Hypoxia-Ischemia (Asphyxia):

Prof. Dr.Abbas Alrabaty

College of medicine
/HMU
Pediatric Department

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Outline

 Objectives
 Introduction
 Etiology

 Pathophysiology And Pathology

 Clinical presentation
 Complication Of Perinatal Asphyxia
 Prognosis

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Objectives

 To identify the importance of fetal monitoring.

 Obstetricians & neonatologist knowledge
interchange are of importance to mange the
neonatal outcome.

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Introduction

 Hypoxia-Ischemia (Asphyxia):
Hypoxia refers to an arterial concentration
of oxygen that is less than normal.

Ischemia refers to blood flow to cells

or organs that is insufficient to maintain
their normal function.
 Hypoxic-ischemic encephalopathy is an important cause
of permanent damage to central nervous system cells,
which may result in

 neonatal death

Or may be manifest later as

 cerebral palsy or
 mental deficiency

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  Meconium stained
baby

Non-vigorous baby
Vigorous baby Depressed nn ,failure
to initiate first breathing

Low Apgar Score At 1st,5th

minutes

mild to moderate asphyxia may 4-7

Less than 3 sever asphyxia need
needs resuscitation
immediate resuscitation

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 Hypoxic-ischemic encephalopathy is an important cause
of permanent damage to central nervous system cells,
which may result in

 neonatal death

Or may be manifest later as

 cerebral palsy or
 mental deficiency

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 Hypoxic-ischemic encephalopathy is an important cause
of permanent damage to central nervous system cells,
which may result in

 neonatal death

Or may be manifest later as

 cerebral palsy or
 mental deficiency

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 Hypoxic-ischemic encephalopathy is an important cause
of permanent damage to central nervous system cells,
which may result in

 neonatal death

Or may be manifest later as

 cerebral palsy or
 mental deficiency

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ETIOLOGY.

Fetal hypoxia may result from

 inadequate oxygenation of
maternal blood as a result of
hypoventilation.
 low maternal blood pressure as
a result of the hypotension
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ETIOLOGY (cont.)

 inadequate relaxation of the uterus to

permit placental filling as a result
of uterine tetany caused by excessive
administration of oxytocin.
 premature separation of the placenta

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  impedance to the circulation of blood
through the umbilical cord as a
result of compression or knotting of
the cord.
 uterine vessel vasoconstriction .
 placental insufficiency

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Chronically hypoxic fetuses may develop intrauterine
growth retardation without traditional signs of fetal
distress (e.g., bradycardia).

Uterine contractions further reduce umbilical

oxygenation, depressing the fetal cardiovascular
and central nervous systems and resulting in low
Apgar scores and postnatal hypoxia in the delivery
13room after birth. 12
 post natal hypoxia may result from:

(1) anemia ,

(2) shock interfere with the transport of oxygen to

vital cells .

(3) a deficit in arterial oxygen saturation resulting

from failure to breath adequately postnatally due
to a cerebral defect, narcosis, or injury.

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  (4) failure of oxygenation of an adequate amount of
blood resulting from severe forms of cyanotic
congenital heart disease or deficient pulmonary
function

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 PATHOPHYSIOLOGY AND
PATHOLOGY
Within minutes of the onset of total fetal hypoxia ;-

 bradycardia, hypotension, decreased cardiac

output, metabolic and respiratory acidosis occur.

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  The initial circulatory response of the fetus is
increased shunting through the ductus
venosus, ductus arteriosus, and foramen ovale
with transient maintenance of perfusion of the
brain,

 heart, and adrenals in preference to the lungs

(due to pulmonary vasoconstriction)

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

 The pathology of hypoxia-ischemia is dependent

upon the affected organ and the severity of the
insult.

 Early congestion, fluid leak from increased

capillary permeability, and endothelial cell
swelling may then lead to signs of coagulation
necrosis and cell death.

 If fetal distress produces gasping, amniotic fluid

18contents aspirated into12the trachea or lungs.
CLINICAL MANIFESTATIONS:

The signs of hypoxia in the fetus are usually noted a

few minutes to a few days before delivery.

1)IUGR with increased vascular resistance may be

the first indication of fetal hypoxia.

2)The fetal heart rate slows, and the beat-to-beat

variability declines.

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 3)fetal scalp blood analysis may
show a pH less than 7.20. The
acidosis is made up of varying

degrees of metabolic or respiratory

components.
These signs should lead to the
administration of high
concentrations of oxygen to the
mother and immediate delivery to
avoid fetal death or central nervous
system damage
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 At delivery :
1)presence of yellow, meconium-
stained amniotic fluid is evidence
that there has been fetal distress

2)infants are frequently depressed

and fail to breath spontaneously

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 Few hours after delivery:
1) the tone change from hypotonia to
extreme hypertonia, or may appear normal.
2)Pallor.
3)cyanosis and apnea.
4)slow heart rate.
5)unresponsiveness to stimulation

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 Complication of perinatal asphyxia HIE

1) Congestive heart failure and cardiogenic

shock.
2) persistent pulmonary hypertension
(persistent fetal circulation)
3) respiratory distress syndrome.
4) gastrointestinal perforation.
5) hematuria, and acute tubular necrosis
6)HIE
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 Case study 1

 At delivery room , the obstetrician informed you

about pregnant women on delivery that there is
fetal distress. The delivery by normal vaginal
delivery the neonate was depressed gasping
respiration and APGAR score at first minute
was 2 after resuscitation at 5th minute the
APGAR was 5 ?
1. Describe the clinical diagnosis of the neonate
2. What are active measures you are going to do
24 for this neonates
 Answers

1. Asphyxia

2. Immediate resusciation

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 Case study 2

 A 2 months old infant presented to your office

with history of birth asphyxia ,family had
concern about the future of this infant,he
delivered prematurely by 4 weeks ,the foetal
monitoring result was bad ,and decision for
cesarean section was late.
 Q1;what other important Question you will ask
in regard to explain the prognosis for family ?

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 Case study 2 cont.

 Would you ask any imaging tulle for diagnosis

confirmation.
 What are important evidences for sever
encephalopathy?

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 PROGNOSIS:

depends on whether

1. its metabolic and cardiopulmonary

complications (hypoxia, hypoglycemia,
shock) can be treated,
2. on the infant's gestational age (outcome is
poorest if infant is preterm),

3. and on the severity of the hypoxic-ischemic

encephalopathy.
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 Severe encephalopathy characterized
by
 Flaccidity
 coma,
 apnea,
 refractory seizures,
 and a marked decrease of cortical
attenuation on CT, is associated with
a poor prognosis.
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 Question ?

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