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Perinatal Asphyxia
By Dr. Abu Bakarr Kanu
Outline
• Review of foetal circulation
• Definition of terms
• Pathophysiology
• Risk factors/Causes
• Assessment
• Investigations
• Complications
• Management
• Questions & feedback
Review of foetal circulation
DISCUSSION………………
Ductus Venosus
Patent Foramen
Ductus Arteriosus
Definition
• A condition in the newborn where there is reduced oxygen saturation
(hypoxaemia) and increased acid in blood (acidaemia) from CO2
retention and lactic acid accumulation.
• The newborn fails to initiate and sustain breathing after birth.
• Hypoxic-ischaemic encephalopathy (HIE) –
• abnormal neurobehavioural state in which the predominant
pathogenic mechanism is impaired cerebral blood flow.
Risk factors
• Impairment of maternal oxygenation
• Decreased blood flow from mother to the placenta
• Impaired gas exchange across the placenta
• Decreased blood flow from placenta to the fetus
• Impaired gas exchange at the fetal tissue level
• Increased foetal oxygen requirement
Aetiology/Predisposing factors
1. Maternal (Prenatal) Factors
• Infection – chorioamnionitis
• Lungs – Pneumonia, Asthmatic attack etc.
• Cardiac – Arrhythmias, heart failure etc.
• Vascular –
• Anaemia due to haemoglobinopathy, poor nutrition & leukaemia
• Diabetes mellitus – due to arteriosclerosis
• Hypertension - due to arteriosclerosis
• Hypoperfusion
Aetiology/Predisposing factors contd.
• Uterus
• Uterine hypertonia
• Malformations
• Uterine rupture
• Others
• Narcotics – via respiratory depression in mother of direct effect on the
baby
• Anaesthetic agent
• Alcohol
Aetiology/Predisposing factors contd.
2. Placental problems
• Abruptio placenta
• Placenta praevia
• Placental insufficiency
3. Foetal factors
• Prematurity – affect respiratory centre
• Postmaturity – due to placental insufficiency
• Developmental anomalies - Diaphragmatic hernia, Hypolplasia, Choanal atresia
• Cord problems : Knotting, compression or Prolapse
• Infection : Congenital
Aetiology/Predisposing factors contd.
4. Delivery factors
• Delayed second stage e.g. prolonged obstructed labour.
• Placental insufficiency
Assessment
• Done using the APGAR score.
• APGAR score is assessed at 1 & 5 minutes though it may be extended to
assess the extent of resuscitation required.
a) 1 minute: To determine the amount of resuscitation.
b) 5minutes: To prognosticate (especially on brain)
If it is low after 5 minutes, the child is likely to have long term sequelae.
APGAR SCORE
Score 0 1 2
Appearance/
colour
Pale or central
cyanosis
Peripheral
cyanosis
Completely pink
Pulse rate /Heart rate Absent < 100 b/min > 100b/min
Grimace/
Irritability
None Grimace Cry /sneezing
Activity
/Muscle tone
Flaccid Some flexion Well flexed
Respiration Absent Weak irregular Regular
Maximal score = 10
Practice
• As the intern oncall in labour ward you were informed that a teenage girl with
severe eclampsia just delivered a baby who is
• limp,
• gasping,
• has blue hands and lips and
• makes no response to stimulation
• had a HR of 120 beats/min by the 1st minute of life.
• You got there by the 5th minute and noted that the baby was now
• breathing normally,
• lips were pink but
• the nurses said all other findings were as before.
• What is this baby’s Apgar score at 1&5mins?
GRADING
Score Grade Management
≥ 7 Resguires no active resuscitation
6 Mild birth asphyxia Suctioning
4 – 5 Moderate birth asphyxia  More suctioning, but avoid
vigorous suctioning to avoid
vagal reflex
 Oxygen by face mask,
occasionally bag & mask
1 – 3 Severe Birth Asphyxia  Clearing of airways
 Endotracheal intubation &
ventilation by bag and mask
Investigations
• Fetal heart rate monitoring
• Fetal scalp blood pH
• Cardiotocography –to assess FHR variability
• Arterial blood gases
• E/U/Cr
• ECG
• Other ancillary investigations as required
Complications
1.Central Nervous system
• Hypoxic IschaemicEncephalopathy (HIE)
• Seizures
• Hypotonia
• Mental retardation
• Learning disability
• Speech disorders
• Cerebral palsy (spastic diplegia, spastic quadriparesis)
• Syndrome of InappropiateADH secretion (SIADH)
• Intracranial haemorrhage
Spastic Diplegia- Usually seen in preterm infants as a result of the high
incidence of IVH & periventricular leukomalacia.
Complications (2)
• Respiratory System
• Respiratory distress syndrome
• Persistent pulmonary hypertension
• Cardiovascular System
• Left ventricular dysfunction -due to myocardial ischaemia
• Patent ductus arteriosus
• Cardiogenic shock
Complications(3)
• Renal
• Acute tubular necrosis –causing haematuria
• Acute cortical necrosis
• Haematuria
• Gastrointestinal
• Necrotising enterocolitis –due to ischaemia which causes bacterial
proliferation
• Liver dysfunction
Complications(4)
• Haemopoeitic
• DIC –due to generalized hypoxia
• Increased risk of infection
• Metabolic
• Hypo or hyperglycaemia
• Hyponatraemia –from renal failure
• Hypocalcaemia
• Acidosis
Hypoxic Ischaemic Encephalopathy
• Most feared complication of perinatal asphyxia
• Impacts on long term neurodevelopmental outcomes
• It is clinically staged by doing a sequential, systematic evaluation of
brain injury
• Sarnat staging commonly used
Level of consciousness
Muscle tone
Tendon reflexes
Seizures
Irritable / hyperalert
Normal or hypertonia
Increased present
Absent
Suck
Moro
Grasp
Oculocephalic (Doll’s eye)
Active
Exaggerated
Normal to exaggerated
Normal
Pupils
Respirations
Heart rate
EEG
Dilated, reactive
Regular
Normal or tachycardia
Normal
Prognosis Good
Sarnat staging of hypoxic – ischemic encephalopathy
Grade 1 (mild)
Level of consciousness Lethargy
Muscle tone Hypotonia
Tendon reflexes Increased
Seizures Present
Suck Weak
Moro Incomplete
Grasp Exaggerated
Oculocephalic (Doll’s eye) Overactive
Pupils Constricted, reactive
Respirations Periodic
Heart rate Bradycardia
EEG Low – voltage periodic
or paroxysmal
Prognosis Variable
Coma
Flaccid
Depressed or absent
Absent
Absent
Absent
Absent
Reduced or absent
Variable or fixed
Ataxic, apnoeic
Bradycardia
Periodic or isoelectric
High mortality and neurologic
disability
Grade 2 (moderate) Grade 3 (severe)
Sarnat staging of hypoxic – ischemic encephalopathy
Management
• Treatment is supportive
• Anticipate need for neonatal resuscitation from maternal obstetric
and labour history (including CTG tracing)
• Maintain breathing and circulation
• Avoid:
• Hypo-or hyperventilation (keep PaC02 in the normal range)
• Hypoxemia
• Hypotension
Management contd.
• Give inotropes for hypotension or myocardial dysfunction
• Maintain normal blood glucose, calcium and magnesium
• Correct metabolic acidosis
• Restrict fluid intake and monitor urine output
• Control seizures
• Avoid overheating, re-warm slowly if hypothermic
• Nutritional support
• Family support
Outcome
• In general:
• A normal neurologic exam and feeding well by 2 weeks of age suggest
good prognosis.
• Mild HIE
• usually normal outcome.
• Moderate HIE
• increased risk for motor and cognitive abnormalities, including cerebral
palsy.
• Severe HIE
• mortality rate 75%.
• 80% of survivors will have neurologic sequelae.
Poor prognostic features
• Persistence of clinical seizures
• Persistently abnormal neurologic exam
• Not feeding orally by 2 weeks of age
• EEG with burst suppression or isoelectric pattern on any day
• Abnormal basal ganglia or marked brain atrophy on MRI
• Poor postnatal head growth
By now we should have…………..
• Reviewed the foetal circulation
• Learnt some related terms
• Listed some risk factors/causes of perinatal asphyxia
• Learnt the parameters of the APGAR score and its application in
perinatal asphyxia
THANKS FOR YOUR ATTENTION
?

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5 Perinatal Asphyxia.pptx9999999999999999999999999999999

  • 1. Perinatal Asphyxia By Dr. Abu Bakarr Kanu
  • 2. Outline • Review of foetal circulation • Definition of terms • Pathophysiology • Risk factors/Causes • Assessment • Investigations • Complications • Management • Questions & feedback
  • 3. Review of foetal circulation DISCUSSION………………
  • 5. Definition • A condition in the newborn where there is reduced oxygen saturation (hypoxaemia) and increased acid in blood (acidaemia) from CO2 retention and lactic acid accumulation. • The newborn fails to initiate and sustain breathing after birth. • Hypoxic-ischaemic encephalopathy (HIE) – • abnormal neurobehavioural state in which the predominant pathogenic mechanism is impaired cerebral blood flow.
  • 6. Risk factors • Impairment of maternal oxygenation • Decreased blood flow from mother to the placenta • Impaired gas exchange across the placenta • Decreased blood flow from placenta to the fetus • Impaired gas exchange at the fetal tissue level • Increased foetal oxygen requirement
  • 7. Aetiology/Predisposing factors 1. Maternal (Prenatal) Factors • Infection – chorioamnionitis • Lungs – Pneumonia, Asthmatic attack etc. • Cardiac – Arrhythmias, heart failure etc. • Vascular – • Anaemia due to haemoglobinopathy, poor nutrition & leukaemia • Diabetes mellitus – due to arteriosclerosis • Hypertension - due to arteriosclerosis • Hypoperfusion
  • 8. Aetiology/Predisposing factors contd. • Uterus • Uterine hypertonia • Malformations • Uterine rupture • Others • Narcotics – via respiratory depression in mother of direct effect on the baby • Anaesthetic agent • Alcohol
  • 9. Aetiology/Predisposing factors contd. 2. Placental problems • Abruptio placenta • Placenta praevia • Placental insufficiency 3. Foetal factors • Prematurity – affect respiratory centre • Postmaturity – due to placental insufficiency • Developmental anomalies - Diaphragmatic hernia, Hypolplasia, Choanal atresia • Cord problems : Knotting, compression or Prolapse • Infection : Congenital
  • 10. Aetiology/Predisposing factors contd. 4. Delivery factors • Delayed second stage e.g. prolonged obstructed labour. • Placental insufficiency
  • 11. Assessment • Done using the APGAR score. • APGAR score is assessed at 1 & 5 minutes though it may be extended to assess the extent of resuscitation required. a) 1 minute: To determine the amount of resuscitation. b) 5minutes: To prognosticate (especially on brain) If it is low after 5 minutes, the child is likely to have long term sequelae.
  • 12. APGAR SCORE Score 0 1 2 Appearance/ colour Pale or central cyanosis Peripheral cyanosis Completely pink Pulse rate /Heart rate Absent < 100 b/min > 100b/min Grimace/ Irritability None Grimace Cry /sneezing Activity /Muscle tone Flaccid Some flexion Well flexed Respiration Absent Weak irregular Regular Maximal score = 10
  • 13. Practice • As the intern oncall in labour ward you were informed that a teenage girl with severe eclampsia just delivered a baby who is • limp, • gasping, • has blue hands and lips and • makes no response to stimulation • had a HR of 120 beats/min by the 1st minute of life. • You got there by the 5th minute and noted that the baby was now • breathing normally, • lips were pink but • the nurses said all other findings were as before. • What is this baby’s Apgar score at 1&5mins?
  • 14. GRADING Score Grade Management ≥ 7 Resguires no active resuscitation 6 Mild birth asphyxia Suctioning 4 – 5 Moderate birth asphyxia  More suctioning, but avoid vigorous suctioning to avoid vagal reflex  Oxygen by face mask, occasionally bag & mask 1 – 3 Severe Birth Asphyxia  Clearing of airways  Endotracheal intubation & ventilation by bag and mask
  • 15. Investigations • Fetal heart rate monitoring • Fetal scalp blood pH • Cardiotocography –to assess FHR variability • Arterial blood gases • E/U/Cr • ECG • Other ancillary investigations as required
  • 16. Complications 1.Central Nervous system • Hypoxic IschaemicEncephalopathy (HIE) • Seizures • Hypotonia • Mental retardation • Learning disability • Speech disorders • Cerebral palsy (spastic diplegia, spastic quadriparesis) • Syndrome of InappropiateADH secretion (SIADH) • Intracranial haemorrhage
  • 17. Spastic Diplegia- Usually seen in preterm infants as a result of the high incidence of IVH & periventricular leukomalacia.
  • 18. Complications (2) • Respiratory System • Respiratory distress syndrome • Persistent pulmonary hypertension • Cardiovascular System • Left ventricular dysfunction -due to myocardial ischaemia • Patent ductus arteriosus • Cardiogenic shock
  • 19. Complications(3) • Renal • Acute tubular necrosis –causing haematuria • Acute cortical necrosis • Haematuria • Gastrointestinal • Necrotising enterocolitis –due to ischaemia which causes bacterial proliferation • Liver dysfunction
  • 20. Complications(4) • Haemopoeitic • DIC –due to generalized hypoxia • Increased risk of infection • Metabolic • Hypo or hyperglycaemia • Hyponatraemia –from renal failure • Hypocalcaemia • Acidosis
  • 21. Hypoxic Ischaemic Encephalopathy • Most feared complication of perinatal asphyxia • Impacts on long term neurodevelopmental outcomes • It is clinically staged by doing a sequential, systematic evaluation of brain injury • Sarnat staging commonly used
  • 22. Level of consciousness Muscle tone Tendon reflexes Seizures Irritable / hyperalert Normal or hypertonia Increased present Absent Suck Moro Grasp Oculocephalic (Doll’s eye) Active Exaggerated Normal to exaggerated Normal Pupils Respirations Heart rate EEG Dilated, reactive Regular Normal or tachycardia Normal Prognosis Good Sarnat staging of hypoxic – ischemic encephalopathy Grade 1 (mild)
  • 23. Level of consciousness Lethargy Muscle tone Hypotonia Tendon reflexes Increased Seizures Present Suck Weak Moro Incomplete Grasp Exaggerated Oculocephalic (Doll’s eye) Overactive Pupils Constricted, reactive Respirations Periodic Heart rate Bradycardia EEG Low – voltage periodic or paroxysmal Prognosis Variable Coma Flaccid Depressed or absent Absent Absent Absent Absent Reduced or absent Variable or fixed Ataxic, apnoeic Bradycardia Periodic or isoelectric High mortality and neurologic disability Grade 2 (moderate) Grade 3 (severe) Sarnat staging of hypoxic – ischemic encephalopathy
  • 24. Management • Treatment is supportive • Anticipate need for neonatal resuscitation from maternal obstetric and labour history (including CTG tracing) • Maintain breathing and circulation • Avoid: • Hypo-or hyperventilation (keep PaC02 in the normal range) • Hypoxemia • Hypotension
  • 25. Management contd. • Give inotropes for hypotension or myocardial dysfunction • Maintain normal blood glucose, calcium and magnesium • Correct metabolic acidosis • Restrict fluid intake and monitor urine output • Control seizures • Avoid overheating, re-warm slowly if hypothermic • Nutritional support • Family support
  • 26. Outcome • In general: • A normal neurologic exam and feeding well by 2 weeks of age suggest good prognosis. • Mild HIE • usually normal outcome. • Moderate HIE • increased risk for motor and cognitive abnormalities, including cerebral palsy. • Severe HIE • mortality rate 75%. • 80% of survivors will have neurologic sequelae.
  • 27. Poor prognostic features • Persistence of clinical seizures • Persistently abnormal neurologic exam • Not feeding orally by 2 weeks of age • EEG with burst suppression or isoelectric pattern on any day • Abnormal basal ganglia or marked brain atrophy on MRI • Poor postnatal head growth
  • 28. By now we should have………….. • Reviewed the foetal circulation • Learnt some related terms • Listed some risk factors/causes of perinatal asphyxia • Learnt the parameters of the APGAR score and its application in perinatal asphyxia
  • 29. THANKS FOR YOUR ATTENTION
  • 30. ?

Editor's Notes

  1. IVH- Intraventricular haemorrhage