1. Authored by: Susan Bishop, RNC-OB, MN
Multiple Gestation
Authored by:
Susan Bishop, RNC-OB, MN
Perinatal Outreach Coordinator MultiCare Regional Perinatal Outreach Program

2. Incidence of Multiples
Currently 3% of all births (95% twins)
Naturally occurring twins 1 in 80 pregnancies
Naturally occurring triplets 1 in 8000 pregnancies
 incidence in African descent
 incidence in Asian descent
(7 – Mandy & Weisman)

3. Between 1980-2004 Incidence of Twins Increased by 70%
(8 – Simpson & Creehan)

4. HOM* increased by 500% *HOM=Higher Order Multiples
(8 – Simpson & Creehan)

5. Factors Associated with Multiple Gestation
Delayed childbearing: AMA
75% increase
Higher levels of Follicle Stimulating Hormone
Greater use of fertility services
ART (assisted reproductive technology)
OI (ovulation induction) 400% triplets/HOM
(1 – ACOG, 7 – Mandy & Weisman, 8 – Simpson & Creehan)

6. Physiology of Twinning
Monozygotic (MZ) – fertilization of a single ovum that subsequently divides into 2 or more zygotes (31% incidence)
Cell splits between day 4-day 12
Genetically the same: physical characteristics, sex, blood type hair & eye color
Dizygotic (DZ) – fertilization of multiple ova (67% incidence)
Two separate eggs/two separate sperm
No more alike than other siblings born to the same parents
(8 – Simpson & Creehan)

7. Monozygotic Twins (8 – Simpson & Creehan)
Egg division timing determines Placentation
< 4 days post-fertilization = Dichorionic Diamniotic
4-8 days post-fertilization=Monochorionic Diamniotic
8-13 days post-fertilization=Monochorionic Monoamniotic
>13 days post-fertilization=conjoined twins
(8 – Simpson & Creehan)

8. Dizygotic Twins
(8 – Simpson & Creehan)

9. Triplets
(8 – Simpson & Creehan)

10. Diagnosis of Multiple Gestation
1st trimester ultrasound
>5weeks chorionicity
>6weeks fetal number
>8weeks amnionicity
Highly accurate at weeks
Clinical Exam
Fundal height 2-4 cm > estimated GA
Leopolds/FHR
Subjective symptoms
Fatigue, hyperemesis, increased appetite/wt gain, FM, exaggerated pregnancy discomforts, “feel different”
(8 – Simpson & Creehan)

11. Maternal Changes GI Hematologic Cardiovascular Respiratory
Hyperemesis/N&V; reflux
Hematologic
Plasma volume  by %=dilutional anemia/iron deficiency anemia
Cardiovascular
HR/stroke volume;  risk pulmonary edema; supine aortocaval compression
Respiratory
>tidal volume and oxygen consumption; more alkalotic arterial pH; > dyspnea and SOB
Musculoskeletal
Symptoms earlier in pregnancy; back/ligament pain
Dermatologic
PUPPP (Pruritic urticarial papules and plaques of pregnancy) 3% twins/14% triplets
GI – 50% have N/V in 1st trimester; 20% persistant N/V throughout pregnancy
-double risk of hyperemesis with highest incidence of hyperemesis mix of male/female fetuses
M/S – use support garments, good body mechanics, supportive pillows, rest.
Derm
Dermatosis PUPPP r/t abd distention - redness anditching in abdominal striae and urticarial papules on lower abdomen. Fetal DNA has been detected in the dermis of affected women, which sugeests that fetal-maternal cell trafficking and immune phenomena play a role
(8 – Simpson & Creehan)

12. Maternal Complications
Preterm Labor – 50% twins, 76% triplets, 90% quads
Education important!
Serial U/S with assessment of cervical length
Fetal fibronectin testing
Tocolytics, corticosteriod therapy, bedrest
Hypertension
Preeclampsia develops earlier and is more severe
HELLP may present with atypical signs/symptoms
ART multiple pregnancies at higher risk
Compared to singletons – more likely to experience more frequent and sever complications: infants are smaller, born earlier, less likely to survive the 1st year of life and more likely to suffer lifelong disability.
Cervix shorter than 25mm at 24 weeks gestation best predictor of delivery before 32, 35 and 37 weeks of gestation and significantly more common in twin gestations.
Fetal Fibronectin – high-molecular-weight extracellular matrix glycoprotein that is normally found in fetal membranes, placental tissues and amniotic fluid. It’s presence in cervical-vaginal fluids at concentrations higher than 50 mg/mL is abnormal and has been shown to predict preterm delivery in single gestations. Data unclear on multiples.
(1 – ACOG, 6 – Jones, 7 – Mandy & Weisman, 8 – Simpson & Creehan)

13. Maternal Complications (continued)
PPROM – increased rate; shorter latency to birth time
Gestational Diabetes
Intrahepatic Cholestasis – 2-5 x greater
Abruptio Placenta
Pulmonary Embolism
Acute Fatty Liver
PPROM – usually presenting sac, but can be nonpresenting esp. after amnio.
Pulmonary Embolism – leading cause of maternal death in the US and around the world and thromboembolism is 6 rimes more likely during pregnancy or the puerperium than in the nonpregnant state. Factors most commonly associated with thromboembolism are multiple pregnancy, C/S delivery, delivery prior to 36 weeks gestation, BMI of 25 or >, and maternal age of 35 years or older; all more common in multiple gestation – BEDREST also increased risk.
Acute Fatty Liver – severe coagulopathy, hypoglycemia and hyperammonemia (pancreatitis DI pp)
Intrahepatic cholestasis of pregnancy is a cholestatic disorder characterized by pruritus, elevated serum aminotransferase and bile acid levels, and spontaneous relief of signs and symptoms within 2–3 weeks after delivery.1 The pruritus is often generalized but commonly starts on the palms of the hands and the soles of the feet before spreading in an ascending pattern. Jaundice typically develops 1–4 weeks after the onset of pruritus but occasionally can be the initial symptom. Serum aminotransferase activity is 2-fold to 10-fold higher than normal in 20–60% of patients with pruritus and may exceed 1,000 units/L in exceptional cases. The most specific and sensitive marker of intrahepatic cholestasis of pregnancy is serum bile acid above 10 micromoles/L.2 Intrahepatic cholestasis of pregnancy usually occurs during the third trimester of pregnancy but has been reported from 20 weeks of pregnancy. Adverse fetal outcomes of intrahepatic cholestasis of pregnancy include preterm delivery, meconium staining of amniotic fluid, fetal distress, and intrauterine fetal demise (0.4–4.1%), particularly when associated with fasting serum bile acid levels above 40 micromoles/L.3 The disorder is thought to be caused by a combination of hormonal, genetic, and environmental factors, although the exact etiology remains unknown
(1 – ACOG, 6 – Jones, 7 – Mandy & Weisman, 8 – Simpson & Creehan)

14. Fetal Risks/Complications
Mortality increased with plurality and late GA
Late GA – accelerated placental aging and earlier lung maturation in multiples
(Jones, 7 – Mandy & Weisman, 8 – Simpson & Creehan)

15. Fetal Risks/Complications (continued)
MZ twin mortality 3-10x than DZ twins
Intrauterine demise is usually cord entanglement
Greater incidence of congenital anomolies such as:
Neural tube defects
Urinary tract malformations
Discordant birth weight (20%)
Twin to Twin Transfusion Syndrome
(7 – Mandy & Weisman)

16. Discordant Growth
Weight of one multiple differs significantly from that of the other(s) by  25%
More common in Mono chorionic twins
Twin to Twin Transfusion Syndrome
Also effected by maternal age, parity, sex discordance and gestational age.
Discordance ranging from 15-40% has been considered predictive of an adverse outcome
TTTS – 10-15% MC twins Donor/recipient results in wide discordance in fetal growth and amniotic fluid volumes. DX by U/S Recipient larger fetus poly, large umbilical cord, abdominal circumference, kidneys and bladder leading to CV decompensation with cardiomegaly, tricuspid regurgititation and ventricular hypertrophy, hydrops, polycythemia/jaundus thrombosis after birth.
Donor twin small with oligo, severe growth restrion with anemia, hypovolemia and renal insufficiency, severe oligo “stuck twin”, pulmonary hypoplasia and deformations. Outcome poor if untreated mortality %. Neurodevelopmental issues.
(7 – Mandy & Weisman)

17. Twin-to-Twin Transfusion Syndrome
Almost exclusively occurs in monochorionic (1 placenta) diamniotic (2 amniotic sacs) pregnancies
Unequal balance of blood flow between the two fetuses due to placental vascular anastomoses within the placenta allowing one twin to transfuse the other
20% growth discordance, poly/oligo, discrepancy in cord size, cardiac dysfunction &/or abnormal cord Doppler studies
Staging: I-V
Amnioreduction (AR) Serial aspiration of large volumes of amniotic fluid (2-3 liters) from the recipient’s amniotic sac. Disadvantage: potential need for multiple procedures with increased risk for maternal/fe5tal injury and/or infection.
Amniotic Sep-TOS-tomy – intentional perforation of the intertwin membrane in an effort to allow amniotic flujid volumes to equalize between the donor and recipient twins. Advantages: offers relief of symptoms, only one procedure vs. serial amnioreductions. Disadvantage: creating hole too large crating a monoamniotic sac (increased risk of cord entanglement)
Fetoscopic Laser Photocoagulation – camera/laser coagulates the vascular anastomoses interrupting the vascular communication b/w the twins
Fetoscopoic Cord Coagulation – selectively occludes the umbilical cord of one twin by coagulating the vessels in that twin’s cord. Vessels b/w donor and 5the placenta are preserved. Recipient twin demises.
(5 – Jackson & Mele, 7 – Mandy & Weisman)

18. TTTS

19. TTTS Management Treatment options: Maternal dietary management
Amnioreduction
Septostomy
Photocoagulation
Umbilical cord occlusion
Maternal dietary management
Patient education, support
(5 – Jackson & Mele, 7 – Mandy & Weisman)

20. Reduction Amniocentesis Septostomy
Selective Vessel Laser Ablation
Umbilical Cord Occlusion/Ablation

21. Initial case series and cohort studies on amnioreduction, endoscopic laser, and microseptostomy as treatment for TTTS, regardless of Quintero staging, suggest that neonatal outcomes are improved with all 3 techniques, compared with the baseline morbidity and mortality risks seen in cohorts with no therapy. Neonatal survival is 37–60% with serial amnioreduction in most case series and has been reported as high as 82%.2,3,52,53 Furthermore, neurologic damage occurred in 17–33% of fetuses who were treated with amnioreduction. Series of endoscopic laser therapy for TTTS report neonatal survival in the range of 55–73%, with a rate of neurologic damage in the range of 4–18% in treated infants.45,54–56 Septostomy of the dividing membrane for TTTS treatment is reported to be associated with >80% neonatal survival rate.33 Neonatal neurologic morbidity is not reported in the early microseptostomy data. Thus, current evidence indicates that endoscopic laser coagulation, amnioreduction, and microseptostomy involve the least risk of death to the pregnant woman, relative to observation with no intervention, low or manageable risk for maternal morbidity and disability, and low or manageable risk to future pregnancies

22. Fetal Risks/Complications (continued)
Intrauterine Growth Restriction (IUGR)
Due to placental insufficiency and competition for nutrients
Fetal growth rates  at:
30-32 weeks (twins)
29 weeks (triplets)
(7 – Mandy & Weisman)

23. Fetal Loss
Spontaneous loss early in multiple pregnancy associated with bleeding
“Vanishing Twin”
Fetal death  20 weeks gestation
Surviving twin at  risk of fetal death, neonatal death and severe long-term morbidity.
Survival is inversely related to time death occurred and survivors of opposite-sex twin pairs more likely to survive than same-sex twin pairs.
Fetal death – 20% severe neurological defect (CP)
(7 – Mandy & Weisman)

24. ( Fuller & Fuller)

25. Fetal Surveillance Fetal Activity Assessment
Serial NSTs – BPP if nonreactive
Doppler velocimetry
Close assessment for possible complications
Doppler studies especially for growth discordancies.
(8 – Simpson & Creehan)

26. Laboring with Multiples
Must occur in facility capable of emergent C/S and neonatal resuscitation
Capability of monitoring all fetuses simultaneously and continuously
Qualified personnel in numbers required to care for all neonates
Ultrasound at bedside
VBAC possible
Qualified: Anesthesia, 2 OBs 2-3 l*d nurses, 1-2 neonatologists, a NICU team for each infant, 1 or 2 anesthsia staff.
(1 – ACOG, 6 – Jones, 7 – Mandy & Weisman, 8 – Simpson & Creehan)

27. Management of Multiple Birth
Route: Vaginal or C/S
Dependant on presentation and number!
Twin: VV/ VB/ BB
HOM=C/S
(2 – Chasen & Chervenak)

28. Management of Multiple Birth (continued)
Timing of delivery is controversial.
Lowest fetal death rates of twins weeks
Lowest fetal death rates for triplets weeks
FLM testing may be required
Dependant on pregnancy course and type of twin pairings
(6 – Jones, 7 – Mandy & Weisman, 8 – Simpson & Creehan)

29. Management of Multiple Birth
IV access, Type & Screen
Prepare for PP Hemorrhage BEFORE delivery!
Continuous monitoring of all
Bedside U/S on admission to determine/confirm fetal lie
Delivery in OR for all twins and HOMs
6-25% C/S for B after vaginal delivery of A
(1 – ACOG, 2 – Chasen & Chervenak, 8 – Simpson & Creehan)

30. Delivery of Multiples
Each must have own bed, own team, own identifier (bracelets)
Double check bands before, during and after delivery!
Prepare to differentiate cords and send placentas to pathology
Vag Del: After delivery of Twin A be prepared with U/S to confirm lie and stabilize Twin B.
Twin B at higher risk of perinatal mortality when delivered vaginally
When > 36 weeks gestation and most likely due to mechanical problems (compound presentation, cord prolapse, abruption)
Continue to monitor Twin B!
May need pitocin, C/S if problems develop
(2 – Chasen & Chervenak, 8 – Simpson & Creehan)

31. Delivery of Multiples (continued)
Nonreassuring FHR Twin B
VE – assess dilatation and check for presence of cord!
Bedside U/S
Prepare for forceps or vacuum assist
External version/internal rotation/extraction for transverse or footling breech
Interval >30 minutes associated with poorer outcomes
C/S via general anesthesia for deterioration
(2 – Chasen & Chervenak, 8 – Simpson & Creehan)

32. Postpartum Hemorrhage – count on it! Physical & Emotional Stress
Twin EBL avg 1000 mL
Twice as likely to need transfusion
Fundal checks!
Uterine Atony -> act quickly
Physical & Emotional Stress
Muscle Atrophy/Endurance
Breastfeeding
(8 – Simpson & Creehan)

33. Triplets and HOM
Increased Gestational Diabetes, pre-eclampsia, PTL, Pregnancy Associated HTN
Common discordant growth
Increased risk of velamentous insertion of cord
BPPs weekly from 30 weeks on
Increased risk of PP Hemorrhage (10-35%)
Velamentous insertion – vessels often run between the chorion and amnion without the protection of Wharton’s jelly. Vasa previa = the fetal vessels traverse the membranes in the lower uterine segment and cover the cervical os and occurs in approximately 1:5000 pregnancies.
(2 – Chasen & Chervenak 6 – Jones, 7 – Mandy & Weisman)

34. Resources & References
American College of Obstetricians & Gynecologists (2004) Multiple Gestation: Complicated Twin, Triplet, and High-Order Multifetal Pregnancy, ACOG Practice Bulletin Number 56.
Chasen, ST & Chervenak, FA (2009) Delivery of twin gestations, UpToDate online
Creasy, RK & Resnick, R (2004) Maternal-Fetal Medicine: Principles and Practice (5th ed.) Philadelphia: Saunders.
Gilbert, ES (2007) Manual of High Risk Pregnancy & Delivery (4th ed.) St. Louis: Mosby.
Jackson, KM & Mele, NL (2009) Nursing for Women’s Health, Twin-to-twin transfusion syndrome: what nurses need to know, 13 (3), p
Jones, D (2008) Triplet pregnancy: Mid and late pregnancy complications and management, UpToDate online
Mandy, GT & Weisman, LE (2009) Multiple Births, UpToDate online
Simpson, KR & Creehan, PA (2008). AWHONN Perinatal Nursing (3rd ed). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins.