3. Asphyxia
Deprivation of oxygen to a newborn that lasts long enough
during the birth process to cause damage to the brain.
- Inadequate tissue perfusion
- Failure to meet the metabolic demands of the tissue
= inadequate oxygen supply and waste removal
4. Asphyxia
In the first minutes following birth:
….if the newborn does not expand its lungs and
establish effective ventilation and perfusion:
• Arterial blood PO2↓
• Arterial blood PCO2↑
• pH↓
Importance of First Breath!
5. Asphyxia leads to….
• Persistence of the fetal circulatory pattern:
- High Pulmonary vascular resistance
- Ductus arteriosus remains wide open with a right to left
shunt
• Once the process has started:
- self-perpetuating with progressive acidosis
- increasing and persistent pulmonary vascular constriction
• The central event: pulmonary vascular constriction in
response to hypoxia and acidosis…..in response to not
breathing
6. Asphyxia: Cause and Consequence
• Deprivation of oxygen to a newborn that lasts long enough during the birth
process to cause damage to the brain.
• Hypoxia can also damage heart, lungs, etc.
• But brain damage is the most severe and the least likely to recover
completely.
• If she survives, the damage to the brain can cause either
a. mental problems, such as developmental delay or mental retardation, or
b. physical problems, such as spasticity.
• Note!! Spastic diplegia and the other forms of cerebral palsy almost
always feature asphyxiation during the birth process as a major factor.
7. Epidemiology
• Birth asphyxia is the cause of 23% of all neonatal deaths
worldwide.
• It causes 920,000 neonatal deaths every year and is associated
with another 1.1 million intrapartum stillbirths.
• More than a million “survivors” develop problems such as
cerebral palsy, mental retardation, learning difficulties, and
other disabilities.
9. High Risk for Asphyxia
Maternal Labor/Delivery Fetal Conditions
Primigravida >35yrs Instrumented delivery Prematurity
Diabetes Breech, abnormal posit Postmaturity
Hypertension, Renal Dx Cesarean section Multiple gestation
Anaemia Hb<10g/dl Prolonged labour Acidosis
Abruptio, placenta
praevia, antepartum
haemorrhage
Prolapse of umbilical cord Abnormal fetal heart rate or
rhythm
Alcohol and drugs Cord compression Meconium stained liquor
Previous neonat. death Maternal hypotension Polyhydramnios
Prolonged rupture of
membranes
Sedatives given IUGR, Macrosomia, Fetal
malformations
10. Fetal Distress
• Can be determined by a partograph.
• Partograph: synchronous recording of uterine contractions
and fetal heart rate.
11. Prognosis
• Fetal cardiotocograph (CTG) may be abnormal, but is
poor at assessing the severity of asphyxia unless it is
profound.
• However, when normal, the CTG is highly predictive of
the absence of asphyxia problems in the neonate.
• Fetal blood sampling or cord blood analysis may
identify a metabolic acidosis, but is also poor at
predicting neonatal outcome unless the acidosis is very
severe.
• Low Apgar scores at 1 and 5 minutes, reflecting
delayed onset of respiration and circulatory failure at
birth, are also poor at predicting outcome, but if the
score remains low (5 or less) at 10 minutes of age, the
risk of long-term disability or mortality is nearly 50%.
12. Anticipation of the need for
resuscitation...
• For many babies the need for resuscitation
cannot be anticipated before delivery.
• Therefore, be prepared for resuscitation
at every delivery!!!
13. Apgar score
Score
Sign 0 1 2
Heart rate Absent Slow <100 >100 per min
Respiration Absent Slow,
irregular
Good, crying
Muscle tone limp Some flexion Active flexion
Reflex
response
No response grimace Cough,
sneeze
Color Blue, pale Blue hands,
pink body
Completely
pink
14. APGAR
• Low 1 minute Apgar score: reflects intrapartum problems.
• Low 5 minute Apgar score: reflects failure to establish
ventilation and circulation immediately.
• Low 10 minute Apgar score: indicates failure of early
resuscitation.
15. Classical pattern:
• After a short period of fast breathing, apnoea sets in (primary
apnoea).
• During primary apnoe the heart rate also falls (bradycardia),
muscle tone decreases (floppy child).
• If asphyxia continues, the heart rate falls further, blood
pressure falls, hypotonia worsens – and a series of deep gasps
occurs.
• The gasps get slower, irregular, stop…… this is the secondary
apnoea.
16. Pathophysiology in the newborn
• Brain hypoxia and ischemia:
1. due to systemic hypoxemia (ventilation)
2. and reduced cerebral blood flow (CBF) (perfusion)
• Hypoxic tissues begin anaerobic metabolism and produce
metabolic acids.
• When bicarbonate to buffer acids is not adequately available,
acidosis occurs (lactic acidosis).
17. Initial compensatory adjustment….
When the newborn is not breathing..
• Increase in cardiac output.
• Redistribution of cardiac output (essential
organs): brain, heart, and adrenal glands.
• Blood pressure (BP) increase (due to release of
epinephrine) further enhances this compensatory
response. Attempt to keep up perfusion pressure
in vital organs.
• With prolonged asphyxia and failure of
compensatory mechanisms, cerebral blood flow
falls, leading to ischemic brain injury.
18. Cerebral Blood Flow
• CBF is maintained at a constant level despite a wide range in
systemic BP - cerebral autoregulation.
• If the early compensatory adjustments fail, the CBF can
become pressure-passive, i.e. brain perfusion depends on
systemic BP.
• If BP then falls, CBF falls below critical levels and brain injury
occurs.
19. Consequences of reduced cerebral
blood flow:
Intracellular energy failure.
• During the early phases of brain injury: brain
temperature drops, release of neurotransmitters
(gamma-aminobutyric acid transaminase
(GABA).
• This reduces cerebral oxygen demand,
transiently minimizing the impact of asphyxia.
• The magnitude of the final neuronal damage
depends on duration and severity of the initial
insult plus reperfusion injury.
20. Reperfusion
• During the reperfusion period, free radical
production increases due to activation of
enzymes (cyclooxygenase, xanthine oxidase).
• Free radicals can lead to lipid peroxidation as
well as DNA and protein damage and can
trigger apoptosis.
• Finally, free radicals can combine with nitric
oxide (NO) to form peroxynitrite, a highly toxic
oxidant.
21. Secondary energy failure
• Following the initial phase:
• Cerebral metabolism may recover following
reperfusion, only to deteriorate in a secondary
energy failure phase.
• This new phase starts at about 6-24 hours after the
initial injury.
• The damage increases over next 24-48 hours and
then starts to resolve thereafter.
• In the infant, the duration of this phase is correlated
with adverse neuro-developmental outcomes.
22. Abnormal neuro-
developmental outcomes
a. Mortality rate ↑
b. Neuro-developmental outcomes:
• Mental development index (MDI)
• Psychomotor development index (PDI)
• Disabling cerebral palsy
• Epilepsy
• Blindness
• Severe hearing impairment
• Probably Attention Deficit Hyperactivity disorders
23. non predictive values………
• Abnormal fetal heart rate patterns, prolonged
labor, meconium-stained fluid, a low 1-minute
Apgar score have no predictive value for long-term
neurologic injury – if the child is without signs of
encephalopathy and seizures after birth.
• It is important to provide proper resuscitation,
support the newborn, and allow time for
evaluation - always.
24. Hypoxic-ischaemic
encephalopathy (HIE) Clinical
Presentation
• Describes the clinical manifestation of brain
injury starting immediately or up to 48 hours
after asphyxia, whether antenatal,
intrapartum or postnatal.
• Mild HIE
• Moderate HIE
• Severe HIE
25. Mild hypoxic-ischemic
encephalopathy
• Muscle tone: slightly increased, deep tendon
reflexes brisk during the first few days.
• Transient behavioral abnormalities: poor feeding,
irritability, or excessive crying or sleepiness.
Responds excessively to stimulation.
• May have staring of the eyes and hyperventilation
• Findings normalize within 2 days of life.
26. Moderately severe HIE
• The newborn shows marked abnormalities of tone and
movement:
• Lethargy, with significant hypotonia and diminished deep
tendon reflexes.
• The grasping, Moro, and suckling reflexes sluggish or
absent. Unable to feed
• Apneas.
• Seizures may occur within the first 24 hours of life.
• Full recovery within 1-2 weeks is possible.
Better long-term outcome.
Cave: An initial period of mild hypoxic-ischemic
encephalopathy may be followed by sudden
deterioration.
27. Morbidity
Surviving moderately severe hypoxic-ischemic
encephalopathy:
• 30-50% serious long-term complications
• 10-20% have minor neurological morbidities.
Infants with mild hypoxic-ischemic encephalopathy
tend to be free from serious CNS complications
28. Severe hypoxic-ischemic
encephalopathy
• Coma is typical. No response to any physical stimulus.
• Breathing irregular, often requires ventilatory support.
• No normal spontaneous movements or response to
pain. Generalized hypotonia and depressed deep
tendon reflexes.
• Neonatal reflexes (sucking, swallowing, grasping,
Moro) absent.
• Disturbances of ocular motion (deviation of the eyes,
nystagmus, loss of "doll's eye" movements).
• Pupils may be dilated, fixed, or poorly reactive to light.
29. Severe…
• Seizures occur early, resistant to treatment;
frequency increases during the 24-48 hours (second
day) - phase of reperfusion injury.
• The fontanels may bulge (cerebral edema).
• Irregularities of heart rate and blood pressure (BP) are
common during the period of reperfusion injury, as is
death from cardio-respiratory failure.
30. Infants who initially survive
severe hypoxic-ischemic
encephalopathy…
• The level of alertness improves by days 4-5 of
life.
• Hypotonia and feeding difficulties persist,
requiring tube feeding for weeks to months.
31. Other Organs affected
• Heart
Myocardial contractility ↓, severe hypotension.
• Lungs
Severe pulmonary hypertension.
• Renal
Renal failure: oliguria; water and electrolyte imbalances.
• Liver
Liver enzymes↑, hyperammonemia, coagulopathy.
Peristalsis↓, gastric emptying↓. Unable to be fed.
• Hematologic
Neutropenia or neutrophilia, thrombocytopenia, and
coagulopathy.
32. Mortality/Morbidity
• Some infants with severe neurologic disabilities die
early (e.g. from aspiration pneumonia).
• As many as 80% of infants who survive severe
hypoxic-ischemic encephalopathy develop serious
complications, 10-20% develop moderately serious
disabilities, few are relatively healthy.
33. Assessment of the Newborn
with Birth Asphyxia
• Observation of posture and spontaneous
movements. Asymmetry is a subtle sign of
hemiparesis; focal features are abnormal.
• Moro reflex : asymmetry is seen in peripheral
lesions (e.g. brachial plexus injury).
• Total absence or paucity of spontaneous
movements with no reaction to painful stimuli and
generalized hypotonia, indicates brainstem
dysfunction or severe diffuse cortical damage.
34. Spasticity
• Spasticity: commonly in the distal parts of the extremities.
• All fingers are flexed with the thumb under the second to fifth fingers
(cortical thumbs).
• Sustained ankle clonus (more than 5-10 beats).
• However: the initial motor manifestation will be flaccid hypotonia
with spasticity later developing.
35. Hypotonia
• When assessing muscle tone, consider state of
arousal and prematurity.
• The infant looks like a “rag doll” when supported
by a hand under the chest (vertical and horizontal
suspension).
• Head lag is demonstrated by traction of the hands
in a supine position.
36. Tone and Posturing
• Increased axial extensor tone with arching of the back and neck
extension = opisthotonus.
• Early sign of spasticity:
scissoring = extreme hip adduction with stimulation
or crying.
37. Seizures
• HIE is the most frequent cause of neonatal seizures.
• Usually 12-24 hours after birth,
• Difficult to control with anticonvulsants.
• Seizures are often focal or multifocal.
• Observation often reveals clonic rhythmic
contractions. (Note: Limb flexion or extension does
not suppress the clonic seizure, unlike jitteriness and
benign myoclonus).
• Newborns don't have generalized seizures due to
immaturity of the neuronal pathways connecting
both halves of the brain.
41. Management
• Skilled resuscitation and stabilization of asphyxiated
newborns will minimize brain damage.
• Respiratory support.
• Treatment of clinical seizures with anticonvulsants.
• Fluid restriction because of transient renal
impairment
• Treatment of hypotension by volume and inotropic
support
• Monitoring and treatment of hypoglycaemia and
electrolyte imbalance.
42. Perfusion and Blood Pressure
Management
• Mean blood pressure (BP) above 35-40 mm Hg
is necessary to avoid decreased cerebral
perfusion. Hypotension is due to myocardial
dysfunction, capillary leak syndrome, and
hypovolemia;
• Hypotension should be promptly treated.
Dopamine or dobutamine can be used to
achieve adequate cardiac output in these
patients.
43. Treatment of Seizures
• Self-limited, only first days of life; but may
compromise ventilation, oxygenation, and blood
pressure (early death).
• Seizures: contribute to brain injury, increase the risk
of subsequent epilepsy.
• Drugs: phenobarbitone, phenytoin, and
benzodiazepines. Phenobarbitone effective in only
up to 50%, Phenytoin additional 15% efficacy.
• Benzodiazepines(diazepam or lorazepam)have
additional efficacy.
• Prophylactic phenobarbitone debatable!
44. Hypothermia Therapy
• Extensive experimental data: mild hypothermia (3-
4°C below baseline temperature) applied within a
few hours (no later than 6 h) of injury is
neuroprotective.
• Possible mechanisms include
(1) reduced metabolic rate and energy depletion;
(2) decreased excitatory transmitter release;
(3) reduced alterations in ion flux;
(4) reduced vascular permeability, edema, and
disruptions of blood-brain barrier function.
45. Clinical aspects of therapeutic
hypothermia
• Inclusion criteria:
• 36 weeks gestation or more; birth weight 2000 g or more, younger
than 6 hours at admission
• Apgar score of 5 or less at 10 minutes after birth, or severe acidosis
pH<7, or continued need for resuscitation at 10 minutes after birth
• Clinically :
Lethargy, coma; abnormal tone; abnormal reflexes; absent
spontaneous activity; autonomic dysfunction [including
bradycardia, abnormal pupils, apneas]; and clinical evidence of
seizures.
46. Feeding
• Moderately severesevere hypoxic-ischemic encephalopathy):
nothing by mouth (NPO) during the first 3 days of life or until
alertness improves.
• Enteral feeds should be carefully initiated (about 5 mL every 3-
4 h). Infants should be monitored carefully for signs and
symptoms of necrotizing enterocolitis.
47. Outpatient Care
• Goal: to detect impairments and promote early
intervention.
• Growth parameters including head circumference.
• Abnormal neurologic findings or feeding difficulties:
intensive follow-up.
• Ophthalmologist: routine.
• Hearing testing in infants at risk for hearing loss.
• Infants with mild hypoxic-ischemic encephalopathy
generally do well; require no specialized follow-up.
48. Prognosis
• Most helpful criteria:
• Lack of spontaneous breathing within 20-30 minutes
of birth is almost always associated with death.
• The presence of seizures: an ominous sign, particularly
if frequent and difficult to control.
• Abnormal neurological findings persisting after 7-10
days indicate poor prognosis (hypotonia, rigidity,
weakness).
• Persistent feeding difficulties (abnormal sucking and
swallowing): significant CNS damage.
• Poor head growth during the first year of life: sensitive
parameter in predicting neurologic deficit.
