FETAL & NEONATAL

ASPHYXIA
 DEFINITION

 Fetal asphyxia is a state of

inadequate oxygenation and
inadequate elimination of CO2, which
if allowed to be continued, will result
in metabolic acidemia (umbilical
arterial blood pH < 7.2).
 PATHOPHYSIOLOGY
 The fetal respiratory centers in the
medulla are inhibited by higher
centers in the diencephalon.
 The mild temporary anoxia at birth
(due to stoppage of the placental
circulation) depresses the higher
cortical centers, thus releasing the
medullary centers from inhibition.
 PATHOPHISIOLOGY
The medullary centers become
stimulated by:
 a. Sensory stimuli from the skin,
muscles & joints;
 b. Relative increase in carbon
dioxide concentration
(chemoreceptors)
 c. Rise in blood pressure at birth
(pressor receptors).
 PATHOPHYSIOLOGY
 However, if the anoxia is marked or
prolonged, the lower respiratory centers
in the medulla together which the
vasomotor centers become paralyzed
leading to asphyxia & shock.
 Thus, if prompt resuscitation is not done
at an early stage, the irreversible
damage to the respiratory center will
result in failure of all attempts at
recovery.
 ONSET of
RESPIRATION(causes)
 Mild temporary anoxia at birth (due to
stoppage of placental circulation), which
depresses higher cortical centers thus
releasing medullary centers from
inhibition.
 Physical stimulation: afferent sensory
stimuli from the skin, muscles & joints.
 The compression of the fetal thorax
incident to vaginal delivery & the
expansion that follows delivery may be
an auxiliary factor in the initiation of
respiration.
 Aetiology of Intrauterine fetal
distress (asphyxia)
I - MATERNAL CAUSES: (conditions
leading to imperfect oxygenation
of maternal blood)
 Severe anemia, Hemorrhage &
shock, Respiratory failure, and
heart failure.
 Eclamptic convulsions, advanced
pulmonary T.B., pneumonia, and
pulmonary edema.
 Aetiology of intrauterine
asphyxia ( cont….)
II- PLACENTAL CAUSES:
 Placental compression: interfering with its
circulation as in tonically contracted
uterus, prolonged labour after rupture of
the membranes or as a method of control
of bleeding in placenta previa.
 Placental separation as in accidental
hemorrhage.
 Placental insufficiency e.g. extensive
degeneration, multiple infarcts &
abnormally small placenta.
 Aetiology (cont…)
III- CAUSES IN THE UMBILICAL CORD:
Obstruction of the circulation, which may
be due to:
 Tight coils around the neck.
 True knots of the cord.
 Prolapsed cord.
 Compression of the vessels by haematoma
of the cord or by blades of the forceps.
 Rupture of vasa praevia.
 Aetiology ( cont…)
IV-PROLONGED COMPRESSION OF THE
FETAL HEAD:
This will cause edema and ischemia, which
interfere with the blood supply of the
medulla leading to depression of the
respiratory center. Prolonged compression
may be due to:
 Contracted pelvis (C/P disproportion).
 Rigid perineum.
 Intracranial hemorrhage.
 Forceps application for a long time.
 Depressed fracture
 CLINICAL FEATURES
1-F.H.R. >160 (tachycardia), or <100
(bradycardia, which is more
dangerous) or irregular.
2-Delay of return of the FHR to their
normal rate after uterine
contraction. (FHR normally slows
down during the uterine
contraction, and returns rapidly to
normal after it ends).
 Clinical features
3-If continuous electronic monitoring of the
fetal heart rate and uterine contractions
is available, the following criteria would
suggest fetal distress:
a-Late deceleration (see assessment of fetal
well being).
b-Variable deceleration.
C-Loss of beat-to-beat variation in fetal heart
rate.
d-A sinusoidal fetal heart rate pattern.
 Clinical features
3-Passage of meconium in cephalic
presentations, due to relaxation of
the anal sphincter due to anoxia &
­­ intestinal peristalsis.
4-Fetal acidosis: Detected by taking
blood samples from the scalp of the
fetus during labour; pH below 7.2
indicates fetal asphyxia (N. 7.25-
7.35).
 MANAGEMENT OF
INTRAUTERINE ASPHYXIA
Try to eliminate the cause if possible:
 The patient should be turned onto her side: this
may relieve either umbilical cord compression,
or alleviate poor return of blood to maternal
heart caused by occlusion of the maternal aorta
or IVC by the gravid uterus.
 Oxytocin infusion, if started, should be
discontinued to _ uterine activity & improve
placental perfusion.
 Any hypotension should be corrected by
position change, intravenous hydration or
vasopressor treatment if severe hypotension
due to induction anesthesia develops
 Management
2-Oxygen (100%) should be
administered to the mother by
facemask.
3-Atropine given to the mother may be
beneficial in some cases of fetal
bradycardia.( of no proven value )
4-If the situation improves, careful
follow up; preferably by the aid of
electronic fetal monitoring is
essential.
 Management
5-If fetal distress is not relieved within
several minutes, immediate
delivery is indicated. Vaginal
examination is done to detect
degree of cervical dilatation,
presentation, position & to rule out
cord prolapse & the fetus is
delivered by:
 Breech extraction or forceps if the
cervix is fully dilated.
 C.S., if cervix is not fully dilated.
CAUSES OF POSTNATAL ASPHYXIA
(ASPHYXIA NEONATORUM
1-Persistence of a state of severe
intrauterine asphyxia after birth.
2-Obstruction of respiratory passages
by mucus, amniotic fluid, blood or
meconium.
3-Paralysis of cardiorespiratory
centers, due to cerebral
hemorrhage.
 Cont…
4-Depression of the respiratory centers by
drugs (morphine or pethidine) or
narcotics & anesthetics given during
labour.
5-Congenital malformations: e.g. congenital
atelectasis of the lungs or congenital
abnormality in respiratory or circulatory
system.
6-Prematurity (R.D.S.).
7-Congenital debility.
 CLINICAL FEATURES OF
ASPHYXIA NEONATORUM:
# With initial oxygen deprivation the
new born develops rapid breathing
pattern followed by a period of
APNEA. .:
# Clinically, primary and
secondary apnea, are
indistinguishable.
The older classification of asphyxia
neonataorum into asphyxia Livida
and asphyxia Pallida has been
abandoned and is nowadays
 Postnatal asphyxia
 Primary apnea: It represents the
initial phase of apnea
 Secondary apnea: If oxygen
deprivation persists
 CLINICAL ASSESSMENT
(APGAR SCORE)
Virginia Apgar (1953)In this
system the child’s condition is
assessed one minute and five
minutes after birth utilizing
five features
 APGAR score
 1. Appearance (color)
 2. Pulse (heart rate)
 3. Grimace (reflex irritability)
 4. Activity (muscle tone)
 5. Respiration (respiratory effort)

Either 0, 1 or 2 is given for each

clinical feature and a total degree out
of ten is given for the 5 clinical
features.
Apgar score should be done at one and
5 minutes after birth

 1. One minute Apgar score:

determines the need for immediate
resuscitation
 2. Five minutes Apgar score is useful
index of the effectiveness of
resuscitation methods, when low is
indicative of infant at higher risk of
morbidity and mortality (prognostic)
 IMPORTANCE
 1. One minute Apgar score:
determines the need for immediate
resuscitation
 2. Five minutes Apgar score is useful
index of the effectiveness of
resuscitation methods, when low is
indicative of infant at higher risk of
morbidity and mortality (prognostic)
 MANAGEMENT OF ASPHYXIA
NEONATORUM
PROPHYLAXIS:
 1.
Proper antenatal care for
detection and proper management of
probable cause of intrauterine
asphyxia.
Management ( prophylaxis)
2. Proper intranatal care:
 Careful observation of FHR.
 Avoid operative trauma (forceps)
 Avoid morphia within 3 hours before
labor
 Proper oxygenation during
anesthesia
 Cont..
 Episiotomy is strongly recommended
especially for breech and premature
infants.
 Proper delivery of the after coming
head
 Vitamin K for all premature and
breech deliveries
 Aspiration of the mucus and
meconium from fetal larynx before it
starts breathing.
 ACTIVE MANAGEMENT
(ACTIVE RESUSCITATION
 Resuscitation of the new born is an
excellent example of a team work that
needs cooperation and harmony between
each member, namely the obstetrician,
the neonatologyst, the anaesthesiologyst
and the nursing team.
 The first few minutes in the new born's
life may be crucial in determining both its
potential for survival and its future health
performance which may not be revealed
except after several months or even
 Active management
1-Clearing the air passages: Holding the
infant from the feet and aspirating mucus
from the mouth and upper pharynx by a
rubber catheter.
 N.B.: The infant's head should
not be lowered if intracranial
hemorrhage is suspected.
1-Warming the infant:Warming is
necessary to decrease oxygen
requirements and to avoid attacks of
apnea.
 Active Management
3-Oxygen therapy : When necessary, may
be supplied by:
 Small mask or stream in front of the
mouth and nose (O2 saturation …).
 Endotracheal tube is indicated if:
– 1 minute Apgar score < 3
– Persistent Apnea.
– Persistent Bradycardia < 100.
4-Artificial respiration: by:

 Endotracheal tube with intermittent

positive pressure insufflation

 Mouth to mouth breathing until

endotracheal tube is available.
 Active Management
5-Cardiopulmonary resuscitation:

Cardiac resuscitation together with

Endotracheal entubation (or mouth to
mouth breathing)
– No audible heart beats or
– Heart rate < 100.
– Thumbs are put at the junction of lower and
middle 1/3 of sternum to compress the chest
gently 100 times per minute.
 Active Management
6-Use of Drugs:
 Nalorphine: ½ mg into umbilical vein if
asphyxia is due to morphia.
 Sodium bicarbonate 8.4%: If the infant
develops acidosis with severe asphyxia.
 Epinephrine: May be used for cardiac
resuscitation (if absent heart beats).
 Up to 0.5 cc are injected either into umbilical
vein or intracardiac
 Antibiotics: To prevent pneumonia
especially if resuscitation has been difficult.