2. INTRODUCTION
Asphyxia neonatorum is a condition of respiratory
failure in in the newborn, it occurs due to inadequate
intake of oxygen before, during, or just after birth
(inadequate gases exchange by respiratory system).
It is also termed as “Birth asphyxia “ which implies the
inability of the newborn baby to establish regular
respiration following birth.
It’s a medical emergency, steps should be taken to
establish respiration→preventing long-term damage and
fatality.
NB:Asphyxia-A condition arising when the body is deprived of O2,caused unconsciousness or death;
suffocation.
Neonatorum: It is derived from English word “Neonate” means a newborn baby aded less than 28
days(4 weeks).
3. Epidemilogy
Birth asphyxia is the most common medical
emergency in newborn babies.
It is also the leading cause of neonatal mortality and
morbidity.
WHO estimates that globally, between 4 & 9 million
newborns suffer birth asphyxia/year
1.2 million deaths and about the same number of
infants who develop severe disability.
WHO estimates for global neonatal deaths caused by
birth asphyxia are 29% (2002).
BA was one of the main causes of neonatal death at
KCMC. Those admitted due to birth asphyxia at KCMC,
41% of them died in the ward. BA was diagnosed on the
basis of Apgar score.
5. Maternal Factors :
I. Inadequate oxygenation of maternal blood
- hypoventilation during anaesthesia
- respiratory failure -Worsening of blood oxygenation in mother
- cyanotic heart disease
- severe anaemia/ Heart Failure
- maternal smoking
2.Hypotension
- complication of spinal anaesthesia
- vena cava and Aorta compression by gravid uterus.
6. 3.Uterine tetany
- excessive Oxytocics
- lack of uterine relaxation to allow placental filling
4.Hypertension (PIH)→placental insufficiency
5.Eclampsia -Unequal blood supply of the maternal part of placenta ( hypertension of any
etiology in mother)
6. Bleeding →↓BP → shock
7. Diabetes Mellitus
7. Fetal factors :
1.Malpresentation eg. Breech
2.CPD → prolonged / obs labour / difficult labour
3.Multiple Births
4.Severe Fetal Anaemia- hydrops
5.Postmaturity→ meconium aspiration/ block
6.Infection –increase oxygen demand
7.Congenital malformations (dysmorphism) Failure of respiratory efforts of the newborn (iatrogenic – drug
induced, caused by congenital malformations).
8.SGA
8. Placental :Disturbances of gaseous exchange through the
placenta (placental abruption, placental presentation)&
Blood flow interraption through the umbilical cord (tight umbilical
cord entanglement around of a neck - loop of cord)
1.Abruptio placenta
2.Placenta praevia
3.Cord prolapse
4.Cord
entanglement/compressi
on
5.Twin to twin
transfusion
9. Pathophysiology
The brain is a highly metabolic organ: constitutes 2%
of the bwt but consumes > 15% of energy (Adenosine
triphosphate-ATP).
It is highly dependent on cerebral blood flow for
aerobic respiration. Cessation for 10-15 sec → coma
It has limited anaerobic respiration
Most of the energy is needed by neurons when pumping
ions through their membranes
During excessive brain activity neuronal metabolism can
increase by 100-150%
10. Pathophysiology cont:
When fetal asphyxia happens, the body will show a self-defended mechanism
which redistribute blood flow to different organs called “inter-organs shunt” in
order to prevent some important organs including brain, heart and adrenal
glands from hypoxic damage.
If energy supply is limited for longer and acidic substances accumulate, the
capillary wall gets damaged and leaky, associated with increased capillary
pressure
This leads to swelling of brain cells, followed by decreased blood flow and
ischemia.
Ischemia triggers arteriolar dilatation again, increasing capillary pressure,
worsening the edema
Edema prevents oxygen delivery to the cells
Final stage: death of brain cells
Hypoxic cellular damages:
Reversible damage(early stage):
Hypoxia may decrease the production of ATP, and result in the cellular
dysfunctions . But these change can be reversible if hypoxia is reversed (corrected)
in short time.
11. Pathophysiology cont…
Irreversible damage(late stage):
Persistent hypoxia leads to irreversible cellular
damage characterized by hypoxemia(abnormal
low level of O2 in the blood) and marked loss of
Cerebral blood flow auto regulation, increased
cellular damage and cellular energy dependent
pump(Na+/K+ ATPase in the plasma membrane
which transport ions and small molecules against
their concentration gradients).
12. Pathophysiology cont….
Progressive Hypoxia leads to:
Primary apnea
Impaired breathing with normal muscular tone
or hypertonia, tachycardia (fast heart rate), and
hypertension
Happens early and shortly; as an auto regulatory
mechanism to maintain vital organs perfusion.
13. Pathophysiology cont:
Secondary apnea
Features of severe hypoxemia due to lack or
unsuccessful resuscitation, usually result in
organs dysfunction.
Other damages:
a. Persistent pulmonary hypertension (PPHN)
b. Hyper/hypoglycemia
c. Hyperbilirubinemia
d. Electrolyte imbalances hyponatremia and hypocalcemia
16. APGAR SCORE
Discovered by American anesthesiologist in 1959 – Virginia
APGAR
This is the first test performed to the newborn at delivery
room
It evaluates quick physical assessment of the newborn & if
any need of extra care
A: activity(muscular tension)
P: pulse(heart rate)
G: grimace(reactive ability)
A: appearance(skin color)
R: respiration
17. APGAR SCORE TABLE
Sign 0 1 2
A
Activity (Muscle
Tone)
flaccid
Arms and Legs
Flexed(some
flexion)
Active
Movement
P Pulse Absent Below 100 bpm Above 100 bpm
G
Respond to
stimulation
(Reflex
Irritability)
No Response Grimace Cry (withdraw)
A
Appearance
(Skin Color)
Blue-gray, pale
all over
Normal, except for
extremities
Normal over
entire body
R Respiration Absent Slow, irregular
regular, strong
cry
18. Diagnosis
Score is given at 1st and 5th minute
At 1st min→ measures how well the newborn infant
tolerated the birth processing
and the 5th min→ measures how well the newborn
infant is adapting to the outside environment.
SCORE < 7 AT FIFTH MINUTE→ BIRTH ASPHYXIA
20. However,
APGAR SCORE ISA POOR SURROGATE(non conclusive) OF BA
Eg: Prematurity
Therefore:
American College of Obstetricians and Gynecologists25 and the American
Academy of Pediatrics, a neonate is labeled
to be asphyxiated if the following conditions are satisfied:
(1) Umbilical cord arterial pH less than 7;
(2) Apgar score
(3)Neonatal neurologic manifestations (eg, seizures, coma, or hypotonia)
(4) Multisystem organ dysfunction, eg, cardiovascular, gastrointestinal,
hematologic, pulmonary, or renal system.
Thus hypoxia or asphyxia should be labeled as a cause of disability and handicap
only when the neonate demonstrates the four perinatal findings listed
21. Management-Resuscitation 1st minute counts (Golden)
ABCDE resuscitation
A (air way)
B (breathing)
C (circulation)
D (drug)
E (evaluation)
Five initial steps of Resuscitation:
Drying
Provision of warmth
Positioning
Suction
Tactile stimulation
22. Airway
1/ open airways by placing the head in the neutral
position-Head up, jaw thrust& hyperextension of the
neck
2/ clear the secretions from the airway by suctioning as
soon as possible
3/ if meconium-stained-deep tracheal suctioning should
be performed to removal of all the meconium to avoid
chemical pneumonitis - MAS
23. Breathing
1/ ensure face mask covers nose & mouth connect to
oxygen bag
2/ establish respiration of 30-40/min with chest wall
movement
3/ No response consider advanced airway
management-intubation & mechanic ventilation
24. Breathing
1/ ensure face mask covers nose & mouth connect to
oxygen bag
2/ establish respiration of 30-40/min with chest wall
movement
3/ No response consider advanced airway
management-intubation & mechanic ventilation
25. Circulation
1/ if heart rate <60/bpm, start external cardiac
compression
2/ Ratio 3:1 ( 90 compressions to 30
bpm)
26. Drugs
1/ In profound bradycardia, give adrenaline(1:10000, 0.1-0.3ml/kg) by
endotracheal tube or umbilical vein
2/ if no response, intravenous fluid (saline, albumin, plasma, blood) with
10ml/kg
3/ In case of acidosis, give 5% sodium bicarbonate (SB) with 3-5ml/kg
4/ Apneic and mum was given opiods consider using naloxone (0.1mg/kg)
5/ Dextrose 10% during prolonged resuscitation
NB:Control seizures (give phenobarbitone/phenytoin), check RBG to R/O
hypogycemia, if seizures at day2-3 mostly due to hypocalcemia& Control
brain edema ( don’t overload with fluids, maintenance for age)
27. Complications of birth asphyxia
Early
Seizure
Poor feeding
Infections
Renal failure
Feature of multi organ involvement
CNS: HIE, ICH
RS: MAS, RDS, pulmonary
hemorrhage
CVS: heart failure, cardiac shock
GIS: NEC, stress gastric ulcer
Others: hypoglycemia,
hypocalcemiia, hyponatremia
Late
Vision and hearing
impairment
Learning difficulties and
mental retardation
Cerebral palsy and epilepsy
28. Hypoxic Ischemic encephalopathy
HIE is cellular damage that occurs within the central
nervous system(the brain and spinal cord) from
inadequate oxygen.
It results into ↑ mortality→↑sudden infant death
syndrome (SIDS)
If there are no signs of HIE in the first 48 hours
after birth, they are unlikely to occur later
31. Sarnat Stages of HIE
Mild: hyperalert,
hyperexcitable, normal muscle
tone, no seizures (Sarnat Stage
I)
Moderate: hypotonia, decreased
movements, and often seizures
(Sarnat II)
Severe: stuporous, flaccid, and absent primitive
reflexes, usually with seizures (Sarnat III)
32. TABLE 1
The HIE scoring chart
Score
Sign 0 1 2 3
Tone Normal Hyper Hypo Flaccid
LOC Normal Hyper alert Lethargic Coma
Fits None Infrequent < thrice /day Frequent < thrice /day
Posture Normal Fisting/cycling Strong distal flexion Decerebrate
Moro Normal/partial Absent
Grasp Normal Poor Absent
Sucking Normal Poor Absent/bites
Respiration Normal Hyperventilation Brief apnoea IPPV(apnoea)
Fontanel Normal Not full tense Tense
Total
LOC, Level of Consciousness; IPPV, Intermittent Positive Pressure Ventilation
33. Neonatal hypoxic-ischemic
encephalopathy staging
Stage 1 Stage 2 Stage 3
Consciousness Hyperalert Lethargic Stuporous
Neuromuscular Normal Mild hypotonia Flaccid
Reflexes Weak to normal Weak Absent
Pupils Dilated Constricted Variable
Heart rate Tachycardia Bradycardia Variable
Secretions Sparse Profuse Variable
Gastrointestinal
motility
Normal or
decreased
Increased Variable
Convulsions None Common Common early, less
common late
Duration <24 hours 2-14 days Weeks
49
34. A score of 0 is normal
a maximum score is 22 which signifies the worst
possible status of HIE.
Infants scoring 1–10 are considered to have mild HIE,
11–14 have moderate
15–22 have severe HIE.
35. Investigations using imaging
CT-SCAN- good in older children than neonates because of high water
content of the neonatal brain, which reduces contrast between normal
and injured tissue.
BRAIN USSpresence of hyperechogenic basal ganglia or cystic
degeneration of the white matter on sonograms is predictive of a poor
outcome
-however about 50% of sonograms are normal in neonates with HIE
- Doppler increases the specificity and sensitivity
MRI- most sensitive and promising technique in neonates.
-White matter and gray matter injuries can be detected with MR imaging
in both term and preterm neonates.
-Documented patterns include absence of the normal signal intensity in
the posterior limb of the internal capsule, bilateral abnormalities within
the basal ganglia and thalami, loss of gray/white matter differentiation
in the hemispheres, and highlighting of the cerebral cortex.
36. Prognosis
Clinical predictors of poor outcome –
1. Refractory seizures.
2. Neurological deficit at the end of first week.
3. -Mild encephalopathy → high probability of being
completely normal
-Moderate encephalopathy →20 to 35 percent risk of later
sequelae from the insult,
although those whose neurologic examinations are
completely normal within one week have a good likelihood of
normal outcome
-Severe encephalopathy →75 percent risk of dying in the
neonatal period, and among survivors, an almost universal risk
of sequelae exists
37. Prevention
1.Anticipation is the key in prevention and management of
asphyxia by the provision of adequate perinal care & early
intervention of BA
