and Intrauterine Growth Retardation
● If birthweight 2.2-2.5kg refer to the Paediatric Registrar at delivery. They may elect
to leave the baby under obstetric care with instructions as for intrauterine growth
retardation.
● If birthweight is <10% for gestation or if infant looks especially thin and
malnourished (this is a subjective assessment), one hourly blood glucose and 4
hourly for 24 hours, 3 hourly feeds (complements will probably be necessary and
may be ordered from the outset).
● If the blood glucose is <2.6mmol/L, the baby should be fed complement NIF and
blood glucose repeated in one hour. If the repeat blood glucose is <2.6mmol/L
refer back to Paediatric Registrar.
● If a blood glucose is <2.2mmol/L immediate referral is necessary.
See guideline on hypoglycaemia
Prematurity
● These infants must be referred to the Paediatric Registrar who may decide
(especially >36 weeks) to leave them under obstetric care. Where there is doubt
about gestation, refer to registrar for their opinion.
Temperature Control
● Hypothermia is a major problem with low birthweight and growth retarded infants.
These infants should be wrapped well and kept in a warm room with no drafts.
● Temperature of <36.5°C are abnormal and re-warming efforts should be carried
out.
● If the temperature is below 36.2°C in the first 24 hours, the baby should be placed
in an incubator in the ward nursery, and if not up above 36.8°C in 4 hours, refer to
the Paediatric Registrar.
● Temperature instability after the first day should be referred to the Paediatric
Registrar.
Note: Hypothermia is often the first sign of sepsis and the possibility of
major infection should always be considered.
Sepsis Risk Factors at Delivery
● Prolonged rupture of membranes

● Gestation <37 weeks
● Maternal pyrexia
● Fetal tachycardia
● Offensive liquor (meconium exposure)
Take swabs at delivery (ear/axilla/gastric aspirate) and ask for a differential

on a full blood count. Request AC temperature and respiratory recordings.
If the white blood count shows a left shift (band forms and immature forms
>20% of total neutrophils), if the respiratory rate is >60/minute or the
temperature is >37.5°C, or swabs subsequently grow Group B
Streptococcus refer to the Paediatric Registrar.
If two or more risk factors present, or the baby has symptoms other than the
above, immediate referral is necessary.
Risk Factors for Group B Streptococcal Sepsis
● PROM
● Prematurity
● Amnionitis
● Previously affected infant
● Twins
● Known GBS colonisation
If mother has any of these risk factors then the guidelines for NWH
suggests antibiotics in labour.
Jaundice
(see also Neonatal Jaundice on the Postnatal Ward)
● Jaundice requires Paediatric evaluation in the following situations and whenever

there is a possibility that hyperbilirubinaemia may be indicated or cause pathology:
1. Clinically present before 24 hours of age.
2. Whenever other symptoms/signs of illness are present.
3. When the serum bilirubin is >200mmol/L on the second day of life.
4. When the serum bilirubin is >250mmol/L.
5. When jaundice is of late onset (7-10 days or later) or is prolonged
with serum bilirubin >200mmol/L after 7-10 days of life.
● If a jaundiced baby requires phototherapy then a Paediatric referral and

assessment is mandatory.
● At the time of Paediatric referral, a request should be made to blood bank for the
baby's blood group and Coomb's results.
● A full blood count and film comment is also helpful at this stage, but may await a
Paediatric assessment.
Heart Murmurs
● If the baby is well then a chest x-ray and ECG should be carried out and then
referral to a Paediatric registrar should be undertaken.
● If the baby is tachypnoeic, cyanosed, or unwell, the baby should be referred
immediately to the Paediatric Registrar.
Cord Flare
● This may indicate the presence of early omphalitis although commonly is due to
cord-clamp irritation of abdominal skin.
● If there are no other signs of sepsis (fever, tachycardia, paronychia, skin pustules
elsewhere or induration), check FBC, do umbilical and groin swabs, and observe.
● If other signs of sepsis are present, refer to Paediatric Registrar immediately for
full septic screen and treatment.
guideline.
Assessment of Prolonged and Late-Onset Jaundice Reviewed by Carl Kuschel
June
2004
Definition Assessment Management References
Definition
● Prolonged jaundice is defined as

❍ >14 days in term infants
❍ >21 days in preterm infants
● Persisting jaundice is more common in breastfed infants than artificially-fed infants.

At least 9% of breastfed infants are still jaundiced at 28 days of age. 1
2
● Jaundiced breast-fed infants who are well are unlikely to have serious disease.
However, a diagnosis of breast milk jaundice is a diagnosis of exclusion, after
investigation as below.
● In artificially-fed infants, prolonged jaundice should be aggressively investigated.
● Jaundice which has not previously been apparent and then appears after day 7
should be investigated carefully.
Assessment
● Physical examination, including evaluation of growth and feeding since birth

● Examination of stool colour and enquiry about urine colour
● Total bilirubin AND conjugated fraction
● Full blood count and blood film
❍ To evaluate for haemolytic anaemia and possible infection.
● Thyroid function tests (TSH and T4)

❍ The newborn screening test in NZ screens for congenital hypothyroidism
and evaluates only TSH.
❍ This test is less reliable in preterm infants, and does not screen for
hypopituitary hypothyroidism.
● Urine sample for microscopy and culture
❍ Be aware that a bag urine may yield ambiguous results which may require
further (potentially invasive or unnecessary) investigation.

● Glucose-6-phosphate dehydrogenase screen (in selected infants).
● Check that the Newborn Screening Test has been done.
Notes: ● Liver function tests are not indicated unless there is a conjugated
hyperbilirubinaemia. LFTs are often abnormal in the newborn period in
breastfed infants with no pathological cause for jaundice.
● A Coomb's test is not required if the baby is not anaemic, did not have
early jaundice, and does not have evidence of haemolysis on the FBC.
Management if Baby is Well and Investigations are Normal
● The phototherapy charts are not validated in infants of this age. Bilirubin levels
which are above treatment levels at 4 days may not require phototherapy at 14
days.
● If approaching treatment levels, recheck the bilirubin within 1-2 days to ensure that
it is decreasing.
❍ Otherwise repeat weekly or less often as indicated by clinical examination.
❍ If persistent, recheck the conjugated fraction
● Parents may need reassurance that the jaundice itself is not harmful. They should
be asked to contact their GP or LMC if they have concerns about their baby’s
growth or health.
● Although temporary cessation of breastfeeding may reduce or eliminate prolonged
jaundice associated with breast milk, we do not currently recommend this.
Management if Any Investigations are Abnormal
● The baby may have a pathological cause for jaundice and urgent further
assessment is indicated.
References
1 Crofts DJ, Michel VJ-M, Rigby AS, Tanner MS, Hall DMB, Bonham JR. Assessment of stool colour in
community management of prolonged jaundice in infancy. Acta Paediatr 1999;88:969-74.
2 Hannam S, McDonnell M, Rennie JM. Investigation of prolonged neonatal jaundice. Acta Paediatr 2000;89
(6):694-7.
Chest Radiographs Abdominal Radiographs Long lines Skeletal Surveys Contact Details
● Tubes, catheters and wires should be displaced, as much as possible from the area of
interest.
Chest Radiographs
● The first chest radiograph includes a rolled lateral unless there are mitigating circumstances (such
as a baby who is too unstable to be handled excessively).
● Lateral chest radiographs are usually not required subsequently unless checking on the position of
chest drains. These lateral films are done as a shoot through lateral so that the infant is not lying on
the tubing.
● AP and lateral films, for assessment of the position of umbilical lines, include the abdomen and
chest.
Ministry of Health
NZ Government Abdominal Radiographs
● Abdominal films, in cases of suspected obstruction or NEC, include both an AP view, and a left
side down decubitus view that must include the right hemidiaphragm/right lower chest.
©Copyright
● Consideration should be given to obtaining a prone abdominal film to define lower obstruction, or
Published: 11/04/2006
lateral film to assess for peritoneal calcification, at the time of the original abdominal series.
Long Lines
● For long lines inserted below the groin, a babygram (AP chest and abdomen) is appropriate.
● For long lines inserted from the arms or head, an AP chest with the head turned away from the site
of insertion is appropriate.
● Contrast is used in all longline films (the registrar or NS-ANP will inject 0.5-1.0ml of non-ionic
contrast medium using sterile technique).
Skeletal Surveys
● Skeletal survey for infection includes:

❍ Babygram to include chest, and abdomen, shoulders and hips
❍ Both arms AP
❍ Both legs AP
❍ Hands and feet and other views (e.g. spine/skull) only if there is local swelling or erythema
● Skeletal survey for syndromes or dysmorphic babies includes:

❍ AP and lateral skull
❍ Chest AP and lateral if not already done (includes thoracic spine)
❍ Lateral lumbar, sacral, and cervical spine
❍ Abdomen/pelvis on the same film
❍ Left leg, foot, arm and hand
(Right side only if there is definite asymmetry)

● Skeletal survey for post mortems
❍ AP whole body (skull to toes)
❍ Lateral radiograph (skull to sacrum)
❍ Lower limbs - hips to feet with the legs in a frog position lateral
Contact Details
● Radiographer
❍ 0730 to 2400hr Monday to Friday
❍ 0830-2400hr Saturday, Sunday and Public Holidays
❍ Page 93-4040
At other times call the operator and ensure you ask for the NICU on-call radiographer/
MRT.
❍ When calling in the on-call radiographer, please consider whether the radiograph can be
delayed until the radiographers on during the day are available (i.e. 0730hr on weekdays,
0830hr on weekends)
● Starship Hospital radiologist: 25130 (online reporting) or 25134 (reception)
● Radiology registrar beeper, evenings until 2200hr: 93-5210
● Radiology registrar beeper, nights: 93-5954
Dr Rita Teele (Starship Radiology) and Dr Carl Kuschel

April 2006
guideline.
Reticulocyte Count
Reviewed by
● It is useful to know the reticulocyte count in infants who were born prematurely if
the haemoglobin is low and at about the level at which one might consider
transfusion.
● If the reticulocyte count is high suggesting the infant is actively making red cells,
one might defer transfusion unless there were other special reasons for
proceeding.
● The reticulocyte count may be expressed as an absolute number or as a
percentage of the red blood cells.
To convert number of reticulocytes to %
● Divide absolute reticulocyte count (reticulocytes x 109/L) by 10

● Then divide the answer by the red blood cell count (RBC x 1012/L)
Normal Range for Reticulocyte Counts
The reticulocyte count – range (%) and (x109/L) in the first 3 months of life
in term infants*
Age % x 109/L
1 day 3.0-7.0 110-445
7 days <0.1-1.3 <10-80
4 weeks <0.1-1.2 <10-65
8 weeks 0.1-2.9 <10-125
12 weeks 0.4-1.6 15-75
>12 weeks 0.2-2.0 10-105
* Data from various sources, based on microscope counts
References
1 Paediatric Haematology. Eds Lilleyman JJ, Hann I, Churchill Livingstone 1992.

Retinopathy of Prematurity Reviewed by Carl Kuschel and David Knight
June
2005
Which Babies are Screened? Classification System When are Babies Screened? Examination
Transfer to Another Hospital Follow-up References Related Documents
Which Babies are Screened?
● All babies <1250g birth weight, or

● ≤29 weeks gestation, or
● Selected infants >1250g and >29 weeks with an unstable clinical course who are believed to be at high risk
by their attending neonatologist.
● Click here to open the screening form in use (available through the ADHB intranet only).
Classification System
Photographic images courtesy of Dr Shuan Dai, Ophthalmologist, Auckland District Health Board
Stage 1 Demarcation line -a flat, thin, whiteish, clear-cut

demaraction between vascularised and avascular retina
(normal retina has a tenuous, non-linear, feathery border)
Stage 2 Elevated ridge - demarcation line now has "3"
dimensions
Stage 3 Neovascularisation - extra-retinal, fibrovascular

proliferative tissue
Stage 4 Retinal detachment - may be exudative and/or

tractional, and may be partial or total
Stage 5 Not part of the international classification system but

used clinically to denote a total retinal detachment
Plus Disease Presence of dilatation and turtuosity of the posterior pole

blood vessels. This is associated with severe disease
and poor outcomes.
It is more likely to occur with higher stages and lower
zones.
When are Babies Screened?
● 4-6 weeks post-natal, or between 31 and 33 weeks gestation, whichever is the earlier.
● Then every 2-4 weeks until vascularisation has progressed into Zone III.
● Infants with ROP or immature vessels in Zone I should be seen 2- weekly until normal vascularisation has
proceeded to Zone III or the risk of attaining threshold conditions has passed.
● The database schedules the first appointment on all babies <1250g or <30 weeks.
❍ The appointment date is printed on the problem list.
❍ The timing is as follows:
<26 weeks 1st Thursday after 30 weeks PMA

26 weeks 1st Thursday after 31 weeks PMA
27-28 weeks 1st Thursday after 32 weeks PMA
29-31 weeks 1st Thursday after 33 weeks PMA
≥32 weeks 1st Thursday when over 3 weeks old
Examination
● It is the responsibility of medical and NS-ANP staff to ensure that the examinations are scheduled at
appropriate ages.
● Administer Cyclopentolate 0.5% (Cyclogyl) and Phenylephrine 2.5% one drop in each eye ½ hour and ¼
hour before examination.
● The ophthalmologist records the appearance of the retina and comments on its maturity. Further
appointments are made until the retina is mature.
Transfer to Another Hospital
● Details of eye examinations and recommendations for further examinations MUST be included in transfer
letters.
● Note should be made of which zone the retina is vascularised to as this will influence follow-up
arrangements.
Follow-up
● This is arranged by the ophthalmologist seeing the baby.
References
1 Retinopathy of Prematurity: guidelines for screening and treatment. The report of a Joint Working Party of the Royal College of
Ophthalmologists and the British Association of Perinatal Medicine. Early Human Development 1996;46:239-58.
2 Screening Examination of Premature Infants for Retinopathy of Prematurity. A joint statement of the American Academy of Pediatrics, the
American Association for Pediatric Ophthalmology and Strabismus, and the American Academy of Ophthalmology. Pediatrics
2001;108:809-811.
3 NH and MRC Expert Panel on Perinatal Morbidity, Draft report 1993. Australia.
4 Reynolds JD. Retinopathy of prematurity. Pediatr Ophthal 1996; 9(2):149-159.

guideline.
Protocol for the Management of Infants at Risk of Reviewed by David Knight, Carl
SARS Kuschel, Lucille Wilkinson
(Obstetric Physician), Judy
(Severe Acute Respiratory Syndrome) Gilmour (Infection Control) and
Lesley Voss (Paediatric Infectious
Diseases)
Date last edited: January 10, 2006
Preparation prior to Immediate Care of the Investigations and other

Postnatal Care
Delivery Infant Management
This guideline applies to those infants whose mothers are confirmed as or

suspected of having SARS.
There is little information available about infants who have been born to pregnant women
who have had SARS. There are reports in the media of infants suspected of having
SARS, although these infants were also premature and may have had morbidity related to
1-3
other neonatal problems.
This protocol is subject to change as new information about management of this condition
becomes available. Other resources which should be consulted include the ADHB
Intranet guidelines on SARS which also has links to other websites.
Preparation prior to Delivery
1. Delivery Unit staff will clear Delivery Room 13 of non-essential equipment.

2. A mobile resuscitation table and equipment is put in Room 13.
3. Neonatal Registrar or NS-ANP is called for the delivery, in time to put on protective
clothing.
4. Newborn staff will put on personal protective apparel before entering Room 13.
a. This includes hat, goggles, impermeable gown, and gloves.
b. Use an N95 mask. A N100 mask is not needed.
Immediate Care of the Infant
1. The midwife hands the baby to the Neonatal Registrar or NS-ANP in the
connecting room between Delivery Room 12 (containing the mother) and Delivery
Room 13.
2. The baby is resuscitated if necessary.
3. The baby remains in Delivery Room 13 while stabilised.
Postnatal Care of the Infant
1. When stable, the baby is washed.

2. Carefully dispose of soiled baby wraps into yellow topped linen bag.
3. The Neonatal Registrar or NS-ANP will carefully remove the personal protective
equipment and perform hand hygiene. Both chlorexidine 4% soap for hand
washing and alcohol hand gel are good protection against viruses.
4. The Registrar or NS-ANP will put on a new gown and gloves to take the baby to
NICU. A N95 mask should be worn if the baby is unwell.
5. The baby is then taken to a side room in NICU (Room 15)
❍ Within the isolation room, an incubator is not indicated for isolation
measures alone and a cot may be sufficient

6. Notify Infection Control.
7. Strict and careful handwashing procedures (using 4% Chlorhexidine soap or
alcohol hand gel) should be followed.
8. Care in NICU is with gown and gloves, but no mask is needed (unless the baby
has respiratory symptoms).
9. The baby does not receive breast milk.
❍ Mother should be encouraged to express, but the breast milk is discarded
until she is non-infectious.

10. There are no visitors allowed (family contacts will be SARS contacts).
11. If the baby has respiratory distress, stricter precautions are needed.
❍ A N95 mask is suitable for short exposures.
❍ A N100 for prolonged exposures such as primary nurse or for procedures
such as suctioning, intubating or taking a nasopharyngeal aspirate. (The

N100 mask is reusable after decontamination . Do not discard).
❍ Staff contact should be kept to a minimum.
12. Babies can be discharged with the mother when the mother and baby are well
enough to go home. Ensure Public Health are notified.
13. Parents should be instructed to seek medical attention should the mother or baby
develop any signs or symptoms of disease within 10 days after delivery.
Investigations and other Management
1. No investigations are indicated if the baby is clinically stable and there are no other
indications for tests.
2. Inform the Paediatric Infectious Diseases specialist about the baby, regardless of
how well the baby is. This can be done in normal working hours, unless there are
clinical concerns.
3. If there are any clinical concerns about the baby, then send
❍ FBC for differential and blood film
❍ Blood cultures
❍ Chest radiograph
❍ Viral studies, specifically looking for the SARS coronavirus, namely

■ Nasopharyngeal aspirate or tracheal aspirate for virus identification
(immunofluoresence, PCR for SARS coronavirus, and viral culture)
■ Urine viral culture
■ Faecal specimen
■ Blood for serology (will need subsequent convalescent sample)
Do not send viral samples for SARS in the Lamson tube. They
must be taken to the laboratory by an orderly.
❍ CSF samples for bacterial and viral (PCR for Herpes and enteroviruses)
analysis may be considered on an individual case-by-case basis

4. If the baby is unwell, start antibiotics in order to cover other potential bacterial
causes of illness.
References
1 http://www.smh.com.au/articles/2003/04/25/1050777391317.html
2 http://chealth.canoe.ca/health_news_detail.asp?channel_id=60&news_id=6837
3 http://www.salon.com/news/wire/2003/04/16/sars_babies/
guideline.
Management of Neonatal Seizures Reviewed by Malcolm Battin
January
2001
History, Examination, and

Types of Seizures Indication for Treatment Usual Sequence of Therapy
Investigation
EEG Maintenance Therapy Duration of Therapy References
The incidence of neonatal seizures in term infants is 0.7-2.8 per 1000 live births and is
higher in the preterm population 1-4. In term infants hypoxic-ischemic encephalopathy is
the most common cause, but other causes include intracranial haemorrhage, infection,
metabolic abnormalities, CNS malformations and drug withdrawal.
Types of Seizures
The clinical manifestations of neonatal seizures differ from those in older children. Five
major varieties are described:
● subtle
● generalised tonic
● multifocal clonic
● focal clonic, and
● myoclonic.
Jitteriness is not a seizure but is frequently confused with one and may be a sign of
cerebral irritation.
History, Examination, and Investigation
● It is important to obtain a careful perinatal history and perform a physical

examination.
● Hypoglycaemia or meningitis should be recognised and treated promptly.
● Investigation should include:
❍ blood glucose
❍ FBC and PCV

❍ Blood gas
❍ sodium, potassium, magnesium, calcium and phosphate.
❍ Further investigation including lumbar puncture, cerebral ultrasound,
metabolic screen and CT or MRI will depend on the individual case.
Indication for Treatment
● Untreated seizures may continue for extended periods of time, interfere with
ventilation or precipitate cardiovascular collapse.
● Cardio-respiratory compromise may impair cerebral vascular autoregulation and
predispose to secondary brain injury.
In general if seizure duration >3 min or frequency or >3 per hour treatment
is required.
● Ensure that ventilation and perfusion are adequate and any

hypoglycaemia is corrected.
● Drugs should be given intravenously to achieve a rapid onset of
action and predictable blood levels.
Usual Sequence of Therapy
1 Phenobarbitone 20 mg/kg loading dose (slow IV infusion over 30 mins)
● If the initial 20 mg/kg dose is ineffective, additional doses of 5-10 mg/Kg

can be administered until either seizures have ceased or a total dose of
5
40 mg/Kg has been given.
2 Phenytoin 20 mg/kg (slow IV infusion over 30 mins, i.e < 1 mg/kg/min)
● Cardiac rate and rhythm should be monitored during the infusion.
3 Paraldehyde 200-400 mg/kg IV
6
● Infuse over 2 hours in a 5% solution made up in 5% dextrose .
OR Clonazepam 100-200 micrograms/kg (intravenously over 30 seconds)
● and if control not achieved then Clonazepam intravenous infusion 10-30

micrograms/kg/hour.
OR Midazolam 0.05 to 0.15mg/kg as a slow push over 5 minutes
● can be repeated 2-4 hourly as required or given as a continuous infusion

(10-60micrograms/kg/hour)
● Convert to maintenance therapy when seizures controlled (usually not >48hrs

infusion) 7.
● N.B. If there are recurrent seizures with no obvious cause consider pyridoxine
dependency.
❍ A therapeutic trial of pyridoxine IV 50 -100 mg may be helpful (this may be
considered during EEG).
EEG
● It is not necessary to defer therapy until an EEG can be obtained. However, EEG
may assist in confirming that subtle phenomena are seizures or to determine if a
paralysed infant is having seizures.
● The interictal EEG may be useful in estimating prognosis particularly in HIE.
Maintenance Therapy
● Phenobarbitone 3-6 mg/kg/day. IV, IM, or oral.

● Phenytoin 3-8 mg/kg/day IV only (oral absorption is erratic)
● Maintenance therapy should begin 12 hrs after the loading dose and is given
divided q 12 hrs.
● Drug levels are important when these drugs are used for maintenance.
● Slow elimination rates in asphyxiated infants, secondary to hepatic and/or renal
involvement, may lead to drug accumulation.
● Also maintenance administration of phenytoin is difficult because of its nonlinear
kinetics and rapid decrease in elimination rates in the first weeks of life.
Duration of Therapy
● Optimal duration of therapy depends principally on the likelihood of recurrence of

seizures.
● Following HIE there is a low risk of seizure recurrence after early withdrawal of
8
anticonvulsant in the neonatal period .
❍ Hence, it is usual to discontinue the anticonvulsant prior to discharge.
● However, infants with prolonged or difficult seizures and those who continue to
show abnormality on EEG may benefit from continuing treatment (usually
monotherapy with phenobarbitone).
● The neurodevelopmental outcome depends on the cause of seizures. Major
cerebral malformations have a poor prognosis whilst the outcome from HIE,
infection, and metabolic abnormalities will be variable. It is important that all infants
with neonatal seizures receive adequate follow up.
References
1 Curtis PD, Matthews TG, Clarke TA, et al. Neonatal seizures: the Dublin Collaborative study. Arch Dis
Child 1988;63:1065-8.
2 Lanska MJ, Lanska RJ, Baumann, RJ, Kryscio RJ. A population based study of neonatal seizures in
Fayette County, Kentucky. Neurology 1995;45:724-32.
3 Lien JM, Towers CV, Quilligan EJ et al. Term early-onset neonatal seizures: obstetric characteristics,
etiologic classifications, and perinatal care. Obstet Gynecol 1995;85:163-9.
4 Scher MS, Aso K, Beggarly ME, et al. Electrographic seizures in preterm and full-term neonates: clinical
correlates, associated brain lesions, and risk for neurologic sequelae. Pediatr 1993;91:128-34.
5 Gilman JT, Gal P, Duchowny MS, Weaver RL, Ransom JL. Rapid sequential phenobarbital treatment of
neonatal seizures. Pediatr 1989;83:674-8.
6 Koren G, Butt W; Rajchgot P, et al. Intravenous paraldehyde for seizure control in newborn infants.
Neurology 1986;36:108-11
7 Evans D, Levene M. Neonatal Seizures. Arch Dis Child. 1998;78:F70-75
8 Hellstrom Westas L, Blennow G, Lindroth M, Rosen I, Svenningsen NW. Low risk of seizure recurrence
after early withdrawal of antiepileptic treatment in the neonatal period. Arch Dis Child 1995;72: F97-101
guideline.
Single Umbilical Artery Reviewed by Carl Kuschel
December
2004
Single Umbilical Artery (SUA) is a common congenital abnormality, often also called a 2-
vessel cord. Isolated SUA occurs in up to 2% of all liveborn infants.1 It may be detected
antenatally, or discovered upon examination of the infant at delivery.
The majority of SUA occur as an isolated anomaly. However, SUA may be associated
with other structural or chromosomal anomalies.2 The risk of a chromosomal abnormality
is 10-times higher in infants with a SUA.3
The median incidence of other major abnormalities in liveborn infants with a SUA is
approximately 27% (range 21.6-32.2%). [1] The median incidence of occult renal
abnormalities (vesicoureteric reflux, hypoplastic kidneys, absent kidney, or multicystic
kidney) in otherwise normal infants with SUA in this meta-analysis was 5%.
In the absence of previously demonstrated physical abnormalities on antenatal ultrasound

screening, there is little yield in obtaining investigations following delivery in infants
4
without examination findings suggesting other anomalies.
Recommendations
1. Check if antenatal ultrasound scans demonstrated any other abnormalities

2. Examine the baby for dysmorphic features, abdominal masses, or cardiac disease
3. If no other abnormalities are found on examination, no investigations are required.
4. If there is suspicion of other abnormalities, appropriate investigations (imaging,
karyotype) should be arranged.
References
1 Thummala MR, Raju TNK, Langenberg P. Isolated single umbilical artery anomaliy and the risk for
congenital malformations: a meta-analysis. J Pediatr Surg 1998;33:580-5.
2 Gossett DR, Lantz ME, Chisholm CA. Antenatal diagnosis of single umbilical artery: Is fetal
echocardiography warranted? Obstet Gynecol 2002;100:903–8
3 Prucka S, Clemens M, Craven C, McPherson E. Single umbilical artery: What does it mean for the fetus? A
case-control analysis of pathologically ascertained cases. Genet Med 2004:6(1):54–7.
4 Parilla BV, Tamura RK, MacGregor SN, Geibel LJ, Sabbagha RE. The clinical significance of a single
umbilical artery as an isolated finding on prenatal ultrasound. Obstet Gynecol 1995;85:570-2.
guideline.
Skeletal Surveys in Neonates

Reviewed by Rita Teele
(Paediatric Radiology)
October 2004
When ordering a skeletal survey, the particular radiographs taken will depend on the
indication. On the form, you will need to specify "Skeletal Survey - Syndromes" or
"Skeletal Survey - Infection"
Syndromes: ● AP and lateral skull. (Currently only lateral is done)

● Chest AP and lateral if not already done (includes
thoracic spine)
● Lateral lumbar, sacral, and cervical spine
● Abdomen/pelvis on the same film
● Left leg, foot, arm and hand
(Right only if there is definite asymmetry.)
Infection: ● Babygram to include chest, and abdomen,

shoulders and hips
● Both arms AP
● Both legs AP
● Hands and feet and other views (e.g. spine/skull)
only if there is local swelling or erythema.
The radiographer is to check all surveys with a radiologist.

First Foods for
Premature Babies
Guidelines on starting solids for caregivers of ex premature babies
Barbara Cormack, Neonatal/Paediatric Dietitian
Auckland City Hospital
Auckland District Health Board
Choosing the right time to start introducing solid food

has been a dilemma for centuries. This decision can be
even more difficult for babies who were born prematurely.
The Window of Opportunity

There is a reasonably small window of opportunity to start
your baby on solids. Too soon (before 16 weeks postnatal
age) and there is an increased risk of allergy and anaemia
because the gut is not ready. Most babies do not yet have
enough control over their tongues and mouth muscles. Instead of swallowing the food, they push
their tongues against the spoon or the food. This tongue-pushing reflex helps babies when they
are breastfeeding or drinking from a bottle. Most babies lose this reflex at about 4 months of age.
Too late (after 7- 10 months postnatal age) and your baby may have developed a resistance to
having anything but milk in his or her mouth. There is also a risk of anaemia with starting solids late
because a baby is born with only enough iron stores to last about 6 months and after that needs
to get iron from food. If your baby was born prematurely, use the following points to help you
decide if he or she is ready:
Earliest time - themid point between 16 weeks from birth and 16 weeks from the expected due
date. Use the chart later in this pamphlet to help you work this out.
• Assess your baby's progress with the "Eating readiness cues for introduction of solids" chart
• Latest time - Before 7 months after birth
Developmental Cues
Introducing solids will be much easier if your baby:
• Can hold his or her head up well, sit up
• Leans towards food when it is offered and opens his or her mouth
• Appears to be able to eat from a spoon
• Doesn’t immediately push food out of his or her mouth although for some preterm babies
this may not be a useful indicator especially if other cues indicate the baby is ready.
Other reliable cues are increasing demands for feeds and an appetite that is clearly not satisfied
with milk alone.
Baby’s first solids

At first you may want to pick a time when you do not have many distractions. However, keep in
mind that as your child gets older he or she will want to eat with the rest of the family.
§ Give the milk feed first and offer solids as a top up
§ Start solids with one new food at a time
§ First try plain soft foods such as baby rice or infant cereal, pureed apple, pear, apricot, peach
or mashed ripe banana
• Try one teaspoon first and gradually increase as the baby wants more
• When baby is having 3 to 4 teaspoons at a meal it is time to add a second meal at a different
time of day
§ Try one new food every 4 to 5 days. If they don’t like it the first time, leave it for a few days and
try again. Sometimes a baby will need to try a new food ten times before they will like it.
§ It is important for preterm babies to be offered lumpy foods by the time they are 9 months old.
Eating readiness cues for introduction of solids – Preterm Babies
Weight Physical Sensory Mealtime Mouth Learning
Baby’s When baby: When placed When baby: When hungry or When baby’s: When baby’s:
Cues • Weighs on stomach, • Puts hands and wants more food Mouth: • Mouth
5kg or more baby can: toys baby: • Opens easily movements
• Hold head easily and • Frequently cries when steadily
up frequently • Leans forward as spoon improve
• Support in the mouth food approaches touches lips during the
weight on • Explores fingers, • Reaches for food or as food first week
forearms thumbs and fists or approaches of spoon
• Push up on with great parent’s hand feeding
arms interest • Opens mouth Tongue:
with straight • Does not
elbows When satisfied or protrude
wants to stop • Moves gently
NB. Some eating: back
premature • Turns head or and forth as
babies may body food
not be able to away from food enters mouth
do this well – • Loses interest in
look at other food Food:
cues too. • Pushes food or • Stays in
parent’s hand mouth
away • Can be
• Closes mouth moved to
When sitting on • Looks distressed or back of
parent’s lap, cries mouth and
baby can: swallowed
• Hold head • Is not
up “recycled”
• Keep head
control
led
when tipped
• Sit with less
help
• Reach out
for toy
What The baby Baby is Baby is seeking Baby knows if he or Baby has Baby is
they who is developing important she wants to eat developed the development
mean growing good control information about and how much type of tongue ally ready,
rapidly and of head and texture, and is food is needed. pattern both
always seems trunk, which developing an necessary for physically
hungry may support mouth acceptance of moving food to and
need extra skills for eating. objects in the the back of emotionally,
calories from front of the mouth. the mouth and for foods in
solids to swallowing. addition to
support breast milk or
growth and formula.
satisfy
hunger.
How Look for When feeding, Give the baby Let baby be the Use favourite “Tune in” and
parents other place baby in toys that provide leader in showing mouth objects watch for
can development a secure, different mouth what he or she (e.g. fingers) as eating cues
help al cues of upright or sensations. This needs. the first that show
eating slightly reclined prepares the “spoon”. This when baby is
readiness. position. This child’s mouth for helps baby development
makes it easier the varying learn to suck ally ready for
for the child to textures of solid and swallow foods in
relax and use foods and food more addition to
good mouth acceptance of a easily. breast milk or
support. spoon. formula.
Adapted from “Eating Readiness Cues for Supplemental Feeding”, Pediatric Basics, Number 61, Summer
1992
Premature Babies Feeding Guide
Fill in these dates to help you decide when to start Date
Birth date
Due date
16 weeks after Birth date
16 weeks after Due date
The earliest date to start considering
solids but many babies will not be ready Mid point between
yet. Check “Eating Readiness for Solids” the two dates above
chart
Definitely ready to start solids by this date 7 months after birth date
Your baby’s start date
Breastfeed or formula first, then offer solids. Use a small teaspoon and put the food in the middle of their
tongue. Pureed smooth and creamy, no lumps, lukewarm, one food at a time. Try one new food every 4
to 5 days. If they don’t like it the first time, leave it for a few days and try again.
Baby rice or infant cereal - This is a good first food because it is iron fortified.
Fruits - Pureed apple, pear, ripe banana, peach, apricot
Vegetables - Pureed kumara, potato, pumpkin, , marrow, carrot, avocado
About one month after starting solids Date

Start offering solids at three meals a day
Offer drinks from a cup sometimes
Begin adding some pureed or finely minced iron containing foods
Meats - Chicken, lamb, liver, kidney, egg yolk
More vegetables - Courgette, yam, parsnip, taro, puha, broccoli, cauliflower
More fruits - Melon, nectarines, plums, nashi pears (remove skins and seeds)
About 2 to 3 months after starting solids Date

Offer solids before breast feed or formula
Learning to drink from a cup instead of a bottle (about 9 months)
Soft, cut up finely, minced or mashed and offer finger foods
Around this age, babies start to learn to chew. The texture of foods can change fairly quickly from
smooth to mashed with small soft lumps, e.g. finely minced meat. Learning to chew with their gums or
teeth is very important as it strengthens jaw muscles, promotes healthy teeth and ensures a smooth
progression to family foods.
• Bread, pasta, rusks, crackers, wheat cereals, oatmeal, semolina, junior muesli
• More meats - Beef, fish, soya foods
• More vegetables - Silverbeet, spinach, peas, beans, tomato, cabbage, creamed corn
• More fruits - Orange, kiwifruit, pineapple, berries
• Some dairy foods- Yoghurt, cottage cheese, grated cheese, custard
• Other foods - White bread or plain crackers, fine porridge
Leave until 12 months corrected age Date

Introduce cows milk as a primary drink around 12 months of age
Limit the total quantity of milk to 600 - 1000mls/day (600mls milk/day for a toddler is enough). This allows
your child to get hungry so he/she will be more willing to eat solid foods.
Muesli, honey, egg white, peanut butter, shellfish, pork
If allergies run in the family delay introducing cow’s milk, cheese, yoghurt, soya foods, wheat rye, oats,
fish, egg white, citrus fruit, strawberries, tomato and chocolate until after 12 months.
Why is iron important for premature babies?
Premature babies have lower iron stores at birth than term infants and therefore a higher risk of
iron deficiency. Iron is needed to make red blood cells, which carry oxygen throughout the body.
It also plays an important role in immunity, brain development and growth. Babies who do not get
enough iron will become tired, faint, pale, and uninterested in play. Low iron levels in the body
may cause anaemia. To improve blood iron levels babies need a variety of iron containing foods
everyday.
What are the best sources of iron?
Babies & Toddlers
• Red meats such as beef and lamb
• Offal meats such as liver and kidney (try pate on toast)
• Chicken
• Pork, fish and shellfish (later)
• Offer cold meats such as ham or chicken as a snack
As well as meat, try serving other foods, which contain iron:

• Iron-fortified breakfast cereals (check the label to see if iron is added)
• Leafy green vegetables eg. spinach, parsley, broccoli
• Eggs
• Dried fruit
Vitamin C helps iron to be absorbed by the body, so try to include a serve of vitamin C rich food
such as fruits (especially citrus fruit, kiwifruit, strawberries, rockmelon and paw paw) and
vegetables (especially tomato, broccoli and capsicum) with meals. For example serve:
• Vegetables or a salad with meals
• Serve fruit for dessert
• Add a dash of orange juice to baby's pureed vegetables
For more information about starting solids, see your Plunket Nurse or a copy of Healthy Eating for
Babies and Toddlers from Birth to Two Years, PHC, Wellington April 1995. Code 6004
(available from Plunket nurse or GP).
July 2004
References
King, C. (1998) Weaning preterm infants on to solids: When, why and how? Journal of Neonatal Nursing
4(6):7,8,10,11.
Rea, J (1997) Introduction of beikost to the preterm infant: A phenomenological study, Journal of
Neonatal Nursing Volume 3, Issue 6. November 1997
Shaw V, Lawson M. Clinical Paediatric Dietetics, 2nd Edition, London: Blackwell Science Ltd, 2001,
Chapter 5
guideline.
Specialist Responsibilities Reviewed by Carl Kuschel
November
2005
Ward Rounds Level 3 Level 2/PIN Postnatal Wards

On Call Weekends Call Elsewhere
Ward Rounds
Weekends
Monday Tuesday Wednesday Thursday Friday and Public
Holidays
Specialist Specialist Specialist Specialist Specialist Specialist
Level 3
0830 0930 0900 0830 0830 0830
Specialist Specialist Specialist Registrar
Level 2
0830 0900 0830 0830
Multi-
Specialist Registrar as
PIN disciplinary
0830 needed
1130
Afternoon
Specialist on call
Handover
1600hr
Round
Night
Specialist on call as needed
Handover
2100hr
Round
Level 3 on Service
● Level 3 ward round attended daily by specialist. All babies in Level 3 are reviewed.
● Specialist on service available on the Grafton site from 8:30 - 16:00.
● Available to review new admissions or unstable babies during the day.
● Attends resident teaching at 1230hr on Mondays.
● Chairs Neonatal Grand Round at 0830hr on Tuesdays.
● Attends Antenatal ward round at 1200hr on Wednesdays (Ward 96/98).
● Is available for antenatal consultations for infants likely to be admitted to Level 3.
Level 2/PIN on Service
● Specialist on service available on the Grafton site each morning and at least 2-3
afternoons each week.
● All babies on Level 2 reviewed by specialist 3 times weekly.
● Level 2 new admissions discussed with Level 2 specialist and reviewed if
necessary.
● PIN/Level 2 Multidisciplinary Round at 1130hr on Monday.
❍ This round will involve the PIN registrar, the PIN FLN, lactation consultant,
speech language therapist, and social workers.
Postnatal Wards
● Covered by the Level 2 specialist. The registrar for PIN is the doctor who should
be called first to review babies seen by the postnatal ward SHO.
● ADAPT team infants are generally looked after by either Carl Kuschel or Simon
Rowley during the week. On weekends, they may be reviewed by the neonatal
SHO, NS-ANP, or registrar.
On Call
● One specialist on call out of normal working hours.

● Available to be contacted by cell phone or pager.
● On call and available to attend within 20 minutes.
● If a second specialist is required, the on-call specialist will ring colleagues as
available.
Weekends
● Level 3 round at 0830hr.

● Level 2 round following this. The registrar or fellow will have already commenced
this ward round.
● PIN does not require a full round on the weekend, but the FLN or CCN should alert
the registrar or fellow of any infants that need to be seen.
● Level 3 hand-over round at 2100hr or review in evening, as required.
Other Call Elsewhere
● Some specialists work at other hospitals or facilities.

● While on duty or on call at National Women’s, specialists will not be on call or on
duty at outside hospitals or facilities.
guideline.
Suctioning Reviewed by Charge Nurse

Overview Newborn
July
2004
Overview
Purpose ● The following recommended best practice outlines the methods of

suctioning in Newborn Services to ensure safety of the baby.
Scope ● Applies to all Nurses in Newborn Services.
Associated Type Document Title(s)

Documents
Newborn ● Oxygen Administration
Services
References ● Askin, D,F. (1997) Acute respiratory Care of the
Neonate. Petaluma, CA: NICU INK (2nd ed.)
● Blackwood, B. (1999) Normal Saline instillation
with endotracheal suctioning: primum non nocere
(first do no harm). Journal of Advanced Nursing, 29
(4), 928-934
● Neonatal Intensive Care Nursing. London,
Routledge pg 114-115
● Hansen, Contemporary Diagnosis and
management of Neonatal Respiratory Diseases.
USA: Handbooks for Healthcare (2nd ed.)
● Wrightson, D.D, 1999. Suctioning Smarter:
Answers to Eight Common Questions about
Endotracheal Suctioning in Neonates. Neonatal
Network. The Journal of Neonatal Nursing. 18 (1)
51-55.
guideline.
Guidelines for the use of Exogenous Surfactant in Reviewed by Malcolm Battin

NICU
January
2000
Infants 30 weeks and Infants above 30

Background Indications and Usage Administration
Under weeks
Dosage Procedure Precautions Adverse Reactions References
See also Survanta Drug Protocol

See also Exogenous Surfactant Administration in Level 2
Background
● The administration of exogenous surfactant to newborn infants with or at risk of

Respiratory Distress Syndrome (RDS) is now an established practice.
● Although clinical trials have used different preparations and entry criteria,
improvements in ventilatory requirements, survival rates and air leak are
consistently reported with both prophylactic and rescue treatment.
● A small additional benefit, however, is reported from early (prophylactic)
administration when compared to rescue therapy .
Indications and Usage
● We are currently using Survanta, a natural bovine lung extract containing

phospholipids, neutral lipids, and fatty acids.
● It is indicated for both prevention and treatment (‘rescue’) of RDS in premature
infants.
● Survanta significantly reduces the incidence of RDS, mortality due to RDS and air
leak complications although use in infants less than 600g or greater than 1750 g
birthweight has not been evaluated in controlled trials.
Infants 30 weeks and Under
● Surfactant therapy should be used early (<2 hours if possible) in ventilator

dependent babies.
● As soon as the baby is on NICU and the doctor/NS-ANP is confident of the ET
tube position, administer the first dose.
● If surfactant is not given early, the baby should receive surfactant if they have a
diagnosis of probable RDS and/or an a/A ratio of <0.22.
Infants above 30 Weeks
● Exogenous surfactant should be used when a diagnosis of respiratory distress

syndrome is clearly established and the a/A ratio is <0.22.
Administration
● Exogenous surfactant should be administered by a registrar, NS-ANP or specialist

experienced in neonatal respiratory management.
● Infants should be monitored by pulse oximetry and ECG as transient desaturation
and/or bradycardia may occur during administration.
● Also marked improvements in oxygenation and lung compliance may occur within
minutes of administration therefore careful observation and rapid changes in
ventilator management may be needed to avoid hyperoxia.
Dosage
● Each dose of Survanta is 100mg of phospholipids/kg birthweight (4ml/kg).

● Two doses of Survanta are usually given 6 -8 hours apart provided the baby is still
intubated.
● Further doses should be discussed with the neonatologist but up to four doses can
be administered in the first 48 hours of life (i.e. no more frequently than every 6
hours).
Procedure
● Place the infant in the supine position

● Cut a 5 French end-hole catheter so the tip will protrude just beyond the end of the
endotracheal tube (ETT)
● Draw up the Survanta and attach the catheter to the syringe
● Insert the catheter into the ETT and administer the surfactant as rapidly as
tolerated
● After administration hand bag or increase ventilation until the baby is stable
● High frequency oscillation will not adequately disperse the surfactant so for babies
ventilated on HFOV hand bagging is necessary
● Suction should be avoided for 4 hours (unless absolutely indicated for a blocked
ETT)
● Following surfactant administration ventilator requirements may rapidly improve
and ventilation should be adjusted appropriately
Precautions
● Transient bradycardia or oxygen desaturation may occur. If necessary, stop the
dosing procedure and initiate hand bagging or increase the pressure from the
ventilator. After the infant has stabilized, resume the dosing procedure.
Adverse Reactions
● Endotracheal tube blockage and pulmonary haemorrhage are potential

complications of surfactant administration.
References
1 Corbet A, Bucciarelli R, Goldman S et al: Decreased mortality rate among small premature infants treated
at birth with a single dose of synthetic surfactant: a multicenter controlled trial. J Pediatr 1991;118: 277-84
2 Bose C, Corbet A et al: Improved outcome at 28 days of age for very low birth weight infants treated with a
single dose of synthetic surfactant. J Pediatr 1990;117:947-53.
3 Soll RF, Hoekstra RE, Fangman JJ: Multicenter trial of single-dose modified bovine surfactant extract
(Survanta) for prevention of respiratory distress syndrome. Pediatrics 1990; 85: 1092-1102.
4 Kendig JW, Notter RH, Cox C et al: A comparison of surfactant as immediate prophylaxis and as rescue
therapy in newborns of less than 30 weeks' gestation. N Engl J Med 1991; 324: 865-871.
5 Horbar JD, Wright LL, Soll RF, et al. A multicenter randomized trial comparing two surfactants for the
treatment of neonatal respiratory distress syndrome. J Pediatr. 1993; 123(5): 757-66
guideline.
Use of Surfactant in Non-Ventilated Infants on Level 2 Reviewed by Simon Rowley
January
2001
See also Guideline on Exogenous Surfactant Use
Criteria for Considering Surfactant Use
● Clinical and/or radiological evidence of RDS.

● Gestational age ≥32/40.
● Age less than 72 hours.
● Current CXR available.
● Increasing requirements, e.g.. FiO2 > 50%, pH < 7.25, PaO2 < 7.0, PaCO2 > 7.0,
(or A/a < 0.22).
● Arterial line in situ.
Unlikely Candidates
● Birth asphyxia.
● Pneumonia.
● Pneumothorax.
● Severe malformations.
● Prolonged ROM >5 days.
● Meconium Aspiration Syndrome
The Process
● Discuss with Level 2 Specialist and Charge Nurse.

● One to one nursing recommended for the duration of the administration and
observations.
● Inform Level 3 staff.
● Registrar or NS-ANP intubates and administers appropriate dose, hand ventilates
until stable (less than ½ hour).
● Extubate to CPAP .
● If possible Registrar to remain on Unit for ½ hour post extubation.
● ABG before and ½ hour after .
● If no improvement post-surfactant, discuss with Consultant (? repeat CXR/?IPPV) .
References
1 Verder H et al. Surfactant Therapy and Nasal Continuous Positive Airway Pressure for Newborns with
Respiratory Distress Syndrome. New Engl J Med Oct 20 1994; 331(16).
guideline.
Neonatal Surgery Reviewed by Charge Nurse -

Introduction Newborn
September
2004
Purpose Scope Index of Related Documents Associated Documents
Purpose
The following policies and recommended best practices outlines the way in which babies
with surgical anomalies are cared for in Newborn Services.
Scope
This document applies to all Nurses who care for babies with surgical anomalies in
Newborn Services.
The table below indicates other documents associated with this policy.

References 1. Blumer, J (1991); A Practical Guide to Paediatric Intensive
and Texts Care, 3rd Edition.
2. Davies, L & Mann, M 1983; Heart Children.
3. Fanarof, A & Martin, J 1987; Neonatal - Paediatric
Medicine Diseases of the Fetus & Infant.
4. Harjo, J. Kenner, C & Brueggemeyer (1988); Neonatal
Surgery : A Nursing Perspective.
5. Knight, D (Aug 1995); Patent Ductus Arteriosus
(Information Sheet)
6. Kolbe, A 1992; Notes from lectures on:
❍ Diaphragmatic hernia
❍ Gastroschisis/omphalocele
❍ Necrotising enterocolitis
7. Leape, L.L (1987); Patient Care in Paediatric Surgery.

8. Leape, L & Holder, T in Sabiston, D (1991); Textbook of
Surgery.
9. Marieb, E 1989; Human Anatomy & Physiology.
10. Neonatal Network Oct 92 Neonatal Short Bowel Syndrome
11. Neonatal Network Feb 93 Diaphragmatic Hernia
12. Neonatal Network Apr 94 Cricoid Split
13. Neuroservices Unit, Akd Hosp Notes on Hydrocephalus.
14. Price, E 1996. Neuroservices Unit, Ak Hosp Meningocele,
Postoperative care
15. Rowley, S 1992 Notes from lecture - Intraventricular
Haemorrhage
16. Saunders, WB 1992; Textbook of Paediatrics, 14th edition.
17. Kenner, C 1998. Comprehensive Neonatal Nursing A
Physiologic Perspective.
Surgical Neonates Reviewed by Carl Kuschel, John Beca (PICU),

Provision and Location of Intensive Care and Philip Morreau (Paediatric Surgery)
November
2004
Location of Intensive Care Infants older than 7 days or with acute infections Referral Processes
24B High Dependency Unit Post-operative Surgical Review Index of Related Documents
Location of Intensive Care
All surgical neonates who require intensive care in the neonatal period will be looked after before and after surgery in NICU.
The exceptions to this are:
● Infants with congenital

diaphragmatic hernia
❍ Delivery will be
attended by the
Neonatal Team
and they will be
stabilised in NICU
and then
transferred as
soon as
practicable to
PICU for ongoing
management.
❍ This will generally
be after vascular
lines have been
inserted and
radiographs
taken, and we
would anticipate
that babies move
to PICU within 1-2
hours of birth.
● Infants with a paediatric

surgical problem (e.g.
bowel anomaly) whose
predominant problem is
congenital heart disease
will be transferred to
PICU.
● Infants with airway

problems will be
managed in PICU.
● Infants with abdominal

wall defects who develop
an abdominal
compartment syndrome
with renal impairment
will be transferred to
PICU.
These guidelines will need to be flexible. There will be times when one or other unit is full and requires assistance. In addition,
some infants with conditions which would normally require admission to PICU may be initially managed in NICU if they are
premature.
Infants older than 7 days or with acute infections
● Infants older than 7 days who have been discharged home and present with a condition requiring surgery will be admitted
to ward 24B and receive their intensive care support in PICU.
● Babies who clearly have acute infections will be admitted to PICU or 24B in preference to NICU.
● If babies who have been in NICU are transferred to ward 24B and subsequently require further intensive care, they will be
admitted to PICU if they have been discharged from NICU for more than 72 hours.
Referral Processes
● Referral to the surgical service for urgent consultation or where there are concerns about the clinical condition of the
infant will continue to be neonatal specialist to surgical specialist.
● Non-urgent referrals (for example, inguinal hernias awaiting elective repair) may be referred from NICU registrar or Nurse
Specialist to surgical registrar.
Ward 24B High Dependency Unit
● Placement of surgical neonates requiring high dependency care will continue on the surgical ward.
● However, the Neonatal Team will consult as needed and advise over medical management.
Post-operative Surgical Review
● The surgical team involved in the surgical care will regularly visit the NICU in the post-operative period until the baby no
longer requires surgical involvement or until the baby is transferred out of NICU.
● Infants born at Middlemore Hospital who require surgical procedures will be looked after post-operatively in the ACH
NICU (some infants may be transferred to the ACH NICU prior to surgery if indicated).
❍ Once these infants no longer need surgical review, they will be transferred back to Middlemore NICU
guideline.
Thermal Environment and Growth in Preterm Infants Reviewed by Dr Claire West
October
2001
The thermal environment is an important factor in the neonatal care of preterm infants,
with effects on mortality and metabolic rate in these infants.
● It has been known for many years that low birthweight infants raised in subthermo-
neutral conditions grow more slowly than those in thermo-neutral conditions, if
each group receives identical feeding (120cal/kg/day).
● The infants are able to make up this difference when given a caloric supplement
1
sufficient to match the calculated cost of the cold-induced metabolic rise. Using
computer controlled incubator systems, improved caloric efficiencies for growth
2
has been reported.
● There is limited scientific evidence for when to move the healthy growing preterm
infant from a relatively warm incubator to a bassinet at room temperature.
● A study of healthy preterm infants moved to bassinets at different points - either a
weight of 1600-1700g, or 1800-1900g, showed the rate of weight gain correlated
with gross energy intake only and did not differ between the two groups. However,
the rate of growth of skin folds increased dramatically after infants were moved
from the incubator. This faster deposition of subcutaneous fat implies that the
distribution of energy to fat, as opposed to muscle, visceral and skeletal growth,
may be regulated by the thermal environment. This could represent an adaptation
for better insulation against cold, however, the authors speculate that this may
3
divert growth from other organs.
These factors should be taken into account when the decision is made to move an infant
from an incubator to a bassinet. Consideration of appropriate clothing including head
cover is important. Can a baby increase its oral intake sufficiently, and is increased
growth of fat better than growth of other vital organs?
References
1 Glass et a1. BioI Neonate 14 : 324; 1969.
2 Perstein et al. Pediatrics 57 : 494; 1976.
3 Heimler et a1. Pediatrics 68 : 82; 1981

guideline.
Neonatal Thrombocytopenia Reviewed by Alan Groves and

Carl Kuschel
April
2003
Background Incidence Aetiology Risks of Thrombocytopenia

Platelet Transfusion
References
Guidelines
Please see also Neonatal Alloimmune Thrombocytopenia
Background
● Thrombocytopenia is extremely common in the NICU setting, occurring in up to a

quarter of admissions, but while the disorder is frequently seen it should not be
dismissed without consideration of its significance.
● Thrombocytopenia can be a marker of underlying disease as well as an obvious
risk factor for haemorrhage.
Incidence
● The incidence of thrombocytopenia depends on its definition as well as the

subgroup of infants examined.
● Although preterm neonates tend to have slightly lower mean platelet counts than
term infants and adults, a lower limit of ‘normal’ of 150 x 109/L still applies.
❍ Around 2% of healthy term infants will fall below this level, with many more
sick preterm infants having low counts.
Aetiology
Causes of thrombocytopenia are best separated by time of presentation into fetal, early
<3 days) and late.
Timing Most Common Aetiology Less Common Aetiology

Fetal ● Alloimmune ● Severe rhesus disease
● Congenital infection (e.g. ● Congenital/inherited (e.g.
CMV, toxoplasma, rubella) Wiskott-Aldrich syndrome)
● Aneuploidy (e.g. trisomies
18, 13, 21, or triploidy)
● Autoimmune (e.g. ITP,
SLE)
Early-Onset ● Placental insufficiency (e.g. ● Congenital infection (e.g.

Neonatal GPH, IUGR, diabetes) CMV, toxoplasma, rubella)
(<72 hours) ● Perinatal asphyxia ● Thrombosis (e.g. aortic,
● DIC renal vein)
● Alloimmune ● Bone marrow replacement
● Autoimmune (e.g. congenital leukaemia)
● Kasabach-Merritt syndrome
● Metabolic disease (e.g.
propionic and
methylmalonic acidaemia)
● Congenital/inherited (e.g.
TAR, Congenital
Amegakaryocytic
Thrombocytopenia [CAMT])
Late-Onset ● Late-onset sepsis ● Congenital infection (e.g.

Neonatal ● NEC CMV, toxoplasma, rubella)
● Autoimmune
● Kasabach-Merritt
Phenomenon
● Metabolic disease (e.g.
propionic and
methylmalonic acidaemia)
● Congenital/inherited (eg
TAR, CAMT)
Fetal Thrombocytopenia
Is most commonly due to Neonatal Alloimmune Thrombocytopenia. Congenital infection

and chromosomal abnormalities are the other principal considerations.
Early-Onset Neonatal Thrombocytopenia
This is common in preterm infants following pregnancies complicated by impaired

placental function or fetal hypoxia (which may impair fetal/infant platelet production).
These infants show a typical pattern of low/low-normal platelet counts at birth (100-200 x
109/L), with levels falling to a nadir of 50-100 x 109/L at 4-5 days. Counts generally return
to normal at 7-10 days. Clinically stable preterm infants following this pattern have only a
very low risk of bleeding if platelet count remains above 50 x 109/L.
Early-onset neonatal thrombocytopenia without an obvious precipitant is much more of a

concern, and may be due to Neonatal Alloimmune Thrombocytopenia, with its high risk of
haemorrhage. Neonatal Autoimmune Thrombocytopenia is due to maternal platelet
autoantibodies (i.e. mothers are also at risk of thrombocytopenia), principally from ITP
and SLE. Infants with this disorder are at only low risk of significant haemorrhage (<1%),
but should have platelet count monitored daily. If count falls to <30 x 109/L, consider
intravenous immunoglobulin therapy.
Late-Onset Neonatal Thrombocytopenia
● Thrombocytopenia presenting in a neonate after the first 3 days of life should be

presumed to be due to sepsis or NEC until proven otherwise.
In such cases platelet count often drops rapidly, and to levels of 50 x 109/L or below.
Once the precipitant is controlled levels rise again over 5-7 days. These infants are at
significant risk of haemorrhage, though the benefit of transfusing with platelets isn’t clear-
cut (see platelet transfusion guidelines)
Risks of Thrombocytopenia
Thrombocytopenia increases the risk of bleeding, but this risk is hard to quantify for
individual infants. A few factors guide decision to transfusion:
● Neonates with active bleeding should be transfused to maintain platelet count

above 100 x 109/L.
● Other thresholds at which to transfuse depend on the perceived risk of
haemorrhage.
● Infants with NAIT should be considered separately as they are at relatively higher
risk at the same platelet count when compared to other aetiologies.
● Prophylactic platelet transfusion has not been shown to reduce morbidity in
neonates.
❍ Infants receiving transfusions have poorer outcomes (which may be due to
only the sickest neonates being transfused).

● Haemopoietic growth factors such as thrombopoietin and interleukin-11 have not
been shown to raise neonatal platelet counts significantly in a clinically useful time
period.
Platelet Transfusion Guideline
Many centres have developed consensus-based guidelines for platelet transfusion while
1
awaiting strong evidence for timing of intervention.
Platelet Count
Action
(x109)
<30 ● Transfuse if bleeding
● Consider transfusion in all other cases
30-49 ● Transfuse if bleeding

● Consider transfusion if:
❍ <1000g and <7 days
❍ Clinically unstable (e.g. fluctuating
BP)
❍ Previous major bleeding (e.g.
Grade 3-4 IVH, pulmonary

haemorrhage)
❍ Current minor bleeding
❍ Concurrent coagulopathy
❍ Requiring surgery or exchange
transfusion
50-99 ● Transfuse only if bleeding
>99 ● Do not transfuse
References
1 Roberts, I.A. and N.A. Murray, Thrombocytopenia in the newborn. Curr Opin Pediatr, 2003. 15(1): p. 17-23.
2 Murray, N.A., Evaluation and treatment of thrombocytopenia in the neonatal intensive care unit. Acta
Paediatr Suppl, 2002. 91(438): p. 74-81.
3 Sola, M.C., A. Del Vecchio, and L.M. Rimsza, Evaluation and treatment of thrombocytopenia in the
neonatal intensive care unit. Clin Perinatol, 2000. 27(3): p. 655-79.
guideline.
Guidelines on Investigation of Infants born to Reviewed by Salim Aftimos and

Mothers with Thyroid Disorders Wayne Cutfield
November
2002
For infants of mothers with Graves disease
● Request T4 on baby on day 3 and day 7.

● If T4 is abnormal, obtain a venous sample for T4, TSH, and if sufficient serum also
include T3.
● If there is any doubt on interpreting the results consult the Paediatric endocrine
service.
For all other infants of mothers with thyroid disorders
● Unless previously specified by the paediatric endocrinologist, request a Guthrie

test, and write on card to please send report to the requesting doctor. This will
ensure that a report is sent back within 2 days.
guideline.
Readmission for Top-Up Transfusion Reviewed by David Knight
January
2001
Occasionally, a baby will need a top-up blood transfusion after discharge from NICU or
PIN. These procedures are elective, and the decision will usually be made by the
specialist.
1. Discuss the timing of admission with the Clinical Charge Nurse.

2. Arrange for blood to be available
❍ Up to 4 months of age, it is not necessary to give blood bank a new
specimen, provided they have had a sample from the mother at birth.
❍ If there is no maternal sample, or if over 4 months of age, a sample for
cross match should be taken from the baby. If feasible, have this done
before the baby is admitted.
3. The baby is admitted to a side room on NICU as a day case. Admissions should
be arranged so that the transfusion is completed during the day.
4. Babies who are unwell and/or have possible infections are not to be readmitted to
NICU. If such a baby needs a top-up transfusion, this should be arranged with
Starship.
TRAINEE INTERNS IN NEONATAL PAEDIATRICS
Dr. Malcolm Battin, Dr Frank Bloomfield, and Professor Jane Harding.
Table of Contents
1. Introduction
2. Objectives
3. Levels of Newborn Care
4. Clinical Duties
5. Rotations at the different hospitals
6. General Reading Topics
7. Neonatal References on the Web
8. Other References
Ministry of Health
Click here to open a copy of the Log of Practical Experience in Neonatal Paediatrics
NZ Government
Introduction
©Copyright
Published: 11/01/2006 ● Neonatal paediatrics is intended to form some 30% of the whole 6-week attachment in Obstetrics
and Gynaecology.
● The experience in Neonatal Paediatrics will vary depending on the hospital. However, all trainee
interns should spend the equivalent of one week working with babies requiring special care. In
addition you should become familiar with the management of the normal baby during your
obstetrics rotation.
● It is essential that all Trainee Interns complete the blue form, Log of Experience in Neonatal
Paediatrics, by the end of their rotation in Neonatal Paediatrics. A failure to do so would result in
incomplete requirements for graduation. Please remember to have both your supervising registrar/
Neonatal nurse practitioner (NS-ANP) (if applicable) and the consultant Neonatologist or
Paediatrician sign these forms before turning them in. These forms are available in the Trainee
Intern Section of the O&G Folder, which was handed out during the 5th year. Alternatively a copy of
the form can be downloaded from this web site.
guideline.
Transfer of Infants from NICU to the Postnatal Ward Reviewed by Carl Kuschel
after a Brief Admission to NICU

July 2002
It is a priority for well infants to be with their mothers as soon as possible. Therefore, it
may be appropriate for infants who have required a brief admission to NICU to be
transferred to a postnatal ward without being reviewed by a specialist.
● Babies are not to be discharged directly to home from the NICU without review
by or consultation with the neonatologist on duty.
In general, infants who can be transferred without review by a specialist are those whose
transient problems with adaptation to extrauterine life have resolved. The problems most
likely to lead to a brief admission to NICU include hypoglycaemia, respiratory distress,
and mild hypoxic-ischaemic encephalopathy.
Infants can be transferred to the postnatal floor if
● Respiratory distress has settled and the infant is well oxygenated in room air
● Staff are satisfied with the infant's efforts at feeding
● Hypoglycaemia has resolved with oral feeds
● Any signs of mild HIE have resolved
● the Clinical Charge Nurse agrees with a decision to discharge the infant from the
NICU
Infants should be transferred under Paediatric care for later review by the paediatric SHO
or registrar. It may also be appropriate for blood glucose monitoring, and/or temperature
or respiratory observations to continue in the postnatal ward.
guideline.
Neonatal Transport Reviewed by David Knight
January
1998
Referrals from North

National Guidelines
Retrieval Shore and Waitakere Transports Urgent Retrievals
on Transfers
Hospitals
National Women’s has a Neonatal Transport Service to retrieve babies from outlying
hospitals and transport babies to other hospitals.
Retrieval
● Calls should be directed to the specialist on duty / on call.

● If a Registrar or NS-ANP receives a referral, it must be discussed with the
specialist (including out of hours). During normal working hours, the specialist is
either the Level 3 or the Level 2 specialist, depending on the type of referral.
● Contact the Newborn Clinical Charge Nurse (Pager 93 5744).

❍ She/he is responsible for organising an escort nurse, the equipment, the
ambulance and the aeroplane if necessary.
● The specialist decides on the medical escort.

● It will usually be one of the Level 3 or Level 2 registrars or an NS-ANP.
● Out of hours, cover of the unit during the transport should be discussed by the
specialist.
● RMOs (and NS-ANPs) will not be left with an unsafe workload when providing
cross cover for a transport.
Referrals from North Shore and Waitakere Hospitals
● Babies from these two hospitals have always been assessed by a paediatrician
prior to referral. Most babies are then transported in by staff from those hospitals.
● However, with sick or unstable babies if requested, National Women’s will send
out a transport team.
● When requesting a transport team, the Waitemata specialist will contact the Level
3 specialist in normal working hours and, at other times the Level 3 Registrar/NS-
ANP (who will then liase with the Level 3 specialist).
● Referrals for admission to Level 2, brought in by Waitemata staff usually go to the
Level 2 Registrar).
Transports
● Transports to other hospitals are usually elective.

● They are arranged by the medical team and the Newborn Clinical Charge Nurse.
● Babies on assisted ventilation or sick unstable babies will need a medical as well
as nursing escort.
Urgent Retrievals
● National Women’s has never had a neonatal "flying squad".

● The transport service is essentially to retrieve babies, stabilising them before
transport.
● It is the responsibility of the referring service to resuscitate and treat a baby until
our transport team arrives.
● However, we will attempt to respond urgently when required. The likely response
time should be discussed with the referring practitioner, to give him/her a realistic
idea of when our team is likely to arrive.
● Make sure that the referral to the St John’s Ambulance service is flagged Priority
One.
Umbilical Artery and Vein Catheterisation Reviewed by Carl Kuschel
Updated May
2001
Umbilical Venous Catheters Umbilical Artery Catheters Other Related Documents References
See also radiology images of UAC and UVC placement
● Umbilical vessels are relatively accessible in the newborn infant, particularly the very small and
very large infants.
● As a general rule, infants less than 1000g should have an umbilical venous catheter (UVC)
inserted on day 1.
● An umbilical arterial catheter (UAC) may be indicated if the infant has significant respiratory
disease (ventilated or >40% oxygen) or is likely to require significant blood sampling over the
first few days of life.
● Larger infants with significant respiratory distress may also require a UAC.
● Larger infants, especially sick infants, should have a UVC inserted. A double-lumen catheter
may be indicated if the infant requires significant support (see Catheter Choice below").
● Contraindications
❍ Omphalitis
❍ Omphalocele
❍ Necrotising enterocolitis (Consultants may choose to use UVC/UAC)
❍ Peritonitis
Umbilical Venous Catheters
Anatomy
● The umbilical vein is 2-3cm long and 4-5mm in diameter

● From the umbilicus, it passes cephalad and a little to the right. It joins the left branch of the
portal vein after giving off several large intrahepatic branches.
● The ductus venosus arises from the point where the UV joins the left portal vein.
Position
● It can be difficult to pass the catheter through the ductus venosus. There are some manoeuvres
that can assist in placement. These include:
❍ pulling the catheter back to about 4-5cm, then advancing the catheter whilst rotating the
catheter clockwise
❍ passing another catheter down beside the already mal-placed catheter. The path of the
second catheter may be through the ductus venosus.

❍ Do not force a catheter in if there is resistance.
● In an emergency, a UVC that remains in the portal circulation may be withdrawn until it lies in
the umbilical vein. Solutions which are not isotonic can be infused through this for a short
period of time until more suitable access is obtained.
3
Catheter size
● <1500g: 3.5F
● >1500-3500g: 5F
Catheter Choice
For infants who are term or near-term and sick enough to require central access (for example, sepsis,
MAS or PPHN), a 5F double-lumen UVC should be inserted.
For infants <1000g, a 3.5F double-lumen catheter should be considered if the infant is likely to need
inotropes or multiple infusions. This will be decided on an individual basis.
Insertion Distance
● If the shoulder-to-
umbilicus distance is
measured, the catheter
can be inserted the
appropriate distance
according to the graph on
2
the right .
● Remember to measure
from the skin at the base
of the stump where it
connects to the anterior
abdominal wall.
● Remember to add the
length of the umbilical
stump to the distance
inserted.
● Another method is to
calculate the distance
according to the weight of
the baby. See the graph
below to evaluate UVC
position.
❍ An approximation
of this is to use
the calculation of:
UVC length (cm) =
(1.5 x birthweight
6
(kg)) + 5.5
or half the UAC
length (calculated
6
below) + 1cm
Complications from UVC insertion include 3

Infection Thromboembolic Catheter Catheter Other
Malpostioned in Malpositioned in
the Heart and portal system
Great Vessels
● Pericardial ● Necrotising ● Perforation
effusion or enterocolitis of peritoneum
cardiac ● Perforation of colon ● Obstruction of
● Hepatic necrosis pulmonary
tamponade venous return (in
● Cardiac infants with
arrhythmias TAPVD)
● Thrombotic ● Plasticizer in
endocarditis tissues
● Haemorrhagic ● Portal
pulmonary hypertension
infarction ● Electrical hazard
● Hydrothorax (improper
(UVC lodged in or grounding of
perforating equipment, or
pulmonary vein) conduction of
current through
fluid filled
catheter).
Umbilical Artery Catheters
Anatomy
● The umbilical arteries are the direct continuation of the internal iliac arteries.
● A catheter passed into an umbilical artery will usually (but not always) enter the aorta via the
internal iliac artery.
● Occasionally it will pass into the femoral artery via the external iliac artery or into the gluteal
arteries.
❍ The femoral artery or gluteal artery are unsuitable sites for sampling, infusion, or blood
pressure monitoring.
Position
● There are two potential positions for the UAC. These are described as "high" or "low".
3
❍ The high position is at the level of thoracic vertebral bodies T6-T9. This position is
above the coeliac axis (T12), the superior mesenteric artery (T12-L1), and the renal
arteries (L1). This position is essentially "above the diaphragm".
3
❍ The low position is at the level of lumbar vertebral bodies L3-L4. This position is below
the structures as above, and is above the aortic bifurcation (L4-L5). The inferior
mesenteric artery arises from L3-L4. This position is essentially "above the bifurcation".
● Our preference is for UACs to be in the high position. If this is not achieved, the catheter can
always be withdrawn to a low position.
● There is debate over whether one position is better. The Cochrane Systematic Review 4
suggests that a high position is preferred as it is associated with fewer obvious vascular
complications, a probable reduction in the incidence of aortic thrombus, and longer catheter life.
Catheter Size 3
● <1200g: 3.5F
● >1200g: 5F
● Never use an 8F UAC
Insertion Distance
● If you know the length of the

infant, you can refer to the
graph on the right which
relates UAC distance to total
5
body length.
● This will result in placement
at approximately T8.
● Note that of all the birth
measurements, length is the
least reliable.
● Another option - and

one which is
particularly good if
you forget to measure
the shoulder-to-
umbilicus length - is
to calculate the
insertion distance
using the birthweight
and referring to the
6
graph on the right ,
or using the formula:
UAC distance
(cm) =
(birthweight
(kg) x3) + 9.
● The top lines on the

graph to the right are
for UAC position.
● The bottom lines on
the graph to the right
are for UVC position.
❍ The curved
lines above
and below the
straight lines
are the 95%
confidence
intervals.
● It does no harm to
insert the line a
centimetre further
than calculated, as
the line can be pulled
back slightly if
needed. However,
you should avoid
inserting the UAC so
far that it needs to be
removed from the
carotid or subclavian
arteries.
Complications from umbilical catheterisation include 3
Malpositioned Vascular accident Equipment related Other

catheter
● Vessel ● Thrombosis ● Broken catheter ● Haemorrhage
perforation ● Embolism/Infarction ● Transection of catheter ● Infection
● Refractory ● Vasospasm ● Plasticizer in tissues ● Necrotising
hypoglycaemia ● Loss of extremity ● Improper groudning of enterocolitis
(if catheter tip opposite ● Hypertension electronic equipment ● Intestinal necrosis or
coeliac axis) ● Paraplegia ● Conduction of current perforation
● Peritoneal perforation ● Heart failure (from through fluid-filled ● Transection of
● False aneurysm aortic thrombosis) catheter omphalocoele
● Air embolism ● Herniation of appendix
through umbilical ring
● Cotton fibre embolus
● Wharton-jelly embolus
● Hypernatraemia
Index of ● Umbilical catheterisation

Other ● Measurement of Central Venous Pressure via UVC
Related
Documents
References
1 Phelps DL, Lachman RS, Leake RD, O W. J Pediatr 1972; 81:337
2 Dunn PM. Arch Dis Child 1966;41:71
3 Fletcher MA, MacDonald MG, Avery GB. Atlas of procedures in Neonatology. JB Lippincott Co, Philadelphia 1983.
4 Barrington KJ. Umbilical artery catheters: catheter position (Cochrane Review). In: The Cochrane Library, Issue 4, 2000:
Update Software.
5 Rosenfeld W, Biagtan J, Schaeffer H, et al. Evaluation of graphs for insertion of umbilical artery catheters below the
diaphragm. J Pediatr 1981; 98:628.
6 Shukla H, Ferrar A. Rapid estimation of insertional length of umbilical catheters in newborns. Am J Dis Child 1986;
140:786.
guideline.
Urinary Catheterisation Reviewed by Charge Nurse -

Newborn
October
2005
Overview Catheterisation of Male Infants Catheterisation of Female Infants

Documentation Catheter Removal Minimisation of Trauma
Overview
Purpose ● This following policy/ recommended best practice outlines,

insertion of and care of a baby with an indwelling urinary
catheter.
Scope ● Applies to all medical and nursing staff working in Newborn

Services.
Associated ● Neonatology, a Large Clinical Manual, 4th Ed (1999).

documents ● Gray (1996) Atraumatic Urethral Catheterisation of
Children. Pediatric Nursing 22 (4) 306-310.
● Urine measurement and urinalysis
Catheterisation of Male Infant by Dr/NS-ANP
Follow the steps below to catheterise a male infant
Step Action
1 Do not use feeding tubes as urinary catheters.
2 Place infant supine, with the thighs abducted.
3 Clean the penis with antiseptic solution starting at meatus and moving down
the shaft of the penis.
4 Put on sterile gloves and drape the area.
5 Apply sterile KY lubricant to catheter tip.
6 Stabilise the penis with non-dominant hand, perpendicular to the body.
7 Gently insert the catheter into the meatus until urine is seen in the catheter.
8 Slight resistance may be felt as the catheter passes through the external
sphincter. Hold the catheter in place with minimal pressure – generally spasm
will relax after several minutes allowing easy passage.
NEVER FORCE THE CATHETER.
9 Connect to closed urinary collection system.
10 To prevent dislodgement, tape catheter securely to lower abdomen, rather than
the leg to help decrease stricture formation caused by pressure on the
posterior urethra.
Catheterisation of Female Infant
Follow the steps below to catheterise a female infant
Step Action
1 Place infant supine, with the thighs abducted.
2 Separate the labia and clean the area around the meatus with antiseptic
solution using anterior-to-posterior strokes.
3 Put on sterile gloves and drape the area.
4 Apply sterile KY lubricant to tip of the catheter.
5 With non-dominant hand spread the labia and identify the urethra.
6 Gently insert catheter until urine is visible in catheter tubing.
7 If catheter is accidentally inserted into vagina, leave in place and insert new
catheter anterior to the first catheter.
8 Connect to closed urinary collection system.
9 Secure the catheter by taping to infant’s leg.
Nursing Documentation/Care Post Insertion
● Document the size, type of catheter used and the time and date of insertion in
multidisciplinary notes.
Removal of Urinary Catheter
Follow the steps below to remove a urinary catheter
Step Action
1 The catheter is removed as soon as possible as requested by medical staff/NS-
ANP.
2 Gently withdraw catheter.
3 Document in multidisciplinary notes and on nursing chart time and date
catheter removed.
4 Observe and document urine output accurately after removing catheter.
5 Every 24hrs record urine output in ml/kg/hr.
Minimisation of Trauma
Step Action
1 Feeding tubes are not used as urinary catheters. Due to their construction of
more rigid material and their longer lengths as compared to urethral catheters
they can knot or cause trauma (ref: Smith AB, Adams LL. Insertion of indwelling urethral
catheters in infants and children: a survey of current nursing practice. Pediatric Nursing 1998 May-June;24
(3):229-34)
2 Do not force catheter.

3 Do not insert catheter further than length recommended as this could result in
kinking or knotting of the catheter.
4 Secure the catheter to prevent pulling.
guideline.
Urine Measurement and Urinalysis in Newborn Reviewed by Charge Nurse -

Services Newborn
October
2005
Overview Urine Measurements Urinalysis
Overview
Purpose ● The following policy/recommended best practice outlines

practice with regard to measuring and ward testing urine in
the Newborn Service
Scope ● Applies to all nursing staff working in Newborn Services.
Associated ● Evaluating the Kidney and Renal Function. In: Rudolph's

documents Pediatrics (20th Ed). Rudolph AM, Hoffman JIE, Rudolph
CD (Eds). Appleton and Lange, Conn, 1996. (p.1331-
1335).
● Urinary catheterisation
Urine Measurements
The following infants should have urine output monitored in the NICU.
Step Action
1 All babies admitted to Level 3 in their first 5 days of life.
2 All babies who suffered intrauterine or intrapartum asphyxia.
3 Infants with cardiac anomalies including symptomatic PDA.
4 Infants with any renal impairment/anomaly identified on ultrasound e.g. reflux.
5 Hydropic/oedematous infants.
6 Muscle relaxed infants.
7 Infants with renal failure.
8 Babies receiving the following medications:
● Diuretics
● Indomethacin
● Inotropes
● Steroids
Urine testing
The following infants should have regular urine testing:
Step Action
1 Infants less than 1000g
2 Infants less than 28 weeks gestation.
3 Infants receiving:
● Steroids
● Insulin
● Indomethacin
guideline.
Collection of Urine Specimens to Exclude Urinary Reviewed by Dr Belinda Austin

Tract Infection
December
1997
This guideline is intended for situations where therapy needs to be commenced within two
days. For other purposes, e.g. monitoring for infection in asymptomatic infants with renal
tract anomalies, infection screen in 'well' infants with risk factors, a bag urine may suffice
if negative on culture.
1. A suprapubic aspiration should be attempted. This should be performed prior to

handling the baby for any other invasive procedure. The method is as described in
any major Paediatric text.
2. If this is unsuccessful and other investigations can be delayed, a cloth nappy
should be put on and the aspiration re-attempted after 30-45 minutes as long as
the nappy is still dry.
3. If no urine has been collected after two attempts at aspiration of if therapy needs to
be commenced urgently, then a collection by urethral catheterisation should be
attempted.
4. Catheterisation should be performed by a member of the medical or nursing staff
who is familiar with the technique. A suitably sized plastic tube should be used.
This would most commonly be a 5 French feeding tube or a 3.5 umbilical catheter.
5. If difficulties are encountered passing the catheter, particularly in a baby boy, the
catheter should not be forced because of the risk of urethral trauma.
6. Ideally the first couple of drops of urine from the catheter should be discarded and
the remainder collected for analysis.
guideline.
Vascular Malformation Clinic Reviewed by Carl Kuschel
January
2001
A Vascular Malformation Clinic has been commenced at Starship Children's Hospital. It is

held in the Outpatient Department of Starship Hospital approximately 4 times a year.
Clinicians involved include:
● Plastic Surgeons
● Paediatric Surgeons
● ENT Surgeons
● Dermatologists
● Radiologists
● Pathologists
The clinic is coordinated by Mr Philip Morreau. In the first instance please contact Mr
Morreau's Secretary in order to refer patients to the clinic.
Telephone : 09 307 4949 ext 6098

Email: margarett@adhb.govt.nz
guideline.
Drainage of Ventricular Reservoirs Reviewed by Ana Kennedy,

Malcolm Battin, and Mr Andrew
Law (Neurosurgery)
August
2003
Indications Contraindications Aims of Treatment Equipment

Precautions Technique Complications References
Indications
● Clinical symptoms of increased intracranial pressure. Symptoms may include

❍ Apnoea, bradycardia
❍ Poor feeding
❍ Somnolence
❍ Hypotonia
● Ultrasound evidence of progressive ventriculomegaly
Contraindications
● Low circulating blood volume

● Cellulitis or abrasion over reservoir site
● Sunken fontanelle
Aims of Treatment
● To decrease progressive ventriculomegaly

● To allow head growth at a rate of <1cm per week
Click here to open a graph of ventricular ● Boys

index plotted against head circumference ● Girls
for:
Equipment
● Chlorhexidine or Povidine-Iodine skin preparation solution

● 25 gauge butterfly needle (may need 23g if CSF tenacious)
● Standard infant lumbar puncture set
● Sterile drapes to allow for maintenance of a sterile field
Precautions
1. Maintain strict asepsis.

2. Monitor and correct serum electrolytes every other day if more than 10ml removed
daily.
3. Be prepared to provide rapid fluid replacement should infant not tolerate large
volumes removed. Replace fluid removed with intravenous normal saline.
4. If skin breakdown occurs, select insertion site away from broken area.
5. Do not place IVs on same side of scalp.
Technique
1. Consider the use of Sucrose for analgesia if the baby meets the criteria.
2. Place the infant with head in neutral position in anticipation of a 20 to 25 minute
procedure.
3. Cut any long hair that interferes with the surgical area but do not shave operative
area.
4. Wearing sterile gloves, clean skin with chlorhexidine (or Povidine-Iodine) over the
reservoir and a surrounding circle of skin with a diameter of 4cm.
❍ Use light but firm contact.
❍ Allow to dry (2 minutes).
5. Position sterile drape to maintain a sterile field.

6. Cut the hub from the butterfly tubing.
7. Insert butterfly needle through skin just into reservoir bladder.
❍ Select an insertion site different from the one most recently used.
❍ Angle needle at 30 to 45 degrees from the skin.
❍ The base of the reservoir is metal so cannot be punctured.
7. Allow the cerebrospinal fluid (CSF) to drip into the CSF collection bottles. As the
pressure reduces, the flow rate will reduce accordingly and this should be used as
a guide for to when cease the procedure.
8. Limit total volume of CSF drained at each tapping to no more than 30ml or 15ml/kg
(whichever is less).
❍ The initial puncture should not exceed 10ml in volume and can be
increased on sequential taps at a rate of not more than 5ml/day.

9. Sample CSF for culture, cell count, glucose and protein every three days.
❍ If fluid is blood-stained (from old haemorrhage), biochemical analysis may
not be helpful.
❍ Culture dark fluid every three days.
10. Remove needle and hold firm pressure for 2 minutes or until CSF leakage from
skin stops.
11. Repeat drainage at intervals dictated by clinical response +/or ultrasound markers.
Repeat once a day but as often as twice daily. Aim to improve daily volume
sufficient to prevent progressive ventriculomegaly.
❍ The volume taken off each day should result in initial concavity of the
fontanelle, with some overlapping of the cranial sutures.

❍ If the sutures are still overlapping and the fontanelle concave the following
day, the interval between aspirations should be lengthened appropriately.

12. Follow response with cranial ultrasound scans.
Reservoirs are seldom removed even if they are no longer needed.
Complications
● Local skin breakdown

● Hypovolaemia
● Hypoproteinaemia
● Hyponatraemia (check electrolytes every 2-3 days)
● Wound or reservoir infection
● CSF leak from puncture site
● Obstruction of ventricular catheter
● Ventriculitis
● May precipitate further haemorrhage if large amounts of CSF removed
References
1 Fletcher M A, MacDonald M G, Schoonover V: Atlas of Procedures in Neonatology 1993. Lippincott

Williams & Wilkins.
2 Whitelaw A. Neonatal hydrocephalus - clinical asessment and non surgical treatment. In Fetal and
Neonatal Neurology and Neurosurgery. Eds Levene MI, Chervenak FA, Whittle M. Publisher - Churchill
LIvingstone 2001
guideline.
Vitamin K prophylaxis and Vitamin K Deficiency Reviewed by Peter Nobbs

Bleeding
May
2003
Recommendations Dosage Informed Consent Vitamin K Deficiency

Risk of Haemorrhagic
Haemorrhagic Disease of
Disease and Oral vs IM Potential Risks of Vitamin K Side Effects of Vitamin K
the Newborn
Vitamin K
Obtaining Konakion MM
References
Paediatric
Introduction
Purpose: This document has been formulated to provide recommendations for staff
working at National Women's Hospital, with regard to Vitamin K prophylaxis and
haemorrhagic disease of the newborn.
Scope: This document applies to all medical, nursing and midwifery staff working within
National Women's maternity and newborn services.
Associated documents: The table below indicates other documents associated with
this policy.

Board Policy ● Informed Consent
Hospital Policy ● N/A

Other ● Consensus Statement ‘Vitamin K prophylaxis in
the Newborn’. Fetus and Newborn Committee of
the Paediatric Society of NZ, The NZ College of
Midwives (Inc.), The NZ Nurses Organisation, The
Royal NZ College of General Practitioners, The
Royal NZ College of Obstetricians and
Gynaecologists. August 2000
● Patient Information :
Vitamin K for the Prevention of Haemorrhagic
disease of the Newborn – Information for parents.
● Guide statement and recommendations on
Vitamin K administration to newborn infants to
prevent Vitamin K deficiency bleeding in infancy:
The Royal Australasian College of Physicians
2001.
Supporting ● Refer to references at the conclusion of this

Literature document.
Recommendations
The August 2000 consensus statement of Fetus and Newborn Committee of the
Paediatric Society of NZ, The NZ College of Midwives (Inc.), The NZ Nurses
Organisation, The Royal NZ College of General Practitioners, The Royal NZ College of
Obstetricians and Gynaecologists recommends that all babies receive vitamin K
prophylaxis.
Dosages for IM and Oral Vitamin K
The recommended route of administration is intramuscular, being given at birth, and that
this should be as a single IM injection:
● Term babies 0.5-1mg IM soon after birth

● Preterm 0.5mg IM soon after birth
Parents should be advised that with intramuscular injection, the risk of haemorrhagic
disease of the newborn is extremely low.
If parents do not consent to IM but consent to oral vitamin K, this needs to be given in 3
separate doses according to the following regime:
● 2mg oral soon after birth

● 2mg oral at 3-7 days
● 2mg oral at 6 weeks
Parents should be advised that even with full compliance with this regime, cases of
Haemorrhagic Disease of the Newborn (HDN) are rare but still occur. Surveillance and
reporting of any bleeding is therefore important. The at risk time is up until the infant is
receiving something other than breastmilk in their diet.
If the infant vomits or regurgitates within 1 hour of an oral dose, this dose should be
repeated.
One difficulty with oral vitamin K is ensuring that repeat doses are administered. They are
often omitted. This is the responsibility of the LMC and the parents. Repeated doses
lowers further the risk of late HDN.
Informed Consent
The administration of vitamin K should have been discussed with the parents by the LMC
prior to labour or delivery. If paediatric staff are at the delivery the LMC should inform
them of the parents’ decision.
Verbal consent is necessary for vitamin K administration and is to be documented

in the Mother’s clinical record at the time of antenatal discussion and on the
delivery summary. Parents should be provided with the hospital information
booklet on vitamin K.
● Any change in consent to the route of administration should be clearly documented

on the Blue card or in the clinical record.
● If vitamin K is not given to these or any infants under paediatric supervision, this
should be discussed with the paediatric specialist on service.
Background
Vitamin K Deficiency
● Newborn babies have low levels of vitamin K. They have low plasma
concentrations and low levels of vitamin K dependent clotting factors. This
deficiency intensifies in the days after birth. Newborn levels are considerably lower
than maternal levels.
● Severe vitamin K deficiency can develop quickly in breast fed infants and can
result in the appearance of classic HDN during the first week of life or late HDN
during the first two months of life. Both forms of the disease can be severe,
causing brain damage and death.
● This situation is very unlikely to occur in formula fed infants as the levels of vitamin
K are higher in formula milk.
Haemorrhagic Disease of the Newborn

Early: ● Occurs in babies of mothers on anticonvulsants, especially
phenobarbitone and phenytoin or maternal coumarin products.
● It can also occur if mother is on anti-tuberculous therapy
(rifampicin and isoniazid). Two series reported bleeding (some
very serious) in the babies of 14 of 21 mothers and 8 of 111
mothers. Women in this situation should be treated with oral
1
vitamin K 20mg/day for 2 weeks prior to delivery.
Classical: ● Usually bleeding between day 2 and 5.

● Incidence of 0.4 to 0.7/100 births with no vitamin K prophylaxis.
● Bleeding sites include intracranial, gastrointestinal and umbilical
haemorrhage.
Late: ● 2-12 weeks of age.

● Usually occurs in breast fed babies who have not received
vitamin K.
● Bleeding can be severe, with half being intracranial.
● This is often associated with cholestatic liver disease, however
this liver disease may be asymptomatic and bleeding is the first
clinical manifestation.
Risk of Haemorrhagic Disease and Oral vs IM Vitamin K
The Risk of Haemorrhagic Disease (HDN)
● The known risk factors for HDN are:

❍ Maternal anticonvulsant, especially phenobarbitone and phenytoin
❍ Surgery
❍ Breastfed infants
● Some authors have recommended policies of selective vitamin K administration to

‘high risk’ infants. There is no basis for their definition of ‘high risk’ (Babies with
traumatic delivery, low birthweight and sick babies are traditionally thought to be at
greater risk).
13
● Late HDN occurs almost exclusively in breast fed infants.
Oral vs IM Vitamin K
● Oral vitamin K does not fully protect against late haemorrhagic disease.
● Data is available from Australia and Europe. The topic has recently been
extensively reviewed and the data and recommendations of this policy reflect upon
12 13
these studies. , .
15
Australia Europe
Expressed as rate per
100,000 babies
No Vitamin K 34.4
1 does of oral Konakion(R) 20
2 doses of 2mg oral 5
Konakion MM(R)
3 doses of oral Konakion 4.1 2.6
(R)
3 doses of 2mg oral 0.44

Konakion MM(R)
1 dose of IM Konakion(R) 0.2 0.0
Potential Risks of Vitamin K
There are now 10 studies investigating whether there is an association between vitamin K
and childhood cancer. There is no proven risk of cancer or leukaemia. A risk of solid
tumours can almost definitely be ruled out but a small risk of leukaemia cannot be
excluded. 1-10
Six studies showed no link with cancer. In the studies that show an increased risk of
cancer or leukaemia, the vitamin K policies were to administer IM vitamin K or any vitamin
K to selected babies only. Some of the findings may be explained by there being other
6 7 13
risk factors associated with these selected babies. , ,
There is no established risk of childhood cancer with IM vitamin K. Any small and
unproven risk has to be balanced against the known risk of developing classic and late
HDN with potentially fatal or debilitating outcomes if either no vitamin K is administered or
even if the oral route is chosen. An additional advantage of the IM route is now a long
established time of usage with this with no proven safety issues. The oral empirical route
had not been in place for many years and there is still a chance of some as yet unknown
risk that may become apparent with time. This must be balanced against the proven risk
of serious bleeding in a small but not easily identifiable group of babies with either no
vitamin K or the oral regimes.
Supporting Literature
● Golding’s original study showed an association between childhood cancer and

maternal smoking and drug administration to the baby (vitamin K was the
2
commonest drug; there was no information whether this was oral or IM).
● A case-control study by the same authors showed an increase risk of childhood
cancer after IM vitamin K administration, but not oral vitamin K. The confidence
3
intervals of IM vs oral vitamin K overlapped.
4
● A study of 54,000 deliveries in USA found no link with childhood cancer.
● A study of 1,384,000 babies in Sweden showed no link between IM vitamin K and
5
childhood cancer.
● Two case controlled studies of 132 and 272 children with cancer did not support
6 7
an increased risk of cancer in babies given IM vitamin K. ,
● A population based case-control study of 515 children in Scotland did not support
a relationship between IM vitamin K and childhood cancer. 8
● Borderline significant association between IM vitamin K and childhood cancer
found in a case controlled study in England. Possibly explained by an effect of
9
abnormal delivery.
● An ecological study by the same authors found there was unlikely to be an
10
increased risk of childhood cancer attributable to vitamin K given to newborns.
● Another case control-study of 685 children with cancer showed no relationship
between IM vitamin K and all cancer or leukaemia, but there was an association
with leukaemia developing in the 1st 6 years. These cases/controls were born in
hospitals that gave vitamin K only to ‘at risk’ babies. However, no association was
11
found in babies from hospitals that give all babies vitamin K.
Side Effects of Vitamin K
These are largely confined to local effects and the side effects of an IM injection.
Exacerbation of jaundice and haemolysis does not occur with the doses now used or the
naturally occurring lipid soluble vitamin K1 (Konakion(R) ). These were problems years
ago with water-soluble vitamin K given in very large doses. IV administration can produce
local reactions. The MM preparation is relatively new.
Risks associated with the injection technique include infection, irritation of the injection
site or nerve and muscle damage as the Vitamin K injection must be given deeply into the
muscle. These are very rare complications.
Obtaining Konakion MM Paediatric
General Information
● Konakion MM Paediatric 2mg in 0.2ml ORAL or injection is held in the Pharmacy

Imprest Cupboard on Wards 32, 33, 34, Delivery Unit, Theatre and NICU.
● When this preparation is prescribed orally the second and third doses may need to
be administered after the baby has been discharged from hospital.
● This is to be documented on the discharge summary, Tamariki Ora booklet and on
referral to the Well Child provider.
● If National Women's is the LMC or providing postnatal care, the second and third
doses required after patient discharge must be administered or supervised by the
midwife carrying out the postnatal homecare visits.
● Administration of all doses is to be documented in the baby’s clinical record.
● The person doing the six week check is to be informed if the baby needs oral
vitamin K.
● The GP should also be made aware of:
❍ baby who has not had any vitamin K
❍ whether baby had oral or IM dose.
Dispensing & Administration of 2nd and 3rd doses
● For babies under the care of ADHB Domino Midwives, or Home Care Midwives the
second and third doses can be administered from ADHB stock as follows:
● Vit K (PO) is prescribed on an ADHB Drug Chart with a patient label

attached.
● Fax the chart to Pharmacy (fax 3801).
● Indicate on the chart if the Midwife is to collect the medication from
Pharmacy, alternatively the medication can be sent to a ward.
(Drugs can not be issued directly to patients.)
● Pharmacy will dispense the medication with the understanding that
the administration is undertaken or supervised by the Domino
Midwife or Homecare.
Obtaining Konakion Out of Pharmacy Hours
● If oral Konakion is required outside pharmacy hours it will be necessary to contact

the On Call Pharmacist through the Duty Manager.
References
1 von Kries R. Neonatal vitamin K prophylaxis: the Gordian knot still awaits untying. BMJ 1998; 316: 161-2
2 Golding J. Factors associated with childhood cancer in a national cohort study. Br J Cancer 1990; 62: 304-
8.
3 Golding J. Childhood cancer, intramuscular vitamin K, and pethidine given during labour. BMJ 1992; 305:
341-46.
4 Klebanoff MA, The risk of childhood cancer after neonatal exposure to vitamin K. N Engl J Med 1993; 329:
905-8
5 Ekelund H, Administration of vitamin K to newborn infants and childhood cancer. BMJ 1993; 307: 89-91
6 Ansell P, Childhood leukaemia and intramuscular vitamin K: findings from a case-control study. BMJ 1996;
313: 204-5
7 von Kries R, Vitamin K and childhood cancer: a population based case-control study in Lower Saxony,
Germany. BMJ 1996; 313: 199-203.
8 McKinney PA. Case-control study of childhood leukaemia and cancer in Scotland: findings for neonatal
intramuscular vitamin K. BMJ 1998; 173-7.
9 Passmore SJ. Case Controlled studies of relationship between childhood cancer and neonatal vitamin K
administration. BMJ. 1998; 316: 178-84.
10 Passmore SJ. Ecological studies of relation between hospital policies on neonatal vitamin K administration
and subsequent occurrence of childhood cancer. Br Med J 1998; 316: 184-9
11 Parker L. Neonatal vitamin K administration and childhood cancer in the north of England: retrospective
case-control study. Br Med J 1998; 316: 189-93
12 Cornellison M., et al. Prevention of Vitamin K deficiency bleeding: efficacy of different multiple oral dose
schedules of Vitamin K. European J of Paed 1997; 156: 126-130.
13 Zipursky A. Prevention of Vitamin K deficiency in a newborn. Brit J Haematology 1999; 104: 430-437.
14 von Kries A.. Oral mixed mycellular Vitamin K for the prevention of late Vitamin K deficiency bleeding. Arch
Dis Child Fetal Neonatal Ed. 2003; 88: F109-112.
15 Loughnan P, et al. The frequency of late onset haemorrhagic disease (HD) in Australia with different
methods of prophylaxis, 1993-1997. An update. J Paediatr Child Health 1999;38:A8.
guideline.
Weighing Babies in NICU Reviewed by Jean Bertram and

Tracey Gyde (CNEs)
June
2005
Weight on Admission to
Level 3 Infants Level 2 Infants Additional Notes
NICU
Weight on Admission to NICU
All babies are to have a weight on admission to NICU.
● Infants who have been weighed in theatre or delivery unit do not need to be
reweighed on admission to NICU within the first 24 hours.
● All infants who are more than 24 hours old must have a new weight taken on
admission to NICU.
Level 3 Infants
● Level 3 infants are to be weighed on alternate days unless a specific order for daily
weighs is initiated after discussion on ward round.
● Infants are weighed from day 5 unless requested earlier by medical staff.
● Infants are not weighed routinely if they have:
❍ chest drains in situ
❍ are being ventilated on High Frequency Oscillatory Ventilation
● The nursing weight chart is not required unless a specific medical request to
document each weight.
Level 2 Infants
● To be weighed twice weekly on Sundays and Wednesdays unless a specific order

for alternate day or daily weighs is initiated after discussion on ward round
● Infants are weighed from day 5 unless requested earlier by medical staff.
Additional ● When there are concerns over weight gain/weight loss for any
notes baby in the service, a nursing weight chart will be completed
showing each weight clearly. This chart will be an important
document for both medical and nursing carers.
Weight Conversion Calculator

Kilograms- to- Pounds and Pounds- to- Kilograms © Carl Kuschel
June 2004
Weight in
1 Kg equals 2.2046 lb
grams g
Weight in
1 lb equals 454g; 1 oz = 28.3g
Pounds lb oz
Calculate Reset
guideline.
Zinc Deficiency in Neonates Reviewed by Barbara Cormack

(Dietitian)
July
2004
Risk Factors Signs Treatment References
● Most Zinc is accumulated during the 3rd trimester of pregnancy.

● After iron it is the most likely trace element to be deficient.
Risk Factors
● Premature birth
● Vegan/vegetarian mother (or a mother who has stopped eating red meat during
pregnancy)
● Accelerated growth - growth is the major determinant of Zinc requirement
● Thiazide diuretics - hydrochlorthiazide increases excretion of Zinc
● Dexamethasone - may impair Zinc absorption
● Unusually low ALP (a Zinc dependent enzyme important for bone metabolism,
which is often high in premature babies with osteopenia)
● Low albumin-Zinc is transported bound to albumin so mild hypoalbuminaemia may
alter serum Zinc concentration
● Large stool or ostomy output - short bowel syndrome etc.
Signs of Zinc Deficiency
● Zinc <7.5 mmol/L is highly suggestive of deficiency (reference range 12-20) but it
is acknowledged there are problems with reliability of measuring serum zinc
● Growth failure - adequate energy and protein intake
● Diminished food intake usually due to reduced ability to taste and smell - loss of
appetite
● Skin lesions
● Poor wound healing
● Hair loss
● Protein synthesis
● Immune function
● If severe - diarrhoea, behaviour changes, skin lesions, poor growth
NB: The only definite method of diagnosing Zinc deficiency is to note the clinical and
biochemical responses to Zinc supplementation.
Guidelines for the Treatment of Zinc Deficiency
2
If poor growth and serum zinc is <8 mmol/L Tsang recommends double or triple the RDI
(1.2mg/kg/day X 2 or 3)
1. Prescribe Zinc Sulphate - 1 to 2 mg elemental Zinc/kg/day

2. Ensure an adequate intake of Zinc from feeds;
❍ If <2.5kg Fortified EBM or Preterm formula
❍ If >2.5kg Unfortified EBM or Term formula (not Soy)
3. Monitor serum Zinc weekly.

4. Treatment is continued until biochemical indexes are normal and growth has
improved
References
1 Groh-Wargo S, Thompson M, Hovasi Cox J, Hartline J. Nutritional Care for High-Risk Newborns, 3rd
Edition, Illinois, Precept Press, 2000
2 Tsang R, Lucas A, Uauy R, Zlotkin S. Nutritional Needs of the Preterm Infant. Scientific Basis and Practical
Guidelines. London: Caduceu Medical Publishers, 1993
● By following the links to the left, you are acknowledging that you have read and
understood the disclaimer below.
● All guidelines and protocols have been written primarily for use within
the NICU of National Women's Health and take into account the best
available evidence at the time of their creation and review, as well as
current recommended best practices.
● Protocols and guidelines are reviewed regularly and altered as required.
● All care has been taken to ensure the accuracy of these guidelines and
protocols.
● No responsibility or liability is accepted for the use or misuse of these
protocols and guidelines outside of National Women's Health Newborn
Ministry of Health Intensive Care Unit.
NZ Government ● The electronic version is the only version which is in current use.
● The use of printed copies of protocols and guidelines held within this
website does not guarantee that they are still valid and in current use.
©Copyright ● The reader should take all due care to ensure that the information
Published: 26/01/2006 contained within the following pages is accurate.
● Note: Auckland District Health Board Policies and Procedures are
available only through the Intranet site
Neonatal Trials Register
Trials in Progress Correlations of bedside

Ultrasound scans to
EEG monitoring with LessMAS
determine longline position
detailed EEG recordings
INIS COIN Methadone and
(International Neonatal (CPAP or Intubation) neurological outcomes
Immunotherapy Study)
Recently Temporal changes in DASVC EEG and longterm

Completed Trials EEGand Prediction of (Descending Aorta and outcomes in preterm Head USS reporting
White Matter Injury SVC) infants
DART
Steroid Follow-Up Study ACTORDS (Dexamethasone - A Dexamethasone Dose Trial
Randomised Trial)
Selective Head Cooling
Ministry of Health for Perinatal Asphyxia
ACTOMgSO4 SGA Study
NZ Government
Trials being
considered: BOOST 2 and POST-ROP
©Copyright
Published: 11/01/2006
Study Name Correlations of bedside EEG monitoring with detailed EEG recordings
Local Claire West, Malcolm Battin, Jane Harding

Investigators
Aim To determine the usefulness of bedside EEG monitoring techniques in term

infants at risk of seizures.
Comments
Study Name LessMAS (Lavage of Exogenous Surfactant Suspension for Meconium Aspiration
Syndrome)
Local Multicentre internation trial co-ordinated from Melbourne (Associate Professor

Investigators Peter Dargaville)
Local participants: Malcolm Battin, Carl Kuschel.
Aim To determine whether lavage with surfactant in term infants with MAS results in
improved respiratory outcomes.
Comments This multicentre RCT aims to recruit babies with severe MAS. Babies will be
randomised to a lavage procedure using diluted surfactant, or to continued
treatment without lavage.
Inclusion criteria:
● Term infants <24 hours old and >2.0kg

● Respiratory failure secondary to MAS
● Mechanical ventilation with MAP >12cm H2O
● Alveolar-arterial oxygen difference >450mmHg
Exclusion criteria:
● Severe neonatal encephalopathy

● Major congenital anomalies
● Known or suspected structural cardiac disease
● Extreme cardiorespiratory instability precluding large volume lung lavage
Link to the LessMAS website
Study Name The usefulness of cardiac ultrasound in determining longline tip position
Local Kitty Bach, Nicky Webster, Alan Groves, Carl Kuschel, Malcolm Battin
Investigators
Aim To evaluate whether cardiac ultrasound scans can accurately determine the
position of long line tips.
Comments There is much debate about the reliability of radiographic studies in determining
longline position. As inappropriately placed line tips can result in significant
complications, this study aims to demonstrate whether ultrasound scanning can
determine tip position as reliably as other available methods.
Study Name INIS - International Neonatal Immunotherapy Study
Local Multicentre international trial co-ordinated in Australasia from Sydney (Professor

Investigators Wiliam Tarnow-Mordi)
Local investigators: Ana Kennedy, Malcolm Battin, Frank Bloomfield, Jane
Harding.
Aim To evaluate whether the use of immunoglobulin in infants with clinical sepsis
results in improved long-term survival without disability.
Click here to open the INIS study page.
Comments There is evidence to suggest that the treatment of life-threatening sepsis with
immunoglobulin may improve survival in neonates. This multicentre randomised
study seeks to answer this, looking at long-term outcome in infancy.
The website for the trial is based at
www.npeu.ox.ac.uk/INIS
Study Name Temporal changes in Electroencephalography and prediction of neonatal white

matter injury by Spectral Edge Frequency
Local Claire West, Malcolm Battin, Jane Harding

Investigators
Aim In infants <32 weeks gestation we aim to examine:
1. The relationship between the electrophysiologic response to injury,

ultrasound imaging and neurodevelopmental outcome.
2. The changes in electrophysiologic response over time and relate them to
recovery from injury and normal maturational changes.
3. The changes in electrophysiology that occur with the physiologic changes
(heart rate, respiratory rate and oxygen saturation) that occur frequently
during the care of premature infants.
Comments This is an extension of the study "
Prediction by EEG of neurodevelopmental outcomes in preterm infants
We will be studying a larger range of gestational ages (<32 weeks) over the period
of their admission to determine maturational changes in addition to examining the
ability of the EEG to predict long-term neurodevelopmental outcome. Concurrent
download of physiologic data with the EEG will allow the relationship between
these to be examined.
This study has ceased enrolling as the sample size has been met.
Study Name DASVC Study (Descending Aortic and Superior Vena Caval Flows
Local Alan Groves, Carl Kuschel, David Knight, Jon Skinner

Investigators
Aim To measure descending aortic and superior vena caval blood flow in newborn
term and preterm babies using Doppler ultrasound
Comments The DASVC trial will assess the accuracy and reproducibility of these relatively
new measures of blood flow, as well as trying to correlate them with clinical
outcomes and other haemodynamic measures.
Study Name Prediction by EEG of neurodevelopmental outcomes in preterm infants
Investigators Claire West, Malcolm Battin
Aim To examine the relationship between the electrophysiologic response to injury,

ultrasound imaging and neurodevelopmental outcome in preterm infants of <28
weeks gestational age using a real-time EEG analytical system.
Comments Ultrasound imaging within the first week may not identify those infants who
subsequently develop white matter injury. Thus alternative methods for early
detection of white matter insult need to be explored. Recent studies in preterm
fetal sheep show that a marked slowing of cortical electrical activity was
associated with the development of lesions within the underlying white matter
tracts. There has also been interest in the use of EEG to predict the presence and
timing of white matter injury in preterm infants.
Study Name Head Ultrasound Reporting in Preterm Infants
Investigators Jane Harding, Deborah Harris, Phil Weston
Aim To determine the extent to which variability in head ultrasound scanning and
reporting might account for variation in the rate of periventricular haemorrhage
reported from different neonatal units.
Comments Data collected from all newborn intensive care units in Australasia shows that
there is a wide variation in the rate of IVH. However some of this variation may be
due to different techniques use in obtaining, storing and reporting the scans. This
is a multicentre study in which a selection of scans from each unit are copied and
reread to determine how much of the variation is technical, and how much may be
due to differences in treatment or the populations of babies treated.
Study Name COIN - CPAP or Intubation in Premature Infants
Investigators Co-ordinated from Melbourne (Professor Colin Morley).

Local investigators: David Knight and Jane Harding
Aim To evaluate whether the use of CPAP or IPPV in preterm infantswith respiratory
distress from birth leads to reduced respiratory morbidity.
Comments Despite the introduction of nasal CPAP to many units over recent years, there is
little evidence in the literature evaluating benefit (or harm). This large mulitcentre
trial aims to randomise infants at birth to CPAP or intubation. The primary
outcome will be the incidence of Chronic Lung Disease.
Study Name Neurological outcomes of infants exposed to Methadone during pregnancy.
Investigators Lianne Woodward, Terrie Inder, Trecia Wouldes, Carl Kuschel
Aim To examine neuroanatomical brain development in infants exposed to methadone,

specifically examining effects on health and neurological development.
Comments Methadone has been shown to have therapeutic advantages for women but the
effects on the fetus are less well defined. Infants are generally more premature,
smaller, and have smaller heads than infants born to polydrug using or non-drug
using mothers. The smaller head circumference appears to persist into childhood
and raises concerns about the potential to affect neurodevelopmental outcomes.
This study will undertake quantitative MRI studies of infant brains, and will
correlate neonatal findings with subsequent longterm neurological outcomes.
Study Name Steroid Follow-Up Study
Investigators Jane Harding, Anthony Rodgers, Stuart Dalziel, Natalie Walker
Aim To determine the longterm effects of antenatal exposure to glucocorticoids.
Comments Steroids are given to women at risk of preterm birth to help mature their baby's
lungs. This treatment was first developed at National Women's Hospital in a study
by Professors Liggins and Howie in the late 1960s and early 1970s. In this study
the babies (now adults) whose mothers participated in the original trial are being
followed up to determine whether there are any longterm effects on their health.
Study Name ACTORDS Trial

Local Jane Harding, Malcolm Battin, Coila Bevan
Investigators
Aim To investigate the effects of repeated doses of antenatal steroids on neonatal

growth, HPA axis, and cardiovascular system.
Comments The ACTORDS trial is a large multicentre trial of repeated doses of antenatal
steroids. In addition to collecting the basic neonatal data required for the trial we
have an add-on component studying neonatal growth, endocrine and
cardiovascular effects.
Study Name DART - Dexamethasone - A Randomised Trial
Enrolment in this study has now ceased at the instruction of the

Steering Committee due to low recruitment.
Investigators Multicentre international trial co-ordinated from Melbourne (Associate Professor

Lex Doyle)
Local investigators: Carl Kuschel, Jane Harding
Aim To evaluate whether postnatal steroid use (Dexamethasone) leads to improved

long-term outcomes (neurodevelopmental status at 2 years)
Comments There has been increasing concern over recent years about steroid use. Although
the used of postnatal Dexamethasone reduces time spent on ventilation and may
reduce CLD, there are concerns about disability rates associated with its use.
This study seeks to answer the question of whether the use of dexamethasone to
facilitate weaning is associated with long term benefit or harm.
Study Name Comparison of two dosing regimes of Dexamethasone for the Prevention of
Chronic Lung Disease
This study has ceased enrolling as the DART study has been entered.
Investigators Jane Harding, Carl Kuschel, David Odd, Damien Armstrong
Aim To compare a 6-week course of Dexamethasone against an individualised course

in infants at risk of CLD.
Comments Postnatal steroids commenced between 7 and 14 days in infants who are
ventilated have been shown to significantly reduce mortality and the incidence of
CLD. The 42-day course has been shown to be effective when compared with
shorter courses, but there is a general reluctance to prescribe such a long course
for infants who may have a dramatic effect within a few days of the drug
commencing. This study randomises infants to a 42-day course or to an
individualised course – the latter of which weans to a low-dose much more rapidly.
Study Name Selective Head Cooling following Perinatal Asphyxia
Investigators Malcolm Battin
Aim To determine whether selective head cooling in term infants with moderate to
severe HIE results in improvements in 18 month neurodevelopmental outcome
and survival.
Comments Inclusion criteria
● >36 weeks GA
● Encephalopathy
plus ONE of the below
● Continued need for resuscitation at 10 mins of age

● Cord / arterial pH < 7.00
● Base deficit > 16 mmol/l
Study Name ACTOMgSO4 Trial
This study has ceased enrolling.
Investigators Lesley McCowan, Jane Harding

International Coordinator: Prof Caroline Crowther (Adelaide)
Aim To determine whether administration of magnesium sulphate to women about to

deliver very a preterm infant reduces the risk of the child developing cerebral palsy
or developmental delay.
Comments Retrospective studies have reported that magnesium sulphate given to pregnant
women may help protect their babies from developing cerebral palsy. This large
multicentre trial randomised >1000 women about to deliver at <30 weeks
gestation to magnesium sulphate or placebo infusion within 24h of delivery.
Recruitment is complete and follow-up of the babies is under way. Results are
expected in late 2003/early 2004
Study Name SGA Study
This study has ceased enrolling.
Investigators Jane Harding, Lesley McCowan
Aim To determine antenatal and perinatal predictors of outcome in children born small
for gestational age
Comments Children who grow poorly before birth are at increased risk of growth and
developmental problems in childhood, and of developing heart disease and
diabetes as adults. However it is difficult to predict which children will do well, and
which will have difficulties. In this longitudinal study some 200 babies who were
small from before birth are being followed with regular measurements of their
growth and development to 6 years of age. Identification of factors which predict
future problems in these children will allow early intervention in the future.
Future Trials Under Consideration
Study Name BOOST 2 and POST-ROP
Investigators Multicentre international trial with Australasian involvement
Aim To determine appropriate oxygen targets in preterm infants

Comments Oxygen is the commonest neonatal therapy. Unfortunately, very premature infants
are particularly sensitive to its toxic effects. The optimum range of oxygen
saturation in the first few weeks is unknown and no randomised controlled trial
(RCT) has addressed this question. High arterial oxygen levels predispose to
retinopathy of prematurity (ROP), the leading cause of blindness and visual
disability in newborns. High inspired oxygen concentrations exacerbate neonatal
chronic lung disease (CLD), which is associated with poor growth, neuro-
developmental impairment and long term respiratory morbidity. However,
insufficient oxygen leads to poor growth and neuro-developmental impairment.
This study aims to enrol 1300 infants.
Last updated January 11, 2006

guideline.
Blood and Blood Products Authorised by Charge Nurse -

Pre-Administration Checking Newborn
April
2006
Step Action
1 The unit of blood/plasma must be checked by a Registered Nurse with a
current IV certificate and checked by a RN or Enrolled Nurse, Registered
Obstetric Nurse with current IV certificate.
2 Check Agreement for Treatment (CR0111) form is signed by parent.
3 Check maternal antibody status and baby’s blood group if known.
4 Baby’s identity - the baby’s identification band is checked against front sheet of
clinical records.
5 Swinging label is checked with baby identity and component issue form.
6 Swinging label is checked with label on bag for donation number, donation
group, expiry date and/or collection date to determine age of blood. MUST BE
LESS THAN 35 DAYS OLD. To limit donor exposure, dedicated units may be
available for small babies who will require up to eight transfusions in the first
four weeks of life.
7 Check blood is leukodepleted.
8 The unit of blood/plasma/platelets is checked for abnormalities (visual
inspection).
9 Check prescription order and amount to be given (blood transfusion/IV fluid
balance chart).
10 Administration of each paediatric pack should take no longer than 2 hours –
no exceptions. If the amount of blood required must be given over 3 hours, a
further pack of blood will need to be obtained from blood bank.
guideline.

Administration Newborn
April
2006
Step Action
1 No substance is to be added to blood or blood products.
2 Ensure blood syringe is not left in contact with heat source (e.g. under radiant
heater or in incubator)
3 If baby is charted Frusemide give via the injection port. (Flush with saline
before and after giving Frusemide.)
4 Rotate syringe periodically to prevent pooling of red cells.
guideline.

Monitoring and Documentation Newborn
April
2006
Monitoring Documentation
Monitoring
Follow the steps below to ensure safety of the baby during transfusion.
Step Action
1 All blood transfusions will be documented using a blood transfusion/IV Fluid
Chart (pink chart CR5541).
2 Before commencement of blood, baseline recordings of temperature, heart
rate, respirations and blood pressure will be taken and then repeated 15
minutes after commencement of blood.
3 Temperature, heart rate and BP will be recorded every 30 minutes.
Documentation
Follow the steps below regarding documentation of the transfusion.
Step Action
1 When checking the unit of blood, the swinging label is checked and signed by
both Nurses.
2 Ensure that donation number (sticky label) is placed in the patients
clinical record as proof of transfusion.
guideline.

Transfusion Reactions Newborn
April
2006
Transfusion Reactions Management
Transfusion Reactions
Type of Symptoms and Signs

Reaction
Febrile ● Pyrexia, rigors.
Circulatory ● Increase in blood pressure, heart rate and respirations.

Overload ● Pulmonary oedema, dyspnoea, increase in urinary output
Allergic ● Urticaria, facial oedema, dyspnoea, hypotension
Haemolytic ● Collapse with hypotension.

● Shock, pyrexia, rigors, haemoglobinuria, haemoglobinaemia,
oliguria, later uraemia.
Infected Blood ● Pyrexia, profound collapse and shock, pallor, dyspnoea, low
blood pressure, rapid pulse.
Management of Transfusion Reactions
● Follow the steps below to manage the baby’s reaction to blood and blood products.
Step Action
1 STOP THE TRANSFUSION IMMEDIATELY.
2 The Nurse contacts the Doctor/NS-ANP immediately the baby manifests
any sign of reaction.
3 Babies vital signs must be recorded and documented.
4 Maintain patency of cannula using a new giving set and 0.9% sodium
chloride.
5 Check label and recipient ID information is correct.
6 Send NZBS Notification and Investigation of Adverse Transfusion form and
the blood product with IV giving set attached in a plastic bag to the Blood
Bank immediately to allow investigation of the cause of the reaction.
7 Notify Blood Bank by phone; discuss urgency of follow-up tests and further
transfusion needs.
8 Take a sample of baby’s blood (from a different vein). Blood group
serology and EDTA – in purple top tube - send to Blood Bank. FBC +
serum biochemistry.
9 Consider need for blood cultures is sepsis suspected. Blood gases if
respiratory distress present. Urine check for haemoglobinuria.
Coagulation screen if bleeding.
10 Parents of baby are informed.
guideline.
PHYTOMENADIONE
Reviewed by Dr Peter Nobbs and Dorothy Cooper
Vitamin K, Konakion
March 1997
Dose and Administration
Prophylaxis
1. Intramuscular (Preferred route) 0.5 - 1 mg at birth.
Treatment
1. 1 mg IM. Repeat as necessary.
Indications
1. Prophylaxis and therapy of haemorrhagic disease of the newborn.

2. Treatment of hypoprothrombinaemia secondary to factors limiting absorption or
synthesis of vitamin K.
1. Severe hepatic dysfunction.

2. Bleeding disorders that are not vitamin K dependent.
Clinical Pharmacology
Phytomenadione is a synthetic preparation of vitamin K. The presence of vitamin K is

essential for the formation within the body of prothrombin, factor VII, factor IX, and factor
X. Lack of vitamin K leads to increased tendency to haemorrhage.
Vitamin K does not counteract the anticoagulant action of heparin.

Systemic availability after IM administration is about 50%.
The primary distribution compartment corresponds to the plasma volume. Vitamin K is

highly bound (90%) to human plasma protein. Metabolism is hepatic, by degradation.
Vitamin K is bound to glucuronic acid and excreted in the bile and urine. Less than 10% is
excreted unchanged in the urine. It is not significantly stored in the body and is
synthesised by the bacterial flora of the intestine. The elimination half-life in the plasma is
1.5 - 3 hours.
Possible Adverse Effects
1. Pain, swelling and nodules at injection site.

2. Jaundice, kernicterus with large doses.
3. Bronchospasm.
4. Rapid IV injection can cause flushing of the face, sweating, cyanosis, peripheral
vascular collapse, death.
Special Considerations
1. Antagonises the activity of dicoumarol and its derivatives.

2. Will not counteract the anticoagulant action of heparin.
3. Intravenous administration should be reserved for potentially fatal haemorrhage.
4. Measure prothrombin time if giving repeated doses.
5. Prothrombin synthesis takes up to 2 hours to occur following parenteral
administration of vitamin K.
6. Efficacy of treatment with vitamin K is decreased with liver disease.
7. Heparin may be used to reverse overdose.
guideline.
PARACETAMOL Reviewed by Dr Salim Aftimos, Brenda Hughes, Robyn

Wilkinson, Sanya Mirkov
July 2000
Panadol, Pamol Caution about use in 1st 24 hours amended January 2003
Addition of vaccination as an indication June 2005
For all neonates, including preterm:
4
1. Oral: 10 mg/kg/dose 6 hourly.
4
2. Rectal: 20 mg/kg/dose 8 hourly.
Indications
1. Analgesia
2. Pyrexia
3. Post-operative pain relief
4. Irritable or unsettled behaviour following vaccination.
Precautions
1. Known hypersensitivity to paracetamol

2. Moderate or severe pain
3. Use in preterm infants, especially very immature infants
4. Impaired hepatic or kidney function
5. Use in the 1st 24-hours after birth (see "Special Considerations").
Paracetamol has analgesic and antipyretic actions but only weak anti-inflammatory
properties. The drug inhibits prostaglandin biosynthesis in conditions associated with low
levels of cellular peroxides (pain, fever).
Due to metabolic immaturity, neonatal clearance of paracetamol is different from adults.

Sulphate conjugation is well developed in a neonate and is the major metabolic pathway
for paracetamol clearance. Glucuronidation clearance is not well developed and plays a
minor role in paracetamol clearance in neonates. With maturation these clearance
pathways for paracetamol change. The usual adult ratio of 2:1 glucuronide to sulphate
4
conjugates of paracetamol is achieved by 12 years of age.
Neonatal gastric pH is almost neutral, and although this favours absorption of

paracetamol the stomach is not an optimal entry point to the circulation. 4 Paracetamol,
therefore, is ideally absorbed from the small intestine where the large surface area, ideal
blood flow and permeability favour absorption of the majority of drugs. Absorption from
this area, however, depends on gastric emptying which is slow and erratic in a neonate.
Slow absorption of paracetamol in infants less than three months has been demonstrated.
4
Hepatotoxicity in children from paracetamol ingestion has been demonstrated and there is
4
the potential for this to occur in neonates. The enzyme systems P450 CYP2E1, 1A2,
3A4 are responsible for forming paracetamol toxic metabolites. Despite a low activity of
P450 CYP 2E1 in neonates, toxic metabolites can still be formed.
1. Adverse effects occur rarely, but may include skin rash, fever, thrombocytopenia,
leucopenia, neutropenia, pancytopenia, agranulocytosis.
2. Overdosage may lead to severe liver damage and occasionally acute renal tubular
necrosis.
3. Hypersensitivity reactions have been reported. These include urticaria, dyspnoea,
hypotension, angioedema.
1. Clinical experience in neonates, especially those preterm, is limited.

2. Caution in the 1st 24 hours for treatment of "pain" related to birth. Infants who are
unsettled should be assessed clinically and not assumed to be in pain secondary
to birth.
3. Management of paracetamol overdose and/or toxicity: activated charcoal,
acetylcysteine or oral methionine. Contact Starship Emergency Department.
4. Consider a dose of paracetamol prior to administration of vaccines. Repeat doses
may be required for hyperthermia and irritability.
guideline.
PARACETAMOL
Reviewed by Dr Salim Aftimos, Brenda Hughes, Robyn
Wilkinson, Sanya Mirkov
Panadol, Pamol
July 2000
Management of Paracetamol Administration
Description
● Panadol ® oral suspension 120mg/ 5 ml (sugar free, alcohol free).

● Suppositories: 25 mg and 50 mg.
Prescription
● Charted on prescription chart in mg/dose.
Administration
1. Oral: Shake well before use. Do NOT dilute.
Observation and Documentation
1. Monitor for signs of adverse effects

2. Assess for toxicity: CNS stimulation, excitement
3. Evaluate baby's need for, and response to medication.
Storage
● Suspension: Room Temperature <25°C.

● Suppositories: Room Temperature or refrigerate.
Selected References
1 Levy G, Khanna NN, Soda DM, et al. Pharmacokinetics of acetaminophen in the human neonate;
Formation of acetaminophen glucuronide and sulfate in relation to plasma bilirubin concentration and D-
glucaric acid excretion. Paediatrics 1975; 55:818.
2 Miller RP, Roberts RJ, Fischer LJ. Acetaminophen elimination kinetics in neonates, children, and adults.
Clin Pharmacol Ther 1975; 19:284.
3 Knight J, Saunders R (eds). New Ethicals Compendium. Auckland, Adis Press 1992, p328-329.
4 Anderson BJ, Woollard GA, Holford NHG. A model for size and age changes in the pharmacokinetics of
paracetamol in neonates, infants and children. Br J Clin Pharmacol. In press. 2000 .
5 Medicines for Children. Royal College of Paediatrics and Child Health. London: RCPCH Publications
Limited, 1999.
● Drugs are indexed alphabetically by their generic name. Trade names are included for user reference.
● Some of the drugs listed below do not have protocols available. This is either because they have been withdrawn (in
which case, hard copies are available through Carl Kuschel) or because protocols are currently under construction.
Those without protocols are not underlined.
Generic Trade Generic Trade Generic Trade
Acyclovir Zovirax IV Erythromycin EES Pancuronium Pancuronium

sodium ethylsuccinate bromide bromide
Adenosine Adenocor Erythromycin Erythromycin DBL Paracetamol Panadol,
lactobionate Pamol
Adrenaline Adrenaline Erythropoietin Recormon , Paraldehyde Paraldehyde
hydrochloride (Recombinant Exprex, Epoetin
Human)
Amikacin Amikin Phenobarbitone Gardenal
sulphate sodium sodium
Amiloride Midamor Fentanyl citrate Sublimaze Phenylephrine Metaoxedrine
hydrochloride
Aminophylline Aminophylline Ferrous gluconate Fergon Phenytoin sodium Dilantin
Amiodarone Cordarone X Ferrous sulphate Ferro-liquid Phytomenadione Vitamin K,
hydrochloride Konakion
Amoxycillin Ibiamox Flucloxacillin Floxapen, Piperacillin sodium Pipril
sodium Flucloxin
Amphotericin B Fungizone Fluconazole Diflucan Poractant alpha Curosurf
Atropine Atropine Flucytosine Alcobon Potassium chloride Potassium
sulphate
Frusemide Frusemide DBL, Propranolol Inderal
Lasix hydrochloride
Benzylpenicillin Crystapen, Prostaglandin E1 Paediatric
Penicillin (Alprostadil) Prostin VR
Sodium
Biochemie
Beractant Survanta Gaviscon Gaviscon Pyridoxine Vitamin B6
hydrochloride
Budesonide Pulmicort Gentamicin Gentamicin DBL
sulphate
Glucagon Glucagen hypokit Ranitidine Zantac
hydrochloride
Caffeine Caffeine Rifampicin Rifampin
Calcium Calcium Heparin sodium Heparin
gluconate gluconate
Carbamazepine Tegretol Hydrochlorothiazide Hydrochlorothiazide Salbutamol Ventolin,
Respax
Cefaclor Ceclor Hydrocortisone Solu-cortef Sodium bicarbonate Sodium
sodium succinate bicarbonate
Cefotaxime Claforan Sodium Chloride Sodium
sodium Infusion Chloride
(links to fluid
guideline)
Cefoxitin Mefoxin Ibuprofen Brufen Sodium Intal
sodium cromoglycate
Ceftazadime Fortum Imipenem / Primaxin Sodium nitroprusside Nipride
pentahydrate Cilastatin sodium dihydrate (DBL)
Ceftriaxone Rocephin Indomethacin Indocid Sodium polystyrene Resonium A
disodium sulphonate
Cefuroxime Zinacef Insulin (neutral) Actrapid penfill Sotalol hydrochloride Sotacor
sodium
Cephalothin Keflin Intralipid 20% Intralipid Spironolactone Aldactone
Chloral Hydrate Ipratropium Atrovent Sucrose 66.7% Syrup BP
bromide (Medical Guideline)
Chloramphenicol Chloromycetin Isoprenaline Isoproterenol, Suxamethonium Ethicholine
sodium hydrochloride Isuprel chloride
succinate
Chlorothiazide Chlorothiazide
Chlorpromazine Largactil Lignocaine Xylocaine Thiopentone sodium Pentothal
hydrochloride
Cisapride Prepulsid Ticarcillin disodium Tarcil
Clonazepam Rivotril Magnesium Magnesium Tolazoline Priscoline
sulphate hydrochloride
Cotrimoxazole Meropenem Merrem Trichloroacetaldehyde Chloral hydrate
(links to HIV hydrate
guideline)
Cyclopentolate Cyclogyl Metoclopramide Maxolon Tromethamine THAM
Metronidazole Metronidazole
(Baxter)
Dexamethasone Dexamethasone Miconazole Daktarin Urokinase Ukidan
sodium DBL,
phosphate Decadron
Diazepam Valium Midazolam Hypnovel
Diazoxide Hyperstat Morphine Morphine Vancomycin Vancocin CP
(Oral)
Digoxin Lanoxin Morphine sulphate Morphine Vitadol C Vitadol C
(IV)
Dobutamine Dobutrex Vitamin K Konakion
hydrochloride (Phytomenadione)
Dopamine Dopamin Naloxone Narcan
Doxapram Dopram Neostigmine Neostigmine
methylsulphate
Nestargel Nestargel
Netilmicin sulphate Netromycin
Nitric oxide Nitric oxide
Nitroprusside Nipride
Noradrenaline Levophed
Nystatin Mycostatin, Nilstat
Last edited Monday, 09 January 2006
guideline.
ACYCLOVIR
Reviewed by Dorothy Cooper and Dr Carl Kuschel
Zovirax IV
September 1999
1. 10 mg/kg/dose IV infusion by syringe pump over one hour.
Postmenstrual
Postnatal Age Dosing Interval
Age
(days) (hr)
(weeks)
0 to 28 24
≤29
>28 12
0 to 14 24
30 to 36
>14 12
≥37 All 8
● Increase dose interval if significant renal impairment.

● Reduce dose if severe renal failure (serum creatinine greater than 130 umol/L, or
creatinine clearance less than 10 ml/minute per 1.73 m2): 5 mg/kg q24h.
Indications
1. Neonatal herpes simplex infections (especially if CNS and pulmonary involvement).

2. Neonatal varicella zoster infections.
Precautions
1. Not usually advisable with second or third degree AV block, or sinus node
dysfunction.
2. Caution in patients capable of rapid AV conduction.
3. Adenosine may be a mild bronchoconstrictor. Caution may be required in patients
with a tendency to bronchoconstriction. However, adenosine does have a half-life
of less than 10 seconds.
Contraindications
1. Hypersensitivity to acyclovir.
2. Caution in preterm infants, especially extreme immaturity.
3. Caution in infants with renal dysfunction or renal failure.
Antiviral agent which is highly active in vitro against herpes simplex (types 1 and 2) and
varicella zoster viruses. Preferentially taken up by infected cells and then phosphorylated
to the active compound acyclovir triphosphate. Acts as an inhibitor of, and substrate for,
the herpes specified DNA polymerase. Prevents further viral DNA synthesis without
affecting normal cellular processes. Toxicity to mammalian host cells is low.
Oral absorption of acyclovir is limited (bioavailability 15-30%) and may involve a saturable
process, but does not appear to be altered by food. Widely distributed throughout the
body fluids and tissues. CSF concentrations approximately 50% that of plasma. Low
binding (9-24%) to human plasma protein. Eliminated, mainly unchanged via the kidney,
primarily by glomerular filtration. Elevated serum concentrations may be reduced by
haemodialysis.
1. Very few adverse effects have been reported in clinical studies.

2. Venous irritation, soft tissue injury at site of IV injection.
3. Gastrointestinal disturbances (nausea, vomiting).
4. Reversible neurological reactions are rare.
5. Transient renal dysfunction and crystalluria.
1. Check renal function prior to commencing therapy. Modify dosing regime if serum
creatinine elevated.
2. Risk of transient renal dysfunction and crystalluria is minimised by slow infusion
rates and adequate patient hydration.
3. Monitor renal function during course of therapy.
4. Resistant viral strains may emerge during long term therapy.
5. Not compatible with dopamine, dobutamine and morphine.
6. There is NO evidence acyclovir will stop transmission of the virus.
7. Acyclovir is compatible with breastfeeding.
8. Do not administer by bolus IV injection IM or SC.
9. Sodium content 4.2mEq/g.
guideline.
ADENOSINE Reviewed by Dr Pat Clarkson, Robyn Wilkinson, Brenda

Hughes, Lejla Brkic
Adenocor January 1999

Reviewed By Dr Jon Skinner, October 1999
7 8
1. Initial dose 0.05 – 0.10 mg / kg ,
2. Increase by 0.05mg/kg/dose to a maximum of 0.25mg/kg/dose (this
is likely to be effective in 90% of cases)
3. Administered by direct IV injection over 1-2 seconds followed by a
rapid sodium chloride 0.9% flush.
Indications
1. Diagnosis and treatment of tachyarrhythmias

2. Other antiarrhythmic medication may be required to prevent recurrence of
tachyarrhythmias
Precautions
1. Not usually advisable with second or third degree AV block, or sinus node
dysfunction
2. Caution in patients capable of rapid AV conduction.
3. Adenosine may be a mild bronchoconstrictor. Caution may be required in patients
with a tendency to bronchoconstriction. However, adenosine does have a half-life
of less than 10 seconds.
Drug Interactions
A drug interaction may occur when a baby is taking other drugs concomitantly.
Adenosine +:
Caffeine, 1
An increase in the adenosine dose may be required .The
Theophylline,
Aminophylline methylxanthines may oppose the antiarrhythmic effects of
adenosine by their antagonistic effect on adenosine receptors.
Beta blockers Not used concomitantly without specialist consultation
Adenosine depresses conduction through the AV node. This action can interrupt re-entry
circuits involving the AV node and restore normal sinus rhythm in patients with
paroxysmal supraventricular tachycardia. It does not have a negative inotropic action.
Adenosine is an endogenous nucleoside primarily formed as a degradation product of

adenosine triphosphate. As an intermediate metabolite in several biochemical pathways,
adenosine contributes to the regulation of numerous physiologic processes, including
platelet function, coronary and systemic vascular tone, and lipolysis in adipocytes. The
duration of electrophysiologic and clinical effects are extremely short, < 10 seconds.
Adenosine is rapidly taken up by most types of cells including cellular elements of the
blood and vascular endothelium, where it is rapidly degraded by deamination to inosine
and subsequently to hypoxanthine. Total clearance from plasma occurs within < 30
seconds.
1. Atrial fibrillation or atrial flutter with rapid ventricular rate

2. Bradycardia, varying degrees of AV block, premature ectopic beats.
3. Dyspnoea, (frequent but transient).
4. Flushing, (common).
5. Chest pain in children and adults
7
6. Apnoea (rare)
1. Ideally administered via a central venous line or large peripheral vessel.

2. Administration through an umbilical artery catheter should be discouraged as the
drug is metabolised systemically and metabolised prior to delivery to the heart.
3. Once the effects of adenosine have been noted, it is usually necessary to institute
long term anti arrhythmic therapy.
guideline.
ADRENALINE Reviewed by Dr Carl Kuschel, Dorothy Cooper

HYDROCHLORIDE
August 1998
Adrenaline Micrograms changed to nanograms June 2002
Instructions regarding CVL December 2002
IV push
1. 0.1-0.3 ml/kg 1:10,000 concentration by IV push, or intracardiac.
Intratracheal
1. 0.3ml/kg 1:10,000 concentration. Repeat dose every 3-5 minutes as necessary.
Continuous infusion
1. 100-300 nanograms/kg/minute (0.1-0.3micrograms/kg/minute). Start at 100

nanograms/kg/minute (0.1micrograms/kg/minute) and titrate to desired response
to a maximum of 1000 nanograms/kg/minute (1microgram/kg/minute).
2. Use 1:10,000 concentration (0.1mg/ml) to prepare continuous infusion.
3. Usual dilution 0.3 mg/kg in 50ml D5W, D10W, NS.
● Use as a continuous infusion should be discussed with Consultant on call.

● Give through a Central Venous Line (UVC, Longline, or Surgical CVL)
Slow IV push/intracradiac
1. 0.1-0.3ml/kg/minute, 1:10,000 concentration.
Indications
1. Acute cardiovascular collapse (bradycardia, asystole).

2. Can be used as a second or third line inotrope.
3. Short-term use for cardiac failure resistant to other drug management.
1. Hypersensitivity to sympathomimetics.
2. Shock.
3. Caution in infants with cardiovascular disease, hypertension.
Adrenaline, a catecholamine, stimulates alpha and beta receptors. It increases heart rate,
increases myocardial contractility, automaticity and conduction velocity. Adrenaline also
increases systemic vascular resistance (via constriction of arterioles), and increases
blood flow to skeletal muscle, brain, liver and myocardium. It decreases renal blood flow
by 40%. Pulmonary resistance may increase, although the major effect of adrenaline is to
redistribute blood from the systemic to pulmonary circulation and thereby increase
pulmonary pressure.
Adrenaline must be given parenterally to reach pharmacologically effective concentrations

because it is rapidly metabolised in the gastrointestinal tract and liver. Its vasoconstrictive
properties account for the slow rate of absorption from subcutaneous or intramuscular
administration sites. The major portion of adrenaline is rapidly metabolised by the same
enzyme systems that metabolise endogenous catecholamines.
1. Venous irritation, soft tissue injury at the site of IV infusion.

2. Cardiac arrhythmias (PVCs and ventricular tachycardia).
3. Renal vascular ischaemia with decreased urine formation.
4. Severe hypertension with intracranial haemorrhage.
5. Pulmonary oedema.
6. Hyperglycaemia related to the inhibition of insulin secretion and conversion of
glycogen reserves.
7. Hypokalaemia.
1. Always use as a 1:10,000 concentration (0.1 mg/ml) for individual doses.

2. If possible, correct acidosis before administration of adrenaline to enhance the
effectiveness of the drug.
guideline.
AMIKACIN SULPHATE
Reviewed by Dr Carl Kuschel, Brenda Hughes, Rob
Ticehurst, and Robyn WIlkinson
Amikin
November 2003
1. 15mg/kg IV as a daily dose every 24 hours, given as an infusion over 30 minutes

4 , 6, 7, 8
Indications
1. Suspected or proven late-onset neonatal sepsis.
1. Hypersensitivity to amikacin/other aminoglycosides.

2. Extreme caution in neonates with renal dysfunction.
3. Caution in concurrent therapy with cephalosporins, potent diuretics such as
frusemide and neuromuscular blocking agents.
4. Concurrent administration with other ototoxic and/or nephrotoxic drugs.
5. Patients with muscular disorders eg. myasthenia gravis. The curare-like effect at
the neuromuscular junction, which may occur with aminoglycosides, can aggravate
1
the muscle weakness in these conditions.
1, 4
Amikacin is a semi-synthetic aminoglycoside antibiotic which is thought to distribute

mainly into extracellular fluid in neonates. It is 11% protein bound (adults) and excreted
unchanged predominantly by glomerular filtration in the kidneys. The half life is 7-14
hours in babies (postmenstrual age < 30 weeks) and 4-7 hours at a postmenstrual age of
40 weeks.
Amikacin has in vitro activity against gram-negative organisms (including Pseudomonas

spp., Proteus spp., Klebsiella, Enterobacter, Serratia spp., Citrobacter, E.Coli.) and gram-
positive Staphylococcus aureus including the methicillin-resistant strains. When indicated,
concomitant therapy with a penicillin type drug may be necessary to cover for gram-
positive organisms such as Streptococci.
1, 5
1. Ototoxicity, both vestibular and auditory, is seen mainly with co-existing renal
impairment, high doses of amikacin and/or prolonged therapy. The risk is
increased with dehydration and previous/current exposure to another ototoxic
agent. Amikacin affects auditory function to a greater extent than gentamicin.
Aminoglycoside induced ototoxicity is usually irreversible.
2. Renal impairment, azotemia, oliguria.
3. Hepatotoxicity.
4. Laboratory test interference may occur with: bilirubin (↑), Na+ (↓), K+ (↓), Platelets
(↓), and others (see data sheet).
1, 2, 3
Drug Interactions
Frusemide ● Possible increased risk of nephrotoxicity and

ototoxicity.
Indomethacin ● Possible increase in amikacin levels.
Pancuronium and other ● Possible increase and prolongation of neuromuscular

neuromuscular blocking blockade. Risk possibly increased with co-existing
agents renal disease and hypocalcaemia, and those with pre-
exisiting muscular weakness. Amikacin has a lower
neuromuscular blocking potential than gentamicin.
Vancomycin, gentamicin ● Possible potentiation of nephrotoxicity and ototoxicity.

(and other
aminoglycosides)
1. Monitor: renal function, hydration

Check levels on the 3rd dose, and then every 3-5 days as required.
4
Serum levels :
❍ Peak 20-30mg/L (1 hour following the commencement of the infusion; 30
minutes after the infusion ceases)

❍ Trough <8mg/L
2. Adjust dose and/or dose intervals in infants with suspected/proven renal
impairment, or reduced clearance due to extreme immaturity.
3. If significant renal impairment, consider stopping Amikacin.
guideline.
AMILORIDE
Reviewed by Dr Carl Kuschel, Dorothy Cooper
Midamor
August 1998
1. 0.4mg/kg/day PO.
Commonly 1 mg mane in term newborn.
Indications
1. Adjunct to thiazides or frusemide to conserve potassium.

2. Not used as primary diuretic.
1. Infants with hyperkalaemia.

2. CAUTION use in renal or hepatic impairment.
3. CAUTION use in renal impairment in infants receiving digoxin therapy. Possible
increase in serum digoxin levels.
4. CAUTION with concomitant administration of IVN. May cause possible metabolic
acidosis.
5. AVOID supplemental potassium.
Amiloride hydrochloride is a weak diuretic with potassium sparing properties. It also

exhibits natriuretic and hypotensive effects. It is chemically unrelated to other known
diuretics. Amiloride acts directly on the distal renal tubule of the nephron to inhibit sodium-
potassium ion exchange. Unlike spironolactone, amiloride does not competitively inhibit
aldosterone and its diuretic activity is independent of aldosterone.
It is completely absorbed from the gastrointestinal tract. Simultaneous administration of

food decreases gastrointestinal absorption from about 50% to about 30%. The drug has
large extravascular distribution. It is not significantly bound to human plasma protein.
Amiloride is not metabolised and is eliminated by the kidney (50%) and in the faeces
(about 40%).
Onset of action about 2 hours and its diuretic action reaches a peak in 6 - 10 hours and
may persist for about 24 hours.
1. Hyperkalaemia (Signs and symptoms: lethargy, paralysis of the extremities,

bradycardia, shock and ECG abnormalities.
2. Hyponatraemia.
3. Gastrointestinal disturbances (nausea, vomiting, diarrhoea or constipation).
4. Metabolic acidosis.
5. Transient elevation in BUN and serum creatinine.
6. Rash.
1. Monitor urea and electrolytes frequently when commenced. Anticipate

hyperkalaemia, hyponatraemia.
2. It should be given with care to patients likely to develop metabolic acidosis.
3. Amiloride has been shown to increase serum digoxin levels.
4. Safety and efficacy of amiloride in children alone or in combination with
hydrochlorothiazide has not been established.
5. Avoid supplemental potassium.
6. Decreased diuretic effectiveness with NSAIDS avoid concomitant use.
guideline.
AMIODARONE HYDROCHLORIDE Reviewed by Brenda Hughes, Dr Carl Kuschel, Dr Jon

Skinner (Paediatric Cardiology) and Karen Anderson-
Hawke (NS-ANP)
Cordarone X
June 2005
● Amiodarone should be used only on the direction of a paediatric

cardiologist.
Intravenous 1,2
1. Loading dose: 25 microgram/kg/minute for 4 hours, then

Maintenance dose: 5 to 15 microgram/kg/minute
Oral 1,2
1. 4mg/kg/dose every 8 hours for one week, then

2. 4mg/kg/dose every 12 hours for one week, then
3. 4mg/kg/dose once daily.
Note: if converting from IV infusion to oral dosing, use 4mg/kg/dose and consult
cardiologist for oral dose frequency.
Indications
1. Control of ventricular and supraventricular arrhythmias including those associated

with Wolff-Parkinson-White syndrome.
Contraindications
1. Hypersensitivity to amiodarone or iodine.

2. Sinus bradycardia.
3. Sino-atrial heartblock.
4. Severe respiratory failure.
5. >Circulatory collapse, severe systemic hypotension, cardiogenic shock, 2nd or 3rd
degree AV block.
Precautions
1. Hepatic disease
2. Pulmonary disease
3. Thyroid disorders
4. Hypotension, AV block, left ventricular dysfunction, heart failure, bradycardia,
myocardiopathy
5. Electrolyte imbalance
6. Preterm infants less than 32 weeks gestation (the injection contains benzyl alcohol
which was associated with the “gasping syndrome” with symptoms of hypotension,
bradycardia, gasping respiration, cardiovascular collapse and death).
Drug Interactions
Digoxin ● Reduce digoxin maintenance dose by half. If loading digoxin,

use a full loading dose, then half maintenance dose. Monitor
digoxin levels.
Flecainide ● Use carefully. Reduce flecainide dose.
Diuretics ● Risk of hypokalaemia.
Corticosteroids ● Risk of hypokalaemia.
Amphotericin ● Risk of hypokalaemia.
Phenytoin ● Monitor phenytoin levels. Phenytoin level may increase and

amiodarone decrease
Sotalol ● Possible increase in QT interval
Erythromycin IV ● Possible increase in QT interval
Beta-blockers ● Not recommended with amiodarone because of possible

and Calcium increase in bradycardia, AV block, and myocardial depression.
Channel Blockers
Anaesthetic ● Use cautiously.
agents
Amiodarone is a Class III antiarrhythmic agent. Its broad spectrum of activity is due to
prolongation of the action potential duration and refractory period of the atrial, nodal and
ventricular tissues. It is extensively distributed into body tissues, accumulating in muscle
and fat. Oral absorption is erratic, and may lead to a wide range in bioavailability. Des-
ethyl amiodarone is an active anti-arrhythmic metabolite. For both parent drug and
metabolite, biliary excretion with some enterohepatic recycling, is the major elimination
route; there is very little urinary excretion.
Adverse effects are common. Many are dose-related and decrease with a dose reduction.
Possible adverse effects include:
1. Bradycardia, hypotension (possible with rapid infusion rates, or with prolonged

use), arrhythmias, heart failure.
2. Fatigue, peripheral neuropathy, tremor.
3. Nausea, vomiting, constipation.
4. Corneal deposits, visual disturbances.
5. Photosensitivity, blue-grey discolouration of the skin.
6. Hepatotoxicity, pulmonary toxicity.
7. Hypothyroidism or hyperthyroidism due to iodine content of injection.
8. Venous irritation (when administered peripherally at concentrations > 2mg/ml.).
1. Reduce dose in liver disease.

2. Administration via a central venous catheter is recommended. Can be
administered via a peripheral line.
3. Monitor:
1. Magnesium, potassium – take baseline levels.
2. LFTs, thyroid function – take baseline levels.
3. INR.
4. ECG and pulse oximetry – monitor continuously.
5. Perform daily 12-lead ECG (for QTc interval).
guideline.
AMOXYCILLIN
Reviewed by Dr Carl Kuschel, Brenda Hughes, Dr Arthur
Morris, Rob Ticehurst, and Robyn Wilkinson
Amoxil, Ibiamox
February 2001
8,9
Suspected Sepsis: 25mg/kg/dose IV

Severe Sepsis +/- Meningitis: 50mg/kg/dose IV
Postmenstrual Postnatal Dosing

Age Age Interval
(weeks) (days) (hr)
0 to 28 12
<29
>28 8
0 to 14 12
30 to 36
>14 8
0 to 7 12
37 to 44
>7 8
>45 All 6
Indications
1. Empirical therapy for infants with risk factors for sepsis or suspected sepsis.
Usually administered in combination with gentamicin, cefoxitin, cefotaxime, or
netilmicin.
2. Specific therapy for Streptococcus agalactiae, Streptococcus faecalis, Listeria
monocytogenes.
Contraindications
1. Hypersensitivity to penicillins/cephalosporins.
Precautions

2. Caution in infants with liver, renal or gastrointestinal disease.
Amoxycillin is a broad spectrum penicillin with antibacterial activity against certain gram
negative and gram positive organisms. It is in activated by penicillinases including those
produced by Staphylococcus aureus, E.coli, Pseudomonas, Klebsiella, and Enterobacter.
6
Widely distributed at varying concentrations in human body tissues and fluids. Very little
passes into the CSF unless the meninges are inflamed. Low binding to human plasma
protein. Half-life (adults) of 1 to 1.5 hours, which would be extended in the neonate. 7
Excreted mainly unchanged by the kidneys.

2. Pain, soft tissue injury at site of IM injection.
3. Gastrointestinal disturbance (nausea, vomiting, diarrhoea).
4. Maculopapular rash, non-specific rashes and skin eruptions.
5. Fever, pruritis, urticaria.
6. Seizures (encephalopathy with high doses greater than 400 mg/kg/day).
1. May give concurrently with aminoglycoside therapy for synergistic effect.

Administer separately as simultaneous administration may cause inactivation.
2. Reduce dose in suspected renal dysfunction.
3. Sodium content 2.6 mmol/g.
guideline.
AMPHOTERICIN
Reviewed by Dr Carl Kuschel, Brenda Hughes, Robyn
Wilkinson
Fungizone
September 2000
1. Initial dose: 0.1-0.3 mg/kg IV infusion over 2-6 hours.

2. Maintenance dose: 0.5-1 mg/kg IV every 24 hours or every 72 hours.
(0.3 mg/kg if used concurrently with flucytosine).
Infuse over 2-6 hours.
3. May need to treat for 4-6 weeks. Dose does need to be reduced with pre-existing
impaired renal function. However, if GFR falls below 10% of normal during
therapy, withhold dose for 2-5 days.
Indications
1. Systemic candidiasis.
2. Congenital candidiasis.
3. Other systemic fungal infections.
1. Hypersensitivity to amphotericin B.
2. Minor, superficial fungal infections.
4. Caution in infants with renal, hepatic or gastrointestinal dysfunction.
Amphotericin B is a polyene antifungal antibiotic that is active against a wide range of

yeasts and yeast-like fungi including Candida albicans. The mechanism of action
depends on its binding to a sterol moiety, ergosterol, present in the membrane of
sensitive fungi. May be fungicidal or fungistatic, depending on the drug concentration
obtained and the sensitivity of the fungus.
Absorption from the gastrointestinal tract is negligible, even with very large doses. After IV
administration only a small percentage of the drug remains in the plasma compartment.
High binding (> 90%) to human plasma protein. CSF concentrations of amphotericin B
are only 2-4% of the serum concentrations. Details of tissue distribution and metabolism
of amphotericin B are not known. No comprehensive studies of pharmacokinetics have
been reported for infants. Drug may accumulate in tissues to a significant concentration
and be excreted renally for months.
Dosage schedules for amphotericin B have been devised following observations of

toxicity with large doses and other clinical experiences. The initial dose is doubled on
each subsequent day until the desired dosage is achieved. The usual maintenance dose
is 0.5-1.0 mg/kg IV given daily or every other day over 2-6 hours. Recommended
therapeutic serum concentrations of amphotericin B range between 0.2 and 0.5 mg/L. No
objective data exists regarding the appropriate length of therapy required, although most
infants have been treated for an average of 40 days (range 14-70 days). Amphotericin is
frequently employed in combination with flucytosine.
1. Venous irritation, soft tissue injury at IV injection site.

2. Fever.
3. Gastrointestinal disturbances (nausea, vomiting, haemorrhagic gastroenteritis).
4. Hypocalcaemia.
5. Anaemia (common), thrombocytopaenia, neutropenia (rare).
6. Nephrotoxicity.
7. Cardiovascular toxicity.
8. Seizures.
9. Acute liver failure.
Interactions
1. Corticosteroids enhance potassium depletion.

2. Digoxin increases risk of digitalis toxicity in potassium depleted patients.
3. Flucytosine synergistic effect.
4. May increase renal toxicity with other nephrotoxic drugs.
1. Amphotericin B should be used primarily for treatment of infants with progressive

and potentially fatal fungal infections.
2. Amphotericin must be used under close clinical supervision. Toxic manifestations
are not fully characterised.
3. Starting doses have ranged from 0.1 to 0.3 mg/kg given IV over a period of 2-6
hours. The dose is increased by 0.1-0.2 mg/kg/day, as tolerated, until a maximum
of 1 mg/kg/day is achieved. The usual maintenance dose is 0.5-1.0 mg/kg/day
given daily or every other day over 2-6 hours.
4. Recommended therapeutic serum concentrations of amphotericin range between
0.2 and 0.5 mg/L. However, serum levels are not routinely measured because of
uncertainties with their interpretation.
guideline.
ATROPINE SULPHATE
Atropine
August 1998
1. 10-30 micrograms/kg/dose IV over 1 minute, IM or ETT (ETT route to be used only

if IV route not possible).
2. Dose may be repeated every 10-15 minutes to achieve desired effect, with a
maximum total dose of 40 micrograms/kg.
Indications
1. Severe sinus bradycardia, particularly when parasympathetic influences on the

heart (digoxin, beta blocker drugs, hyperactive carotid sinus reflex) predominate.
2. To reduce the muscarinic effects of neostigmine when reversing neuromuscular
blockade.
3. Prevention of reflex bradycardia during intubation.
1. Known hypersensitivity to atropine.

2. Abdominal distension with decreased peristalsis and/or intestinal obstruction.
3. Gastroesophageal reflux.
4. Obstructive uropathy.
5. Congenital glaucoma.
6. Caution in patients with Down's Syndrome.
Atropine, a naturally occurring alkaloid, is an anticholinergic agent. Acts by competitive

inhibition of the actions of acetylcholine on muscarinic receptors. Increases heart rate by
decreasing the effects of the parasympathetic system while increasing the effects of the
sympathetic system. Vagal influences on the gastrointestinal tract are partially inhibited by
atropine. Motor activity in the stomach and small and large intestines is reduced.
Oesophageal sphincter tone is reduced. Salivary secretion is inhibited. Atropine relaxes
bronchial and bronchiolar smooth muscle, thereby reducing airway resistance and
increasing dead space by 30%.
Rapid absorption from intestinal tract but not the stomach. Pharmacological activity of
parenteral administration is 2-3 times greater than enteral administration. Low binding
(20%) to human plasma protein. Excreted mainly unchanged via the urine.
Rapid onset of action. Peak effects: cardiovascular (12-16 minutes), gastrointestinal tract
(1-2 hours). Duration of action 4-6 hours.
1. Tachycardia
2. Urinary retention
3. Impaired gastrointestinal motility
4. Hyperthermia
5. Hot, dry scarlet flushed skin
6. Cardiac arrhythmias
7. Dry mucous membranes, dry mouth
1. Limited use in newborn infants. Should not be used in neonatal resuscitation.

2. Management of atropine toxicity: stop atropine, treat anticholinergic symptoms with
physostigmine 0.5 mg by slow IV infusion.
3. Sodium chloride content 9mg.
guideline.
BENZYLPENICILLIN
Crystapen, Pencillin Sodium

Biochemie September 1998
1. 15-30 mg/kg/dose IV infusion over 15-30 minutes or IM.

2. 60mg/kg/dose for severe sepsis and meningitis.
Add an aminoglycoside if tolerance is suspected/confirmed.

Age Age Interval
(weeks) (days) (hr)
0 to 28 12
≤29
>28 8
0 to 14 12
30 to 36
>14 8
0 to 7 12
37 to 44
>7 8
≥45 All 6
Indications
1. Neonatal infections caused by susceptible organisms - streptococci (non

enterococcal), gonococci, congenital syphilis.

Benzylpenicillin has bacteriostatic/bacteriocidal actions (depending on its concentration)

against most gram positive bacteria and gram negative cocci. Also active against some
spirochaetes and actinomycetes. Action through inhibition of biosynthesis of cell wall
mucopeptide. Its action is inhibited by the enzyme penicillinase, produced during the
growth of certain micro-organisms.
Well absorbed following intramuscular injection. Widely distributed at varying

concentrations in body tissues and fluids. Very little passes into the CSF unless the
meninges are inflamed. Moderate binding (45-65%) to human plasma protein. Rapidly
excreted via the kidney, mainly unchanged. Tubular excretion is inhibited by probenecid.
Reduction in serum concentrations can be achieved by haemodialysis. Half life 5-6 hours
in healthy newly born preterm infants and 2 hours in full term babies > 1-2 weeks old.

4. Non specific rashes and skin eruptions.
5. Fever, pruritis, urticaria.

Administer separately as intravenous administration may cause inactivation.
2. Adjust dose in suspected renal dysfunction (usually by lengthening the dosing
interval).
3. Sodium content 1.7 mmol/gm.
guideline.
BERACTANT
Reviewed by Dr Simon Rowley, Dorothy Cooper
Survanta
August 1996
1. Survanta 4 ml/kg via endotracheal tube. Usually administer a second dose after 6 -
12 hours.
Doctor / NS-ANP to administer. Further doses should be discussed with the

Consultant but up to 4 doses can be administered in first 48 hours of life (i.
e, no more frequently than every 6 hours).
● Inject in boluses through 6 FG catheter inserted into ETT.

● Judge size of boluses according to baby’s tolerance.
● Ventilate between boluses for baby to recover.
● Administer over a few minutes, as fast as baby tolerates it.
● Baby supine and flat throughout.
Indications
Intubated Infant in Level 3
1. Moderately severe respiratory distress syndrome.

2. <= 30 week babies either administer early or same criteria as (3) below
3. > 30 weeks. Diagnosis of RDS and an a/A ratio of <0.22.
Non ventilated infant in Level 2 (baby intubated for Surfactant administration as per
Guideline ). Decision whether baby is transferred to Level 3 made by CCN on duty.
1. Clinical/radiological evidence of respiratory distress syndrome.

2. Gestational age >32/40.
3. Age <72 hours.
4. Current chest radiograph available.
5. Increasing requirements e.g. FiO2 >50%, pH <7.25, PaO2 <7.0, CO2 >7.0 (or a/A
<0.22).
6. Arterial line in situ.
1. Use in < 600g infants not established.

2. Hindu parents. Discuss with specialist and get consent.
Natural New Zealand bovine lung extract with added phospholipids. Exogenous
surfactant decreases surface tension, improves lung compliance and lung water
clearance.
Survanta is cleared into lung tissue within hours. The lipids enter endogenous surfactant
pathways.
No information is available on metabolism of the bovine surfactant proteins.
1. Instability during administration.

2. Possible ETT blockage.
3. Rapid changes in lung compliance and blood gases.
4. Slight increased risk of pulmonary haemorrhage.
5. Increased risk of nosocomial infections.
1. Should be used only after consultation with specialist.

2. Doctor /NS-ANP to administer.
3. Monitor O2 saturation, ECG continuously and blood gases and adjust ventilator/
oxygen appropriately. Inspect Survanta for discolouration prior to use.
4. Suction prior to administration if necessary.
guideline.
BUDESONIDE
Reviewed by Dr Simon Rowley, Dr Innes Asher, Dorothy
Cooper
Pulmicort
September 1996
1. Starting dose 0.5 mg (12 hourly) for six weeks until improved and stable.
2. Usual maintenance dose 0.25 mg 12 hourly.
3. If no response increase to 0.5 mg 12 hourly.
Indications
1. Infants with severe chronic lung disease with bronchial hyper-reactivity. Consider
use via a spacer. Contact Pharmacy or Asthma Nurse re availability of a spacer.
1. Known sensitivity to budesonide.

2. Caution neonates with fungal and viral infections in the airways.
3. Caution neonates who are being transferred from oral corticosteroids to
budesonide.
4. Caution, may need to wean dose, not stop suddenly.
Budesonide is a potent, nonhalogenated corticosteroid. Budesonide has shown a

favourable relation between local anti-inflammatory effect and systemic corticoid side
effects over a wide dose range. This is explained by an extensive (90%) first-pass
metabolism of budesonide in the liver after systemic absorption ie any drug deposited on
the oral buccal mucosa will be rapidly eliminated from the body. Budesonide has shown
anti-inflammatory effect and is manifested as decreased bronchial obstruction.
A proportion of the drug may be swallowed. The percentage of the inhaled dose reaching
the lung will depend upon the method and delivery of the nebulised budesonide. After a
single dose of budesonide, improvement of the lung function is achieved within a few
hours. The duration of effect is more than 12 hours. Full effect is not achieved until after a
couple of days.
Budesonide is protein-bound 88%. Vd is 4.3 L/kg and half-life is 2 hours.
1. Posterior subcapsular cataracts.

2. Mild irritation in the throat.
3. Candida infection in the oropharynx.
4. Facial skin irritation.
5. Bronchoconstriction (rare).
6. Gastrointestinal (nausea and vomiting).
1. Ideally before starting, do short synacthen test.
● Short Synacthen Test:

Give synacthen as 250 mcg/1.73 m2 injected intramuscularly. Cortisol levels at "0"
minutes and 60 minutes. Repeat synacthen test the day after budesonide stopped.
If response is poor, should repeat 2-4 weeks later.
guideline.
CAFFEINE Reviewed by Dr David Knight, Robyn Wilkinson, Brenda

Hughes, Colin McFarlane
Caffeine November 1999

April 2003 (change in timing of maintenance dose)
34
Loading Dose 25mg/kg total in two divided

(caffeine base) doses
IV 2 doses of 12.5mg/kg/dose
caffeine base 1 hour apart, each
over 30 minutes
Oral 2 doses of 12.5mg/kg/dose
caffeine base 2 hours apart with
feeds
Maintenance 6mg/kg/dose IV or PO every 24
dose hours at 06:00 hours:
(caffeine base)
Note: If Loading Dose given
before 22:00hr, maintenance dose
should be given at 06:00 the next
day day. If Loading Dose given
after 22:00hr, then miss the next
06:00 dose and give a day later (i.
e. between 24 and 32 hours after
the loading dose)
Indications
1. Apnoea of prematurity
2. Respiratory stimulation to assist extubation.
1. Known hypersensitivity to caffeine

2. Caution in very immature infants
3. Caution in neonates with liver and/or gastrointestinal tract disease
4. Caution in neonates with fits or tachyarrhythmia
Caffeine is a member of the group of chemically related alkaloids known as

methylxanthines. Almost all organ systems can be influenced by the methylxanthines,
although the predominant site of activity involves the central nervous system and the
cardiovascular system. Three major cellular actions of the methylxanthines have been
suggested: translocation of intracellular calcium, increasing accumulation of cyclic
nucleotides (particularly cyclic 3'S' AMP), and blockage of receptors for adenosine.
Pharmacological effects of caffeine include: stimulation of medullary respiratory centres,

generalised enhancement of CNS cellular response to stimulation, increased heart rate,
decreased peripheral vascular resistance, increased cerebral vascular resistance, smooth
muscle relaxation, skeletal muscle stimulation, stimulation of gastrointestinal secretions,
and diuresis. Caffeine may increase diaphragmatic contractility. The pharmacological
mechanisms proposed for the alteration of neonatal apnoea include: increased sensitivity
of medullary respiratory centre to CO2, increased afferent nerve traffic to brain stem,
increased catecholamine response, stimulation of central inspiratory drive, improved
skeletal muscle contraction, improved metabolic homeostasis, and improved oxygenation
via increased cardiac output and decreased hypoxaemic episodes. Caffeine, when
compared to theophyllines with equal efficacy, has fewer side effects. Caffeine has a
wider therapeutic to toxic ratio and is administered once a day because of its long half-
life. Serious problems are rare and only occur in large overdose but would include
neurological abnormalities such as tremor, seizures and hypertension, cardiac
abnormalities such as tachyarrhythmias. Side effects are rare at levels <400μmol/ml.
Oral administration results in very good bioavailability. There is little evidence that food
delays absorption of caffeine. Caffeine is metabolised by the liver cytochrome oxygenase
system which is induced by phenobarbitone and phenytoin. Levels may be increased by
enzyme inhibitors such as cimetidine.
1. Failure to gain weight

2. Hyperglycaemia
3. Gastrointestinal disturbances (nausea, vomiting, abdominal distension)
4. Irritability, sleeplessness, jitteriness
5. Cardiac arrhythmias, tachycardia, rarely bradycardia
6. Diuresis and dehydration
7. Tachypnoea
8. Hyperreflexia, seizures
1. Half-life very long (t½>100hrs). A baby will need respiratory monitoring for several
days after discontinuing.
2. Rapid infusion of caffeine may precipitate cardiac arrhythmias.
3. Routine levels are not necessary on stable babies. Serum levels should be
obtained if toxicity is suspected or if a baby continues to have apnoea and has not
previously had an optimal level documented. Levels should not be checked within
6 hours of previous dose. Order levels the day before assay is to be done and do
at 0830 hours. Therapeutic range is: 135-200 μmol/L, toxicity is unlikely at <400
μmol/L. 4 Note that the assay is not very accurate and has a coefficient of
variation of 15%.
4. Treatment of serious caffeine toxicity: activated charcoal 1 gm/kg as a slurry by
gavage tube every 2-4 hours. Avoid sorbitol-containing preparations - they may
cause osmotic diarrhoea.
5. If infant is on phenobarbitone clearance of caffeine is increased, therefore
decrease dose interval from 24 hourly to 12-18 hourly.
guideline.
CALCIUM GLUCONATE
Reviewed by Brenda Hughes, Rob Ticehurst, and Dr Carl
Kuschel
Calcium gluconate
June 2003
7 13
1. Urgent IV Correction , : 0.23-0.46mmol/kg (1-2ml/kg of calcium gluconate
10%) by slow IV injection of diluted solution over 10 minutes.
The infant requires ECG monitoring during the infusion.
6 11
2. Maintenance IV Treatment , : 0.5 - 1.0 mmol/kg/day as an IV infusion.
12
3. Oral : 1mmol/kg/day of elemental calcium in divided doses.
7
Indications
1. Treatment of symptomatic hypocalcaemia (serum Ca2+ <1.7mmol/L, ionised Ca2+

<0.64 mmol/L).
9
Contraindications
1. Hypercalcaemia.
2. Severe hypercalcuria.
3. Severe renal disease
9
Precautions
1. Impaired renal function

2. Cardiac disease
3. Diseases associated with elevated vitamin D concentrations.
4. Dehydration or electrolyte imbalance.
9
Calcium activates many enzymatic reactions and is essential in a number of physiological
processes including the transmission of nerve impulses; contraction of cardiac, smooth &
skeletal muscle; renal function; respiration; and blood coagulation. Bone calcium is in
constant exchange with plasma calcium. Bone contains 99% of the body calcium , with
the remaining 1% distributed between the intracellular and extracellular fluids. If dietary
deficiency, or other means, causes an imbalance of calcium in the body, the bone stores
of calcium may be depleted to accommodate the body’s more acute needs. Ionised
calcium is the physiologically active form of calcium. Approximately 45% of serum calcium
is bound to plasma protein. Acidosis leads to increased levels of ionised calcium, and
alkalosis decreases the levels. Calcium is excreted in the faeces as unabsorbed calcium,
plus that excreted via the bile duct.
7 ,8
1. Extravasation of intravenous injection can cause cutaneous necrosis or calcium

deposition.
2. Arrhythmias
3. Rapid administration is associated with bradycardia or cardiac asystole.
4. Gastric irritation and diarrhoea may occur during oral therapy.
7,8
1. Avoid intra-arterial and subcutaneous administration. Never give intramuscularly.

2. Adjust dose in renal failure.
3. Monitor: plasma calcium
4. Late hypocalcaemia (4-10 days after birth) is usually associated with increased
tone, jitteriness, and multiofcal seizures in an otherwise well infant. Seizures are
usually associated with serum Ca2+<1.7 mmol/L and ionised Ca2+<0.64mmol/L.
Often there is hypomagnesaemia (Mg2+ <0.68mmol/L) and ECG changes (QTc
>0.2 sec). In any infant presenting with late, symptomatic hypocalcaemia,
consider investigation of maternal calcium homeostasis (especially
hyperparathyroidism).
5. Treatment of asymptomatic neonatal hypocalcaemia is controversial.
guideline.
CEFACLOR
Ceclor
September 1998
1. 10-20 mg/kg/day PO nocte prophylaxis.

2. 40 mg/kg/day as 3 divided doses as treatment
Indications
1. Prophylaxis against urinary tract infections.

2. Treatment e.g. otitis media.
1. Hypersensitivity to penicillin or cephalosporins.
Semisynthetic second generation cephalosporin antibiotic for oral administration. Usually

active against the following organisms: Staphylococci species, Streptococcus pyogenes,
Streptococcus pneumoniae, Escherichia coli, Proteus spp, Klebsiella spp, Haemophilus
influenzae (including most beta lactamase producing ampicillin resistant strains),
Neisseria gonorrhoeae, and several anaerobic bacteria (excluding Bacteroides fragilis).
Note that Pseudomonas spp and most strains of enterococci, enterobacter spp, indole
positive proteus and serratia spp are resistant to cefaclor. Action results from inhibition of
synthesis of cell wall mucopeptides.
Cefaclor is well absorbed after oral administration, whether taken with food or while
fasting. However, when taken with food, the peak concentration is less and occurs later
than that observed when the medicine is administered to fasting subjects. Widely
distributed throughout body fluids and tissues. Does not penetrate the CSF.
Approximately 60-85% of the drug is excreted unchanged in the urine. Elevated serum
concentrations may be reduced by haemodialysis.
1. Rash, fever and urticaria.

2. Gastrointestinal disturbances (nausea, vomiting, diarrhoea, candidiasis).
3. Transient fluctuations in leucocyte count, eosinophilia, thrombocytopaenia.
4. False/positive Coomb's test, 40-75%.
5. Transient slight elevations in AST, ALP, or serum creatinine.
6. Stevens-Johnson Syndrome, toxic epidermal necrolysis.
7. Hyperactivity, somnolence.
8. False/positive urine glucose determination on Clinitest.
Interactions
Chloramphenicol - antagonistic effect do not use together.
1. The safety and effectiveness of cefaclor for use in infants less than one month of
age has not been established.
2. False/positive reaction for glucose in the urine may occur with Clinitest tablets.
3. Forced diuresis, peritoneal dialysis, haemodialysis or charcoal haemoperfusion
have not been established as beneficial for an overdose of cefaclor.
guideline.
CEFOTAXIME SODIUM
Reviewed by Dr Peter Nobbs, Brenda Hughes, Robyn
Wilkinson, Colin MacFarlane
Claforan
October 1999
9 9
1. 50-100mg/kg/dose (to a maximum of 200 mg/kg/day I.V. over 3 to 5 minutes ,
10
, or IM.
2. The higher doses are used in severe sepsis and meningitis.

Age* Age Interval
(weeks) (days) (hr)
0 to 28 12
≤29
>28 8
0 to 14 12
30 to 36
>14 8
0 to 7 12
37 to 44
>7 8
≥45 All 6
* PMA at the time of prescribing.
Indications
1. Neonatal meningitis.
2. Empirical therapy in infants with suspected sepsis who have previously received
multiple courses of antibiotics.
Contraindications
Precautions
1. Infants with liver, renal or gastrointestinal disease.

4
2. Use of high doses in those infants receiving aminoglycosides or frusemide .
Drug Interactions
+Phenobarbitone = Increase in skin rashes
Broad spectrum third generation cephalosporin antibiotic. At therapeutic doses it is active,

in vitro, against gram positive organisms such as staphylococci (including penicillinase
resistant strains), Streptococcus pyogenes, Streptococcus pneumoniae (Streptococcus
faecalis is resistant); and Gram negative organisms such as Enterobacter, Klebsiella,
4
Haemophilus influenza, and E.coli . There is only moderate activity against
7
Pseudomonas .
Poor oral absorption. Widely distributed at varying concentrations in human body tissues
and fluids. Usually penetrates the CSF in levels above the MIC of common sensitive
organisms when meninges are inflamed: CSF concentrations are considerably lower than
7
plasma. Cefotaxime is about 40% bound to plasma protein (in adults) . Metabolised in
the liver to an active compound, desacetylcefotaxime. Renal excretion with 20-36% of the
7
drug unchanged in urine. Cefotaxime and metabolites are excreted by haemodialysis .
Elimination half life is prolonged in neonates.

2. Pain, soft tissue injury at IM injection site.
3. Rash, pruritus, urticaria.
4. Gastrointestinal disturbance (nausea, diarrhoea); pseudomembranous colitis.
5. Neutropenia, thrombocytopenia, eosinophilia, leucopenia.
6. Positive Coombs test.
7. Transient elevation of hepatic enzymes.
4
8. Superinfection with non-susceptible organisms including fungi .
1. Monitor renal and hepatic function.
7
2. Reduce dose in suspected renal dysfunction .
3. Reduce dose in suspected liver dysfunction (only if there is concurrent renal
8
impairment) .
4. Sodium content 2.1mmol/g of cefotaxime.
guideline.
CEFOXITIN SODIUM
Reviewed by Dr Carl Kuschel, Brenda Hughes
Cefoxitin DBL, Mefoxin

September 1998
1. 50 mg/kg/dose IV injection over 3-5 minutes, or IM.

Age Age Interval
(weeks) (days) (hr)
0 to 28 12
<29
>28 8
0 to 14 12
30 to 36
>14 8
0 to 7 12
37 to 44
>7 8
>45 All 6
Indications
1. Empirical therapy for infants with risk factors for sepsis, or suspected sepsis.
Usually administered in combination with amoxycillin.
Bacteriocidal semisynthetic beta-lactam cephalosporin antibiotic for parenteral

administration. Has broad spectrum of antibacterial activity against gram positive and
gram negative pathogens, both aerobic and anaerobic. Cefoxitin is not active against
Listeria monocytogenes, Streptococcus faecalis, Pseudomonas spp, and most strains of
enterococci. Action is by inhibition of bacterial wall synthesis.
Widely distributed at varying concentrations in human body tissues and fluids. Very little
passes into the CSF unless the meninges are inflamed. Moderate binding (70%) to
human plasma protein. It is excreted virtually unchanged via the kidneys. Tubular
excretion is inhibited by probenecid.

5. Anaemia, neutropaenia, thrombocytopaenia.
7. Elevation of serum creatinine.
8. Super-infection with non susceptible organisms including fungi.
9. Hypotension.
1. Cefoxitin at high dosage should be given with caution to those infants receiving
aminoglycosides or potent diuretics.
interval).
4. May be associated with false positive glycosuria, falsely high serum creatinine
(using Jaffe technique), and a false elevation of urinary 17-hydroxycorticosteroids.
guideline.
CEFTAZADIME PENTAHYDRATE
Reviewed by Dorothy Cooper
Fortum
September 1998
1. 30-50 mg/kg/dose IV infusion by syringe pump over 30 minutes, or IM.

Age Age Interval
(weeks) (days) (hr)
0 to 28 12
<29
> 28 8
0 to 14 12
30 to 36
> 14 8
0 to 7 12
37 to 44
>7 8
>45 All 6
Indications
1. Infections caused by organisms resistant to other antibiotics, including

aminoglycosides and many cephalosporins.
1. CNS infections with Streptococcal faecalis, Pseudomonas aerogenosa.

Bacteriocidal third generation cephalosporin antibiotic which is resistant to most beta-
lactamases and is active against a wide range of gram positive and gram negative
bacteria. Inactive against Streptococcus faecalis, many staphylococci and many strains of
Bacteroides fragilis. A useful anti-pseudomonal agent, especially in combination with
aminoglycosides or penicillin. Active by inhibiting cell wall mucopeptide synthesis.
Poor oral absorption. Widely distributed at varying concentrations in human body tissues
and fluids. Very little passes into the CSF unless the meninges are inflamed. Low binding
(10%) to human plasma protein. Ceftazadime is not metabolised in the body. Excreted via
the kidney. Reduction in serum concentrations can be achieved by peritoneal dialysis/
haemodialysis. Serum half life in neonates is 4-10 hours.

4. Gastrointestinal disturbance (nausea, vomiting and diarrhoea).
5. Neutropaenia, thrombocytopaenia, eosinophilia.
6. Positive Coombs test.
1. Ceftazadime at high dosage should be given with caution to those infants receiving
aminoglycosides or potent diuretics.
interval).
guideline.
TRICHLORACETALDEHYDE
HYDRATE Reviewed by Dorothy Cooper
Chloral hydrate February 1997
Dose and administration
1. 25-50 mg/kg/day divided into 4-6 doses PO. Administer after feeding to reduce
gastric irritation.
Indication
1. Restlessness requiring sedation.
1. Known hypersensitivity to chloral hydrate.

2. Pain.
3. Caution in infants with respiratory distress.
4. Caution in preterm infant, especially extreme immaturity.
5. Caution in infants with hepatic or renal impairment.
Trichloracetaldehyde hydrate is a central nervous system depressant (sedative and

hypnotic). The action of the drug is confined to the cerebral hemispheres. The drug has
virtually no effect upon REM sleep. Has no analgesic properties.
Well absorbed from the gastrointestinal tract and distributes widely in the body (Vd 1-2 L/
kg). Hepatic metabolism by alcohol dehydrogenase to trichloroethanol, an active
metabolite. Moderate binding (35-40%) of trichloroethanol to human plasma protein.
Elimination via the kidney as a glucuronide. Clearance is very variable in neonates.
Elimination half life 8-64 hours (mean 37 hours).
Relatively safe sedative and hypnotic drug. Lethal therapeutic-toxic ratio is lower than for
diazepam. Onset of action 30-60 minutes. Duration of action 4-8 hours.
Possible Adverse Reactions
1. Gastric irritation
2. Respiratory depression
3. Vasodilation, hypotension, cardiac arrhythmias, myocardial depression.
4. CNS depression
5. Paradoxical excitement (especially if given to neonates with pain).
1. Chloral hydrate should be used cautiously in neonates. Tolerance and physical

dependence possible with prolonged use. Review continuing use at frequent
intervals.
2. Accumulation of major metabolites may occur with long-term administration,
especially in very immature neonates, or those with hepatic and/or renal
dysfunction.
guideline.
CHLORAMPHENICOL SODIUM
SUCCINATE Reviewed by Dorothy Cooper
Chloromycetin September 1998
1. Loading dose 20 mg/kg IV infusion by syringe pump over 30 minutes. Maintenance

dose (begin 12 hours after loading dose):
Preterm infants less than 1 2.5 mg/kg/dose

month of age: every 6 hours
Preterm infants over 1 month 5.0 mg/kg/dose
of age: every 6 hours
Full term infants less than 1 5.0 mg/kg/dose
week of age: every 6 hours
Full term infants over 1 week 12.5 mg/kg/dose
of age: every 6 hours
Indications
1. Neonatal CNS infections.

2. After consultation with Paediatric Infectious Disease Consultant.

2. Caution in infants with liver, renal or gastrointestinal dysfunction.
3. Caution in infants with G6PD deficiency.
A wide spectrum bacteriostatic anti-microbial agent. Active against a wide range of gram
negative and gram positive bacteria. It is particularly active against Salmonella typhii and
Haemophilus influenzae. Also active against rickettsial organisms and the
lymphogranuloma-psittacosis group. Acts by inhibition of protein synthesis in intact cells
and in cell free systems. Development of resistance to chloramphenicol appears to be low
in comparison with other antibiotics.
Absorbed rapidly from the gastrointestinal tract. Crosses tissue barriers readily, and
diffuses widely and rapidly through nearly all body tissues and fluids. Chloramphenicol
enters CSF even in the absence of meningeal inflammation. Hydrolysed for release of the
active free base - the site of hydrolysis is unknown. The degree of hydrolysis can be
unpredictable and variable from patient to patient with significant clinical consequences.
Infants during the first month of life appear to hydrolyse the succinate ester less readily
than do older infants and children. Some of the succinate ester is excreted by the kidneys
prior to hydrolysis (9-40%). Free chloramphenicol is metabolised by hepatic glucuronyl
transferases. Of administered or available free chloramphenicol, 85-90% is excreted via
the kidney as the glucuronide.
1. Irritation, soft tissue injury at the site of IV injection.

2. Fever, rash, urticaria and pruritus.
3. Gastrointestinal disturbances (nausea, vomiting, diarrhoea).
4. Haematological disturbances (anaemia, granulocytopaenia, thrombocytopaenia). A
reversible type of bone marrow depression which is dose related, may occur.
There is also an irreversible type of marrow suppression leading to aplastic
anaemia.
5. Neurological disturbances (headache, confusion and delirium, optic and peripheral
neuritis).
6. Grey syndrome (vomiting, refusal to suck, irregular and rapid respiration,
abdominal distension, periods of cyanosis and passage of loose stools, flaccidity,
an ashen grey colour, a decrease in temperature followed by circulatory collapse).
There is no treatment of proved value in managing drug toxicity.
Interactions
1. Anticoagulants, barbiturates, phenytoin, iron salts increase blood level with these
agents.
2. Penicillin synergistic effect may occur.
3. Rifampicin may reduce chloramphenicol levels.
1. Rarely used in the newborn infant.

2. Close monitoring of serum concentration is mandatory. Small changes in dose and
interval can lead to disproportionately large changes in serum concentration.
Therapeutic peak serum concentration 10-25 mg/L.
3. Monitor FBC and reticulocyte counts.
4. Assess hepatic and renal function.
5. Sodium content = 2.25mEq (52mg)/g.
guideline.
CHLORPROMAZINE
HYDROCHLORIDE Reviewed by Dorothy Cooper
Largactil September 1998
Neonatal Abstinence Syndrome
1
1. 2.2-3mg/kg/24 hours (given in divided doses every 6 hours) PO or IM .
2. Use full dosage for 2-4 days. Reduce dosage by approximately 20% every 2-3
2
days according to neonatal abstinence score sheet, if clinical condition permits .
Indications
1. Neonatal abstinence syndrome. Used as a second line drug or alternative to

morphine. Indications for starting treatment are according to the neonatal
abstinence clinical score sheet.
2. In terminal care situations where sedation is needed and secretions are a problem.
Contraindications & Precautions
3
1. Contraindicated in pre-existing CNS depression .
2. Use with caution, or not at all, with impaired liver, kidney, cardiovascular,
cerebrovascular and respiratory function.
3,4
3. Use cautiously with hypothyroidism, acute infections, jaundice and leucopenia .
3
Chlorpromazine is a phenothiazine neuroleptic (antipsychotic) agent . It inhibits
dopamine, has strong sedative effects to which tolerance may develop rapidly, strong
anticholinergic, antiemetic and adrenergic blocking activity, moderate extrapyramidal
3, 6
effects and weak ganglionic block, antihistaminic and antiserotonergic activity .
Chlorpromazine has been used in neonatal opioid abstinence syndrome for sedation and
1,7
to reduce irritability, tremors and gastrointestinal symptoms . Its sedative effect is
prompt and effective.
After oral administration it is readily, but erratically absorbed. Extensive metabolism

occurs in the gut wall and during the first-pass through the liver, hence peak plasma
concentrations are much lower following oral administration than IM.
There may be some enterohepatic recycling. The metabolic pathways are hydroxylation
and conjugation with glucuronic acid, N-oxidation, oxidation of a sulphur atom, and
3,6
dealkylation . (The adult half life = 30 hours). Plasma protein binding is 95-98%
(primarily to albumin). There is wide distribution into body tissues and fluids. After
crossing the blood/brain barrier concentrations achieved in the brain are higher than
those in plasma. Excretion of active and inactive metabolites occurs in the urine and the
bile-elimination of metabolites may be prolonged. Elimination (adults) is biphasic with a
rapid initial phase and a prolonged secondary phase; elimination rate from the brain is
3, 6, 8
unknown .
3
1. Pain and irritation at site of injection .
2. Sedation (tolerance develops rapidly), convulsions (rarely).
3. Tachycardia ECG changes, hypotension, cardiac arrhythmias.
4. Haemolytic anaemia, aplastic anaemia, agranulocytosis, mild leucopenia (high
dose, long term).
5. Gastro-intestinal: Constipation
6. Jaundice: photosensitisation.
7. Hyperglycaemia.
8. Hypo/hyperthermia.
9. Extra pyramidal effects.
10. Possible suppression of cough and gag reflex.
3,4
11. Skin sensitisation and rashes .
Special Considerations & Drug Interactions
1. CNS depressant effect may be enhanced with other CNS depressant drugs, e.g.
sedatives, opiates 3. Infants should be monitored for apnoea.
4
2. Avoid abrupt withdrawal of the drug .
3. Largactil injection contains sodium sulphate which may cause an allergic reaction,
6
e.g., anaphylaxis and/or asthmatic episodes in susceptible patients .
4. Largactil Forte Suspension contains the additives sodium benzoate, sorbitol
(adverse effect = diarrhoea), propylene glycol and povidone K30.
5. Chlorpromazine may cause severe contact dermatitis in sensitised personnel.
3, 4, 6
Nursing staff should avoid skin contact with the drug at administration times .
guideline.
CISAPRIDE
Carl Kuschel
Prepulsid
March 2002
This protocol has been withdrawn
Cisapride should only be prescribed on the direct instructions of the specialist looking
after the baby, after due consideration of the potential adverse effects and the lack of
evidence to support its use in the treatment of Gastro-Oesophageal Reflux Disease in
infants.
A paper copy of the withdrawn protocol is available from the departmental secretary.
guideline.
CYCLOPENTOLATE
Cyclogel September 1998
1. Instil one drop in each eye 30 minutes and 15 minutes before eye examination.
Indications
Is used in conjunction with phenylephrine hydrochloride to dilate the pupil in preparation

for eye examination.
1. All babies at risk of severe ROP (<1250g birthweight or <30 weeks gestation).
2. Intraocular surgery pre and post-operatively.
1. Known hypersensitivity to cyclopentolate hydrochloride.

2. Congenital glaucoma.
3. Increased intraocular pressure.
4. Caution in infants with CNS injury.
Cyclopentolate produces both mydriasis and cycloplegia. As a mydriatic and cycloplegic

cyclopentolate shows its maximum effect 30 - 60 minutes after instillation. Duration 2 - 4
hours. Recovery of accommodation occurs within 24 hours. Binds to melanin in the pupil;
brown eyes may be less responsive to action and require a greater dose. Systemic
absorption can occur and may be minimised by depressing the lacrimal sac for 1-2
minutes after instillation.

1. Photophobia.
2. CNS: irritability, restlessness, seizures.
3. Dry mucous membranes.
4. Flushing, fever.
5. Tachycardia.
6. Urinary retention.
7. Bradycardia caused by intraocular pressure during instilling of drops.
1. Babies are screened:

❍ 4 - 6 weeks postnatally or between 31-33 weeks gestation whichever is
earlier.
❍ Then every 2-4 weeks until vascularisation has progressed into zone III.
❍ Infants with ROP or immature vessels in zone I should be seen two weekly
until normal vascularisation has proceeded to zone III or the risk of

obtaining threshold conditions has passed.
2. Infants with threshold disease should be considered candidates for ablative
therapy of at least one eye within 72 hours of diagnosis.
guideline.
DEXAMETHASONE SODIUM Reviewed by Dr Carl Kuschel, Brenda Hughes, and Robyn

PHOSPHATE Wilkinson
Dexamethasone DBL, Decadron November 2002

DART schedule regime introduced November 2005
For Chronic Lung Disease
The use of Dexamethasone may be considered in infants who are:
● Requiring mechanical ventilation between 7 and 21 days of age,

● In supplemental oxygen, and
● At high risk of neonatal Chronic Lung Disease (CLD)
The recommended course for use in National Women's Health is the course used in the
DART trial.1 Parental consent after explanation of the potential benefits and risks of
treatment will be documented in the clinical notes.
Time Dose Frequency

Days 1 to 3 0.075mg/kg/ 12-hourly
dose
Days 4 to 6 0.050mg/kg/ 12-hourly
dose
Days 7 and 8 0.025mg/kg/ 12-hourly
dose
Days 9 and 10 0.01mg/kg/dose 12-hourly
● Some individuals may receive subsequent doses of 0.01mg/kg/day every 2-3 days
if there is significant deterioration after the tapering of the dose on day 10.
● Repeat courses may be indicated in selected infants with severe CLD.
For subglottic oedema:
1. 0.25 mg/kg/dose IV, PO 8 hourly for 3 doses.

First dose administered approximately 4 hours before the scheduled extubation.
Indications
1. To improve lung function and facilitate extubation in infants requiring prolonged

mechanical ventilation or supplementary oxygen.
2. Subglottic oedema.
1. Known hypersensitivity to corticosteroids and/or dexamethasone.

2. Caution in acute infection, especially systemic fungal infections.
3. Caution with positive sputum cultures for Candida albicans.
4. Caution in gastrointestinal ulceration and renal disease.
Interactions
1. Barbiturates, phenytoin and rifampin decrease cortico-steroid effect.

2. Indomethacin increases the risk of GI bleeding.
3. May decrease the antibody response to vaccines.
Dexamethasone is a synthetic adrenocortical steroid possessing basic glucocorticoid

actions and effects. It is among the most active members of its class, being about 25-30
times as potent as hydrocortisone. At equipotent anti-inflammatory doses,
dexamethasone almost completely lacks the sodium retaining property of hydrocortisone
and closely related derivatives of hydrocortisone. Dexamethasone is readily absorbed
from the gastrointestinal tract. The plasma half-life is 3-4 hours but the biological half-life
is 36-54 hours. The metabolic clearance of dexamethasone is enhanced by the
concurrent administration of phenobarbitone, phenytoin, and other drugs that induce
hepatic enzyme function. Elimination in urine and bile.
Pharmacological effects of dexamethasone are numerous and predominantly affect

metabolism, including glucose homeostasis, promoting catabolism, suppression of the
hypothalamus-pituitary-adrenal axis, suppression of growth. The potential benefits of
dexamethasone on respiratory function may be mediated through a reduction of bronchial
and pulmonary oedema, bronchospasm, reduced inflammation (through inhibition of
prostaglandin and leukotriene synthesis, increased antioxidant activity, and cell
membrane stabilisation).
1. Increased susceptibility to and suppression of the usual symptoms and signs of

infection.
2. Glucose metabolism: hyperglycaemia, glycosuria.
3. Cardiovascular: hypertension, myocardial hypertrophy.
4. Electrolyte disturbances: sodium and water retention, hypokalaemia and
hypocalcaemia.
5. Gastrointestinal: haemorrhage, gastric ulceration and duodenal perforation.
6. Haematological: Leukocytosis, neutrophilia, monocytopaenia, lymphopaenia,
eosinopaenia
7. Skin: Thin fragile skin, impaired wound healing
8. Renal: Nephrocalcinosis, nephrolithiasis
9. Musculo-skeletal: myopathy, osteopenia.
10. Posterior subcapsular cataracts
11. Cessation of linear growth
12. Benign raised intracranial pressure
13. Suppression of adrenal glands (HPA axis)
Special Consideration
1. Several regimens for the use of dexamethasone in chronic lung disease have
been described in the literature. They may be classified as short, intermediate or
long. At present there are few comparative data recording the efficacy and safety
of these regimens.
2. Biochemical and haematological disturbances are common. Urea, electrolytes,
glucose and WBC should be monitored frequently.
3. Use cautiously with potassium-depleting diuretic therapy.
4. Suppression of the HPA axis occurs if dexamethasone is used for longer than one
week. Acute adrenal insufficiency may occur if dexamethasone is abruptly
discontinued. Infants who have received dexamethasone for more than one week
must be weaned over a period of several days.
a. Infants who deteriorate during the weaning phase of their course of
dexamethasone, or shortly after discontinuing dexamethasone, may benefit
from additional dexamethasone.
b. Infants undergoing surgery while receiving dexamethasone must have their
dose increased during the perioperative period.
5. There have been recent concerns about potential long-term adverse
neurodevelopmental effects in preterm infants exposed to postnatal steroids for
treatment or prevention of chronic lung disease.7 The DART study ceased early
due to slow recruitment but did not show a significant differences in the primary
outcome of survival without disability between the dexamethasone and placebo
groups.
6. Systematic reviews have demonstrated that moderately early (7-14 days) steroid
use is associated with a reduction in mortality and in the incidence of CLD.8
Similar reductions in these outcomes are seen with early (<96 hours of age)
steroids.9 Delayed (>21 days) steroid use is not associated with increased
survival but there may be a reduction in CLD.10
7. The reviews of early 9 and delayed 10 steroids have also raised concerns about
long-term outcomes, which are more common in steroid treated infants. There are
insufficient data regarding the long-term outcomes with moderately early steroid
use. However, there may be a decreased risk of neurodevelopmental problems
when steroids are used in infants at high risk of CLD.12
guideline.
DIAZOXIDE
Diazoxide DBL
September 1998
● Note: This is a Section 29 Drug when administered by oral

preparation. This means that a record must be kept of babies to whom
it has been administered, and parents should be informed that it is not
registered for oral use in NZ.
1. 2-5 mg/kg IV for hypertension.

2. 10-15 mg/kg/day p.o divided in 8-12 hourly doses for hypogylcaemia.
3. Doses of >20mg/kg/day often result in hypotension leading to congestive heart
failure.
Indications
1. Hypertensive crisis
2. Hypoglycaemia (due to hyperinsulinaemia)
1. Compensatory hypertension with aortic coarctation or AV shunt.

2. CAUTION use in infants with congestive heart failure.
3. CAUTION in infants with renal insufficiency and impaired carbohydrate metabolism.
Diazoxide is a thiazide but it is nondiuretic and relaxes vascular smooth muscle in the
peripheral arterioles in a mode of action similar to that of nitroprusside. Cardiac output is
increased as blood pressure is reduced.
Hyperglycaemia has been observed in the newborn. Excretion in breast milk - not known.
Diazoxide crosses the placenta and brain barrier. The effect of diazoxide after an IV bolus
is usually maximal within 5 minutes and will persist up to 24 hours. It is highly bound
(>90% to human plasma protein) Vd 0.18L/kg. Elimination is mainly hepatic (80%) and
20% renal. Elimination half life is 15-30 hours. Use during lactation has not been studied.
Use with extreme caution.
1. Sodium and water retention, oedema.

2. Hyperglycaemia.
3. Hypotension.
4. Neonatal jaundice.
5. Gastrointestinal disturbances (nausea and vomiting).
6. Arrhythmias, tachycardia.
7. Cerebral ischemia/convulsions.
8. Blood dyscrasias.
9. Transient cataracts with prolonged use.
1. Is NOT a drug of choice in treatment of hypertensive emergencies in newborns.

2. Extravasation can cause severe inflammatory reaction.
3. Hypokalaemia potentiates the hyperglycaemic effect.
4. Diazoxide causes sodium retention and diuretics may be administered
concomitantly.
5. Concomitant administration with diuretics, anti-hypertensives, phenytoin and
corticosteroids potentiates hyperglycaemia and hypotension.
6. ANTIDOTE: discontinue diazoxide; administer insulin as necessary for
hyperglycaemia; treat hypotension with volume replacement.
guideline.
DIGOXIN
Lanoxin
September 1998
1. Loading dose (digitalisation) is especially recommended when treating arrhythmias.

2. Give over 24 hours as 3 divided doses: Initially half of the total dose is given, then
quarter of total dose every 8-12 hours x 2. Administer by slow IV infusion over 30
minutes.
3. Oral doses should be 25% greater than IV doses.
4. Do not administer IM (causes pain and tissue damage)
Total Loading Dose Maintenance Dose Interval

Postmenstrual IV PO IV PO
Age (weeks) micrograms / micrograms / micrograms / micrograms/ hr
kg kg kg kg
≤29 15 20 4 5 24
30 to 36 20 25 5 6 24
37 to 48 30 40 4 5 12
≥49 40 50 5 6 12
Indications
1. Treatment of heart failure caused by diminished myocardial contractility.

2. Treatment of supraventricular tachycardia, atrial flutter, and atrial fibrillation.
1. Known hypersensitivity to cardiac glycosides.

3. Caution in infants with renal impairment.
4. Caution in infants with acute myocarditis, bradyarrhythmias (especially heart
block).
5. Ventricular dysrhythmias.
6. Pre-existing hypokalaemia may precipitate adverse reactions.
Digoxin is a digitalis glycoside with positive inotropic and negative chronotopic

actions. Increases myocardial catecholamine levels (low doses) and inhibits
sarcolemmal sodium potassium - ATPase (higher doses) to enhance contractility.
Indirectly increases vagal activity, thereby slowing SA and AV node conduction.
Other effects include peripheral, splanchnic, and perhaps pulmonary
vasoconstriction, and reduced CSF production.
Rapid but variable absorption (52-79%) from the gastrointestinal tract. IM

absorption similar variability but IM injection causes pain and local soft tissue
injury. Large distribution volume: Vd in term infant (12-16 L/kg) > preterm infant (4-
6 L/kg). Rapid distribution to peripheral tissue compartments (elimination half life
is reported as 61-170 hours in preterm infants and 35-45 hours in term infants) but
the time to reach steady state is much slower. Serum concentration peaks 30-90
minutes after an oral dose with myocardial peak occurring after 4-6 hours.
Accumulates in the myocardium: myocardial to serum ratio 149:1. Low binding
(20%) to human plasma protein. Probably not significantly metabolised. Eliminated
mainly via the kidneys (75% unchanged) by glomerular filtration and tubular
secretion.
Main pharmacodynamic property of digoxin is its ability to increase the force of

contraction of the myocardium - positive inotropic action. Also slows the heart rate
and produces changes in activity of SA node, the atria, and AV node - negative
chronotropic effect. Inotropic effect occurs within 30 minutes. Non toxic cardiac
effects include shortening of QTC interval, depression of STsegment, diminished
amplitude of T wave, and slowing of heart rate.

2. Lethargy
3. Bradycardia
4. Cardiac arrhythmias (PVCs, PAT with block, bigeminy, sinus arrhythmia,
sinoatrial block, atrioventricular junctional or multifocal ventricular
tachycardia).
5. Toxicity is enhanced by hypokalaemia.
1. Dosing regime determined by maturity and renal function.

2. Serum electrolytes should be stabilised prior to digitalisation. Monitor urea,
electrolytes, creatinine during therapy.
3. Obtain baseline ECG prior to first digitalising dose of digoxin, prior to the
final digitalising dose and at intervals throughout treatment.
4. Serum digoxin levels should be measured during treatment. Obtain
specimen 10 - 12 hours after last loading dose and repeat at intervals.
Repeat after dose changed. Usual therapeutic range 1.0 - 2.6 nmol/L. Serum
levels >4.6 nmol/L are considered to be in the toxic range.
5. Management of digoxin toxicity: stop digoxin, stabilise fluids and
electrolytes, treat arrhythmias.
Interactions
1. Cisapride and metoclopramide may decrease absorption of digoxin.

2. Indomethacin amiodarone, erythromycin and spironolactone may increase
digoxin levels
3. Amiloride inhibits digoxin effect.
4. Amphotericin B, corticosteroids, diuretics and ticarcillin: hypokalaemia or
hypomagnesaemia predisposing patient to digitalis toxicity.
guideline.
DOBUTAMINE HYDROCHLORIDE
Reviewed by Dr Carl Kuschel
Dobutamine DBL, Dobutrex

April 2004
1. 2-25 micrograms/kg/minute by continuous IV infusion.

2. Begin at a low dose and titrate by monitoring effects.
3. Administer via a central line (UVC, Longline, or Surgical CVL). If no central access
available, use a large vein.
4. Usual dilution 30 mg/kg (2.4 ml/kg) dobutamine to make 50 ml with NS or D5W
1 ml/hour = 10 micrograms/kg/minute.
3 x weight (kg) x dose (micrograms/kg/min)

Dobutamine (mg) in 50ml IV solution =
IV rate (ml/hr)
Indication
1. Blood pressure support in infants with shock and hypotension.
1. Hypersensitivity to sympathomimetic amines and sodium metabisulfite.

2. Hypovolaemia should be corrected prior to commencing the drug.
3. Uncorrected tachyarrhythmia.
4. Caution in infants with hypertension, LV outflow tract obstruction.
Dobutamine is a synthetic catecholamine with primarily beta 1 adrenergic activity. It is an

inotropic vasopressor. It increases myocardial contractility, cardiac index, oxygen delivery
and oxygen consumption. It decreases systemic and pulmonary vascular resistance
(adults).
The drug must be administered by continuous IV infusion because of rapid metabolism of

the drug. It is metabolised in the liver to an inactive compound. The onset of action is 1-2
minutes after IV administration with the peak effect occurring in 10 minutes. The half-life
of its drug effect is two minutes.
1. Venous irritation, soft tissue injury at site of IV infusion.

2. May cause hypotension if patient is hypovolaemic.
3. Tachycardia at high dosage.
4. Arrhythmias, hypertension especially systolic pressure and cutaneous
vasodilatation.
5. Gastro-intestinal (nausea and vomiting).
1. Volume loading is recommended before commencing dobutamine infusion.

2. Clinical experience with dobutamine in neonates is limited. Whether dobutamine
has any consistent advantages over dopamine in the treatment of a neonate with
myocardial dysfunction remains to be established.
3. Betablockers may antagonise dobutamine effect.
4. General anaesthetics: greater incidence of ventricular arrhythmias.
5. Dobutamine should not be used with agents containing sodium bisulfite.
guideline.
DOPAMINE HYDROCHLORIDE
Dopamine DBL, Dopamin

April 2004
1. 2-20 micrograms/kg/minute by continuous IV infusion.

2. Begin at a low dose and titrate by monitoring clinical response.
3. Maximum recommended dose 20-50 micrograms/kg/minute.
4. Administer via a central line (UVC, Longline, or Surgical CVL). If no central access
available, use a large vein.
5. Usual dilution 30 mg/kg (0.75 ml/kg) dopamine to make 50 ml with Normal Saline
or D5W
1 ml/hour = 10 micrograms/kg/minute.
3 x weight (kg) x dose (micrograms/

Dopamine (mg) in 50ml IV solution
kg/min)
=
IV Rate (ml/hr)
Indications
1. To improve cardiac output, blood pressure and urine output in critically ill infants
with hypotension.
1. Hypersensitivity to sympathomimetic amines and sulfites.

2. Hypovolaemia should be corrected prior to commencing the drug.
3. Uncorrected tachyarrhythmias.
4. Caution if concurrent with phenytoin.
Dopamine is a sympathomimetic catecholamine which exhibits alpha adrenergic, beta

adrenergic, and dopaminergic agonism. The mechanism of action in neonates is
controversial. Relative effects of dopamine at different doses are uncertain because of
developmental differences in:
● endogenous noradrenaline stores,

● alpha and beta adrenergic, and dopaminergic receptor functions,
● the ability of the neonatal heart to increase stroke volume. Responses tend to be
individualised.
Dopamine is metabolised very rapidly and is effective only when administered

intravenously by continuous infusion. The half-life of dopamine effect is 2 minutes, which
is the same as the other catecholamines. No information available on protein binding.
97% is excreted in the urine as metabolites.
Drug effects are dose dependent:
● Low dose: 2-5 micrograms/kg/minute. Little effect seen on heart rate or cardiac
output. Increased blood flow accompanied by increased urine output.
● Intermediate doses: 5-15 micrograms/kg/minute. An increase in cardiac
contractility and cardiac output results in increased normal blood flow and heart
rate.
● High dose: 15 micrograms/kg/minute. Alpha adrenergic effects begin to dominate:
increased systemic and pulmonary vascular resistance. Decrease in normal
perfusion.
1. Venous irritation, soft tissue injury at the site of IV injection.

2. Tachycardia and tachyarrhythmias, bradycardia.
3. Gastrointestinal upset (vomiting).
4. Vasoconstriction, hypertension.
1. Dosage range is determined by type of desired clinical effect. Start at the lower
end of the desired range and titrate according to clinical response.
2. Volume loading is considered before commencing dopamine infusion.
3. Use with caution in patients with persistent pulmonary hypertension of the
newborn.
4. Suggested treatment for tissue sloughing following IV infiltration: inject a 1 mg/ml
solution of phentolamine into the affected area. The usual amount needed is 1-5
ml, depending on the size of the infiltrate.
5. Dopamine effects are prolonged and intensified by betablockers.
6. General anaesthetic: increased risk of arrhythmias or hypertension.
7. Phenytoin may lower blood pressure.
8. Acidosis decreases effectiveness of dopamine.
guideline.
DOXAPRAM
Reviewed by Dr Carl Kuschel, Dr Malcolm Battin, Brenda
Hughes, and Ana Kennedy
Dopram
April 2004
Continuous Intravenous Infusion
1. Start at 0.5mg/kg/hour and, if necessary, titrate upwards at increments of 0.5 mg/

kg/hour to a maximum of 1.5 mg/kg/hour.
2. Review continuing use on a daily basis. There is some evidence that the effect
may not be sustained.
Indications
1. Apnoea of prematurity unresponsive to caffeine (or aminophylline).

Doxapram is used in conjunction with caffeine (or aminophylline).
Contraindications and Precautions 1, 2, 3
1. Seizures
2. Recent periventricular haemorrhage
3. Cerebral oedema
4. Severe hypertension
5. Cardiac failure
6. Hyperthyroidism
Clinical Pharmacology 1, 2, 3, 4
Doxapram is a respiratory stimulant, acting principally through the central respiratory

centres in the medulla. Stimulation of peripheral carotid chemoreceptors may also
contribute to the respiratory action. The resultant effect is an increase in tidal volume
with an increase in respiratory rate. Doxapram has a quick onset and short duration of
action. A release in catecholamines has been noted following the use of doxapram,
leading to a pressor effect, attributed to an increase in cardiac output rather than a
peripheral vasoconstriction.
Doxapram undergoes extensive hepatic metabolism, with very little free drug appearing in
the urine.
Possible Adverse Effects 1, 2, 3, 7
1. Hypertension is the most common adverse effect seen in preterm infants, and can
7
even occur at low doses. Monitor blood pressure regularly.
2. QTc prolongation, 2nd degree heart block, arrhythmias.
3. Seizures (may be associated with high doses), irritability, flushing, sweating,
involuntary movements, muscle spasm.
4. Respiratory distress
5. Vomiting, diarrhoea, urinary retention.
Drug Interactions 1
1. Caffeine, aminophylline - possible increase in CNS stimulation.
3, 6
1. Do not use in conjunction with mechanical ventilation.

2. Monitor:
❍ B.P. & pulse rate (sudden onset of hypotension or dyspnoea suggests that
doxapram should be stopped)

❍ Blood gases: consider ventilation if there is a deterioration in blood gas
parameters without clinical improvement

3. Watch for accumulation if high doses are infused for more than 36 to 48 hours.
4. Signs of overdose are: excessive pressor effect, tachycardia, skeletal muscle
hyperactivity (tremors), enhanced deep tendon reflexes.
5. Extravasation may lead to thrombophlebitis or local skin irritation.
6. Some preparations of doxapram contain benzyl alcohol as a preservative (e.g.
Wyeth brand of Dopram®). Benzyl alcohol may cause significant metabolic and
neurological disturbance in infants. 8
7. Doxapram is not licensed for use in children. There are limited trials evaluating its
use in neonates for the treatment of apnoea.
guideline.
ERYTHROMYCIN ETHYLSUCCINATE
Reviewed by Dr Carl Kuschel and Dorothy Cooper
EES
September 1998
Dose
5-20 mg/kg/dose 12
Preterm neonates
hourly PO
10-20 mg/kg/dose 12
Term neonates:≤7 days
hourly PO
10-20 mg/kg/dose 8
Term neonates: >7 days
hourly PO
10-20 mg/kg/dose 6
Infants
hourly PO
Administer with EBM/infant formula to enhance absorption and reduce

possible gastrointestinal side effects.
Indications
1. Suspected/proven infection with Mycoplasma pneumoniae, Ureaplasma

urealyticum, and Chlamydia trachomatis.
2. As a substitute for penicillin in situations of significant hypersensitivity to penicillin.
3. Treatment for and prophylaxis against Bordetella pertussis.
1. Known hypersensitivity to erythromycin or other macrolides.

2. Infants with biliary tract obstruction.
4. Caution in infants with jaundice, liver dysfunction, and biliary tract disease.
Bacteriostatic antibiotic which suppresses bacterial protein synthesis. The antibacterial

spectrum is similar to penicillin but extended to include Mycoplasma pneumoniae,
Ureaplasma urealyticum and Chlamydia trachomatis.
Vd 45% of body weight in adults. Antibacterial levels are achievable in all tissues except
brain and CSF. Highly bound (64-98%) to human plasma protein. Hepatic excretion into
bile as active compound. Only 5-15% of administered dose excreted in the active form in
the urine. Limited data are available for pharmacokinetics in neonates. It is reported that
the drug is well absorbed by mouth. Plasma half life is 2-4 hours.
Interactions
● Increase serum digoxin levels.

● Midazolam: increased effect.
● Theophylline decreases erythromycin blood levels and increases theophylline
toxicity. Effect on half life of caffeine has not been clarified.
● Never give erythromycin to a baby receiving cisapride because there is a risk of
arrhythmias.

2. Jaundice, intrahepatic cholestasis.
3. Reversible hearing loss (very high doses).
4. Hypersensitivity reactions (urticaria, mild skin eruptions, anaphylaxis) rare.
1. May antagonise action of penicillins, cephalosporins.

2. Concurrent use with theophylline, phenytoin, carbamapezine, or digoxin may be
associated with elevation in serum levels of these drugs. The dose of these drugs
should be reduced in infants and serum concentrations monitored closely.
3. Reduce dose of erythromycin if extreme immaturity, severe jaundice and/or
hepatic dysfunction.
4. Absorption from the gastrointestinal tract is unpredictable in the very immature
infant. It may be preferable to administer erythromycin intravenously initially for at
least 48-72 hours, or longer, before changing to oral administration.
guideline.
ERYTHROMYCIN LACTOBIONATE
Reviewed by Dr Carl Kuschel and Dorothy Cooper
Erythromycin DBL
September 1998
1. IV infusion by syringe pump over 60 minutes.
Dose
10 mg/kg/dose 6
Preterm neonates:
hourly
Term neonates: ≤7 10-20 mg/kg/dose
days: 12 hourly
Term neonates: >7 10-20 mg/kg/dose 8
days: hourly
10-20 mg/kg/dose 6-
Infants:
8 hourly
Indications
1. Suspected/proven infection with Mycoplasma pneumoniae, Ureaplasma

urealyticum, and Chlamydia trachomatis.
2. As a substitute for penicillin in situations of significant hypersensitivity to penicillin.
3. Treatment for and prophylaxis against Bordetella pertussis.
1. Known hypersensitivity to erythromycin or other macrolides.

4. Caution in infants with jaundice, liver dysfunction, and biliary tract disease.
Interactions
● Increase serum digoxin levels.

● Midazolam: increases effect.
● Theophylline decreases erythromycin blood levels and increases theophylline
toxicity. Effect on half life of caffeine has not been clarified.
● Never give erythromycin to a baby receiving cisapride because there is a risk of
arrhythmia.
Bacteriostatic antibiotic which suppresses bacterial protein synthesis. The antibacterial

spectrum is similar to penicillin but extended to include Mycoplasma pneumoniae,
Ureaplasma urealyticum and Chlamydia trachomatis.
Vd 45% of body weight in adults. Antibacterial levels are achievable in all tissues except
brain and CSF. Highly bound (64-98%) to human plasma protein. Hepatic excretion into
bile as active compound. Only 5-15% of administered dose excreted in the active form in
the urine. Plasma half life equals 2-4 hours.

2. Pain, soft tissue injury at IM injection site. Not suitable for IM administration.
4. Jaundice, intrahepatic cholestasis.
5. Reversible hearing loss (very high doses).
6. Hypersensitivity reactions (urticaria, mild skin eruptions, anaphylaxis) rare.
7. Sudden severe bradycardia after IV administration. Prolongation of QT interval and
ventricular arrhythmias with rapid IV administration.
1. May antagonise action of penicillins, cephalosporins.

2. Concurrent use with theophylline, phenytoin, carbamapezine, or digoxin may be
associated with elevation in serum levels of these drugs. The dose of these drugs
should be reduced in infants and serum concentrations monitored closely.
3. Reduce dose of erythromycin if severe jaundice and/or hepatic dysfunction.
guideline.
ERYTHROPOIETIN
Reviewed by Dr Jutta van den Boom, Dr Simon Rowley,
Brenda Hughes, and Robyn Wilkinson
Recormon, Eprex, Epoetin
July 2003
1. 250 units/kg/dose two-times per week (Monday/Friday) SC. Total weekly dose 500
units/kg.
Continue for 4-6 weeks.
● Please chart appropriate generic name. The particular preparation in use at

present is Recormon (Epoetin beta).
● Although other preparations (Trade name: Eprex - Generic name: Epoetin alpha)
are available, they are not currently in use in National Women's Hospital NICU.
Indications
1. Prevention of blood transfusion in the treatment of anaemia of prematurity

(reduced reticulocyte count, normochromic, normocytic, no haemolysis)
2. Consider treatment in infants with
● birth weight <1200g and/or

● gestation <32/40
● at two weeks of age
● who have not received previous blood transfusions (or have had
early blood transfusions with only one donor exposure)
● falling haematocrit (close to transfusion guidelines - see Guidelines
for Red Blood Cell Transfusion)
● not symptomatic or sick.
● Once a transfusion is required during treatment with erythropoietin, it should be

discontinued.

1. Prescription of erythropoietin should be discussed with the parents and a verbal
consent for treatment needs to be obtained.
Erythropoietin is a natural glycoprotein produced primarily in the kidneys which stimulates

red blood cell production. During fetal life it is mostly produced in the liver. Extremely
premature infants experience a lack of erythropoietin and therefore reduced
erythropoiesis. With administration of exogenous erythropoietin red blood cell production
is stimulated. Historically it has been shown to reduce the number of blood transfusions,
but not within the first two weeks of life. It also has not been shown to avoid transfusions
altogether. It seems to be safe, but not cost effective. The aim of exogenous
administration of erythropoietin is to avoid blood transfusions and/or to reduce donor
exposure). At the same time measures to reduce blood loss (avoid unnecessary blood
tests, development of small volume blood tests) should be initiated and blood transfusions
protocols should be adhered to.
Interactions
1. No known interactions
1. Iron deficiency (which can be prevented by ensuring adequate supplementation).

2. Neutropenia (self-correcting after stopping treatment) may occasionally occur.
3. Thrombocytopenia
4. Thrombocytosis
5. Hypertension
Use in conjunction with
Iron 1. Commence oral iron when on 75% feeds.

2. Dose 6mg/kg/day elemental iron (1ml/kg/day of Ferrous
sulphate [30mg elemental iron per 5ml])
3. Increase iron to 9 or 12 mg/kg/day if ferritin below 100 μg/L.
Note: Patients with chronic lung disease may require less iron
depending on number of transfusions received. Use ferritin level as a
guide to dosage.
Vitamin E 1. Start when oral iron commenced
2. Dose 25 IU/day
3. Given to prevent oxidative haemoloysis of red cells.
4. Do not give simultaneously with iron.
Bloods and 1. FBC (including WBC and platelet count), ferritin and
Monitoring reticulocytes at commencement.
2. FBC and reticulocyte count weekly.
3. Ferritin every second week.
4. Daily blood pressure
guideline.
FENTANYL
Reviewed by Dr Carl Kuschel and Brenda Hughes
Sublimaze
October 2004
1. Sedation and analgesia: 1-4 micrograms/kg/dose IV slow push, IM.

a. For intubation, use 4micrograms/kg
b. Repeat as required (usually every 2-4 hours).
c. May be given as a continuous infusion: 1-5 micrograms/kg/hour.
2. Anaesthesia: 5-50 micrograms/kg/dose.
a. Minor surgery 5-20 micrograms/kg/dose.
b. Major surgery 30-50 micrograms/kg/dose.
50 x weight (kg) x dose (micrograms/kg/

Fentanyl (micrograms) in 50ml IV solution
hour)
=
IV rate (ml/hour)
Usual strength = 2-10 micrograms/ml.
Indications
1. Intubation
2. Analgesia
3. Sedation
4. Anaesthesia
1. Known hypersensitivity to fentanyl and/or other opiates.

2. Bradyarrhythmias.
3. Myasthenia gravis
5. Caution in neonates with hepatic or renal impairment
6. Caution in nonventilated neonates with respiratory distress.
7. Caution in neonates with raised intracranial pressure.
Fentanyl citrate, a narcotic analgesic, is 50-100 times more potent than morphine. Actions
qualitatively similar to those of morphine. Produces a minimum of cortical depression.
Alterations in respiratory rate and alveolar ventilation may last longer than analgesic
effect. No significant cardiovascular effects at usual therapeutic doses.
Rapid distribution with sequestration in fat. Wide variability in distribution volume (Vd 1-13
L/kg). Extensive binding to human plasma protein. Hepatic metabolism. Excretion via the
kidney. Elimination half-life very variable in neonates (6-32 hours). Onset of action almost
immediate with IV administration (7-8 minutes with IM). Peak effect 5-15 minutes
following IV injection. Duration of the analgesic effect 30-60 minutes (1-2 hours with IM).
1. Bradycardia (rapid administration).

2. Respiratory depression.
3. Decrease in physical activity.
4. Physical dependence.
5. Rapid tolerance with prolonged use (>2 days).
6. Nausea and vomiting.
7. Severe muscle rigidity, especially chest wall rigidity. Can be avoided with slow IV
pushes rather than rapid boluses. Have suxamethonium ready.
1. Faster onset of action but shorter duration of action than morphine.

2. Additive effects with other narcotics and/or other central nervous system
depressants.
3. With prolonged use the minimum effective dose may increase as tolerance
develops.
4. After continuous use, discontinue fentanyl over a few days because physical
dependence develops.
5. Management of fentanyl overdose and/or toxicity: discontinue fentanyl, supportive
therapy (ventilation, etc.), naloxone (0.01-0.1 mg/kg/dose IV).
guideline.
FERROUS SULPHATE
Ferro-Liquid
July 2005
● Ferrous sulphate is available in a solution labelled 150mg/5ml, which

provides 6mg of elemental iron per ml.
Prophylaxis
1. 0.5ml/kg/day (3mg/kg/day of elemental iron) in one or two divided doses.
● All infants with a birthweight<1800g or a gestation at birth <32 weeks

❍ Infants outside these criteria should be discussed with a specialist first.
● Commence at 4 weeks of age or on discharge, whichever occurs earliest.
Treatment
1. 1ml/kg/day (6mg/kg/day of elemental iron) in two divided doses.
Indications
1. Prophylaxis for iron deficiency anaemia in low birthweight infants with reduced
body iron stores.
2. Treatment of documented iron deficiency anaemia.
1. Peptic ulcer.
2. Haemolytic anaemias.
Iron is an integral part of haemoglobin. Although the major portion of iron in the body is in
the form of haemoglobin, a small amount is also stored in tissues as haemosiderin and
ferritin, and in blood it is bound to transferrin, a carrier protein.
The intestine is the primary site for both absorption and excretion of iron. Food and
antacid decrease the absorption of iron.
Iron is rigidly conserved in the body. Most of the iron released from breakdown of
haemoglobin in the liver is reused.
1. Gastrointestinal disturbance:
❍ Nausea, vomiting, constipation.
❍ Dark stools (green or black).
❍ Erosion of gastric mucosa.
2. In preterm infants may cause increased red cell haemolysis and haemolytic
anaemia because of low serum values of vitamin E.
3. Lethargy.
4. Hypotension.
5. Acute toxicity: gastrointestinal disturbances worsened, CNS disorders (lethargy),
pallor, cyanosis, shock.
1. Monitor Hb, PCV, reticulocytes.

2. Vitamin C may increase iron absorption.
guideline.
FLUCLOXACILLIN
Floxapen, Flucloxin
September 1998
1. 25-50mg/kg/dose by slow IV injection, IM or PO.
Postmenstrual
Postnatal Age Dose Interval
Age
(days) (hours)
(weeks)
0 to 28 12
≤29
> 28 8
0 to 14 12
30 to 36
> 14 8
0 to 7 12
37 to 44
>7 8
≥45 All 8
Indications
1. Empirical therapy for infants with suspected coagulase negative staphylococcal

sepsis but resistance is now increasingly common. May be administered in
combination with amoxycillin and amikacin until culture results available.
2. Skin and soft tissue infections.
3. Bone and joint infections.
Semi-synthetic narrow spectrum bacteriocidal antibiotic with considerable activity against

penicillinase producing coagulase negative staphylococci and Staphylococcus aureus.
Has little activity against gram negative bacilli. Action through inhibition of biosynthesis of
cell wall mucopeptides.
Well absorbed after oral administration, although absorption is reduced in the presence of
food and unpredictable in neonates. Widely distributed at varying concentrations in
human body tissues and fluids. Very little passes into the CSF unless the meninges are
inflamed. Highly bound (92%) to human plasma proteins. Excreted, mainly unchanged, by
the kidney. Tubular excretion is inhibited by probenecid.

4. Non-specific rashes and skin eruptions.
5. Fever, pruritus, urticaria.

Administer separately as simultaneous administration may cause inactivation, and
precipitation.
interval).
3. Sodium content: Flucloxin 3.9mmol/gm, Floxapen 3.3mmol/gm
guideline.
FLUCONAZOLE
Reviewed by Dr Carl Kuschel, Dr Liz Wilson, Brenda
Hughes, and Robyn Wilkinson
Diflucan
March 2002
1,2.3
1. 6 mg/kg PO/IV every 72 hours (first 2 weeks of life), every 48 hours (weeks 2 to 4)
and every 24 hours (over 4 weeks of age).
Administer IV dose over 30 minutes.
2. Prophylaxis while neutropenic: 3 – 12 mg/kg PO/IV every 72 hours (first 2 weeks
of life), every 48 hours (weeks 2 to 4) and every 24 hours (over 4 weeks of age).
Administer IV dose over 20 - 30 minutes
Indications
1. Treatment of suspected systemic fungal infection and extensive cutaneous and

confirmed Candidiasis once sensitivities confirmed.
Contraindications
1. Hypersensitivity to fluconazole or related azole compounds.
Precautions
1. Impaired renal or hepatic function. Dose reduction recommended in renal

impairment – see "Special Considerations".
Fluconazole is a highly selective inhibitor of fungal cytochrome P-450 sterol C-14 α-

demethylation, thus inhibiting ergosterol synthesis. Ergosterol is an essential component
of the fungal cell membrane, and instability of the cell membrane results in cell death.
It is water-soluble and is well absorbed from the gastrointestinal tract, although it is not
generally used via this route in neonates. Oral absorption is unaffected by food intake. It
has good CSF penetration and is excreted largely unchanged in urine, therefore dose
adjustments are necessary in the presence of impaired renal function. Neonates have a
greater volume of distribution and decreased elimination rates compared to older children
and adults. The plasma half life in neonates is approximately 70 hours (30 hours in
adults). In preterm infants fluconazole was found to have a plasma half life=73 hours (at
3
birth), 53 hours (6 days of age), and 46 hours (at 12 days of age).
3,5
Possible Interactions
Amphotericin Currently not established if the combination is beneficial or of

reduced benefit in terms of antifungal reponse. There is theoretical
antagonism seen in vitro but not in vivo.
Caffeine Possible increase in caffeine levels.
Cisapride Increases risk of arrhythmias
Hydrochlorothiazide Given orally with oral fluconazole may increase fluconazole levels
Midazolam Increases half-life of Midazolam(more likely with higher doses long
term)
Theophylline Raises theophylline levels
Phenytoin Raises phenytoin levels – (measure serum levels and reduce
phenytoin dose if necessary); possible decrease in fluconazole
levels; increase in LFTs
Rifampicin Decreases fluconazole levels, possible increase in LFTs
Zidovudine Increase in zidovudine levels
1. Diarrhoea, flatulence, nausea, rash, increase in LFTs, severe hepatotoxicity in

patients with underlying hepatic disease.
2. Rarely: leukopenia, thrombocytopenia, toxic epidermal necrolysis, Stevens-
Johnson syndrome.
1. Monitor: Renal & hepatic function Consider reducing dose if there is renal
impairment:
❍ Mild to moderate renal impairment: give half normal dose
❍ Moderate to severe renal impairment: give one-third normal dose
2. Do NOT give by IM or direct IV bolus injection. Continuous infusion is not

4
recommended
3. Systemic Candidiasis is rare without evidence of superficial infection or
colonisation.
4. Not effective against some Candida species (i.e. C.krusei, C.glabrata)
5. Amphotericin is still the drug of choice for proven Candida infection until sensitivity
to Fluconazole is confirmed. However, Fluconazole therapy for established
infection can be considered in consultation with the Infectious Diseases service.
guideline.
FLUCYTOSINE
Reviewed by Dr Lesley Voss, Brenda Hughes, Mandy
Hodgson, Ruth Tramschek
Alcobon
January 2000
Oral
8,9
1. 25 - 37.5 mg/kg/dose every 6 hours .
2. The oral route should be the first line option, as the drug is well absorbed by this
route. Use I.V. if N.B.M.
Intravenous
8
1. 25 mg/kg/dose every 6 hours
Indications
1. Congenital candidiasis, candida meningitis, fungal endocarditis, systemic

candidiasis and, systemic fungal infections caused by other sensitive fungi.
2. Usually used in combination with Amphotericin.
Contraindications
1. Known hypersensitivity to flucytosine

2. Known sensitivity to trometamol (excipient in infusion solution).
Precautions
1. Bone marrow depression

2. Preterm infants, especially extreme immaturity.
3. Renal dysfunction.
Drug Interactions
● Amphotericin; Possible decrease in kidney function, resulting in reduced clearance

7
of flucytosine
● Caution with other drugs with nephrotoxic potential.
An antifungal agent with activity against Candida species, Cryptococcus neoformans and
6
the pathogens of chromoblastomycosis . The drug penetrates the cell, is transformed to
5-fluorouracil which interferes with RNA synthesis. Resistance can develop during
treatment and it is recommended that sensitivity tests are conducted before and during
6
treatment . Synergism has been demonstrated in several species of pathogens when
6
flucytosine is combined with amphotericin .
Flucytosine is well absorbed from the gastrointestinal tract. Widely distributed through
5
body tissues and fluids and into the CSF . Low binding to plasma proteins.
Approximately 80-90% of a given dose is excreted, unchanged via the kidney.

2. Rash
3. Gastrointestinal disturbances (vomiting, diarrhoea).
4. Alterations in liver function tests- possibly dose related and reversible.
5
Hepatotoxicity
5. Bone marrow depression: especially leucopenia and thrombocytopenia(usually
associated with toxic blood levels plus concurrent amphotericin administration, and
with renal function impairment. Fatal agranulocytosis and aplastic anaemia have
been reported5 .
1. The oral preparation is unlicensed in New Zealand

2. Usually given in conjunction with amphotericin due to high risk of resistance when
used alone.
3. Monitor:
● Sensitivity of isolate before and during treatment
● Renal Function:
Mild renal failure- extend dose interval to every 12 hours

Moderate renal failure – extend dose interval to every 24 hours
Severe renal failure – dose according to serum levels 8.
● Full blood count and liver function – daily at start of treatment, then twice
weekly
● Therapeutic Drug Monitoring (TDM):
Steady state achieved in approximately one day.

Peak level: 250 – 400 μmol/L. Take level at 15 to 30 minutes after end of I.
V. infusion 10 or 2 hours after an oral dose 11.
Trough level: > 80 μmol/L (to avoid resistance)
6
4. Infusion contains chloride (34.4mmol/250 mL)
guideline.
FRUSEMIDE
Reviewed by Dr Carl Kuschel, Brenda Hughes, and Karen
Anderson-Hawke
Frusemide DBL, Lasix
June 2005
1. Intravenous and oral dosing 1,2,4

Dose Interval
Route Dose
(hr)
IV 1mg/kg/dose 24
<32 weeks
Oral 1-2mg/kg/dose 24
IV 1mg/kg/dose 12-24
≥32 weeks
Oral 1-2mg/kg/dose 12-24
2. Infusion: 3 Maximum dose of 1mg/kg/hour in those infants in whom an

aggressive yet controlled diuresis is required.
Commence at 0.3mg/kg/hour and titrate according to urinary output.
Usual dilution 50mg/kg frusemide to make 50ml with D5W or D10W. 1ml/hour =
1mg/kg/hour.
Indications
1. Fluid overload (iatrogenic, congestive heart failure, renal failure, other).

2. Chronic lung disease.
1. Known hypersensitivity to frusemide.

4. Caution in infants with jaundice.
5. Caution in infants with hyponatraemia and/or hypokalaemia.
Frusemide is a potent loop diuretic with rapid action. The drug inhibits chloride
reabsorption in the ascending limb of the Loop of Henle and inhibits tubular sodium
transport, causing major loss of sodium and chloride. Increased urinary losses of
potassium, calcium and phosphate (large doses only) also occur. Urine pH increases.
Frusemide also increases renal blood flow.
Frusemide is rapidly absorbed from the gastrointestinal tract (bioavailability 60-70%). The
half life in adults is 2 hours, but this is approximately 8 times greater in neonates. It is
approximately 99% bound to plasma proteins, and excreted mainly unchanged by the
kidneys.
6,7
1. Dehydration, hypotension.
2. Gastrointestinal disturbance (oral administration).
3. Hyponatraemia, hypokalaemia, hypochloraemic metabolic alkalosis.
4. Hypercalciuria, hypocalcaemia, nephrocalcinosis.
5. Rash.
6. Ototoxicity (especially in those also receiving nephrotoxic drugs).
7. Nephrotoxicity.
Drug Interactions
Aminoglycosides ● Possible nephrotoxicity and ototoxicity with high dose frusemide

infusions.
Bilirubin ● Frusemide and bilirubin may displace either other from plasma
protein.
Captopril ● Monitor renal function in infants with renal arterial stenosis.
Ceftazidime ● May increase ceftazadime levels.
Digoxin ● Monitor digoxin and potassium levels.
Hydrocortisone ● May lead to a decrease in potassium levels.
Indomethacin ● Decrease in effect of frusemide.

Pancuronium ● Possible increase in neuromuscular blockade.
Phenytoin ● Decrease in frusemide effect.
1. Electrolyte aberrations occur frequently and should be anticipated and monitored.

❍ Sodium, potassium and chloride supplements are usually required with long-
term use of frusemide.

❍ Need to monitor calcium levels with long term use.
2. Dosing regime determined by clinical response and infant's maturity.

3. Placement of an indwelling urinary catheter should be mandatory for infants
receiving continuous infusions of frusemide.
guideline.
GENTAMICIN SULPHATE Reviewed by Dr Carl Kuschel and Brenda Hughes
Gentamicin DBL February 2001

Monitoring levels information changed November 2003
1. Intravenous infusion by syringe pump over 30 minutes, or IM.

2. Loading dose of 4mg/kg.
Postmenstrual
Postnatal Age Dose Interval
Age
(days) (mg/kg/dose) (hours)
(weeks)
≤29 0 to 28 2.5 24
(or significant
asphyxia) > 28 3.0 24
0 to 14 3.0 24
30 to 36
>14 2.5 12
0 to 7 2.5 12
≥37
>7 2.5 8
Indications
1. Empirical therapy for those VLBW infants with risk factors for perinatal sepsis in
the first week of life.
2. Proven neonatal sepsis (pneumonia, septicaemia, urinary tract infections, CNS
infections, skin, bone and soft tissue infection), with bacteria known to be sensitive
(note Staph epidermidis is resistant).
1. Known hypersensitivity to gentamicin/other aminoglycosides.

2. Use in treatment of minor infections.
3. Extreme caution in neonates with renal dysfunction.
4. Caution in concurrent therapy with cephalosporins, potent diuretics such as
frusemide, and neuromuscular blocking agents.
5. Concurrent administration with other ototoxic and/or nephrotoxic drugs.
Bacteriocidal aminoglycoside antibiotic which inhibits bacterial protein synthesis. Active

against a wide variety of pathogenic gram negative and gram positive bacteria, including
Escherichia coli, Enterbacter spp, Pseudomonas aeruginosa, Proteus spp, Serratia spp,
Staphylococcus spp (including penicillin and methicillin resistant strains).
Poorly absorbed by the oral route, variable absorption from intramuscular injection sites.
Diffuses through the plasma and interstitial fluid volumes. Does not penetrate the CSF to
any significant extent. Low binding (25-30%) to human plasma protein. Thought to be
excreted unchanged, eliminated mainly by the kidney. Renal clearance of gentamicin
appears to be slightly less than that of endogenous creatinine. Reduction in serum
concentrations can be achieved by peritoneal dialysis or haemodialysis.

4. Nephrotoxicity.
5. Ototoxicity (vestibular injury irreversible).
6. Neurotoxicity (lethargy, muscle twitching).
7. Blood dyscrasias (rare).
8. Hypersensitivity (rash, urticaria, fever, laryngeal oedema).
1. May be used in combination with other antibiotics if infused separately. Synergistic

effect against several organisms when used with penicillin.
2. Adjust dose and/or dose interval in infants with suspected/proven renal
impairment, or reduced renal clearance due to extreme immaturity.
3. Obtain trough and peak serum levels on the 3rd dose. Repeat if dose changed.
Repeat every 3-5 days. Desired peak level 30 minutes after completion of drug
infusion 5-8 mg/L. Trough level immediately prior to the next dose should be 1-2
mg/L.
guideline.
GLUCAGON
Reviewed by Reviewed by Dorothy Cooper
Glucagen hypokit
September 1996
1. 100 to 300 mcg/kg/dose by slow IV injection over 1 minute: or IM or SC. Maximum

dose 1mcg.
2. Continuous infusion 1-1.5mg/day. Usual dilution add 1mg glucagon to 23ml D5W
or D10W, 1ml/hour = 1mg/day.
Indications
1. To treat hypoglycaemia
a. When dextrose infusion is unavailable.
b. In documented cases of glucagon deficiency.
c. Refractory hypoglycaemia with high dextrose requirements and/or fluid
restriction.
1. Hypersensitivity to protein compounds.
Glucagon stimulates synthesis of cyclic AMP, especially in liver and adipose tissue.
Stimulates gluconeogenesis. In high doses, glucagon has a cardiac inotropic effect.
Inhibits small-bowel motility and gastric acid secretion.
Glucagon is secreted by the alpha-cells of the pancreas and transported via the portal
circulation to the liver where the major portion is bound. From the liver it is excreted into
the bile. A lesser portion is distributed to other organs, particularly the kidneys which have
a high binding capacity for it. It is degraded enzymatically in blood plasma and in the
organs to which it is distributed. Metabolised primarily in the liver.
Increased blood glucose levels occur within 5-30 minutes after injection and fall to normal
or hypoglycaemia levels within 1-2 hours. Half-life is about 5 minutes.
1. Gastro-intestinal disturbances (nausea and vomiting).

2. Tachycardia.
3. Rebound hypoglycaemia (result of insulin release and rebound effect).
4. Hypersensitivity reactions.
5. Anaphylaxis (rare).
6. Hypotension (rare).
7. ? ileus.
1. Supplemental carbohydrates should be ongoing, parenteral or PO.

2. Follow blood glucoses closely.
3. May be of less benefit if liver glycogen stores are low or insulin secretion is
excessive e.g. SGA babies or insulinoma.
guideline.
HEPARIN SODIUM
Reviewed by Dr Carl Kuschel, Ana Kennedy (NS-ANP),
and Dr George Chan (Haematology)
Heparin
May 2005
Maintenance of patency of arterial and/or central venous catheters.
1. Continuous infusion: 0.5 unit/ml of solution for maintenance of patency of arterial

catheters, central venous catheters and umbilical venous catheters.
2. In IVN solutions - all solutions contain 0.5 units/ml.
Intermittent heparin flushes:
1. Peripheral IV lines no longer flushed with heparin - use 0.5ml of 0.9% NaCl Q12H.
2. Longlines, UACs and UVCs are to be primed with and flushed with 0.9% NaCl
during insertion.
After insertion, flush with 0.5ml of 10U/ml Heparin.
3. For intermittent flushing of longlines and CVLs that are luered, use 0.7ml of 10U
Heparin per ml flush after each medication. We strongly recommend removal of
the line if it is no longer required, except under exceptional circumstances.
Full dose heparinisation for

anticoagulation:
1. Loading dose 75 units/kg by IV injection over 10 minutes. Higher loading doses

may need to be considered in special cases but this should be discussed with the
specialist responsible for the patient.
2. Commence maintenance dose at 28units/kg/hour by continuous intravenous
infusion and titrate dose by assessment of clinical effects and clotting studies.
Notes about Titration of Heparin Anticoagulation:
1. Ensure a baseline APTT has been performed.

2. The target APTT for anticoagulation is 50-80 seconds.
3. The normal APTT in term neonates and babies up to 30 days of age is 31-55
seconds.
❍ Note that the upper limit in normal babies overlaps with the target APTT.
This reflects the relative immaturity of neonatal haemostasis.

4. Heparin-induced thrombocytopenia is less common in neonates but the platelet
count should be checked 24-hours after starting the heparin and every 2-3 days
whilst on treatment.
5. Review the need for continuing heparin treatment in 5-7 days and consider other
forms of anticoagulation as appropriate.
APTT Bolus Stop Infusion % Infusion Repeat

(seconds) (u/kg) (min) Rate Change APTT
<40 50 0 +10% 4-6 hours
40-49 0 0 +10% 4-6 hours
50-80 0 0 0 Daily
81-90 0 0 -10% 4-6 hours
91-115 0 30 -10% 4-6 hours
>115 0 60 -15% 4-6 hours
● APTT is used to monitor unfractionated heparin treatment and is reagent/

instrument specific. The current target APTT values from the ADHB laboratory is
50-80 seconds for either the venous or capillary APTT. The laboratory will notify
the clinical area if there is a change in target values but if in doubt please check
with the laboratory.
❍ APTT can be determined on venous blood collects in a citrate tube.
❍ The laboratory also provides a capillary APTT service between 8am and
midnight for heparin monitoring.

Please discuss the capillary APTT service with the laboratory haematologist
through the Haemostasis Section, Haematology Laboratory, as soon as
possible when heparin treatment is being considered.
● If heparin dose adjustment is made as soon as possible after the APTT result is
available, the capillary APTT can be monitored around 8:30am, 1:30pm, 6:30pm,
and midnight, if necessary. APTT outside these hours should be checked on a
venous sample (available 24-hours a day).The dosing protocol above aims to bring
the APTT within the therapeutic range within 24-48 hours, but recent studies
indicate (in adults) provided an adequate dose as stated above the clinical
outcome is the same regardless of whether the APTT is within the therapeutic
range within the specified time.
● APTT monitoring is important to prevent overdose with the associated bleeding
risk.
● Clinical staff are responsible for dose adjustment and informing the laboratory
whether and when the subsequent test is required.
Low Dose Heparin

1. Ensure a baseline APTT has been done.
2. No loading dose is given.
3. The dose is fixed at 10u/kg/hour unless the APTT is unduly prolonged.
4. APTT is checked 4-6 hours after the infusion is commenced and then daily if the
APTT is <45 seconds.
5. If the APTT is 45-50 seconds, reduce the heparin to 8u/kg/hour then check 4-6
hours later.
6. If the APTT is >50 seconds, reduce the heparin to 5u/kg/hour then check 4-6 hours
later.
7. Please see above for APTT monitoring.
Indications
1. Maintenance of patency of arterial catheters, umbilical and central venous

catheters, and luered CVLs and longlines.
2. Neonatal thrombosis.
3. Disseminated intravascular coagulation.
1. Known hypersensitivity to heparin.

2. Presence of uncontrollable bleeding, bleeding tendencies.
3. Intraventricular haemorrhage, gastrointestinal haemorrhage.
4. Thrombocytopaenia < 50 x 109/L.
5. Severe hepatic, biliary or renal dysfunction.
6. Severe hypertension.
7. Eye, brain or spinal cord surgery.
8. Ascorbic acid deficiency.
Heparin activates antithrombin III, which progressively inactivates both thrombin and
factor Xa, key proteolytic enzymes in the formation of fibrinogen and the activation of
prothrombin. Also possesses anticomplementary activity, inhibiting both the classic and
alternative pathways. Not clinically significant at serum heparin levels associated with
therapeutic anticoagulant doses of heparin.
Some oral absorption but lack of anticoagulant effect. Rapidly taken up by endothelial
cells with remainder bound to plasma proteins. Hepatic metabolism. Elimination via the
kidneys (only small quantities of unchanged heparin).
Possible Adverse Reactions
1. Haemorrhage, haematomas.
2. Hypersensitivity reactions (fever, rash, nasal congestion, asthma, anaphylaxis,
alopecia).
3. Transient mild thrombocytopaenia.
4. Renal impairment.
5. Hyperaldosteronism.
1. Maternal heparin therapy is not a contraindication to breast feeding, as heparin

does not pass through breast milk.
2. Management of heparin overdose and/or toxicity:
❍ Stop heparin
❍ Administer protamine sulphate (1 mg per 100 units of heparin received by
infant in previous 3-4 hours IV by slow infusion over 10 minutes. Do not

exceed 5mg/min, maximum dose 50 mg).
guideline.
HYDROCHLOROTHIAZIDE
Created by Brenda Hughes, Tess Camfield, Robyn
Wilkinson, and Dr Carl Kuschel
Hydrochlorothiazide
November 2001
Note: This is NOT Chlorothiazide. Please check the preparation carefully,

particularly if obtained after hours from other paediatric wards or units.
Chlorothiazide is not used in NICU.
4,5,7
1 –2 mg/kg/dose orally every 12 hours.
4
Indications
1. Diuretic for long term control of mild to moderate oedema associated with
congestive heart failure.
2. Diuretic for control of pulmonary oedema in preterm infants with chronic ventilator-
dependent-induced lung disease.
Contraindications 6
1. Severe renal or hepatic dysfunction

2. Anuria.
Precautions 6
1. Decreased renal or hepatic function.

2. Electrolyte imbalance.
Drug Interactions
1. Captopril or Enalapril: possible decrease in renal function or renal failure in

patients with renal arterial stenosis.
2. Digoxin: possible digoxin toxicity if hypokalaemia exists.
3. Indomethacin: decrease in diuretic-induced antihypertensive effect.
4. Sotalol: prolongation of QT interval and development of torsades de pointes,
especially if hypokalaemia exists.
6
Hydrochlorothiazide is a thiazide diuretic. The thiazides are moderately potent diuretics

which act at the proximal end of the distal tubule causing a decrease in reabsorption of
electrolytes and an increase in excretion of sodium and chloride ions with accompanying
water loss. The hypotensive effect is possibly due to a decrease in peripheral resistance.
They are generally not effective in adults with a creatinine clearance of < 30ml/min.
Hydrochlorothiazide is fairly rapidly absorbed from the gastrointestinal tract with a

bioavailability of 65 – 70 % (adults), a half life = 5 to 15 hours (adults) and is
predominantly bound to red blood cells. Elimination half life is dependent on glomerular
filtration rate (creatinine clearance) and is longer than for chlorothiazide. It is excreted
mainly unchanged in the urine.
5, 6
1. Hypokalaemia, hypochloraemic alkalosis, hypomagnesaemia, hypercalcaemia,

hypophosphotaemia, hyponatraemia, hyperglycaemia, hyperuricaemia.
2. Small increase in excretion of bicarbonate due to decrease in carbonic-anhydrase
activity.
3. Zinc deficiency.
4. Possibly kernicterus in very jaundiced babies, as the thiazides compete with
bilirubin for plasma albumin binding sites.
1. The use of spironolactone in combination with chlorothiazide is common. There is,

however, little evidence to support that this results in any clinical benefit in preterm
8
infants with neonatal Chronic Lung Disease.
2. Distal diuretics (eg. hydrochlorothiazide) improve pulmonary mechanics in preterm
8
infants, aged greater than 3 weeks, with chronic lung disease. The use of distal
diuretics reduces the need for Frusemide.
guideline.
HYDROCORTISONE SODIUM
SUCCINATE Reviewed by Dr Jane Harding, Brenda Hughes, and
Dorothy Cooper
Solu-Cortef
August 1996
1. For adrenal crisis: 1mg/kg IM/IV q 4 hourly.

2. For maintenance: 1mg/kg/day PO
Indications
1. Replacement therapy in acute and chronic adrenocortical insufficiency.
Contraindication and Precautions
1. Infection.
2. Abrupt discontinuation in longterm therapy may result in withdrawal-like symptoms.
3. CAUTION concurrent use with amphotericin, potassium depleting diuretics,
indomethacin, theophyllines.
Hydrocortisone is the principle glucorticoid of the human adrenal cortex. The rate of
secretion follows a characteristic diurnal rhythm. Secretion increases in the early hours of
the morning and gradually declines toward late evening.
The three major effects of adrenal steroids are on metabolism, mineral metabolism and
inflammation.
Hydrocortisone is about 25-30 times less potent than dexamethasone.

1. Increased susceptibility to and suppression of the usual symptoms and signs of
infection.
2. Hyperglycaemia, glycosuria.
3. Sodium and water retention.
4. Hypertension.
5. Poor growth.
6. Gastrointestinal disturbance, aggravation of peptic ulcers, bleeding.
7. Hypokalaemia.
8. Hypocalcaemia.
9. Thrombocytopaenia.
10. Interferes with tissue granulation and repair, wound healing.
11. Rash.
12. Osteoporosis.
13. Prolonged use may produce posterior subcapsular cataracts.
1. The manufacturer recommends that Solu-Cortef is contraindicated in premature

infants because it contains benzyl alcohol. Benzyl alcohol has been reported to be
associated with the fatal gasping syndrome in premature infants. However, no
other preparation is currently available.
2. Dangerous to stop if using for adrenal crisis.
3. Infants born to mothers receiving this drug need to be monitored for signs of
hypoadrenalism.
4. Phenobarbitone and phenytoin may increase the clearance of cortico-steroids.
5. Hydrocortisone may increase or decrease theophylline levels.
guideline.
IMIPENEM/CILASTATIN SODIUM
Primaxin
September 1998
1. 25 mg/kg/dose 12 hourly IV infusion by syringe pump over 30 minutes.
Indications
1. Organisms resistant to other antibiotics.

2. Only administered after consultation with Infectious Disease Consultant.
1. Hypersensitivity to any component of this product.

2. Should not be used for meningitis.
3. Imipenem is not active against mycoplasma or chlamydia.
4. CAUTION in babies with CNS disorders.
5. Patients with creatinine clearances of <5 ml/min/1.73 m2.
Imipenem is a beta-lactam antibiotic belonging to the thienamycin group. It is a potent

inhibitor of bacterial cell wall synthesis and is bactericidal against a broad spectrum of
pathogens - Gram positive and Gram negative, aerobic and anaerobic. It may reduce the
likelihood of superinfection with nonsusceptible bacterial species. The spectrum of activity
includes Pseudomonas aeruginosa, Staphylococcus aureus, Streptococcus faecalis and
Bacteroids fragilis. It is broader than that of any other antibiotic studied and includes
virtually all clinically significant pathogens. Imipenem is combined with cilastatin sodium, a
competitive, reversible and specific inhibitor of dehydropeptidase-I-enzyme, the renal
enzyme which metabolises and inactivates imipenem.
Vd is 0.23-0.42 L/kg. Low binding 20% to human plasma protein. Excreted mainly by the
kidney (70%). Liver 30%. The plasma half-life is 1 hour.
Cilastatin is approximately 40% plasma protein bound, is 70-80% excreted in the urine
unchanged and has a plasma half-life of 1 hour.

2. Hypersensitivity reactions (fever, rash).
4. Myoclonic activity and seizures have been reported with high doses.
5. Eosinophilia, leucopenia, neutropenia. A positive Coombs test may develop.
6. Mild increase in serum transaminases, bilirubin, serum alkaline phosphatase,
creatinine and blood urea.
7. Reddish urine discolouration (not significant).
8. Bacterial or fungal superinfections.
9. Seizures in patients with CNS dysfunction.
1. Is not suitable for oral, intramuscular, direct IV injection or continuous infusion.

2. Sodium content 1.6 mmol.
3. Clinical data are insufficient to recommend use in infants < 3 months age without
the special indications of a resistant organism.
4. Avoid concurrent use with beta lactum antibiotics. Possible in vitro antagonism.
5. Avoid concurrent use with gancyclovir may cause seizures.
guideline.
INDOMETHACIN
Reviewed by Dr David Knight and Dorothy Cooper
Indocid
September 1998
1. 200 micrograms/kg/dose as IV infusion by syringe pump over 30 minutes.
Current recommendations for PDA

closure 2:
1. Three doses (200 micrograms/kg/dose) given at 12-24 hour intervals with close
monitoring of urine output. If anuria or severe oliguria occurs, subsequent doses
should be delayed. Dosing interval depends on maturity of the infant.
Postmenstrual Age Dosing Interval

(weeks) (hours)
≤29 18-24
30-36 18-24
>37 8-12
2. Subsequently, 200 micrograms/kg/dose as IV infusion daily to complete 7 days

therapy.
Indications
1. Closure of persistent patent ductus arteriosus.
1. Anuria, severe oliguria (<0.5-1.0ml/kg/hour).

2. Serum creatinine >0.12 mmol/L.
3. Thrombocytopaenia <80 x 109/L.
4. Bleeding phenomena.
5. Necrotising enterocolitis.
6. Known hypersensitivity to indomethacin.
Indomethacin, an indole derivative, is one of the most potent inhibitors of the cyclo-
oxygenase pathway. Inhibits the action of prostaglandin synthetase, and thus inhibits the
synthesis of the prostaglandin E series. Indomethacin is a potent vasoconstrictor and
decreases cerebral, gastrointestinal, and renal blood flow.
Very variable absorption from gastrointestinal tract (10-90%). Indomethacin solutions very
susceptible to chemical decomposition. High binding (95%) to human plasma protein. No
displacement of bilirubin from albumin at usual therapeutic levels. Hepatic metabolism,
elimination via biliary tract and kidneys. Elimination half-life is approximately 30 hours
(range 15-50 hours). Individual differences in rate of distribution, drug metabolism, rate of
renal and biliary excretion, and re-entry of drug into the circulation by enterohepatic
recirculation all contribute to the variability in plasma clearance.
1. Renal impairment
2. Gastrointestinal dysfunction (abdominal distension, gastrointestinal bleeding,
necrotising enterocolitis, gastric perforation, gastric ulceration).
3. Platelet dysfunction and bleeding tendency.
1. Rapid infusions of intravenous indomethacin have been associated with significant

reductions in cerebral blood flow.
2. Careful monitoring of gastrointestinal and renal status is required during a course
of therapy.
guideline.
INSULIN (Neutral)
Reviewed by Dr Carl Kuschel, Robyn Wilkinson, and
Brenda Hughes
Actrapid Penfill
February 2002
1. Continuous IV infusion: 0.01 - 0.1 U/kg/hr (starting dose usually 0.05 U/kg/hr).
Titrate infusion rate according to blood glucose response.
Infusion should not be included in the daily prescribed fluid total. Insulin should be
given in addition to daily fluid intake.
Insulin (units of 1 Unit/ml dilution) to be 50 x weight (kg) x dose (units/kg/hour)

added to 50ml = IV rate (ml/hr)
2. Intermittent dose: 0.1-0.2 U/kg 6-12 hourly SC/IM.
Indications
1. Hyperglycaemia in VLBW infants with persistent glucose intolerance.

2. Hyperkalaemia in critically ill VLBW infants.
1. May rapidly induce hypoglycaemia.

2. Hypersensitivity to insulin (extremely rare).
3. Insulin resistance may develop causing a larger dose requirement.
Insulin enhances uptake of glucose in insulin sensitive tissues, enhances glycogen and
fat synthesis, enhances muscle uptake of amino acids and cellular uptake of potassium. It
inhibits lipolysis and gluconeogenesis. Plasma half-life is short (approximately 9 minutes
in adults), with degradation in liver and kidneys. Absorption from IM or SC doses is
variable.
1. Hypoglycaemia
2. Hypokalaemia
1. If given by infusion, should be via a line that will not need to be flushed (to avoid
boluses) and ideally the same line as is used for dextrose or intravenous nutrition
infusion. This ensures cessation of insulin at the same time as glucose infusion if
the drip tissues, and thus reduces the risk of hypoglycaemia.
2. Incompatible with aminophylline, chlorothiazide, dobutamine, lignocaine,
phenobarbitone, phenytoin, sodium bicarbonate.
3. Effect decreased by drug-induced hyperglycaemia e.g. corticosteroids, thiazide
diuretics, adrenaline, glucagon, thyroid preparations, phenytoin.
4. Adsorbs onto plastic i.e. syringes, extension tubing, filters, and 3-way taps.
5. Is considered safe by National Women’s Hospital Paediatricians to mix insulin and
heparin in the same syringe for administration via a central venous line.
guideline.
IPRATROPIUM BROMIDE
Reviewed by Dr Simon Rowley, Dr Innes Asher, Dorothy
Cooper
Atrovent
September 1996
Dose
0.025 mg/kg/dose as nebulised
Endotracheal
solution 4-6 hourly.
0.0625-0.25 mg/kg/dose as
Via face mask
nebulised solution 4-6 hourly
Indications
1. Bronchospasm in infants with bronchopulmonary dysplasia.
1. Known hypersensitivity to atropine and/or the propellant mixture.

2. Caution in newborn infants with glaucoma
Ipratropium bromide is a quaternary derivative of atropine. Has low lipid solubility. The
drug is a parasympathetic inhibitor (anticholinergic antimuscarinic agent) that blocks the
vagal reflexes which mediate bronchoconstriction. Exerts a local effect on the airways.
Has a high therapeutic ratio, producing bronchodilation without significant effect on other
organ systems.
Systemic absorption after inhalation is very low (bioavailability <5%). Distribution is

limited. Does not cross the blood brain barrier. Low binding (<20%) to human plasma
protein. Some hepatic biotransformation, excretion via the kidneys. Elimination half-life in
the adult is 3-4 hours.
Onset of action 5-30 minutes after inhalation. Peak effect occurs at approximately 60-120
minutes. Duration of action 3-8 hours. Incidence of systemic side effects is extremely low
following inhalation. There is no evidence that in the therapeutic dose range ipratropium
has any adverse effect on sputum viscosity or volume.
1. Dryness of the mouth

2. Irritation and cough
3. Mild reversible accommodation disorder (if the eye is exposed to the drug).
1. There is very little data about the pharmacokinetics and pharmacodynamics of this
drug in the newborn and young infant. Dosage recommendations are largely
empirical.
2. The efficacy of anticholinergic drugs in asthma is inferior to that of b adrenergic
agonists. The use of inhaled anticholinergic drugs should generally be limited to
those patients who do not adequately respond to maximal b adrenergic therapy.
3. The role of ipratropium in the management of bronchodilator responsive
bronchospasm occurring in infants with BPD has not been clearly established.
guideline.
ISOPRENLINE HYDROCHLORIDE Reviewed by Dorothy Cooper
Isoproterenol, Isuprel November 1996

Dose revised to nanograms April 2003
1. 50-500 nanograms/kg/min (0.05-0.5 mcg/kg/min) by continuous IV

infusion.
3 x weight (kg) x dose (mcg/kg/min)

Isoprenaline (mg) in 50ml IV solution =
IV rate (ml/hr)
Indications
1. Low cardiac output and hypotension.

2. Persistent pulmonary hypertension of the newborn.
1. Known hypersensitivity to isoprenaline.

2. Hypovolaemia.
Isoprenaline hydrochloride is a synthetic sympathomimetic amine that is structurally

related to adrenaline. The drug is a B1 and B2 adrenergic agonist with almost no activity
on a receptors. Increases cardiac output by increasing heart rate, contractility and venous
return. Lowers peripheral vascular resistance. Relaxes most smooth muscles, especially
bronchial and gastrointestinal. Decreases pulmonary artery pressure and pulmonary
artery resistance in experimental animals. Stimulates insulin secretion. Metabolised in the
liver and other tissues by catechol-o-methyl transferase. Marked chronotropic and
arrhythmogenic effects. May cause myocardial ischaemia or necrosis.
1. Hypotension
2. Arrhythmias
3. Decreased perfusion to kidney, heart, brain.
4. Tremors, irritability.
5. Gastrointestinal disturbances (nausea, vomiting and diarrhoea).
6. Myocardial necrosis.
1. Titrate infusion rate according to clinical response and/or side effects. May
increase dose every 2-3 minutes until appropriate response obtained.
2. Hypovolaemia, metabolic acidosis should be corrected before infusion commences.
3. Simultaneous administration with adrenaline may lead to serious arrhythmias.
guideline.
MAGNESIUM SULPHATE
Magnesium
September 1996
Initial Dose
1. 200mg/kg dose.
2. Dilute to 8% concentrate in D5W. Infuse IV for 30 minutes. DO NOT exceed 150
mg/minute.
Continuous IV infusion
1. 20 - 50mg/kg/hour. Dilute to 8% concentration in D5W.

2. Usual dilution 4 grams magnesium sulphate to make 50ml with D5W = 80mg/ml
0.25ml x weight = 20mg/kg/hour
Indications
1. Seizures refactory to other anticonvulsant therapy.

2. Hypomagnesaemia.
3. Severe persistent pulmonary hypertension of the newborn unresponsive to other
vasodilation management.
1. Patients with heart block or myocardial damage.

2. CAUTION in patients with impaired renal function and/or electrolyte imbalance.
At high serum concentrations Mg is a potent vasodilator, muscle relaxant and sedative.

Magnesium is the second most common intracellular cation. One half of body Mg is in
bone, one-fourth is in muscle and one-fourth is in soft tissue. About 25% to 30% of total
plasma Mg is bound to protein, 10% to 15% circulates in complex form and 55% to 60%
is ionised.
Readily crosses the placenta and is distributed in mothers milk, however breastfeeding is
not contraindicated. In the newborn Mg absorption occurs in the small intestine: 55% to
75% of ingested Mg normally is absorbed. The main route of Mg loss is through the
kidneys. Serum magnesium concentrations are maintained within a narrow range. At the
three major target organs for hormonal control of Mg homeostasis (bone, intestine and
kidney) the close inter-relationship between Mg and Ca is evident.
An elimination half life of 43.2 hours has been reported in newborn infants whose mothers
received magnesium sulphate. The elimination rate is the same for both preterm and term
infants.
1. ECG changes (prolongation of the atrio-ventricular conduction time, sinoatrial

block and atrio-ventricular block).
2. Circulatory collapse, hypotension.
3. Gastro intestinal disturbances (diarrhoea, abdominal distension, absence of bowel
sounds).
5. CNS depression (central sedation, muscle relaxation, hyporeflexia and decreased
excitability).
6. Calcium and potassium disturbances.
1. Anticipate change in calcium and phosphorus balance.

2. Drug interaction has been reported between magnesium sulphate and gentamicin
(respiratory arrest).
3. Monitor serum magnesium and calcium levels.
4. Antidote for hypermagnesaemia is calcium gluconate.
guideline.
MEROPENEM Reviewed by Dr Malcolm Battin, Dr Lesley Voss

(Paediatric Infectious Diseases), Brenda Hughes,
and Helen Lamb (NSANP)
Merrem
December 2005
Intravenous: Weight <2000g 1

20 mg/kg/dose every 12 hours
40 mg/kg/dose every 12 hours for first 7
Weight >2000g 2
days, then every 8 hours
Indication
1. Systemic sepsis, for use as a second or third line agent. It could be considered
when there is failure of a previous therapy or for those certain situations where
broad cover treatment may be necessary. Use of meropenem must be discussed
with the Infectious Diseases Team.
1. Inflammation at injection site.

2. Caution in infants with impaired renal or hepatic function.
3
3. Caution in infants with history of seizures.
Meropenem, a potent carbapenem antibacterial agent with enhanced beta-lactamase

stability, has antimicrobial activity against Gram-negative, Gram-positive and anaerobic
micro-organisms. The bacterial concentrations are usually within one doubling dilution of
4
the MICs. Meropenem is not licensed for children under 3 months of age, but its efficacy,
5,6,7
safety and tolerability have been studied in this age group. The serum half life is
5
approximately 3 hours in preterm infants and 2 hours in term infants. The
pharmacokinetics of meropenem, for infants and children, are similar to those for adults. It
penetrates most body fluids and tissues including the CSF. Protein binding is minimal,
and elimination is predominantly renal as unchanged drug. The only metabolite, produced
5
by non-specific hydrolysis in plasma of the beta-lactam ring, is inactive.
3
1. Leukopenia, neutropenia, thrombocytopenia and anaemia.
3
2. Inflammation at injection site.
3
3. Vomiting, diarrhoea, and constipation (1%).
3
4. Rash (2%)
3
5. Nephrotoxicity, hepatotoxicity
Interactions
● There are currently no known relevant drug interactions
1. Monitor:
❍ FBC – monitor for thrombocytosis and eosinophilia with prolonged use.
8
❍Renal function - increase dose interval in renal failure.
❍ Hepatic function – at the beginning of treatment, and weekly thereafter.
❍ Vomiting and pseudomembranous colitis – consider alternate antibiotic.
2. Use under close clinical supervision usually after discussion with ID service.
3. Meropenem is not licensed for children <3 months of age.
2
4. The intramuscular route is not recommended.
guideline.
METOCLOPRAMIDE
Maxolon September 1996
1. 0.03-0.1 mg/kg/dose by slow IV infusion over 30 minutes, PO every 6-8 hours.

2. Maximum daily dosage 0.5 mg/kg/day.
Indications
1. Impaired gastric emptying and gastrointestinal motility.

2. Gastroesophageal reflux.
1. Known hypersensitivity to metoclopramide.

2. Pheochromocytoma (may precipitate hypertensive crisis).
3. Caution in neonates with hepatic or renal impairment.
4. Caution in neonates with conditions in which stimulation of gastric motility may be
hazardous (gastrointestinal haemorrhage, mechanical obstruction and/or
perforation).
5. Concurrent use with narcotic may increase respiratory depression, decrease
gastrointestinal motility.
Metoclopramide hydrochloride, a derivative of procainamide, stimulates motility of the

upper gastrointestinal tract. Does not stimulate gastric, biliary or pancreatic secretions.
Mechanism of action is unknown. Has both dopamine antagonistic activity and peripheral
cholinergic effects. Also induces the release of prolactin.
Well absorbed from gastrointestinal tract. Marked variation in bioavailability as a

consequence of very variable first pass metabolism. Large distribution volume (lipid
soluble drug). Low binding (13-22%) to human plasma protein. Hepatic metabolism.
Elimination via the kidney with significant fraction unchanged (40-50%). Rapid onset of
action: 1-3 minutes following an IV dose (10-15 minutes IM; 30-60 minutes PO). Duration
of action 1-2 hours.

2. Hypotension.
3. Cardiac arrhythmias.
4. Restlessness, drowsiness, fatigue, anxiety, agitation.
5. Dystonic reactions and extrapyramidal symptoms.
1. Therapy usually continued for 2-8 weeks.

2. Side effects are usually mild, transient and reversible following discontinuation of
the drug.
3. May increase serum levels of aldosterone and prolactin
4. Management of metoclopramide overdose and/or toxicity: discontinue
metoclopramide, provide supportive therapy for side effects. May administer
diazepam or benadryl for treatment oculogyric crisis.
guideline.
METRONIDAZOLE
Metronidazole (Baxter)
September 1996
1. IV infusion by syringe pump over 30 minutes.

2. Preterm infants less than one month of age: 7.5 mg/kg/dose 12 hourly.
3. All other infants: 7.5 mg/kg/dose 8 hourly.
4. Loading dose of 15 mg/kg is optional.
Indications
1. Suspected/proven anaerobic infection, especially Bacteroides fragilis.

2. Necrotising enterocolitis.
3. Peritonitis.
1. Known hypersensitivity to metronidazole.

3. Caution in preterm infants especially extreme immaturity.
4. Caution in infants with jaundice, liver dysfunction and biliary tract disease.
Metronidazole is active against a wide range of anaerobic micro-organisms, including

Bacteroides species, Fusobacteria, Clostridia, Eubacteria and anaerobic cocci. Also
active against Gardnerella vaginalis, Trichomonas, Entamoeba histolytica, Giardia lamblia
and Balantidium coli. The precise mode of action is not clear. Active metabolites of
metronidazole appear to bind to DNA and disrupt protein synthesis.
Readily absorbed after oral administration. Slower and more variable absorption from the
rectum. Diffuses throughout the body and readily penetrates CSF and cerebral
abscesses. High apparent distribution volume similar to that of total body water. Low
binding (20%) to human plasma protein. Elimination mainly by hepatic biotransformation,
resulting from side chain oxidation, hydroxylation or conjugation of the parent compound.
The major metabolites are active. Elimination half-life remains unchanged in renal failure.
Rapidly removed from the plasma by dialysis.

2. Gastrointestinal disturbance (nausea, vomiting)
3. Peripheral neuropathy, encephalopathy (usually during intensive and/or prolonged
therapy).
4. Neutropenia (moderate, reversible).
5. Hypersensitivity reactions rare (urticaria, skin eruptions, anaphylaxis).
1. Lengthen dosing interval if extreme immaturity, severe jaundice, and/or hepatic

dysfunction.
2. Neonates receiving phenobarbitone metabolise metronidazole at a much greater
rate than normal, reducing half life by approximately 50-75%.
3. Darkening of the urine, due to metronidazole metabolites, has been reported.
4. Serum levels should be measured if toxicity suspected (toxic levels greater than
300 umol/L).
5. Is considered safe by National Women’s paediatricians, that mothers receiving
metronidazole breast feed their babies.
guideline.
MICONAZOLE
Reviewed by Carl Kuschel
Daktarin
May 2006
Oral
1. 25mg (1.25g of gel, equalling 1.25ml) 4 times daily. The initial prescription should
be for a 5 day course.
Intravenous
1. This has not been studied in children and is not available for use at NWH.
Indications
1. Treatment of oral candidiasis (second-line agent after Nystatin).

2. Superficial candidal infections.

2. Caution in infants with hepatic dysfunction.
3. Hypersensitivity to miconazole.
4. Systemic fungal infections.
5. Congenital candidiasis.
5
6. Caution in infants with poor swallowing (potential for airway obstruction).
An imidazole antifungal agent which has shown fungistatic activity against a number of
fungi causing systemic infection. Action depends on its binding to a sterole moiety,
ergosterole, present in the membrane of sensitive fungi. May be fungicidal or fungistatic,
depending on the drug concentration obtained and the sensitivity of the fungus.
Absorption of miconazole from the gastrointestinal tract is low. Small amounts of

miconazole have been detected in saliva.
1. Gastrointestinal disturbances (vomiting and, occasionally, diarrhoea ).

5
2. Potential for airway obstruction in infants with poor swallowing.
3. Other side effects have been described following IV administration in adults,
notably cardiac arrhythmias (with rapid administration), haematological changes
(anaemia, aggregation of erythrocytes, thromocytopenia, thrombocytosis),
transient hyponatraemia, hyperlipidaemia, fever, rash, pruritus, blurring of vision,
dryness of eyes, arthralgia, seizures and transient renal dysfunction.
1. No pharmacokinetic studies of miconazole have been performed in neonates and

young infants.
2. Use of the oral gel in infants <6 months of age is not endorsed by the
5
manufacturer, due to the potential for airway obstruction.
3. Oral miconazole is not indicated in systemic or congenital candidiasis.
4. Oral miconazole is not indicated in the treatment of gastrointestinal candidiasis.
Nystatin is more effective at eradicating yeasts from the gastrointestinal tract.
5. Consider topical application of anti-candidal agent to mother’s nipples when infant
has oral candidiasis.
6. If candidal nappy rash is coexistent, a topical agent should also be used.
guideline.
MIDAZOLAM Reviewed by Dr Carl Kuschel and Brenda Hughes
January 2001
Hypnovel Description information changed to note 2 different
strengths December 2004
1. Slow IV push
50 to 150 micrograms/kg as a slow push over 5 minutes. Can be repeated Q2-4H
as required.
Give lower dose if opiates being administered simultaneously.
2. Continuous intravenous infusion
10-60 micrograms/kg/hour. Dosage can be increased if necessary.

Midazolam (micrograms) in 50ml IV
hour)
solution =
IV rate ml/hour
Indications
1. Sedation/anaesthesia.
2. Anticonvulsant (3rd or 4th line).
1. Known hypersensitivity to midazolam.

2. Shock.
5. Caution when concurrent use with opiates, particularly fentanyl.
6. Caution when concurrent use with other anticonvulsants.
Interactions
1. Concurrent administration with erythromycin promotes accumulation.

2. May alter the depth of and prolong the recovery from concurrent neuromuscular
blockade.
3. Xanthines may decrease the anaesthetic/sedative effect of benzodiazepines. Care
needs to be taken with adding or withdrawing caffeine or aminophylline.
Midazolam, an imidazobenzodiazepine, has anxiolytic, sedative, muscle relaxant and

anticonvulsant actions. Facilitates the action in the brain of gamma aminobutyric acid, a
naturally occurring neurotransmitter. Absorption 30% with oral and 50% with nasal
administration. Rapid and extensive distribution. Highly protein bound. Hepatic
metabolism to active and inactive derivatives, impaired by poor hepatic perfusion . Very
slow elimination via the kidneys. Elimination half-life variable (6-7 hours in infants close to
term, longer in less mature infants), with the major metabolite (1-hydroxymidazolam)
having an even shorter half-life. Rapid onset of action (<3 minutes) and peak sedative
action <20 minutes after IV administration. Anticonvulsant action may be more rapid. The
IV preparation has a pH of 3.
1. Hypotension and reduced cardiac output, particularly when used in combination

with fentanyl.
2. Respiratory depression and apnoea.
3. Hypotonia.
4. Seizures or seizure-like activity may be seen following rapid bolus administration
and in patients with underlying CNS disorders.
5. Cerebral blood flow velocities are reported to decrease transiently in preterm
infants receiving midazolam boluses, possibly reflecting the reduction in blood
pressure.
6. Nasal administration in children and adults has been reported to produce a burning
sensation.
1. Lower doses of midazolam should be considered in neonates with reduced cardiac

output.
2. Development of tolerance and a requirement for higher doses may occur with
prolonged use.
3. Prolonged use may result in neonatal abstinence syndrome.
4. Recent systematic review has suggested that routine use of midazolam for
sedation in ventilated infants is associated with an increased incidence of adverse
9
neurological outcomes.
5. Management of midazolam overdose and/or toxicity: stop midazolam, supportive
therapy (ventilation, volume expansion etc.), consider use of specific antagonist
flumazenil (very limited experience in the neonate).
guideline.
MORPHINE HYDROCHLORIDE
Reviewed by Dr Carl Kuschel, Simon Rowley, and Brenda
Hughes
Morphine
February 2001
Neonatal Abstinence Syndrome
1
1. Start at 500 micrograms/kg/day orally .
This is usually prescribed 6-hourly. Dose may need to be increased
with severe withdrawal before weaning can take place.
2. Reduce dose by 10-15% of the original dose every 2-3 days as
tolerated.
Analgesia
1. Ventilated 100 - 200 micrograms/kg/dose.

2. Non-ventilated 50 micrograms/kg/dose
Indications
1. Neonatal Abstinence Syndrome

2. Sedation
1. Known hypersensitivity to opiates.

2. Hypovolaemia, hypotension.
3. Caution in preterm infants, especially very immature.
4. Caution in neonates with hepatic and renal impairment.
5. Caution in neonates with cardiac arrhythmias.
Morphine hydrochloride is a narcotic analgesic which stimulates opioid receptors in the

central nervous system (mimics actions of encephalins and β endorphins). Produces
respiratory depression by direct effect upon brain stem respiratory centres. No major
effect upon cardiovascular system in analgesic doses. Resistance and capacitance
vessels are dilated by the opioids. Gastrointestinal secretions and motility are decreased
while tone is increased. Stimulates smooth muscle of biliary and urinary tracts.
Well absorbed from gastrointestinal tract but high first pass hepatic metabolism. Low
binding (20%) to human plasma protein. Hepatic metabolism to glucuronide and other
metabolites. Excretion via the kidney - significant amounts of unchanged drug in the
neonate. The pharmacokinetics of morphine in the neonate are very variable.
Variable onset of action after oral administration. Analgesic effects occur with plasma
concentrations around 120ng/ml. Respiratory depression occurs with plasma
concentrations >300ng/ml. In the non-withdrawing baby respiratory depression is more
likely.
2. Gastrointestinal disturbances (vomiting and spilling, ileus, delayed gastric
emptying, cramps, and constipation.
3. Hypotension
4. Physical dependence
1. Morphine is the drug of choice for most situations requiring pain relief
2. Wean slowly after prolonged use of morphine.
3. Management of morphine toxicity: stop morphine, support infant (ventilation,
external cardiac massage, volume expansion etc.), Naloxone (0.1 - 0.2 mg/kg/
dose IM). Naloxone is never used for babies with Neonatal Abstinence
Syndrome.
4. For further information about its use in narcotic withdrawal see Neonatal
Abstinence Guideline.
guideline.
MORPHINE SULPHATE
Reviewed by Dr Carl Kuschel, Brenda Hughes, and Robyn
Wilkinson
Morphine
October 2004
Infusion
Morphine (mg) in 50ml IV solution = hour)
IV rate x 1000
1. Dose is 100 micrograms/kg/hr for 2 hours followed by 25 micrograms/kg/hr

thereafter.
2. Lower infusions of 10 -20 micrograms/kg/hr may be used but have not been shown
to achieve adequate analgesic levels in preterm infants.
Intermittent Dosing
Click here to open the Morphine bolus

quick reference chart
1. 50 - 200 micrograms/kg/dose by slow IV injection, IM or SC. Repeat as required

(usually 4-hourly).
2. Usual starting dose 100 micrograms/kg. Titrate dose against clinical response.
Intermittent dosing may lead to intermittent effect.
3. A bolus of a continuous infusion may be given for short-term additional sedation.
This should be charted on the stat drug chart as:
● Bolus morphine infusion with the strength specified and the volume and dose
specified.
e.g. For a 1kg baby, "Bolus morphine infusion (25 micrograms/kg in 0.5ml) - dose
2ml (100micrograms) IV"
Indications
1. Analgesia
2. Sedation
1. Known hypersensitivity to opiates

2. Hypovolaemia, hypotension
3. Caution in preterm infants, especially very immature
4. Caution in neonates with hepatic and renal impairment
5. Caution in neonates with cardiac arrhythmias
Morphine sulphate is a narcotic analgesic which stimulates opioid receptors in the central
nervous system (mimics actions of encephalins and β endorphins). Produces respiratory
depression by direct effect upon brain stem respiratory centres. No major effect upon
cardiovascular system in analgesic doses. Resistance and capacitance vessels are
dilated by the opioids. Gastrointestinal secretions and motility are decreased while tone is
increased. Stimulates smooth muscle of biliary and urinary tracts.
Well absorbed from gastrointestinal tract but high first pass hepatic metabolism:
parenteral route of administration is preferred. Low binding (20%) to human plasma
protein. Hepatic metabolism to glucuronide and other metabolites. Excretion via the
kidney - significant amounts of unchanged drug in the neonate. The pharmacokinetics of
morphine in the neonate are very variable.
Rapid onset of action after parenteral administration. Peak effect 20-60 minutes. Duration
of analgesic effect variable (may persist up to 7 hours). Analgesic effects occur with
plasma concentrations 100-150 ng/ml. Respiratory depression may occur with plasma
concentrations >300 ng/ml. Accumulation can occur but is rarely a clinical problem.
1. Respiratory depression
2. Gastrointestinal disturbances (ileus and delayed gastric emptying, cramps,
constipation).
3. Hypotension
4. Urinary retention
5. Physical dependence
1. Morphine is the drug of choice for most situations requiring pain relief.
2. Administer parenterally appropriate length of time compatible with the infant's
needs for analgesia and/or sedation.
3. Wean slowly after prolonged use of morphine, greater than 2 weeks.
4. Management of morphine toxicity: stop morphine, support infant, (ventilation,
external cardiac massage, volume expansion etc.), naloxone (0.1 - 0.2 mg/kg/dose
IV, or IM).
5. Naloxone is never used for babies at risk of neonatal abstinence syndrome.
guideline.
NALOXONE HYDROCHLORIDE
Reviewed by Dr Simon Rowley and Dorothy Cooper
Narcan
November 1996
1
1. 0.1-0.2 mg/kg/dose IM (0.25-0.5ml/kg of 0.4 mg/ml concentration) .
May also be given IV, intratracheally or subcutaneously.
May repeat in 3-5 minutes if no response during resuscitation.
Indications
1. Narcotic induced respiratory and CNS depression.

2. Narcotic overdose.
1. Known or suspected naloxone hypersensitivity.

2. Newborns of mothers who are known or suspected to be physically dependent on
opioids. In such cases an abrupt and complete reversal of narcotic effects may
precipitate an acute abstinence syndrome.
3. Not indicated if infant shows no sign of respiratory depression.
4. Has no effect on non-narcotic induced respiratory and CNS depression.
5. Naloxone is an adjuvant therapy to customary resuscitation efforts for narcotic
induced respiratory depression. Other resuscitative measures such as
maintenance of a free airway, artificial ventilation, cardiac massage and
vasopressor agents should be employed as necessary.
6. Caution in infants with tachycardia, congenital heart defects.
Naloxone is a pure narcotic antagonist. It prevents or reverses the effects of opioids,

including respiratory depression, sedation and hypotension. Naloxone does not possess
agonist properties and therefore does not produce respiratory depression,
psychotomimetic affects or pupillary constriction. In the absence of opioids it exhibits
essentially no pharmacological activity. Naloxone antagonises the opioid effects by
competitive inhibition at the opioid receptor sites.
Following parenteral administration naloxone is rapidly distributed in the body. It is

metabolised in the liver, primarily by glucuronide conjugation and excreted in the urine.
When administered intravenously its onset of action is rapid (within 2 minutes); the onset
of action is only slightly less rapid when it is administered subcutaneously or
intramuscularly. The duration of action is dependent upon the dose and route of
administration. Intramuscular administration produces a more prolonged effect than
intravenous administration.
Naloxone has not been shown to produce tolerance nor to cause physical or
psychological dependence. No short-term toxicity has been observed but long-term safety
has not been investigated. There is no clinical experience with naloxone overdosage in
humans.
1. Abrupt reversal of narcotic depression may result in nausea, vomiting, sweating,

tachycardia, increased blood pressure and tremulousness.
2. Tachycardia, hypertension.
3. Gastrointestinal disturbances (nausea, vomiting).
4. Lethargy, tremors.
5. Elevated PTT.
Special Precautions
1. Infants receiving naloxone in the delivery room because of narcotic induced

respiratory depression require observation afterwards. This observation need not
necessarily be on the neonatal unit. See Naloxone guideline.
2. The duration of naloxone antagonism may be less than the clearance of the opiate
being antagonised. This should not be a problem with the intramuscular
administration of naloxone. However, some babies may require a second dose of
naloxone.
guideline.
NEOSTIGMINE METHYLSULPHATE
Reviewed by Dr Carl Kuschel, Robyn Wilkinson, Brenda
Hughes, and Leanne Bratton
Neostigmine
October 2001
Dose and Administration 3, 4, 5, 6, 7
1. Myasthenia gravis
Route Dose
Test Dose: IM 150 microgram/kg
Always have Atropine 20
micrograms/kg available to
control undue salivation.
Alternatively, Edrophonium
may be given (20 micrograms/
kg IV followed, after 30
seconds, by 80 micrograms/kg
IV if no adverse effect [watch
for bradycardia or arrhythmia])
Maintenance: IM or SC 150 micrograms/kg every 6 to
8 hours.
Higher doses (300 micrograms/

kg Q4H may be necessary)
PO An oral dose of Neostigmine
bromide 10-20 times the IM
maintenance dose of
Neostigmine methylsulphate
every 3 hours.
Other longer acting

preparations (e.g.
pyridostigmine) may be
preferable.
2. Reversal of non-depolarising neuromuscular blocking agents (e.g.
pancuronium)
Usually reversed with atropine 20 micrograms/kg IV followed by one (or
occasionally 2) 40 microgram/kg/dose of neostigmine.
Indications
1. Diagnosis and management of transient neonatal and persistent (congenital)

myasthenia gravis.
2. Reversal of the effects of neuromuscular blocking agents.
5
Contraindications
1. Mechanical obstruction of intestinal or urinary tract

2. Peritonitis
5
Precautions
1. Cardiac disease
2. Seizures
3. Hypotension
4. Peptic ulceration
5. Hyperthyroidism
6. Asthma
5
Drug Interactions
Corticosteroids: decrease in anticholinesterase effect of neostigmine. Conversely, the

anticholinesterase effect may be increased after stopping corticosteroids.
Atropine: reversal of muscarinic effect of neostigmine.
Aminoglycoside: neostigmine may reverse the neuromuscular blockade induced by
aminoglycoside antibiotics.
Depolarising muscle relaxants (eg. suxamethonium): prolongation of blockade.
3,4
Neostigmine prolongs and intensifies the physiological activity of acetylcholine by

anticholinesterase activity which is reversible. It is poorly absorbed from the
gastrointestinal tract, and CNS penetration is poor. Neostigmine causes vasodilation,
increased smooth muscle activity, lacrimation, salivation and increased voluntary muscle
tone. It is the preferred agent over edrephonium for the management of neonatal
myasthenia gravis, owing to its more prolonged effect (2 to 4 hours), however does have
a slower onset of action (20 – 30 minutes).

1. Gastrointestinal disturbances (vomiting, abdominal cramps, increased peristalsis).
2. Respiratory depression and/or arrest.
3. Cardiac arrhythmias (especially bradycardia), hypotension, cardiac arrest.
4. Muscle cramps, paralysis, general weakness.
5. Rash.
6. Convulsion, restlessness, coma.
1. Overdosage may cause cholingeric crisis. Keep atropine available to counteract

muscarinic effect.
2. Management of neostigmine overdose and/or toxicity: stop neostigmine,
supportive therapy (ventilation, volume expansion etc.), control convulsions,
consider administration of atropine 20 micrograms/kg IV.
3. Hypersensitivity reactions reversible with atropine 20 micrograms/kg/ IV.
4. Drug therapy for transient neonatal myasthenia gravis is rarely required beyond 8
weeks of age.
5. Reversal of the effects of neuromuscular blocking agents may be incomplete.
Postoperative neonates may demonstrate hypoventilation despite partial reversal
of neuromuscular blockade. These infants require close observation and
monitoring. (Note: many anaesthetists do not attempt to reverse neuromuscular
blockade produced during general anaesthesia).
guideline.
NETILMICIN
Netromycin
July 2000
Dosage and Administration
1. 4 mg/kg/dose 24-hourly
IV infusion by syringe pump over 30 minutes
The dose will be adjusted according to therapeutic drug monitoring protocol below.
May be given IM if IV route not possible
Indications
1. Empirical therapy for those VLBW infants with risk factors for perinatal sepsis after
first week of life.
2. Suspected/proven neonatal sepsis (pneumonia, septicaemia, urinary tract
infections, CNS infections, skin, bone and soft tissue infections).
Contraindications
1. Hypersensitivity to netilmicin/other aminoglycosides.
Precautions
1. Use in treatment of minor infections.

2. Impaired renal function, high dosage or prolonged therapy, increases the risk of
4
nephrotoxicity and ototoxicity . Evidence of nephrotoxicity or ototoxicity requires
dose adjustment or discontinuation of netilmicin.
Drug Interactions
+ potential neurotoxic/nephrotoxic drugs eg: amphotericin, acyclovir, other

aminoglycosides = increased risk of toxicity 4.
+ frusemide = increased risk of ototoxicity 4.
+ cephalosporins = possible increase in nephrotoxicity 4.
Semisynthetic, water-soluble aminoglycoside antibiotic which probably acts by inhibiting

4
bacterial protein synthesis in susceptible organisms. Active against a wide variety of
pathogenic bacteria including Escherichia coli, Enterobacter, Pseudomonas aeruginosa,
Proteus spp, Serratia spp, Staphylococcus spp (including penicillin and methicillin
resistant strains). Distributes into extracellular fluid. Does not penetrate the CSF to any
significant extent. Low binding to human plasma protein. Eliminated mainly by glomerular
filtration.

3. Nephrotoxicity. More likely to occur with renal impairment, prolonged therapy and/
or high doses 4.
4. Ototoxicity. Incidence is low for netilmicin compared with other aminoglycosides,
and is more likely to occur with renal impairment, prolonged therapy and/or high
doses 4.
5. Rarely: tachycardia, hypotension, rash, fever, vomiting and diarrhoea 4.
6. A Fanconi-like syndrome, with aminoaciduria and metabolic acidosis, has been
reported in some adults and children treated with netilmicin 4.
1. Therapeutic Drug Monitoring:

a. Obtain trough and peak serum levels on 2nd dose and every 3-4 days
thereafter if dose unchanged.
b. If concerns about renal function or immaturity of baby, wait for trough level
before administering 2nd dose and performing peak levels - 36-hourly
dosing may be appropriate for some babies.
c. Trough level immediately prior to the next dose should be <2 mg/L. Desired
serum peak level 30 minutes after completion of drug infusion 5-8 mg/L.
d. Repeat trough and peak levels if dose changed - the peak level should be
performed after the next dose if the dose has been increased to ensure an
adequate level.
2. May be used in combination with other antibiotics if infused separately. Synergistic
effect against several organisms when used with penicillins.
3. Patients should be well hydrated during treatment 4.
4. The proprietary preparation contains benzyl alcohol which has been associated
with the "gasping syndrome". See "Description".
5. Abnormal laboratory results may occur: increase in blood sugar, alkaline
phosphatase, AST, ALT, bilirubin, potassium 4. Decrease in haemoglobin 4.
guideline.
INHALED NITRIC OXIDE

Reviewed by Dr David Knight
Nitric Oxide, iNO

February 2001
Nitric oxide (NO) is a gas that is given into the ventilator circuit. It is a potent vasodilator.
When given into the ventilator circuit, it dilates the pulmonary vasculature. It is inactivated
instantly in blood, by reacting with haemoglobin. Therefore it has no action on the
systemic vasculature and therefore (theoretically) on systemic blood pressure.
● Cylinder has 880 parts per million (ppm) in nitrogen

● Add to ventilator circuit between humidifier and baby.
● 100 ml/min added to 10 litres/min ventilator gas flow = 8.7 ppm

● 200 ml/min added to 10 litres/min ventilator gas flow = 17.4 ppm
1. Start on 20ppm (approximately 200ml/min, and increase according to

measurement on Nitric Oxide Monitor)
2. Start on 0.2 litres per minute in 10 litres of 100% O2 = 17.4 ppm
3. Reduce to 0.1 litres per minute: = 8.7 ppm
4. Reduce according to response
5. Doses above 20ppm are not indicated as generally a response is obtained prior to
this.
Indications
1. Persistent pulmonary hypertension of the newborn (proven on clinical grounds or

by echocardiography)
2. Severe respiratory failure
1. None in term infants. This is now considered a recognised practice.

2. Caution in preterm infants. Benefit in preterm infants has not be proven by
randomised studies.
Nitric oxide is endothelial derived relaxing factor (EDRF). It is produced in the

endothelium of blood vessels and diffuses out of the cells. It then enters vascular smooth
muscle cells and activates guanalate cyclase which forms cyclic guanosine
monophosphate (cGMP). This is a smooth muscle relaxer. cGMP is inactivated by cGMP
phosphodiesterase. The half life of NO is 3-6 seconds.
NO is bound to haemoglobin and inactivated to nitosylhaemoglobins and methaemoglobin.
1. Combines with haemoglobin to form methaemoglobin. At clinically used doses

high methaemoglobin levels have not been reported. In overdose, it may be fatal.
If methaemoglobinaemia occurs, check the ventilator circuit, particularly the
delivery and measuring points of iNO.
2. Is a toxic free radical and causes tissue damage. NO is used by macrophages to
kill bacteria. It can theoretically damage the lung through lipid peroxidation. The
precise importance of this has not been elucidated. Produces peroxynitrates which
are toxic to tissue.
3. NO converts to nitrogen dioxide NO2) spontaneously when mixed with oxygen.
High concentration of NO in O2 lasts 6 seconds! At clinical doses (<20 ppm), the
half-life is much longer. NO2 is very toxic.
4. NO is an inhibitor of platelet function. Caution when thrombocytopaenia or
bleeding problem.
guideline.
SODIUM NITROPRUSSIDE
DIHYDRATE Reviewed by Dr David Knight and Dorothy Cooper
Nipride April 1997
1. 0.4-2.0 micrograms/kg/minute by continuous IV infusion.

2. Usual starting dose: 1 micrograms/kg/min; adjust rate as necessary to control BP.
3. Maximum dose: 10 micrograms/kg/min for 10 minutes.
4. Maximum infusion rate for prolonged therapy 2 micrograms/kg/min.
Sodium nitroprusside 5mg added to D5W to make 50ml = 100 micrograms/ml
0.6ml/hr x weight (kg) = 1 microgram/kg/min
Calculation Formula
desired dose (micrograms/

Weight x 60 x kg/min) = rate in ml/hr
Strength of solution
Indications

2. Hypertensive crisis.
3. Severe congestive heart failure.
1. Known hypersensitivity to sodium nitroprusside.

2. Coarctation of the aorta.
3. Arteriovenous fistula.
4. Compensatory hypertension.
6. Caution in infants with hepatic or renal impairment.
7. Caution in infants with raised intracranial pressure.
Sodium nitroprusside is a potent, direct acting vasodilator. Affects arteriolar and venous
smooth muscle equally. Has little effect on gastrointestinal or uterine smooth muscle,
autonomic nervous system or central nervous system.
Rapid distribution to the target tissues (smooth muscle of the arteriolar and venous
vessels). Rapid and complete metabolism within erythrocytes to cyanide and
cyanomethaemoglobin. Metabolism of cyanide to thiocyanate by hepatic enzyme
rhodanase. Repeated enterohepatic circulation. Very slow elimination of thiocyanate by
the kidney (elimination half life 4-7 days).
Very rapid onset of action (1-2 minutes). Toxicity due to accumulation of cyanide and
thiocyanate. Associated with marked vasodilation and hypotension.
1. Hypotension
2. Cyanide toxicity
3. Metabolic acidosis
4. Restlessness, agitation, muscle twitching
5. Vomiting
6. Skin rash
7. Drug intolerance (metabolic acidosis, increased serum lactate and thiocyanate
levels).
8. Methaemoglobinaemia.
9. Raised intracranial pressure.
1. The efficacy and safety of nitroprusside in neonates has not been established.
Clinical experience is limited.
2. Titrate infusion rate against clinical response, especially blood pressure.
3. When discontinuing a nitroprusside infusion reduce the infusion rate steadily over
a period of 10-30 minutes to avoid rebound hypertension.
4. Monitor haemoglobin (nitroprusside binds the haemoglobin), arterial blood gases
for metabolic acidosis.
5. Serum thiocyanate levels should be measured. Toxic levels >2 mmol/L.
6. Management of thiocyanate or cyanide toxicity: stop nitroprusside infusion, infuse
vitamin B12 0.1 mg/kg IV.
guideline.
NORADRENALINE Dr Carl Kuschel, Brenda Hughes, Mandy Hodgson, Rob

Ticehurst (Pharmacy)
April 2000
Levophed Micrograms changed to nanograms June 2002
1. 50-500 nanograms/kg/min (0.05-0.5 micrograms/kg/minute) by continuous IV

infusion via a central venous catheter.
2. Dose is guideline only and must be considered in light of clinical response. Begin
at low dose and titrate to effect. Dosages should be increased or decreased in
small increments only.
3. Administer via a central line (UVC, Longline, or Surgical CVL).
4. Usual dilution 300 micrograms/kg (0.3 ml/kg) noradrenaline to make 50 ml with
D5W.
50 nanograms/kg/min (0.05 micrograms/kg/minute) = 0.5 ml/hour .
3 x weight (kg) x dose (nanograms/

Noradrenaline (mcg) in 50ml IV
kg/min)
Solution =
IV Rate (ml/hr)
Indication
1. Blood pressure support in infants who are not responsive to high dose dopamine (i.
e. (15-20 micrograms/kg/minute).
● Must discuss with the specialist on duty before instituting this treatment.
Contraindications
1. Uncorrected hypovolaemia is an absolute contraindication.

2. Hypertension.
3. Mesenteric or peripheral vascular thrombosis 2.
Precautions
1. Hypoxia or hypercapnia (may cause noradrenaline-induced cardiac arrhythmias).
Drug Interactions
1. Halogenated anaesthetic agents: serious cardiac arrhythmias may occur with

4
concomitant use .
4
2. Digoxin: increased risk of arrhythmias .
4
3. Beta blockers: risk of hypertension .
4
4. Doxapram: risk of hypertension .
Noradrenaline is a catecholamine agent with β-1 and potent α-1 activity. It acts primarily
to raise systemic vascular resistance and therefore blood pressure. It also has a direct
stimulatory action on the myocardium. However, this may be overshadowed by reflex
decreases in cardiac output occasionally manifested by a reduction in heart rate. Marked
bradycardia would be unusual (adults) and indeed heart rate may increase. There is
virtually no published data on the haemodynamic effects in the neonatal age group. There
is no evidence of a beneficial effect on the ratio of pulmonary vascular resistance/
systemic vascular resistance in persistent pulmonary hypertension of the newborn. The
drug must be given by continuous infusion. It is rapidly metabolised and has a half-life of
less than 5 minutes.
1. Extravasation can cause profound local vasoconstriction and tissue necrosis. If

extravasation occurs infiltrate with 5 mg phentolamine mesylate in 10 ml sodium
4
chloride 0.9% using a fine neeedle .
2. May cause large increases in blood pressure. Rapid changes in blood pressure
should be avoided.
4
3. Plasma volume depletion .
4. Arrhythmias, bradycardia. Severe arrhythmias warrant discontinuation of the drug.
4
5. Peripheral ischaemia including gangrene of the extremities .
6. Contains sodium metabisulphite as preservative. This agent can cause
2
hypersensitivity reactions including anaphylactic symptoms .
1. Ensure patient is not hypovolaemic. Correct if necessary before commencing

therapy.
2. Administer via a central venous catheter.
3. Clinical experience with noradrenaline is extremely limited and clinical efficacy and
potential problems are not clearly defined. It is therefore not appropriate as a first
line treatment and should be reserved for intractable hypotension not responsive
to volume loading or high dose dopamine.
4. Safety and efficacy of noradrenaline in paediatric patients has not been
2
established .
guideline.
PANCURONIUM BROMIDE
Pancuronium bromide
February 2001
Dose and administration
1. 100 micrograms/kg IV push, as needed for paralysis.

2. Usual dosing interval is 1-2 hours. Adjust dose as needed based on duration of
paralysis.
Indications
1. Skeletal muscle relaxation or paralysis in infants requiring mechanical ventilation.

2. Proposed desirable effects are improved oxygenation/ventilation, reduced
barotrauma and reduced cerebral blood flow fluctuations.
1. Known hypersensitivity to bromide.

2. Non-intubated infants.
3. Infants in whom tachycardia is undesirable.
4. Caution in infants with fluid and electrolyte imbalance.
5. Caution in infants with pulmonary, hepatic, renal disease.
Pancuronium is a non-depolarising muscle relaxant that competitively antagonises

autonomic cholinergic receptors and also causes sympathetic stimulation. Cardiovascular
effects (increased heart rate and blood pressure) are non-existent or mild. Histamine
release is absent or weak. The drug is partially hydroxylated by the liver, 40% is excreted
unchanged in the urine.
The dose required for neuromuscular blockage (95% depression of twitch height) is
extremely variable: the daily dose ranges between 100 and 1100 mcg/kg/day. The onset
of action is 1-2 minutes. Duration of neuromuscular blockade varies with dose and age.
Acidosis, hypothermia, neuromuscular disease, hepatic disease, renal failure,
cardiovascular disease, aminoglycosides, hypermagnesaemia, hypocalcaemia, and
immaturity potentiate duration of neuromuscular blockage. Alkalosis, hypercalcaemia and
adrenaline antagonise duration of neuromuscular blockage. Infants appear to recover fully
from the effect of pancuronium after 20 hours.
The effects of pancuronium are reversed by neostigmine (60 micrograms/kg) and atropine
(20 micrograms/kg).
1. Hypoxaemia may occur because of inadequate mechanical ventilation and

deterioration in pulmonary mechanics.
2. Tachycardia and blood pressure changes (both hypotension and hypertension)
occur frequently.
3. Increased salivation.
4. Oedema secondary to third-spacing of fluids.
5. Ventricular extrasystole.
6. Muscle wasting and hypotonia associated with prolonged use.
1. The duration of neuromuscular blockage is influenced by acid base status,

electrolyte disturbances, disease states, and a variety of drugs. The duration of
effect may be either shortened or lengthened.
2. The management of pancuronium overdose includes supportive mechanical
ventilation and reversal with neostigmine and atropine.
PARALDEHYDE Reviewed by Dr Malcolm Battin, Brenda Hughes, Gail Glogoski, Robyn

Wilkinson.
Paraldehyde August 1999

May 2000 (administration details only)
Dose and Administration (See "Possible Adverse Effects")
1. Slow intravenous infusion of DILUTED paraldehyde.

2
Administered as a 2 hour infusion .
Dose range is 0.2 to 0.4 ml (pure paraldehyde) /kg as 2 hour infusion. This is equivalent to 4 to 8ml (of DILUTED
SOLUTION ) /kg.– see Administration.
The dose may be repeated to NOT MORE than 0.4ml (pure paraldehyde)/kg in 24 hours.
2. Rectal enema: 0.2 to 0.3ml (of pure paraldehyde)/kg (this volume of paraldehyde must be diluted before
9
administration) - see Administration.
Indications (For term or near term infants)
1. Seizure/status epilepticus refractory to initial therapy with phenobarbitone and phenytoin.
Contraindications
1. Known hypersensitivity to paraldehyde.

5
2. Severe hepatic insufficiency, bronchopulmonary disease , or gastric disease.
Precautions
1. Hepatic dysfunction.
5
2. Cardiovascular disease .
3. Use only freshly opened ampoules. Do not use paraldehyde if it is brownish colour or has a sharp
penetrating odour of acetic acid – this indicates decomposed paraldehyde which is dangerous if administered
5.
.
4. Avoid contact between paraldehyde and rubber; avoid use of plastic syringes because of solvent action of
paraldehyde.
Drug Interactions
Possible concomitant drug therapy
CNS Depressants Possible potentiation of CNS depression.

(e.g. phenobarbitone,
phenytoin)
Paraldehyde is a hypnotic and sedative with anticonvulsant effects. Its possible action is to depress parts of the CNS
including the ascending reticular activating system to cause an imbalance between inhibitory and facilitatory
5
mechanisms . The drug is used to control seizures in infants, including those refractory to phenobarbitone and
phenytoin, and is as effective as phenobarbitone in the emergency treatment of convulsions in children. Adult
metabolism of paraldehyde involves 80% conversion to acetaldehyde, which is oxidised by aldehyde dehydrogenase to
acetic acid. Unmetabolised drug is largely excreted unchanged through the lungs with a smaller amount excreted in the
6
urine . The drug diffuses into the CSF and has a rapid onset of action. At therapeutic doses, paraldehyde has little effect
5
on respiration and blood pressure .
1. Intravenous injection may be hazardous and may cause pulmonary oedema and haemorrhage, hypotension and
5
cardiac dilatation, and circulatory collapse .
2. Rectal administration may result in rectal irritation.
5
3. Skin rash; trembling; unusual sweating .
4. Overdosage manifests as rapid laboured breathing, due to damage to lungs and to acidosis. Respiratory
6
depression and coma; metabolic acidosis, hepatic and renal damage may also occur . Diagnosis of paraldehyde
6
overdose may be aided by the characteristic odour of the drug on the breath .
5. Gastrointestinal irritation.
1. Emergency action for overdosage: Supportive measures:

❍ Ventilation
❍ Correction of hypotension
❍ Correction of metabolic acidosis

guideline.
PHENOBARBITONE SODIUM
Reviewed by Dr Malcolm Battin, Brenda Hughes, Beth
Loe, Vicki Savage
Gardenal sodium
June 1999
1. Loading: 20 mg/kg by slow IV infusion over 30 minutes, or IM.

Additional 5-10 mg/kg loading doses may be given if seizures are not controlled.
9
Maximum loading dose 40 mg/kg .
Maximum rate of administration 1 mg/kg/min.
2. Maintenance: 3-5 mg/kg daily IV, IM or PO as a single dose no earlier than 12-24
8
hours after the loading dose .
Indication
1. Seizures.
Precautions
1. Neonates and infants with respiratory failure.

3. Neonates with hepatic or renal impairment.
Drug Interactions
Possible concomitant drug therapy:
Paracetamol Possible decrease in effect of paracetamol due to induction of

hepatic enzymes by phenobarbitone. Prolonged use of the
combination may lead to liver damage.
Cefotaxime: Increase in skin reaction.

Chlorpromazine: Possible decrease in blood levels of both.
Corticosteroids Increase in clearance of steroid, due to induction of hepatic

enzymes.
Folic acid Possible decrease in phenobarbitone level.
Metronidazole Increase in clearance of metronidazole.
Phenytoin: Possible increase in phenobarbitone level. Phenytoin levels may

increase or decrease. Monitor levels of both drugs. Watch for
phenytoin intoxication if withdrawing phenobarbitone.
Rifampicin Possible increase in clearance of rifampicin
Theophylline Increase in theophylline clearance. Possibly also occurs with

caffeine
Propranolol Increase in clearance (propranolol hepatically metabolised). Sotalol:

not affected (renally cleared).
Phenobarbitone is a central nervous system depressant which is an effective

anticonvulsant. It appears to elevate the seizure threshold and limit the spread of seizure
activity. Mechanism for pharmacological actions is not known. May involve an increase in
inhibitory neurotransmission via enhancement of GABAergic systems.
Absorption virtually complete after PO, IM or rectal administration. Widely distributed with
higher distribution volume in neonates (Vd 0.6-1.0 L/kg) and infants than adults. Low
binding (10-30%) to human plasma protein. Brain/plasma phenobarbitone ratio
approximately 0.7. Ratio decreases with decreasing gestational age. Hepatic metabolism
(50-70%) to inactive metabolite. Elimination via the kidney (20-30%) unchanged. Renal
clearance enhanced by alkaline urine, diminished by acidic urine. Pharmacokinetics
among neonates very variable (elimination half life 40-200 hours).
7
1. At serum levels >40mcg/ml : Sedation, lethargy, drowsiness, slow feeding,
irritability.
7
2. At serum levels >60mcg/ml : Respiratory depression, apnoea.
3. Hypotension; hypothermia; bronchospasm.
4. Folate deficiency or hypocalcaemia with prolonged use.
5. Hepatitis. Monitor liver function tests during prolonged therapy
6. Rash.
7. Necrosis after extravasation, due to alkalinity of injection.
6
1. Therapeutic Drug Monitoring
1. Blood levels: Time to steady state: 10 – 14 days ( possibly longer in
neonates)
2. Sampling time: immediately before next dose.
3. Therapeutic range: 60 – 120 μmol/L
6
2. Measure serum phenobarbitone levels 12-24 hours after the loading dose,
especially if there are breakthrough seizures.
3. Measure levels at regular intervals during maintenance therapy especially if other
drugs are added to the therapy, or if there is a problem with on-going seizures.
4. Discontinue phenobarbitone by slowly reducing the maintenance dose.
5. Management of phenobarbitone overdose and/or toxicity: stop phenobarbitone,
supportive therapy (ventilation, volume expansion etc.). Elimination of
phenobarbitone may be enhanced by alkalisation of the urine and/or diuretic
therapy. Clearance delayed in neonates because of prolonged half life of
phenobarbitone.
guideline.
PHENYLEPHRINE HYDROCHLORIDE
Reviewed by
Metaoxedrine
September 1998
1. Instil one drop in each eye 30 minutes and 15 minutes before eye examination.
Indications
Is used in conjunction with cyclopentolate hydrochloride to dilate the pupil in preparation

for eye examination.
1. All babies at risk of severe ROP (<1250g birthweight or <30 weeks gestation).
2. Intraocular surgery pre and postoperatively.
1. Known hypersensitivity to phenylephrine.

2. Severe hypertension, ventricular tachycardia.
3. Caution in neonates with hyperthyroidism, hypertension, myocardial disease, heart
block, bradycardia, bronchopulmonary dysplasia.
Phenylephrine is a sympathomimetic agent with mainly direct effects on adrenergic

receptors. Produces mydriasis without cycloplegia. It also acts as a conjunctival
decongestant. The effect lasts several hours.
Phenylephrine may lower intraocular pressure temporarily.
Systemic absorption from conjunctival membranes can occur.

Possible Adverse Effect
1. Reflex bradycardia, ventricular dysrhythmias, tachycardia.

2. Excitability, headache, lacrimation, conjunctival allergy.
3. Increase in blood pressure.
4. May cause local discomfort.
1. Solutions stronger the 2.5% are NOT recommended in the newborn.

2. Interactions - beta-blocker: may cause arrhythmias.
3. Babies are screened.
1. 4-6 weeks postnatally or between 31-33 weeks gestation whichever is
earlier.
2. Then every 4-6 weeks until vascularisation has progressed into zone III.
3. Infants with ROP or immature vessels in zone I should be seen two weekly
until normal vascularisation has proceeded to zone III or the risk of attaining
threshold conditions has passed.
4. Infants with threshold disease should be considered candidates for ablative
therapy of at least one eye within 72 hours of diagnosis.
guideline.
PHENYTOIN SODIUM
Reviewed by Dr Malcolm Battin, Brenda Hughes, Julia
Blagburn, Robyn Wilkinson
Dilantin
July 1999
5
1. Loading dose: 20 mg/kg by slow IV infusion over 60 minutes .
6
2. Maintenance dose: 2-4 mg/kg/dose twice a day by slow IV infusion, or PO .
Administer at a rate not faster than 1.0 mg/kg/minute 6.
The maintenance dose needs to be monitored and adjusted according to blood
levels.
Indication
1. Seizures refractory to phenobarbitone therapy alone.
Contraindications
1. Sinus rhythm bradycardia, sinoatrial or atrioventricular block.
Precautions
1. Known hypersensitivity to phenytoin.

2. Neonates with jaundice, respiratory failure, hypotension or heart failure.
4. Neonates and infants with hepatic or renal impairment.
7
Drug Interactions
Phenytoin may increase the Phenobarbitone.

levels of:
Phenytoin may decrease the Paracetamol, caffeine, corticosteroids, diazoxide,
levels or activity of: digoxin, dopamine, fentanyl, frusemide,
theophylline.
Phenytoin levels may be Phenobarbitone, rifampicin, theophylline.

decreased by:
Phenytoin levels may be Fluconazole, ranitidine.

increased by:
Phenytoin levels may be altered Chlorpromazine, benzodiazepines.

by:
Phenytoin levels may be altered Interfere with thyroid function tests, and produce
by: lower than normal values for metyrapone
suppression tests.
Phenytoin is an anticonvulsant with a primary site of action in the motor cortex.

Environmental changes or excessive stimulation can cause a reduction in membrane
sodium gradient. Phenytoin causes an efflux of sodium from neurons and therefore
stabilises the threshold against over-activity in those brain stem centres responsible for
9
the tonic phase of grand mal seizures . Absorption from gastrointestinal tract and
intramuscular injection sites erratic. Phenytoin has high binding (85-90%) to plasma
protein. Bilirubin displaces phenytoin from albumin binding sites resulting in higher
percentage of unbound drug in plasma. Elimination via the kidney. Pharmacokinetics are
dose-dependent over the therapeutic range and unpredictable in the neonate. Relatively
small margin between full therapeutic effect and a minimally toxic dose of phenytoin.
1. Injection is very alkaline –therefore may result in venous irritation and phlebitis.
Avoid extravasation.
2. Observe diluted solution, for crystal formation.
3. Rapid administration may result in hypotension, CNS depression, cardiac
arrhythmias, and impaired cardiac conduction.
4. Gastrointestinal disturbances (nausea, vomiting, constipation).
5. Overdosage may result in hypotension, coma, respiratory depression. Nystagmus
may be an indication of toxicity.
6. Possible interference of Vitamin D and folate metabolism. Megaloblastic anaemia.
7. Hypersensitivity reactions eg. skin rashes. Bullous or purpuric rashes are
indicators to withdraw therapy as they may be symptoms of rare but severe
reactions eg. toxic epidermal necrolysis.
8. Hyperglycaemia.
1. DO NOT administer phenytoin intramuscularly. Crystallisation in muscle results in
erratic absorption and severe pain.
2. If used for maintenance therapy:
1. Monitor: Liver function and full blood count.
6
2. Therapeutic Drug Monitoring (TDM) : Time to steady state: 1 to 2 weeks
(variable).
Serum level (neonate): 40-80 μmol/L .
8
Measure serum phenytoin levels at least 12 - 24 hours after IV loading dose

and at regular intervals during maintenance therapy.
3. Management of phenytoin overdose and/or toxicity: stop phenytoin, supportive
therapy (ventilation, volume expansion, inotropes, and/or anti-arrhythmic agents).
guideline.
PIPERACILLIN SODIUM
Pipril
November 1996
Postmenstrual Age Postnatal Age Dosing Interval

(weeks) (days) (hours)
0 to 28 12
≤29
>28 8
0 to 14 12
30 to 36
>14 8
0 to 7 12
37 to 44
>7 8
45 All 6
Indications
1. Suspected/proven infections caused by Pseudomonas aeruginosa.

2. Use should be restricted to clinical situations in which ticarcillin has expected
disadvantages (need for lower sodium load, hypocalcaemia or platelet dysfunction).
2. Should not be used for gram positive infections.
Broad spectrum semi-synthetic penicillin antibiotic bactericidal against gram positive and
gram negative aerobic and anaerobic organisms. Increased activity against
Pseudomonas aeruginosa and many strains of Klebsiella, Serratia, E. coli, Enterobacter,
Citrobacter and Proteus. Exerts its bacteriocidal action by inhibiting cell wall synthesis.
Piperacillin is inactivated by beta lactamases produced by staphylococci and some gram
negative bacteria.
Poor oral absorption. Widely distributed in human tissues and body fluids. Very little
passes into the CSF unless the meninges are inflamed. Low binding (16%) to human
plasma protein. Excreted, mainly unchanged by the kidney. In the presence of urinary
tract infections, piperacillin appears to undergo some bacterial degradation. The half-life
in neonates is about 220 minutes. Reduction in serum concentrations may be achieved
by dialysis.
1. Venous irritation, soft tissue, injury at IV injection site.

2. Pain, erythema, soft tissue injury at IM injection site.
3. Hypersensitivity reactions (fever, rash).
5. Lethargy, seizures at high doses.
6. Increase in alkaline phosphatase, AST, creatinine.
7. Transient leukopenia, neutropenia, eosinophilia.

interval).
3. Sodium content: 1.8mmol/gm
guideline.
PORACTANT ALPHA
Curosurf
September 2005
1. Curosurf 1.25ml/kg (100mg/kg phospholipid) via endotracheal tube, 4 administered

by a doctor/NS-ANP.
Some infants with severe RDS may receive 2.5ml/kg (200mg/kg phospholipid) 4
on the instruction of specialist.
❍ Inject as a single bolus directly into ETT.
5
❍ Administer rapidly as quickly as the baby tolerates it.
❍ Baby supine and flat throughout.
2. Subsequent doses should not be given less than 6 hours after the preceding dose.
The usual criteria for administering a second dose are:
❍ need for positive pressure ventilation, and
❍ FiO >0.30
2
3. Some infants may require more than 2 doses. This should be on the instruction of
a specialist.
Indications
Intubated Infant in Level 3
1. Moderately severe respiratory distress syndrome.

2. ≤30 week babies either administer as early as possible or same
criteria as below.
3. >30 weeks. Diagnosis of RDS and an a/A ratio of <0.22.
Non ventilated infant in Level 2 (baby intubated for Surfactant

administration as per Guideline). Decision whether baby is transferred to
Level 3 made by CCN on duty.
1. Clinical/radiological evidence of respiratory distress syndrome.
2. Gestational age >32/40.
3. Age <72 hours.
4. Current chest radiograph available.
5. Increasing requirements e.g. FiO2 >50%, pH <7.25, PaO2 <7.0, CO2
>7.0 (or a/A <0.22).
6. Arterial line in situ.
1. Use in infants weighing <700g is not established.

2. Efficacy of poractant in the treatment of Meconium Aspiration Syndrome and
Group B Streptococcal Pneumonia has not been proven and therefore use for
these indications should be regarded as experimental.
A natural porcine surfactant derived from minced pig lungs. Surfactant is extracted using
chloroform or methanol and then purified using liquid-gel chromatography. It is then
sterilised via a high pressure filter system and then finally suspended in an isotonic saline
solution to a final concentration of 80mg/ml phospholipids. It also contains surfactant
apoproteins SP-B and SP-C.
Poractant increases the degree of mechanical stability of the alveoli and reduces surface
tension. A surfactant monolayer is formed at the air-liquid interface, allowing all areas of
lung to expand and contract.
Poractant is absorbed extremely rapidly. Infants typically show a rapid improvement in

oxygenation within minutes of the dose.
1. Instability during administration.

2. Possible ETT blockage.
3. Rapid changes in lung compliance and blood gases.
4. Slight increased risk of pulmonary haemorrhage.
5. Increased risk of nosocomial infections.
1. Should be used after consultation with specialist.

2. Staff need to be careful with vial size selection, as inappropriate vial selection may
result in high wastage and therefore increased cost.
Use the table below as a guide for choosing vial size:
1 dose 2 doses
(100mg/kg) (200mg/kg total)
Infant weight expected expected
Vial size Vial size
≤600g 1.5ml 1.5ml
600g-1200g 1.5ml 3ml
1200g-1800g 3ml 3ml plus 1.5ml
>1800g 3ml 3ml plus 3ml
These are guidelines only and discretion may be needed around choosing an
appropriate vial size for a particular infant.
3. Monitor O2 saturation, ECG continuously and blood gases and adjust ventilator/
oxygen appropriately.
4. Suction prior to administration if necessary but avoid suctioning if possible for 6
hours following doses.
5. Jewish and Muslim parents: use in these populations should be discussed with
parents. Poractant has been used extensively in Israel and as it is not per se
ingested, its use is considered acceptable. Parents should be informed that
alternative non-porcine preparations are not immediately available.
guideline.
POTASSIUM CHLORIDE
Potassium
November 1996
Maintenance treatment
1. 2 mmol/kg/day continuous IV infusion, PO.

2. Follow serum concentrations closely.
Acute treatment of symptomatic hypokalaemia
1. If renal function is adequate 0.5mmol/kg in an hour. Repeat as necessary.

2. Adjust maintenance potassium. Correct hypocalcaemia.
Indications
1. Prevention and treatment of hypokalaemia

2. Bradycardia secondary to hypokalaemia
1. Hyperkalaemia
2. Caution in babies with severe renal impairment and oliguria and renal disease.
3. Caution in babies with severe haemolytic reactions.
4. Caution in babies with cardiac disease.
5. Caution in babies with systemic acidosis.
6. Caution in babies with digoxin intoxication in presence of conduction disturbances.
7. Caution in babies receiving potassium sparing diuretic.
Potassium is the major intracellular cation. Hypokalaemia in critically ill neonates is

usually the result of diuretic therapy, inadequate intake or diarrhoea. Other causes
include congenital adrenal hyperplasia and renal disorders. Alkalosis as well as insulin
infusions will lower serum potassium concentrations by driving the ion intracellularly.
Symptoms of hypokalaemia include neuromuscular weakness and paralysis, ileus, urine
retention, and ECG changes, ST segment depression, low voltage T wave and
appearance of U wave. Hypokalaemia increases digoxin toxicity. Renal mechanisms are
of primary importance in maintaining both total body potassium and plasma concentration
within narrow limits. Oral potassium preparations are completely absorbed.
Hyperkalaemia effects cardiac conduction. ECG changes include tall peaked T waves,
heartblock with widening QRS complex, arrhythmia and cardiac arrest.
Potassium is excreted mainly by the kidneys and is secreted in the distal tubules where it
is involved in the sodium-potassium exchange process. Some potassium is excreted in
the stools and small amounts may also be excreted in the sweat, saliva, bile and
pancreatic juice.
1. Venous irritation, pain, soft tissue injury at the injection site.

2. Gastrointestinal disturbances common (diarrhoea, vomiting, bleeding, abdominal
discomfort).
3. Altered sensitivity to digoxin.
4. Respiratory distress.
5. Hyperkalaemia, indicated by weakness, listlessness, flaccid paralysis,
hypotension, cardiac arrhythmias including heart block and cardiac arrest.
1. Administer IV slowly, maximum infusion rate, 0.5-1mmol/kg/hour.

2. Monitor electrolytes.
3. Dilute potassium before intravenous administration. The literature recommends
dilution to 40mmol/L, i.e, 1mmol/25ml. As this may cause volume overload dilute to
1mmol/12.5ml and piggyback with IV fluids to achieve further dilution.
4. Adequate renal function must be confirmed.
5. Management of hyperkalaemia if K+>7mmol/L unhaemolysed. Refer to
Hyperkalaemia guideline.
guideline.
PROPRANOLOL HYDROCHLORIDE
Reviewed by Dr Patricia Clarkson, Dr Jon Skinner, Brenda
Hughes, Cherry Olsen, Lijla Brkic
Inderal
November 1999
Intravenous
4
1. 20 - 100 mcg/kg by slow IV infusion over 10 minutes every 6 hours
Oral
4
1. 20 -100 mcg/kg/dose 6 hourly
2. Dosage needs to be individualised and will vary depending on both clinical
diagnosis and individual patient metabolism.
Indications
1. Hypoxic spells in Tetralogy of Fallot.

2. Treatment of neonatal thyrotoxicosis.
3. Tachyarrhythmia.
Precautions
1. Use cautiously if there is heart failure.

2. Use cautiously in heart block.
3. Use cautiously in renal or hepatic impairment.
4. Infants with a tendency to bronchospasm.
5. Bradycardia, hypotension, metabolic acidosis, cardiogenic shock
Drug Interactions
Caffeine An increase in propranolol dose may be required. No clear evidence
for this
Chlorpromazine Possible hypotension. (Both drugs inhibit hepatic metabolism of

each other)
Digoxin May lead to bradycardia
Insulin Potential for severe, prolonged hypoglycaemia (reported in adult

diabetics ).
Phenobarbitone May require increase in propranolol dose. (Increase in metabolism

and clearance may occur)
Rifampicin May require increase in propranolol dose. (Increase in hepatic

metabolism)
Theophylline Increase in theophylline levels possible
Thyroid Altered levels of triodothyronine, T3 and thyroxine may occur –

hormones monitor.
Flecainide Possible additive negative inotropic effect. Cardiac depression may

occur
Verapamil Contraindicated in combination with a beta-blocker (negative

inotropic effect)
Propranolol is a non-selective beta-blocker acting on both β1 (mainly heart) and β2

(bronchial tissue) receptors. Blockade of β2 receptors may result in bronchospasm in
some patients. Propranolol has membrane stabilising properties in high doses. It does not
have intrinsic sympathomimetic activity (ISA). It exhibits a negative inotropic effect.
Propranolol is almost completely absorbed from the GI tract (adults) and there is
significant first pass metabolism and hepatic tissue binding with up to 90% of an oral dose
being eliminated. At least one metabolite shows biological activity but the effect on overall
activity is unknown. Metabolites and a small amount of unchanged propranolol are
excreted in the urine. Propranolol is highly protein-bound (80-95%). It is widely distributed
throughout the body with highest levels occurring in the lungs, kidney, brain and heart.
1. Bradycardia.
2. Hypoglycaemia / hyperglycaemia.
3. Hypotension in patients with underlying myocardial dysfunction, precipitation of
heart failure or heart block
4. Gastrointestinal effects (diarrhoea, vomiting, constipation)
5. Thrombocytopenia.
6. Bronchospasm.
1. Monitor: - Blood glucose; Renal, hepatic and haematological studies with

prolonged administration.
2. Have atropine on hand for excessive bradycardia.
3. Have aminophylline on hand for bronchospasm.
4. May mask the signs of thyrotoxicosis
5. Sudden cessation can cause withdrawal (nervousness, tachycardia, sweating,
hypertension).
guideline.
PROSTAGLANDIN E1
(ALPROSTADIL) Reviewed by Dr Jon Skinner, Brenda Hughes, Cherry
Olson, Jo Tatler and Rob Ticehurst
Paediatric Prostin VR
October 2004
1. 5 to 100 nanograms/kg/minute (0.005-0.1 micrograms/kg/minute) by continuous

intravenous infusion.
2. Start with low infusion rate and titrate according to the infant's response. Higher
initial doses are usually no more effective and have a higher incidence of adverse
effects.
3. Maintenance dose may be as low as 5 nanograms/kg/minute (0.005 micrograms/
kg/minute).
Prostaglandin (micrograms) in 50ml IV 3 x weight (kg) x dose (nanograms/kg/min)

solution = IV rate (ml/hr)
Usual dilution 3 - 6 micrograms/ml. In rare situations the strength can be

made up to 20 micrograms/ml. This is however very hyperosmolar. At 3
micrograms/ml, 1ml/hour = 0.05 micrograms/minute.
Indications
Dilatation of ductus arteriosus in infants with ductal dependent congenital heart defects:
1. Transposition of the great vessels.

2. All right sided cyanotic congenital heart defects associated with reduced
pulmonary perfusion.
3. Left sided congenital heart defects including hypoplastic left heart syndrome,
coarctation of aorta and interrupted aortic arch.
Contraindications
3
1. None.
Precautions
1. Respiratory distress. Alprostadil (Prostaglandin E1) should not be used in

3
neonates with Respiratory Distress.
2. Total anomalous venous return with obstruction.
3. Infants with bleeding tendencies (Alprostadil inhibits platelet aggregation).
4. Seizure disorders.
Prostaglandin E1 is a potent vasodilator of all arterioles. Other effects include inhibition of

platelet aggregation, and stimulation of uterine and intestinal small muscle. Alprostadil
(Prostaglandin E1) is rapidly cleared by metabolism, primarily occurring in the lungs, and
3
excretion via the kidney. Maximal drug effect usually seen within 30 minutes in cyanotic
lesion: may take several hours in acyanotic lesions.
3
1.Apnoea.
2.Hypotension.
3.Hyperthermia (transient).
4.Hypoglycaemia.
5.Tachycardia.
6.Bradycardia.
7.Seizures.
8.Diarrhoea.
9.Skin flush secondary to vasodilation- occurs more frequently with intraarterial
administration.
10. Sepsis, cardiac arrest, disseminated intravascular coagulation, hypokalaemia,
oedema, cortical proliferation of the long bones.
● Alprostadil (Prostaglandin E1) is rapidly metabolised and must, therefore, always

be given by continuous intravenous infusion. Vascular access must be secure at
all times and may demand the insertion of a central venous catheter or long line to
ensure continuity of delivery.
● The maintenance dose of the Alprostadil (Prostaglandin E1) infusion is determined
by titration according to the infant's response - oxygenation versus adverse effects.
● Monitor:
❍ Observe respiratory effort closely
❍ Monitor arterial pressure closely. If arterial pressure falls, a bolus of fluid
( 10- 20 ml/kg) is required. It may be necessary to decrease the rate of

infusion.
❍ Pulse oximetry is mandatory due to risk of apnoea and to monitor
therapeutic effect in cyanotic heart disease.

❍ Where there is restricted systemic blood flow, measure efficacy by
monitoring improvement of systemic blood pressure and blood pH, and

femoral pulses/arm-leg BP gradient in aortic coarctation.
❍ Renal function; full Blood Count & platelets frequently.
● Increased infant temperature is not an indication to stop therapy.

guideline.
PYRIDOXINE HYDROCHLORIDE
Vitamin B6
November 1996
For pyridoxine-dependent seizure control
Diagnostic test
1. 50-100 mg/kg IV, IM.
Maintenance dose
1. 2-100 mg/kg daily PO throughout life.

2. High doses may be required during periods of intercurrent illness.
Vitamin B6 deficiency
1. 2-5 mg per day PO.
Recommended daily requirement
1. 0.2-0.5 mg per day.
Indications
1. Diagnosis and treatment of pyridoxine-dependent seizures.

2. Prevention and/or treatment of vitamin B6 deficiency.
1. Known hypersensitivity to vitamin B6.

Pyridoxine-dependent seizures, an autosomal recessive trait, result from a defective

binding of pyridoxine to its apoenzyme, glutamate decarboxylase. The apoenzyme
catalyses the conversion of glutamic acid to gamma aminobutyric acid (GABA) which acts
as an inhibitory neurotransmitter in the central nervous system. Seizure threshold is
lowered in infants with reduced concentrations of GABA. Administration of
pharmacological doses of pyridoxine will correct the GABA deficiency.
Onset of pyridoxine dependent seizures usually occurs within 4 hours of age. The
seizures generally stop within 2-3 minutes following administration of pyridoxine.
Discontinuation of pyridoxine results in recurrence of seizures within 1-7 days in the
neonate and 2-24 days in the older infant. Therapeutic doses of pyridoxine are virtually
without toxicity.
1. Venous irritation, soft tissue injury at the IV injection site.

2. Pain, soft tissue injury at the IM injection site.
3. Nausea, headaches, irritability.
4. Profound sedation.
1. Wherever possible the initial diagnostic administration of pyridoxine should be

accompanied by EEG monitoring. There should be a 30 minute period of
observation after the test dose for the presence of seizure activity. If seizures
persist during the observation period, conventional anticonvulsant therapy should
be instituted.
2. Once a definite response to treatment with pyridoxine has been established,
therapy should be continued indefinitely.
guideline.
RANITIDINE
Zantac
November 1996
1. 1-2 mg/kg/dose 8-12 hourly by slow IV infusion over 30 minutes or orally.
Indications
Safety and efficacy has not been established in children younger than 12 years of age.
1. Treatment of acute gastrointestinal bleeding or stress ulcers.
1. Known hypersensitivity to ranitidine.

2. CAUTION use in neonates with renal or hepatic impairment.
Ranitidine is a highly effective, rapidly acting histamine H2 receptor antagonist. It inhibits

both basal stimulated gastric secretions (volume, acid and pepsin content reduced).
Peak plasma concentration occurs 1-3 hours after oral administration and is not
influenced by food. Bioavailability varies from 40-80%. Ranitidine is widely distributed
throughout the body. Low binding (10-19%) to human plasma protein. Hepatic
biotransformation predominates after oral absorption and undergoes extensive
metabolism on first pass through the liver. 30% is excreted unchanged in the urine. In
contrast, 70% of an IV dose is excreted unchanged in the urine. Normal elimination half-
life in children is 2-3 hours but is prolonged in patients with renal insufficiency. Very
limited data available describing pharmacokinetics and pharmacodynamics in the
newborn.
1. Bradycardia, tachycardia, PVCs.

2. Hepatotoxicity.
3. Gastrointestinal disturbances (nausea, vomiting, constipation, diarrhoea,
abdominal pain).
4. Headache (irritability).
1. Safe use in neonates, infants and children has not yet been determined.
2. May show false positive protein in urine.
3. 3-13 times more potent than cimetidine in inhibiting gastric acid secretion.
guideline.
SALBUTAMOL Reviewed by Dr Simon Rowley, Dr Innes Asher, Dorothy

Cooper
Ventolin, Respax September 1996

Dose for Hyperkalaemia revised July 2003 (Carl Kuschel)
1. Endotracheal: 0.02 mg/kg/dose 4 hourly as nebulised solution. May be repeated

2 hourly.
2. Via face mask: 0.05-0.15 mg/kg/dose 4 hourly as nebulised solution. May be
repeated 2 hourly.
7
3. For hyperkalaemia: 4 micrograms/kg IV over 10 minutes
4. Nebulised initially 2 hourly. Maybe extended to 4-6 hourly with response.
5. Dose as per chart below.
Weight (kg) Dose

3.0 kg 0.15-0.45 mg/dose
3.5 kg 0.17-0.52 mg/dose
4.0 kg 0.20-0.60 mg/dose
4.5 kg 0.22-0.67 mg/dose
5.0 kg 0.25-0.75 mg/dose
5.5 kg 0.27-0.82 mg/dose
6.0 kg 0.30-0.90 mg/dose
Indications
1. Bronchospasm in infants with bronchopulmonary dysplasia.

2. Emergency treatment of hyperkalaemia.
1. Known sensitivity to salbutamol and/or propellant mixture.

2. Caution in infants with hypertension, hyperthyroidism, hypokalaemia.
3. Concurrent use of β blocking agents.
Salbutamol is a selective β-2 adrenoceptor agonist. At therapeutic doses it acts on the β-2
adrenoreceptors of pulmonary bronchial muscle with little or no action on the β-1
adrenoreceptors of cardiac muscle. Salbutamol stimulates the production of intracellular
cyclic AMP, enhancing the binding of intracellular calcium to the cell membrane and
endoplasmic reticulum, resulting in bronchodilation. Also enhances mucociliary clearance.
Activation of the β-2 adreno-receptors opens ATPase channels and drives potassium
from the extracellular to the intracellular space. This both decreases extracellular
hyperkalaemia and increases intracellular potassium, so decreasing the chance of
arrhythmias.
Face mask is not significantly systemically absorbed via the lungs. A proportion of the
dose may be swallowed and can be readily absorbed from the gastrointestinal tract. First
pass metabolism of salbutamol occurs in the liver. About half is excreted in the urine as
an inactive sulphate conjugate, and about 30% is excreted as unchanged salbutamol.
The percentage of the inhaled dose reaching the lung will depend upon the method and
delivery of the nebulised salbutamol. Bronchodilation usually starts within 3-5 minutes
with peak at 15-20 minutes. The duration of effect is approximately 4 hours. Clinical
efficacy of nebulised salbutamol in infants under 18 months, especially very young infants
with bronchopulmonary dysplasia, is uncertain. Side effects from β-2 agonists are largely
due to b adrenoceptor stimulation and depend on dose, cell activity and route of
administration. The important side effects are worsening airway obstruction due to
reduced tone of the airway wall and worsening of ventilation - perfusion missmatch.
Overall, side effects are unusual and rarely result in discontinuation of therapy. There
have been no detailed studies on the side effects of salbutamol in infants and children
with bronchopulmonary dysplasia.
1. Peripheral vasodilation with a reflex tachycardia.

2. Irritability, tremors, hyperactivity.
3. Gastrointestinal disturbance (nausea and vomiting).
4. Paradoxical bronchospasm
5. Paradoxical hypoxaemia.
6. Hypokalaemia.
1. Consider not administering salbutamol when heart rate >180/minute.

2. Under special circumstances the dose may be increased up to 0.5 mg/kg/dose.
Titrate dose against clinical response and side effects. Discuss with Specialist.
3. Although the incidence of all side effects is very low following inhalation, the oral
and parenteral routes commonly induce side effects. The side effects may be so
severe that the drug has to be discontinued.
4. Transient hypoxaemia may occur during the administration of nebulised
salbutamol and therefore it should be administered with oxygen. Watch for signs of
hypoxaemia after delivery for up to 30 minutes.
guideline.
SODIUM BICARBONATE
Sodium Bicarbonate
February 2001
Indications, Dose and Administration
1. Emergency neonatal resuscitation.

1-2mmol/kg by slow IV push.
2. Metabolic acidosis
a. Documented metabolic acidosis during prolonged resuscitation after
establishment of effective ventilation. Administer half calculated dose then
assess need for remainder. Administered by slow IV infusion over 30
minutes.
b. Bicarbonate deficit caused by renal or gastrointestinal losses. Slow
correction orally.
Sodium bicarbonate dose (ml) = base deficit x 0.6 x weight (kg).

0.25-0.50 mmol/kg/hour. Continuous IV infusion.
Doses needs to be individualised and titrated according to response and to
adverse effects (e.g. hypernatraemia)
1. Respiratory or metabolic alkalosis.

2. Not recommended for hypercapnia or hypernatraemic states.
4. Caution in preterm infants. Rapid infusion of hypertonic NaHCO3 has been
incriminated in the pathogenesis of intraventricular haemorrhage in preterm infants.
Sodium bicarbonate is the alkali most frequently employed for correction of metabolic
acidosis. The drug is well absorbed from the gastrointestinal tract. Between 20-50% of an
orally administered dose can be recovered in the form of expired carbon dioxide. The
apparent bicarbonate space has been estimated to be 74% of body weight (range of 37-
134%). Thus calculations of bicarbonate dosage are based on an apparent volume of
distribution of 0.3 to 0.6 L/kg. Bicarbonate is rapidly metabolised to carbonic acid which
rapidly dissociates into water and carbon dioxide. The carbon dioxide is excreted via the
lungs.
1. Venous irritation, soft tissue injury at the site of IV injection.

2. Increased vascular volume, serum osmolarity, serum sodium.
3. Hypercapnia and respiratory acidosis.
4. Hypocalcaemia.
5. Abdominal cramping, nausea, vomiting.
6. Oedema, congestive heart failure.
7. Hyperirritability, tetany.
8. Intraventricular haemorrhage.
1. The osmolarity of molar sodium bicarbonate (8.4%) is approximately 1800 mOsm/

kg H20.
2. The adverse effects of sodium bicarbonate are largely associated with the use of
inappropriately excessive doses, infusion rate or concentrations of sodium
bicarbonate. Some of these side effects, such as intracranial haemorrhage, may
not be specific for sodium bicarbonate.
3. The recommended rate of infusion is no more rapid than 1 ml of bicarbonate IV per
minute.
4. Paradoxical acidosis (intracellular, CSF) may occur. Carbon dioxide diffuses more
readily across cell membranes than bicarbonate, thereby decreasing intracellular/
CSF pH.
guideline.
SODIUM POLYSTYRENE
SULPHONATE Reviewed by Dorothy Cooper
Resonium A February 1997
1. Rectal: 0.5 - 1.0 gm/kg every 20 minutes PRN, have infant retain dose for 15-20
minutes.
Indication
1. Hyperkalaemia (as an adjunct to other therapeutic measures).
1. Hypernatraemia
2. Congestive heart failure
3. Caution in neonates with hypokalaemia and hypocalcaemia.
Sodium polystyrene sulphonate is a cation-exchange resin prepared in the sodium phase

with an in vivo exchange capacity of approximately 1 mmol of potassium per gm. As the
resin passes along the intestine or is retained in the colon, the sodium ions are partially
released and are replaced by potassium ions. For the most part this action occurs in the
large intestine which excretes potassium ions to a greater degree than does the small
intestine. The resin is not totally selective: potassium and small amounts of other cations
such as magnesium and calcium can be lost during treatment. Treatment is slow with
effective lowering of serum potassium taking hours to days.
1. Gastrointestinal disturbances (nausea, vomiting, constipation, diarrhoea).

2. Hypokalaemia
3. Hypocalcaemia
4. Other electrolyte disturbances.
1. Sodium content 100 mg/gm.

2. Administration with sorbitol facilitates passage through GI tract, prevents
constipation.
3. For severe hyperkalaemia (>7.5 mmol/L) consider emergency therapy such as IV
glucose and insulin or IV sodium bicarbonate.
4. Monitor serum electrolytes for hypernatraemia, hypokalaemia, hypocalcaemia.
guideline.
SOTALOL HYDROCHLORIDE Reviewed by Dr Patricia Clarkson, Dr Jon Skinner

(October 1999), Brenda Hughes, Lejla Brkic, Robyn
Wilkinson
Sotacor
January 1999
Administration updated August 2002
IV
3
1. 0.5 to 1.5mg/kg/dose 8-hourly by slow IV infusion over 10 minutes
Oral
36
1. 1 to 2mg /kg/dose 8-hourly. Increase to 4mg/kg/dose if required ,
2. Needs to be individualised
Indications
1. Supraventricular tachycardia
2. Hyperthyroidism
Contraindications
1. Cardiogenic shock.
2. Severe sinus bradycardia.
3. Congenital or acquired long QT syndromes.
4. Hypokalaemia and hypomagnesaemia.
Precautions
1. Tendency to bronchoconstriction.
2. Greater than first degree heart block
3. Heart failure
4. Renal failure – decrease the dose in renal impairment, and discontinue if renal
3
impairment severe
5. Metabolic acidosis.
Drug Interactions
● Possible concomitant drug therapy should be undertaken only in

consultation with paediatric cardiologist
Amiodarone Bradycardia and hypotension (mechanism not established). Monitor

for haemodynamic depression
Diuretics May induce hypokalaemia or hypomagnesemia therefore increasing

the risk of Torsades de Pointes
Flecainide Bradycardia, AV block, cardiac arrest (allow a gap of several days

before starting flecainide)
Chlorpromazine Hypotension
Sotalol has both beta adrenergic receptor blockade and antiarrhythmic properties. It is a
non-selective beta adrenergic blocking agent affecting both beta1 and beta2 receptors. It
has no intrinsic sympathomimetic activity or membrane stabilising activity. It inhibits renin
release. Its beta adrenergic activity causes a reduction in heart rate (negative
chronotropic effect) and a limited reduction in the force of contraction (negative inotropic
effect). This leads to a decrease in myocardial oxygen consumption and cardiac work.
Sotalols antiarrhythmic activity causes a prolongation of the action potential in cardiac
tissue by delaying the repolarisation phase.
When given orally its absorption is minimally affected by food. Sotalol undergoes very
little first pass hepatic metabolism and, in adults, exhibits almost 100% bioavailability after
oral dosing. It is not protein bound, and is hydrophilic with a low incidence of severe CNS
adverse effects. Elimination is primarily by the kidneys with 75% of a dose excreted
unchanged in the urine.
1. Can worsen existing arrhythmias or cause new arrhythmias

2. Bradycardia, heart failure, hypotension, dyspnoea
3. Rash
4. Vomiting, diarrhoea
1. Have atropine on hand for excessive bradycardia.

2. Monitor
❍ Electrolytes, especially potassium and magnesium
❍ QT interval. Caution if QT becomes prolonged especially with increased
dosage
3. Therapeutic drug monitoring is possible.
4. Titrate dose of Sotalol when discontinuing treatment.
guideline.
SPIRONOLACTONE
Aldactone
September 1996
1. 1-3 mg/kg/dose daily PO.
Indications
1. Used in combination with other diuretics in the treatment of congestive heart failure
and BPD (situations of increased aldosterone secretion).
1. Known hypersensitivity to spironolactone

2. Significant impairment of renal function, especially anuria
3. Caution in neonates with severe liver dysfunction
4. Hyperkalaemia
5. Caution in neonates receiving potassium supplements
6. Should not be used concurrently with other potassium sparing agents.
Spironolactone is a specific pharmacological antagonist of aldosterone. Acts primarily

through competitive binding of receptors at the aldosterone dependent sodium-potassium
exchange site in the distal convoluted renal tubule. Causes increased urinary excretion of
sodium and water while potassium is retained. Also has an effect on tubular transported
calcium, resulting in increased urinary calcium excretion. Spironolactone has moderate
anti-androgenic activity in humans.
Well absorbed from the gastrointestinal tract (bioavailability >90%). Very high protein
binding (98%) to human plasma protein. Rapidly and completely metabolised to a large
number of metabolites. The major active metabolite is canrenone which has a slow
clearance. The activity of canrenone is 10-33 % that of spironolactone. Elimination of
canrenone and other metabolites is primarily in the urine (50%) but they also appear in
bile (5-33%).
The onset of action of spironolactone is usually observed 2-3 days after commencement
of therapy. The effects of aldosterone involve the synthesis of protein or peptide
subsequent to its combination with its receptor. The activity of the protein or peptide
persist for 2-3 days. With long-term use of spironolactone the elimination half-life is 13-24
hours. The duration of effect persists for 2-3 days following discontinuation of therapy.

2. Lethargy, irritability.
3. Paraesthesia, weakness, flaccid paralysis and tetany.
4. Rashes
5. Dose dependent androgenic effects (females), gynaecomastia (males).
1. Monitor urea and electrolytes frequently. Anticipate hyperkalaemia, hypocalaemia,

hyponatraemia, transient elevation of urea.
2. Reversible hyperchoraemic metabolic acidosis, usually in association with
hyperkalaemia, has been reported in patients with severe liver dysfunction, even in
the presence of normal renal function.
3. Spironolactone has been shown to increase the elimination half-life of digoxin. May
result in increased serum digoxin levels and subsequent digoxin toxicity.
4. Several reports of possible interference with digoxin radioimmunoassays by
spironolactone, or its metabolites, have appeared in the literature. Neither the
extent nor the potential clinical significance of its interference has been fully
established.
guideline.
SUXAMETHONIUM CHLORIDE
Dr Carl Kuschel and Brenda Hughes
Ethicholine
January 2001
1. 1-2 mg/kg/dose slow IV injection or 2 mg/kg/dose IM.
Indication
1. Short duration muscle relaxation to facilitate intubation.
1. Known hypersensitivity to suxamethonium chloride.

2. Known or suspected deficiency of plasma pseudocholinesterase.
3. Family history of malignant hyperthermia.
4. Hyperkalaemia.
6. Caution in neonates with renal impairment.
7. Caution in neonates with cardiac arrhythmias.
8. Caution in neonates with congenital myopathy.
Suxamethonium chloride (also known as succinylcholine) is a depolarising muscle

relaxant. Action due to initial stimulation then prolonged depolarisation of receptors for
acetylcholine at the neuromuscular junction. Suxamethonium may have a number of
effects apart from skeletal muscle relaxation (hyperkalaemic response, cardiac
arrhythmias).
Poorly absorbed from gastrointestinal tract - must be given IM or IV. Rapidly and
completely hydrolysed by hepatic and plasma pseudocholinesterase. Very rapid onset of
action (1-2 minutes). Continuous administration over a prolonged period of time may
result in irreversible blockage (phase II block). Short duration of action: 3-5 minutes (with
IM administration may be prolonged 10-15 minutes).
1. Bradycardia
2. Hyperkalaemia
3. Prolonged paralysis
4. Phase II (dual) block
5. Hypersensitivity reactions
6. Malignant hyperthermia
1. See Intubation Protocol.

2. Should not be used without additional sedation.
3. Bradycardia common in neonates and children, especially after a second dose of
suxamethonium. May be prevented by administration of atropine 20 mcg/kg prior
to administration of suxamethonium.
4. Suxamethonium causes a transient rise in serum potassium. Usually not a
problem unless serum potassium already very high, or potassium release is
enhanced.
5. Deficiency of pseudocholinesterase may be genetic or acquired. Incidence
approximately 1:2000 in adult population.
6. Management of suxamethonium overdose and/or toxicity is supportive (ventilation,
insulin glucose infusion for hyperkalaemia, antiarrhythmic agents).
guideline.
TICARCILLIN DISODIUM
Tarcil
February 1997
Postmenstrual
Postnatal Age Dosing Interval
Age
(days) (hours)
(weeks)
0 to 28 12
≤29
>28 8
0 to 14 12
30 to 36
>14 8
0 to 7 8
37 to 44
>7 6
≥45 All 6
Indications
1. Suspected/proven Pseudomonas infection. Usually administered concurrently with

an aminoglycoside as separate infusion.
2. Occasionally for resistant strains of other gram negative organisms (combination
therapy with an aminoglycoside).
3. Caution in infants with restricted sodium intake, contains 5.2mEq Na+/gm.
Semisynthetic penicillin antibiotic, bacteriocidal against non penicillinase producing

organisms (all penicillin sensitive organisms and some gram negative organisms).
Particularly useful as an anti-pseudomonal agent. In vitro synergism between ticarcillin
and aminoglycosides against certain strains of pseudomonas has been demonstrated.
Action through inhibition of biosynthesis of cell wall mucopeptide. Ticarcillin is not stable
in the presence of penicillinase. Some strains of pseudomonas have developed
resistance fairly rapidly.
Well absorbed after intramuscular injection. Widely distributed at varying concentrations

in human body tissues and fluids. Very little passes into the CSF unless the meninges are
inflamed. Moderate binding (45%) to human plasma protein. Eliminated via kidney, mainly
unchanged. Tubular excretion is inhibited by probenecid.

3. Skin rashes, pruritus, urticaria.
5. Anaemia, thrombocytopaenia, leukopaenia, neutropaenia and eosinophilia. May
inhibit platelet function.

interval).
guideline.
UROKINASE
Ukidan
March 1997
● This Is a Section 29 Medicine
1. 4400 units/kg IV infusion over 10 minutes. Dose may be repeated once.

2. Use with EXTREME caution. Safe dose in neonates has not been established and
use in neonates is not recommended by manufacturer.
Indication
1. Blocked central venous catheter.
1. Active internal bleeding or recent surgery within 10 days.

2. Not effective in clearing catheters occluded by substances other than blood
products.
4. Retinopathy of prematurity.
5. Arterial hypertension.
Urokinase is a fibrinolytic enzyme isolated from human urine. Its molecular weight is
54000. Urokinase brings about dissolution of blood clots by provoking the activation of
plasminogen. The latter is the inactive precursor of plasmin, the proteolytic enzyme
responsible for the breakdown of fibrin (clots) into peptide molecules which are
dispersible through the bloodstream. Being of human origin, urokinase is non-antigenic in
man.
Plasma half-life 10-20 minutes. Effect usually disappears within a few hours but increased
thrombin time, decreased plasma levels of fibrinogen and plasminogen, and increased
levels of the degradation products of fibrinogen and fibrin may persist for up to 12-24
hours after discontinuation of medication. Potentiates other anticoagulants (heparin).
1. Induced anticoagulant effect.

2. Haemorrhagic complications.
4. Lowered haematocrit.
5. Hypersensitivity reaction (rash, fever, bronchospasm).
6. Rapid lysis of coronary artery thrombi causing atrial or ventricular arrhythmias.
1. Discontinue therapy if spontaneous bleeding occurs.

Generic Infusion Calculator

© Carl Kuschel
December 2003
Note:
● This calculator only uses the information provided.

❍ It cannot determine whether the doses or concentrations are safe or recommended.
❍ It cannot determine what the appropriate diluent fluid is.
❍ Please refer to other sources for compatibility and concentration information.
● We suggest that the prescriber writes "milligrams", "micrograms", and "nanograms" in full.
● We recommend that you manually check the calculated formula to ensure accuracy.
● See also the "Reverse" Infusion calculator which allows you to determine what dose a prepared infusion will
give.
Drug Name:
Enter text so that there is a record of this if the calculation is printed
out.
Drug Concentration:
-Choose- per ml
Baby weight:
grams
Dose:
-Choose- per kg per -Choose-
Infusion Rate:
ml per hour
Volume to make infusion in:
50 ml (Default volume is 50ml)
Calculate Reset
"Reverse" Infusion Calculator

© Carl Kuschel
January 2004
Note:
● This calculator aims to determine what dose is being given from an infusion that is already made up.
● This can be used a a cross-check for babies who come from elsewhere who already have infusions in place, or where
there is uncertainty about the dose that the baby may be receiving.
Drug Name: Enter text so that there is a record of this if the calculation is printed out.
Original Drug Concentration: -Choose- per ml (Concentration of drug as it comes in the packet)
Baby weight: grams (Weight on which current dosing is based)
Original drug amount: ml in the syringe

Volume infusion made up to: ml
Calculate Reset
The Newborn Services Drug Protocols
The Newborn Service Drug Manual was commenced as a combined Nursing/Medical

project in 1990 by Andrew James (Paediatrician) and Dorothy Cooper (Newborn Clinical
Nurse Specialist). Andrew resigned from National Women’s Hospital in 1992 and took up
a position at the Hospital for Sick Children, Toronto, Canada, where he has maintained
his interest in clinical pharmacology in the neonate. Andrew was involved in the
preparation of many of the original protocols.
Dorothy Cooper took over the role of co-ordinator of the Drug Manual once Andrew
departed, but relinquished this role in 1998. Many of the protocols still carry her
contributions.
Brenda Hughes, Clinical Pharmacist, became involved in 1998. Pharmacy involvement is

an essential part of ensuring the accuracy and safety of this manual. Brenda has a
particular interest in compatibility information in neonatal pharmacology.
Many senior nursing staff have also contributed to the drug protocols.
In February 2001, the protocols were published in an intranet format in order to reduce
the risks of staff working off outdated "hard copy" protocols. Requests from Level 1 and 2
neonatal units that referred to National Women's Health to access the web-based
protocols provided the impetus for the entire website to be published on the internet in
August 2001. There has been further development of the many facets of the site,
including the development of drug calculation programmes (David Knight and Carl
Kuschel).
Thanks and Acknowledgements
Current Paediatricians, Malcolm Battin David Knight

National Women’s Frank Bloomfield Carl Kuschel
Hospital Jane Harding Simon Rowley
Previous Paediatricians, Salim Aftimos Andrew James

National Women's Guy Bloomfield Peter Nobbs
Hospital Patricia Clarkson Ian Wright
Tania Gunn
Paediatricians from Innes Asher, Respiratory Paediatrician
other Services Wayne Cutfield, Paediatric Endocrinologist
Jon Skinner, Paediatric Cardiologist
Lesley Voss, Paediatric Infectious Disease Specialist
Liz Wilson, Paediatric Infectious Disease Specialist
Pharmacy Staff Brenda Hughes Beth Loe
Billy Allen Colin McFarlane
Julia Blagburn Sanya Mirkov
Lejla Brkic Jo Tatler
Tess Camfield Rob Ticehurst
Gail Glogoski Ruth Tramschek
Nursing Staff Jean Bertram Cherry Olson
Dorothy Cooper Vicki Savage
Mandy Hodgson Robyn Wilkinson
Ana Kennedy
Thanks also to Carolynn Whiteman, Newborn Services Manager, who has allowed
significant time to be spent by nursing staff in the preparation of these protocols.
Apologies to anyone who may have unwittingly been left off this list.
guideline.
ACYCLOVIR
Reviewed by Dorothy Cooper and Carl Kuschel
Zovirax IV
September 1998
Management of Acyclovir Administration
Description
● White powder for reconstitution 250 mg/vial.

● Reconstituted solution is clear and colourless. It has a pH of about 11.
● (Not available in Neonatal Unit. Contact Pharmacy).
Prescription
● Charted on the prescription chart in mg/dose.
Administration
Slow IV Infusion over 1 hour
1. Reconstitute immediately prior to use with water 10 ml to make 25 mg/ml (2.5%

solution).
2. Do not use if any visible turbidity or if crystals form before or during infusion.
3. Requires further dilution. Using our usual dilution method dilute to 5 mg/ml in D5W,
NS.
4. Filter prior to administration through a Pall 0.22 micron filter.
5. Administer by slow IV infusion over 1 hour using a syringe pump.
6. Compatible with NS, D5W.
7. Do NOT mix with other drugs, IV solutions, blood or blood products.
8. Flush line with NS before and after infusion of acyclovir.
Nursing Considerations
1. Assess IV site carefully before and during infusion of acyclovir.

2. Observe for signs of adverse effects.
3. Monitor fluid balance closely.
Storage
● Not suitable for storage. Refrigeration may cause precipitation.
References
1 O'Brien JJ, Campolle-Richards DM. Acyclovir: An update of its role in antiviral therapy. New Ethicals 1989
(June): 45-65.
2 Askin OL. Clinical pharmacokinetics of acyclovir. Clin Pharmacokinetics 1983; 8:187-201
3 Hintz M, Connor JD, Spectre SA, et al. Neonatal acyclovir pharmacokinetics in patients with herpes virus
infections. Am J Med 1982; 73(1a): 210-4
4 Sullender WM, Arvin AM, Diaz PS, et al. Pharmacokinetics of acyclovir suspension in infants and children.
Antimicrob Agents Chemother 1987; 31:17-22.
5 Englund JA, Fletcher CV, Bowthor HH. Acyclovir therapy in neonates. J Pediatr 1991; 119:129-35.
6 Briggs GG, Freeman RK, Yaffe SJ. Drugs in lactation. Williams and Wilkins 1993 p8.
7 Royal Children's Hospital Melbourne. Paediatric Pharmacopoeia 1994, p4.
8 Nursing 97 Drug handbook. Springhouse 1997 p 163.
9 Pawlak RP, Herfect LAT. Drug administration in the NICU. Neonatal Network 2nd Ed 1991 p9.
guideline.
ADENOSINE Reviewed by Dr Pat Clarkson, Robyn Wilkinson, Brenda

Hughes, Lejla Brkic
Adenocor January 1999

Reviewed By Dr Jon Skinner, October 1999
Management of Adenosine Administration
Description
● Clear colourless solution 3mg/ml in 0.9% sodium chloride in 2ml vials. For IV
administration only.
Prescription
● Each dose is charted on the stat page of the drug chart in mg/dose.
Administration
1. Administered by doctor or NS-ANP with doctor in attendance.

2. Dilute immediately prior to use to 1mg / ml by adding to sodium chloride 0.9%
using our usual dilution method.
3. Filter prior to administration through a 0.22 micron filter
4. Administer by direct IV injection over 1 to 2 seconds.
5. Follow instantaneously with a rapid flush of sodium chloride 0.9%
6. Compatible with sodium chloride 0.9%. Adenosine 1mg/mL compatible with
10
glucose 5%
1. Continuous ECG printout during and immediately after administration IS

ESSENTIAL. File record in patient notes
2. Where practical record blood pressure prior to first dose
3. Continuous cardio-respiratory monitoring. Observe closely for arrhythmia.
4. Monitor and assess patient response to therapy.
5. Observe for signs of adverse effects and arrhythmias
6. Ensure resuscitation equipment available.
Storage
● Unopened, store at room temperature < 25°C. Do NOT refrigerate - may cause
crystallization.
● Used vial not suitable for storage.
References
1 Adenosine Drug evaluation monograph. 1974 - 1993 Micromedex Inc. Vol 78, Exp 11/30/93.
2 Sanofi Winthrop Pty Ltd. When seconds count, count on Adenocor (Product Information) 1995. Oxford
Clinical Communications Australia Pty Ltd.
3 Beral CI. Higher adenosine dosage required for supraventricular tachycardia in infants treated with
theophylline. Clin Pediatrics 1993: 167-168.
4 Paul T, Pfammatter JP. Adenosine. An effective and safe antiarrhythmic drug in pediatrics. Paed.
Cardiology 1997: 18; 118-126.
5 Stockley I. Drug Interactions 4th ed. The Pharmaceutical Press; 1996: London
6 Hansten P, Horn J. Drug Interactions Analysis and Management. Applied Therapeutics Inc.; July 1998:
Vancouver.
7 Crosson J, Etheridge SP, Milstein S, Hesslein PS, Dunnigan A. Therapeutic and diagnostic utility of
Adenosine during tachycardia evaluation in children. Am J Cardiol 1994; 74:155-160
8 Sherwood M, Lau K, Sholler G. Adenosine in the management of supraventricular tachycardia in children J
Paediatr Child Health 1998;34:53-56
9 Ralston M, Knilans T, Hannon D, Daniels S. Use of adenosine for diagnosis and treatment of
tachyarrhythmias in pediatric patients J Pediatr 1994; 124: 139-143
10 Ketkar V, Kolling W, et al. Stability of undiluted and diluted adenosine at three temperatures in syringes
and bags. Am J Health- Syst Pharm 1998; 55: 466-70
guideline.
ADRENALINE HYDROCHLORIDE Reviewed by Dr Carl Kuschel, Dorothy Cooper
August 1998
Adrenaline Micrograms changed to nanograms June 2002
Management of Adrenaline Administration
Prescription
● Slow intravenous push, intratracheal and intracardiac adrenaline are charted on

the stat page of the drug prescription chart in ml/dose.
Continuous Infusions:
Charted on fluid chart giving:
● rate in ml/hour
● dose in nanograms/kg/minute
Also charted on drug chart under continuous infusions giving:
● amount of drug to be added

● base fluid, type and volume
Administration
Administration of Intratracheal Adrenalin for Resuscitation
1. Administered by doctor / NS-ANP or a nurse with neonatal IV Drug Certification.

2. Dilute in 1-2ml of NS.
3. Instil into endotracheal tube. May be repeated as necessary.
Continuous Infusion (Use 1:1000 strength Adrenaline)
1. Administered by a nurse with Neonatal IV Drug Certification.

2. Dilute prior to administration.
3. Do NOT use discoloured solutions.
4. Filter prior to administration through a Pall 0.22 micron filter.
5. Compatible with D5W, D10W and NS. Incompatible with alkaline solutions/drugs.
6. Do NOT mix with other drugs, blood or blood products.
7. Protect from light during administration. Wrap tubing in tinfoil and cover syringe.
8. Administer via a syringe pump.
9. Give through a central venous line (UVC, Longline, or Surgical CVL).
Slow Intravenous Push
1. Is administered by the doctor / NS-ANP. In an emergency situation the nurse may

administer under the direct supervision of the doctor / NS-ANP present.
2. Further dilution is not necessary. Do not use discoloured solutions.
3. Administer IV by slow push over 5 minutes.
4. Filter prior to administration through a 5 micron filter.
5. Compatible with NS, D5W and D10W. Incompatible with alkaline solutions/drugs.
6. Do NOT mix with other drugs, IV solutions, blood or blood products.
7. Flush with NS before and after administration of adrenaline.
Administration of Intracardiac Adrenaline
1. This is a medical staff only procedure.

2. To be administered with a 22 gauge needle.
1. Observe IV site for signs of infiltration.

2. Continuous blood pressure monitoring or 5 minute BP recordings.
3. Continuous cardiorespiratory monitoring.
4. Document vital signs hourly and PRN.
5. Assess need for endotracheal suctioning. Mucous plugs may become more
difficult to dislodge.
Storage
● At room temperature.
● Protect from light.
● Discard ampoule after opening.
● Continuous infusions. No stability data available for dilute solutions of adrenaline.
Change solutions 8 hourly or more frequently if BP not maintained.
References
1 Guys, Lewisham and St Thomas Hospitals, Paediatric Formulary, 3rd Edition 1993, p11.
2 Royal Children's Hospital, Melbourne. Paediatric Pharmacopaeia 11th Edition 1994, p5.
guideline.
AMIKACIN SULPHATE
Reviewed by Dr Carl Kuschel, Brenda Hughes, Rob Ticehurst, and Robyn
Wilkinson
Amikin
November 2003
Management of Amikacin Administration
126
Description , ,
● Amikacin comes repackaged to a concentration of 5mg/ml.

● Supplied as 5ml and 10ml syringes.
● Preservative free but contains sodium metabisulphate.
● pH 4.5.
Prescription
● Doses are charted on the drug prescription chart in mg/dose.
Administration
Slow IV Infusion
1. No further dilution required ( 5mg/ml).

2. For infants <1000 grams administer as close to the intravascular catheter (LL,
UVC, IV) as possible to avoid the need for large NaCl flushes. Note that the
prepared syringes are pre-filtered so no added Pall filter is required.
3. Administer by slow IV infusion over 30 minutes using a syringe pump.
4. Incompatible with Heparin.
5. Do not mix with other drugs, IV solutions, blood or blood products.
6. Flush line with 0.9% NaCl before and after infusion of Amikacin.
7. Compatible with 0.9% NaCl or 5% Dextrose.
1. Monitor trough and peak levels - 1 hour after the infusion commences, 30 minutes
after the infusion ceases.
2. Observe site for extravasation during administration.
3. Observe for signs of renal, hepatic and haematological dysfunction during
prolonged therapy.
Storage
● Store prepared syringes in fridge.

● Opened vials: Use immediately and discard remainder.
References
1 Amikacin Data Sheet. Auckland: Baxter Healthcare Ltd., 2000.

2 Amikin® Data Sheet. Australia: Bristol-Myers Squibb,2001.
3 Stockley I. Drug Interactions 5th ed. London :The Pharmaceutical Press; 2000.
4 Northern Neonatal Network. Neonatal Formulary 3. London: BMJ Books, 2000.
5 Sweetman S (ed.) Martindale: The Extra Pharmacopoeia. (33rd ed). London : Royal Pharmaceutical
Society; 2002.
6 Trissel LA. Handbook of Injectable Drugs (10th edition). American Society of Hospital Pharmacists; 1998:
Bethesda
7 Treluyer JM, Merle Y, Tonnelier S, Rey E, Pons G. Nonparametric population pharmacokinetic analysis of
amikacin in neonates, infants, and children. Antimicrob Agents Chemother 2002; 46:1381-7.
8 Young TE, Mangum B. Neofax. 15th edition. Acorn publishing (Raleigh) 2002. P4-5.
9 Kotze A, Bartel PR, Sommers DK. Once versus twice daily amikacin in neonates: prospective study on
toxicity. J Paediatr Child Health 1999; 35:283-6.
10 Shore K, Morris A. Amikacin as a replacement aminoglycoside for netilmicin for coagulase-negative
staphylococcal sepsis in neonates (letter). NZMJ 2001; 115(1163):216
11 Prober CsG, Yeager AS, Arvin AM. The effect of chronological age on the serum concentrations of
amikacin in sick and preterm infants. J Pediatr 1981; 98:636.
12 Myers MG, Roberts RJ, Mirhij NH. Effects of gestational age, birthweight and hypoxaemia of
pharmacokinetics of amikacin in serum of infants. Antimicrob Agents Chemother 1977; 11:1027.
13 Nursing 97 Drug Handbook 1997 Springhouse p67-8.

Aukland Newborn Guideline PDF

Cargado por

Información del documento

Título original

Derechos de autor

Formatos disponibles

Compartir este documento

Compartir o incrustar documentos

Opciones para compartir

¿Le pareció útil este documento?

¿Este contenido es inapropiado?

Copyright:

Formatos disponibles

Aukland Newborn Guideline PDF

Cargado por

Copyright:

Formatos disponibles

Home | Contact Us | Phone Directory | Search

● Clinical Guidelines are listed alphabetically.

● Paediatric Resources (Starship)

Infant of Diabetic Mothers (Severe Acute Respiratory

INIS Study Syndrome)

Intracranial Haemorrhage ● Seizures

Intravascular catheters ● Sepsis

Intravenous cannulation ● Single Umbilical Artery

● Buffy Coat Concentrates ● Intravenous and Medication ● Skeletal Surveys

● Narcotic depression ● Vaccinations

Generic Trade Generic Trade Generic Trade

Acyclovir Zovirax IV Erythromycin EES Pancuronium Pancuronium

Respiratory Indices Calculator

Oxygenation Index (OI)

Respiratory indices have two main uses:

● All calculations are performed using mmHg.

Ventilation Choose ventilation

Abbreviations in Use in Newborn Services Reviewed by Charge Nurse -

● The following list is an accepted list of abbreviations that can be used in

AB Apex beat N10 Newborn intravenous

ABG Arterial blood gas Na+ Sodium

ETA Estimated time of arrival PROM Prolonged rupture of

HPU Has passed urine SIPPV Synchronised IPPV

Investigation of Infants born to Mothers with HELLP Reviewed by Carl Kuschel,

An association has been demonstrated between long chain 3-hydroxyacyl-CoA-

Guidelines for Screening

In pregnancies complicated by the HELLP syndrome or AFLP,

● Take the Newborn Screening Card at the usual time

A thorough family history is important. Infants should be observed for hypoglycaemia in

● If babies are symptomatic and LCHAD is considered a likely diagnosis, requests

Guidelines for Admissions to NICU, and Discharges Reviewed by Carl Kuschel

Discharge of Low Transfers to and from Level

Guidelines for Admission to 1. Birthweight less than 1250g.

Guidelines for Admission to 1. Low Birthweight - under 2500g.

Discharge of Low Birthweight Infants

Transfers & Discharges from NICU and PIN

Transfers from Level 3

For infants discharged from Level 2

summary in the notes.

All patients discharged from hospital must have:

● No baby is to be discharged from Level 3, Level 2, or PIN without a letter.

❍ It provides a structure for the letter, and makes an attempt at providing a

Guidelines on Admission to NICU from Home Reviewed by Simon Rowley

The general principles are:

1 Ideally babies admitted should be isolated, nursed in incubators or single room.

● Low birthweight (including recent NICU/PIN discharge).

b: Those infants requiring expertise likely to be more appropriately managed at

● Congenital heart disease or severe cyanosis in the absence of other

● Mother and baby admitted to a postnatal ward at National Women’s

A yellow card (detailing perinatal history) is preferred.

Albumex TM4 Authorised by Charge Nurse -

Albumex TM4 Parental Consent Prescribing Dose

● Available in two sizes - 500ml and 50ml.

● 4% albumin is free of risk of transmission of known viral diseases (heat

● Informed consent required.

Prescribing of Albumex TM4

● Prescribed on the blood transfusion/IV fluid chart (CR5541).

● On NZBS requisition form (111F01802)

Checking, Administration, Monitoring, and Documentation

● As for blood and blood products.

● See Transfusion Reactions.

Albumex TM20 Authorised by Charge Nurse -

Albumex TM20 Parental Consent Prescribing Ordering