Hypoxic-ischaemic encephalopathy

Transcription

Queensland Maternity and Neonatal Clinical Guideline: Hypoxic-ischaemic encephalopathy
Document title:
Publication date:
May 2010
Document number:
MN10.11-V4-R15
Replaces document:
MN10.11-V3-R15
Author:
Queensland Maternity and Neonatal Clinical Guidelines Program
Audience:
Health professionals in Queensland public and private maternity services
Exclusions:
All subsets of neonatal encephalopathy except hypoxic-ischaemic
encephalopathy
Review date:
May 2015
Endorsed by:
Statewide Maternity and Neonatal Clinical Network
QH Patient Safety and Quality Executive Committee
Contact:
Queensland Maternity and Neonatal Clinical Guidelines Program
Email: MN-Guidelines@health.qld.gov.au
URL: www.health.qld.gov.au/qcg
Disclaimer
These guidelines have been prepared to promote and facilitate standardisation and consistency of
practice, using a multidisciplinary approach.
Information in this guideline is current at time of publication.
Queensland Health does not accept liability to any person for loss or damage incurred as a result of
reliance upon the material contained in this guideline.
Clinical material offered in this guideline does not replace or remove clinical judgement or the
professional care and duty necessary for each specific patient case.
Clinical care carried out in accordance with this guideline should be provided within the context of
locally available resources and expertise.
This Guideline does not address all elements of standard practice and assumes that individual
clinicians are responsible to:
• Discuss care with consumers in an environment that is culturally appropriate and which
enables respectful confidential discussion. This includes the use of interpreter services
where necessary
• Advise consumers of their choice and ensure informed consent is obtained
• Provide care within scope of practice, meet all legislative requirements and maintain
standards of professional conduct
• Apply standard precautions and additional precautions as necessary, when delivering care
• Document all care in accordance with mandatory and local requirements
This work is licensed under a Creative Commons Attribution Non-Commercial No Derivatives 2.5 Australia licence. To view a copy of this
licence, visit http://creativecommons.org/licenses/by-nc-nd/2.5/au/
© State of Queensland (Queensland Health) 2010
In essence you are free to copy and communicate the work in its current form for non-commercial purposes, as long as you attribute the authors
and abide by the licence terms. You may not alter or adapt the work in any way.
For permissions beyond the scope of this licence contact: Intellectual Property Officer, Queensland Health, GPO Box 48, Brisbane Qld 4001,
email ip_officer@health.qld.gov.au , phone (07) 3234 1479. For further information contact Queensland Maternity and Neonatal Clinical
Guidelines Program, RBWH Post Office, Herston Qld 4029, email MN-Guidelines@health.qld.gov.au phone (07) 3131 6777.
Refer to online version, destroy printed copies after use
Page 2 of 25
Abbreviations
ABG
Arterial blood gas
aEEG
Amplitude integrated electroencephalogram
ACA
Anterior cerebral artery
ADH
Antidiuretic hormone
BGL
Blood glucose level
CNS
Central nervous system
DIC
Disseminated intravascular coagulopathy
ECG
Electrocardiogram
ECHO
Echocardiography
EEG
Electroencephalogram
FBC
Full blood count
FFP
Fresh frozen plasma
HIE
HMD
Hyaline membrane disease
IM
Intramuscular
ISC
Infant servo control
IV
Intravenous
MCA
Middle cerebral artery
mmHg
Millimetres of mercury
MRI
Magnetic resonance imaging
MRS
Magnetic resonance spectroscopy
NEC
Necrotising enterocolitis
NNST
Neonatal screening test
pCO2
Partial pressure of carbon dioxide
pH
Partial pressure of hydrogen ions
PLIC
Posterior limb of the internal capsule
pO2
Partial pressure of oxygen
PPHN
Persistent pulmonary hypertension of the newborn
PPV
Positive predictive value
RCT
Randomised controlled trial
RSQ
Retrieval Services Queensland
VBG
Venous blood gas
Page 3 of 25
Table of Contents
Introduction.....................................................................................................................................7
Differential diagnosis ......................................................................................................................7
2.1
Criteria for the diagnosis of HIE.............................................................................................8
2.2
HIE Staging............................................................................................................................8
3 Management...................................................................................................................................8
3.1
Resuscitation .........................................................................................................................8
3.2
Inter hospital transfer .............................................................................................................9
3.3
Cardiorespiratory ...................................................................................................................9
3.3.1 Respiratory.........................................................................................................................9
3.3.2 Cardiac...............................................................................................................................9
3.4
Infection ...............................................................................................................................11
3.5
Fluid, electrolyte and acid base ...........................................................................................12
3.5.1 Hypoglycaemia ................................................................................................................12
3.5.2 Acidosis............................................................................................................................12
3.5.3 Volume.............................................................................................................................12
3.6
Temperature ........................................................................................................................12
3.6.1 Criteria for cooling............................................................................................................13
3.6.2 Babies excluded from cooling..........................................................................................13
3.6.3 Babies born outside a Level 3 neonatal unit....................................................................13
3.7
Neurologic............................................................................................................................14
3.7.1 Neuroimaging ..................................................................................................................14
3.7.2 Electrophysiology.............................................................................................................14
3.7.3 Seizures ...........................................................................................................................14
3.7.3.1
Management .........................................................................................................15
3.7.4 Physiotherapy and speech pathology..............................................................................15
3.8
Impaired synthetic liver function/consumptive coagulopathy ..............................................15
3.9
Gastrointestinal....................................................................................................................16
3.10 Other investigations .............................................................................................................16
4 Prognosis......................................................................................................................................17
References ..........................................................................................................................................18
Appendix A: Sarnat and Sarnat staging system..................................................................................21
Appendix B: HIE staging......................................................................................................................22
Appendix C: Management of therapeutic hypothermia .......................................................................23
Acknowledgements..............................................................................................................................25
1
2
List of Tables
Table 1. Inotropic therapy.................................................................................................................... 10
Table 2. Antibiotic therapy ................................................................................................................... 11
Table 3. Prognosis............................................................................................................................... 17
Page 4 of 25
Check List A: Criteria for therapeutic hypothermia
Term or near term (greater than or equal to (≥) 35 weeks) baby with a perinatal event and
acidosis. Call RSQ on 1300 799 127 to discuss the need for transfer and therapeutic
hypothermia with a Level 3 Neonatologist

1. Baby must meet all of the following criteria:

Greater than or equal to (≥) 35 weeks

Birth weight greater than or equal to (≥) 1800 g

Able to begin cooling before 6 hours of age

No severe congenital anomaly

Not moribund and with plans for full care
AND

2. Baby must meet either of the following criteria:

Blood gas (cord, arterial blood gas (ABG), venous blood gas (VBG)) within 60 minutes of
birth with: pH less than or equal to (≤) 7.00 and base deficit greater than or equal to (≥)
12 mmol/L
OR if no blood gas is available, BOTH OF:

10 minute Apgar less than or equal to (≤) 5 or assisted ventilation required at birth and
continued for greater than or equal to (≥) 10 minutes

Acute perinatal event (eg. ruptured uterus, placental abruption, cord prolapse, amniotic
fluid embolism, fetal exsanguination from vasa praevia, fetal maternal haemorrhage or
severe fetal bradycardia)
AND

3. Baby must meet either of the following:

Seizures (witnessed by medical or nursing staff)
OR:

Early onset encephalopathy determined by the baby exhibiting a minimum of one
symptom in at least 3 categories as documented below
Category
Moderate encephalopathy
Severe encephalopathy
Level of
consciousness

Lethargic

Stupor or coma
Spontaneous
activity

Decreased activity

No activity
Posture

Distal flexion, complete
extension

Decerebrate
Tone

Hypotonia (focal or
general)

Flaccid
Primitive reflexes

Weak suck or
Incomplete Moro

Absent suck or Moro
Autonomic system

Constricted pupils,
bradycardia or
periodic/irregular breathing

Deviated/dilated/non-reactive
pupils, variable heart rate or
apnoea
Adapted from:
Shankaran S, Laptook AR, Ehrenkranz RA, Tyson JE, McDonald SA, Donovan ER, et al. Whole-body hypothermia for
neonates with hypoxic -ischaemic encephalopathy. N Engl J Med 2005:353(15);1574-84.
Jacobs SE, Hunt R, Tarnow-Mordi WO, Inder TE, Davis PG. Cooling for newborns with hypoxic ischaemic encephalopathy.
Cochrane Database of Systematic Reviews 2007, Issue 4, Art. No.:CD003311. DO1: 10.1002/14651858.CD003311.pub2.
Page 5 of 25
Check List B: Parental advice regarding therapeutic hypothermia
Suggested information that clinicians may wish to use when discussing aspects of HIE and
therapeutic hypothermia with parent(s).
Criteria
Advice to parent(s)
Resuscitation
•
Incidence
•
Consequences
•
•
Prognosis
•
Treatment
•
•
What does the
treatment entail
•
•
•
•
Your baby needed significant resuscitation at birth to help him/her
breathe. He/she appears to have suffered from the effects of lack of
oxygen and blood supply to the brain
About I in 1000 newborn babies suffer from the effects of reduced blood
flow or oxygen supply to their brain around the time of birth
This can result in brain damage from direct injury and also from ongoing
changes that begin around six hours after the injury
These secondary changes are known to increase the amount of brain
injury that occurs
Approximately 30 to 60% of those babies who survive after this degree of
damage to their brain may develop long-term disabilities. These
disabilities include cerebral palsy and severe learning difficulties
In the past there were no treatments to reduce the severity of brain injury
in these newborn babies
Recent research has shown that cooling these babies reduces the
secondary brain injury, increases the chances of survival and reduces the
severity of possible long-term disability
Your baby will receive cooling therapy in addition to standard intensive
care support
Your baby’s temperature will be slowly lowered and kept between 33 to
34°C for 72 hours. Cooling will be achieved by exposing your baby to the
ambient air temperature and with the use of cool gel packs if required
Your baby’s temperature and other vital signs will be closely monitored
throughout the process. If your baby shows any signs of discomfort during
cooling he/she will be prescribed medication to reduce this
After 72 hours of cooling, your baby will be gradually rewarmed to a
temperature of 37°C
Page 6 of 25
1
Introduction
Neonatal encephalopathy and its subset of hypoxic-ischaemic encephalopathy (HIE) are defined
clinically on the basis of a constellation of findings to include a combination of abnormal1:
• consciousness
• tone and reflexes
• feeding
• respiration
• seizures
Encephalopathy can result from a myriad of conditions and may or may not result in permanent
neurologic impairment1:
• Approximately 70% of neonatal encephalopathy is secondary to events arising before the
onset of labour1
• Neonatal encephalopathy attributable to intrapartum hypoxia, in the absence of any other
preconceptional or antepartum abnormalities, is approximately 1.6 per 10,0001
The pathway from an intrapartum hypoxic-ischaemic injury to subsequent permanent neurologic
impairment must progress through neonatal encephalopathy. 1
Perinatal asphyxia can be defined as a condition of impaired blood gas exchange leading to
progressive hypoxaemia and hypercapnia with a significant metabolic acidosis evidenced by an
umbilical artery base deficit greater than 12 mmol/L at birth.2
Classification of the severity of intrapartum fetal asphyxia can be determined by the short term
outcome which is expressed by:
• neonatal encephalopathy and
• other newborn organ system complications2
It is recommended that the terms ‘perinatal asphyxia’, ‘birth asphyxia’ and ‘HIE’ not be used until or
unless there is some available evidence specific to the asphyxial origin for the neurological illness in
the baby.3
2
Differential diagnosis
The differential diagnosis of neonatal encephalopathy includes1:
• HIE
• infection
• prenatal stroke
• intracranial haemorrhage
• congenital brain malformations
• inborn errors of metabolism
• genetic syndromes
HIE is the term used to describe babies who have the spectrum of clinical findings described by
Sarnat and Sarnat4 AND convincing evidence of antepartum or intrapartum hypoxia (criteria as
outlined by the International Cerebral Palsy Taskforce).5
This guideline will focus on the management of HIE and not the other causes of neonatal
encephalopathy.
Page 7 of 25
2.1
Criteria for the diagnosis of HIE
Essential criteria for the diagnosis of HIE in the neonatal period includes5:
• evidence of metabolic acidosis (pH less than 7.00, base deficit greater than or equal to 12
mmol/L in fetal, cord or early neonatal blood samples)
• early onset encephalopathy (fitting the Sarnat and Sarnat criteria)4 in babies born at 34 or
more weeks gestation [refer to Appendix A: Sarnat and Sarnat staging system and
Appendix B: HIE staging]
Criteria that collectively suggest an intrapartum timing (within close proximity to labour and delivery
e.g. 0 – 48 hours) but are not specific to asphyxial insults include5:
• sentinel hypoxic event occurring immediately before or during labour (e.g. ruptured
uterus, placental abruption, cord prolapse, amniotic fluid embolism, fetal exsanguination
from vasa praevia or fetal maternal haemorrhage)5
• sudden and sustained fetal bradycardia or the absence of fetal heart rate variability in the
presence of persistent, late or variable decelerations, usually after a hypoxic sentinel
event when the pattern was previously normal
• Apgar scores of 0 – 3 for longer than 5 minutes
• early evidence of multi system involvement (within 72 hours of birth)
• early imaging study showing evidence of acute non focal cerebral abnormality
2.2
HIE Staging
[refer to Appendix A: Sarnat and Sarnat staging system and Appendix B: HIE staging]
HIE is classified in stages,4 which if applied consistently provide useful information about magnitude
of injury and prognosis. Babies with:
• Stage 1 HIE usually require minimal support and the neurological examination is normal
by Day 3 – 4
• Stage 2 to 3 will be significantly more unwell and the level of support required will depend
upon organ compromise
Assessment of HIE staging should be undertaken as soon as possible after the baby is stabilised so
that therapeutic interventions that will require transfer to a Level 3 neonatal unit can be coordinated
[refer to Check List A: Criteria for therapeutic hypothermia].
3
Management
Clinical management is primarily supportive and is dependent on the extent of organ compromise.
High level evidence6-9 supports the use of therapeutic hypothermia for the treatment of moderate to
severe cases of HIE [refer to section 3.6].
Each baby’s management should be individualised, with close monitoring of cardiorespiratory status
and early identification and treatment of multi-organ system complications where appropriate.
3.1
Resuscitation
Appropriate and timely resuscitation is required to prevent hypoxia, hypercarbia and acidosis. This
may prevent or reduce the clinical severity of HIE [refer to Guideline: Neonatal resuscitation].
Cord blood gases should be measured if possible in every resuscitated newborn baby as the most
objective way to assess the baby’s condition just before birth10:
• Collect umbilical cord arterial blood gases from a clamped cord as soon as possible after
delivery (preferably before 30 minutes, arterial pH and base excess become unstable in a
clamped cord at room temperature after 30 minutes)11
• Blood samples taken for acid base status remain stable in a plastic syringe for up to 30
minutes before analysis11
Page 8 of 25
3.2
Inter hospital transfer
Any baby with moderate to severe HIE must be considered for transfer to a Level 3 neonatal unit for
therapeutic hypothermia or the possibility thereof. Other babies that may need transfer include those
with moderate to severe encephalopathy requiring:
• ventilation
• inotropic support
• any diagnostic tests unavailable at a Level 1 or 2 neonatal unit
Early consultation with a Level 3 Neonatologist is recommended. Management and transfer
discussions can be facilitated by calling Retrieval Services Queensland (RSQ) on 1300 799 127.
3.3
Cardiorespiratory
3.3.1 Respiratory
Monitor for hypoxia, acidosis and hypercarbia. Respiratory distress may have multiple causes
including:
• acidosis
• meconium aspiration
• sepsis
• persistent pulmonary hypertension of the newborn (PPHN)
• hyaline membrane disease (HMD)
Babies with respiratory depression should be intubated and ventilated particularly if:
• there is severe encephalopathy
• there is severe acidosis
• the baby is having frequent seizures
• the baby requires large or frequent doses of anticonvulsant medication
Avoid hyperoxaemia and hypocarbia (severe hyperoxaemia with PaO2 greater than 200 mmHg
and hypocarbia with pCO2 less than 20 mmHg are associated with poor outcome).12
Any concerns regarding respiratory status should be discussed with a Level 3 Neonatologist.
3.3.2 Cardiac
Hypotension (mean arterial blood pressure of less than 35 - 40 mmHg)7 has been associated with
poor outcomes.13,14 Loss of cerebral autoregulation makes hypertension equally hazardous. Acute
tubular necrosis or the presence of inappropriate antidiuretic hormone (ADH) secretion, affect fluid
output, increasing the risk of fluid overload.15
Blood pressure is used in neonatology as a marker for systemic perfusion, however it is a poor
predictor of low cardiac output16 and should not be the only criterion by which systemic perfusion is
monitored.
Page 9 of 25
Assessment should include:
• assessment of peripheral perfusion
• establishment of whether hypotension is symptomatic of another problem including:
o hypovolaemia or blood loss
o sepsis
o high mean airway pressure on mechanical ventilation
• the need for intravenous crystalloid boluses (10 mL/kg of 0.9% Sodium Chloride) if:
o perfusion is poor (capillary refill greater than 3 seconds)
o blood gas lactate is not improving
o mean blood pressure is less than 35 - 40 mmHg7
• the need for echocardiography (ECHO) which may identify hypovolaemia, poor
myocardial contractility and low flow states and should be considered in ventilated babies
after a significant hypoxic-ischaemic insult
If hypotension persists or low flow states are identified on ECHO consider inotropic therapy including:
• Dopamine or Dobutamine [refer to Table 1. Inotropic therapy]
o Inotropes should preferably be administered via an appropriately positioned catheter in
a central vein (e.g. umbilical venous catheter positioned above the ductus venosus).17
A dedicated intravenous line is preferred. Never give inotropes into an arterial
line.18
Table 1. Inotropic therapy
Drug
Dose
Route
Comment
Dopamine
10 micrograms/kg/minute18
IV infusion17,19
Monitor heart rate and intra-arterial
blood pressure17
Prepare a
fresh infusion
every 24
hours17,19
May cause tachycardia and
arrhythmias and increase
pulmonary artery pressure17
Infusion:
(Dilute 30 mg/kg of Dopamine
up to a total of 50 mL with 5%
or 10% Glucose or 0.9%
Sodium Chloride.17 This gives
a Dopamine solution of 600
micrograms/kg/mL. If run at 1
mL/hr this will deliver 10
micrograms/kg/min)18
Dobutamine
10 micrograms/kg/minute18,19
Infusion:
(Dilute 30 mg/kg of
Dobutamine up to a total of
50 mL with 5% or 10%
Glucose or 0.9% Sodium
Chloride.17 This gives a
Dobutamine solution of 600
micrograms/kg/mL. If run at 1
mL/hr this will deliver 10
micrograms/kg/min)18
Use in conjunction with Phenytoin
may cause severe hypotension19
More effective than Dobutamine for
treating hypotension20
IV infusion17,19
Monitor heart rate and intra-arterial
blood pressure17
Prepare a
fresh infusion
every 24
hours17,19
May cause hypotension if baby is
hypovolaemic17
May cause significant respiratory
depression if injected rapidly of if
high dose infusion is used
Tachycardia may occur and
increase pulmonary blood pressure
leading to pulmonary oedema19
Do not mix with Sodium
Bicarbonate19,21
More effective than Dopamine for
treating low cardiac output20
Page 10 of 25
3.4
Infection
Perinatal infection may co-exist with HIE. All babies should have:
• a full blood count (FBC)
• blood cultures
• intravenous antibiotics (Penicillin (Benzylpenicillin, Ampicillin or Amoxicillin)) and
Gentamicin) as soon as possible after birth [refer to Table 2. Antibiotic therapy]
Administer antibiotics in accordance with local/hospital guidelines. In the absence of such
guidelines use the dosage regimen below.
Table 2. Antibiotic therapy
Drug
Dose
Route
Comment
Ampicillin
50 mg/kg/dose
12 hourly17,19
IV – slow push
IM17,19
Increase the dosage interval if
there is renal failure19
60 mg/kg/dose
12 hourly19,22
IV - slow push
IM19
Halve the dose and double the
dose interval if there is renal
failure19
Babies greater than 32
weeks gestation
5 mg/kg 24 hourly19
IV – slow push
(infusion over 30
minutes is not
necessary)19
IM19
Trough level prior to 3rd dose in
babies less than a week old and in
babies with poor renal function19
OR
Benzylpenicillin
AND
Gentamicin
CAUTION
Caution must be exercised in the administration of second and subsequent doses
of aminoglycosides (Gentamicin) to babies who are oliguric. Wait for a trough
level result prior to 2nd dose
Trough level
Comment
Less than or equal to 1 mg/L17,19
Therapeutic17,19
1.1 – 2.3 mg/L17
Extend the dosage interval by 12 hours17
2.4 – 3.2 mg/Ls17
Extend the dosage interval by 24 hours17
Greater than or equal to 3.3 mg/L17
Do not give further doses. Measure level
in 24 hours17
Page 11 of 25
3.5
Fluid, electrolyte and acid base
3.5.1 Hypoglycaemia
Perform an early blood glucose level and correct hypoglycaemia. Babies with Stage 2 to 3 HIE will
require intravenous glucose administration [refer to Guideline: Neonatal hypoglycaemia: assessment
and blood glucose level (BGL) monitoring].
3.5.2 Acidosis
Perform early arterial blood gas and correct:
• respiratory acidosis (hypercarbia and acidosis) with appropriate ventilatory support
• it is possible to correct persistent severe metabolic acidosis in a baby who is appropriately
ventilated with intravenous Sodium Bicarbonate given at a rate of no more than 0.5
mmol/kg per minute.19 Do not give Sodium Bicarbonate to a baby who is not effectively
ventilating (either spontaneously or mechanically) as it causes hypercarbia and worsens
respiratory acidosis. There is no convincing evidence that administration of Sodium
Bicarbonate produces long term benefits in this situation.23
3.5.3 Volume
Many restrict maintenance fluids15,24 to 40 – 50 mL/kg/day until a urine output equal to 1 mL/kg/hr has
been established. Fluid restriction is recommended in standard textbooks to avoid fluid overload and
cerebral oedema, however no RCTs address the use of fluid restriction following perinatal asphyxia.
There is concern that fluid restriction may cause dehydration and hypotension decreasing cerebral
perfusion and causing further brain damage.25 Monitor serum sodium trends to gauge whether more
or less fluids are needed.
•
•
•
3.6
Administer intravenous 10% Glucose in the first 24 hours. Once renal function is stable,
sodium and potassium additives can be commenced if required
If the baby has oliguria/anuria consider:
o urinary catheterisation especially if there is a palpable bladder and/or baby is not
voiding spontaneously
o Dopamine (4 microgram/kg/minute or less)18 if not already receiving inotropic therapy
o withholding second or subsequent dose of aminoglycoside (Gentamicin) antibiotics if
prescribed. Be guided by serum aminoglycoside levels if considering further doses
Assess the fluid balance regularly and check urea, electrolytes and creatinine (there is a
risk of fluid overload and hyperkalaemia)
Temperature
Therapeutic hypothermia (cooling) following a hypoxic-ischaemic insult can benefit certain babies
and is now considered standard care.26
For cooling to provide benefit:
• it must be commenced within 6 hours of birth before secondary reperfusion injury begins27
• it must be discussed with a Level 3 Neonatologist as soon as HIE is suspected to facilitate
commencement of cooling within the critical period [refer to Check list A: Criteria for
therapeutic hypothermia]
• hyperthermia should be avoided2,15,28
• rectal temperature should be maintained at 33.0 – 34.0°C7,8,26
Page 12 of 25
3.6.1 Criteria for cooling
Current evidence and consensus professional opinion supports therapeutic hypothermia (cooling) to
be used for the following babies:
• greater than or equal to 35 weeks gestational age AND
• greater than or equal to 1800 g
• with evidence of moderate to severe encephalopathy [refer to Appendix A: Sarnat and
Sarnat staging system and Appendix B: HIE staging] AND
• with evidence of intrapartum hypoxia indicated by at least two of the following:
o Apgar score of less than or equal to 5 at 10 minutes
o needing mechanical ventilation or ongoing resuscitation at 10 minutes of age
o cord, arterial or venous blood gas with pH of less than or equal to 7.00 and base
deficit of greater than or equal to 12 mmol/L within 60 minutes of birth
3.6.2 Babies excluded from cooling
Babies that were excluded from RCTs for therapeutic hypothermia included babies:
• less than 35 weeks gestation6,7,26
• with a birth weight less than 1800 grams7,26
• where cooling could not be started within 6 hours of birth6,7,26
• with major congenital abnormalities6,7,26 including:
o suspected neuromuscular disorders
o suspected significant chromosomal abnormalities
o life threatening abnormalities of the cardiovascular or respiratory systems
• so severely affected that there was little hope for normal outcome7,26 i.e. moribund or in
extremis (e.g. very low blood pressure or severe acidosis unresponsive to treatment)
There is no evidence of any therapeutic benefit from cooling for these babies and cooling is still
considered experimental (i.e. not standard care). Any decision to cool these babies should be made
by a Level 3 Neonatologist after discussion where possible with the parent(s).
3.6.3 Babies born outside a Level 3 neonatal unit
All babies who require cooling should be referred to a level 3 neonatal unit as early as possible.
Where cooling is advised the referring unit should:
• stop active warming by turning off the heater:
o monitor and measure the axillary or rectal temperature every ½ hour, commence
continuous skin temperature monitoring if able. Maintain the temperature between
33.0 – 34.0°C by passive cooling only (heater off)
• turn the heater on if the axillary or rectal temperature is less than 33.5 °C and continue to
closely monitor the axillary/rectal temperature
Do not delay passive cooling to await the arrival of the transport/retrieval team. Active cooling will
only be started once the retrieval team arrives at the referring unit.
Page 13 of 25
3.7
3.7.1
Neurologic
Neuroimaging
•
•
3.7.2
Electrophysiology
•
•
3.7.3
Cranial ultrasound:
o With middle cerebral artery (MCA) and anterior cerebral artery (ACA) Doppler should
be considered in the first 48 hours. Although not sensitive, any persistent changes in
the basal ganglia or abnormal cerebral artery Doppler are specific for poor neuromotor
outcome.29 There is a lack of evidence from RCTs regarding the value of these tests in
a baby undergoing therapeutic hypothermia
Magnetic resonance imaging (MRI):
o Should be considered in babies with moderate to severe neonatal encephalopathy and
performed at approximately one week of age.30 Neonates who develop signs of HIE
following an acute sentinel event (e.g. placental abruption) sustain bilateral and
usually symmetrical lesions within the basal ganglia and thalami, and exhibit an
abnormal appearance in the posterior limb of the internal capsule (PLIC). Abnormality
seen in the PLIC is a an excellent predictor of abnormal outcome31
o Earlier MRI may be considered in order to make decisions about the withdrawal of
intensive care in the severely unwell baby
A formal EEG should be considered in the presence of moderate and severe
encephalopathy or seizures
amplitude-integrated electroencephalogram (aEEG) may be considered. It enables
extended monitoring of cerebral electrical activity, seizure detection and outcome
prediction32,33
Seizures
•
•
HIE is the most common cause of early onset neonatal seizures.24 Approximately 30% of
babies with HIE have seizures which usually occur in the first 24 hours after birth and may
be difficult to control. The early onset of seizures may predict a poorer
neurodevelopmental outcome independent of the severity of hypoxic-ischaemic brain
injury34
Electrolyte abnormalities and multi system complications may coexist. Localised
ischaemic events may result in focal clonic seizures. It is important to exclude other
causes of seizures which include:
o intracranial haemorrhage (approximately 15%)
o neonatal stroke
o intracranial infections
o metabolic abnormalities
o central nervous system malformations
o drug withdrawal
o hypoglycaemia (always check the BGL of all babies who present with seizures)
Page 14 of 25
3.7.3.1 Management
• 30-90% of seizures are subclinical and up to 50% of clinical seizures may not be
detected35,36
• 66% of electrographic seizures do not have overt clinical signs35
• Anticonvulsants may not treat electroencephalographic seizures even if effective for
clinical seizure activity35,37
• Seizures should be treated to reduce the risk of additional injury, however little consensus
exists regarding the optimal treatment protocol.38 Ensure that ventilation and
cardiovascular status are stable and monitored before giving anticonvulsant therapy
• Anticonvulsant therapy should be given intravenously to achieve a rapid onset of action
and predictable blood levels [refer to Guideline: Neonatal seizures39]. Recommended
anticonvulsant therapy includes40:
o Phenobarbitone (first line treatment)
o Phenytoin
o Midazolam
o Clonazepam
• Refer to Guideline: Neonatal seizures for anticonvulsant therapy administration
information
Drug levels are important when maintenance doses of these drugs are used. Slow elimination rates
secondary to hepatic and/or renal injury may lead to drug accumulation.
Duration of drug therapy depends on the likelihood of seizure recurrence:
• following HIE there is a low risk of seizure recurrence after early withdrawal of
anticonvulsant in the neonatal period41
• anticonvulsant treatment may be withdrawn once seizures are controlled and the
neurological examination is normal42
• babies with prolonged or difficult seizures and those with abnormality on EEG may benefit
from continuing anticonvulsant treatment, however there is a lack of evidence from RCTs
to address duration of treatment
3.7.4 Physiotherapy and speech pathology
Neurological examination of the baby, including assessment of tone, movement, and oromotor
responses (cough, gag, suck and swallow), are valuable in order to track progress and can assist in
the decision to:
• commence oral feeding
• provide parents and staff with handling and positioning strategies
Prechtl’s Method on Qualitative Assessment of General Movements43 is a tool that may be used to
assess the baby’s neurological status to help determine appropriate early neurodevelopmental
intervention.
3.8
Impaired synthetic liver function/consumptive coagulopathy
Disseminated intravascular coagulopathy (DIC) is a significant risk after hypoxic injury to the liver.27
Liver function tests (LFTs) should be monitored regularly.
If there is evidence of bleeding or petechiae, perform platelet level and coagulation profile. Consider:
• fresh frozen plasma (FFP) and
• a second dose of Vitamin K
Page 15 of 25
3.9
Gastrointestinal
Do not feed during therapeutic hypothermia and only recommence feeds after rewarming.
Commence feeding after assessment of the severity of asphyxia and associated system
complications including:
• whether the baby is being cooled
• respiratory distress
• encephalopathy
• hypotension
• renal impairment
Feed intolerance is common as gut circulation may have been compromised, this may increase the
risk for necrotising enterocolitis (NEC)27:
• Breast milk is preferable
• Feeds should be introduced gradually
3.10 Other investigations
• Calcium, magnesium, glucose
• Serum lactate
To exclude other causes of neonatal encephalopathy consider:
• C-reactive protein
• Lumbar puncture
• Liver function tests
• Coagulation profile
• Serum for chromosome analysis, ammonia, amino acids
• Urine for amino and organic acids, ketones, reducing substances
• Early newborn screening test (NNST) if metabolic/genetic disorders suspected. Repeat
the NNST when it would normally have been collected
Page 16 of 25
4
Prognosis
Clinical
Table 3. Prognosis
Test
Timing
Outcome
Sarnat and
Sarnat4
Early onset neonatal
encephalopathy is the
best single predictor of
long-term outcome2
Severity of the acute encephalopathy predicts the overall risk of
death and severe handicap45
Stage 1 HIE – normal neurologic outcome in greater than 90% of
cases45
Quick recovery is
associated with a better
outcome44
Seizures
34
Early onset of seizures
Stage 2 HIE – incidence of poor outcomes ranges from 30 - 60%45
Stage 3 HIE – poor neurologic outcome (death or severe disability
45
in almost all cases)
May predict a poorer neurodevelopmental outcome, independent of
the severity of hypoxic-ischaemic brain injury34
May assist with outcome prediction43
Dubowitz/
Prechtl43
Time to
spontaneous
respiration
Greater than 30 minutes46
Overall risk of death or severe handicap 72%46
EEG
First few days of life after
HIE47
Background EEG abnormalities, detected in the first few days of life
after HIE can provide prognostic information even in babies treated
with hypothermia47
Grade of abnormality predicts the rate of death or severe
handicap46
Severe abnormality (burst suppression, low voltage or
46
isoelectric) - 95%
Moderate abnormality (slow wave activity) - 64%46
Mild or no abnormality 3.5%46
Persistence of EEG abnormalities at 1 month of age is
associated with a higher risk of neurologic sequelae47
Electrophysiology
aEEG
aEEG at an early age
(within several hours after
birth) can differentiate
between babies with later
severe neurologic deficits
and babies with mild
deficits or normal
outcomes48-50
The course of aEEG background activity adds to the prognostic
50
value of aEEG monitoring in asphyxiated babies
Normalisation of initially abnormal background patterns (burst
suppression, continuos low voltage, flat trace) by50:
• 6 hours of age is predictive of good outcomes – positive
49
predictive value (PPV) 91%
• 24 hours of age is less predictive of good outcome – PPV
49
61%
• severely abnormal patterns persisting beyond 24 hours are
50
predictive of adverse neurological outcomes
• adverse outcome is x 19 more likely when abnormal
background pattern (burst suppression or worse) occurs
50
between 24 – 36 hours
• onset of sleep wake cycling within 36 hours of birth, is
predictive of good neurodevelopmental outcome – PPV
92.1%51
Radiology
Background is affected by several medications and must be
considered when interpreting the aEEG trace52
Cerebral
artery
Doppler
12 +/- 2 hours29
Severe increase in mean cerebral blood flow velocity post hypoxia,
is predictive of Stage 3 HIE with poor neurologic outcome (death or
severe disability) in 100%29
MRI/magnetic
resonance
spectroscopy
(MRS)
7 – 10 days of age53
Both sensitive and specific for outcome prediction53
Grade 1 changes – normal outcome 100%
Grade 3 changes – death or severe disability 100%
Page 17 of 25
References
1. ACOG, Executive Summary. Neonatal encephalopathy and cerebral palsy: Defining the pathogenesis and
physiology. 2003 [Available from:
http://www.acog.org/from_home/Misc/neonatalEncephalopathy.cfm?printerfriendly=yes
2. Low JA. Intrapartum fetal asphyxia: definition, diagnosis, and classification. Am J Obstet Gynecol. 1997;
176(5):957-9.
3. Bax M, Nelson KB. Birth asphyxia: a statement. World Federation of Neurology Group. Dev Med Child
Neurol. 1993; 35(11):1022-4.
4. Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress. A clinical and
electroencephalographic study. Arch Neurol. 1976; 33(10):696-705.
5. MacLennan Alistair. A template for defining a causal relation between acute intrapartum events and cerebral
palsy: international consensus statement. BMJ. 1999; 319:1054-9.
6. Azzopardi D, Brocklehurst P, Edwards D, Halliday H, Levene M, Thoresen M, et al. The TOBY Study. Whole
body hypothermia for the treatment of perinatal asphyxial encephalopathy: a randomised controlled trial. BMC
Pediatr. 2008; 8:17.
7. Gluckman P, Wyatt J, Azzopardi D, Ballard R, Edwards A, Ferriero D, et al. Selective head cooling with mild
systemic hypothermia after neonatal encephalopathy: multicentre randomised trial. Lancet. 2005;
365(9460):663-70.
8. Shankaran S, Laptook AR, Ehrenkranz RA, Tyson JE, McDonald SA, Donovan EF, et al. Whole-body
hypothermia for neonates with hypoxic-ischemic encephalopathy. N Engl J Med. 2005; 353(15):1574-84.
9. Shankaran S, Pappas A, Laptook AR, McDonald SA, Ehrenkranz RA, Tyson JE, et al. Outcomes of safety
and effectiveness in a multicenter randomized, controlled trial of whole-body hypothermia for neonatal hypoxicischemic encephalopathy. Pediatrics. 2008; 122(4):e791-8.
10. Australian Resuscitation Council. Neonatal Guidelines
[updated February 2006. Available from: www.resus.org.au/
11. Lynn A, Beeby P. Cord and placenta arterial gas analysis: the accuracy of delayed sampling. Arch Dis Child
Fetal Neonatal Ed. 2007; 92(4):F281-5.
12. Klinger G, Beyene J, Shah P, Perlman M. Do hyperoxaemia and hypocapnia add to the risk of brain injury
after intrapartum asphyxia? Arch Dis Child Fetal Neonatal Ed. 2005; 90(1):F49-52.
13. Bada HS, Korones SB, Perry EH, Arheart KL, Ray JD, Pourcyrous M, et al. Mean arterial blood pressure
changes in premature infants and those at risk for intraventricular hemorrhage. J Pediatr. 1990; 117:607-14.
14. Miall-Allen VM, de Vries LS, Whitelaw AG. Mean arterial blood pressure and neonatal cerebral lesions. Arch
Dis Child. 1987; 62(10):1068-9.
15. Kattwinkel J, editor. Textbook of Neonatal Resuscitation. 5th ed. Chicago: American Academy of
Paediatrics and American Heart Association; 2006.
16. Kluckow M, Evans N. Relationship between blood pressure and cardiac output in preterm infants requiring
mechanical ventilation. J Pediatr. 1996; 129:506-12.
17. Young T, Mangum B. Neofax. A manual of drugs used in neonatal care. 21 ed. Montvale: Thompson
Reuters; 2008.
18. Davies MW, Cartwright D. Common drugs and infusions. In: Davies MW, Cartwright D, Inglis G, editors.
Pocket notes on neonatology
2ed. Marrickville: Churchill Livingstone; 2008.
19. Hey E. Neonatal Formulary. Drug use in pregnancy and the first year of life. 5 ed. Massachusetts: Blackwell
Publishing Ltd; 2007.
20. Osborn D, Evans N, Kluckow M. Randomized trial of dobutamine versus dopamine in preterm infants with
low systemic blood flow. J Pediatr. 2002; 140(2):183-91.
Page 18 of 25
21. Burridge N, editor. SHPA. Australian Injectable Drug Handbook. 4 ed: Health communication Network;
2008.
22. Shann F. Drug doses. 14 ed. Parkville: Intensive Care Unit, Royal Children's Hospital; 2008.
23. Beveridge CJ, Wilkinson AR. Sodium bicarbonate infusion during resuscitation of infants at birth. Cochrane
Database Syst Rev. 2006; (1):CD004864.
24. Perlman J. Intervention strategies for neonatal hypoxic-ischaemic cerebral injury. Clinical Therapeutics.
2006; 28(9):1353-65.
25. Kecskes Z, Healy G, Jensen A. Fluid restriction for term infants with hypoxic-ischaemic encephalopathy
following perinatal asphyxia. Cochrane Database Syst Rev. 2005; (3):CD004337.
26. Jacobs S, Hunt R, Tarnow-Mordi W, Inder T, Davis P. Cooling for newborns with hypoxic ischaemic
encephalopathy. Cochrane Database Syst Rev. 2007; (4):CD003311.
27. Zanelli S, Stanley D, Kaufman D. Hypoxic-ischaemic encephalopathy. eMedicine. 2008 [Available from:
http://emedicine.medscape.com/article/973501-overview
28. Laptook A, Tyson J, Shankaran S, McDonald S, Ehrenkranz R, Fanaroff A, et al. Elevated temperature after
hypoxic-ischemic encephalopathy: risk factor for adverse outcomes. Pediatrics. 2008; 122(3):491-9.
29. Ilves P, Talvik R, Talvik T. Changes in Doppler ultrasonography in asphyxiated term infants with hypoxicischaemic encephalopathy. Acta Paediatrica. 1998; 87(6):680-4.
30. Ment LR, Bada HS, Barnes P, Grant PE, Hirtz D, Papile LA, et al. Practice parameter: neuroimaging of the
neonate: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice
Committee of the Child Neurology Society. Neurology. 2002; 58(12):1726-38.
31. Srinivasan L, Rutherford MA. MRI of the newborn brain. Paediatrics and Child Health. 2008; 18(4):183-95.
32. Toet MC, Hellstrom-Westas L, Groenendaal F, Eken P, de Vries LS. Amplitude integrated EEG 3 and 6
hours after birth in full term neonates with hypoxic-ischaemic encephalopathy. Arch Dis Child Fetal Neonatal Ed.
1999; 81(1):F19-23.
33. Spitzmiller RE, Phillips T, Meinzen-Derr J, Hoath SB. Amplitude-integrated EEG is useful in predicting
neurodevelopmental outcome in full-term infants with hypoxic-ischemic encephalopathy: a meta-analysis. J
Child Neurol. 2007; 22(9):1069-78.
34. Glass HC, Glidden D, Jeremy RJ, Barkovich AJ, Ferriero DM, Miller SP. Clinical neonatal seizures are
independently associated with outcome in infants at risk for hypoxic-ischemic brain injury. J Pediatr. 2009;
155(3):318-23.
35. Murray DM, Boylan GB, Ali I, Ryan CA, Murphy BP, Connolly S. Defining the gap between electrographic
seizure burden, clinical expression and staff recognition of neonatal seizures. Arch Dis Child Fetal Neonatal Ed.
2008; 93(3):F187-91.
36. Malone A, Ryan C, Boylan G, Connolly S. Ability of medical staff to accurately distinguish neonatal seizures
from non-seizure movements. Irish Journal of Medical Science. 2005; 14(2e3).
37. Painter MJ, Scher MS, Stein AD, Armatti S, Wang Z, Gardiner JC, et al. Phenobarbital compared with
phenytoin for the treatment of neonatal seizures. N Engl J Med. 1999; 341(7):485-9.
38. Silverstein F, Jensen F, Inder T, Hellstrom-Westas L, Hirtz D, Ferriero DM. Improving the treatment of
neonatal seizures: National Institute of Neurological Disorders and Stroke Workshop Report. Pediatr. 2008;
153(1):12-15e1.
39. Queensland Maternity and Neonatal Clinical Guidelines Program. Neonatal seizures. Guideline No.
MN10.23-V1-R16. Queensland Health. 2010.
40. Rennie JM, Boylan GB. Neonatal seizures and their treatment. Curr Opin Neurol. 2003; 16:177-81.
41. Hellstrom WL, 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 Fetal Neonatal Ed. 1995; 72:F97-101.
42. Evans D, Levene M. Neonatal seizures. Arch Dis Child Fetal Neonatal Ed. 1998; 78(1):F70-5.
Page 19 of 25
43. Prechtl HF, Ferrari F, Cioni G. Predictive value of general movements in asphyxiated full term infants. Early
Hum Dev. 1993; 35(2):91-120.
44. Carli G, Reiger I, Evans N. One-year neurodevelopmental outcome after moderate newborn hypoxic
ischaemic encephalopathy. J Paediatr Child Health. 2004; 40(4):217-20.
45. Murray DM, Boylan GB, Ryan CA, Connolly S. Early EEG findings in hypoxic-ischemic encephalopathy
predict outcomes at 2 years. Pediatrics. 2009.
46. Perlman JM, Risser R. Can asphyxiated infants at risk for neonatal seizures be rapidly identified by current
high-risk markers? Pediatrics. 1996; 97(4):456-62.
47. Mariani E, Scelsa B, Pogliani L, Introvini P, Lista G. Prognostic value of electroencephalograms in
asphyxiated newborns treated with hypothermia. Pediatr Neurol. 2008; 39(5):317-24.
48. Azzopardi D, Guarino I, Brayshaw C, Cowan F, Price-Williams D, Edwards AD, et al. Prediction of
neurological outcome after birth asphyxia from early continuous two-channel electroencephalography. Early
Hum Dev. 1999; 55(2):113-23.
49. van Rooij LG, Toet MC, Osredkar D, van Huffelen AC, Groenendaal F, de Vries LS. Recovery of amplitude
integrated electroencephalographic background patterns within 24 hours of perinatal asphyxia. Arch Dis Child
Fetal Neonatal Ed. 2005; 90(3):F245-51.
50. ter Horst HJ, Sommer C, Bergman KA, Fock JM, van Weerden TW, Bos AF. Prognostic significance of
amplitude-integrated EEG during the first 72 hours after birth in severely asphyxiated neonates. Pediatr Res.
2004; 55(6):1026-33.
51. Osredkar D, Toet MC, van Rooij LG, van Huffelen AC, Groenendaal F, de Vries LS. Sleep-wake cycling on
amplitude-integrated electroencephalography in term newborns with hypoxic-ischemic encephalopathy.
Pediatrics. 2005; 115(2):327-32.
52. Hellstrom-Westas L, Rosen I. Continuous brain-function monitoring: state of the art in clinical practice.
Semin Fetal Neonatal Med. 2006; 11(6):503-11.
53. Jyoti R, O'Neil R, Hurrion E. Predicting outcome in term neonates with hypoxic-ischaemic encephalopathy
using simplified MR criteria. Pediatr Radiol. 2006; 36(1):38-42.
54. Gunn AJ, Gluckman PD, Gunn TR. Selective head cooling in newborn infants after perinatal asphyxia: a
safety study. Pediatrics. 1998; 102(4 Pt 1):885-92.
55. Thoresen M, Whitelaw A. Cardiovascular changes during mild therapeutic hypothermia and rewarming in
infants with hypoxic-ischemic encephalopathy. Pediatrics. 2000; 106(1 Pt 1):92-9.
56. Azzopardi D, Robertson NJ, Cowan FM, Rutherford MA, Rampling M, Edwards AD. Pilot study of treatment
with whole body hypothermia for neonatal encephalopathy. Pediatrics. 2000; 106:684-94.
57. Gilman JT, Gal P, Duchowny MS, Weaver RL, Ransom JL. Rapid sequential phenobarbital treatment of
neonatal seizures. Pediatrics. 1989; 83:674-8.
58. Fary R, Smith R, editors. RWH Neonatal Pharmacopoeia. 2 ed. Melbourne: Pharmacy Dept, Royal
Women's Hospital Melbourne; 2005.
Page 20 of 25
Appendix A: Sarnat and Sarnat staging system
The staging system proposed by Sarnat and Sarnat in 19764 is often useful in classifying the degree
of encephalopathy. Stages 1, 2, and 3 correlate with the descriptions of mild, moderate, and severe
encephalopathy described in Appendix B: HIE staging.
Stage 1
Stage 2
Stage 3
Hyperalert
Lethargic or obtunded
Stuporous
Muscle tone
Normal
Mild hypotonia
Flaccid
Posture
Mild distal
flexion
Strong distal flexion
Intermittent decerebration
Stretch reflexes
Overactive
Overactive
Decreased or absent
Segmental myoclonus
Present
Present
Absent
Suck
Weak
Weak or absent
Absent
Moro
Strong, low
threshold
Weak, incomplete, high
threshold
Absent
Oculo vestibular
Normal
Overactive
Weak or absent
Tonic neck
Slight
Strong
Absent
Autonomic function
Generalized
sympathetic
Generalized
parasympathetic
Both systems depressed
Pupils
Mydriasis
Miosis
Variable, often unequal,
poor light reflex
Heart rate
Bronchial and salivary
secretions
Gastrointestinal
motility
Tachycardia
Bradycardia
Variable
Sparse
Profuse
Variable
Normal or
decreased
Increased, diarrhoea
Variable
Seizures
None
Common, focal or
multifocal
Uncommon (excluding
decerebration)
Electroencephalogram
findings
Normal
(awake)
Early: low-voltage
continuous delta and theta
Later: periodic pattern
(awake)
Seizures: focal 1-to 1-Hz
spike-and-wave
Early: periodic pattern
with Isopotential phases
Later: totally isopotential
Duration
Less than 24
hours
2 – 14 days
Hours to weeks
Level of consciousness
Neuromuscular control
Complex reflexes
Page 21 of 25
Appendix B: HIE staging
Clinical manifestations and course vary depending on the severity of HIE27
Mild HIE (Stage 1)
•
•
•
Muscle tone may be increased slightly and deep tendon reflexes may be brisk during the first
few days
Transient behavioural abnormalities, such as poor feeding, irritability, or excessive crying or
sleepiness, may be observed
By 3 - 4 days of life, the central nervous system examination findings become normal
Moderate HIE (Stage 2)
•
•
•
•
•
•
The baby is lethargic, with significant hypotonia and diminished deep tendon reflexes
The grasping, Moro, and sucking reflexes may be sluggish or absent
The baby may experience occasional periods of apnoea
Seizures may occur within the first 24 hours of life
Full recovery within 1 - 2 weeks is possible and is associated with a better long-term
outcome
An initial period of well-being or mild HIE may be followed by sudden deterioration,
suggesting ongoing brain cell dysfunction, injury, and death; during this period, seizure
intensity might increase
Severe HIE (Stage 3)
•
•
•
•
•
•
•
•
Stupor or coma is typical. The baby may not respond to any physical stimulus
Breathing may be irregular, and the baby often requires ventilatory support
Generalized hypotonia and depressed deep tendon reflexes are common
Neonatal reflexes (e.g. sucking, swallowing, grasping, Moro) are absent
Disturbances of ocular motion, such as a skewed deviation of the eyes, nystagmus, bobbing,
and loss of "doll's eye" (i.e. conjugate) movements may be revealed by cranial nerve
examination
Pupils may be dilated, fixed, or poorly reactive to light
Seizures occur early and often and may be initially resistant to conventional treatments. The
seizures are usually generalized, and their frequency may increase during the 24 - 48 hours
after onset, correlating with the phase of reperfusion injury. As the injury progresses,
seizures subside and the EEG becomes isoelectric or shows a burst suppression pattern. At
that time, wakefulness may deteriorate further, and the fontanelle may bulge, suggesting
increasing cerebral oedema
Irregularities of heart rate and blood pressure are common during the period of reperfusion
injury, as is death from cardiorespiratory failure
Babies who survive HIE
•
•
The level of alertness improves by days 4 - 5 of life
Hypotonia and feeding difficulties may persist, requiring tube feeding for weeks to months
Multiorgan dysfunction
Multiorgan systems involvement is a hallmark of HIE. Organ systems involved following a hypoxicischaemic event include the following:
•
•
•
•
•
Heart (43 – 78%). May present as reduced myocardial contractility, severe hypotension,
passive cardiac dilatation and tricuspid regurgitation
Lungs (71 – 86%). Babies may have severe pulmonary hypotension requiring assisted
ventilation
Renal (46 – 72%). Failure presents as oliguria and during recovery as high output tubular
failure leading to significant water and electrolyte imbalances
Liver (80 – 85%). Elevated liver function tests, hyperammonemia, and coagulopathy can be
seen. This may suggest possible gastrointestinal dysfunction. Poor peristalsis and delayed
gastric emptying are common, necrotising enterocolitis is rare. Intestinal injuries may not be
apparent in the first few days of life or until feeds are initiated
Haematologic (32 – 54%). Disturbances include increased nucleated red blood cells,
neutropenia, or neutrophilia, thrombocytopenia and coagulopathy. Severely depressed
respiratory and cardiac function and signs of brainstem compression suggest a life
threatening rupture of the vein of Galen (i.e. great cerebral vein) with a haematoma in the
posterior cranial fossa
Page 22 of 25
Appendix C: Management of therapeutic hypothermia
Care system:
• Nurse baby on an open cot that has a radiant warmer. Venous and arterial catheters
should be inserted
Monitoring:
Monitoring throughout the cooling and rewarming period should include:
• continuous invasive blood pressure monitoring
• continuous oxygen saturation
• continuous respiratory monitoring
• continuous electrocardiograph (ECG)
• documented hourly observations including:
o oxygen saturation
o heart rate and blood pressure
o respiration rate
o urine output
• daily investigations (and more frequently if abnormal):
o blood gases, electrolytes, glucose and lactate (may all be obtained from the blood gas
sample)
o full blood count including platelets (which may be sampled from an arterial line)
• continuous amplitude integrated electroencephalography (aEEG) commenced as soon as
possible, if available. This is prognostic and may assist in guiding therapy (treatment of
significant electrical seizures may lessen excitotoxic damage)
Cooling:
Cooling should be started (within 6 hours of birth) after the baby has been assessed and stabilised
and then continued for 72 hours:
• Measure core temperature continuously (for both passive and active cooling) by a
thermistor inserted very gently (using appropriate lubricants ) 5 cm into the rectum and
taped to the thigh
• Lower core temperature to between 33.0 - 34.0 °C7,8,26
• Achieve cooling primarily by exposing the baby to the ambient air temperature which
includes:
o turning the radiant warmer off
o nursing the baby naked with no:
nappy or wraps
sheepskin or water bag
occlusive wrap
o cool packs may be applied as needed:
cool packs (covered with a cotton/other appropriate cover) around 10 °C (taken
from the fridge, NEVER the freezer) may be applied to the back of the neck and
head, and across the torso
• Active cooling should be:
o reduced when the rectal temperature falls below 34.5 °C, by removing one/some/all
cool packs
o stopped when the rectal temperature falls below 34.0 °C, by removing all cool packs
• If the temperature falls below 33.0 °C, manually adjust the heater output on the radiant
warmer to maintain the target rectal temperature greater than or equal to 33.0 °C
• If the baby is ventilated maintain the humidifier temperature at the temperature
recommended by the manufacturer
Sedation/pain relief
If the baby shows any signs of distress (they tend to shiver a lot), consider:
• Morphine or Midazolam (if ventilated)
• Paracetamol (give per rectum, the presence of the rectal thermistor does not inhibit
administration)
Page 23 of 25
Consider ceasing cooling if there is:
• persistent hypoxaemia in 100% oxygen
• life threatening coagulopathy
• an arrhythmia requiring medical treatment (not sinus bradycardia)
Feeding:
No enteral feeds are to be given during cooling
Rewarming:
After 72 hours, re-warming should occur at a rate not exceeding 0.5 °C every 2 hours:
• This may be achieved by nursing the baby on Infant Servo Control (ISC) mode. The
lowest setting that can be achieved on ISC is 34.5 °C, therefore manual heater increases
will need to be carefully managed until ISC settings can be used
• Increase the desired set temperature by 0.1 °C every 20 minutes. This will leave a further
20 minutes within that 2 hour period before needing to resume increasing the set
temperature
• The target rectal temperature is 37 °C
• Babies will take up to 12 hours to rewarm
• Rectal probe measurements may cease after the baby has reached the target rectal
temperature and maintained this temperature with stability for 6 hours
• Prevent rebound hyperthermia which is detrimental. Use of a specific rewarming chart
documenting exact time periods and increments required, may assist in ensuring that the
baby is rewarmed accurately and safely
Cooling risks:
Complications of therapeutic hypothermia are infrequent and symptoms may also be related to the
effects of the original asphyxial insult on all systems.
• There have been no serious adverse effects reported54-56
• Adverse effects which are transient and reversible with warming include26:
o sinus bradycardia
o hypotension requiring inotropic treatment
o increased oxygen requirement
o thrombocytopaenia
Follow up:
• Consider a magnetic resonance imaging (MRI) brain scan at approximately one week of
age
• If the baby dies the value of an autopsy should be discussed with parent(s)
• All babies with grade 2 to 3 HIE, and all babies who have received therapeutic
hypothermia as treatment for HIE, should be enrolled in a long term neurodevelopmental
assessment program
Page 24 of 25
Acknowledgements
The Maternity and Neonatal Clinical Guidelines Program gratefully acknowledge the contribution of
Queensland clinicians and other stakeholders who participated throughout the guideline development
process particularly:
Working Party Clinical Lead
Dr Lucy Cooke, Mater Health Services, Brisbane
Working Party Members
Dr Gary Alcock, Neonatologist, The Townsville Hospital
Glen Alexander, Clinical Nurse Consultant, Logan Hospital
Ms Tanya Beaumont, Acting Clinical Network Coordinator, Central Maternity and Neonatal Network
Ms Maxine Ballinger, Midwife, Rockhampton
Dr David Cartwright, Neonatologist, Royal Brisbane and Women’s Hospital
Greg Coulson, Neonatal Nurse Practitioner, Mackay Base Hospital
Ms Megan Davidson, Midwifery Unit Manager, Mt Isa Hospital
Dr Mark Davies, Neonatologist, Royal Brisbane and Women’s Hospital
Dr Glenn Gardener, Director MFM, Mater Health Services, Brisbane
Dr John Gavranich, Director of Paediatrics, Ipswich
Dr Glenn Harte, Paediatrician, Pindara Private Hospital
Ms Karen Hose, Clinical Nurse Consultant, Royal Brisbane and Women’s Hospital
Dr Derek Jackson, Clinical Nurse, Gold Coast
Dr Pieter Koorts, Neonatologist, Royal Brisbane and Women’s Hospital
Dr David Knight, Director Neonatology, Mater Health Services, Brisbane
Ms Naid Lumsden, Statewide Maternity and Neonatal Clinical Network Coordinator
Ms Naoni Ngenda, Physiotherapist, Royal Brisbane and Women’s Hospital
Ms Michelle Doidge, Centre for Healthcare Related Infection Surveillance and Prevention (CHRISP),
Brisbane
Dr Peter Schmidt, Neonatologist, Gold Coast Hospital
Andrew Shearman, Neonatal Critical Care Scientist, Mater Health Services, Brisbane
Ms Jacqueline Smith, Neonatal Nurse Practitioner, The Townsville Hospital
Ms Mary Tredinnick, Pharmacist, Royal Brisbane and Women’s Hospital
Professor David Tudehope, Neonatologist, Mater Health Services, Brisbane
Dr Tim Warnock, Consultant Paediatrician Child &Youth Health, Far North Queensland
Dr Judy Williams, Paediatrician, Bundaberg
Program Team
Associate Professor Rebecca Kimble, Director, Queensland Maternity and Neonatal Clinical
Guidelines Program
Ms Joan Kennedy, Principal Program Officer, Queensland Maternity and Neonatal Clinical Guidelines
Program
Ms Jacinta Lee, Program Officer, Queensland Maternity and Neonatal Clinical Guidelines Program
Mrs Catherine van den Berg, Program Officer, Queensland Maternity and Neonatal Clinical
Guidelines Program
Steering Committee, Queensland Maternity and Neonatal Clinical Guidelines Program
Page 25 of 25

Hypoxic-ischaemic encephalopathy

Transcription

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