Birth Asphyxia: Walter Otieno Consultant Paediatrician

Birth asphyxia
Walter Otieno
Consultant Paediatrician
Objectives
• Understand the assessment & care of normal
birth
• Familiar with the pathogenesis of birth asphyxia
• Know Apgar score & ABCDE resuscitation
• Familiar with the complication of severe
asphyxia
Background
• Birth asphyxia is defined as a reduction of oxygen delivery
and an accumulation of carbon dioxide owing to cessation of
blood supply to the fetus around the time of birth.
• This is pathologic condition referred to neonate who have no

spontaneous breathing or represented irregular breathing
movement after birth. Usually caused by perinatal hypoxia. It
is emergency condition and need quickly treatment
(resuscitation)
Criteria for asphyxia
Intrapartum distress, as indicated by:

– fetal bradycardia
– meconium-stained amniotic fluid
– an Apgar score of 6 or less at five minutes
– need ventilation and oxygen immediately after
birth
– blood pH value of 7.20 or less
Aetiology
 Pathologically, any factors which interfere with the circulation between
maternal and fetal blood exchange could result in perinatal asphyxia.
These factors can be maternal factor, delivery factor and fetal factor
• Maternal factor:
Maternal illness (anemia, diabetes, nephritis, heart disease), maternal
infection, PROM, PIH, APH, substance abuse,
• Delivery condition:
Abruption of placenta, placenta previa, prolapsed cord, premature
rupture of membranes, sedative drugs
• Fetal factor:
Multiple birth, congenital or malformed fetus, prolonged labor,
intrauterine infections.
Pathophysiology
Hypoxic cellular damages:

a. Reversible damage(early stage):
Hypoxia may decrease the production of ATP, and result in the

cellular functions . But these change can be reversible if hypoxia is
reversed in short time.
b. Unreversible damage:
If hypoxia exist in long time enough, the cellular damage will become
unreversible that means even if hypoxia disappear but the cellular
damages are not recovers. In other words, the complications will happen.
Pathophysiology
Primary apnea
Breathing stop but normal muscular tone or hypertonia, tachycardia and
hypertension
Secondary apnea
Features of severe asphyxia or unsuccessful resuscitation, usually result in
damage of organs function.
Other damages:
a. Persistent pulmonary hypertension (PPHN)
b. Hyper/hypoglycemia
c. Hyperbilirubinemia
Clinical manifestations
fetal heart rate: tachycardia then bradycardia
fetal movement: increase then decrease
amniotic fluid: meconium-stained
APGAR SCORE
Score 0 1 2
Heart rate none <100 > 100
Respiration none irregular regular
Muscle tone limp reduced normal
Response to none grimaced cough
stimulation
Color of trunk white blue pink
Degree of asphyxia:
Apgar score 8~10: no asphyxia
Apgar score 4~8: mild/cyanosis asphyxia
Apgar score 0~3: severe/pale asphyxia

Complications
CNS: HIE, ICH
• RS: MAS, RDS, pulmonary hemorrhage, persistent
fetal circulation, pulmonary hypertension
• CVS: myocardial injury, heart failure, cardiac shock
• GIS: NEC, stress ulcer
• Kidneys: Acute renal failure, renal venous
thrombosis, Acute tubular necrosis
• Others: hypoglycemia, hypocalcemia, hyponatremia
Diagnosis
Evidence of fetal distress
Fetal metabolic acidosis
Abnormal neurological state
Multiorgan involvement
Management
• ABCDE resuscitation
• A (air way)
• B (breathing)
• C (circulation)
• D (drug)
• E (evaluation)
Basic algorithm for newborn resuscitation
Drugs
profound bradycardia, give adrenaline (1:10000, 0.1-
0.3ml/kg) by endotracheal tube or umbilical vein
if no response, intravenous fluid (saline, albumin,

plasma, blood) with 10ml/kg
if acidosis, give 5% sodium bicarbonate with 3-5ml/kg
if bradypnea, consider using naloxone (0.1mg/kg)

Hypoxic Ischemic Encephalopathy
(HIE)
• The brain damage after perinatal asphyxia and
the most severe condition showed high
mortality or remain cerebral complications
such as mental retardation & cerebral palsy.
Pathophysiology
• Cerebral blood flow
early stage: normal (intraorgans shunt)
then slow down (selective vulnerability)
finally ischemia
• Cerebral metabolism
Clinical manifestations
Excitation: hyperalert, irritable, hypertonia,

tachycardia, tachypnea, seizure, etc
Depression: coma, hypotonia, bradycardia,

bradypnea, unresponsibility, etc
Classification
• Mild(stage I): hyperalert, irritable, normal muscular

tone & reflex, no seizure, normal EEG
• Moderate(stage II): lethargy, hypotonia, weak

sucking & Moro response, often seizure, EEG+
• Severe(stage III): coma, absent muscular tone &

reflex, persistent seizure, EEG++
Management
Generalized treatment:
– Ventilation: CPAP, CMV, HFOV
– Circulation: Dopamine/Dobutamine
– Energy: normal glucose
– Fluid: restriction < 60-80ml/kg/d
Management
Control of seizures:
– Phenobarbital
loading dose 15-20mg/kg, iv maintenance dose 3-5mg/kg, iv
Cerebral edema & high pressure
– Furosemide , Mannitol 0.5g/kg, iv, q8-12h

Prognosis
• Depends on severity

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Birth asphyxia

• This is pathologic condition referred to neonate who have no

Intrapartum distress, as indicated by:

Hypoxic cellular damages:

Hypoxia may decrease the production of ATP, and result in the

Features of severe asphyxia or unsuccessful resuscitation, usually result in

damage of organs function.

a. Persistent pulmonary hypertension (PPHN)

fetal movement: increase then decrease

amniotic fluid: meconium-stained

Apgar score 8~10: no asphyxia

Apgar score 4~8: mild/cyanosis asphyxia

Apgar score 0~3: severe/pale asphyxia

Evidence of fetal distress

Fetal metabolic acidosis

Abnormal neurological state

if no response, intravenous fluid (saline, albumin,

if acidosis, give 5% sodium bicarbonate with 3-5ml/kg

if bradypnea, consider using naloxone (0.1mg/kg)

Excitation: hyperalert, irritable, hypertonia,

Depression: coma, hypotonia, bradycardia,

• Mild(stage I): hyperalert, irritable, normal muscular

• Moderate(stage II): lethargy, hypotonia, weak

• Severe(stage III): coma, absent muscular tone &

Cerebral edema & high pressure

– Furosemide , Mannitol 0.5g/kg, iv, q8-12h

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