Intrapartum Care and Fetal Monitoring Flashcards

1
Q

Labor and delivery goals

A
  • Safe birth for mother and baby
  • Empowering experience for woman and her family
  • Comfortable(???)
  • Manage complications if they arise, remembering that birth is a normal, natural process, not a disease process
  • Support family interaction and bonding
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2
Q

clinical management - triage

A
  • Time of onset of contractions, frequency, bleeding, ROM
  • Med/OB hx, pregnancy complications, allergies, meds, last PO intake
  • GBS status
  • Vital signs, urine dip
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3
Q

Group B strep

A
  • Gram positive cocci that colonizes 15-30% of pregnant women (GU and GI tract)
  • An important cause of illness in infants, pregnant women, and adults with underlyling medical conditions
  • 70% rate of vertical transmission to fetus once membranes rupture
  • The most common cause of neonatal sepsis
    • Babies have respiratory symptoms that resemble RDS
  • Risk factors for neonatal transmission include premature delivery, prolonged ROM, maternal fever in labor, multiple gestation
  • Asymptomatic in women, though some may have GBS induced UTIs
    • If discovered prenatally treat with antibiotics and note in chart
    • Woman with GBS bacturiuria will automatically be considered GBS+ in the 3rd trimester and not require additional testing
  • GBS Management
    • Test all women in clinic with a vaginal and rectal swab at 35-37 weeks
    • Women who test positive are not treated prenatally
    • Offer prophylactic antibiotics in labor to decrease the rate of transmission to the baby
      • PCN G 5 million units IV loading dose then 2.5 mil units q 4hrs until delivery
      • Ampicillin 2 grams IV, then I gram IV q 4 hours as second choice, “four hours before delivery”
    • Indications for antibiotic prophylaxis:
      • Positive screening cx for GBS (vagina or rectum)
      • Positive hx of birth of an infant with early-onset GBS disease
      • GBS bacteriuria during current pregnancy
      • Unknown antepartum cx status AND
        • Intrapartum fever >100.4F or
        • Preterm labor < 37 weeks, or
        • Prolonged ROM >18 hours or
      • Intrapartum rapid NAAT positive for GBS
  • Maternal intrapartum GBS chemoprophylaxis has resulted in a significant reduction in early onset GBS disease (>80% of cases)
  • GBS positive women (treated) have 1/4000 chance of GBS disease in baby, 1/200 (if not treated intrapartum)
  • In the US, widespread use of GBS screening/intrapartum abx prophylaxis has resulted in a substantial decrease in early onset GBS infections (infection within 6 days after birth)
  • 1993: (Prior to active efforts at prevention) Early onset GBS infection 1.5 per 1000 births.
  • 2006: 0.4 per 1000 births
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4
Q

rupture of membranes

A
  • Antenatally/preterm (preterm premature rupture of membranes (PPROM)) <37 wks
  • At term but before the onset of labor (premature rupture of membranes (PROM))
  • Spontaneously at onset of or during labor (SROM)
  • Via practitioner (amniotomy or artificial rupture of membranes (AROM))
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5
Q

amniotic fluids

A
  • Check color, odor, presence of blood
  • Meconium staining
    • Term or post term fetuses are developmentally able to move their bowels and may do so spontaneously causing meconium stained fluid
    • Stressed/hypoxic baby will also pass meconium
    • Occurs about 20% of the time
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6
Q

meconium

A
  • Thick, black-green, odorless material first demonstrable in the fetal intestine during the third month of gestation.
  • Results from the accumulation of debris (desquamated cells from the intestine/skin, GI mucin, lanugo hair, fatty material from vernix caseosa), amniotic fluid, intestinal secretions, and bile pigments.
  • Meconium is sterile, but may stimulate the release of cytokines/vasoactive substances leading to cardiovascular and inflammatory responses in the fetus/newborn
  • Meconium Management
    • If light meconium, expectant management, amnioinfusion?
    • Thick or dark meconium requires peds notification
      • Will probably desire suctioning the nares/mouth immediately after delivery of head, before delivery of body
      • Will prepare for possible intubation immediately after delivery to visualize below the vocal cords for meconium aspiration
  • Clinical significance
    • Meconium aspiration syndrome
      • Occurs 2-10% of infants born through meconium stained fluid
      • Greatest risk in postmature infants and SGA infants
      • Mechanical obstruction and chemical pneumonitis leading to serious pulmonary hypertension
      • Frequently fatal
      • May suffer long term neurological defects
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7
Q

fetal monitoring

A
  • Assessment of the fetus during labor is a challenging task.
  • Rationale for monitoring: FHR patterns are indirect markers of the fetal cardiac and medullary responses to blood volume changes, acidemia, and hypoxemia
  • Virtually all obstetrical organizations advise monitoring the FHR during labor. This position is largely based upon the experience of experts and medico-legal precedent.
  • 2013 systematic review of 13 RCTs (>37,000 high and low risk women)
  • Compared continuous EFM to intermittent auscultation, found no significant difference regarding:
    • Perinatal mortality
    • Cerebral palsy
    • Neurodevelopmental impairment at 12 months
    • Apgar scores <4 at 5 minutes
    • NICU admission
  • But… Continuous EFM was associated with an extra 12 caesarean sections, and 25 operative(assisted) deliveries per 1000 births
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8
Q

electronic fetal monitoring

A
  • Monitors fetal well being, tolerance of labor, occurrence of uterine contractions
  • Primary indicator of fetal well being per neurologic status and normal cardiac response
  • Accelerations – “Accels” - a reassuring indicator of fetal well-being (fetus NOT acidotic)
  • Baseline FHR 110-160bpm
  • Moderate (beat to beat variability is reassuring
  • May be absent due to sleep
  • Decels - periodic FHR changes associated with
  • contractions
    • Early, Late, or Variable
  • Sinusoidal pattern –rare and ominous (anemia, or severe hypoxia)
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9
Q

fetal heart rate deceleration patterns

A
  • Early decelerations – indicator of head compression.
    • Returns to baseline at end of contraction
    • Not indicative of distress, normal fetal response/vagal stimulation, slowing of FHR
  • Variable decelerations – indicates cord compression.
    • Acute fall in FHR/rapid downslope/variable recovery phase. Generally associated with favorable outcome
  • Late decelerations – associated with uteroplacental insufficiency
    • Begins at/after peak of contraction
    • Persistent, late decels potentially ominous, requires further evaluation of fetal pH
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10
Q

EFM internal monitor

A
  • Fetal electrocardiogram — bipolar spiral electrode inserted into fetal scalp/second reference electrode is placed upon the maternal thigh to eliminate electrical interference.
  • Detects fetal ECG) and calculates the FHR
  • Very clear signal - provides accurate measurement of beat-to-beat variability, artifact kept to a minimum
  • Used when the externally derived tracing is difficult to interpret because of poor technical quality. (fetus or mother is frequently changing position, multiple gestations.)
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11
Q

emergency interventions for nonreassuring patterns

A
  • Call for assistance
  • Administer O2 via tight fitting mask
  • Change maternal position (lateral or knees/chest
  • Administer fluid bolus (lactated Ringer’s)
  • Perform vaginal exam, fetal scalp stimulation
  • Consider tocolysis for uterine tetany or hyperstimulation
  • Discontinue oxytocin if used
  • Consider amnioinfusion (for variable decels)
  • Determine if operative intervention is warranted/how urgently
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12
Q

fetal surveillance

A
  • Vibroacoustic Stimulation (VAS)
  • Startles baby - Should ellicit accels
  • Procedure stimulates the fetus to move, shortening the duration of time needed to produce an acceleration, without compromising the predictive value of a reactive NST.
  • No evidence-based standards for performing this procedure
  • Can also be used intrapartum if fetus has little FHR variability to determine sleeping baby vs hypoxic
  • Vibroacoustic Stimulation (VAS)
  • Uses artificial larynx held at belly to startle baby into activity through sound and vibration
  • Performed antepartum or intrapartum if fetus has little FHR variability to determine sleeping baby vs hypoxic
  • Goal is to identify fetus at risk of intrauterine death/asphyxia
  • PMH, family hx, genetic hx, psychosocial hx will all help identify risk factors
  • Indications for testing include, GDM, HTN/preeclampsia, multiple gestation, decreased fetal movement, hx of prior stillbirth, increased risk for stillbirth, postdates pregnancy, amniotic fluid abnormalities, fetal growth restriction
  • Fetal movement (FM) awareness, “kick counts”
  • FHR, variability
  • Uterine growth
  • Palpable movement 17-20 weeks “quickening”, fetal movement decreases in response to hypoxia
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13
Q

pulmonary maturity

A
  • Amniotic Fluid Analysis (Amnio or vaginal if ROM) – Testing to determine pulmonary maturity:
    • biochemical tests and biophysical tests
  • All are better at predicting the absence, rather than the presence, of respiratory distress
    • Lamellar body count (most common) –direct measurement of surfactant production
  • Analyze lecithin:sphingomyelin (L:S) ratio (pulmonary secretions into amniotic fluid)
    • Should be 2:1 if mature
  • Phosphatidyglycol (PTG) presence signifies mature (present after 35 weeks)
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14
Q

fetal surveillance sonograms

A
  • Confirm GA, number of fetuses, placental location, fetal growth, R/o anomalies, AFI, Doppler velocimetry
  • Nuchal translucency 10-14 wks – most useful marker (trisomy 21), Turners, heart defects, cystic hygroma, single umbilical artery
  • Anatomic scan
  • Fetuses with abnl karyotypes often have anatomic anomalies
  • Trisomy, triploidy, monosomy, 90% involve chromosomes 21, 18,13, X or Y
  • Abnormal U/S markers can be associated with normal fetuses and should be correlated with prenatal diagnostic testing. Isolated “soft” markers are identified in 11-17% of normal fetuses.
  • “Soft” markers include: Increased nuchal translucency, absent nasal bone, echogenic bowel, pyelectasis, shortened long bones, echogenic intracardiac focus.
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15
Q

Nonstress test (NST)

A
  • Most common cardiotocographic method of antepartum fetal assessment. There are no direct maternal or fetal risks from nonstress testing – does not require oxytocin or contractions
  • Higher rates of FN and FP rates than CST
  • Neurologically intact, oxygenated fetus will have ≥2 15 bpm each lasting ≥ 15s accelerations above baseline in 20 min of monitoring
  • “Reactive” meets or exceeds criteria
  • “Nonreactive” is nonreassuring finding
  • Nonreactive or inconclusive usually requires f/u w/ BPP or contraction stress test (CST)
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16
Q

Contraction stress test (CST)

A
  • Most accurate predictor of uteroplacental insufficiency – a hypoxic fetus will demonstrate recurrent late decels
  • More expensive, takes more time, high false positives
  • Can be used from 26 weeks on
  • Used to f/u on NST
  • Can cause labor
  • Uses oxytocin (pitocin) or nipple stimulation to create uterine contractions
  • Criteria: 3 UCs/10 min, felt or not
  • Negative (good): FHR stable, no late decels
  • Positive (bad): repetitive late decels with each UC
  • Equivocal: unable to obtain satisfactory tracing
  • Hyperstimulation (UCs q <2 min)
  • Few false negatives, many false positives
17
Q

biophysical profile (BPP)

A
  • Combined with electronic fetal monitoring nonstress test (NST)
  • Fully oxygenated fetus that is neurologically intact will demonstrate:
    • Muscle tone
    • Gross movement
    • Respiratory activity
    • And will have:
      • An adequate AFI
      • A reactive NST
18
Q

Rh isoimmunization

A
  • Infrequently seen presently with advent of Rh immune globulin (Rhogam) antenatally and postpartum
  • Still occurs in countries where prophylaxis is not widely available
  • Red cells of the fetus or newborn are destroyed by maternally-derived alloantibodies
  • When an Rh(D) negative mother carries an Rh(D) positive fetus
  • Rh blood system consists of numerous other antigens, most commonly C, c, E, e, and G
  • Ethnic variation of phenotypically Rh(D) negative:
  • Basques — 30 to 35 %
  • Caucasians in North America and Europe — 15 %
  • African Americans — 8 %
  • Africa — 4 to 6 %
  • India — 5 %
  • Native Americans and Inuit Eskimos — 1 to 2 %
  • Japan — 0.5 %
  • Thailand — 0.3 %
  • China — 0.3 %
  • Peripheral blood smear shows multiple spherocytes which are small, dark, dense hyperchromic red cells without central pallor (arrows). These findings are compatible with hereditary spherocytosis or autoimmune hemolytic anemia.
  • Complications can be lethal or carry serious morbidity
    • Alloimmune hemolytic disease of the newborn (HDN) aka erythroblastis fetalis (when it is of the fetus)
    • Clinical manifestations of alloimmune HDN range from mild, self-limited hemolytic disease (eg, hyperbilirubinemia with mild to moderate anemia) to severe life-threatening anemia (eg, hydrops fetalis).
  • Hyperbilirubinemia — Less severely affected infants typically present with unexpected hyperbilirubinemia within the first 24 hours of life.
  • The degree of anemia varies depending upon type of HDN.
  • Some infants with Rh or some minor blood group incompatibilities can present with symptomatic anemia that require RBC transfusion.
  • Hydrops fetalis — Infants present with skin edema, pleural/pericardial effusion, or ascites.
  • Infants with Rh(D) and some minor blood group incompatibilities, such as Kell (most immunogenic antigens after Rh and ABO blood group systems), are at risk for hydrops.
  • Neonates with hydrops may present at delivery with shock/ require emergent transfusion.
19
Q

prevention with rhogam (anti-D immunoglobulin)

A
  • Not given to women who are already D alloimmunized, or biologic father CONFIRMED to be Rh Negative, consider genetic counseling
  • AB screen at first prenatal visit
  • AB screen again at 28 wees, Prophylaxis at 28 weeks
  • After possible placental trauma, SAB, induced abortion, invasive prenatal diagnostics, ectopic, TAB, fetal demise, molar pregnancy
  • Within 72 hours post partum of delivery of D-positive newborn
20
Q

risk categories

A
  • Antigens that cause IgM antibodies
    • Cannot cross placental barrier, only IgG
    • Generally innocuous
      • A, P(1), Le (a), M, I, IH and Sd(a)
      • Lewis antibodies and some I and IH are prevalent
      • Some Lewis have IgG component but rarely cause clinical disease
21
Q

isoimmunization

A
  • Antigen poorly expressed fetal red blood cells
    • Some IgG antibodies capable of causing significant hemolytic transfusion reactions in adults are not clinically important in the fetus because their corresponding antigens are not well developed at birth: Lu(b), Yt(a), and VEL
  • gM antibodies to A and B develop early in life but do not cross placenta, however IgG ABO antibodies exist, particularly in group O mothers exposed to a non O fetus. Hemolysis is more a problem for neonate, not fetus. Most common in group B African-American fetuses
  • Isoimmunization Management
    • Serial amniocentesis to check fetal effects
    • Possibly deliver before term if fetus affected
    • In severe cases, fetal transfusion
    • Antenatal care and the prevention of maternal Rh sensitization have significantly reduced the number of infants born with severe manifestations of alloimmune HDN.
    • Postnatal management for affected infants is focused on treating the anemia and hyperbilirubinemia caused by hemolysis of neonatal RBCs.
22
Q

alloantibodies

A
  • High risk antigens
    • Responsible for the majority of HDN cases including anti-c, anti-D, anti-E and anti-Kell
    • Anti-Kell antibodies are responsible for approximately 10% of cases of severe antibody-mediated anemia in fetuses and newborns
    • Requires intrauterine or direct fetal transfusion during pregnancy or exchange transfusion postpartum