ASPHYXIA NEONATRUM
By: Temesgen D (MSc)
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At the end of the session you will be able to:
•Define asphyxia neonatrum
•Discuss the etiopathologyof Asphyxia
•Describe pathophysiology of Asphyxia neonatrum
•Describe the clinical features of asphyxia neonatrum
•Discuss how to diagnose and treat asphyxia neonatrum
•Manage neonate with asphyxia neonatrum
Session Objectives
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Perinatal Asphyxia…
•As a result of anaerobic glycolysis lactate is produced and will
accumulate in the brain, heart and other tissues with a resultant effect
of metabolic acidosis (evidenced by low cord PH< 7).
•Manifestations of perinatal asphyxia are low APGAR score <3 at 10
th
minute and abnormal muscle tone
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Perinatal Asphyxia…
Perinatal asphyxia is often the continuation of antepartum or
intrapartum event
It is a significant cause of perinatal death (50%).
Incidence of asphyxia varies depending on the gestational age
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Placental insufficiency
The placenta, as a respiratory organ of the fetus, fails functionally
either due to anatomical changes or due to inadequacy of utero-
placental circulation such as:
Premature placental separation
Hypertensive disorders in pregnancy
Cord compression
Vascular anomalies in cord, etc.).
A. Continuation of Intrauterine Hypoxia
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Maternal hypoxic states:
The maternal diseases such as:
•Anemia
•Eclampsia
•Cyanotic cardiovascular disorders
•Status asthmaticus
•Dehydration and
•Hypotension
A. Continuation of Intrauterine Hypoxia…
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B. Prenatal and IntranatalMedication to the Mother
Morphine, pethidine and anaestheticagents depress the respiratory
centers directly and the chance of development of asphyxia is
increased.
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C. Birth Trauma to the Neonate
Malpresentation such as breech, oblique lie, occipitoposterioroften
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.
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D. Postnatal factors
Postnatalasphyxiaissecondarytopulmonary,cardiovascularand
neurologicalabnormalitiesoftheneonate.
Theseoftenoverlap,makingisolationofasinglecausativefactor
difficult
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Clinical Features
•The clinical features depend upon:
Etiology
Intensity and duration of oxygen lack,
Plasma carbon dioxide excess and
Subsequent acidosis
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APGAR score VsClinical features
•The APGAR score is related to the status of oxygenation of the fetus at or
immediately after birth.
•Long-term neurological correlation is obtained at the 5 minute score which is
of more value.
•In cases where the score remains significantly depressed at 5 minutes, it
should be evaluated again after 15 minutes.
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Newborn Arterial Blood Gases (Normal Value)
•Normal range of arterial blood gas values for a term newborn are :
Pa O2 50–80 (mm Hg);
Pa CO2 35–45 mm Hg;
HCO3 24–26 mEq/L and
pH 7.35-7.45
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Pathophysiology of Birth Asphyxia
•Initial response is hyperapneaand 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).
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Management
•Management of perinatal asphyxia can be divided into two:
1.Prophylactic
2.Definitive
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1. Prophylactic
a)Antenatal detection of high-risk patients;
b)Thorough fetal monitoring to ensure early detection of fetal distress and
timely delivery;
c)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;
d)Cautious administration of anesthetic agents and sedatives during labor;
e)Cooperation between obstetric and pediatric staff since delivery;
f)Avoidance of difficult or traumatic delivery
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•HIE is a type of brain dysfunction that occurs when the brain
doesn't receive enough oxygen or blood flow for a period of time.
•HIE refers to the characteristic neurological manifestationsin
newborns which develop soon after birth following perinatal asphyxia.
Hypoxic Ischemic Encephalopathy (HIE)
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Classification of HIE
ClinicalspectrumsofHIEincludesmild,moderateorsevereaccordingtoSaranatstagesofHIE
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Before Birth: Sign of fetal distress
•Fetal heart rate changes
•Meconium stained amniotic fluid
•Fetal acidosis : scalp blood pH < 7.2
•Weak cord pulsation, if cord is prolapsed.
After Birth:
Clinical Features
APGAR score
Diagnosisof Asphyxia
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Differential Diagnosis
Brain tumors
Developmental defects
Genetics of Methylmalonicacidemia
Genetics of Propionic acidemia
Infections
Neuromuscular disorders including neonatal myopathy
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•Drugs are needed for a persistent HR < 60bpm even after ventilation and
chest compression.
•Epinephrine: 10 mg /kg ( 0.1 ml/kg of 1:10,000 solution) is given IV
when there is persistent bradycardia.
•It may be repeated every 5 minutes.
•Maximum dose is 30 mg/kg IV
•Sodium bicarbonate to treat metabolic acidosis (pH < 7.2) IV (4 ml/kg
of 0.5mEq/ml, 4.2% solution) is given.
Drugs used for Asphyxia (Resuscitation)
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•Reversal of narcotic drug is needed when mother has been given Pethidineor
Morphinewithin three hours of delivery.
•Naloxone100 mg/kg is given to the baby by IV, IM or endotracheal.
•Volume expansion is needed when blood pressure is low and tissue perfusion is
poor.
•Normal saline, whole blood, 5% albumin or packed red blood cells (10 ml/ kg) IV
is given.
•Antibiotics: to guard against pneumonia which is liable to develop after prolonged
resuscitation.
Drugs used in Resuscitation
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