birth asphyxia

1. Birth Asphyxia
Presenter:
Dr Subodh Kumar Shah
1st year Resident
Pediatric
Moderator
Assoc. Prof. Dr. Sunil Kumar Yadav
Department of Pediatrics and Adolescent
Medicine
Nobel Medical College & Teaching Hospital

2. Contents
• Introduction
• Definition
• Etiology
• Pathophysiology
• HIE
• Diagnosis
• Management

3. Perinatal Asphyxia:
• There is no universal definition of perinatal
asphyxia.
• Depending on the setting, different criteria are taken
into consideration
• Perinatal asphyxia is an insult to the fetus or newborn
due to lack of oxygen(hypoxia) or lack of perfusion
(ishchemia) to various organs.
• It is often associated with tissue lactic acidosis and
hypercarbia.
• 2

4. Definition:
It refers to a condition during pregnancy and labor in which
impaired gas exchange leads to;
Hypoxemia, and
Hypercarbia.
Fetal acidosis,
 It is evidenced by fetal acidosis as measured in umbilical arterial
blood pH <7.0
[Cloherty and Stark’s Manual of Neonatal Care ;pg .820]

5. • National Neonatology Forum (NNF) of India defined
perinatal asphyxia as gasping or no breathing at 1 minute
or Apgar Score of 4 or less at 1 minute.
WHO :
• Failure to initiate and sustain breathing at birth.

6. Diagnosing Criteria
• Prolonged metabolic or mixed academia (pH <7) on an umbilical
arterial blood sample
• Persistent APGAR score of 0-3 for >5 mins
• Neurological manifestations: e.g.- seizure, coma, hypotonia or
HIE in the immediate neonatal period
• Evidence of multi organ dysfunction in the immediate neonatal
period
• 3
• These are the Essential Criteria recommended by the American Academy of Pediatrics

7. ApgarScoring:

8. • Severe perinatal asphyxia
APGAR score at 1 min is 0–3.
• Mild and moderate perinatal asphyxia
Apgar score at 1 min is 4-7 .
International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10 WHO
Version 2016), P20 Intrauterine hypoxia, P21 Birth asphyxia.

9. ComplicationsofPerinatalAsphyxia :
Immediate Complications: Multi-organ damage
May end up with long term sequelae
May lead to immediate death
• Long term sequelae

10. ImmediateComplications

12. Long TermSequelae:
Cognitive delay
Cerebral palsy
Dystonia
Seizure disorders
Hemiparesis or Quadriparesis/plegia
Visual and auditory processing difficulty

13. HIE :Hypoxic Ischemic Encephalopathy
• Abnormal neurologic behavior in the neonatal period arising as
a result of a hypoxic-ischemic event.
• It is an important cause of permanent damage to CNS tissues
that may result in neonatal death or manifest later as cerebral
palsy or developmental delay.
• It is the term used to designate the clinical and neuropathological
findings of an encephalopathy that occurs in a full term infant
who has experienced a significant episode of intrapartum
asphyxia.

14. HIE:
• About 20-30% of infants with HIE die in the neonatal period, and ≈ 33-50% of
survivors are left with permanent neurodevelopmental abnormalities (cerebral
palsy, mental retardation).
• The greatest risk of adverse outcome is seen in infants with severe fetal
acidosis (pH <6.7) (90% death/impairment) and a base deficit
>25mmol/L (72% mortality).
• Multiorgan failure can occur
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15. Neurological pattern of HIE:
Premature newborns :
 Selective subcortical neuronal necrosis
 Periventricular leukomalacia
 Focal and multifocal ischemic necrosis
 Periventricular hemorrhage or infarction
Term newborns
 Selective cortical neuronal necrosis (spastic CP)
 Status marmoratus of basal ganglia and thalamus(choreo-athetoid CP)
 Parasagittal cerebral injury (spastic quadreperesis)
 Focal and multifocal ischemic cerebral necrosis ( hemiparesis, cognitive defect,
seizure)

16. RiskFactors:
• Inadequate
oxygenation
of maternal
blood
• Low BP
• Oxytocin-
contraction of
uterus
Maternal Uteroplacental
• Premature
separation
• Knotting of
cord -
impedance to
the
circulation
• Placental
insufficiency
• Failure of
oxygenation
• Severe
anemia-blood
loss or
hemolysis
• Shock
Fetal

17. Etiology
• Cardiacarrest
• Asphyxiation
• Severe
anaphylaxis
• Statusepilepticus
• Hypovolemic
shock
• Placental
abruption
• Cord prolapse
• Uterine rupture
• Hyperstimulation
with oxytocic
agents
• Fetomaternal
hemorrhage
• Twin totwin
transfusion
• Severe
isoimmune
hemolytic disease
• Cardiac
arrhythmia
Maternal Uteroplacental Fetal

22. Pathophysiology
Other organs
(pericardium,
pleura, heart,
adrenal,
meninges etc.)
Increased
capillary
permeability
Fluid leak
and
congestion
Coagulation necrosis

28. Pathophysiology: BrainDamage
Hypoxia and ischemia
Increased lactate and inorganic phosphate
Accumulation of cytotoxic product
Cerebral edema
Increased shunting(diving seal reflex)

30. Clinical Manifestations:Asphyxia
Intrauterine growth restriction
Fetal bradycardia
Meconium stained liquor
Depressed infant
Hypotonic
Pallor
Cyanosis
Apnea
Unresponsive to
stimulation
Seizure due to brain
edema in 24hr after birth

31. DIAGNOSIS
Perinatal assessment of risk
 includes awareness of preexisting maternal or fetal problems
 placental and fetal conditions ascertained by
- Ultrasonographic examination,
- Biophysical profile and
- Non stress tests
Umbilical cord or first blood gas determination
• Serum CK-BB may be increased in asphyxiated newborns
within 12 hours of the insult.
• Others-Protein S-100,NSE and urine markers.

32. Diagnosis
MRI is the preferred imaging modality in neonates
with HIE
CT scans are helpful in identifying focal hemorrhagic lesions, diffuse
cortical injury, and damage to the basal ganglia;
CT has limited ability to identify cortical injury during the 1st few days of
life.
Ultrasonography has limited utility in evaluation of hypoxic injury in the
term infant; it is the preferred modality in evaluation of the preterm
infant.
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33. A- MRI showing focal neuronal injury; B- Diffuse weighted MRI
showing HIE

34. StagingofHIEin terminfants: Sarnat& Sarnat
Signs Stage 1 Stage 2 Stage 3
Level of
consciousness
Hyperalert Lethargic Stuprous/coma
Muscle tone Normal Hypotonic Flaccid
posture Normal Flexion Decerebrate
Tendon Reflex Hyperactive Hyperactive Absent
Myoclonus Present Present Absent
Moro reflex strong weak Absent
Pupils Mydriasis Miosis Unequal
Seizure None Common Decerebration
EEG findings Normal Low voltage Burst suppression
Duration <24hr 24hr-14days Days to weeks
Outcome Good Variable Death/severe deficit

37. Management of HIE
Selective cerebral or whole body (systemic) therapeutic hypothermia reduces
mortality or major neurodevelopmental impairment in term and near-term infants
with HIE.
core temperature of 33.5oC within the 1st 6 hr after birth
Note: Prevent hyperthermia first
Phenobarbital, the drug of choice for seizures, is given with an intravenous loading dose
(20 mg/kg); additional doses of 5-10 mg/kg (up to 40-50 mg/kg total) may be needed.
Phenytoin (20 mg/kg loading dose) or lorazepam (0.1 mg/kg) may be needed for
refractory seizures.
Additional therapy for infants with HIE includes supportive care directed at management
of organ system dysfunction

38. Summary of potential neuroprotective
strategies

40. Prognosis
Depends upon the timing and severity of the insult
Initial cord or initial blood pH <6.7 have a 90% risk for death or severe
neurodevelopmental impairment at 18 month of age
Apgar scores of 0-3 at 5 min
High base deficit (>20-25 mmol/L)
Decerebrate posture
Lack of spontaneous activity
Increased
risk for
death or
impairment