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PERINATALASPHYXIA
BY: MRS. PRECILLA C. STEPHEN
PERINATAL ASPHYXIA
(HYPOXIC ISCHEMIC ENCEPHALOPATHY)
 Perinatal asphyxia, more appropriately known as hypoxic-ischemic encephalopathy, is characterized by clinical
and laboratory evidence of acute or subacute brain injury due to asphyxia.
 The primary cause of this condition are systemic hypoxemia and/or reduced cerebral blood flow (CBF).
 Birth asphyxia causes 23% of all neonatal death worldwide.
 Severe hypoxia results in anaerobic glycolysis and lactic acid production first in the peripheral tissues
(muscle and heart) and then in the brain
 Ischemia (lack of sufficient blood flow to all or part of an organ) is both a cause and a result of hypoxia.
DEFINITON
 An insult to the fetus or new-born due to lack of oxygen (hypoxia) and /
or lack of perfusion (ischemia) to various organ.
INCIDENCE
 1-1.5%
 20% of perinatal deaths
 Increased risk in IDM
 Toxemic mothers
 IUGR
 Breech
 Postmature
ETIOLOGY
 90% Antepartum / Intrapartum
 10% Postpartum
FACTORS
MATERNAL
 Hypertension – chronic /pre-eclampsia
 Diabetes, anaemia, malnutrition
 Heart disease, bronchial asthma
 Hypotension
 Intrauterine infections
 Prolonged and difficult 2nd stage of labour
 Drug addiction
 Toxaemia
CORD ACCIDENTS: Prolapse/ true knots/ compression
OBSTETRIC FACTOR: placental previa, cord prolapse, PROM, polyhydramnios, placental
insufficiency, chorioamnionitis
INTRAPARTU, CONDIITONS: Abnormal placentation, prolonged delivery, difficult delivery,
post term delivery, forceps delivery
FETAL OR NEONATAL CONDITION: Prematurity, RDS, MAS, Sepsis, pneumonia,
haemolytic diseases, cardiac or pulmonary anomalies
NEONATAL RESUSCITATION EQUIPMENT
 Suction equipment – Bulb syringe/ mechanical suction and tubing suction catheter 5F
or 6F, 10F or 12F, 8F feeding tube and 20ml syringe meconium aspirator
 Bag and mask equipment
 Intubation equipment
 Medications: Epinephrine 1/10,000, isotonic crystalloid, naloxone hydrochloride,
dextrose 40%, normal saline, umbilical vessel catheterization supplies
 Miscellaneous : Gloves, radiant warmer, linens, stethoscope, oropharyngeal airway
HOW DOES A BABY RECEIVE O2 BEFORE BIRTH?
 All oxygen diffuse across the placental membrane from the mother’s blood to
the baby blood
 Only a small fraction of the fetal blood passed through the fetal lungs
 Alveoli is filled with fluid
 The blood vessels in the fetal lung are markedly constricted
 Most of the blood flow through the ductus arteriosus into the aorta
AFTER BIRTH
 No connection to the placenta
 A baby get oxygen from the lung
1. The fluid in the alveoli is absorbed into the lungs tissue and replace by air
2. The umbilical artery and vein clamped – increases blood pressure
3. Oxygen increases in the alveoli – relaxation of blood vessel in the lungs
4. The ductus arteriosus begin to constrict – more blood flow through the lungs –
oxygen increases to tissues
SYSTEMIC MANIFESTATIONS
 Brain (28%) – HIE, ICH, apnoeic attack, seizures
 Heart (25%) – Arrhythmia, myocardial damage, CCF
 Lungs (23%) – Meconium aspiration, pulmonary haemorrhage, pneumonia
 Kidney (50%) – Hematuria, ARF
 GIT – NEC, Paralytic ileus
 Hematologic – DIC, hyperbilirubinemia, sepsis
 Endocrine – SIADH, Adrenal haemorrhage
 Metabolic – Hypoglycaemia, hypocalcaemia, hyperbilirubinemia
SARNAT AND SARNAT CLASSIFIED HIE INTO 3 GRADIES
 Grade I (mild)
 Grade II (moderate)
 Grade III(severe)
GRADE I HIE
 Alternating period of lethargy, irritability, hyper alertness
 Poor feeding
 Increased muscle tone
 Increase heart rate
 Pupils- dilated
 No seizures
 Symptoms resolve in 24 hours
GRADE II HIE
 Lethargy
 Poor feeding, depressed gag reflex
 Hypotonia
 Bradycardia
 50-70% neonates display seizures usually in the first 24 hour after birth
GRADE III
 Coma
 Flaccidity
 Absent reflexes
 Pupil – fixed, slight reactive
 Apnoea, bradycardia, hypotension
 Seizures are uncommon but if present they are intractable
LATE EFFECTS
 Microcephaly
 MR
 Developmental delay
 Cerebral palsy
 Epilepsy
 Visual, hearing impairment
 Behavioural disturbances
DIAGNOSTIC EVALUATION
Perinatal
 Awareness of problems and high risk
 Fetal movement count
 Fetal BPP
 Monitor FHR
 Progress of Labor
 Fetal scalp – pH
 Presence of Meconium
MANAGEMENT
 Prevention is the best management
 Timing is very crucial and a few minute of delay can lead to death or life long
suffering from handicap
 Maintain oxygenation and acid base balance
 Ventilation – for hypoxia and hypercapnia
 Maintain cerebral perfusion
 Correction of hypoglycaemia and hypocalcaemia
 Temperature maintenance
 Control of seizure – Anticonvulsants drug
 Cardiac effects – Ionotropes
 Renal effects – Dopamine
 Administer phenobarbital 20mg/kg IV over 5 minute, it can be increased in dose 5mg/kg
every 5 min until seizures are controlled or uuntil maximum dose 40mg/kg is reached.

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Perinatal asphyxia in Neonatal

  • 2. PERINATAL ASPHYXIA (HYPOXIC ISCHEMIC ENCEPHALOPATHY)  Perinatal asphyxia, more appropriately known as hypoxic-ischemic encephalopathy, is characterized by clinical and laboratory evidence of acute or subacute brain injury due to asphyxia.  The primary cause of this condition are systemic hypoxemia and/or reduced cerebral blood flow (CBF).  Birth asphyxia causes 23% of all neonatal death worldwide.  Severe hypoxia results in anaerobic glycolysis and lactic acid production first in the peripheral tissues (muscle and heart) and then in the brain  Ischemia (lack of sufficient blood flow to all or part of an organ) is both a cause and a result of hypoxia.
  • 3. DEFINITON  An insult to the fetus or new-born due to lack of oxygen (hypoxia) and / or lack of perfusion (ischemia) to various organ.
  • 4. INCIDENCE  1-1.5%  20% of perinatal deaths  Increased risk in IDM  Toxemic mothers  IUGR  Breech  Postmature
  • 5. ETIOLOGY  90% Antepartum / Intrapartum  10% Postpartum
  • 6. FACTORS MATERNAL  Hypertension – chronic /pre-eclampsia  Diabetes, anaemia, malnutrition  Heart disease, bronchial asthma  Hypotension  Intrauterine infections  Prolonged and difficult 2nd stage of labour  Drug addiction  Toxaemia
  • 7. CORD ACCIDENTS: Prolapse/ true knots/ compression OBSTETRIC FACTOR: placental previa, cord prolapse, PROM, polyhydramnios, placental insufficiency, chorioamnionitis INTRAPARTU, CONDIITONS: Abnormal placentation, prolonged delivery, difficult delivery, post term delivery, forceps delivery FETAL OR NEONATAL CONDITION: Prematurity, RDS, MAS, Sepsis, pneumonia, haemolytic diseases, cardiac or pulmonary anomalies
  • 8. NEONATAL RESUSCITATION EQUIPMENT  Suction equipment – Bulb syringe/ mechanical suction and tubing suction catheter 5F or 6F, 10F or 12F, 8F feeding tube and 20ml syringe meconium aspirator  Bag and mask equipment  Intubation equipment  Medications: Epinephrine 1/10,000, isotonic crystalloid, naloxone hydrochloride, dextrose 40%, normal saline, umbilical vessel catheterization supplies  Miscellaneous : Gloves, radiant warmer, linens, stethoscope, oropharyngeal airway
  • 9. HOW DOES A BABY RECEIVE O2 BEFORE BIRTH?  All oxygen diffuse across the placental membrane from the mother’s blood to the baby blood  Only a small fraction of the fetal blood passed through the fetal lungs  Alveoli is filled with fluid  The blood vessels in the fetal lung are markedly constricted  Most of the blood flow through the ductus arteriosus into the aorta
  • 10. AFTER BIRTH  No connection to the placenta  A baby get oxygen from the lung 1. The fluid in the alveoli is absorbed into the lungs tissue and replace by air 2. The umbilical artery and vein clamped – increases blood pressure 3. Oxygen increases in the alveoli – relaxation of blood vessel in the lungs 4. The ductus arteriosus begin to constrict – more blood flow through the lungs – oxygen increases to tissues
  • 11. SYSTEMIC MANIFESTATIONS  Brain (28%) – HIE, ICH, apnoeic attack, seizures  Heart (25%) – Arrhythmia, myocardial damage, CCF  Lungs (23%) – Meconium aspiration, pulmonary haemorrhage, pneumonia  Kidney (50%) – Hematuria, ARF  GIT – NEC, Paralytic ileus  Hematologic – DIC, hyperbilirubinemia, sepsis  Endocrine – SIADH, Adrenal haemorrhage  Metabolic – Hypoglycaemia, hypocalcaemia, hyperbilirubinemia
  • 12. SARNAT AND SARNAT CLASSIFIED HIE INTO 3 GRADIES  Grade I (mild)  Grade II (moderate)  Grade III(severe)
  • 13. GRADE I HIE  Alternating period of lethargy, irritability, hyper alertness  Poor feeding  Increased muscle tone  Increase heart rate  Pupils- dilated  No seizures  Symptoms resolve in 24 hours
  • 14. GRADE II HIE  Lethargy  Poor feeding, depressed gag reflex  Hypotonia  Bradycardia  50-70% neonates display seizures usually in the first 24 hour after birth
  • 15. GRADE III  Coma  Flaccidity  Absent reflexes  Pupil – fixed, slight reactive  Apnoea, bradycardia, hypotension  Seizures are uncommon but if present they are intractable
  • 16. LATE EFFECTS  Microcephaly  MR  Developmental delay  Cerebral palsy  Epilepsy  Visual, hearing impairment  Behavioural disturbances
  • 17. DIAGNOSTIC EVALUATION Perinatal  Awareness of problems and high risk  Fetal movement count  Fetal BPP  Monitor FHR  Progress of Labor  Fetal scalp – pH  Presence of Meconium
  • 18. MANAGEMENT  Prevention is the best management  Timing is very crucial and a few minute of delay can lead to death or life long suffering from handicap  Maintain oxygenation and acid base balance  Ventilation – for hypoxia and hypercapnia  Maintain cerebral perfusion
  • 19.  Correction of hypoglycaemia and hypocalcaemia  Temperature maintenance  Control of seizure – Anticonvulsants drug  Cardiac effects – Ionotropes  Renal effects – Dopamine  Administer phenobarbital 20mg/kg IV over 5 minute, it can be increased in dose 5mg/kg every 5 min until seizures are controlled or uuntil maximum dose 40mg/kg is reached.