Guideline: Hypoglycaemia-Newborn - CKN · Web view3. Thorton P, Stanley C, De Leon D, Harris D,...

MaternityandNeonatalClinicalGuideline

Hypoglycaemia–Newborn (V6) v0.05

Queensland Health

Queensland Clinical Guideline: Hypoglycaemia–Newborn

Refer to online version, destroy printed copies after use of 61


Document title: Hypoglycaemia–newborn

Publication date: Review publication date Month 2019

Document number: MN18.8-V6-R24

Document supplement:The document supplement is integral to and should be read in conjunction with this guideline.

Amendments: Full version history is supplied in the document supplement.

Amendment date: Full review of original document published in August 2013

Replaces document: MN13.8-V5-R18

Author: Queensland Clinical Guidelines

Audience:Health professionals in Queensland public and private maternity and neonatal services

Review date: Month 2019

Endorsed by:Queensland Clinical Guidelines Steering Committee

Statewide Maternity and Neonatal Clinical Network (Queensland)

Contact:Email: [email protected]

URL: www.health.qld.gov.au/qcg

Disclaimer

This guideline is intended as a guide and provided for information purposes only. The information has been prepared using a multidisciplinary approach with reference to the best information and evidence available at the time of preparation. No assurance is given that the information is entirely complete, current, or accurate in every respect.

The guideline is not a substitute for clinical judgement, knowledge and expertise, or medical advice. Variation from the guideline, taking into account individual circumstances, may be appropriate.

This guideline does not address all elements of standard practice and accepts that individual clinicians are responsible for:

Providing care within the context of locally available resources, expertise, and scope of practice

Supporting consumer rights and informed decision making, including the right to decline intervention or ongoing management

Advising consumers of their choices in an environment that is culturally appropriate and which enables comfortable and confidential discussion. This includes the use of interpreter services where


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necessary

Ensuring informed consent is obtained prior to delivering care

Meeting all legislative requirements and professional standards

Applying standard precautions, and additional precautions as necessary, when delivering care

Documenting all care in accordance with mandatory and local requirements

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Version Control

Date Version Comment Updated by

9/8/2018 0.01 First draft Stephanie Sutherns

14/9/2018 0.02 Following discussion with clinical leads Stephanie Sutherns



11/2/2019 0.05 Version for distribution to working party Stephanie Sutherns



Flow Chart: Preventative care of the well at risk newborn baby

Well at risk newborn babyIf baby is symptomatic or screening BGL < 2.6 mmol/L–refer to

Flowchart: Management of hypoglycaemic newborn baby

At birth Assess for risk factors Keep baby warm

o Dry babyo Early skin to skino Maintain temperature 36.5 ºC– ºC

Initiate feeds within – minutes of birtho Discuss feeding cueso Feed at least 3 hourly or more frequentlyo Gavage feed if baby < 35 weeks

Avoid separation of mother and babyo Discuss preventative care with parents

Symptomatic or unwell babyMay have one or more signs Poor feeding Tremors/jitteriness Apnoea Cyanosis Irregular, rapid breathing Seizures Altered LOC–irritability,

lethargy, stupor, coma Hypotonia Weak or high pitched cry

Effective first feedSymptomatic or

unwell orBGL < 1.5 mmol/L

Ongoing care Keep baby warm Continue skin to skin contact Feed

o Feed at least 3 hourly or more frequently BGL screening:

o 1st–before second feed not longer than 3 hours of age

o 2nd–before third feed not longer than 6 hours of age

o If normal– every – hours pre-feed for 24 hours

Routine observations for 24 hourso Temperatureo Heart rateo Respirationso Colour/perfusiono LOCo Tone

Yes

No

Feedingo Assist breast feeding

mothers with attachment and hand expression

o Give baby colostrum/EBM if available

o Assist formula feeding baby

If concerned, re-check BGL

BGL � mmol/L

Continue usual care Cease BGL monitoring if:

o BGL � mmol/L for 24 hourso Baby feeding effectivelyo Baby is well and has not required IV

glucose

Refer to Flowchart : Management of hypoglycaemic newborn baby – mmol/ L

Medical/NNP review Admit to neonatal unit Refer to Flowchart: Neonatal

hypoglycaemia BGL< 1.5 mmol/L

Yes

BGL– mmol/L

Temperature– ºC or labile Baby of diabetic mother Preterm < 37 weeks gestation Inadequate feeding SGA < 10th centile LBW < 2500 g

Risk factors

Suspected syndromes Maternal medications– beta

blockers; dexamethasone; oral hypoglycaemics

Family history of metabolic disorders

LGA > 95th centile Severe intrapartum asphyxia/

resuscitation at birth Post-mature baby Polycythaemia

No

No

Yes

If baby< 35 weeks and/or < 37 weeks gestation and/or < 2500 g admit to neonatal unit

Conf

irm B

GL

< 2.

6 m

mol

/L a

t any

tim

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blo

od g

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achi

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orat

ory

Yes

No

BGL blood glucose level, IV intravenous, LBW low birth weight, LGA large for gestational age,



LOC level of consciousness, NNP neonatal nurse practitioner, SGA small for gestational age,

< less than, ≥ greater than or equal to



Flow Chart: Management of hypoglycaemic newborn baby (BGL 1.5–2.5 mmol/L)

Management of hypoglycaemic newborn babyBGL1.5 mmol/L– mmol/L

If baby well and > 35 weeks gestation–give glucose gel 40% 0.5 mL/kg orally prior to feed (maximum 2 doses per episode up to 6 doses in total)

Feed immediately:o Give oral or enteral EBM (if available) or formula o 60 mL/kg/ day

Notify medical officer/NNP Repeat BGL 30 minutes after glucose gel

BGL – mmol/LBGL < 1.5 mmol/L,

unrecordable or symptomatic baby

BGL � mmol/L

Monitor BGL – hourly pre-feed for first 24 hours

BGL � mmol/L

Discharge and follow-up As per underlying cause May require long-term follow-up May require 6 hour fast and BGL

monitoring test prior to discharge

Continue usual care Cease BGL monitoring if:

o BGL � mmol/L for 24 hourso Baby feeding effectively

If term baby, enteral feeding discontinued

o Baby is well and not requiring IV therapy

Notify medical officer/NNP Admit to neonatal unit Refer to Flowchart:

Neonatal hypoglycaemia–BGL < 1.5 mmol/L or unrecordable

BGL increasingAND > 2 mmol/L after

glucose gel regimen

Yes

No

NoYes

Yes

Baby¶s weight Dose to be administered

Glucose gel 40% (0.5 mL/kg)

1 mL– g– g 1.1mL– g 1.2 mL

2.5 mL

– g 1.3 mL– g– g

1.4 mL1.5 mL1.6 mL– g

– g 1.7 mL– g 1.8 mL– g 1.9 mL– g 2.0 mL– g– g 2.2 mL– g 2.3 mL– g– g

2.4 mL

2.1 mL

Yes

No

No

Yes

Conf

irm B

GL

< 2.

6 m

mol

/L a

t any

tim

e in

blo

od g

as m

achi

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oC a

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Abbreviations: BGL blood glucose level, CVL central venous catheter, EBM expressed breast milk, IV intravenous, NNP neonatal nurse practitioner, PoC point of care, UVC umbilical venous catheter, < less than, ≥ greater than or equal to



Flow Chart: Management of neonatal hypoglycaemia (baby symptomatic or BGL < 1.5 mmol/L)

Management of neonatal hypoglycaemia–symptomatic or BGL < 1.5 mmol/L

Do not delay treatment Urgent medical review/consider neonatologist consultation Confirm BGL in blood gas machine, PoC analyser or

laboratory Admit to neonatal unit Collect diagnostic samples for hypoglycaemia screen Urgent treatment

o Glucose – mL/kg bolus IV, then repeat BGL after 30 minutes and if required, further 1 mL/kg bolus IV

o IV infusion glucose 10% at 60 mL/kg/day to giveglucose at 4.2 mg/kg/min

o If IV access delayed, give glucagon 200 microg/kg IM As required

o Increase IV glucose rate in 20 mL/kg/day increments (e.g. 60 to 80 mL/kg/day)

Risk of fluid overload— mL/kg/day maximum on day 1 of life (monitor serum sodium levels)

o Increase IV glucose concentration to 12% or step-wise to higher concentration

If > 12% glucose administer by UVC/CVL BGL

o Repeat 30 minutes after: Commencing/any changes to glucose concentration Medication administration (for hypoglycaemia)

o Repeat hourly until � mmol/L then, – hourly Feeds–continue if not contraindicated

Diagnostic samplesBlood–during hypoglycaemic episode Insulin, cortisol, growth hormone Ketones–ßOH butyrate Adrenocorticotrophic hormone Free fatty acids Acyl-carnitine profile Blood gas (including electrolytes,

glucose, haemoglobin, haematocrit and lactate)

Urine–post-hypoglycaemic episode Metabolic screen

Check BGL before feeds Gradually reduce IV therapy as

enteral feeds increase If no IV glucose and BGL �

mmol/L prior to 3 consecutive feeds cease monitoring

Discharge and follow-up As per underlying cause May require long-term follow-up May require 6 hour fast and BGL

monitoring test prior to discharge

YesBGL � mmol/L for > 12 hours

Consult with neonatologist/endocrinologist Discuss pharmacological intervention:

o Glucagon: 200 microg/kg IV, IM or subcut bolus then – microgram/kg/hour IV infusion

o Hydrocortisone: – mg/kg 6 hourly IV or oralo Diazoxide: Initial dose 5 mg/kg/dose bd oral AND

Hydrochlorothiazide: – mg/kg/dose bd oralo Octreotide:2– microgram/kg – hourly subcut

IV glucose > 10 mg/kg/min orBaby >72 hours of age or

BGL difficult to control

NoNo

Yes

Conf

irm B

GL

< 2.

6 m

mol

/L a

t any

tim

e in

blo

od g

as m

achi

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oC a

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ory

mL/kg/day

14% 5.8 7.8 9.7 11.7

16% 6.7 8.9 11.1 13.3

18% 7.5 10 12.5 15

20% 8.3 11 13.9 16.7

12% 5 6.7 8.3 10

10% 4.2 5.6 6.9 8.3

Glucose mg/kg/minute

% 60 80 100 120

Abbreviations: BGL blood glucose level, CVL central venous line, IM intramuscular, IV intravenous, NNP neonatal nurse practitioner, subcut subcutaneous, UVC umbilical venous catheter,Refer to online version, destroy printed copies after use of 61


> greater than, < less than, ≥ greater than or equal to



Abbreviations

BGL Blood glucose level

CI Confidence interval

EBM Expressed breast milk

FGR Fetal growth restriction

GDM Gestational diabetes mellitus

IM Intramuscular

IM Intramuscular

IV Intravenous

LGA Large for gestational age

MCADD Medium chain acyl-CoA dehydrogenase deficiency

MRI Magnetic resonance imaging

NICU Neonatal intensive care unit

PICC Peripherally inserted catheter

RR Relative risk

SGA Small for gestational age

UVC Umbilical venous catheter

Definitions

Trophic feeds Minute volumes of feed to stimulate the gastrointestinal tract1



Table of Contents

1 Introduction................................................................................................................................... 91.1 Normal physiology................................................................................................................91.2 Definition............................................................................................................................ 10

2 Babies at risk.............................................................................................................................. 112.1 Causes............................................................................................................................... 11

2.1.1 Maternal risk factors.......................................................................................................112.2 Baby risk factors and causes..............................................................................................12

3 Identification................................................................................................................................ 133.1 Screening and assessment of at risk baby.........................................................................133.2 Clinical signs......................................................................................................................14

4 Management............................................................................................................................... 154.1 Prevention.......................................................................................................................... 154.2 Initial management.............................................................................................................164.3 Glucose gel........................................................................................................................ 174.4 Ongoing management........................................................................................................184.5 Intravenous glucose...........................................................................................................194.6 Medications........................................................................................................................20

4.6.1 Medicines....................................................................................................................... 205 Persistent hypoglycaemia...........................................................................................................22

5.1 Indications for further investigation and management........................................................225.3 Interpretation of investigations............................................................................................235.4 Ongoing management........................................................................................................235.6 Six hour fast test.................................................................................................................24

6 Sequelae of hypoglycaemia........................................................................................................257 Discharge planning..................................................................................................................... 25References......................................................................................................................................... 26Appendix A Growth charts..................................................................................................................28Appendix B Glucose 40% gel doses..................................................................................................30Appendix C Glucose infusion rates (GIR) and concentrations...........................................................31Appendix D Investigations for neonatal hypoglycaemia.....................................................................32Acknowledgements............................................................................................................................ 33

List of Tables

Table 1. Clinical hypoglycaemia.........................................................................................................10

Table 2. Maternal risk factors.............................................................................................................11

Table 3. Baby risk factors and causes................................................................................................12

Table 4. Screening............................................................................................................................. 13

Table 5. Clinical signs.........................................................................................................................14

Table 6. Prevention............................................................................................................................ 15

Table 7. Initial management...............................................................................................................16



Table 8. Glucose gel........................................................................................................................... 17

Table 9. Ongoing management..........................................................................................................18

Table 10. IV fluids............................................................................................................................... 19

Table 11. Short term medicines..........................................................................................................20

Table 12. Medicines long-term...........................................................................................................21

Table 13. Pathological hypoglycaemia...............................................................................................22

Table 14. Investigations interpretation................................................................................................23

Table 16. Six hour fast test................................................................................................................. 24

Table 17. Sequelae............................................................................................................................ 25

Table 18. Discharge planning.............................................................................................................25



1 Introduction1.1 Normal physiology During fetal life glucose, lactate and amino acids are the principal sources of energy. The fetus receives glucose from the mother with fetal plasma glucose concentrations 70–80% of the maternal level. The fetal insulin level is independent of the mother’s level, as insulin does not cross the placenta, but it is dependent on the fetal blood glucose level. During the last trimester of pregnancy when there is rapid growth, energy stores (particularly muscle and fat in adipose tissue) are laid down in preparation for birth.2

Blood glucose levels (BGL) in healthy term newborn babies fall in the first two hours of life during transition to extra-uterine life. An asymptomatic, transient and mildly low BGL after birth is normal.3 It occurs due to the transition from continuous transplacental glucose supply from the mother in-utero, to an intermittent supply from milk feeds.

Physiological transition beginning immediately after birth includes:

Endocrine changes–plasma insulin levels fall and catecholamines and pancreatic glucagon are released and the essential enzymes for glycogenolysis, gluconeogenesis, lipolysis and ketogenesis are switched on2

Glycogenolysis–production of glucose by the liver when stored glycogen is broken down to form pyruvate in response to increased epinephrine and glucagon concentrations and falling insulin levels2

Glycogenesis–plasma glucose levels are maintained by glucose synthesis from non-carbohydrate sources, for example glycerol, lactate, pyruvate and glucogenic amino acid precursors and occurs during the first 8–12 hours of life when glycogen stores are depleted2,4

Stimulation of appetite and adaption to fast and feed cycle and promotion of oxidative fat metabolism using lipid from fat stores and milk feeds4

o Delay in the first feed by the baby for 3–6 hours after birth results in approximately 10% of babies not maintaining their plasma glucose levels above 1.7 mmol/L5.

o Concentrations of free fatty acids, lactate and ketones as substrate for metabolism are raised in response to breast feeding

The nadir usually falls to 2.2 mmol/L in the first two to four hours of life then, by four to six hours of age stabilises at 2.5–4.4 mmol/L (up to 6.2 mmol/L)4. Over subsequent days the mean BGL rises slowly to concentrations seen in older children and adults5.

Glucose levels in the blood are maintained during postprandial and postabsorptive states by balancing glucose utilisation with endogenous glucose production. Counter-regulation is the process in the fasted state where the body makes glucose available.2 Babies have a two to three times higher glucose utilisation rate per unit of body mass compared with adults due to the disproportionately larger brain size relative to body mass.3

This normal physiological transitional response is different from disorders resulting in persistent or recurrent hypoglycaemia.6



1.2 Definition

Table 1. Clinical hypoglycaemia

Aspect Consideration

Context

The blood glucose level in babies, changes in the first hours after birth

Generally, hypoglycaemia is defined as:

o BGL less than 2.6 mmol/L7-9

o If BGL less than 1.5 mmol/L or unrecordable–severe

o Symptomatic baby (refer to Table 5. Clinical signs )

Clinical hypoglycaemia

BGL low enough to cause signs of impaired brain function10 (refer to Table5. Clinical signs)

Not defined based on specific BGL10 as:

o Not possible to identify single BGL that causes brain injury

Injury extent influenced by other factors including extent and duration of hypoglycaemia, and availability and ability to use other substrates such as lactate, fatty acids and ketones

o Specific brain response thresholds to hypoglycaemia vary across different BGL

Factors influencing clinical significance

Infection

Inborn errors of metabolism

Hyponatraemia

Neonatal encephalopathy due to perinatal asphyxia

Conditions associated with diminished hepatic glucose production11

o Cold stress

o Congenital heart disease; congestive heart failure

o Intrauterine growth restriction

o Prematurity

o Perinatal stress/hypoxia

o Sepsis

Clinical standards

Screen all at risk babies

Avoid separation of mother and baby unless admission to neonatal unit is required for investigation and management

Screen baby with glucometer with electrochemical sensor that uses



glucose oxidase test strips12

Collect blood samples:

o Heel prick (do not squeeze poorly perfused heel) or venepuncture for screening

o Venepuncture for diagnostic tests including BGL (when indicated)

o Do not take samples from intravenous or intra-arterial lines infusing glucose

o Ensure adequate drawback of fluid and blood from indwelling lines administering other solutions, for example sodium chloride 0.9%

Refer to Queensland Clinical Guideline Standard care13



2 Babies at risk2.1 CausesGenerally, neonatal hypoglycaemia is caused by one or more of:

Increased levels of insulin (regulatory hormone)2,11,14-17

Increased glucose utilisation11

Inadequate glucose supply2,11

Inadequate body stores (glycogen, fat)17-19

Decreased levels of counter-regulatory hormones (e.g. growth hormones, cortisol, adrenergic)11,14,16,17

Disorders of glycogen metabolism (glycogenolysis)11,15,19

Disorders of glucose production (gluconeogenesis)11,15,18,19 Babies at risk may or may not present with signs of hypoglycaemia (refer to Table 5. Clinical signs). The number and type of risk factors needs to be considered when planning the management for the baby. Extra vigilance is required for babies who have multiple risk factors and/or are born to women with gestational diabetes mellitus (GDM) or if there is a sibling or other family member with a history of a metabolic disorder such as medium chain acyl-CoA dehydrogenase deficiency (MCADD).

Where there is impaired metabolic adaptation there may be impaired glucose and ketone body production. This includes preterm babies, intrauterine growth restriction, perinatal hypoxia/ischaemia and poorly controlled GDM. These babies require prevention, diagnosis and management of hypoglycaemia to reduce the risk of harm.2

2.1.1 Maternal risk factors

Table 2. Maternal risk factors


Maternal medications

Beta-blockers5,20 (aOR 1.68, 95% CI. 1.50–1.89)20, for example propranolol, atenolol, labetalol

Insulin21

Oral hypoglycaemic agents5 given for non-diabetes conditions such as polycystic ovarian syndrome

Maternal antenatal betamethasone22-24 may cause transient fetal adrenal suppression if administered to women after 36 weeks gestation within 24 hours of birth25 or multiple courses

Maternal diabetes

Poor maternal diabetes control and macrosomic baby

Maternal diabetic control rather than type or treatment (diet, oral hypoglycaemic medicines or insulin) of diabetes is the important factor15,26,27

Known family history

Family history of genetic form of hypoglycaemia3,18 or congenital hyperinsulinaemic disorder

Sibling or parent with:



o MCADD

o Other fatty acid oxidation defect

Intrapartum glucose IV

IV glucose administration greater than 20 g/hour causing transient hyperinsulinaemia

o For example, Hartmann’s solution with glucose 5% if greater than 400 mL/hour or glucose 10% at greater than 200 mL/hour

Maternal conditions Maternal pre-eclampsia/ eclampsia or hypertension



2.2 Baby risk factors and causesSome risk factors, for example fetal growth restriction, predispose a baby to hypoglycaemia through several mechanisms.

Table 3. Baby risk factors and causes


Increased glucose utilisation

Increased glucose requirements:

o Temperature 36–36.4º C less than 36º C

o Birth asphyxia3,15,18

o Infection2,5

o Congenital heart disease

o Respiratory disease

Fetal growth restriction (FGR)–less than 2500 g at term gestation or less than 10th centile 3,14,17–refer to Appendix A Growth charts

Perinatal asphyxia3,15,18–acidosis (e.g. cord pH less than 7.0, base deficit less than 12); need for prolonged resuscitation

Polycythaemia/hyperviscosity3,5,14

Seizures18

Inadequate glucose supply

Delayed or inadequate feeding

Intravenous (IV) therapy–abrupt cessation or rapid weaning of glucose infusion including infusion infiltration in baby

Inadequate body stores

Inadequate substrate stores or ability to use

FGR–less than 2500 g at term gestation or less than 10th centile15,19–refer to Appendix A Growth charts )

Preterm2–less than 37 weeks 5,15or post-mature

Maternal use of beta-blockers20 or terbutaline5

Severe hepatic dysfunction

Increased levels of insulin

Large for gestational age (LGA)14,17; small for gestational age (SGA)3,5,14–refer to Appendix A Growth charts

Hyperinsulinaemia17; persistent neonatal hyperinsulinaemia hypoglycaemia19; congenital hyperinsulinaemia2

Erythroblastosis15, for example haemolytic disease of the newborn2,5

Leucine sensitivity

Islet cell hyperplasia or dysfunction; insulinoma



Beckwith-Wiedemann Syndrome15,19

Perinatal asphyxia or stress3,5,14

In-utero hyperglycaemia in poorly controlled maternal diabetes2,3,5,14

Intrapartum maternal administration of IV glucose greater than 20 g/hour15

Decreased levels of counter-regulatory hormones

Impaired glucose homeostasis from endocrine disorders:

o Panhypopituitarism17

o Growth hormone deficiency17

o Adrenocorticotrophic hormone (ACTH) unresponsiveness28, adrenal haemorrhage, congenital adrenal hyperplasia

Suspected syndromes and endocrine disorders:

o Midline defects–facial anomalies, micropenis, midline brain anomalies (detected antenatally), for example absent septum pellucidum, corpus callosum

Congenital anomalies

Beckwith-Wiedemann syndrome/exomphalos2,3,15,29

Other major congenital anomalies or congenital anomaly syndromes14,15

Disorders of glycogenolysis

Inborn errors of carbohydrate metabolism15,17,19

o Glycogen storage disease types 1 (von Gierke’s), III and IV

Disorders of gluconeogenesis

Inborn errors of carbohydrate metabolism15,17,19, (e.g. galactosaemia)

Inborn errors of amino acid metabolism15,17,19, (e.g. maple syrup urine disease; proprionicidaemia; methylmalonicacidaemia)

Inborn errors of fatty acid oxidation17,30, (e.g. medium chain acyl-coenzyme A dehydrogenase deficiency; long chain 3-hydroxy acyl-coenzyme A deficiency)

Unknown or mixed causes

Hypothyroidism21

Meconium aspiration syndrome3,5,14

Iatrogenic–from erroneous or malicious administration of insulin2



3 Identification3.1 Screening and assessment of at risk baby

Table 4. Screening


Physical assessment5,26,31

Identify if baby is:

o LGA–greater than 95th centile or greater than 4500 g 18,19

o SGA18,19 less than 2500 g at term gestation or less than 10th centile

o Refer to Appendix A Growth charts

Undertake complete physical assessment to identify signs associated with neonatal hypoglycaemia

Refer to Table 5. Clinical signs

Refer to Queensland Clinical Guideline Routine newborn assessment32

BGL screening asymptomatic baby

Screening times:

o 1st before second feed not later than 3 hours of age

o 2nd screen before third feed not later than 6 hours of age

o If normal (greater than 2.6 mmol/L) screen before every second feed–every four to six hours pre-feed for 24 hours depending on feeding frequency

Screen baby who has risk factors

o Preterm11 baby less than 37 weeks gestation

o Baby is LGA, SGA or FGR

o Temperature11,18–labile or less than 36 ºC per axilla

o Poor feeding5

o Baby of diabetic mother11,18,19–poorly controlled and or macrosomic baby

o Maternal hypertension or pre-eclampsia/eclampsia18,19

o Birth asphyxia; meconium aspiration syndrome5,18

o Polycythaemia18

o Postmature baby5

o Baby of mother treated with beta adrenergic medications or oral hypoglycaemic medications5



o Family history of genetic form of hypoglycaemia5

o Suspected or known congenital syndromes18; abnormal physical features5

BGL screening

Provide adequate pain relief to baby for blood sampling, (e.g. oral sucrose or breast milk)

Capillary blood may be used for screening

Use glucose meter suitable for neonatal samples

If screening BGL less than 2.6 mmol/L or borderline result in baby with significant risk factors or clinical signs of hypoglycaemia, validate by diagnostic test using point of care analyser, blood gas analyser or laboratory specimen in fluoride oxalate tube

o If tested BGL less than 2.6 mmol/L refer to Table 7. Initial management



3.2 Clinical signsHypoglycaemia can be asymptomatic.5 Measure the BGL and consider the clinical signs in the differential diagnosis. Clinical signs may overlap or be concurrent with other newborn disorders.

Table 5. Clinical signs


Neurogenic17

Jitteriness11 or persistent tremor11

Breathing irregular and rapid

Sweating

Irritability

Pallor

Neuroglycopenic17

If neurological signs present then this may represent severe hypoglycaemia5

Poor feeding

Hypotonia–floppiness11

Abnormal cry–weak or high-pitched11

Seizures

Changes in level of consciousness–stupor, coma11

Lethargy11, apathy

Other Apnoea11; bradycardia; cyanosis; tachypnoea11

Hypothermia11



4 ManagementAny baby with BGL less than 1.5 mmol/L or unrecordable, or who is symptomatic requires urgent management and further investigation. A staged approach to management and further investigation is indicated in a hypoglycaemic baby with a BGL greater than or equal to 1.5 mmol/L.

4.1 Prevention

Table 6. Prevention

Aspect Recommendation/good practice point

At birth

Keep baby warm–maintain temperature 36.5–37.5ºC per axilla

Dry baby

Early skin to skin contact if appropriate

Routine observations

Initiate feeds early2,17,19 within 30–60 minutes of birth

Discuss feeding cues with mother

Feed at least 3 hourly or more frequently as baby requires2

If baby less than 35 weeks admit to neonatal unit and commence gavage feeds

Breast feed2 (preferably) or expressed breast milk

o Assist woman with colostrum/breastmilk expression

Formula feed if this is maternal choice or with consent if breast milk not available, commence at:

o If normal or no risk baby 30–40 mL/kg/day

o If high risk baby at 60–75 mL/kg/day as tolerated

Baby less than 37 weeks gestation or low birth weight

Admit to neonatal unit as per local protocols

Prevent/manage hypothermia

If baby’s clinical condition allows, give early and frequent feeds

o Commence gavage feeds as indicated

Manage other conditions as required

Feeding

Breast feed if baby’s condition allows

If enteral feeding not possible or contraindicated:

o Commence IV glucose 10% at 60 mL/kg/day (refer to Table 10. IV fluids)

Provides 4.2 mg/kg/minute of glucose

Complementary feeds of expressed breast milk (EBM) or formula not Refer to online version, destroy printed copies after use of 61


required in first 24 hours unless:

o One BGL less than 2 mmol/L OR

o Two or more BGL are less than 2.6 mmol/L

If complementary feed required give–

o Minimum 7.5 mL/kg/feed (based on 60 mL/kg/24 hours on day one)

If baby breastfeeding well and BGL in normal range halve complementary feeding quota

If BGL greater than or equal to 2.6 mmol/L in first 24 hours–continue breastfeeding and cease complementary feeds

Symptomatic or unwell baby

If baby becomes symptomatic or unwell:

o Medical/NNP review

o Admit baby to neonatal unit

Refer to Table 7. Initial management



4.2 Initial management

Table 7. Initial management


Management of well baby (feeding)

If BGL 1.5–2.5 mmol/L and baby is greater than or equal to 35 weeks gestation, well and feeding

o Give glucose gel 40%33 and feed baby (refer to Table 8. Glucose gel)

o Feed at least 3 hourly

If BGL less than 1.5 mmol/L admit to neonatal unit and commence glucose 10% IV infusion (refer to Table 10. IV fluids)

BGL 1.5–2.5 mmol/L and poor feeding

Give glucose gel and feed baby (refer to Table 8. Glucose gel)

Notify medical officer/NNP

Consider other observations regarding general condition of baby

If BGL less than or equal to 2 mmol/L

o Admit to neonatal unit17

o Commence IV therapy (refer to Table 10. IV fluids)

o Continue breast feeding if baby able

If BGL greater than 2 mmol/L and less than or equal to 2.6 mmol/L:

o Administer glucose gel 40% (refer to Table 8. Glucose gel

o Feed baby immediately

Give oral or enteral colostrum or EBM, or formula

Give 90 mL/kg/day (12 mL/kg)

o If BGL greater than 2 mmol/L and increasing

Continue feeding baby and monitoring BGL

BGL less than 1.5 mmol/L, unrecordable or baby symptomatic

Do not delay treatment

Admit to neonatal unit

Confirm screening BGL in blood gas machine, point of care analyser or laboratory15,16

Collect diagnostic blood and urine samples (refer to Table 13. Pathological)

Urgently commence IV therapy

o Refer to Table 10. IV fluids

If IV/UVC access delayed–administer glucagon 200 micrograms/kg IM



injection (refer to Table 11. Short term medicines)

o Contact NeoRESQ for advice regarding cannulation options

Repeat BGL after 30 minutes of glucose 10% IV infusion commenced or glucagon administered

o Hypoglycaemia non-responsive to glucagon may be due to glycogen storage disease

Continue feeds if not contraindicated

Consider any formula in total fluid volume

Cease BGL monitoring

Cease if:

o BGL is greater than or equal to 2.6 mmol/L for greater than 24 hours

o Baby is feeding effectively

Baby well and not requiring glucose IV



4.3 Glucose gel

Table 8. Glucose gel

Aspect Consideration/recommendation

Context

Effective adjunct to oral feeding9,34

A single buccal dose (200mg/kg) 0.5 mL/kg of glucose 40% gel reduces incidence of hypoglycaemia (RR 0.68; 95% CI 0.47–0.99, p = 0.04)35

Reduces incidence of hypoglycaemia35 compared with placebo administration (RR 0.79; 95% CI 0.64–0.98, p = 03; number needed to treat = 10, 95% CI 5–115)35

Reduces admission to NICU for hypoglycaemia (RR 0.46; 95% CI 0.21–1.01, p = 0.05)

Treatment with glucose gel does not affect neurosensory outcome at two years of age9

Dose

If BGL 1.5–2.5 mmol/L–administer glucose 40% gel and continue feeds9

Dose of glucose 40%:

o 0.5 mL/kg (200 mg/kg)

o For specific doses for different weight ranges, refer to

Appendix B Glucose 40% gel doses If BGL 1.5–2.5 mmol/L:

o Administer dose and feed baby (breast, EBM or formula at 60 mLs/kg/day)

o Re-check BGL 30 minutes after administration of gel

If BGL 2–2.5 mmol/L after first dose of gel:

o Administer repeat dose and feed baby (breast, EBM or formula)

Assess and supervise baby’s feeding

o Re-check BGL 30 minutes after administration of gel

If BGL less than 2 mmol/L after second dose of gel:

o Admit baby to neonatal unit for IV glucose and feed

o Maintain baby’s temperature

o Assess for any other signs

o Consider the nature of the baby’s risk

Consider continuing up to 6 doses (within first 48 hours of life) if:

o Baby’s clinical examination by doctor or NNP is normal AND



o Baby is asymptomatic AND

o Baby is feeding well AND

o Prefeed BGL is greater than 2 mmol/L AND

o BGL is rising after each glucose gel dose

Admit to neonatal unit if:

o Baby has risk factors and requires a third consecutive dose

Consider discussing with a neonatologist

Administration

To administer9:

o Dry baby’s buccal mucosa with gauze

o Rub into buccal mucosa

Feed baby

Feeding Breast feeding reduces requirement for repeated glucose gel doses (OR=0.52, 95% CI 0.28–0.94)9

Criteria to escalate

Notify medical officer or NNP after gel administered if:

o BGL remains less than 2.6 mmol/L

o Baby becomes unwell or is feeding poorly

Admit to neonatal unit

o BGL less than 2.6 mmol/L despite 2 doses of glucose gel 40% and EBM or formula feed

o BGL less than 1.5 mmol/L at any time

o Baby becomes unwell or is feeding poorly



4.4 Ongoing managementIf greater than 8 mg per minute of glucose required, consider administering glucagon earlier to minimise interference with the establishment of breast feeding, avoid fluid overload and lessen pancreatic over stimulation with high glucose delivery.

Table 9. Ongoing management


Ongoing

Refer to Table 13. Pathological

If required, increase volume of fluid administered

o An increase of 20 ml/kg/day provides a 33% increase in glucose

o Check sodium level

If low prepare a solution with increased glucose concentration for equivalent glucose delivery rate, and reduce fluid intake

Refer to Table 10. IV fluids and

Appendix C Glucose infusion rates (GIR) and concentrationsIncrease the concentration of glucose to12% or step-wise to higher concentration as required

o Glucose 12% provides a 20% increase in glucose

o If IV infusion required is greater than 12% insert umbilical venous catheter (UVC) or central line

Optimal BGL:

o 3.0 mmol/L in first 24 hours

o 4.0 mmol/L after 48 hours or as advised by neonatologist or paediatric endocrinologist36

o If required increase volume to 100 mL/kg/day maximum in first 24 hours36

o Consider risk of fluid overload

o Review serum sodium and other electrolyte levels regularly

If not contraindicated continue trophic feeds

Repeat BGL 30 minutes after any changes to concentration or volume of glucose administered to confirm response

BGL Measure:

o Hourly until greater than or equal to 2.6 mmol/L

o Then every 4–6 hours

If greater than or equal to 3 mmol/L for 12 hours on first day of life or



greater than or equal to 4 mmol/l on second day:

o Gradually reduce IV glucose as enteral feeds increase

o Check BGL prefeed

o If full feeds achieved and BGL consistently greater than or equal to 3 mmol/L (first day) or greater than or equal to 4 mmol/L after first day, can be ceased

Further investigations and management

Consider further investigations and pharmacological intervention5 if:

o IV glucose rate greater than or equal to 8 mg/kg/minute OR

o Baby is more than 48 hours of age OR

o Baby presents with hypoglycaemia for the first time after 24 hours

o BGL is difficult to control

Refer to Table 11. Short term medicines

Refer to Table 13. Pathological hypoglycaemia

Consider consulting with a neonatologist

Cease BGL monitoring

Cease BGL monitoring if:

o Complementary feeds or IV glucose not required and BGL now greater than or equal to 2.6 mmol/L for 24 hours or

o Complementary feeds and/or IV glucose were required and now ceased, and BGL now greater than or equal to 2.6 mmol/L prior to 3 consecutive normal feeds



4.5 Intravenous glucose

Table 10. IV fluids


Context

IV glucose indicated if:

o BGL less than 1.5 mmol/L or unrecordable and/or

o Baby has any signs consistent with severe hypoglycaemia

If greater than 12% glucose required administer via central catheter– umbilical vein catheter or peripherally inserted central catheter (PICC)

Regimen

Urgently:

o Administer glucose 10% IV 1 mL/kg (100 mg/kg) as bolus dose15

o Recheck BGL after 30 minutes and if indicated repeat dose at 1 mL/kg

If IV access delayed, administer glucagon (refer to Table 11. Short term medicines)2

Use bolus doses of glucose sparingly except where severe or symptomatic hypoglycaemia

o Commence glucose 10% IV infusion at 60 mL/kg37 to give 4.2 mg/kg/minute of glucose

Calculate IV glucose in mg/kg/minute (refer to

Appendix C Glucose infusion rates (GIR) and concentrationsBaby with hyperinsulinaemia may require higher glucose concentration2

Baby with endocrine deficiency or inborn error of metabolism more likely to require only 4–6 mg/kg/minute of glucose

As required:

o If severe or persistent hypoglycaemia increase the fluid volume before the concentration as this will result in an immediate change in glucose delivery rate

o Increase IV glucose in 20 mL/kg/day increments (e.g. 60 mL/kg/day to 80 mL/kg/day)

o Administer glucagon (refer to Table 11. Short term medicines)

o Increase IV glucose concentration to 12 % or step-wise to a higher concentration21 and/or

o If hyponatraemic or fluids 100mL/kg/day on day one insert, central venous line when time allows for administration of increased concentration and reduced volume

o Refer to

Appendix C Glucose infusion rates (GIR) and concentrationsConsider risk Refer to online version, destroy printed copies after use of 61


of fluid overload (refer to Table 9. Ongoing management)

o If baby is day one of life, 100 mL/kg/day total fluid intake is maximum baby is likely to tolerate without developing fluid overload

o Continue oral feeds if not contraindicated

o Review serum sodium levels regularly

General principles of weaning treatment:

o Wean IV glucose and increase to full feeds (appropriate for day of age), then

o Wean glucagon (if used), then

o Wean hydrocortisone (if used)

o If trouble weaning, consult with neonatologist or paediatric endocrinologist

Calculation for glucose infusion rate (mg/kg/min)38

Glucose infusion rate (mg/kg/minute)=Concentration%×rate (mL /hour)

¿¿

OR

Glucose infusion rate (mg/kg/minute)=Concentration%×rate(mL /kg)/day ¿ ¿

144



4.6 Medications

4.6.1 MedicinesIf BGL does not normalise after oral glucose gel 40% or IV glucose consider other medication to manage hypoglycaemia. Take blood samples immediately before commencing medications while the baby is hypoglycaemic. Consider discussion with a neonatologist.

Table 11. Short term medicines


Glucagon*15,39,40

Dose and route:

o Bolus: 200 microgram/kg IV, IM injection or subcutaneous injection during hypoglycaemic episode,

Administer IM or subcutaneously if IV access not immediately available (within 10 minutes) then,

o Infusion: 10–20 microgram/kg/hour IV infusion preferably via UVC or PICC–can be given short-term through a peripheral IV line

Compatibility:

o Glucose 5%, sodium chloride 0.9%

Incompatibilities:

o Calcium containing solutions

Mode of action:

o Increases gluconeogenesis and glycogenolysis15–only of benefit when liver glycogen is present

o Effective for babies of diabetic mothers or other hyperinsulinaemic conditions

o Blood glucose level should rise within one hour of commencing infusion

Precautions:

o Less likely to be effective in SGA or FGR babies (due to lower glycogen stores)

Side effects include:

o Paradoxical insulin secretion at high dose

o Nausea and vomiting15

Hydro-cortisone*41-44

Dose and route:

o 1–2 mg/kg IV 6 hourly then change to oral once BGL is stabilised

o Taper dose when BGL stabilises

Compatibility:



o Glucose 5%, glucose 10%, sodium chloride 0.9%

Incompatibilities:

o Midazolam, phenobarbital, phenytoin

Mode of action:

o Reduces peripheral glucose utilisation

o Increases gluconeogenesis

o Has a slow response than glucagon

Precautions:

o May mask signs of infection

o Can cause hypertension

o Avoid concurrent use of indomethacin (risk of gastrointestinal perforation)

Side effects:

o Related to dose and duration of treatment

*Refer to an Australian pharmacopoeia for complete drug information



Table 12. Medicines long-term


Diazoxide15,45-48*

Dose and route:

o 5 mg/kg/day orally in 2–3 doses

Indication:

o Persistent hypoglycaemia–

Use to facilitate weaning from glucose infusion

Long-term management

Compatibility:

o Do not dilute or mix with other drugs

o Incompatibilities:

o Hartmann’s or Ringer’s solutions

Mode of action:

o Glycogenolytic hormone that inhibits insulin release from the pancreas

Precautions:

o Concurrent hydrochlorothiazide usually given for fluid retention

o Usually administered orally

o Commence in consultation with paediatric endocrinologist

o Administer hydrochlorothiazide (see below)

o Do not administer by intramuscular or subcutaneous injection

o May cause pain along the injected vein when given IV

o Avoid extravasation

o Monitor blood pressure

o Weigh daily

Side effects:

o Fluid retention, abdominal discomfort, hypotension, hypertrichosis; less commonly–fever, eosinophilia, leukopenia

o Persistent pulmonary hypertension

Hydro-chlorothiazide*

49,50

Dose and route:

o 1–2 mg/kg/day in 2 divided doses



Mode of action:

o Diuretic–use in conjunction with diazoxide

o Inhibits pancreatic release of insulin from the pancreas

Side effects:

o Hypokalaemia, hypochloraemia and other electrolyte abnormalities

o Displaces bilirubin from albumin (caution in significantly jaundiced babies)

Octreotide*15,51-55

Dose and route:

o Initially administer 2–5 microg/kg/dose subcutaneously 6–8 hourly

Compatibility:

o Glucose 5%, sodium chloride 0.9%

Incompatibility:

o No information

Mode of action:

o Binds to somatostatin receptors leading to inhibition of insulin

Precaution:

o Consult with paediatric endocrinologist

o Has been associated with necrotising enterocolitis in babies with or without co-morbidities

Side effects:

o Bradycardia, nausea, abdominal pain, vomiting, diarrhoea, tachyphylaxis15

*Refer to an Australian pharmacopoeia for complete drug information



5 Persistent hypoglycaemia 5.1 Indications for further investigation and managementFurther investigations and management are required for severe, persistent, recurrent or atypical hypoglycaemia2,14,27. It is recommended to investigate the underlying mechanism for the hypoglycaemia to identify the specific treatment.3 If further investigations are required early discussion with a neonatologist is indicated to advise regarding paediatric endocrinology consultation and need for retrieval to a tertiary neonatal unit.

Table 13. Pathological hypoglycaemia


Indications for further investigation

Symptomatic hypoglycaemia14,26 or need for glucose IV to treat after 48 hours of age5,14

Seizures or altered level of consciousness

Inability to consistently maintain pre-prandial BGL greater than 2.6 mmol/L up to 48 hours of age and 4 mmol/L after 48 hours56

Severe hypoglycaemia

o Low BGL (less than 1.5 mmol/L in first 6 hours of life) if not baby of diabetic mother

o Persistent or recurrent hypoglycaemia despite glucose IV greater than or equal to 8 mg/kg/minute57

o Required treatment with medication

Late hypoglycaemia

o BGL less than 2.6mmol/L onset after 24 hours of life

o Early onset persistent or any hypoglycaemia recurrent after 72 hours

Presence of associated abnormalities (e.g. midline facial malformations, microcephalus; exomphalos)26

Unusual presentation or with no known risk factors

Family history of:

o Genetic hypoglycaemia

o Inborn errors of metabolism (parent or sibling) e.g. MCADD17 or other fatty acid oxidation defect (e.g. LCHAD)

o Sudden infant death syndrome26

o Reye’s syndrome26

o Developmental delay26

Investigations2,3,57 Refer to



Appendix D Investigations for neonatal hypoglycaemia Blood

o Take pathology specimens immediately before treatment while baby is hypoglycaemia

o Insulin, cortisol, growth hormone, adrenocorticotrophic hormone

o Ketones–beta hydroxybutyric acid

o Free fatty acids

o Acyl-carnitine profile

o Blood gas (including electrolytes, glucose, haemoglobin, haematocrit and lactate)

Urine–metabolic screen

o First sample after hypoglycaemic episode

o Do not wait to start treatment while collecting sample

5.2



5.3 Interpretation of investigations

Table 14. Investigations interpretation


Hyper-insulinaemic state3

If any detectable insulin when hypoglycaemic

Confirmed by absence of free fatty acids and beta hydroxy-butyrate

Usually transient but may be persistent and require long-term treatment

In absence of maternal diabetes, consult with neonatologist or paediatric endocrinologist

Cortisol3,26,58

If more than 200 nmol/L–likely to be a normal response

o May be blunted in preterm baby

If lesser response–suggestive of hypothalamic, pituitary or adrenal dysfunction

o Seek neonatologist or paediatric endocrine consultation urgently

Growth hormone26

If more than 20 milliunits per mL–normal response

o May be blunted in preterm baby

If lesser response–suggestive of hypothalamic, pituitary or adrenal dysfunction

o Seek neonatologist or paediatric endocrine consultation urgently

Ammonia

If greater than 50 micromol/L consider metabolic disorder (e.g. urea cycle defect)59

o Consult with neonatologist or paediatric metabolic physician

Severe, persistent or recurrent hypoglycaemia

If endocrine disorder not identified

o Consult with neonatologist or paediatric metabolic specialist

5.4 Ongoing managementTable 15. Ongoing management


Consultation

Endocrinologist, metabolic specialist or both

If hypoglycaemia:

o Severe, recurrent or prolonged or lasts longer than 48 hours refer to endocrinologist17

o Persists despite standard treatment refer to metabolic specialist17

Severe or Persistent hypoglycaemic conditions may result in neurological damage if:



persistent hypoglycaemia

o Mild but recurrent hypoglycaemia or

o Feeds are delayed or interrupted (e.g. due to recurrent illness)

Exclude persistent hypoglycaemic conditions

o Persistent hyperinsulinaemic conditions31

o Endocrine deficiencies (e.g. hypopituitarism, hypoadrenalism

o Inborn errors of metabolism

Fasting test

Prior to discharge

Six hours duration unless otherwise recommended by endocrinologist or metabolic specialist

Refer to Table 16. Six hour fast test

5.5



5.6 Six hour fast test

Table 16. Six hour fast test

Aspect ConsiderationContext Identifies baby requiring additional investigation or management3

Indications

Family history of hypoglycaemia or congenital anomalies suggestive of pituitary or adrenal disorder to:

o Screen for persistent hypoglycaemic disorder despite normal previous BGLs

o Ensure baby can maintain BGL greater than or equal to 4 mmol/L after discharge3

History of clinically significant hypoglycaemia (requiring IV glucose or medication) to:_ENREF_3

o Ensure baby can maintain BGL above 3.3. mmol/L6 after discharge

o Screen for persistent disorder

BGL

Check at 4, 5 and 6 hours post feed (omit further feeds during test)

If BGL less than 3 mmol/L at any time

o Perform investigations as to the cause and then feed baby

If baby symptomatic between scheduled BGL measures

o Check BGL early

If low–perform investigations and feed baby

If baby asymptomatic and BGL greater than or equal to 3 mmol/L throughout–finish test and feed baby



6 Sequelae of hypoglycaemiaTable 17. Sequelae


Context

Both symptomatic and asymptomatic hypoglycaemia may lead to adverse neurodevelopment outcome when compared with euglycaemic babies60

MRI:

o More instructive than the severity or duration of hypoglycaemia as prognostic indicators of later outcomes61

o Features similar for transient versus recurrent or prolonged hypoglycaemia61

Neuro-developmental outcome

Cognitive impairment more likely than motor impairment61

May present in neonatal period as encephalopathy with62:

o Poor feeding

o Lethargy

o Seizures

o Hypothermia

o Respiratory distress

Hypoglycaemic encephalopathy:

o Usually injury to posterior region of brain typically the occipital cortex62 or parietal lobes61

o Develops in white matter61

o May follow neonatal focal or generalised seizures resulting from symptomatic hypoglycaemia29

Potential short and long-term sequelae include:

o Head growth suboptimal consistent with white matter injury61 intellectual disability, learning difficulties, behavioural difficulties29, visual co-ordination

o Hemiplegic cerebral palsy or spastic quadriplegia; milder motor problems29

o Visual impairment29



7 Discharge planningTable 18. Discharge planning


Discharge planning

Consider six hour fast with BGL monitoring to exclude:

o Persistent hyperinsulinaemic conditions

o Endocrine deficiencies

o Inborn errors of metabolism3,5

o Refer to Table 16. Six hour fast test

If in doubt, discuss with neonatologist, paediatric endocrinologist or metabolic specialist

Discharge criteria

Baby less than 48 hours of age and pre-prandial BGL is greater than 2.6 mmol/L for three feed-fast cycles

Baby more than or equal to 48 hours of age and pre-prandial BGL is greater than 4 mmol/L for three feed-fast cycles6

Six hour fast test performed (if indicated) and baby able to maintain BGL

Parent education

Discuss causes, risks, potential sequelae and management

Include signs that require escalation and the escalation plan

Provide parent information brochure

Follow-up

Usual follow-up with general practitioner and child health nurse

If symptomatic, severe, recurrent or atypical hypoglycaemia:

o Follow up by paediatrician or neonatologist

o Endocrinologist or metabolic specialist follow-up as indicated

Reducing risk in subsequent pregnancies

Maternal lifestyle–healthy weight and diet management

Genetic counselling/family history

Glycaemic/diabetes management

Refer to Queensland Clinical Guideline Gestational diabetes63



ReferencesSources cited within this reference list may be available to working party members upon request (subject to copyright and licencing restrictions). Contact QCG for further information.

1. McClure RJ. Trophic feeding of the preterm infant. Acta Paediatrica (Oslo, Norway: 1992). Supplement 2001;90(436):19-21.

2. Hawdon JM. Postnatal metabolic adaptation and neonatal hypoglycaemia. Paediatrics & Child Health. 2016;26(4):135-9.

3. Thorton P, Stanley C, De Leon D, Harris D, Haymond MW, Hussain K, et al. Recommendations from the Pediatric Endocrine Society for evaluation and management of persistent hypoglycemia in neonates, infants and children. The Journal of Pediatrics 2015;167(2):238-45.

4. Güemes M, Rahman SA, Hussain K. What is a normal blood glucose? Archives of Disease in Childhood. 2016;101(6):569.

5. Rosance P, Garcia-Prats J, Wolfsdorf JI, Kim M. Pathogenesis, screening, and diagnosis of neonatal hypoglycemia. [Internet]. Watham MA: UpToDate Inc; 2017 [cited 2018 July 20]. Available from: https://www.uptodate.com/.

6. Rosance P, Garcia-Prats J, Wolfsdorf JI, Kim M. Management and outcome of neonatal hypoglycemia. [Internet]. Watham MA: UpToDate Inc; 2017 [cited 2018 July 20]. Available from: https://www.uptodate.com/.

7. Dixon K. Definition and monitoring of neonatal hypoglycaemia: a nationwide survey of NHS England Neonatal Units. Arch Dis Child Fetal Neonatal E 2017;102(1):F92-3.

8. Harding JE, Harris DL, Hegarty JE, Alsweiler JM, McKinlay CJD. An emerging evidence base for the management of neonatal hypoglycaemia. Early Human Development 2017;104:51-6.

9. Harris D. What happens to blood glucose concentrations after oral treatment for neonatal hypoglycemia? Journal of Pediatrics 2017;190(November):136-41.

10. Puchalski M, Russell T, Karlsen A. Neonatal hypoglycaemia. Is there a sweet spot? Crit Care Nurs Clin N Am 2018;30:467-80.

11. Cowett R, Loughead J. Neonatal glucose metabolism: differential diagnoses, evaluation and treatment of hypoglycemia. Neonatal Network. 2002;21(4):9-19.

12. Screenivasa B, Kumar G, Screenivasa B. Comparative study of blood glucose levels in neonates using glucometer and laboratory glucose oxidase method. Curr Pediatr Res 2015;19:29-32.

13. Queensland Clinical Guidelines. Standard care. Guideline No. MN18.50-V1-R23. [Internet]. Queensland Health. 2018. [cited 2018 September 12]. Available from: http://www.health.qld.gov.au

14. Adamkin DH. Neonatal hypoglycemia. Seminars in Fetal and Neonatal Medicine 2017;22(1):36-41.

15. Kallem VR, Pandita A, Gupta G. Hypoglycemia: when to treat? Clinical Medicine Insights. Pediatrics 2017;11:1-9.

16. Li T, Stuart A, Beardsall K. Glucose monitoring and management in the NICU–how are we doing? Infant 2017;13(5):182-6.

17. Thompson-Branch A, Havranek T. Neonatal hypoglycemia. Pediatrics in Review 2017;38(4):147-57.

18. Adamkin D, American Academy of Pediatrics Committee on Fetus and Newborn. Postnatal glucose homeostasis in late-preterm and term infants. Pediatrics. 2011;127(3):575-9.

19. Stomnaroska-Damcevski O, Petkovska E, Jancevska S, Danilovski D. Neonatal hypoglycemia: a continuing debate in definition and management. Prilozi Section of Medical Sciences. 2015;36(3):91.


http://www.health.qld.gov.au/

https://www.uptodate.com/



20. Bateman BT, Patorno E, Desai RJ, Seely EW, Mogun H, Maeda A, et al. Late pregnancy beta-blocker exposure and risks of neonatal hypoglycemia and bradycardia. Pediatrics. 2016 [cited 2018 April 16]; 138(3):e20160731. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5005024/ DOI:10.1542/peds.2016-0731.

21. Oden J, Bourgeois M. Neonatal endocrinology. Indian Journal Of Pediatrics 2000;67(3):217-23.

22. Aydin M, Deveci U, Hakan N. Neonatal hypoglycemia associated with the antenatal corticosteroids may be secondary to fetal adrenal suppression. The Journal of Maternal-Fetal & Neonatal Medicine 2015;28(8):892.

23. Pettit KE, Tran SH, Lee E, Caughey AB. The association of antenatal corticosteroids with neonatal hypoglycemia and hyperbilirubinemia. The Journal of Maternal-Fetal & Neonatal Medicine 2014;27(7):683-6.

24. Rosenbloom JI, Lewkowitz AK, Tuuli MG. Risks and benefits of antenatal late-preterm corticosteroids. JAMA Pediatrics 2018;172(7):615-6.

25. Sifianou P, Thanou V, Karga H. Metabolic and hormonal effects of antenatal betamethasone after 35 weeks of gestation. The Journal of Pediatric Pharmacology and Therapeutics 2015;20(2):138-43.

26. Despande S, Platt M. The investigation and management of neonatal hypoglycaemia. Seminars in Fetal & Neonatal Medicine 2005;10:351-61.

27. Williams A. Neonatal hypoglycaemia: clinical and legal aspects. Seminars in Fetal & Neonatal Medicine 2005;10:363-8.

28. Rozance PJ, Hay WW. Hypoglycemia in newborn infants: features associated with adverse outcomes. Neonatology 2006;90(2):74-86.

29. Arhan E, Öztürk Z, Serdaroğlu A, Aydın K, Hirfanoğlu T, Akbaş Y. Neonatal hypoglycemia: a wide range of electroclinical manifestations and seizure outcomes. European Journal of Paediatric Neurology. 2017;21(5):738-44.

30. Merritt J, Vockley J. Overview of fatty acid oxidation disorders. [Internet]. Waltham MA: Uptodate Inc; August 2018 [cited 2018 September 12]. Available from: https://www.uptodate.com/.

31. Goel P, Choudray S. Persistent hyperinsulinemic hypoglycemia of infancy: an overview of current concepts. Journal of Indian Association of Pediatric Surgeons 2012;17(3):99-103.

32. Queensland Clinical Guidelines. Routine newborn assessment Guideline No. MN14.4.V4.R19. [Internet]. Queensland Health. 2015. [cited 2016 February 26]. Available from: http://www.health.qld.gov.au

33. Harris DL, Weston PJ, Signal M, Chase JG, Harding JE. Dextrose gel for neonatal hypoglycaemia (the Sugar Babies Study): a randomised, double-blind, placebo-controlled trial. Lancet 2013;382(9910):2077-83.

34. Hegarty JE, Harding JE, Crowther CA, Brown J, Alsweiler J. Oral dextrose gel to prevent hypoglycaemia in at-risk neonates. Cochrane Database of Systematic Reviews. 2017 [cited 2018 March 16]; Issue 7. Art. No.: CD012152(7). Available from: http://dx.doi.org/10.1002/14651858.CD012152.pub2 DOI:10.1002/14651858.CD012152.pub2.

35. Hegarty JE, Harding JE, Crowther CA, Brown J, Alsweiler J. Oral dextrose gel for the prevention of hypoglycaemia in newborn infants. Cochrane Database of Systematic Reviews. 2016 [cited 2018 March 16]; Issue 7. Art. No.: CD012152(4). Available from: http://dx.doi.org/10.1002/14651858.CD012152 DOI:10.1002/14651858.CD012152.pub2.

36. Mater Health Services. Procedure-Hypoglycaemia in newborn babies. 2018.

37. Harris DLM, Battin MRM, Weston PJM, Harding JEM. Continuous glucose monitoring in newborn babies at risk of hypoglycemia. Journal of Pediatrics, 2010;157(2):198-202.

38. Auckland District Hospital Board. Fluids and electrolytes. Newborn Services Clinical Guideline. [Internet]. 2007 [cited 2018 April 11]. Available from: http://www.adhb.govt.nz/newborn/guidelines/nutrition/fluidsandglucose.htm.


http://www.adhb.govt.nz/newborn/guidelines/nutrition/fluidsandglucose.htm

http://dx.doi.org/10.1002/14651858.CD012152

http://dx.doi.org/10.1002/14651858.CD012152.pub2

http://www.health.qld.gov.au/


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5005024/


39. Australian Injectable Drugs Handbook. Nicolette Burridge, Keli Symons, editors. Glucagon. 7th ed. [Internet]. New South Wales: Society of Hospital Pharmacists of Australia (SHPA); 2018 [cited 2018 May 3]. Available from: https://aidh.hcn.com.au.

40. Therapeutic Goods Australia (TGA). Glucagon. [Internet]. Canberra: Australian Government; 2015. Available from: https://www.tga.gov.au/.

41. Australian Medicines Handbook. Hydrocortisone. [Internet]. Adelaide: Australian Medicines Handbook Pty Ltd; 2018 [cited 2018 May 3]. Available from: http://amhonline.amh.net.au/

42. Wilker R. Hypoglycemia and hyperglycemia. In: Cloherty J, Eichenwald E, Hansen A, Stark A, editors. Manual of Neonatal Care. 7th ed. Philadelphia PA: Lippincott Williams & Wilkins; 2012. p. 292-3.

43. Davies M. Hypoglycaemia. In: Davies M, Cartwright D, Inglis G, editors. Pocket Notes on Neonataology. 2nd ed. Sydney: Churchill Livingstone Elsevier; 2008. p. 79.

44. NeoFax/Pediatrics. Hydrocortisone. [Internet]. Greenwood Village, Colorado, USA 2017 [cited 2018 May 3]. Available from: http://www.micromedexsolutions.com/.

45. Australian Injectable Drugs Handbook. Nicolette Burridge, Keli Symons, editors. Diazoxide. 7th ed. [Internet]. New South Wales: Society of Hospital Pharmacists of Australia (SHPA); 2018 [cited 2018 May 3]. Available from: https://aidh.hcn.com.au.

46. British National Formulary for Children (BNFC) online. Diazoxide. [Internet]: Royal Pharmaceutical Society; 2018 [cited 2018 May 3]. Available from: https://www.medicinescomplete.com/.

47. DrugBank. Diazoxide. [Internet]. Canada: DrugBank; 2018 [cited 2018 May 3]. Available from: https://www.drugbank.ca/drugs/DB01119.

48. Therapeutic Goods Australia (TGA). Diazoxide. [Internet]. Canberra: Australian Government; 2012 [cited 2018 May 3]. Available from: https://www.tga.gov.au/.

49. Australian Medicines Handbook Children's Dosing Companion. Hydrochlorothiazide. [Internet]. Adelaide: Australian Medicines Hanbook Pty Ltd; 2018 [cited 2018 May 3]. Available from: http://amhonline.amh.net.au/

50. NeoFax/Pediatrics. Hydrochlorothiazide. [Internet]. Greenwood Village, Colorado, USA 2018 [cited 2018 May 3]. Available from: http://www.micromedexsolutions.com/.

51. Australian Injectable Drugs Handbook. Nicolette Burridge, Keli Symons, editors. Octreotide. 7th ed. [Internet]. New South Wales: Society of Hospital Pharmacists of Australia (SHPA); 2018 [cited 2018 August 9]. Available from: https://aidh.hcn.com.au.

52. Laje P, Halaby L, Adzick N, Stanley C. Necrotizing enterocolitis in neonates receiving octreotide for the management of congenital hyperinsulinism. Pediatric Diabetes 2010;11:142-7.

53. McMahon A, Wharton G, Thorton P, De Leon D. Octreotide use and safety in infants with hyperinsulinism. Pharmacoepidemiology and Drug Safety 2017;26:26-31.

54. Reck-Burneo CA, Parekh A, Velcek FT. Is octreotide a risk factor in necrotizing enterocolitis? Journal of Pediatric Surgery 2008;43(6):1209-10.

55. Therapeutic Goods Australia (TGA). Octreotide. [Internet]. Canberra: Australian Government; 2018 [cited 2018 May 3]. Available from: https://www.tga.gov.au/.

56. Lord K, De León D. Hyperinsulinism in the neonate. Clinics in Perinatology 2018;45(1):61-74.

57. Gilbert C. Investigation and management of congenital hyperinsulinism. British Journal of Nursing 2009;18(21):1306-10.

58. Hussain K, Hindmarsh P, Aynsley-Green A. Neonates with symptomatic hyperinsulinemic hypoglycemia generate inappropriately low serum cortisol counterregulatory hormonal responses. The Journal of Clinical Endocrinology & Metabolism 2003;888(9):4342-7.


https://www.tga.gov.au/

https://aidh.hcn.com.au/

http://www.micromedexsolutions.com/

http://amhonline.amh.net.au/


https://www.drugbank.ca/drugs/DB01119

https://www.medicinescomplete.com/


http://www.micromedexsolutions.com/

http://amhonline.amh.net.au/




59. Sunehag A, Wolfsdorf JI, Hoppin A. Treatment and complications of persistent hyperinsulinemic hypoglycemia of infancy. [Internet]. Waltham MA: UpToDate Inc; March 2018 [cited 2018 April 13]. Available from: https://www.uptodate.com/.

60. Mahajan G, Mukhopdhyay K, Attri S, Kumar P. Neurodevelopmentatl outcome of asymptomatic hypoglycemia compared with symptomatic hypoglycemia and euglycemia in high-risk neonates. Pediatric Neurology 2017;74:74-9.

61. Burns CM, Rutherford MA, Boardman JP, Cowan FM. Patterns of cerebral injury and neurodevelopmental outcomes after symptomatic neonatal hypoglycemia. Pediatrics. 2008;122(1):65.

62. Likeman M. MRI brain imaging in neonates. Paediatrics and Child Health. 2014;24(9):407-12.

63. Stanley CA, Rozance PJ, Thornton PS, De Leon DD, Harris D, Haymond MW, et al. Re-evaluating transitional neonatal hypoglycemia: mechanism and implications for management. The Journal of Pediatrics 2015;166(6):1520-5.




Appendix A Growth charts Growth chart for girls



Growth chart for boys



Appendix B Glucose 40% gel doses

Baby’s weight Dose of glucose 40% gel 0.5mL/kg (200mg/kg) for buccal administration

2000–2080 g 1 mL

2081–2280 g 1.1 mL

2281–2480 g 1.2 mL

2481–2680 g 1.3 mL

2681–2880 g 1.4 mL

2881–3080 g 1.5 mL

3081–3280 g 1.6 mL

3281–3480 g 1.7 mL

3481–3680 g 1.8 mL

3681–3880 g 1.9 mL

3881–4080 g 2.0 mL

4081–4280 g 2.1 mL

4281–4480 g 2.2 mL

4481–4680 g 2.3 mL

4681–4880 g 2.4 mL

4881–5080 g 2.5 mL



Appendix C Glucose infusion rates (GIR) and concentrationsHow to calculate GIR (mg/kg/minute)

GIR(mg /kg/minute)=% glucose beinginfused × rate of infusion (mL /hour)Weight×6

Example–GIR for 4.5 kg baby having 100mL/kg of 12 % glucose (18.75 mL/hour)

GIR(mg /kg/minute)=% glucose beinginfused × rate of infusion (mL /hour)Weight×6

¿12%×18.75mL /hour¿ ¿4.5kg×6

¿8.34mg /kg/minute

How to calculate increased concentrations of glucose

Glucose concentration required

Glucose 10% volume(100 mg/mL)

Glucose 50% volume(500mg/mL)

12% 95 mL 5 mL

14% 90 mL 10 mL

16% 85 mL 15 mL

18% 80 mL 20 mL

20% 75 mL 25 mL

Formula to increase concentration of 10% glucose and make a 100 mL solution

Step1.Volumeof highconcentrationmL= total volume mL×(desired concentration%− lower concentration%)(highconcentration%−lower concentration% )

Step2.Volumeof lowconcentrationmL=desired volumemL−highconcentration volumemL

Step3.Volumeof desired concentrationmL=highconcentrationmL+lowconcentrationmL

Example–to prepare 100 mL of 12% glucose for infusion

Step1.Volumeof highconcentrationmL=100mL×(12%−10%)(50%−10%)

=20040

=5mL

Step2.Volumeof lowconcentrationmL=100mL−5mL=95mL



Step3.100mL=5mL (50% )+95mL(10% )

For comparison of mg/kg/minute by concentration of glucose and volume of fluid being infused refer to

Flow Chart: Management of neonatal hypoglycaemia (baby symptomatic or BGL < 1.5 mmol/L)

Notes:

Glucose 50% contains 50 grams per 100 mL or 0.5 grams per 1 mL Glucose 10 % contains 10 grams per 100 mL or 0.1 grams per 1 mL Rounding final volumes of each concentration of glucose up and down may be required

for practical purposes Remove the volume of 50% glucose from the bag of 10% glucose before adding the 50%

glucose solution



Appendix D Investigations for neonatal hypoglycaemia Test/sample type Volume Container guide Specimen collection Insulin

Cortisol

Growth hormone

900 μL

Red cap (serum no gel) X 2

OR

Green cap (lithium heparin) X 2

If high haematocrit (> 0.55 %)–collect third tube

Ketones 200 μL Red cap (serum no gel)

Adrenocorticotrophic hormone

400 μLPink cap (EDTA)

Free fatty acids 100 μL Red cap (serum no gel)

Acyl-carnitine profile1–2 filled spots OR Newborn screening card

Label Acyl-carnitane profile

In addition to newborn screening test (NST)

o Send routine NST as usual

150 μL Green cap (lithium heparin)

Lactate

Glucose1 mL

Grey cap (fluoro-oxalate) Can be combined with blood gas

Blood gas including:

o Electrolytes

o Haemoglobin

0.5 mL Blood gas syringe or capillary tube Send specimen on ice to laboratory



o Haematocrit

o

Plasma amino acid profile

100 μLGreen cap (lithium heparin)

Ammonia 500 μL Pink cap (EDTA)

Pyruvate Contact pathology service prior to collection

Urine 10 mLYellow lid specimen container Treatment can start while collecting specimen

Store and transport at 4 ºC

For complete blood profile collect:

1400 μL in red cap microcontainers

900 μL in pink cap microcontainers

150 μL in green cap microcontainer

0.5 mL in capillary tube or blood gas syringe

Abbreviation: μL–microlitre



AcknowledgementsQueensland Clinical Guidelines gratefully acknowledge the contribution of Queensland clinicians and other stakeholders who participated throughout the guideline development process particularly:

Working Party Clinical Leads

Ms Karen Hose Nurse Practitioner, Royal Brisbane and Women’s Hospital

Professor Helen Liley, Neonatologist, Mater Mother’s Hospital, Brisbane

QCG Program Officer

Ms Stephanie Sutherns

Working Party Members

Dr Gary Alcock, Neonatologist, The Townsville Hospital

Mrs Seija Argyros, Neonatal Nurse Practitioner, Royal Brisbane and Women's Hospital

Mrs Maxine Ballinger, Clinical Nurse Consultant, Rockhampton Hospital

Miss Chase Becker, Clinical Nurse and Registered Midwife, Amana Hospital

Ms Jan Becker, Registered Midwife, Amana Hospital and Sunshine Coast Private Hospital

Mrs Judith Benton, Clinical Nurse Consultant, The Townsville Hospital

Mrs Bebra Byrt, Clinical Nurse Midwife, Buderim Private Hospital

Mrs Katie Cameron, Consumer Representative, Maternity Consumer Network

Dr David Cartwright, Neonatologist, Royal Brisbane and Women's Hospital

Ms Nicole Chappell, Registered Midwife/Registered Nurse, Logan Hospital

Dr Manbir Chauhan, Neonatologist, Gold Coast University Hospital

Ms Li-an Collie, Nurse Educator, Royal Brisbane and Women's Hospital

Associate Professor Louise Conwell, Paediatric Endocrinologist, Queensland Children's Hospital

Dr Jan Cullen, Director of Paediatrics, Logan Hospital

Dr Mark Davies, Neonatologist, Royal Brisbane and Women's Hospital

Mrs Allison Davis, Midwife, Mackay Base Hospital

Mrs Carla Dillon, Caseload Midwife, Goondiwindi Hospital

Mrs Carole Dodd, Registered Midwife/Clinical Nurse, Caboolture Hospital

Doctor Joy Domingo-Bates, Neonatal Fellow, Mater Mother's Hospital and Royal Brisbane and Women's HospitalRefer to online version, destroy printed copies after use of 61


Mr Raymond Doro, Clinical Nurse, Redland Hospital

Mrs Julie Dunsmuir, Clinical Nurse Consultant, Gold Coast University Hospital

Dr Christopher Edwards, General Paediatrician, Bundaberg Base Hospital

Miss Isabelle Fassbind, Pharmacist, Royal Brisbane and Women's Hospital

Mrs Anndrea Flint, Neonatal Nurse Practitioner, Redcliffe Hospital

Mrs Nicol Franz, Registered Nurse, Caboolture Hospital

Dr Jessica Gaughan, Senior Medical Officer and Rural Generalist, Emerald Hospital

Dr Leigh Grant, Obstetrician and Gynaecologist, Rockhampton Hospital

Mrs Danielle Groves, Registered Nurse/Registered Midwife, Hervey Bay Hospital

Mrs Linda Hackett, Clinical Nurse, Bundaberg Hospital

Mrs Marnina Hales, Registered Nurse/Registered Midwife, Logan Hospital

Ms Julia Hannan, Registered Nurse/Registered Midwife, Sunshine Coast University Hospital

Ms Leah Hardiman, Consumer Representative, Maternity Choices

Dr Shivanand Hebbandi, Paediatrician, Redland Hospital

Mrs Julianne Hite, Clinical Nurse/Neonatal Nurse Educator, Rockhampton Hospital

Mrs Donna Hovey, Neonatal Clinical Facilitator, Central West Hospital and Health Service

Mrs Anne Illingsworth, Clinical Nurse Consultant, The Townsville Hospital

Mrs Danika Imhoff, Registered Nurse, Royal Brisbane and Women's Hospital

Prof Guan Koh, Clinical Director, The Townsville Hospital

Mrs Helen Kross, Clinical Nurse/Midwife, Ayr Health Service

Dr Prasanna Kumar, Neonatologist, The Townsville Hospital

Mrs Karen Langford, Clinical Nurse Consultant, Royal Brisbane and Women's Hospital

Miss Christine Latimer, Clinical Nurse Consultants, The Townsville Hospital

Mrs Katharine Lawlor, Nurse Unit Manager, Logan Hospital

Mrs Joanne Lawrence, Registered Midwife, Cairns Hospital

Miss Donna Martin, Nurse Unit Manager, Mount Isa Hospital

Mrs Colette Mcintyre, Clinical Nurse Consultant, Royal Brisbane and Women's Hospital

Ms Sandra Mcmahon, Practice Development Midwife, Gold Coast University Hospital

Ms Melissa Melville, Nurse Unit Manager, Royal Brisbane and Women's Hospital

Ms Amanda Merchant, Clinical Nurse Consultant, Mater Mothers' Hospital

Ms Debbie Mitchell, Midwifery Educator/Baby Friendly Health Initiative Co-ordinator, Emerald HospitalRefer to online version, destroy printed copies after use of 61


Miss Janene Moore, Neonatal Nurse Practitioner Candidate, Mackay Base Hospital

Mrs Sumant Naidu, Sonographer/Team Leader, Logan Hospital

Dr Parvin Niknafs, Registered Midwife, Gold Coast University Hospital

Dr Kristin O'Connor, Neonatal Fellow, Royal Brisbane and Women's Hospital

Ms Jacqueline O'Neill, Midwife, Toowoomba Base Hospital

Ms Marian Rigney, Associate Nurse Unit Manager, Redland Hospital

Ms Teresa Sander, Registered Midwife, Rockhampton Hospital

Miss Brittany Schoenmaker, Registered Nurse, Royal Brisbane and Women's Hospital

Dr Sonia Shah, Paediatrician, Buderim Private Hospital

Mrs Chris Sheppard, Registered Midwife/Registered Nurse, Caboolture Hospital

Dr Prasanna Shirkhedkar, Paediatrician, Caboolture Hospital

Ms Elise Stanton, Registered Nurse, Royal Brisbane and Women’s Hospital

Miss Ashleigh Sullivan, Registered Midwife/Registered Nurse, Toowoomba Base Hospital

Ms Linda Thomasson, Clinical Midwife/Lactation Consultant, Bundaberg Hospital

Ms Natasha Torrielli, Perioperative Midwife, Royal Brisbane and Women's Hospital

Dr Jean Pascal Tshamala, Principal House Officer, Gladstone Hospital

Ms Nicole Utley, Registered Midwife, Royal Brisbane and Women's Hospital

Dr Lizelle Weber, Director of Neonatology, Sunshine Coast University Hospital

Ms Louise Wilkins, Lactation Consultant, Logan Hospital

Ms Amanda Wolski, Registered Midwife, Logan Hospital

Queensland Clinical Guidelines Team

Associate Professor Rebecca Kimble, Director

Ms Jacinta Lee, Manager

Ms Stephanie Sutherns, Clinical Nurse Consultant

Ms Cara Cox, Clinical Nurse Consultant

Ms Emily Holmes, Clinical Nurse Consultant

Dr Brent Knack, Program Officer

Steering Committee



Funding

This clinical guideline was funded by Healthcare Improvement Unit, Queensland Health


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