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Year 4 GOSH > Antenatal Problems 1 > Flashcards

Antenatal Problems 1 Flashcards

1
Q

What are some risk factors for hyperemesis gravidarum?

A
  • Multiple pregnancies
  • Molar pregnancies
  • First pregnancy
  • Hormone administration e.g. infertility treatment
  • Raised BMI

Due to higher levels of hCG

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2
Q

What are some signs/symptoms of hyperemesis gravidarum?

A

Usually 1st trimester

  • Nausea and vomiting
  • Weight loss
  • Excess salivation, ptyalism (inability to swallow saliva)
  • Reduced urine output
  • Epigastric pain
  • Haematemesis (mallory-weirs tears)
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3
Q

What are some maternal and foetal complications of hyperemesis gravidarum?

A

Maternal

  • 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

Foetal
- IUGR if mother loses 10%+ of body weight

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4
Q

What is the diagnostic triad of hyperemesis gravidarum?

A
  1. More than 5% pre-pregnancy weight loss
  2. Dehydration
  3. Electrolyte imbalances
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5
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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6
Q

DDx of hyperemesis gravidarum? When would you be more suspecting of alternative diagnosis?

A

Particularly consider if the symptoms start after week 10

  • Gastroenteritis
  • Cholecystitis
  • Hepatitis
  • Pancreatitis
  • Peptic ulcer
  • Pyelonephritis
  • Metabolic cause eg diabetic ketoacidosis
  • Neurological cause eg migraine
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7
Q

What is the treatment hyperemesis gravidarum?

A

Admit if not tolerating oral fluids

IV fluids - 0.9% NaCl + KCl as guided by electrolyte monitoring (daily U&Es)

Antiemetics

  • 1st line: cyclizine 50mg TDS
  • 2nd line: metoclopramide 10mg TDS

If vomiting unresponsive to fluids and antiemetic, consider a trial of corticosteroids:
- Prednisolone 40-50mg PO daily in divided doses
OR
- Hydrocortisone 100mg/12hr IV

IV thiamine if prolonged

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8
Q

Define:

  • SGA

- Severe SGA

A

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

Severe SGA = birth weight less than 3rd centile

Can either be constitutionally small (not pathological) or IUGR (placenta or non-placenta mediated)

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9
Q

What can cause placental insufficiency?

A
  • Low pregnancy-weight
  • Nutritional status
  • Substance abuse
  • Altitude (lower oxygen = smaller baby)
  • Pre-existing disease
  • Pregnancy-related disease eg Diabtes/hypertension
  • Infections
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10
Q

What are the main antenatal complications of SGA?

A

Antenatal

  • Stillbirth
  • Preterm labour
  • Low birth weight linked with sudden infant death syndrome
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11
Q

How may SGA present? What would indicate need for referral for USS?

A

Serial measurements of symphysis fundal height may be reduced or slow down

Refer for USS if:

  • Single SFH measurement < 10th centile
  • SFH is 2cm less than gestation
  • Static growth
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12
Q

What investigation is used to assess growth velocity? What indicates constitutionally small vs IUGR?

A

USS

Estimated foetal weight is plotted
If baby remains in same growth centile as it grows, suggests it is constitutionally small
If baby drops down centiles indicates IUGR

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13
Q

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

A

8-10 weeks = crown-rump length

16-20 weeks = biparietal diameter

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14
Q

What is the primary surveillance tool for SGA foetus? What is the management using this?

A

UAD (uterine artery doppler)

  • If normal UAD, growth scans and UAD should be carried out every 2-3 weeks - if UAD remains normal, aim for IOL at 37 weeks
  • If high resistance on UAD, review growth scans and UAD weekly - aim to prevent in utero damage associated with placental dysfunction whilst maximising the gestation to avoid prematurity complications
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15
Q

Define:

  • LGA

- Macrosomia

A

LGA = above 90th centile in weight for gestation

Macrosomia = excessive intrauterine growth beyond a specific threshold regardless of gestational age (birth weight > 4000 or 4500g)

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16
Q

What are some causes of LGA?

A
  • Gestational DM (most common)
  • Gestational trophoblastic disease
  • Constitutional
  • Obesity
  • Fetal abnormality
  • Intrauterine infection
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17
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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18
Q

What is polyhydramnios?

A

Increased liquor (increased amniotic fluid)

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19
Q

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

A
  • Normal maternal blood glucose
  • Normal placenta
  • Normal liquor volume
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20
Q

What are some potential complications of LGA?

A
  • Dystocia (obstructed labour) especially shoulder dystocia - brachial plexus injury
  • Birth trauma - perineal tearing, blood loss, damage to coccyx
  • Hypoglycaemia of baby after delivery
  • Left colon syndrome = self-limiting condition where temporary bowel obstruction occurs (mimicks Hirshsprung’s disease)
  • Hyperbilirubinaemia
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21
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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22
Q

What is the management of LGA?

A
  • Position adjustment during birth to reduce need for episiotomy
  • Induction of labour if gestational diabetes
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23
Q

What is prolonged pregnancy?

A

Pregnancy that exceeds >42wks gestation (294 days)

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24
Q

What happens beyond 41 weeks gestation?

A
  • Increased potential for placental insufficiency - higher risk of foetal acidaemia and meconium aspiration in labour
  • Neonatal hypoglycaemia - reduced oxygen and nutrient transfer due to placental degradation can deplete foetal glycogen stores
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25
Q

How common is prolonged pregnancy?

A

Common (3-10%)

Recognised cause of increased morbidity and mortality

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26
Q

What are some risk factors for prolonged pregnancy?

A
  • Nulliparity
  • Maternal age > 40
  • Previous prolonged pregnancy
  • High BMI
  • Family history of prolonged pregnancies
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27
Q

What is the main risk of prolonged pregnancy?

A

The rate of stillbirth rises exponentially after 37/40 gestation

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28
Q

What interventions may be done in prolonged pregnancy?

A
  • Membrane sweeps - offered from 40+0 in nulliparous women and 41+0 in parous women
  • Induction of labour - offered between 41+0 and 42+0 weeks - IOL in nulliparous women may fail to establish labour and lead to c section
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29
Q

What investigations should be done in prolonged labour?

A

Confirm EDD (most accurate is 1st trimester USS between 11+0 and 13+6 weeks)

Assess RF which may be an indicator to induce close to EDD:

  • Pre-eclampsia
  • DM
  • Antepartum haemorrhage
  • IUGR associated with placental insufficiency

USS assessment of growth and amniotic fluid volume

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30
Q

What is a cephalhematoma? What are the 2 main causes?

A

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)

Causes:

  • Assisted delivery - forceps, Ventouse
  • Prolonged labour

Goes away weeks-months

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31
Q

Which clotting disorder is most common in young women?

What does it make young women at risk of?

A

Antiphospholipid syndrome = combination of arterial and venous thrombosis and bleeding

Makes young women at high risk of foetal loss

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32
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

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33
Q

What is asymmetrical IUGR? What is often the cause?

A

Foetal hypoxia and hypoglycaemia leads to shunting of blood flow to vital foetal organs (brain, heart, adrenal glands) and bypassing other organs (liver, muscle, fat tissue)

= ‘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

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34
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
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35
Q

How does pre-eclampsia lead to IUGR?

A

Pre-eclampsia occurs due to poor placental perfusion, secondary to abnormal placentation
Due to impaired trophoblast invasion in the first stage of pregnancy, the remodelling of the spiral arteries is incomplete so they are constricted meaning there is a high resistance to blood flow into the placenta
The mother’s BP increases to ensure the foetus is sufficiently supplied, which leads to leaky blood vessels and microthrombosis
The consequence of vasoconstriction and microthrombosis is chronic hypoperfusion of the placenta, leading to placental insufficiency which ultimately results in IUGR

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36
Q

List some foetal 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
37
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
38
Q

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

A

If delivery occurs between 24 and 35+6 weeks, antenatal corticosteroids should be given for foetal lung maturity then labour induced 48 hours later
Continuous foetal heart rate monitoring is required from onset of contractions

39
Q

What is placenta accreta?

A

Serious pregnancy condition in which the placenta grows too deeply into uterine wall (attachment of the placenta to the myometrium, due to a defective decidua basalis)
Usually the placenta detaches from uterine wall after childbirth, however in placenta accrete part/all of it remains attached, which can cause post-partum haemorrhage

40
Q

What is placenta praevia? What are the different types?

A

= Low-lying placenta

Low-lying placenta (type 1) - lower edge of the placenta lies less than 2cm from internal cervical os

Marginal praevia (type 2) - placenta reaches the internal cervical os

Partial praevia (type 3) - placenta partially covers the internal os

Complete praevia (type 4) - placenta completely covers the internal os

41
Q

What is the main risk factor for placenta praevia? List some other risk factors too

A

Previous Caesarean section - main risk factor; risk increases with number of previous CS

Others:

  • High maternal age
  • High parity
  • Smoking
  • Cocaine use during pregnancy
  • Previous spontaneous or induced abortion
  • History of endometritis
42
Q

How does placenta praevia usually present?

A

May be an incidental finding on routine anomaly scan

Sudden, painless, bright red vaginal bleeding starting after 28wk (3rd trimester) that stops spontaneously after 1-2 hours

!!! Do not do a VE - would cause haemorrhage !!!

43
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
44
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 USS improve accuracy of placental localisation
45
Q

How is placenta praevia managed if it presents pre-term depending on whether the placental position is known or not?

A

Bleeding with unknown placental position:

  • ABCDE, resuscitate, stabilise
  • Perform urgent USS if stable
  • If bleeding not controlled, immediate C-section

Bleeding with known placenta praevia:

  • ABCDE, resuscitate, stabilise
  • Corticosteroids if between 24-34 weeks
  • If bleeding not controlled, immediate C-section
46
Q

Which placenta praevia are more likely to resolve spontaneously and why?

A

Partial, marginal, and low-lying may resolve
After 28 weeks, migration can occur due to the development of the lower uterine segment

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

47
Q

What is vasa praevia?

A

Fetal vessels lie over the internal os

48
Q

Anatomy of fetal membranes

A 
Innermost = amnion
Outermost = chorion

Together form the amniotic sack

49
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 2 different sperm and simultaneously implanting and developing

These foetuses have separate amniotic membranes and plants = diamniotic dichorionic

50
Q

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

A

Dizygotic twins

51
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

52
Q

Which type of monozygotic twin is the most common?

A

Monochorionic diamniotic = two thirds

Twins share a placenta but have individual amniotic sacs

53
Q

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

A

<3 days = morula

Dichorionic, diamniotic (DCDA - separate placenta and amnion)

= 30%

54
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%

55
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%

56
Q

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

A

> 12 days = formed embryonic disc

Monochorionic, monoamniotic
Conjoined twins

= very rare (<0.1%

57
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%
58
Q

What is clomiphene?

A

Ovulatory stimulant
It inhibits hypothalamic oestrogen receptors, which blocks the normal negative feedback effect of oestrogen, so there is increased secretion of GnRH from hypothalamus and increased FSH and LH from anterior pituitary which stimulate ovulation

59
Q

What are some fetal risks associated with multiple pregnancy?

A
  • Preterm labour
  • IUGR in 25%
  • Miscarriage - especially with monochorionic twins
  • Congenital abnormalities with monochorionic twins e.g. NTD, cardiac abnormalities, GI atresia
  • Twin-to-twin transfusion syndrome - monochorionic twins
  • Vanishing twin syndrome = one twin apparently reabsorbed at an early gestation (1st trimester)
60
Q

What are some maternal risks associated with multiple pregnancy (vs singleton) - antenatal and birth complications?

A

Antenatal

  • Hyperemesis gravidarum
  • Anaemia = greater increase in blood volume causing a dilution effect, and more iron and folic acid are needed
  • Pre-eclampsia = 5x greater risk with twins
  • Gestational diabetes
  • Polyhydramnios

Birth complications

  • Prolonged first stage of labour
  • Premature placental abruption after birth of first foetus
  • Prolapsed cord
61
Q

What occurs in twin-to-twin transfusion syndrome (TTTS)?

A

In monochorionic twins they share the placenta so blood is flowing in one direction from one twin to the other - this means blood is being transferred from donor twin to recipient twin

Recipient twin suffers fluid overload
Donor twin suffers high output cardiac failure
Both twins are at risk of developing heart failure and hydrops fetalis

62
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

63
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

64
Q

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

A
  • Hypovolaemic
  • Anaemic
  • Oligohydramnios = appear ‘stuck’ to placenta or uterine wall
  • Growth restriction
65
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
66
Q

What is fetal hydrops?

A

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

67
Q

Which twin is more at risk in TTTS?

A

The ‘recipient’ twin

68
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

69
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
70
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

71
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
72
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

73
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

74
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
  • High dose folic acid - 5mg
  • Iron supplementation
  • 75mg aspirin OD for high risk women
  • Extra growth scans to detect discordant growth
  • OGTT at 28 weeks
75
Q

What are the different methods and gestations by/at which multiple pregnancies are delivered?

A

MCDA - delivery at 36-37 weeks
MCMA - elective CS at 32 weeks

Dichorionic - delivery at 38 weeks

For labour: first twin must be cephalic and must be no CI e.g. two previous CS

Triplets / higher order multiples usually delivered by CS

76
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

77
Q

When is gestation most accurately determined by USS?

A

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

78
Q

What on USS can determine whether the IUGR is due to placental insufficiency or not? Explain why

A

Ratio of head circumference and abdominal circumference shows if foetus is symmetrical/asymmetrically small - asymmetrically small foetus is more likely to be caused by placental insufficiency

Foetal hypoxia and hypoglycaemia leads to shunting of blood flow to vital foetal organs (brain, heart, adrenal glands) and bypassing other organs (liver, muscle, fat tissue)

Placental insufficiency can result in impaired foetal kidney function, resulting in reduced amniotic fluid volume

79
Q

What preventative interventions can be taken to reduce risk of complications from SGA?

A
  • Optimise maternal disease
  • Promote smoking/alcohol cessation
  • Start women at high risk of pre-eclampsia on 75mg aspirin
80
Q

What foetal measurements are used to assess growth on USS?

A
  • BPD: biparietal diameter
  • HC: head circumference - more commonly used than BPD
  • AC: abdominal circumference
  • FL: femur length
81
Q

What factors make up the Biophysical Profile (BPP) that indicates foetal hypoxia?

A

Foetal breathing movements
Foetal movements
Foetal tone
Amniotic fluid volume

82
Q

What 2 indices does UAD produce? What does it mean if they are high?

A 
Pulsatility index (PI)
Resistance index (RI)

If they’re high it suggests there is resistance to flow in the placenta and that the placenta is not working/growing properly

83
Q

On UAD, what would indicate need for delivery of baby?

A

Absent or reversed end-diastolic flow because it shows that there is either no blood flow or the blood flow is backwards in diastole

These essentially indicated reduced placental function

84
Q

If IOL is declined in prolonged pregnancy (between 41+0 and 42+0), what is the management plan?

A

Offer twice weekly CTG monitoring and USS with amniotic fluid measurement to identify any foetal distress
If foetal distress noted, conduct emergency c-section

85
Q

What is the main difference in presentation between placenta praevia and placental abruption?

A 
Praevia = painless
Abruption = painful
86
Q

If placenta praevia is diagnosed incidentally and the woman is not in labour, what is the management plan?

A
  • Monitor with USS
  • Give advice about pelvic rest i.e. no penetrative sex
  • Advise to go to hospital if significant vaginal bleeding
87
Q

What is the management of placenta praevia if presenting at full term depending on location of placenta?

A

Placenta > 20mm from internal os

  • Trial of labour and vaginal delivery
  • If any significant haemorrhage or foetal distress, emergency CS

Placenta overlapping internal os

  • Elective C-section at 37-38 weeks
  • Urgent C-section if woman goes into labour
88
Q

What is the classic triad of vasa praevia?

A
  1. Rupture of membranes
  2. Painless vaginal bleeding
  3. Foetal bradycardia
89
Q

What is the main risk factor for vasa praevia?

A

IVF

Year 4 GOSH (16 decks)

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