Fetal distress

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

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

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

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

Chronic

Fetal

distress

Pathogenesis

IUGR

(intrauterine growth retardation)

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

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)

Clinical manifestation

Chronic fetal distress

(1) Placental function

(24h E3<10mg or E/C<10)

(2) FHR

(3) BPS

(4) Fetal movement

(5) Amnioscopy

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

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

Neonatal Asphyxia

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

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.

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).

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.

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

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.

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.

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(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

b. Secondary apnea

Features of severe asphyxia or

unsuccessful resuscitation, usually

result in damage of organs function.

Pathophysiology(III)

Other damages:

a. Persistent pulmonary hypertension (PPHN)

b. Hyper/hypoglycemia

c. Hyperbilirubinemia

Clinic manifestations

Fetal asphyxia

fetal heart rate: tachycardia bradycardia

fetal movement: increase decrease

amniotic fluid: meconium-stained

Clinic manifestations

• Apgar score:

A: appearance(skin color)

P: pulse(heart rate)

G: grimace(reactive ability)

A: activity(muscular tension)

R: respiration

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

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

Diagnosis

1/ Evidence of fetal distress

2/ Fetal metabolic acidosis

3/ Abnormal neurological state

4/ Multiorgan involvement

Management

• ABCDE resuscitation

• A (air way)

• B (breathing)

• C (circulation)

• D (drug)

• E (evaluation)

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

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

Circulation

1/ if heart rate <60/bpm, start

external cardiac compression

with fingers

2/ ratio 3:1 ( 90 compressions to

30

bpm)

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)

Evaluation

Evaluate the result of

resuscitation to determine if

more rescue necessary:

– If not good, repeat the resuscitation

– If good, transmit baby to NICU

Remember

In the whole resuscitation,

the most important step is

A --- clean up completely the

airway