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MANAGEMENT OF
BIRTH ASPHYXIA
Presenter :Dr Jecinter Modi-Juma
OUTLINE
 Diagnosis
 Management principles
 Follow up
 Complications
 Summary
WHY IS IT IMPORTANT?
 Occurs in 1-6 per 1000 live term births in
developed countries
 Number 5 leading cause of under 5 mortality
 Significant cause of cerebral palsy and
developmental delay
WHAT SHOULD BE DONE
1) Early recognition of maternal risk factors
2) Decision on when and where to deliver
3) Close surveillance of high risk labor
PRENATAL DETECTION OF RISK OF ASPHYXIA:
.
Only possible in half of cases
Predictors of low Apgar score:
 Fetal movement counting
 Non-stress test
 Fetal biophysical profile
 Abnormal fetal heart rate (FHR) recording
 Fetal scalp Ph monitoring- is the best but invasive
DIAGNOSIS
 History , physical examination and laboratory
tests
 Profound metabolic or mixed acidemia (pH < 7)
in an umbilical artery blood sample, if obtained
 Persistence of an Apgar score of 0-3 for longer
than 5 minutes
 Neonatal neurologic sequelae (
 Multiple organ involvement
AAP / ACOG criteria for asphyxia severe enough to cause
neurological injury
INVESTIGATIONS
 Physical examination: according to Sarnat and
Sarnat criteria
 To rule out multi organ damage
 Rule out other causes of CNS dysfunction
 Prognosis
 Monitoring of progress
LABORATORY TESTS
 Blood gas analysis
 Renal function tests and electrolytes
 Liver function Tests
 Coagulation test
 Monitoring of blood sugars
 Cardiac enzymes
IMAGING
 Cranial Ultrasound
 CT
 MRI
 EEG
TREATMENT
 Prevention of intrauterine asphyxia
 Supportive treatment
 Treatment of complications
 Neuroprotective strategies
SUPPORTIVE TREATMENT
 Aim is to avoid any further brain injury
 Initial newborn resuscitation and stabilisation ensures
adequate oxygenation and ventilation using bag mask
ventilation
 Several clinical trials : room air resuscitation for infants with
perinatal asphyxia is as effective as resuscitation with 100%
oxygen.
 Infants resuscitated with room air have been shown to have
lower circulating ROS
 International Liaison Committee on Resuscitation (ILCOR)
recommendations include initiating neonatal resuscitation with
concentrations of oxygen between 21-100%
VENTILATORY SUPPORT
 Incase of respiratory failure, start mechanical
ventilation aiming at PO2 (80-100mmHg) and
PCO2 (35-45mmHg) within normal.
 Hyperoxia/hypoxia and hypercabia/hypocabia may
cause further injury to the brain.
PERFUSION
 Maintain adequate perfusion by use of intravenous fluids
 Maintain blood pressure within normal
 Correct deficit by slow infusions of N/S
 Monitor urine output: 1ml/kg/hr
 Ensure normal hematocrit >40%
 Monitor CVP
METABOLIC SUPPORT
 Monitor electrolytes Na+,K+,Cl-, calcium,
magnesium and correct the abnormalities
 These are usually deranged in ATN and in SIADH
 Maintain RBS at 3.3- 5.5 mmol /L
 Maintain normal acid base balance
HYPERTHERMIA MANAGEMENT
 Avoid hyperthermia
 For 1 degree increase in temprature = 3-4 fold
increase in risk of death/disability
 In therapeutic hypothermia aim to get core (rectal)
temperature to 33-35⁰ C for 72 hours
 Followed by gradual rewarming for the next 6-8
hours
HYPERTHERMIA MANAGEMENT
 It has been shown from randomized trials that
cooling 3-4°C below baseline temperature applied
within a few hours not later than 6 h of injury is
neuroprotective
 Whole body cooling VS head cooling
 This form of therapy is still under investigation
MECHANISM OF ACTION OF THERAPEUTIC
HYPOTHERMIA
 Reduced metabolic rate and energy depletion
 Decreased excitatory transmitter release
 Reduced vascular permeability, edema, and
disruptions of blood-brain barrier function
 Reduced alterations in ion flux
 Reduced apoptosis due to hypoxic-ischemic
encephalopathy
POSSIBLE COMPLICATIONS OF HYPOTHERMIA
RX
 Coagulation defects, leukocyte malfunctions,
pulmonary hypertension, worsening of metabolic
acidosis, and abnormalities of cardiac rhythm,
especially during rewarming.
 These are still controversial and under investigation
SEIZURE CONTROL
 Common in moderate to severe asphyxia
 Causes further brain injury and future risk of
epilepsy
 Usually self –limited and confined to early days of
life.
 Start with phenobarbitone loading dose at 20mg/kg
, can repeat after 15 minutes if no response
 Phenytoin used if no response to phenobarbitone
 Other drugs: benzodiazepines like midazolam and
clonazepam
 Complicates ventilation, oxygenation and blood
pressure control
DIET
 Generally kept NPO in the first 3 days of life in
moderate to severe asphyxia till level of
consciousness improves
 Start with trophic enteral feeds at 5mls 3 hourly
and increase based on individual progress
 Watch for signs of NEC
 Parenteral nutrition
POTENTIAL NEUROPROTECTIVE
STRATEGIES
FUTURE THERAPIES
1) Monosialogangliosides
–Cell membrane constituents
2) Growth factors
–Nerve growth factor
–Insulin-like growth factor
3)Gene therapy
–Bcl-2 (potent inhibitor of cell death pathways)
4) Intracellular calcium buffering
–Calbindin-D28k (intracellular calcium-binding protein which
acts as a mobile calcium buffer)
5) Anti-NMDA receptor immunization
PREDICTORS OF OUTCOME
 Failure to establish respiration by 5 minutes of life
 Apgar score of 3 or less at 5 minutes
 Onset of seizures with in 12 hours
 Refractory seizures
 Stage III HIE
 Persistent oliguria (<1 ml/kg/hr) for the first 36 hrs
of life
 Inability to establish oral feeds by 1 wk
 Abnormal EEG & failure to normalize by D7
 Abnormal CT, MRI in neonatal period
FOLLOW UP
 Goal: detect impairments and intervene early
 Monitor growth
 Neurologic examination to identify those who
require intensive follow-up
 Visual and hearing tests
 Multidisciplinary
REFERENCES
 Averys Neonatology 6th Edition
 Medscape
 Nelsons Textbook of paediatrics 19th Edition

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Management of Asphyxia

  • 1. MANAGEMENT OF BIRTH ASPHYXIA Presenter :Dr Jecinter Modi-Juma
  • 2. OUTLINE  Diagnosis  Management principles  Follow up  Complications  Summary
  • 3. WHY IS IT IMPORTANT?  Occurs in 1-6 per 1000 live term births in developed countries  Number 5 leading cause of under 5 mortality  Significant cause of cerebral palsy and developmental delay WHAT SHOULD BE DONE 1) Early recognition of maternal risk factors 2) Decision on when and where to deliver 3) Close surveillance of high risk labor
  • 4. PRENATAL DETECTION OF RISK OF ASPHYXIA: . Only possible in half of cases Predictors of low Apgar score:  Fetal movement counting  Non-stress test  Fetal biophysical profile  Abnormal fetal heart rate (FHR) recording  Fetal scalp Ph monitoring- is the best but invasive
  • 5. DIAGNOSIS  History , physical examination and laboratory tests  Profound metabolic or mixed acidemia (pH < 7) in an umbilical artery blood sample, if obtained  Persistence of an Apgar score of 0-3 for longer than 5 minutes  Neonatal neurologic sequelae (  Multiple organ involvement AAP / ACOG criteria for asphyxia severe enough to cause neurological injury
  • 6. INVESTIGATIONS  Physical examination: according to Sarnat and Sarnat criteria  To rule out multi organ damage  Rule out other causes of CNS dysfunction  Prognosis  Monitoring of progress
  • 7. LABORATORY TESTS  Blood gas analysis  Renal function tests and electrolytes  Liver function Tests  Coagulation test  Monitoring of blood sugars  Cardiac enzymes
  • 9. TREATMENT  Prevention of intrauterine asphyxia  Supportive treatment  Treatment of complications  Neuroprotective strategies
  • 10. SUPPORTIVE TREATMENT  Aim is to avoid any further brain injury  Initial newborn resuscitation and stabilisation ensures adequate oxygenation and ventilation using bag mask ventilation  Several clinical trials : room air resuscitation for infants with perinatal asphyxia is as effective as resuscitation with 100% oxygen.  Infants resuscitated with room air have been shown to have lower circulating ROS  International Liaison Committee on Resuscitation (ILCOR) recommendations include initiating neonatal resuscitation with concentrations of oxygen between 21-100%
  • 11. VENTILATORY SUPPORT  Incase of respiratory failure, start mechanical ventilation aiming at PO2 (80-100mmHg) and PCO2 (35-45mmHg) within normal.  Hyperoxia/hypoxia and hypercabia/hypocabia may cause further injury to the brain.
  • 12. PERFUSION  Maintain adequate perfusion by use of intravenous fluids  Maintain blood pressure within normal  Correct deficit by slow infusions of N/S  Monitor urine output: 1ml/kg/hr  Ensure normal hematocrit >40%  Monitor CVP
  • 13. METABOLIC SUPPORT  Monitor electrolytes Na+,K+,Cl-, calcium, magnesium and correct the abnormalities  These are usually deranged in ATN and in SIADH  Maintain RBS at 3.3- 5.5 mmol /L  Maintain normal acid base balance
  • 14. HYPERTHERMIA MANAGEMENT  Avoid hyperthermia  For 1 degree increase in temprature = 3-4 fold increase in risk of death/disability  In therapeutic hypothermia aim to get core (rectal) temperature to 33-35⁰ C for 72 hours  Followed by gradual rewarming for the next 6-8 hours
  • 15. HYPERTHERMIA MANAGEMENT  It has been shown from randomized trials that cooling 3-4°C below baseline temperature applied within a few hours not later than 6 h of injury is neuroprotective  Whole body cooling VS head cooling  This form of therapy is still under investigation
  • 16. MECHANISM OF ACTION OF THERAPEUTIC HYPOTHERMIA  Reduced metabolic rate and energy depletion  Decreased excitatory transmitter release  Reduced vascular permeability, edema, and disruptions of blood-brain barrier function  Reduced alterations in ion flux  Reduced apoptosis due to hypoxic-ischemic encephalopathy
  • 17. POSSIBLE COMPLICATIONS OF HYPOTHERMIA RX  Coagulation defects, leukocyte malfunctions, pulmonary hypertension, worsening of metabolic acidosis, and abnormalities of cardiac rhythm, especially during rewarming.  These are still controversial and under investigation
  • 18. SEIZURE CONTROL  Common in moderate to severe asphyxia  Causes further brain injury and future risk of epilepsy  Usually self –limited and confined to early days of life.  Start with phenobarbitone loading dose at 20mg/kg , can repeat after 15 minutes if no response  Phenytoin used if no response to phenobarbitone  Other drugs: benzodiazepines like midazolam and clonazepam  Complicates ventilation, oxygenation and blood pressure control
  • 19. DIET  Generally kept NPO in the first 3 days of life in moderate to severe asphyxia till level of consciousness improves  Start with trophic enteral feeds at 5mls 3 hourly and increase based on individual progress  Watch for signs of NEC  Parenteral nutrition
  • 21. FUTURE THERAPIES 1) Monosialogangliosides –Cell membrane constituents 2) Growth factors –Nerve growth factor –Insulin-like growth factor 3)Gene therapy –Bcl-2 (potent inhibitor of cell death pathways) 4) Intracellular calcium buffering –Calbindin-D28k (intracellular calcium-binding protein which acts as a mobile calcium buffer) 5) Anti-NMDA receptor immunization
  • 22. PREDICTORS OF OUTCOME  Failure to establish respiration by 5 minutes of life  Apgar score of 3 or less at 5 minutes  Onset of seizures with in 12 hours  Refractory seizures  Stage III HIE  Persistent oliguria (<1 ml/kg/hr) for the first 36 hrs of life  Inability to establish oral feeds by 1 wk  Abnormal EEG & failure to normalize by D7  Abnormal CT, MRI in neonatal period
  • 23. FOLLOW UP  Goal: detect impairments and intervene early  Monitor growth  Neurologic examination to identify those who require intensive follow-up  Visual and hearing tests  Multidisciplinary
  • 24. REFERENCES  Averys Neonatology 6th Edition  Medscape  Nelsons Textbook of paediatrics 19th Edition