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
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
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
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))
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
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
- Meconium aspiration syndrome
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
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)
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
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.)
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
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
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)
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.
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)
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