11-evaluation Of Fetal Well-being Sept01

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Antenatal & Intrapartum Fetal Monitoring

Objectives of Evaluation • • • • • •

Location Viability Number Biometry(size, growth) Placental exam Amniotic fluid volume assessment

• • • • •

Morphology Biophysical profile Adaptation to stress Lung Maturity Prediction of hypoxicacidotic insults

Tools of Evaluation 1. 2. 3. 4. 5.

History. Physical Exam. Pregnancy test. Ultrasound. Doppler: Auscultation; Blood flow studies.

6. Biochemical screening tests.

Tools of Evaluation 7. Invasive procedures: Amniocentesis, cordocentesis, Chorionic villous sampling and other sampling. 8. Electronic fetal heart rate (FHR) monitoring. 9. Tests of acid-base balance.

History • • • •

Amenorrhea Pain & bleeding in first trimester Pregnancy symptoms Significant past obstetrical and general history

• Fetal movement first felt at 16-20 weeks “Quickening”. – Fetal sleep cycle. • Pain, bleeding, leaking in 2nd and 3rd trimester.

Physical exam • • • •

General: BP, Temp, edema, anemia Size of uterus Signs of abortion Abdominal obstetrical examination – Uterine fundal growth • 12 weeks: just above pubis • 20-24 weeks at umbilicus (variable) • 24-34 weeks: SFH (cm) = gestational age (wks)

Physical exam • FHR auscultation starting at 11-12 weeks by daptone – FHR in early gestation may reach 160-170 bpm, – Subsequently become less (120-160) due to autonomic maturation. – Do not confuse other sounds e.g. fetal movement, maternal uterine pulse

Laboratory Investigations • Pregnancy test – Urine β HCG – Serum β HCG: level normally doubles every 48 hrs. • Routine Investigations – CBC – Blood group and Rh type – Rh antibodies – VDRL, Rubella, Hepatitis – FBS – Urine r/m and c/s – Other tests according to case e.g. APL in recurrent abortions, RFT in renal disease …etc. • •

Ultrasound in First Trimester • • • •

Location of gestational sac Number of fetuses Viability of fetus Nuchal translucency: chromosomal abnormalities.

Ultrasound in First Trimester Vaginal Ultrasound (TVS)

Interauterine Sac

Cardiac Pulsation

Abdominal Ultrasound (TAS)

5 weeks 6 weeks β HCG > 1200 IU/L β HCG > 5000 IU/L

6 weeks

7 weeks

Ultrasound in 2nd & 3rd Trimesters • 16-20 weeks (≈ 18 weeks) – Number of fetuses – Presentation – Viability – Amniotic fluid volume – Placental localization – Fetal biometry – Basic morphological surveillance – Detailed morphological exam, if required • Fetal echocardiography if high risk congenital heart disease.

Prenatal screening tests • 3 biochemical tests: α -fetoprotein, β -HCG & S. estriol • Tests risk of chromosomal abnormalties, mainly trisomy 21, but not diagnsotic. • Diagnosis confirmed by ultrasound and/or amniocentesis. • Done where abortion laws are permissive. Not practiced in Kuwait.

Invasive Procedures Chorionic villous sampling Amniocentesis Cordocentesis • Not practiced in Kuwait on routine basis for religious issues. • Reserved for diagnosis if anomalies present on ultrasound. • Amniocentesis and cordocentesis are used for diagnosis and management of other diseases e.g. Rh Isoimmunization, hydrops, suspected infection.

• Complications of procedure: – Fetal loss: CVS 1%, Amnio 0.5%, Cordo 2-3% – Bleeding – Infection – Membrane rupture

Doppler Study In cases of utero-placental insufficiency, fetal blood flow redistribution occur more to (less resistance) fetal brain, heart and adrenals and less to (less resistance) abdominal viscera and lower limbs. Therefore, measurements of fetal umbilical artery blood flow (represents lower body flow) and cerebral artery flow may show this asymmetrical changes.

Doppler Study • Systolic:diastolic ratio indicates the resistance index • Decreased diastolic flow, becoming absent or even reversed correlates with the severity of impaired blood flow.

Degrees of Placental Insufficiency Normal Flow

Decreased diastolic flow (Mild)

Absent diastolic flow (Moderate)

Reversed diastole (Severe)

Tests of Fetal Lung Maturity Lecithin-to-Sphingomyelin (LS) Ratio • L & S are phospholipids components of surfactants. • Lung maturity is related to surfactant maturity. • Before 34 weeks, L & S are present in amniotic fluid in similar concentrations. • After 34 weeks, L begins to rise relative to S. • Increased Respiratory distress if LS ratio is < 2 • LS ratio sample is obtained by amniocentesis

Tests of Fetal Lung Maturity Phosphatidylglycerol (PG) • PG enhances surfactant function. • Identification of PG in amniotic fluid assures, but not absolutely, against respiratory distress. • PG is not present in (so not contaminated by) blood, meconium, or vaginal secretions so can be sampled by amniocentesis or directly from AF in the vagina.

Biophysical profile (BPP) Fetal movement ≥ 3 times

No 0 30 0

Breathing movement ≥ seconds Tone: ≥ 1 limb flexion-extension Amniotic fluid perpendicular



Reactive Non-stress test

2

cm

Yes 2 2

0

2

0

2

0 2 Total 10

Biophysical profile (BPP) • Total score of 8 or 10 is normal • Total score of 6 is equivocal and should be repeated in 12-24 hours • Total

score

of

4

or

less

abnormal, consider delivery soon.

is

Electronic Fetal Heart Rate Monitoring

A. Contraction stress test (CST) B. Non-Stress Test

Contraction stress test (CST) • Marginally adequate fetal oxygenation with the uterus at rest will be transiently worsened by uterine contractions resulting in fetal hypoxemia and late deceleration. • Contractions may be induced by I.V. oxytocin or nipple stimulation • Most used in USA but not very popular elsewhere because of its risk.

Antenatal Assessment

Reactive Pattern Baseline FHR 120-160 bpm ∀ ≥ 2 accelerations in 20 minutes • Acceleration amplitude > 15 beats lasting > 15 seconds • Variability 15 beats (5-10 beats in premature fetuses) • No periodic or significant decelerations (>30 beats)

Non-Reactive Pattern • Lack of reactive criteria over 40 minutes. • Always of concern ante-partum & delivery is generally indicated.

Intrapartum (During Labour) Fetal Monitoring

Fetal Hypoxemia and Hypoxia • • • •

Transient and repetitive even at the level of CNS Extremely common during normal labor. Generally well tolerated by the fetus. Levels that are ominous to an infant or adult are commonly seen in normal newborns. • Only when hypoxia and resultant metabolic acidemia reach extreme levels is the fetus at risk for long-term neurologic impairment.

• Fetal oxygen extraction from the maternal circulation is well adapted even with the additional stress of normal labor and delivery. • Insufficient fetoplacental unit resulting from labor or intrapartum complications may compromise fetal oxygenation. • Oxygen delivery is critically dependent on uterine blood flow.

Factors that decrease placental blood flow • Uterine contractions • Maternal position • Conduction anesthesia • Pathologic situations: Preeclampsia, abruptio placentae, chorioamnionitis, and others. • Cord compression by entanglement, oligohydramnios, knots, or prolapse. • Susceptible fetuses

Fetal CNS, Hypoxia and FHR H

y p

o

N

S

C S

y m

p F

a H

x ia

t h P e a t ir c a

s y m

p

R

r a

n

A

lt e

t io

Methods of Intrapartum Monitoring Oxygen Saturation

H

Biophysical Profile

C S

y m

p F

Monitoring of FHR & Uterine Contractions (Cardiotocography)

Umbilical Blood Gases

Scalp pH or Lactic Acid

a H

y p

o

N

S

x ia

Vibroacoustic Stimulation a t h e t ic

t h P e a t i rc a

s y m

p

R

r a

n s

A

lt e

t io

Fetal ECG Monitoring Intermittent Auscultation

Amnioinfusion

Monitoring of FHR & Uterine Contractions (Cardio-toco-graphy)

Patterns of The FHR • • • • • • •

Normal Pattern Baseline Tachycardia/Bradycardia Reduced Variability Early Decelerations Late Decelerations Variable Decelerations Other Patterns e.g Sinusoidal

FHR Accelerations • Are common periodic changes in labor and are nearly always associated with fetal movement. • Virtually always reassuring and almost always confirm that the fetus is not acidotic at that time.

Variability • A useful indicator of fetal CNS integrity. • May serve as a barometer of the fetal response to hypoxia. • In most situations, decelerations of the FHR will precede the loss of variability, indicating the cause of neurologic depression.

Variability • Factors such as a fetal sleep cycle or medications may decrease the activity of the CNS and the variability of the FHR. • Decreased variability in the absence of decelerations is unlikely to be due to hypoxia.

Early Decelerations • Benign changes caused by fetal head compression. • Seen in the active phase of labor. • They are usually shallow and symmetrical. • Reach their nadir at the same time as the peak of the contraction.

Baseline Tachycardia • Tachycardia may be associated with: – Severe and prolonged fetal hypoxia – maternal fever – Fetal anemia – Intraamniotic infection i.e. chorioamnionitis – congenital heart disease – Hyperthyroidism

Prolonged Deceleration • An isolated, abrupt decrease in the FHR to levels below the baseline that lasts at least 60-90 seconds. • Always of concern and may be caused by virtually any mechanism that can lead to fetal hypoxia.

Variable Decelerations • Umbilical cord compression or, occasionally, head compression. • Abrupt onset and return • Vary in depth, duration, and shape.

Variable Decelerations • Frequently preceded and followed by small accelerations of the FHR. • Coincide in timing and duration with the compression which coincides with the timing of the uterine contractions.

Variable Decelerations • Generally associated with a favorable outcome. • Non-reassuring if: – Persistent. – Progressively deeper to less than 70 bpm lasting greater than 60 seconds. – Persistently slow return to baseline .

Late Decelerations • U-shaped, gradual onset and return, usually shallow 10-30 beats per minute. • Reach their deepest point after the peak of the contraction. • A result of CNS hypoxia; in more severe cases, it may be the result of direct myocardial depression.

Sinusoidal Heart Rate Pattern • Regular oscillation of the baseline long-term variability resembling a sine wave, lasting at least 10 minutes. • Rare and associated with: – Severe chronic fetal anemia – Medications: e.g. pethidine – Severe hypoxia and acidosis.

CTG prediction of neonatal outcome • Highly sensitive but non-specific resulting in many unnecessary interventions. • Cesarean section rates had risen after introduction of CTG without major impact on neonatal outcome.

Intermittent Auscultations • Fetal

monitoring

by

intermittent

auscultation has been shown to be equally effective to electronic FHR monitoring in predicting fetal outcome with less need for cesarean sections.

Fetal Scalp pH Testing • Gold standard test of acid-base status. • Management: • pH > 7.25

Reassuring

• pH < 7.2

Immediate delivery

• pH 7.2-7.25

Repeat after 20-30 minutes

• Used in only 10% of obstetric centers. • Invasive, labour-intensive, requires repetitions.

Other tests: Limited evidence & use • Amnioinfusion • Vibroacoustic Stimulation • Oxygen Saturation • Scalp Lactic Acid • Fetal ECG Monitoring

Management of abnormal FHR pattern 1. Turn patient onto side to alleviate vena cava compression. 2. Discontinue intravenous oxytocin. 3. Apply 100% oxygen to mother by face mask.

4. Correct maternal hypertension. 5. Vaginal examination to rule out prolapsed cord. 6. Consider

fetal

determination.

scalp

blood

sampling

for

pH

7. Search for the cause – Late decelerations: excessive uterine contractions, maternal hypotension, or maternal hypoxemia. – Severe variable or prolonged decelerations: • Umbilical cord prolapse • Rapid descent of the fetal head • Cord compression

8. With decreased variability, consider fetal scalp stimulation.

9. With

prolonged

bradycardia

unresponsive

to

other

maneuvers or late decelerations with worsening fetal acidosis (pH <7.20), consider immediate delivery.

10.The decision to intervene depends on: – Assessment of the likelihood of severe hypoxia and the possibility of metabolic acidosis – The estimated time to spontaneous delivery.

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