Fetal Distress (2)
Transcript of Fetal Distress (2)
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Fetal distress
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Fetal distress is defined as depletion
of oxygen and accumulation of carbon
dioxide,leading to a state of “hypoxia
and acidosis ” during intra-uterine life.
Definition
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Maternal factors1) Microvascular ischaemia(PIH)
2) Low oxygen carried by RBC(severe anemia)
3) Acute bleeding(placenta previa, placental
abruption)
4) Shock and acute infection
5) obstructed of Utero-placental blood flow
Etiology
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Placenta、umbilical factors
1) Obstructed of umbilical blood flow
2) Dysfunction of placenta
3) Fetal factors
4) Malformations of cardiovascular system
5) Intrauterine infection
Etiology
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Hypoxia、accumulation of carbon dioxide
↓Respiratory Acidosis
↓FHR↑ → FHR ↓→ FHR ↑
↓Intestinal peristalsis
↓Relaxation of the anal sphincter
↓Meconium aspiration
↓Fetal or neonatal pneumonia
Pathogenesis
Acute fetal distress
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Chronic
Fetal
distress
Pathogenesis
IUGR
(intrauterine growth retardation)
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Clinical manifestation
Acute fetal distress
(1)FHR
FHR>180 beats/min (tachycardia)
<100 beats/min (bradycardia)
(LD) Repeated Late deceleration
Placenta dysfunction
(VD) Variable deceleration
Umbilical factors
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Clinical manifestation
Acute fetal distress
(2) Meconium staining of the amniotic fluid grade I、II、III
(3) Fetal movement
Frequently→decrease and weaken
(4) Acidosis
FBS (fetal blood sample)
pH<7.20
pO2<10mmHg (15~30mmHg)
CO2>60mmHg (35~55mmHg)
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Clinical manifestation
Chronic fetal distress
(1) Placental function
(24h E3<10mg or E/C<10)
(2) FHR
(3) BPS
(4) Fetal movement
(5) Amnioscopy
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Management
Remove the induced factors actively
Correct the acidosis: 5%NaHCO3 250ML
Terminate the pregnancy
(1) FHR>160 or <120 bpm
meconium staining (II~III)
(2) Meconium staining grade III
amniotic fluid volume<2cm
(3) FHR<100 bpm continually
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Management
Terminate the pregnancy
(4) Repeated LD and severe VD
(5) Baseline variability disappear with LD
(6) FBS pH<7.20
Forceps delivery
Caesarean section
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Neonatal Asphyxia
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Aim & Claim
• Understand the assessment & care of
normal birth
• Familiar with the pathogenesis of birth
asphyxia
• Hold of Apgar score & ABCDE
resuscitation
• Familiar with the complication of
severe asphyxia
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Definition
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.
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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).
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Etiology
Pathologically, any factors which
interfere with the circulation between
maternal and fetal blood exchange
could result in the happens of perinatal
asphyxia. These factors can be
maternal factor, delivery factor and
fetal factor.
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Etiology—High Risk Factors
• Maternal factor:
hypoxia, anemia, diabetes, hypertension,
smoking, nephritis, heart disease, too old or
too young,etc
• Delivery condition:
Abruption of placenta, placenta previa,
prolapsed cord, premature rupture of
membranes,etc
• Fetal factor:
Multiple birth, congenital or malformed
fetus,etc
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Pathophysiology
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 from
hypoxic damage.
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Pathophysiology(I)
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.
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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.
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Pathophysiology(II)
Asphyxia development:
a. Primary apnea
breathing stop but normal muscular tone or
hypertonia, tachycardia (quick heart rate),
and hypertension
Happens early and shortly, self-defended
mechanism,could not be damage to organ
functions if corrected quickly
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b. Secondary apnea
Features of severe asphyxia or
unsuccessful resuscitation, usually
result in damage of organs function.
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Pathophysiology(III)
Other damages:
a. Persistent pulmonary hypertension (PPHN)
b. Hyper/hypoglycemia
c. Hyperbilirubinemia
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Clinic manifestations
Fetal asphyxia
fetal heart rate: tachycardia bradycardia
fetal movement: increase decrease
amniotic fluid: meconium-stained
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Clinic manifestations
• Apgar score:
A: appearance(skin color)
P: pulse(heart rate)
G: grimace(reactive ability)
A: activity(muscular tension)
R: respiration
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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
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Degree of asphyxia:
Apgar score 8~10: no asphyxia
Apgar score 4~8: mild/cyanosis asphyxia
Apgar score 0~3: severe/pale asphyxia
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Clinic manifestations
Complications:
CNS: HIE, ICH
RS: MAS, RDS, pulmonary hemorrhage
CVS: heart failure, cardiac shock
GIS: NEC, stress gastric ulcer
Others: hypoglycemia, hypocalcemia,
hyponatremia
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Diagnosis
1/ Evidence of fetal distress
2/ Fetal metabolic acidosis
3/ Abnormal neurological state
4/ Multiorgan involvement
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Management
• ABCDE resuscitation
• A (air way)
• B (breathing)
• C (circulation)
• D (drug)
• E (evaluation)
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Airway
1/ open by placing the head in the neutral
position
2/ clean up completely amniotic fluid from
the airway by suction with syringe as
soon as possible
3/ if meconium-stained, tracheal
cathetershould be placed to ensure
meconium to be removed
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Breathing
1/ ensure face mask covers nose &
mouth connect to oxygen bag
2/ establish respiration of 30-40/min
with chest wall movement
3/ if no response, intubation &
mechanic ventilation is necessary
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Circulation
1/ if heart rate <60/bpm, start
external cardiac compression
with fingers
2/ ratio 3:1 ( 90 compressions to
30
bpm)
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Drugs
1/ if 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/ if acidosis, give 5% sodium bicarbonate (SB) with 3-5ml/kg
4/ if bradypnea, consider using naloxone (0.1mg/kg)
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Evaluation
Evaluate the result of
resuscitation to determine if
more rescue necessary:
– If not good, repeat the resuscitation
– If good, transmit baby to NICU
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Remember
In the whole resuscitation,
the most important step is
A --- clean up completely the
airway
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