BIRTH ASPHYXIA
Dr.Jacob kuruvilla
INTRODUCTION
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Hypoxic-ischemic encephalopathy (HIE) is an important
cause of brain injury in the newborn and can result in
long-term devastating consequences.
Perinatal hypoxia is a vital cause of long-term neurologic
complications varying from mild behavioural deficits to
severe seizure, mental retardation, and/or cerebral palsy
in the newborn.
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Understanding of hypoxic ischemic injury is handicapped
by the lack of generally accepted definition.
Asphyxia - Impairment of placental or pulmonary gas
exchange resulting in hypoxemia, hypercapnia and a
mixed respiratory and metabolic acidosis
Hypoxia - condition in which the body or a region of the
body is deprived of adequate oxygen supply.
Ischaemia - restriction in blood supply to tissues, causing
a shortage of oxygen and glucose needed for cellular
metabolism (to keep tissue alive)
Neonatal encephalopathy - is a clinical term used to
describe an abnormal neurobehavioral state that consists
of a decreased level of consciousness with abnormalities
in neuromotor tone.
The essence of this is a simultaneous
occurrence of hypoxia and ischemia and the
term hypoxic ischemic insult is now
preferred.
DEFINITION
Hypoxic ischemic encephalopathy(HIE) refers to the CNS
dysfunction associated with perinatal asphyxia.
It is an abnormal neurobehavioral state in which the
predominant pathogenic mechanism is impaired cerebral
blood flow that may result in neonatal death or CNS
dysfunction.
Etiology of HIE
• Maternal:
– Cardiac arrest
– Asphyxiation
– Severe anaphylaxis
– Status epilepticus
– Hypovolemic shock
• Uteroplacental:
– Placental abruption
– Cord prolapse
– Uterine rupture
– Hyperstimulation with
oxytocic agents
• Fetal:
– Fetomaternal hemorrhage
– Twin to twin transfusion
– Severe isoimmune hemolytic
disease
– Cardiac arrhythmia
TIMING OF HIE
20%
Antepartum
35%
Antepartum/
Intrapartum
30%
Intrapartum
10%
Postpartum
INCIDENCE
PATHOPHYSIOLOGY OF HIE
ASPHYXIA-PATHOPHYSIOLOGY
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Intrapartum Asphyxia results in:
– Diminished Oxygen Content in Blood
– Increased Carbon dioxide
– Acidosis
– Decrease blood pressure
Loss of Normal Cerebrovascular auto regulation
resulting in pressure-passive Flow
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Results in decreased perfusion Of brain and
hypoxic neuronal injury
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Following Resuscitation - Repurfusion Injury and
IVH
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MECHANISM OF INJURY
Mechanism of injury following
hypoxia-ischemia
Insults e.g.
Asphyxia
Impaired
perfusion
Opportunity for
neuronal
rescue
Primary
neuronal
death
Cytotoxic mechanisms
Delayed
neuronal Death
/Reperfusion
Injury
CLINICAL FEATURES & DIAGNOSIS :
ANTEPARTUM
-Fetal distress : if fetal distress detected it cannot be
assumed that the insult has occurred during labor .
A fetus that has sustained a hypoxic –ischemic insult before
labor may not be able to mount the normal physiological
coping responses during labor .
CLINICAL FEATURES & DIAGNOSIS :
INTRAPARTUM
Apgar scores : prolonged depression of Apgar is related to
major neurological disability .
APGAR Score:
Total Score = 10
score 7-10 normal
score 5-6 mild birth asphyxia
score 3-4 mod. birth asphyxia
score 0-2 severe birth asphyxia
●The problems with using Apgar score as a marker of HIE
are:
●Apgar score may be low because of causes other than
birth asphyxia, e.g. prematurity, maternal sedation,
neuromuscular disorder, etc.
●Apgar score has a poor correlation with the long term
outcome. However, the extended Apgar score recorded 20
minutes after birth has much better specificity for the
prediction of both early death and disability
● A low 1 or 5-minute Apgar score alone does not correlate
with the infant’s future outcome
CLINICAL FEATURES & DIAGNOSIS
:INTRAPARTUM
Acidosis : is associated with poor outcome in combination
with abnormal fetal heart rate pattern, depressed apgar
scores and encephalopathy
Sarnat Clinical Stages of Perinatal Hypoxic
Ischemic Brain Injury
Sarnat Clinical Stages of Perinatal Hypoxic
Ischemic Brain Injury
Hematologic (32-54%)
Disturbances include increased nucleated RBCs,
neutropenia or neutrophilia, thrombocytopenia,
and coagulopathy. Severely depressed
respiratory and cardiac functions and signs of
brainstem compression suggest a lifethreatening rupture of the vein of Galen (ie,
great cerebral vein) with a hematoma in the
posterior cranial fossa.
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Infants who survive severe hypoxic-ischemic
encephalopathy
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The level of alertness improves by days 4-5
of life.
Hypotonia and feeding difficulties persist,
requiring tube feeding for weeks to months.
Exclusion of alternative causes of Neonatal
Encephalopathy
INVESTIGATIONS
Study
Serum electrolyte
Markedly low serum sodium, potassium, and chloride levels in the
presence of reduced urine flow and excessive weight gain may
indicate acute tubular damage or (SIADH) secretion, particularly
during the initial 2-3 days of life.
Renal function
Serum creatinine levels, creatinine clearance, and BUN levels
Cardiac & liver enzymes
Assess the degree of hypoxic-ischemic injury to other organs
Coagulation system
Prothrombin time, partial thromboplastin time, and fibrinogen levels.
ABG
Assess acid-base status and to avoid hyperoxia and hypoxia as well as
hypercapnia and hypocapnia.
To correct acidosis
Others
Screen for infection (± lumbar puncture), Tests for congenital
infection ,Investigation for metabolic or genetic disorders, lactate,
pyruvate
Imaging studies:- Cranial USG
-Convenient, noninvasive, relatively low-cost and non –
radiation screening examination of the hemodynamically
unstable neonate at the bedside.
-Doppler study and resistive index (RI) provide additional
information on cerebral perfusion.
-Sustained asphyxia & ICH or diffuse cerebral edema results in
increased RI and is indicative of a poor outcome .
Cranial MRI
- The most sensitive and specific imaging technique for
examining infants with suspected hypoxic-ischemic brain injury.
- Hypoxic-ischemic injury (deep grey matter,cortex)demonstrates
characteristic T1 hyperintensity and variable T2 intensity.
- Ischemic injury generally results in T1 hypointensity &T2
hyperintensity (white matter)due to ischemia-induced edema.
Standard EEG
- Generalized depression of the background rhythm and
voltage, with varying degrees of superimposed seizures,
are early findings.
MANAGEMENT
Clinical management is primarily supportive and is
dependent on the extent of organ compromise. High level
evidence supports the use of therapeutic hypothermia for
the treatment of moderate to severe cases of HIE;
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
Monitoring :
1) Vitals parameters
2) Accurate record of the urine output
3) If required blood gases analysis can be done .
4) Periodic blood biochemistry such as:
5) Blood sugar charting (2 hourly x 2 ,then 4 hrly on
the 1st day and 6 hrly thereafter .
6) Hematocrit – (6 to 8 hrly for the first 2 days ,the
once a day)
7) Serum sodium,potssium and calcium (once a day).
8) Assessment of the of sensorium,tone,seizures
autonomic disturbances and reflexes should be done
every 4 to 6 hours
MANAGEMENT-LABOUR ROOM
Resuscitation
Appropriate and timely resuscitation is required to prevent
hypoxia, hypercarbia and acidosis. This may prevent or reduce
the clinical severity of HIE.
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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 birth.
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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)
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Blood samples taken for acid base status remain stable in a
plastic syringe for up to 30 minutes before analysis
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MANAGEMENT-NICU
CARDIORESPIRATORY
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.
Assessment should include:
• Assessment of peripheral perfusion
• Establishment of whether hypotension is symptomatic of another
problem including
-Sepsis
-Hypovolaemia or blood loss.
-High mean airway pressure on mechanical ventilation
The need for intravenous crystalloid boluses (10 mL/kg of 0.9% Sodium
Chloride) if:
– Perfusion is poor (capillary refill greater than 3 seconds)
– Blood gas lactate is not improving
– Mean blood pressure is less than 35 - 40 mmHg
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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 hypoxicischaemic insult.
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If hypotension persists or low flow states are identified on ECHO
consider inotropic therapy including:
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– Dopamine or Dobutamine
– Inotropes should preferably be administered via an appropriately
positioned catheter in a central vein (e.g. umbilical venous
catheter positioned above the ductus venosus).
– A dedicated intravenous line is preferred. Never give inotropes
into an arterial line
INFECTION
Perinatal infection may co-exist with HIE. All babies should
have:
A full blood count (FBC)
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Blood cultures
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Intravenous antibiotics (Penicillin (Benzylpenicillin,
Ampicillin or Amoxicillin)) and Gentamicin) as soon as
possible after birth.
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Fluid, electrolyte and acid base Management
Hypoglycaemia
●Perform an early blood glucose level and correct hypoglycaemia.
Babies with Stage 2 to 3 HIE will require intravenous glucose
administration
●Acidosis
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Perform early arterial blood gas and correct
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Respiratory acidosis (hypercarbia and acidosis) with
appropriate ventilatory support
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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
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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.
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There is no convincing evidence that administration of Sodium
Bicarbonate produces long term benefits in this situation.
VOLUME
Many restrict maintenance fluids to 40 – 50 mL/kg/day until a
urine output equal to 1 mL/kg/hr has been established.
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Fluid restriction is recommended to avoid fluid overload and
cerebral oedema, however no RCTs address the use of fluid
restriction following perinatal asphyxia.
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There is concern that fluid restriction may cause dehydration
and hypotension decreasing cerebral perfusion and causing
further brain damage.
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Monitor serum sodium trends to gauge whether more or less
fluids are needed.
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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:
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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) 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 MANAGEMENT
•Therapeutic hypothermia (cooling) following
a hypoxic-ischaemic insult can benefit certain
babies and is now considered standard care
•For cooling to provide benefit:
•It must be commenced within 6 hours of birth
before secondary reperfusion injury begins.
SEIZURE MANAGEMENT
HIE is the most common cause of early onset neonatal
seizures.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 hypoxicischaemic brain injury
• Electrolyte abnormalities and multi system complications may coexis
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
• 30-90% of seizures are subclinical and up to 50% of clinical seizures
may not be detected
• 66% of electrographic seizures do not have overt clinical signs
• Anticonvulsants may not treat electroencephalographic seizures
even if effective for clinical seizure activity
• 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 .Recommended
anticonvulsant therapy includes:
o Phenobarbitone (first line treatment)
o Phenytoin
o Midazolam
o Clonazepam
GIT SYMPTOMS MANAGEMENT
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:
Breast milk is preferable
Feeds should be introduced gradually
PHOTOTHERAPY
Most often the babies will present with hyperbilirubinemia so Phototherapy will be required.
Hyper-bilirubinemia due to:
-Lack of feeding
-Liver injury
-Increased hemolysis
-hypotension
- Supportive Care in Patients with Hypoxic-ischemic
Encephalopathy
- Most infants with severe hypoxic-ischemic encephalopathy need
ventilatory support during first days of life.
- The role of mechanical ventilation is to maintain the blood gases and
acid-base status in the physiological ranges and prevent hypoxia,
hyperoxia, hypercapnia, and hypocapnia.
Important point in ventilator seting is to avoid hyperoxia (inc o2 free
radicals) and hypocapnia (dec. Cerebral perfusion)
- Infants with hypoxic-ischemic encephalopathy are also at risk for
pulmonary hypertension and should be monitored. Nitric oxide (NO) may
be used according to published guidelines.
Cerebral Palsy & HIE
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There has been considerable debate regarding the
contribution of HIE to the prevalence of Cerebral
Palsy
Incidence of cerebral palsy is largely unchanged
despite increasing obstertric intervention and better
obstetric care.
It has been suggested that the brain have been
significantly impaired by the events during pregnancy
and birth asphyxia is just a final insult making a
relatively small contribution to the burden of damage
- Intrapartum asphyxia may be first
presentation of cerebral palsy if this
prenatal insult impairs the ability of the
fetus to cope with physiological stress
of labor
- It is postulated that If the asphyxia is severe
enough to cause brain injury, it often causes
multi organ failure leading to neonatal
death.
PREDICTORS OF OUTCOME
The presence of one or more of the following features has been
found to be a predictor of poor neurodevelopmental outcome
in the long term.
1. Failure to establish respiration by 5 minutes of life
2. Apgar score of 3 or less at 5 minutes
3. Onset of seizures with in 12 hours
4. Refractory seizures
5. Stage III HIE
6. Persistent oliguria ( <1 ml/kg/hr) for the first 36 hrs of life
7. Inability to establish oral feeds by 1 wk
8. Abnormal EEG & failure to normalize by D7
9. Abnormal CT, MRI, MRS in neonatal period
REFERENCES
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Roberton’s textbook of Neonatology 4th edition
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Avery Disease of Newborn
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Manual of newborn Care Cloherty et al seventh Edition
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NNF guidelines
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AIIMS WHO Neonatology protocols
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Care of newborn : Meharban Singh
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Queensland Maternity and Neonatal Clinical GuidelineHypoxic ischaemic encephalopathy (2010)