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Birth asphyxia
Definition
• Non establishment of satisfactory respiration at birth.
• Literal meaning : stopping of pulse
• There is impaired blood gas exchange if persists leads to progressive
hypoximia, hypercapnia and metabolic acidosis.
• It is a significant cause of perinatal death about 50%
Diagnosis
• Profound acidemia (pH <7) on umbilical cord arterial blood sample
• Persistence of an apgar score 0-3 for > 5 minutes
• Neurological manifestations– hypotonia, coma, seizures in immediate
neonatal period
• Evidence of multi organ dysfunction
Fetal respiration
• Breathing activity observed at 11 weeks of IUL
• Following birth, fluid filled lung becomes organ of gas exchange.
Requirements are:
a. Establishment of pulmonary circulation
b. Establishment of ventilation
c. Diffusion of O2 and CO2 through alveolar-capillary membranes
Development of lungs
• ( 1 ) Foregut ventral diverticulum formation—4th week
• (2) Pseudoglandular period 8th–16th weeks
• (3) Canalicular period 17th–27th weeks
• (4) Saccular period—24th– 38th weeks
• (5) Alveolar period at or after 36 weeks.
• With the first breath the neonate must overcome the following
resistances for the expansion of the lungs.
• These are
(i) Viscosity of the lung fluid
(ii) Lung tissue resistance
(iii) The forces of surface tension at the air-liquid interface
IMPORTANT FACTORS THAT OPERATE TO
OVERCOME THE LUNG RESISTANCE
1. Increased fluid absorption and less fluid secretion by the alveolar
cells with the onset of labor.
2. Thoracic squeeze during delivery.
3. Marked increase in pulmonary lymph flow.
4. Removal of fluid via pulmonary circulation. In a normal birth the
process is completed within 2 hours. Babies born by cesarean and
premature infants have delayed lung fluid absorption.
Surfactants
• Type 2 Respiratory epithelium produce surfactant
• Surfactants reduce surface tension of the alveolus.
• The harmones and growth factors that augment surfactant
production are:
glucocorticoids, thyroid hormone, thyrotrophin releasing hormone
(TRH), prolactin, cyclic adenosine monophosphate (cAMP) and
epidermal growth factor.
Composition of surfactants
• Picture of the chart
• Antenatal glucocorticoids:
- If given before 34 weeks, reduces RDS by 70%
- Effect starts after 24 hours and lasts for 7 days
- Other uses:
Maturation of CVS, CNS and GI systems
Reduces the risk of periventricular or intraventricular hemorrhage
Reduces the risk of necrotizing enterocolitis
Etiopathogenesis
• Continuation of intrauterine hypoxia (placental insufficiency)
• Maternal medications
• Birth trauma
• Postnatal factors
A. Continuation of intrauterine hypoxia
(placental insufficiency)
• The placenta,
due to anatomical changes or due to inadequacy of uteroplacental
circulation (such as premature placental separation, circumvallate
placenta, hypertensive disorders in pregnancy, abnormal labor, cord
compression, vascular anomalies in cord, etc.).
• Maternal hypoxic states: The maternal diseases such as anemia,
eclampsia, cyanotic cardiovascular disorders, status asthmaticus,
dehydration and hypotension.
Maternal medications
Medications depress the respiratory centers directly and the chance of
development of asphyxia is increased.
• Morphine
• Pethidine
• Anaesthetic agents
Birth trauma
• Malpresentation such as breech, oblique lie, occipitoposterior often
requires manipulative and operative vaginal delivery (forceps or
ventouse).
• Prolonged second stage of labor in contracted pelvis, often causes
asphyxia.
• Increased intracranial tension → cerebral edema and congestion →
increased intracranial pressure → asphyxia.
Postnatal factors
• Postnatal asphyxia is secondary to pulmonary, cardiovascular and
neurological abnormalities of the neonate.
Clinical features
• The clinical features depend upon the etiology, intensity and duration
of oxygen lack, plasma carbon dioxide excess and subsequent acidosis
• According to the intensity of clinical features they have been classified
previously as
asphyxia livida (stage of cyanosis)
asphyxia pallida (stage of shock)
• But at present, according to the parameters denoted by Apgar, (Dr
Virginia Apgar—1953) a scoring procedure has been designed for
better understanding of the clinical state.
• Apgar score
• Majority of infants born with an Apgar score > 4 by 10 min., do not
develop cerebral palsy (CP).
• 75% children who develop CP have normal Apgar score at birth.
• Apgar score alone should not be taken as an evidence of neurological
damage.
• Cord blood pH can assess fetal oxygenation status better.
Clinical sequelae of birth asphyxia
• Initial response is hyperapnea and hypertension → primary apnea →
gasping attempt to breathe → (if unresolved) → secondary apnea →
bradycardia and shock → diminished cerebral blood flow → cerebral
hemorrhage → hypoxic ischemic encephalopathy (HIE) → (if severe)
→ either death or disability (if the baby survives).
Neonatal diagnosis
• EEG may help to detect severity of asphyxial injury
• CT can detect cortical neuronal injury several weeks after asphyxial
insults
• USG is the method of choice for routine screening to detect IVH,
necrosis of basal ganglia and thalamus. It is superior to CT
• MRI: best method to diagnose hypoxic brain injury within 24 hours of
the insult. It has no radiation exposure
• Others: Magnetic resonance spectroscopy and proton MRS and near
infrared spectroscopy.
Prophylactic management
(1) Antenatal detection of high-risk patients
(2) Scrupulous fetal monitoring to ensure early detection of fetal
distress and timely delivery
(3) Intrapartum use of electronic fetal monitoring and scalp blood pH
assessment when indicated. Scalp blood pH < 7.0 is a substantial
evidence of prolonged intrauterine asphyxia
(4) Judicious administration of anesthetic agents and sedatives during
labor
(5) Cooperation between obstetric and pediatric staff since delivery
(6) Avoidance of difficult or traumatic delivery.
Definitive management
• Apgar rating—classically, the evaluation of the cardiopulmonary
status in the newborn has been assessed by Apgar rating at 1 and 5
minutes after birth.
• Heart rate, skin color and respiratory activity provide the most
accurate evaluation and the need of resuscitation.
• Normal value: 7–10
Babies with Apgar score7–10
Pink, breathing regular, HR > 100.
• The oropharynx and the nasopharynx are to be cleared off any mucus
by suction.
• Dry the infant and place under radiant heat source.
• Oxygen is administered only when required.
• The condition is reassessed at 5 minutes and if found normal, the
infant should be given to mother
Babies with Apgar score 4–6
Peripheral cyanosis, breathing irregular, HR < 100.
— Baby may follow primary apnea.
— Place under a radiant heater, dry the baby.
— The baby is put flat or slight head down position.
— Immediate suction of the oropharynx and nasopharynx is done
either by mucus sucker or by suction apparatus (mechanical or
electrical) whichever is available. — Stimulus to back and sole (gentle
rubbing).
Babies with Apgar score 4–6
-- Simultaneously, oxygen (100%) is administered at a rate of 5 L/min.
by bag and mask at a pressure range of 30–40 cm H2 O
— Intermittent positive pressure ventilation (IPPV) is given if necessary.
— Support should be continued until respirations are spontaneous,
color improves and the heart rate is > 100 bpm.
Such an infant may be acidotic but it is corrected spontaneously after
respiration is established
If the above measures fail (secondary apnea)
• Oral suction followed by tracheal intubation is done.
• The tracheal tube is connected to resuscitation bag through which
oxygen is administered at the rate of 5–8 liters/ minute.
• Intermittent positive pressure ventilation (IPPV) is maintained at the
rate of 40–60/minute. Gentle external cardiac massage is performed
if the heart rate is < 60/min.
• When there is history of administration of a central depressant drug
such as pethidine or morphine to the mother within 3 hours of
delivery, suitable antidote, e.g. naloxone hydrochloride 100 µg/kg IM
(single dose) and may have to be repeated
Babies with Apgar score below 4
central cyanosis, no breathing, HR < 100
• Tracheal intubation and intermittent positive pressure ventilation
must be started immediately.
• If intermittent positive pressure ventilation is nor available, gentle
mouth to-mouth respiration is life saving.
• For circulation to maintain, cardiac massage is given if after intubation
and ventilation with 100% O2 for 30 sec. the heart rate remains < 60
bpm
• Drugs used in resuscitation:
Drugs are needed for a persistent HR < 60 bpm even after ventilation
and chest compression. Drug of choice is epinephrine
Other drugs are given as needed
• Meconium aspiration syndrome (MAS): Endotracheal intubation and
suctioning is performed with a negative pressure of 80–100 mm Hg.
This procedure may be repeated.
Infant resuscitation bag and mask
PROGNOSIS
• Depends on:(1) Maturity of the baby
(2) Duration and intensity of hypoxia and acidosis as evidenced by Apgar
score and blood pH—higher the score, normal the pH, better is the
prognosis
(3) Facilities for immediate and competent management of a compromised
baby. Most survivors of perinatal asphyxia do not have any major sequelae.
Factors for increased risk of neurological sequelae are:
(i) Apgar score of 0–3 at 20 min. of age
(ii) Presence of multi organ failure (oliguria > 24 hours of life)
(iii) Severity of the neonatal neurological syndrome. Severe HIE carries
mortality about 80%
(iv) Presence of neonatal seizure
COMPLICATIONS:
Immediate:
• Cardiovascular–hypotension, cardiac failure
• Renal–acute cortical necrosis, renal failure
• Liver function–compromised
• Gastrointestinal–ulcers and necrotising enterocolitis
• Lungs–persistent pulmonary hypertension
• Brain–cerebral edema, seizures.
COMPLICATIONS:
Delayed
• Retarded mental and physical growth
• Epilepsy–up to 30 percent in severe asphyxia
• Minimal brain dysfunction
Questions
1. Which of the following is not a diagnostic criteria of birth asphyxia?
a. Profound acidemia (pH <7) on umbilical cord arterial blood sample
b. Persistence of an apgar score 0-3 for > 5 minutes
c. Neurological manifestations– hypotonia, coma, seizures in
immediate neonatal period
d. Evidence of multi organ dysfunction
e. None of the above
• Breathing activity is observed at
a. 14 weeks of life
b. 11 weeks of life
c. 12 weeks of life
d. 16 weeks of life
• Surfactants are produced by
a. Type 1 pneumocytes
b. Type 2 pneumocytes
c. Goblet cells
• Which is the antidote of choice for pethidine or morphine ?
a. Naloxone
b. Naltrexone
c. Nalmefene
d. None of the above
• pethidine or morphine to the mother within 3 hours of delivery,
suitable antidote, e.g. naloxone hydrochloride
• Calculate the APGAR score
Baby with pulse rate of 96bpm, with weak cry on stimulation, only
extremities are blue,. The baby has active movements. It has strong cry.
7
Thank you..

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Birth asphyxia 1.pptx

  • 2. Definition • Non establishment of satisfactory respiration at birth. • Literal meaning : stopping of pulse • There is impaired blood gas exchange if persists leads to progressive hypoximia, hypercapnia and metabolic acidosis. • It is a significant cause of perinatal death about 50%
  • 3. Diagnosis • Profound acidemia (pH <7) on umbilical cord arterial blood sample • Persistence of an apgar score 0-3 for > 5 minutes • Neurological manifestations– hypotonia, coma, seizures in immediate neonatal period • Evidence of multi organ dysfunction
  • 4. Fetal respiration • Breathing activity observed at 11 weeks of IUL • Following birth, fluid filled lung becomes organ of gas exchange. Requirements are: a. Establishment of pulmonary circulation b. Establishment of ventilation c. Diffusion of O2 and CO2 through alveolar-capillary membranes
  • 5. Development of lungs • ( 1 ) Foregut ventral diverticulum formation—4th week • (2) Pseudoglandular period 8th–16th weeks • (3) Canalicular period 17th–27th weeks • (4) Saccular period—24th– 38th weeks • (5) Alveolar period at or after 36 weeks.
  • 6. • With the first breath the neonate must overcome the following resistances for the expansion of the lungs. • These are (i) Viscosity of the lung fluid (ii) Lung tissue resistance (iii) The forces of surface tension at the air-liquid interface
  • 7. IMPORTANT FACTORS THAT OPERATE TO OVERCOME THE LUNG RESISTANCE 1. Increased fluid absorption and less fluid secretion by the alveolar cells with the onset of labor. 2. Thoracic squeeze during delivery. 3. Marked increase in pulmonary lymph flow. 4. Removal of fluid via pulmonary circulation. In a normal birth the process is completed within 2 hours. Babies born by cesarean and premature infants have delayed lung fluid absorption.
  • 8. Surfactants • Type 2 Respiratory epithelium produce surfactant • Surfactants reduce surface tension of the alveolus. • The harmones and growth factors that augment surfactant production are: glucocorticoids, thyroid hormone, thyrotrophin releasing hormone (TRH), prolactin, cyclic adenosine monophosphate (cAMP) and epidermal growth factor.
  • 9. Composition of surfactants • Picture of the chart
  • 10. • Antenatal glucocorticoids: - If given before 34 weeks, reduces RDS by 70% - Effect starts after 24 hours and lasts for 7 days - Other uses: Maturation of CVS, CNS and GI systems Reduces the risk of periventricular or intraventricular hemorrhage Reduces the risk of necrotizing enterocolitis
  • 11. Etiopathogenesis • Continuation of intrauterine hypoxia (placental insufficiency) • Maternal medications • Birth trauma • Postnatal factors
  • 12. A. Continuation of intrauterine hypoxia (placental insufficiency) • The placenta, due to anatomical changes or due to inadequacy of uteroplacental circulation (such as premature placental separation, circumvallate placenta, hypertensive disorders in pregnancy, abnormal labor, cord compression, vascular anomalies in cord, etc.). • Maternal hypoxic states: The maternal diseases such as anemia, eclampsia, cyanotic cardiovascular disorders, status asthmaticus, dehydration and hypotension.
  • 13. Maternal medications Medications depress the respiratory centers directly and the chance of development of asphyxia is increased. • Morphine • Pethidine • Anaesthetic agents
  • 14. Birth trauma • Malpresentation such as breech, oblique lie, occipitoposterior often requires manipulative and operative vaginal delivery (forceps or ventouse). • Prolonged second stage of labor in contracted pelvis, often causes asphyxia. • Increased intracranial tension → cerebral edema and congestion → increased intracranial pressure → asphyxia.
  • 15. Postnatal factors • Postnatal asphyxia is secondary to pulmonary, cardiovascular and neurological abnormalities of the neonate.
  • 16. Clinical features • The clinical features depend upon the etiology, intensity and duration of oxygen lack, plasma carbon dioxide excess and subsequent acidosis • According to the intensity of clinical features they have been classified previously as asphyxia livida (stage of cyanosis) asphyxia pallida (stage of shock)
  • 17. • But at present, according to the parameters denoted by Apgar, (Dr Virginia Apgar—1953) a scoring procedure has been designed for better understanding of the clinical state. • Apgar score
  • 18. • Majority of infants born with an Apgar score > 4 by 10 min., do not develop cerebral palsy (CP). • 75% children who develop CP have normal Apgar score at birth. • Apgar score alone should not be taken as an evidence of neurological damage. • Cord blood pH can assess fetal oxygenation status better.
  • 19. Clinical sequelae of birth asphyxia • Initial response is hyperapnea and hypertension → primary apnea → gasping attempt to breathe → (if unresolved) → secondary apnea → bradycardia and shock → diminished cerebral blood flow → cerebral hemorrhage → hypoxic ischemic encephalopathy (HIE) → (if severe) → either death or disability (if the baby survives).
  • 20. Neonatal diagnosis • EEG may help to detect severity of asphyxial injury • CT can detect cortical neuronal injury several weeks after asphyxial insults • USG is the method of choice for routine screening to detect IVH, necrosis of basal ganglia and thalamus. It is superior to CT • MRI: best method to diagnose hypoxic brain injury within 24 hours of the insult. It has no radiation exposure • Others: Magnetic resonance spectroscopy and proton MRS and near infrared spectroscopy.
  • 21. Prophylactic management (1) Antenatal detection of high-risk patients (2) Scrupulous fetal monitoring to ensure early detection of fetal distress and timely delivery (3) Intrapartum use of electronic fetal monitoring and scalp blood pH assessment when indicated. Scalp blood pH < 7.0 is a substantial evidence of prolonged intrauterine asphyxia (4) Judicious administration of anesthetic agents and sedatives during labor (5) Cooperation between obstetric and pediatric staff since delivery (6) Avoidance of difficult or traumatic delivery.
  • 22. Definitive management • Apgar rating—classically, the evaluation of the cardiopulmonary status in the newborn has been assessed by Apgar rating at 1 and 5 minutes after birth. • Heart rate, skin color and respiratory activity provide the most accurate evaluation and the need of resuscitation. • Normal value: 7–10
  • 23. Babies with Apgar score7–10 Pink, breathing regular, HR > 100. • The oropharynx and the nasopharynx are to be cleared off any mucus by suction. • Dry the infant and place under radiant heat source. • Oxygen is administered only when required. • The condition is reassessed at 5 minutes and if found normal, the infant should be given to mother
  • 24. Babies with Apgar score 4–6 Peripheral cyanosis, breathing irregular, HR < 100. — Baby may follow primary apnea. — Place under a radiant heater, dry the baby. — The baby is put flat or slight head down position. — Immediate suction of the oropharynx and nasopharynx is done either by mucus sucker or by suction apparatus (mechanical or electrical) whichever is available. — Stimulus to back and sole (gentle rubbing).
  • 25. Babies with Apgar score 4–6 -- Simultaneously, oxygen (100%) is administered at a rate of 5 L/min. by bag and mask at a pressure range of 30–40 cm H2 O — Intermittent positive pressure ventilation (IPPV) is given if necessary. — Support should be continued until respirations are spontaneous, color improves and the heart rate is > 100 bpm. Such an infant may be acidotic but it is corrected spontaneously after respiration is established
  • 26. If the above measures fail (secondary apnea) • Oral suction followed by tracheal intubation is done. • The tracheal tube is connected to resuscitation bag through which oxygen is administered at the rate of 5–8 liters/ minute. • Intermittent positive pressure ventilation (IPPV) is maintained at the rate of 40–60/minute. Gentle external cardiac massage is performed if the heart rate is < 60/min. • When there is history of administration of a central depressant drug such as pethidine or morphine to the mother within 3 hours of delivery, suitable antidote, e.g. naloxone hydrochloride 100 µg/kg IM (single dose) and may have to be repeated
  • 27. Babies with Apgar score below 4 central cyanosis, no breathing, HR < 100 • Tracheal intubation and intermittent positive pressure ventilation must be started immediately. • If intermittent positive pressure ventilation is nor available, gentle mouth to-mouth respiration is life saving. • For circulation to maintain, cardiac massage is given if after intubation and ventilation with 100% O2 for 30 sec. the heart rate remains < 60 bpm
  • 28. • Drugs used in resuscitation: Drugs are needed for a persistent HR < 60 bpm even after ventilation and chest compression. Drug of choice is epinephrine Other drugs are given as needed • Meconium aspiration syndrome (MAS): Endotracheal intubation and suctioning is performed with a negative pressure of 80–100 mm Hg. This procedure may be repeated.
  • 30.
  • 31. PROGNOSIS • Depends on:(1) Maturity of the baby (2) Duration and intensity of hypoxia and acidosis as evidenced by Apgar score and blood pH—higher the score, normal the pH, better is the prognosis (3) Facilities for immediate and competent management of a compromised baby. Most survivors of perinatal asphyxia do not have any major sequelae. Factors for increased risk of neurological sequelae are: (i) Apgar score of 0–3 at 20 min. of age (ii) Presence of multi organ failure (oliguria > 24 hours of life) (iii) Severity of the neonatal neurological syndrome. Severe HIE carries mortality about 80% (iv) Presence of neonatal seizure
  • 32. COMPLICATIONS: Immediate: • Cardiovascular–hypotension, cardiac failure • Renal–acute cortical necrosis, renal failure • Liver function–compromised • Gastrointestinal–ulcers and necrotising enterocolitis • Lungs–persistent pulmonary hypertension • Brain–cerebral edema, seizures.
  • 33. COMPLICATIONS: Delayed • Retarded mental and physical growth • Epilepsy–up to 30 percent in severe asphyxia • Minimal brain dysfunction
  • 34. Questions 1. Which of the following is not a diagnostic criteria of birth asphyxia? a. Profound acidemia (pH <7) on umbilical cord arterial blood sample b. Persistence of an apgar score 0-3 for > 5 minutes c. Neurological manifestations– hypotonia, coma, seizures in immediate neonatal period d. Evidence of multi organ dysfunction e. None of the above
  • 35. • Breathing activity is observed at a. 14 weeks of life b. 11 weeks of life c. 12 weeks of life d. 16 weeks of life
  • 36. • Surfactants are produced by a. Type 1 pneumocytes b. Type 2 pneumocytes c. Goblet cells
  • 37. • Which is the antidote of choice for pethidine or morphine ? a. Naloxone b. Naltrexone c. Nalmefene d. None of the above • pethidine or morphine to the mother within 3 hours of delivery, suitable antidote, e.g. naloxone hydrochloride
  • 38. • Calculate the APGAR score Baby with pulse rate of 96bpm, with weak cry on stimulation, only extremities are blue,. The baby has active movements. It has strong cry. 7