The infant in choice c presents with signs of moderate encephalopathy after a known perinatal hypoxic event and meets criteria for therapeutic hypothermia based on guidelines. The other infants presented do not meet criteria either due to prematurity, mild encephalopathy findings, or presenting outside the time window.

1. Birth Asphyxia
(PERINATAL ASPHYXIA)
Dr. Jwan Ali Ahmed AlSofi

2. Contents
Pathophysiology
Causes
Clinical presentation
Treatment
Prognosis

3. PERINATAL ASPHYXIA
• Is a mixture of hypoxia, hypercapnia, and a combination of both
respiratory and metabolic acidosis.

4. Pathophysiology:
•Asphyxia results in a series of changes in the fetus
and newborn, corresponding to changes in the pH of
the blood.
•Interruption in blood flow and oxygen supply will
result in the fetus or newborn transitioning to
anaerobic respiration, with a resultant buildup of
lactic acid, leading to a decrease in the pH of the
blood and an acidotic state.

5. Causes of Perinatal Asphyxia
Maternal
• 1. Decreased
uterine blood
flow
• 2. Maternal
hypotension
• 3. Regional
anesthesia
• 4. Eclampsia
• 5. Abnormal
uterine
contractions
Placental
• 1. Infarcts
• 2. Premature
separation
(abruption)
• 3.
Inflammatory
changes
Fetal
• 1. Cord
compression
(nuchal,
prolapsed) or
entanglement
(twins)
• 2. Breech
presentation
• 3. Anemia
• 4.Hypovolemia
(in utero blood
loss)
Neonatal
• 1.Hypovolemia
• 2. Apnea
related to
drug-induced
depression
(narcotics,
magnesium)
• 3. Congenital
anomalies of
the airway and
lung
• 4. Prematurity

7. CLINICAL MANIFESTATIONS:

8. Signs before delivery:-
•The signs of hypoxia in the fetus are usually noted a
few minutes to a few days before delivery.
1. IUGR with increased vascular resistance may be
the first indication of fetal hypoxia.
2. The fetal heart rate slows, and the beat-to-beat
variability declines.
3. Fetal scalp blood analysis may show a pH less
than 7.20. The acidosis is made up of varying
degrees of metabolic or respiratory components.

9. Action
•These signs should lead to
1. Administration of high concentrations of oxygen
to the mother
2. And immediate delivery to avoid fetal death CNS
damage.

10. Signs at delivery:-
1. Presence of yellow, meconium-stained amniotic
fluid is evidence that there has been fetal
distress.
2. Infants are frequently depressed and fail to
breath spontaneously.

11. Signs Few hours after delivery:-
1. The tone change from hypotonia to extreme
hypertonia, or may appear normal.
2. Pallor.
3. Cyanosis and apnea.
4. Slow heart rate.
5. Unresponsiveness to stimulation.

13. Clinical Presentation
1. Apnea
2. Vascular redistribution
3. Hypoxic-ischemic brain injury

14. Apnea:-
1. Primary apnea:
• Primary apnea can result from acidosis secondary to decreased fetal
circulation.
• It is often recoverable with stimulation.
• It may progress into a period of gasping and, without intervention, may
develop into secondary apnea.
2. Secondary apnea:
• Results after a more prolonged period of decreased oxygenation and will lead
to a decreased heart rate, as well as additional cardiovascular compromise if
not corrected.
• Secondary apnea can only be corrected with improved ventilation, usually
via positive-pressure ventilation (PPV) through a mask or endotracheal tube.
• Because after delivery of an infant it is impossible to differentiate between
primary apnea and secondary apnea, assume the infant is in secondary
apnea and begin resuscitation immediately .

16. • The asphyxiated infant passes through a series of events:
1. rapid breathing and fall in heart rate
2. primary apnea
3. irregular gasping, further fall in heart rate and drop in blood pressure
4. secondary apnea
• Most infants in primary apnea will resume breathing when stimulated.
• Once in secondary apnea, infants are unresponsive to stimulation.

17. Vascular redistribution:
Eventually, prolonged asphyxia results in decreased cerebral blood flow, which
can lead to hypoxic-ischemic brain injury.
Prolonged periods of decreased systemic blood pressure and perfusion can result in
end-organ damage in other systems as blood is shunted away from some organs to
maintain cerebral perfusion.
Kidney— AKI with ↑ creatinine levels and abnormal
urine production (e.g., polyuria, oliguria, and/or anuria)
GI tract— ischemic bowel injury; may increase the risk
of necrotizing enterocolitis in at-risk infants.
Persistent hypercarbia, hypoxemia, and/or acidosis may lead to decreased systemic
blood pressure and loss of autoregulation of the cerebral blood flow.
The hypercapnia, hypoxemia, and acidosis that result from asphyxia will initially
cause a redistribution of blood flow to the heart, brain, and adrenal glands.

18. • Prolonged intrauterine hypoxia may result in periventricular
leukomalacia(PVL).
• Pulmonary arterioles smooth muscle hyperplasia may develop,
predisposes the infant to pulmonary hypertension.
• If fetal distress produces gasping, the amniotic fluid contents
(meconium, squamous, lanugo) are aspirated into the trachea or
lungs.

20. Hypoxic-ischemic encephalopathy
• This occurs after a hypoxic or ischemic event resulting in
asphyxia, shortly before or at the time of delivery.
• Is an important cause of permanent damage to central
nervous system cells, which may result in:
1. Neonatal death
Or may be manifest later as:
2. Cerebral palsy
3. Mental deficiency

21. Hypoxic-ischemic brain injury- Mechanism
1. Primary energy failure
- Occurs Immediately after the insult,
- there is a depletion of (ATP),.
- Results in immediate necrotic cell death, from which the brain metabolism may
be able to recover.
- Necrosis occurs after cellular membrane breakdown (from lack of ATP) results in
the leakage of cellular contents, resulting in inflammation and necrotic cell
death.
2. Secondary energy failure
- Occurs if the injury is sufficiently severe, after a brief period of attempted
recovery.
- may occur hours to days after the initial insult (usually, 6–48 hours).
- Glutamate, an excitatory amino acid, accumulates in the extracellular space due
to increased production, as well as decreased reuptake by damaged cells.
- This results in an increased Ca2+ influx and activation of degradative enzymes,
as well as reactive oxygen species, which lead to delayed, apoptotic cell death.

22. • This will lead to Neonatal neurologic abnormalities :
• hypotonia to extreme hypertonia , or may appear normal .
• Multiple organ involvement :
• congestive heart failure,
• pulmonary hypertension,
• respiratory distress syndrome,
• gastrointestinal perforation ,
• acute tubular necrosis
• hematuria.

23. Definition of hypoxic-ischemic encephalopathy (HIE) due to perinatal
asphyxia, as given by the American Academy of Pediatrics (AAP) and
American College of Obstetrics and Gynecology (ACOG):
1. Significant metabolic or mixed acidosis in an umbilical arterial
sample.
2. pH <7.00 or BE > −12— high-risk fetal compromise
3. Apgar score of <4 for longer than 5 minutes
4. Neonatal neurologic abnormalities
5. Multiple organ involvement
6. Umbilical venous blood—reflects supply from placenta (blood
from placenta to fetus): average pH, 7.20–7.40; Po2, 30 mm Hg;
Pco2, 40 mm Hg; base excess (BE) = −3
7. Umbilical artery blood – reflects condition of fetus (blood
returning from fetus to placenta): average pH, 7.15–7.35; Po2, 16
mm Hg; Pco2, 55 mm Hg; BE = −3

24. Severe encephalopathy characterized by:
1. Flaccidity
2. Coma
3. Refractory seizures
4. Apnea
5. a marked decrease of cortical attenuation on CT,
 Is associated with a poor prognosis.

25. Apgar scores
• This developed to provide a more consistent and objective way to
describe the condition of an infant in the delivery room .
• Can be used to
1. describe the infant’s condition
2. response to delivery room interventions.
• Scores assigned at 1 and 5 minutes after birth.
• If the score remains less than 7 at 5 minutes, score should continue
to be assigned every 5 minutes until 20 minutes of life.
• Poor scores have been shown to be associated with increased
mortality, but scores are not predictive of long term neurologic
outcome.

29. Treatment:

30. Immediate resuscitation
of the neonate
Therapeutic cooling

31. Immediate resuscitation of the neonate
1. AIRWAY AND VENTILATION
• Establishing a patent and secure airway that allows for adequate ventilation is crucial in the
successful resuscitation of the neonate because most episodes of bradycardia will respond
to improved ventilation.
• Most infants can be effectively ventilated with a bag and mask device and do not require
the placement of an advanced airway, such as a laryngeal mask airway or endotracheal
intubation.
• Intubation for direct suctioning of meconium below the cords is no longer recommended.
2. Chest compressions
• should be coordinated with ventilation breaths in a 3:1 (compression-to-breath) ratio.
• The goal is for 120 events in a 60-second period—that is, 90 compressions and 30 breaths.
• Indicated when HR remains less than 60 bpm after at least 30 seconds of PPV that inflates
the lungs (effective ventilation)
3. Drug used in resuscitation: is epinephrine in 0.1mg/ml concentration
(1:10000), this is the only concentration that should be used in neonatal
resuscitation
• The volume given during resuscitation is 0.1-0.3ml/kg/dose IV or 0.5-1ml/kg /dose via
endotracheal tube (0.01–0.03 mg/kg/dose IV or 0.05–0.1 mg/kg/ dose via ETT).

32. Therapeutic cooling
• Therapeutic head and whole-body cooling have shown improved
neurodevelopmental outcomes in infants with moderate to severe encephalopathy
at birth.
• The goal of therapies, such as whole-body cooling, is to prevent the onset or lessen
the impact of secondary energy failure by
1. Decreasing cellular metabolism in the brain,So Suppress cell death by
decreasing proapoptotic proteins and increasing antiapoptotic proteins and
neurotropic factors.
2. Suppress inflammation by decreasing activated microglia and neutrophils,
decreasing reactive oxygen species and proinflammatory cytokines
• Criteria for diagnosis of HIE that qualify neonates for therapeutic cooling include
clinical and biochemical components :
1. History of perinatal asphyxia event
2. Evidence of acute acidosis on umbilical artery gas
3. Apgar < 5 at 10 minutes or continued need for mechanical ventilation at 10 minutes after birth.
Neurologic criteria
1. Seizure
2. Or evidence of moderate to severe encephalopathy on examination (must have at least three to
six components in the moderate to severe category )

34. Prognosis:
•Depends on whether:
 It’s metabolic and cardiopulmonary complications (hypoxia,
hypoglycemia, shock) can be corrected or not.
On the infant's gestational age (outcome is poorest if infant is
preterm).
And on the severity of the hypoxic-ischemic encephalopathy.
•The outcome ranges between normal to severe in the
form of cerebral palsy, seizure, deafness.

35. Cases - MCQS

36. • At delivery room, the obstetrician informed you
about a pregnant woman on delivery, that there is
fetal distress. The delivery was by normal vaginal
delivery, the neonate was depressed, gasping
respiration and APGAR score at first minute was 2
after resuscitation at 5th minute the APGAR was 5.
1.Describe the clinical diagnosis of the neonate.
2.What are active measures you are going to do for
this neonates.

37. 1. Asphyxia
2. Immediate resuscitation

38. • A 2 months old infant presented to your office with history of
birth asphyxia, family had concern about the future of this
infant, he delivered prematurely by 4 weeks, the fetal
monitoring result was bad, and decision for cesarean section
was late.
• What other important Question you will ask in regard to
explain the prognosis for family?
• Would you ask for any imaging tools for diagnosis
confirmation. MRI
• What are important evidences for severe encephalopathy?

39. • Clinical manifestations of fetal hypoxia includes:
1. Normal birth weight
2. Normal beat to beat variation
3. Metabolic acidosis only
4. Increased vascular resistance
Answer: d
• There will be IUGR, acidosis could be metabolic or respiratory or both components
and beat to beat variation declines.

40. CASE-1
• You are called to the delivery of a 39-week infant, with no known
maternal complications of pregnancy. Meco- nium was noted at the
time of delivery. You arrive in the delivery room ∼1 minute after birth
and find the infant is on a warmer, apneic, and being vigorously
stimulated by nursing staff. The HR is noted to be less than 100
bpm. Of the following, which is the most appropriate next step to
improve the patient’s heart rate?
a. Continue vigorous stimulation of the patient
b. Deep-suction the posterior pharynx
c. Provide positive-pressure ventilation via bag-mask ventilation
d. Intubate the patient
e. Obtain umbilical access and administer intravenous epinephrine

41. CASE1
• c. This patient is likely in secondary apnea.
• The appro- priate next step is to provide effective positive-pressure
ventilation.
• Continuous stimulation is unlikely to induce spontaneous respirations
and improvement in heart rate in this infant.
• Deep suctioning may fur- ther exacerbate bradycardia by inducing a
vagal nerve stimulatory response.
• If the patient does not respond to effective bag-mask ventilation,
obtaining a more secure airway and administration of epinephrine
may become necessary, but not before a period of effective positive-
pressure ventilation and chest compressions has been attempted.

42. • CASE-2. Based on current evidence and practice guidelines, which of the
following describes an infant who would most benefit from therapeutic whole-
body cooling?
a. 33-week infant born due to maternal preeclampsia, required intubation at birth,
Apgar scores—1 at 1 minute, 3 at 5 minutes, 8 at 10 minutes
b. 37-week infant born after prolonged shoulder dysto- cia, Apgar scores—1 at 1
minute, 3 at 5 minutes, 8 at 10 minutes—and an arterial cord gas of pH 6.98/ CO2
88 mmHG/PaO2 24 mmHg/ Bicarbonate 20 mmol/L/base excess–17 who at 1 hour
of age appears hyperalert, with mildly increased tone, a weak suck, HR of 190
beats/min, and respiratory rate (RR) of 75 breaths/min.
c. 39-week infant born after uterine rupture, Apgar scores—1 at 1 minute, 3 at 5
minutes, 8 at 10 minutes—and an arterial cord gas of pH 6.98/CO2 88 mmHG/PaO2
24 mmHg/ Bicarbonate 20 mmol/L/ base excess–17 who at 1 hour of age appears
coma- tose, remains intubated, is lethargic, with decreased activity, hypotonia,
incomplete Moro reflex and suck, and intermittent spontaneous respirations on the
ventilator.
d. 37-week infant, now 12 hours old, found in mother’s room to be unresponsive
and received CPR with two doses of epinephrine before spontaneous return of cir-
culation.

43. case2
• c. The infant in choice c presents with signs of moder- ate
encephalopathy after a known perinatal hypoxic event and is most
likely to have a neurologic benefit from whole-body cooling.
• The infant in (b) has also experienced a significant hypoxic event at
birth but shows signs of only mild encephalopathy on examina- tion
and therefore does not meet the criteria for whole- body cooling.
• The infant in (a) is preterm; cooling in this population has not yet
been established to be beneficial.
• The infant in (d) had an unwitnessed hypoxic event 12 hours after
birth; whole-body cooling for neonates who experience this type of
arrest is not the standard of care.

44. CASE-3
• Which of the following is the preferred dose of
epineph- rine to be given during a neonatal
resuscitation?
a. 0.01-mL/kg/dose of a 1:10,000 solution IV
b. 0.5-mL/kg/dose of a 1:1000 solution via ETT
c. 0.0-mL/kg/dose of a 0.1-mg/mL solution (1:10,000)
IV
d. 1-mL/kg/dose of a 1:10,000 solution via ETT

45. Case 3
• c. This is the preferred dosage and route of administra- tion for
epinephrine during a neonatal resuscitation.

46. 4
• Which of the following is an advantage of a self-
inflating bag over a T-piece resuscitator?
a. It can administer PPV without a source of compressed air
or oxygen
b. It can provide PEEP when applied continuously to the
face
c. It provides consistent PIP and PEEP with each breath,
with minimal variation between breaths
d. It can be used to deliver oxygen concentrations > Fio2
21%

47. 4
• 4. a. Of the most commonly used devices used in neona- tal
resuscitation, the self-inflating bag is the only device that can deliver
positive-pressure breaths without being attached to a source of
compressed air or flow.
• A self-inflat- ing bag cannot deliver PEEP unless additional valves or
mechanisms are attached to the device, whereas a T-piece
resuscitator can. Additionally, the benefit of a T-piece resuscitator is
that it will deliver consistent PIP and PEEP to the patient, provided
that a good seal is made between the mask and the patient’s face
and/or the ETT remains in place. Both devices can deliver PPV with
an increased Fio2 concentration if attached to an oxygen source.

48. 5
• The hypercapnia, hypoxemia, and acidosis that result
from asphyxia will initially cause a redistribution of
blood flow to which organs?
a. Heart, kidneys, and adrenal glands
b. Heart, intestines, and brain
c. Heart, brain, and adrenal glands
d. Brain, intestines, and kidneys
e. Brain, kidneys, and heart

49. 5
• c. The hypercapnia, hypoxemia and acidosis that result from asphyxia
will initially cause a redistribution of blood flow to the most vital
organs, the heart, brain and adrenal glands.

50. 6
• Which of the following is a feature of primary
energy failure from hypoxic brain injury?
a. Occurs 6−48 hours after hypoxic injury
b. Necrotic cell death
c. Apoptosis
d. Decreased glutamate reuptake by damaged cells
e. Increases in cerebral ATP stores

51. 6
• b. Necrotic cell death occurs after primary energy failure due to
depletion of cerebral ATP stores and inactivation of the Na/K
membrane pumps. Secondary energy failure occurs 6−48 hours after
the initial hypoxic injury and results in decreased glutamate reuptake,
which leads to the induction of apoptosis.

52. The END