Antepartum surveillance techniques

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Antepartum surveillance techniques
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Indication

• Diabetes mellitus
• Hypertensive disorders (chronic hypertension,
  preeclampsia)
• Renal disease
• Collagen vascular disorders
• Maternal thyrotoxicosis
• Severe anemia or maternal hemoglobinopathies
• Isoimmunization
• Prior unexplained fetal demise
• Third-trimester vaginal bleeding
• Premature rupture of membranes
• Maternal perception of decreased fetal movements
• Postdate pregnancy (gt41 weeks)
• Elevated maternal serum AFP (normal amniotic
  fluid AFP)
• Abnormal or irregular fetal heart rate on
  auscultation
• Selected fetal anomalies (e.g., gastroschisis)
• Multiple gestation
• Intrauterine growth restriction
• Amniotic fluid abnormalities (oligohydramnios or
  polyhydramnios

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Fetal movement monitoring

• A decrease in fetal movements often precedes
  fetal death, in some cases by several days.
• Around 1618 weeks gestation, most women become
  cognizant of fetal activity, and this perception
  appears to be at its maximum by 2832 weeks.
• Awareness of fetal movements will vary from
  patient to patient, and is also affected by other
  maternal, fetal, and uterine factors
• In general, patients perceive about 80 of
  ultrasonographically visualized fetal movements.

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Factors influencing maternally perceived fetal
movements

• Maternal
• Activity
• Obesity
• Ingestion of medications or drugs that depress
  (e.g., methadone) or increase (e.g., cocaine)
  fetal movements
• Fetal
• Behavioral states
• Gestational age
• Congenital anomalies (e.g., neuromuscular
  disorders, fetal akinesia
• syndrome)
• Duration of fetal movements
• Uterine
• Placental location
• Amniotic fluid volume

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• A popular approach is to have the patient lie on
  her left side and count distinct fetal movements.
• Counting 10 movements in a period of up to 2h is
  felt to be reassuring.
• If the count is nonreassuring or decreased,
  further assessment is recommended (such as NST
  with AFV assessment or BPP), and the physician
  should be contacted immediately.
• The relationship between decreased fetal activity
  and poor perinatal outcome has been well
  established

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Dangers of decrease fetal movement

• 35 risk of Stillbirths
• Poor neonatal condition at birth
• Abnormal labor FHR patterns
• Cesarean for fetal distress
• 5-min Apgar scores 6.
• Fetal growth restriction was almost 10 times
  higher than that of the active group

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Contraction stress test (CST)

• Designed to detect uteroplacental insufficiency
  before fetal compromise, this test is based on
  the response of the FHR to uterine contractions.
• It relies on the premise that fetal oxygenation
  will be transiently worsened by contractions.
• In the suboptimally oxygenated fetus, the
  resultant intermittent worsening in oxygenation
  will, in turn, lead to the FHR pattern of late
  decelerations.

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• Lying in a lateral recumbent position, the
  patient has an external fetal monitor record both
  the FHR and uterine contractions simultaneously
  for a 20- to 30-min interval.
• If the patient is spontaneously contracting, and
  the frequency is 3 contractions/10 min, and the
  duration of each contraction is 45s, then
  uterine stimulation is not required

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• If these criteria are not met
• nipple stimulation
• exogenous oxytocin can be used .
• Once adequate contractions are achieved, the
  oxytocin infusion is discontinued.
• The CST should be avoided when there is a
  contraindication to labor
• prior myomectomy
• classical Cesarean section scar
• placenta previa or placental abruption,
• Premature rupture of membranes (PROM),
• Current preterm labor
• Multiple gestations
• Incompetent cervix.

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• The most common result is a negative CST, which
  indicates adequate fetal oxygenation in the
  presence of contractions.
• It has also been consistently associated with a
  good fetal outcome.
• One group reviewed data from their institution
  along with the literature, and found that the
  incidence of antepartum fetal death (within 1
  week of a negative CST) was 0.20.7.11
• The literature suggests that there is a low
  incidence (lt1) of antepartum fetal death within
  1 week of testing.
• In general, a positive CST implies uteroplacental
  insufficiency and has been associated with
  adverse perinatal outcome and an increased
  incidence of intrauterine demise

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Nonstress test (NST)

• This testing modality is based on the premise
  that the heart rate of the fetus that is not
  acidemic or neurologically depressed will
  temporarily accelerate with fetal movement.
• FHR reactivity is felt to be a good indicator of
  normal fetal autonomic function and well-being
  it depends on normal neurological development and
  normal integration of the central nervous system
  (CNS) control of FHR.
• The purpose of the NST is to identify both normal
  fetuses and those with asphyxia/hypoxia.
• NST (compared with the CST) has the advantages of
  time, easier interpretability, and lack of
  contraindications.

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Reactive trace

• The tracing is categorized as reactive (normal)
  or nonreactive.
• The most common definition is 2 FHR
  accelerations which peak, but do not necessarily
  remain, at least 15 beats per minute (b.p.m.) in
  amplitude above the baseline, and last 15 s from
  baseline to baseline within a 10- or 20-min
  period, with or without fetal movement

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Nonreactive trace

• Causes
• Most commonly associated with a sleep cycle
• CNS depression (including).
• Fetal acidemia Fetal hypoxia, asphyxia
• Gestational age
• Drugs depressants (narcotics, phenobarbital),
  betablockers (propranolol)
• Smoking

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• Routine NST interpretation does not take
  gestational age into account however, this is an
  important consideration, as preterm fetuses are
  less likely to have FHR accelerations in
  association with fetal movements.
• In summary, while a reactive NST is usually
  associated with good outcomes, most fetuses who
  do not show accelerations during an NST are also
  not compromised.

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Vibroacoustic stimulation (VAS)

• This method may elicit FHR accelerations by
  utilizing an artificial larynx (positioned on the
  maternal abdomen over the fetal vertex) with a
  stimulus of 12 s being applied.
• This may be repeated up to three times (at 1-min
  intervals) for progressively longer durations (of
  up to 3 s) to elicit accelerations.
• The normal fetal response to VAS includes not
  only FHR accelerations, but also increases in
  long-term FHR variability and gross body
  movements.

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Consequences of nonreactive after VAS

• Increased rates of intrapartum fetal distress
• Fetal growth restriction
• Low Apgar scores
• Gestational age appears to affect the FHR
  response to VAS, with a maturational response as
  gestation advances

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Biophysical profile (BPP)

• The BPP is performed using real-time
  ultrasonography to assess multiple fetal
  biophysical activities, as well as AFV.
• The observation is continued until either normal
  activity is seen or 30 consecutive minutes of
  scanning have elapsed.
• The BPP is unique in that it assesses both acute
  (FHR reactivity, fetal breathing movements, fetal
  movements, fetal tone) and chronic markers (AFV)
  of fetal condition.
• The fetus will respond to central
  hypoxemia/acidemia by altering its movement,
  tone, breathing, and heart rate pattern.

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Amniotic fluid volume (AFV) assessment

• Amniotic fluid (AF) is essential to pregnancy,
  providing a compartment for normal development,
  growth, and movement of the fetus.
• AFV is a chronic marker of fetal well-being, and
  a normal AFV also protects the fetus from cord
  compression during fetal activity or uterine
  contractions.
• This volume changes during pregnancy at 22
  weeks, the average AFV is 630 mL, and this
  increases to 770 mL at 28 weeks.
• Between 29 and 37 weeks, there is little change
  in volume, which averages 800mL.
• Beyond 39 weeks, AFV decreases sharply (averaging
  515mL at 41 weeks). Once a patient becomes
  postdate, there is a 33 decline in AFV per week,
  consistent with clinical observations of an
  increased incidence of oligohydramnios in
  post-term gestations

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• In the second half of pregnancy, the main sources
  of AF include fetal urine excretion (especially)
  and fluid secreted by the fetal lung.
• Fetal urine production rates appear to be in the
  range of nearly 1 L/day near term.
• The primary pathways for fluid removal are fetal
  swallowing (mainly) and intramembranous
  absorption into fetal blood perfusing the fetal
  surface of the placenta.

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• The uterus divided into four quadrants (linea
  nigra and umbilicus divide the uterus into
  right/left halves and upper/lower halves
  respectively), the vertical diameter of the
  largest pocket in each quadrant (umbilical cord
  free) is measured.
• The summation of all four quadrant numbers equals
  the AFI (in cm) (Fig. 32.5). In low-risk
  pregnancies, the mean AFI was 16.2 5.3 cm

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Polyhydramnios

• Polyhydramnios (pathologic accumulation of AF),
  which is defined as an AFI gt 25cm, occurs in
  0.21.6 of the general population.
• It is associated with increased maternal and
  perinatal morbidity and mortality .
• The causes of polyhydramnios depend on its
  severity.

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Causes of polyhydramnios

• Fetal malformations gastroschisis, duodenal
  atresia
• anencephaly
• Genetic disorders
• Diabetes
• Rhesus (Rh) sensitization
• Congenital infections.
• Fetal swallowing impairment

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Potential complications associated with
polyhydramnios.

• Premature labor
• Placental abruption
• Puerperal hemorrhage
• Perinatal mortality
• Maternal respiratory difficulties

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Oligohydramnios

• Oligohydramnios (reduced AFV) occurs in 5.537.8
  of pregnancies, and is significant because of its
  known association with adverse pregnancy outcome
• umbilical cord occlusion
• Fetal distress in labor
• Meconium aspiration
• Operative deliveries
• Stillbirth .

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Causes

• Intrauterine growth restriction
• Urinary tract malformations
• Postdate pregnancies
• Ruptured membranes.
• Placental insufficiency.

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Potential consequences of oligohydramnios

• Umbilical cord compression
• Meconium-stained amniotic fluid
• Fetal demise
• Deformation syndrome
• Pulmonary hypoplasia
• Maternal or neonatal infection

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Alpha-Fetoprotein Testing

• Alpha-fetoprotein (AFP) is a protein synthesized
  first by the yolk sac and then primarily by the
  fetal liver. The fetal AFP level increases until
  about 20 weeks and then declines to term.
• The normal AFP levels in maternal serum continue
  to rise until around 32 weeks.
• Alterations in AFP levels in either amniotic
  fluid or maternal serum have multiple possible
  etiologies.
• In general, an increase in maternal serum AFP is
  due to leaking of fetal AFP through an opening
  in the fetal skinthat is, an open neural tube
  defect or an open ventral wall defect.

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Normative levels of MSAFP are dependent on many
factors

• Gestational age
• Maternal age
• Race
• Weight
• Diabetes
• Therefore, careful assessment of gestational age
  and accurate reporting of maternal factors to the
  lab play a part in getting accurate screening
  results.

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• The placenta also plays a role in elevated MSAFP
  levels.
• If the placenta is large or malpositioned, more
  AFP may cross into the maternal circulation
• A placental defect may also allow an abnormal
  amount of fetal AFP to pass from the fetal blood
  to the maternal serum

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 Multiple Marker Screening

• Multiple marker screening most commonly consists
  of
• MSAFP,
• hCG,
• unconjugated estriol,
• Both trisomy 21 (Down syndrome) and Edwards
  syndrome (trisomy 18) have increased detection
  rates with multiple marker screening.
• In trisomy 21, hCG levels are high, while estriol
  and AFP levels are relatively decreased.
• In trisomy 18, all three values are low.
• These tests are well demonstrated to increase the
  detection rates of chromosomal abnormalities,
  identifying about 60 percent of fetuses with
  trisomies 21 or 18.