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Extra 5 (e) > Antenatal Problems 1 > Flashcards

Antenatal Problems 1 Flashcards

1
Q

What is hyperemesis gravidarum?

A

Excessive vomiting in pregnancy causing severe dehydration, weight loss or electrolyte disturbance / ketosis

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2
Q

What are some risk factors for hyperemesis gravidarum?

A
  • Multiple pregnancies
  • Molar pregnancies

Due to higher levels of hCG

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3
Q

What are some signs/symptoms of hyperemesis gravidarum?

A

Usually 1st trimester

  • Vomiting
  • Weight loss
  • Muscle wasting
  • Dehydration
  • Ptyalism (inability to swallow saliva)
  • Hypovolaemia
  • Electrolyte imbalance
  • Behaviour disorders
  • Haematemesis (mallory-weirs tears)
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4
Q

What are some maternal complications of hyperemesis gravidarum?

A
  • Liver and renal failure
  • Hyponatraemia and rapid reversal of hyponatraemia leading to central pontine myelinosis
  • Thiamie deficiency can lead to Wernicke’s encephalopathy
  • Can be fatal if untreated
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5
Q

What are some fetal complications of hyperemesis gravidarum?

A
  • IUGR

- Fetal death in cases of Wernicke’s encephalopathy

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6
Q

What investigations are done in hyperemesis gravidarum?

A
  • Urinalysis = detect ketones
  • MSU to exclude UTI
  • FBC = raised haemaocrit
  • U&Es to exclude hypokalaemia or hyponatraemia
  • LFTs = transaminases may be abnormal and albumin may be low
  • US to diagnose multiple pregnancies or a molar pregnancy
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7
Q

How common is hyperemesis gravidarum?

A

Rare (0.1-1%)

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8
Q

Ddx of hyperemesis gravidarum?

A
  • GI cause eg gastroenteritis / ileus
  • Metabolic cause eg diabetic keoacidosis
  • Neurological cause eg migraine
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9
Q

What is the treatment hyperemesis gravidarum?

A
  • Admit if not tolerating oral fluids
  • IV fluids (NaCl or Hartmanns but avoid dextrose containing fluids as can precipitate Wernickes encephalopathy)
  • Daily U&Es (replace K+ if needed)
  • NBM for 24hrs then introduce light diet as tolerated
  • Antiemetics if IV fluids and electrolyte treatment not helping:
 = metoclopramide 10mg/8hr PO/IM/IV
OR
= cyclizine 50mg/8hr PO/IM/IV
OR
= Prochloperzaine 12.5mg IM/IV TDS or 5mg PO TDS
  • Thiamine (either thiamine hydrochloride 25-50mg PO TDS or thiamine 100mg IV infusion weekly)
  • If vomitng unresponsive to fluids and antiemetic, consider a trial of corticosteroids:

= prednisolone 40-50mg PO daily in divided doses
OR
= hydrocortisone 100mg/12hr IV

  • May need psychological support
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10
Q

What is SGA?

A

Small for gestational age = an infant born with a birth weight less than 10th percentile

Severe SGA = less than 3rd centile

Can either be constitutionally small or IUGR

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11
Q

What are some intrinsic factors affecting fetal growth?

A

Maternal factors:

  • Maternal height and weight
  • Parity (nulliparity smaller)
  • Ethnic group (asian smaller vs Caucasian or Afro-carribean)

Fetal factors:

  • Sex (F smaller)
  • Multiple pregnancy
  • Genes/inherited conditions
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12
Q

What are some extrinsic factors affecting fetal growth?

A

Maternal:

  • Social class
  • Nutritional status
  • Altitude (lower oxygen = smaller baby)
  • Pre-existing disease
  • Pregnancy-related disease eg DM/HTN
Fetal
- Nutrition = most common problem is antiphospholipid syndrome
- Teratogens 
- Infective
= viral: rubella, CMV, Hep A, B
= protozoan: toxoplasmosa
Others = listeria, syphilis
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13
Q

What are the risks of SGA?

A

Inc risk:

  • Cerebral palsy
  • Preterm delivery (iatrogenic and spontaneous)
  • Maternal risk greater as pre-eclampsia may exist and CS is more often used
  • May be reduced fetal movements
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14
Q

How may SGA present?

A
  • Serial measurements of symphysis fundal height may be reduced or slow down
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15
Q

What investigations should be done for SGA?

A
  • USS makes diagnosis = gestation most accurately determined by USS before 20wk as assumption all foetuses are similar size until that point.

Natural variation in size after this point makes accurate dating difficult and estimate required from menstrual dates

  • BP and urinalysis for pre-eclampsia
  • To determine which SGA are IUGR = serial USS and umbilical artery doppler
  • Infection or chromosomal abnormalities are investigated using fetal blood sampling or amniocentesis
  • CTG only abnormal when severe compromise of fetal distress is present
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16
Q

What are the most reliable measurements between:
8-10 weeks
16-20 weeks

A

8-10 weeks = crown-rump length

16-20 weeks = biparietal diameter

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17
Q

How should SGA be managed?

A
  • Fortnightly growth checks
  • The small but consistently growing fetus with normal umbilical artery doppler values does not need intervention

If fetal compromise at term:
- SGA with abnormal doppler values should be delivered beyond 36wk by induction / CS

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18
Q

What is LGA?

A

Large for gestational age = macrocosmic

Excessive intrauterine growth beyond a specific threshold regardless of gestiantional age. Usually >4000 - 4500g (above 95th percentile)

(approx 1.7% babies)

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19
Q

What are some causes of LGA?

A
  • Gestational DM (most common)
  • Gestational trophoblastic disease
  • Fetal abnormality
  • Intrauterine infection
  • Constitutional
  • Excessive maternal weight gain during pregnancy can increase fetal weight
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20
Q

How does gestational DM increase fetal weight?

A

Mother’s increased blood glucose circulates to the baby which in response produces insulin = fetal pancreatic cell hyperplasia leads to hyperinsulinaemia and fat deposition

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21
Q

What is polyhydramnios?

A

Increased liquor (increased amniotic fluid)

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22
Q

What must normal in order for an LGA to be considered constitutional?

A
  • Normal maternal blood glucose
  • Normal placenta
  • Normal liquor volume
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23
Q

What are some risks of LGA?

A
  • Infants at greater risk of perinatal morbidity and long term metabolic complications
  • Dystocia (obstructed labour) esp shoulder dystocia
  • Birth trauma (perineal tearing, blood loss or damage to coccyx
  • Glucose regulation problems:
    1) hypoglycaemia of baby after delivery
    2) Inc incidence of birth defects
    3) Resp distress
  • Left colon syndrome = self-limiting condition where temporary bowel obstruction occurs
  • Hyperbilirubinaemia
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24
Q

What can shoulder distocia cause?

A

May result in the collar bone being broken or damage to brachial plexus

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25
Q

What investigations should be done for LGA?

A
  • Glucose tolerance test (check for gestational DM)
  • If polyhydraminos is found in the absence of gestational DM, fetal infection may be cause so check IgM and IgG to toxoplasma, rubella, CMV and herpes
  • USS
  • CTG
  • Umbilical artery doppler not useful unless pre-eclampsia or IUGR develop
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26
Q

What is the management of LGA?

A
  • Position adjustment during birth to reduce need for episiotomy
  • Induction may be required esp if gestational DM
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27
Q

What is prolonged pregnancy?

A

Pregnancy that exceeds >42wks gestation (294 days)

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28
Q

What happens beyond 41 weeks?

A

Placental function may decline, reducing supply of oxygen and nutrients to fetus

Increased risk of meconium aspiration and neonatal hypoglycaemia

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29
Q

How common is prolonged pregnancy?

A

Common (3-10%)

Recognised cause of increased morbidity and mortality

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30
Q

What are some risk factors for prolonged pregnancy?

A
  • One previous prolonged pregnancy = 30% risk of another

- History of two = 40% risk of another

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31
Q

When are EDD unreliable?

A
  • Uncertainty of LMP
  • Irregular periods
  • Recent use of COCP
  • Contraception during lactational amenorrhoea
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32
Q

What are some risks of prolonged pregnancy?

A
  • Increased risk of intrapartum and early neonatal death
  • Meconium aspiration and assisted ventilation
  • Oligohydraminos
  • Macrosomia, shoulder dystocia and fetal injury
  • Cephalhaematoma
  • Fetal distress in labour
  • Neonatal hypothermia, hypoglycaemia, polycythaemia and growth restriction
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33
Q

What interventions may be done in prolonged pregnancy?

A
  • Induction of labour

- Operative delivery

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34
Q

What investigations should be done in prolonged labour?

A

Confirm EDD (most accurate is 1st trimester USS)
Assess RF which may be an indicator to induce close to EDD:
- Pre-eclampsia
- DM
- Antepartum haemorrhage
- IUGR associated with placental insufficiency

Fetal monitoring:

  • USS assessment of growth and amniotic fluid volume
  • CTG after 42wk
  • Report reduced fetal movements
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35
Q

How should prolonged pregnancy be managed?

A

Offer ‘stretch and sweep’ at 41wks

  • During internal examination, sweep a finger around the cervix
  • This should separate membranes of amniotic sac from the cervix which will stimulate prostaglandin release which may kick-start labour

Offer IOL between 41-42wks:
- Reduce perinatal mortality and risk of CS

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36
Q

What is a cephalhematoma?

A

One of the most common cranial injuries that an infant may suffer esp during a forceps-assisted delivery or vacuum extraction. Can result from prolonged labour

= Swelling of an infants scalp as a result of haemorrhaging or collection of blood between infant’s skull, most commonly parietal or occipital bone and periosteum (a tough thin tissue that surrounds the bone)

Goes away weeks-months

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37
Q
  • MOVE THIS CARD *

What is antiphospholipid syndrome?

A

AI disorder characterised by arterial and venous thrombosis, adverse pregnancy outcomes (both for mother and fetus) and raisied levels of antiphospholipid (aPL) antibodies

Mechanism known - possibly aPL lead to complement activation / activation of vascular endothelium

38
Q

What is symmetrical IUGR?What is often the cause?

A

Fetus whose entire body is proportionally small and tensds to be seen with very early onset IUGR

Often due to chromosomal abnormalities

39
Q

What is asymmetrical IUGR? What is often the cause?

A

Seen with an undernourished fetus who is compensating by directing most of its energy to maintaining the growth of vital organs such as the brain and heart at the expense of the liver, fat and muscle

= ‘head-sparing effect’ leads to normal head size with small abdo circumference and thin limbs

Often due to placental insufficiency. If it occurs for too long, the fetus loses its ability to sufficiently compensate and head growth too becomes affected

40
Q

List some maternal causes for IUGR (6)

A
  • Chronic maternal disease eg HTN, CVD, CKD
  • Substance abuse eg alcohol, drugs, smoking
  • AI disease eg antiphospholipid syndome
  • Genetic disorders eg phenylketonuria
  • Poor nutrition
  • Low socio-economic status
41
Q

List some placental causes for IUGR (5)

A
  • Abnormal trophoblast invasion eg pre-eclampsia or placenta accrete
  • Infarction
  • Placenta praevia
  • Tumours eg chorioangiomas
  • Abnormal umbilical cord or cord insertion eg two vessel cord
42
Q

How does pre-eclampsia lead to IUGR?

A

Conversion of maternal spiral arteries into competent vessels essential for development of normal placenta. This requires invasion of trophoblasts into sub-endometrial area and spiral arteries.

In preeclampsia = shallow trophoblast invasion and unconverted narrow spiral arteries leading to fetal hypoxia that causes endothelial injury that ultimately leads to maternal HTN, oedema and proteinuria

43
Q

NEED TO MOVE ALL THESE CARDS UP

List some fetal causes of IUGR (4)

A
  • Genetic abnormalities eg Trisomy 13, 18 or 21, Turner’s syndrome, Triploidy
  • Congenital abnormalities eg cardiac (tetralogy of Fallot), gastrochisis
  • Congenital infection eg CMV, rubella, toxoplasmosis
  • Multiple pregnancies
44
Q

What are some risks of IUGR?

A
  • Preinatal mortality 6-10x greater
  • Cerebal palsy 4x greater
  • 30% stillborns are IUGR

Increased risk of:

  • Intrapartum fetal distress and asphyxia
  • Meconium aspiration
  • Emergency CS
  • Necrotising enterocolitis
  • Impaired neurodevelopment
  • Hypoglycaemia and hypocalcaemia
45
Q

What investigations are done for IUGR?

A

US criteria (ideally wk 8-13):

  • Elevated FL:AC
  • Elevated HC:AC
  • Unexplained oligohydramous
  • BP and urinalysis (check for pre-eclampsia)
  • To determine SGA vs IUGR = serial US and umbilical artery doppler used (if increased flow to MCA = head sparing effect)
  • Amniocentesis or fetal blood sampling to test for infection or chromosomal abnormalities
  • Test for syphilis or malaria in high risk pop
  • CTG used but only abnormal when severe fetal distress present
46
Q

What is the management of IUGR between 24+0 and 35+6?

A

Women with an SGA/IUGR between 24+0 - 35+6 where delivery is being considered should receive a course of antenatal corticosteroids = stimulates surfactant production in fetal lungs

47
Q

What is the management of IUGR when there is fetal compromise at preterm?

A

Aim to prevent in utero demise / neurological damage associated with ongoing placental dysfunction whilst maximising gestation to avoid complications of prematurity’
= thus intervention varies with gestation

Generally:

  • Review IUGR with abnormal dopplers twice a week, if absent end diastolic flow = mothers admitted for steroids (if pre-34 wks) and daily CTG
  • At severely preterm, delivery delayed until 34 wks or until CTG is abnormal
  • Severe IUGR = deliver by CS
48
Q

What is placenta accrete?

A

Serious pregnancy condition in which the placenta grows too deeply into uterine wall. Usually the placenta detaches from uterine wall after childbirth, however in placenta accrete part/all of it remains attached = can cause severe blood loss after delivery

49
Q

What is placenta praevia?

A

= Low-lying placenta

Placenta is inserted wholly or in part to lower segment of the uterus

  • Major = placenta covers internal os of cervix
  • Minor / partial = if the leading edge is in the lower segment but not covering the os

Placenta praevia and placental abruption = most important causes of antepartum haemorrhage (more than half the cases)

50
Q

What are some RF for placenta praevia? (9)

A
  • Hx placenta praevia
  • Previous CS
  • Inc age
  • Inc parity
  • Smoking
  • Cocaine use during pregnancy
  • Previous spontaneous or induced abortion
  • Deficient endometrium eg hx of endometritis
  • Assisted conception
51
Q

How may placenta praevia present?

A

May be an incidental finding on routine anomaly scan

  • Painless bleeding starting after 28wk (but spotting may occur earlier)
  • Usually sudden and profuse but of short duration (rarely life threatening)
52
Q

What are some risks of placenta praevia?

A
  • 14x more likely to bleed in antenatal period
  • Inc risk preterm labour
  • More likely to have abnormal lie eg oblique / transverse
53
Q

How is placenta praevia diagnosed?

A
  • Clinical suspicion should be high in any woman with vaginal bleeding after 20wk gestation, high presenting part, abnormal lie and painless bleeding provoked by sexual intercourse
  • US provides definitive diagnosis
  • Transvaginal scans improve accuracy of placental localisation
54
Q

How is placenta praevia managed? (Minor and major)

A

Minor:

  • May be able to deliver vaginally
  • Placental edge less than 2cm from os indicates need for CS (esp if posterior or thick)
  • If head engaged at time of planned CS, TVS can be used

Major:

  • Need CS
  • No penetrative intercourse
  • Tocolytics should not be used
  • If experienced a bleed, should stay in hospital from 34wks
  • If no bleed can remain at home but advised to attend hospital immediately if experiencing any bleed, contractions or pain
56
Q

What is vasa praevia?

A

Fetal vessels lie over the internal os

57
Q

How common are multiple pregnancies?

A

1 in 34 babies are a twin or triplet

58
Q

Anatomy of fetal membranes

A 
Innermost = amnion
Outermost = chorion

Together form the amniotic sack

59
Q

What % of twins are dizygotic? What is the mechanism?

A

= 75% twins

  • Non-identical
  • Twins can be of different sex

Result of two separate ova being fertilised by different sperm and simultaneously implanting and developing

These foetuses have separate amniotic membranes and plants = diamniotic dichorionic

60
Q

Which type of twin is most affected by predisposing factors such as age and ethnicity?

A

Dizygotic twins

61
Q

What % of twins are monozygotic? What is the mechanism?

A

= 25% twins

  • Genetically identical
  • Always same sex

Result of an already developing single embryo dividing into two

Whether they share the same amniotic membrane and/or chorion depends on the stage of development when the embryo divides

62
Q

Which type of monozygotic twin is the most common?

A

Monochorionic diamniotic = two thirds

63
Q

If monozygotic twins divide <3 days what is the result?

A

<3 days = morula

dichorionic, diamniotic (DCDA - separate placenta and amnion)

= 30%

64
Q

If monozygotic twins divide 4-7 days what is the result?

A

4-7 days = blastocyst

monochorionic, diamniotic (MCDA - shared placenta but separate amnions)

= 70%

65
Q

If monozygotic twins divide 8-12 days what is the result?

A

8-12 days = implanted blastocyst

monochorionic, monoamniotic (MCMA - shared placenta but single amniotic sac)

= <1%

66
Q

If monozygotic twins divide >12 days what is the result?

A

> 12 days = formed embryonic disc

conjoined twins

= very rare

67
Q

What factors increase the likelihood of a multiple pregnancy? (6)

A
  • Prev multiple pregnancy
  • FH
  • Inc number of births
  • Inc maternal age
  • Ethnicity (eg inc in Nigerians, dec in Japanese)
  • Assisted reproduction:
    1) Clomiphene - 10%
    2) Intrauterine insemination (IUI) = 10-20%
    3) IVF with two embryo transfer = 20-30%
68
Q

What is clomiphene?

A

Ovulatory stimulant

69
Q

How can twins present? (4)

A
  • Uterus is larger than expected for dates
  • Hyperemesis gravidarum
  • 3/more fetal poles may be palpable >24wk
  • Two fetal hearts may heard on auscultation
70
Q

What are some fetal risks associated with multiple pregnancy?

A
  • Preterm labour = main cause of perinatal morbidity and mortality:

40% twins deliver before 37wks
10% twins deliver before 32wks

  • Inc risk of miscarriage = esp with monochorionic twins
  • Inc risk of congenital abnormalities with monochorionic twins eg NTD, cardiac abnormalities, GI atresia
  • IUGR in 25%
  • Also inc risk still birth, disability (mainly due to low birthweight/prematurity), cerebal palsy
  • Vanishing twin syndrome = one twin apparently reabsorbed at an early gestation (1st trimester)
71
Q

What are some maternal risks associated with multiple pregnancy (vs singleton)?

A
  • Hyperemesis gravidarum
  • Anaemia = greater inc in blood volume causing a dilution effect, and more iron and folic acid are needed
  • Pre-eclampsia = 5x greater risk with twins
  • Gestational DM
  • HTN
  • Polyhydramnios
  • APH and PPM
  • Operative delivery
  • Financial / psychological impacts = incidence of post natal depression higher
72
Q

What is twin to twin transfusion syndrome (TTTS)?

A

Caused by abnormal vascular anastomoses within the placenta which redistribute the fetal blood = blood from ‘donor’ twin is transfused to the ‘recipient’ twin

73
Q

How common is TTTS? Is it dangerous?

A

Affects 5-25% monochorionic twins and left untreated has 80% mortality and 10% handicap risk in surviving twin

74
Q

What course can TTTS take during pregnancy?

A

Can occur acutely at any stage but more commonly takes a chronic course, which can lead to severe fetal compromise at a gestation too early to consider delivery

75
Q

What are the effects of TTTS on the ‘donor’ twin?

A
  • Hypovolaemic
  • Anaemic
  • Oligohydramnios = appear ‘stuck’ to placenta or uterine wall
  • Growth restriction
76
Q

What are the effects of TTTS on the ‘recipient’ twin?

A
  • Hypervolaemic
  • Polycythaemic
  • Polyhydramnios
  • Large bladder
  • Evidence of fetal hydrops = ascites, pleural and pericardial effusion
77
Q

What is fetal hydrops?

A

Abnormal accumulation of fluid in two or more fetal compartments including ascites, pleural effusion, skin oedema

78
Q

Which twin is more at risk in TTTS?

A

The ‘recipient’ twin

79
Q

How should TTTS be managed?

A

Monochorionic twins require more intensive monitoring to look for signs of TTTS:
- Fortnightly serial USS from 12 wks at specialist fetal medicine unit

80
Q

What are the treatment options for TTTS?

A
  • Laser ablation of placental anastomoses = associated with lower risk of neonatal handicap
  • Selective foeticide by cord occlusion = reserved for refractory disease
  • Serial amnioreductions = symptomatic relief only
  • Septostomy = allows equilibrium between the two amniotic sacs
81
Q

What are the effects of a dichorionic intrauterine death of a twin during each trimester?

A

The death of one twin in the 1st trimester / early part of the 2nd does not appear to adversely affect the remaining fetus

Loss in the late part of the 2nd / 3rd usually precipitates labour = 90% having delivered in 3 weeks

82
Q

What are the effects of a monochorionic intrauterine death of a twin during each trimester?

A

Subsequent death / severe damage from hypovolaemia follows in 25% where on of the pair dies - due to shared circulation

Little evidence that immediate delivery decreases risk of brain injury

83
Q

What is the maternal risk of an intrauterine death of a twin?

A

Increased risk of DIC as thromboplastin are released into the circulation

84
Q

What are the intrapartum (labour) risks of multiple pregnancy?

A
  • Malpresentation
  • Fetal hypoxia in 2nd twin after delivery of the 1st
  • Cord prolapse
  • Operative delivery
  • PPH

Rarely:

  • Cord entanglement = MCMA twins only
  • Head entrapment with each other = ‘locked twins’
85
Q

What investigations are done for multiple pregnancies?

A
  • USS = vast majority diagnosed at USS in 1st trimester (at dating scan or nuchal translucent scan)
  • Chorionicity = allows risk stratification. Done best by USS in 1st trimester / early 2nd
86
Q

What are the key indicators for chorionicity?

A

Dichorionic:

  • Obviously widely separated sacks or placentae
  • Membranes insertion showing the lambda sign
  • Foetuses of different sex (dizygotic)

Absence of lambda sign <14wks = monochorionic

87
Q

How can chorionicity be determined postnatally?

A
  • Macropscopic and microscopic examination of membranes
  • Analysis of RBC markers
  • DNA probes
88
Q

What follow-up scans should be offered in multiple pregnancy?

A 
18wks = growth discrepancy +/- fetal abnormality screening (if pt wishes)
24wks = growth (average weight for twins is 10% lighter than singletons)

+ Every 2-4wks thereafter depending on chorionicity to determine growth measurements, more freq if significant size discordance

89
Q

What is the antenatal care management for multiple pregnancy?

A

All multiple pregnancies are high risk = consultant lead

  • Establish chorionicity = most accurately in 1st trimester
  • Early USS for any indication of multiple pregnancy
  • Iron and folate supplements
  • Detailed anomaly scan
  • Serial growth scans: 28, 32, 36 for dichorionic
  • More freq antenatal checks (inc risk of pre-eclampsia)
  • Discuss mode of delivery
  • Establish presentation of leading twin by 34wks
  • Consider induction at 38wks
  • More intensive monitoring required for monochorionic twins, esp <24wks or higher multiples = refer to specialist fetal medicine team
90
Q

What is the labour management of multiple pregnancies?

A

Mode of delivery:

  • Second twin is at increased risk of perinatal mortality but not currently the case that all twins should be delivered by CS
  • For labour: first twin must be cephalic and must be no CI eg two previous CS
  • Triplets / higher order multiples usually delivered by CS
  • Some advise CS for monochorionic twins
91
Q

Describe the process of labour and delivery of multiple pregnancy

A
  • Twins are usually induced at 38 wks (many deliver spontaneously before this)
  • IV access and G&S for mother
  • Continuous CTG monitoring (fetal distress more common)

NB CTG imperative after delivery of 1st twin to avoid hypoxia in 2nd

  • FSE useful to monitor leading twin and the other abdominally
  • Leading twin should be delivered the same as singleton (2nd constantly monitored throughout)
  • After 1st baby delivered, the lie of the second twin should be checked and gently ‘stabilised’ by gentle palpation of abdo which VE performed to assess the station of the presenting part

NB once the presenting part enters the pelvis and the membranes can be broken, the second twin is usually delivered within 20 mins of the first

  • USS should be available at all times during delivery
  • Oxytocin may be helpful if contractions diminish after delivery of 1st twin
  • If fetal distress in 1st twin = forceps or ventouse, if inappropriate = CS or breech extraction (after internal podalic version)
  • If inc risk of uterine atony = syntometrine and prophylactic oxytocin infusion recommended
92
Q

What is the management of fetal abnormality in multiple pregnancy?

A

Where one twin has an abnormality - selective termination should be discussed

  • In DC twins = can be by intracardiac injection of KCL (potassium chloride)
  • In MC twins = cord must be occluded as circulation is shared and death/damage to remaining twin may follow

Both (esp cord occlusion) risk miscarriage

NB termination of pregnancy can be performed up to 34wks so that delivery ensues and remaining twin will survive

93
Q

Which placenta praevia are more likely to resolve spontaneously?

A

Partial, marginal, and low-lying may resolve (placental migration)

It is less likely to occur if the placenta is posterior or if there has been a previous CS

Extra 5 (e) (12 decks)

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