Perinatal Asphyxia lecture.ppt

Dr. Sabona Lemessa (Assistant Professor of Pediatrics &
Child Health, JUMC)
Perinatal Asphyxia and Hypoxic-Ischemic
Encephalopathy
8/12/2022
Sabona Lemessa, MD+
1

Objectives
 Describe etiology, epidemiology, pathophysiology and
pathogenesis of perinatal asphyxia
 Explain clinical features and diagnostic criteria and
prognostic factors
 Explain management principles
 Explain steps of neonatal resuscitation
 Explain preventive measures
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Introduction
 Hypoxia - refers to decreased arterial concentration of
oxygen.
 Anoxia - is a term used to indicate the consequences of
complete lack of oxygen
 Ischemia - refers to blood flow to cells or organs that is
insufficient to maintain their normal function.
 Perinatal period - defined as the period from the 28th
wk of gestation through the 7th day after birth.
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 Encephalopathy – clinical term that describes an altered level of
consciousness at the time of examination.
 Hypoxic ischemic encephalopathy – etiologic term to describe
encephalopathy caused by ischemia and /or hypoxia.
 Hypoxic ischemic brain injury – biochemical , EEG, neuroimaging
or pathologic evidence of brain injury caused by hypoxia and/or
ischemia.
 Perinatal asphyxia – is a perinatal insult to the fetus or newborn
due to hypoxia and/or ischemia of various organs leading to
physiologic and/or biochemical organ changes.
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Perinatal Asphyxia (PNA)
 Insult to the fetus/neonate due to hypoxia and/or
ischemia to various organs
 “perinatal asphyxia“ a condition in the neonate where
there is the following combination:
o An event or condition during the perinatal period that
is likely to severely reduce oxygen delivery and lead
to acidosis; and
o A failure of function of at least two organs (may
include lung, heart, liver, brain, kidneys and
hematological) consistent with the effects of acute
asphyxia. 8/12/2022
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Cont…
 Consider PNA in our set up if:-
 Low first minute APGAR (0-3)
 Hypotonic and
 Seizure
 Exceptional cases
Preterm babies
Babies who had birth trauma
Babies with congenital neurologic al anomalies
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Epidemiology
 Incidence is 1-2% in developed countries
 Incidence is much higher in developing countries
as high as 10-30% in different studies
 Indirectly related with GA & birth weight
 Responsible for around 23% of perinatal deaths
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Causes of Neonatal Deaths in Ethiopia,
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Etiologies and risk factors
 Placental insufficiency(90%)-inability of the placenta to provide
O2 & remove CO2 & H from the fetus
 10% is due to Cardiovascular, Pulmonary and neurologic diseases
 Antepartal events (20%)
 Intrapartum (70%)
 Postpartal Asphyxia (10%)
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cont…
Antepartal events (20%) Intrapartum (70%)
 Maternal hypotension
 Severe anemia
 Cardiopulmonary diseases
 Placental abruption
 Maternal hypertension
 Preeclampsia/eclampsia
 Maternal diabetes
 Problems with
umbilical circulation
(E.g. Cord prolapse)
 Meconium aspiration
 Prolonged labor
(maternal/ fetal
causes)
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Cont…
Postpartal Asphyxia (10%)
 Prematurity
 Cardiovascular abnormalities
 Pulmonary malformations
 Neurologic abnormalities
 Severe infections
 Bleeding, shock
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Cont…
 Generally, risk factors for perinatal asphyxia can be
classified as:
a. Impairment of maternal oxygenation
b. Decreased blood flow from mother to placenta
c. Decreased blood flow from placenta to fetus
d. Increased fetal oxygen requirement
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Pathophysiology
Deprivation of O2
• Fast breathing
• Respond to
stimulation
primary apnea
• gasping respiration
• Bradycardia
• Hypotension
Secondary apnea
• Needs intensive
resuscitation
Perinatal
asphyxia
•Shifting of blood to vital organs
(brain and heart)
•Hypoxic-Ischemic damage to
multiple organs
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Cont…
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 Major sequel of PNA encompassing spectrum of
neuropathology & neurological features:-
Hypoxia
Impairs cerebral oxidative metabolism & myocardial
depression
Reduced Cardiac output
Reduced Central Perfusion Pressure
Brain ischemia
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Anaerobic glycolysis (lactic acidosis);
loss of cerebral vascular auto-regulation
further reduction of cardiac function
which aggravates tissue ischemia
impairs glucose delivery to tissues
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 Prolonged hypoxia:
Failure of oxidative phosphorylation & ATP production
Impairs ion pumps (Na-K ATPase) and produce excitatory amino
acids (neurotransmitters)
 NaCl & Ca++ enters the cell causing osmolar load which
induces neuronal death
 Ca activates proteases, lipases and endonucleases leading to
cell death
.
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Neuropathology
 Biochemical & physiologic consequences of perinatal hypoxic-
ischemic insults lead to major neurologic lesions:
 Selective neuronal necrosis:-
Cerebral cortex: hippocampus
Diencephalon: thalamus, hypothalamus, lateral geniculate
bodies
Basal ganglia: caudate, putamen
Brainstem: cochlear nuclei, motor nuclei of cranial nerves,
reticular formation
Cerebellum: purkinje cells
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 Status Marmoratus:-
 Neuronal loss (necrosis of thalamic nuclei and basal ganglia)
 Hypermyelination of Basal ganglia (caudate, putamen) and
thalamus
 Parasagittal cerebral injury:-
 Mostly in term neonates
 “water-shed” areas of involvement
 Periventricular leukomalacia:-
 Necrosis of white matter adjacent to the lateral ventricle
 Common in preterm neonates
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TOPOGRAPHY OF BRAIN INJURY IN TERM INFANTS WITH HIE AND CLINICAL
CORRELATES
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Clinical manifestations
 Intrauterine growth restriction with increased vascular
resistance may be the 1st indication of fetal hypoxia
 Target organs includes:-
kidneys(50%)
CNS(28%)
CVS(25%)
Pulmonary(23%)
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cont…
 Depression of the neonate at birth with a low APGAR score and
acidosis,
 Multiple organ involvement
 Hypoxic ischemic encephalopathy (HIE)
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Multiple organ system dysfunction
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HIE-Sarnat staging
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Diagnosis
1. Perinatal assessment of risk-
awareness of pre-existing maternal or fetal problems
Changing placental and fetal conditions
2. Low Apgar scores and need for resuscitation in the delivery
room
are common but not sufficient to diagnose HIE/perinatal
asphyxia.
If the Apgar score is >6 by 5 minutes, perinatal asphyxia is
not likely.
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cont…
 low Apgar score may caused by:-
depression from maternal anesthesia or analgesia,
birth trauma, infection,
cardiac or pulmonary disorders, and
neuromuscular and other central nervous system (CNS)
disorders or malformations.
3. Umbilical cord or first blood gas determination
The pH and base deficit on the cord or first blood gas are
helpful
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Cont…
4. Clinical presentation and differential diagnosis-
Asphyxia is likely, and other causes are less likely if the following
are present:
o Prolonged (>1 hour) antenatal acidosis
o Fetal HR <60 beats per minute
o Apgar score ≤3 at ≥10 minutes
o Need for positive-pressure ventilation or first cry delayed
>5 minutes
o Seizures within 12 to 24 hours of birth
o Burst suppression or suppressed background pattern on
EEG or amplitude-integrated electroencephalogram (aEEG)
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MANAGEMENT
 Perinatal management of high-risk pregnancies
 Supportive care,
 correct metabolic abnormalities
 Directed at the organ system manifestation
 Ventilatory support
 Hemodynamic stabilization
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Perinatal management of high-risk pregnancies
 Fetal HR abnormalities detection
 Measurement of fetal scalp pH is a better determinant of fetal
oxygenation than PO2
 Close monitoring of the progress of labor with awareness of other
signs of in utero distress is important.
 mobilize the perinatal team for a newborn who could require
immediate intervention.
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Postnatal management of neurologic effects of asphyxia
 Ventilation- CO2 should be maintained in the normal range
Hypercapnia and Excessive hypocapnia (CO2 <25 mm Hg)
should be avoided
 Oxygenation- Hypoxemia should be treated with supplemental
O2 and/or mechanical ventilation
 Temperature- Passive cooling by turning off radiant warmer is an
effective way to initiate TH
Hyperthermia should always be avoided
 Perfusion-in order to maintain adequate cerebral perfusion
pressure
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Cont…
 Maintain physiologic metabolic state
Hypocalcemia
Hypoglycemia- blood glucose level should be kept
between
• Judicious fluid management
both fluid overload and inadequate circulating volume
should be avoided.
Fluid should be restricted (2/3 of daily maintainance)
Keep NPO for severe PNA (for 48 hrs)
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Cont…
 Control of seizures- Seizures generally start within 12 hours of
birth,
Increase in frequency, and then usually resolve within days,
although seizures may persist in severe cases.
Seizures caused by HIE can be extremely
difficult to control
 usually caused by hypoglycemia,
hypocalcaemia, and hyponatremia and
ischemic injury to the brain.
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Acute anticonvulsant management
 Hypoglycemia and hypocaelcemia should be corrected
 Phenobarbitone: loading dose of 20 mg/kg IV may be
followed by increments of 10 mg/kg IV to a total of 40 mg/kg,
Maintenance dose should be started at 5 mg/kg/day divided
twice daily.
 Phenytoine:- Loading dose is 20 mg/kg;
maintenances dose is 4-6 mg/kg daily.
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NEUROPROTECTIVE STRATEGIES
 Therapeutic hypothermia- whole body or selective
head cooling
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Cont…
 reduce the core (rectal) temperature to 33-34º C for 72 hours in a
constant manner
 Indication :-
Infants 36 weeks or more gestation and
birth weight of >1800gm
Age less than 6hours at admission.
Evidence of moderate to severe encephalopathy.
Infant must have 2 or more of the following- o APGAR score of 5
or less at 10 minutes,
Cord or arterial pH <7 or base deficit of 12 or more within 60
minutes of birth ventilation or resuscitation at 10 minutes.
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Perinatal Asphyxia Follow up chart
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Prevention of prenatal asphyxia
 The minimum preventive measure which is provided
during perinatal period is much better than a
sophisticated care provided to an asphyxiated new
born.
 Prenatal assessment of changing fetal and placental
condition by clinical assessment and ultrasonography
 Fetal Biophysical profile
 Monitor progress of labor
 Effective neonatal resuscitation
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 Failure to establish respiration by 5 minutes
 Apgar 3 or less in 5 minutes
 Onset of Seizure in 12 hrs
 Refractory convulsion
 Inability to establish oral feed by 1 wk
 Abnormal EEG & failure to normalize by 7 days of life
 Abnormal CT, MRI in neonatal period
PREDICTORS OF POOR NEURO DEVELOPMENTAL OUTCOME
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Prognosis of HIE
 Stage I(mild HIE) 98- 100% of newborns will have a normal
neurological outcome and < 1% mortality
 Stage II(moderate HIE) 20-37% of them die or have abnormal
neurodevelopmental outcome
 Stage III (Severe HIE) death is more likely survivors would have
one or more major neurodevelopmental disability such as:-
Cerebral palsy, intellectual disability, hearing loss
visual impairment or epilepsy.
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Reference
 Cloherty and Stark’s, Manual of Neonatal Care south Asian
edition.
 Nelson text book of pediatrics 21st Edition.
 Martin: Fanaroff and Martin's Neonatal Perinatal
Medicine, 8th ed.
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Thank you!
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Perinatal Asphyxia lecture.ppt

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